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Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has a cohort study or clinical trial

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have any cohorts or clinical trial

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has a control, double-blind, or comparison patient group

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have any comparison patient group

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has human subjects

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have human subjects

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study contains population size or sample size information

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not contain population size information

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have any quantitative outcomes

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has a target drug

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have a target drug

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study has a target disease

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

This study does not have a target disease

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has a cohort study or clinical trial

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have any cohorts or clinical trial

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has a control, double-blind, or comparison patient group

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have any comparison patient group

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has human subjects

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have human subjects

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study contains population size or sample size information

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not contain population size information

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have any quantitative outcomes

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has a target drug

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have a target drug

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study has a target disease

A comparative trial of lisinopril and nifedipine in mild to moderate hypertension in general practice.

to compare lisinopril and nifedipine in the management of essential hypertension in 52 patients in general practice with respect to the obtaining of target diastolic blood pressure and freedom from side effects. an open label, parallel randomised trial over an eight week period. lisinopril and nifedipine were found to effectively lower diastolic blood pressure with the latter having a significantly higher level of withdrawals and clinical side effects. lisinopril is equivalent to nifedipine in its hypertensive effect and has a better side effect profile.

This study does not have a target disease

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has a cohort study or clinical trial

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have any cohorts or clinical trial

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has a control, double-blind, or comparison patient group

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have any comparison patient group

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has human subjects

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have human subjects

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study contains population size or sample size information

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not contain population size information

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have any quantitative outcomes

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has a target drug

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have a target drug

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study has a target disease

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

This study does not have a target disease

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has a cohort study or clinical trial

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have any cohorts or clinical trial

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has a control, double-blind, or comparison patient group

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have any comparison patient group

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has human subjects

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have human subjects

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study contains population size or sample size information

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not contain population size information

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have any quantitative outcomes

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has a target drug

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have a target drug

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study has a target disease

Intentional early delivery versus expectant management for preterm premature rupture of membranes at 28-32 weeks' gestation: A multicentre randomized controlled trial (MICADO STUDY).

Preterm premature rupture of fetal membranes (PPROM) exposes the fetus to preterm birth, and optimal timing for delivery is controversial. The aim of this study was to compare intentional early delivery ("active management") with expectant management in very preterm birth (28-32 weeks). We conducted a prospective randomized controlled trial with intent-to-treat analysis, at 19 tertiary-care hospitals in France and 1 in Geneva, Switzerland. Inclusion criteria were women age ≥18 years, PPROM at 28^0/7 to 31^6/7 weeks' gestation, singleton pregnancy. Exclusion criteria were maternal/fetal indications for immediate delivery. All participants received prophylactic antibiotics (amoxicillin + gentamicin) and two doses of corticosteroids. Women in expectant management delivered at 34 weeks, sooner if medically indicated. Women in active management delivered 24 h after the second steroid dose. The primary outcome measure was a composite of neonatal death/severe adverse events: periventricular leukomalacia, intraventricular hemorrhage, sepsis, oxygen requirement at 36 weeks, and necrotizing enterocolitis. The secondary outcome was clinical chorioamnionitis. The trial was stopped prematurely, due to recruitment difficulties. Of 360 women assessed, 139 (40% of calculated sample size) were randomized: 70 to expectant management, 69 to active management. Mean gestational age at PPROM was similar in both groups (30 ± 1.3 vs. 30.2 ± 1.2 weeks, respectively). There were 35 cases of medical/suspected complications requiring delivery in expectant management vs. 4 in active management. Mean latency between PPROM and delivery was 11.7 ± 9.8 vs. 2.8 ± 0.6 days, respectively; P < 0.0001 (median 8.4 (1.8-44.2) vs. 2.7 (1.9-4.3)). There were more caesarean deliveries in active than expectant management (80% vs. 60%, respectively; P < 0.01). There were 2 chorioamnionitis cases, both in expectant management. One baby died in expectant management; 2 in active management (one with heart defect). There was no significant difference in sepsis rates. The combined neonatal death/severe adverse events measure was 12.9% for expectant management and 13.0% for active management (OR 0.98; 95% CI: 0.33-2.93, P = 0.97). For PPROM at 28-32 weeks, and with antenatal antibiotic and steroid therapy, there were no observed differences in neonatal health when comparing expectant management to early delivery. As expected, expectant management resulted in higher gestational age and birth weight. However, our study was underpowered to draw firm and reliable conclusions.

