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Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study contains population size or sample size information

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study does not contain population size information

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

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

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study does not have any quantitative outcomes

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study has a target drug

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study does not have a target drug

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study has a target disease

Inspiratory muscle training during treatment with corticosteroids in humans.

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

This study does not have a target disease

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study has a cohort study or clinical trial

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have any cohorts or clinical trial

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

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

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have any comparison patient group

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study has human subjects

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have human subjects

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study contains population size or sample size information

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not contain population size information

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

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

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have any quantitative outcomes

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study has a target drug

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have a target drug

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study has a target disease

Failure of remission induction by glucocorticoids alone or in combination with immunosuppressive agents in IgG4-related disease: a prospective study of 215 patients.

The aim of this study was to assess the outcomes of remission induction in patients with IgG4-related disease (IgG4-RD) in our cohort, and to investigate the characteristics, prognosis, and risk factors in the patients failed of remission induction. We prospectively enrolled 215 newly diagnosed patients with IgG4-RD, who were initially treated with glucocorticoid (GC) alone or in combination with immunosuppressive agents (IM), and had at least 6 months of follow up. The therapeutic goals of remission induction were defined as fulfilling each of the following after the 6-month remission induction stage: (1) ≥ 50% decline in the IgG4-RD responder index (RI); (2) GC tapered to maintenance dose; and (3) no relapse during GC tapering. The patients not achieving the therapeutic goals were considered to have failed of remission induction. There were 26 patients in our cohort who failed of remission induction, including 16 (20.8%) on GC monotherapy, and 10 (7.2%) on combination therapy comprising GC and IM. The lacrimal gland and lung were most common sites of remission induction failure. Among the patients who relapsed during remission induction stage, 52.9% had secondary relapse during follow-up. Eosinophilia, higher baseline RI, more than five organs involved and dacryoadenitis were risk factors for remission induction failure with GC monotherapy, and the incidence of remission induction failure was 71.4% in the patients with more than three risk factors. After 6-month treatment, the patients who failed of remission induction had significantly higher erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and IgG4. In our cohort, 20.8% of patients failed of remission induction with GC monotherapy, while 7.2% of patients failed of remission induction with combination therapy comprising GC and IM.

This study does not have a target disease

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study has a cohort study or clinical trial

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have any cohorts or clinical trial

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

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

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have any comparison patient group

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study has human subjects

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have human subjects

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study contains population size or sample size information

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not contain population size information

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

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

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have any quantitative outcomes

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study has a target drug

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have a target drug

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study has a target disease

[Exercise performance after long-term administration of enalapril or metoprolol. A randomized double-blind study of hypertensive leisure-time sportsmen].

A randomized double-blind trial was conducted in 36 leisure-time sportsmen (mean age 40.1 +/- 5.4 years) with mild or moderate essential hypertension (WHO groups I or II) to find out whether an 8-week antihypertensive treatment with daily 10-20 mg enalapril or 100-200 mg metoprolol changed their exercise performance. This was measured by bicycle spiroergometry together with determination of lactate levels, before and at the end of the treatment period. Maximal oxygen uptake rose by 1.86 ml/kg.min during enalapril administration and by 1.06 ml/kg.min at the individual anaerobic threshold. But under metoprolol these parameters fell by 6.57 ml/kg.min and 4.61 ml/kg.min, respectively. After treatment with these two drugs 3 and 15 patients, respectively, had the sensation of greater exercise performance at identical exercise levels. The differences in exercise between the two drugs using the stated three primary criteria were statistically significant. The Watt-time product decreased in only one of the patients of the enalapril group, but in 17 of the metoprolol group. Only metoprolol significantly reduced exercise heart rate. Both drugs caused a similar fall in systolic blood pressure during exercise.

This study does not have a target disease

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study has a cohort study or clinical trial

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have any cohorts or clinical trial

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

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

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have any comparison patient group

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study has human subjects

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have human subjects

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study contains population size or sample size information

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not contain population size information

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

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

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have any quantitative outcomes

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study has a target drug

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have a target drug

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study has a target disease

Angiotensin II receptor antagonists role in arterial hypertension.

Angiotensin II receptor blockers represent a class of effective and well tolerated orally active antihypertensive drugs. Activation of AT(1) receptors leads to vasoconstriction, stimulation of the release of catecholamines and antidiuretic hormone and promote growth of vascular and cardiac muscle. AT(1) receptor blockers antagonise all those effects. Losartan was the first drug of this class marketed, shortly followed by valsartan, irbesartan, telmisartan, candesartan, eprosartan and others on current investigation. All these drugs have the common properties of blockading the AT(1) receptor thereby relaxing vascular smooth muscle, increase salt excretion, decrease cellular hypertrophy and induce antihypertensive effect without modifying heart rate or cardiac output. Most of the AT(1) receptor blockers in use controlled blood pressure during the 24 h with a once-daily dose, without evidence of producing tolerance to the antihypertensive effect and being with low incidence of side effects even at long term use. Monotherapy in mild-to-moderate hypertension controls blood pressure in 40 to 50% of these patients; when a low dose of thiazide diuretic is added, 60-70% of patients are controlled. The efficacy is similar to angiotensin-converting enzyme (ACE) inhibitors, diuretics, calcium antagonists and beta-blocking agents. AT(1) receptor blockers are specially indicated in patients with hypertension who are being treated with ACE inhibitors and developed side effects such as, cough or angioedema. The final position in the antihypertensive therapy in this special population and other clinical situations, such as left ventricular hypertrophy, heart failure, diabetes mellitus and renal disease, has to be determined