This study does not have a target disease

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has a cohort study or clinical trial

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have any cohorts or clinical trial

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has a control, double-blind, or comparison patient group

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have any comparison patient group

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has human subjects

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have human subjects

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study contains population size or sample size information

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not contain population size information

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have any quantitative outcomes

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has a target drug

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have a target drug

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study has a target disease

Rapid corticosteroid taper versus standard of care for immune checkpoint inhibitor induced nephritis: a single-center retrospective cohort study.

Current guidelines for treatment of immune checkpoint inhibitor (ICI)-induced nephritis are not evidence based and may lead to excess corticosteroid exposure. We aimed to compare a rapid corticosteroid taper to standard of care. Retrospective cohort study in patients with ICI-induced nephritis comparing a rapid taper beginning with 60 mg/day prednisone and tapered to 10 mg within 3 weeks to a historical control group that began 60 mg/day tapered to 10 mg within 6 weeks (standard of care). Renal recovery was defined as creatinine returning to within 1.5-fold baseline. The log-rank test compared the differences in time to renal recovery between the groups. We report rates of renal recovery at 30, 60 and 90 days, and timing and outcomes of ICI rechallenge. Thirteen patients received rapid corticosteroid taper and 14 patients received standard of care. Baseline characteristics were similar between groups. The median time to ≤10 mg/day prednisone was 20 days (IQR 15-25) in the rapid-taper group compared with 38 days (IQR 30-58) in the standard-of-care group. There was no significant difference in the time to renal recovery between the groups, though numerically higher numbers of patients recovered by 30 days, 11 (85%) in the rapid-taper arm versus 6 (46%) in the standard of care arm. Exposure to other nephritis-causing medications (proton pump inhibitor or trimethoprim-sulfamethoxazole) during the corticosteroid taper was more common in the standard of care group, 9 (64%) versus rapid-taper group, 2 (15%), and was associated with longer time to renal recovery, 20 days (IQR 14-101) versus 13 days (IQR 7-34) in those that discontinued nephritis-causing medications. Fifteen (56%) of patients were rechallenged with ICIs, and only two (13%) developed recurrent nephritis. Patients with ICI-induced nephritis have excellent kidney outcomes when treated with corticosteroids that are tapered over 3 weeks.

This study does not have a target disease

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has a cohort study or clinical trial

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have any cohorts or clinical trial

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has a control, double-blind, or comparison patient group

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have any comparison patient group

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has human subjects

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have human subjects

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study contains population size or sample size information

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not contain population size information

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have any quantitative outcomes

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has a target drug

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have a target drug

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study has a target disease

Prophylaxis in gynaecological surgery: a prospective randomized comparison between single dose prophylaxis with amoxycillin/clavulanate and the combination of cefuroxime and metronidazole.

A prospective randomized comparison of a single pre-operative dose of 2.2 g amoxycillin/clavulanate versus the combination of 1.5 g cefuroxime plus 0.5 g metronidazole was conducted in 467 women, who underwent gynaecological surgery. The incidence of febrile morbidity, urinary tract infection, wound infection and the use of post-operative antimicrobial agents was similar in the two groups. Amoxycillin/clavulanate is as effective as a combination of cefuroxime and metronidazole and less expensive.

This study does not have a target disease

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has a cohort study or clinical trial

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have any cohorts or clinical trial

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has a control, double-blind, or comparison patient group

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have any comparison patient group

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has human subjects

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have human subjects

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study contains population size or sample size information

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not contain population size information

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have any quantitative outcomes

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has a target drug

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have a target drug

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study has a target disease

A placebo-controlled clinical trial of regular monotherapy with short-acting and long-acting beta(2)-agonists in allergic asthmatic patients.

Some recent studies suggest that regular beta(2)-agonist use may result in inadequate control of asthma. It has been hypothesized that this occurs particularly in allergic asthmatic patients exposed to relevant allergens. Moreover, it is still unclear whether this occurs during the use of both short-acting and long-acting beta(2)-agonists. Asthmatic patients (n = 145) allergic to house dust mite (HDM) were randomly allocated to monotherapy with a short-acting beta(2)-agonist (SA; n = 48), a long-acting beta(2)-agonist (LA; n = 50), or placebo (n = 47), double blind, double dummy. The study covered three periods: (1) a 4-week run-in period, in which no changes took place; followed by (2) cessation of treatment with asthma medication including inhaled corticosteroids, introduction of allergen avoidance measures (active/placebo treatment) to lower HDM exposure in the active group, and an 8-week washout period to adjust patients to these changes; followed by (3) a 12-week study medication period. At the start of the 12-week medication period, and every 4 weeks thereafter, spirometric measurements (FEV(1) and provocative concentration of histamine causing a 20% fall in FEV(1) [PC(20)]) were performed. Peak flow and asthma symptoms were recorded daily. Additionally, at the start and every 6 weeks thereafter, dust samples were collected from mattresses and living room and bedroom floors to assess HDM (der p 1) concentrations. Effects on FEV(1), PC(20), peak flow, and asthma symptoms were analyzed with repeated-measurement analysis and corrected for the exposure to HDM allergens. There were no significant differences among the three medication groups after 12 weeks for FEV(1). However, a significant decrease in mean FEV(1) percent predicted (95% confidence interval [CI]) was observed within the SA group: - 6.6 (- 10.4 to - 2.8) (p = 0.0002). A decrease in geometric mean PC(20) (95% CI) of - 1.2 (- 1.96 to - 0.44) doubling concentration was observed within the SA group (p = 0.05). No significant changes in FEV(1) and PC(20) were observed > 12 weeks within the LA group or the placebo group. There were neither changes in peak flow and asthma symptom scores among the three medication groups nor within the groups. Moreover, none of the parameters showed interactive effects with allergen exposure. There were no significant differences among the three medication groups for FEV(1) and PC(20). The within-treatment group comparison showed a significant small decline in FEV(1) for the SA group (but not for the LA group), which could indicate that monotherapy with SAs might have negative effects on FEV(1). This was not seen during regular use of LAS: No clear pathophysiologic mechanism can explain these findings at the moment. Relatively high or low exposure to allergens did not alter these findings.

This study does not have a target disease

Efficacy of the Natural Clay, Calcium Aluminosilicate Anti-Diarrheal, in Reducing Medullary Thyroid Cancer-Related Diarrhea and Its Effects on Quality of Life: A Pilot Study.

Medullary thyroid cancer (MTC)-related diarrhea can be debilitating, reduces quality of life (QOL), and may be the only indication for initiating systemic therapy. Conventional antidiarrheal drugs are not always helpful and may have side effects. Calcium aluminosilicate antidiarrheal (CASAD), a natural calcium montmorrilonite clay, safely adsorbs toxins and inflammatory proteins associated with diarrhea. It was hypothesized that CASAD would reduce the severity of diarrhea and improve QOL in MTC patients. This was a prospective pilot trial (NCT01739634) of MTC patients not on systemic therapy with self-reported diarrhea of three or more bowel movements (BMs) per day for a week or more. The study design included a one-week run-in period followed by one week of CASAD ± a two-week optional continuation period. The primary endpoint was efficacy of one week of CASAD treatment in decreasing the number of BMs per day by ≥20% when compared with the baseline run-in period. Secondary objectives included tolerability and safety and the impact on QOL using the MD Anderson Symptom Inventory-Thyroid questionnaire (MDASI-THY). Ten MTC patients (median age = 52 years, 70% female, 80% white) were enrolled. All had distant metastases, and median calcitonin was 5088 ng/mL (range 1817-42,007 ng/mL). Ninety percent had received prior antidiarrheals, and 40% of these had used two or more drugs, including tincture of opium (30%), loperamide (50%), diphenoxylate/atropine (20%), colestipol (10%), or cholestyramine (10%). Of seven evaluable patients, four (56%) had ≥20% reduction in BMs per day. Six out of seven patients discontinued their prior antidiarrheals. Best response ranged from 7% to 99% reduction in mean BMs/day from baseline. Five out of seven patients considered CASAD a success, and they opted for the two-week continuation period. Improvements in diarrhea and all six interference items assessed by MDASI-THY were noted at weeks 1 and 3. Total interference score was significantly improved at three weeks compared with baseline (p = 0.05). An oral levothyroxine absorption test was performed in one patient; malabsorption of levothyroxine was not observed. Adverse events included flatulence (40%), bloating (10%), heartburn (10%), and constipation (10%). CASAD is a promising strategy for treatment of MTC-related diarrhea. In this small pilot study, improvements in frequency and quality of diarrhea as well as QOL were noted. Further studies in this population are warranted.

This study has a cohort study or clinical trial

Efficacy of the Natural Clay, Calcium Aluminosilicate Anti-Diarrheal, in Reducing Medullary Thyroid Cancer-Related Diarrhea and Its Effects on Quality of Life: A Pilot Study.

Medullary thyroid cancer (MTC)-related diarrhea can be debilitating, reduces quality of life (QOL), and may be the only indication for initiating systemic therapy. Conventional antidiarrheal drugs are not always helpful and may have side effects. Calcium aluminosilicate antidiarrheal (CASAD), a natural calcium montmorrilonite clay, safely adsorbs toxins and inflammatory proteins associated with diarrhea. It was hypothesized that CASAD would reduce the severity of diarrhea and improve QOL in MTC patients. This was a prospective pilot trial (NCT01739634) of MTC patients not on systemic therapy with self-reported diarrhea of three or more bowel movements (BMs) per day for a week or more. The study design included a one-week run-in period followed by one week of CASAD ± a two-week optional continuation period. The primary endpoint was efficacy of one week of CASAD treatment in decreasing the number of BMs per day by ≥20% when compared with the baseline run-in period. Secondary objectives included tolerability and safety and the impact on QOL using the MD Anderson Symptom Inventory-Thyroid questionnaire (MDASI-THY). Ten MTC patients (median age = 52 years, 70% female, 80% white) were enrolled. All had distant metastases, and median calcitonin was 5088 ng/mL (range 1817-42,007 ng/mL). Ninety percent had received prior antidiarrheals, and 40% of these had used two or more drugs, including tincture of opium (30%), loperamide (50%), diphenoxylate/atropine (20%), colestipol (10%), or cholestyramine (10%). Of seven evaluable patients, four (56%) had ≥20% reduction in BMs per day. Six out of seven patients discontinued their prior antidiarrheals. Best response ranged from 7% to 99% reduction in mean BMs/day from baseline. Five out of seven patients considered CASAD a success, and they opted for the two-week continuation period. Improvements in diarrhea and all six interference items assessed by MDASI-THY were noted at weeks 1 and 3. Total interference score was significantly improved at three weeks compared with baseline (p = 0.05). An oral levothyroxine absorption test was performed in one patient; malabsorption of levothyroxine was not observed. Adverse events included flatulence (40%), bloating (10%), heartburn (10%), and constipation (10%). CASAD is a promising strategy for treatment of MTC-related diarrhea. In this small pilot study, improvements in frequency and quality of diarrhea as well as QOL were noted. Further studies in this population are warranted.

This study does not have any cohorts or clinical trial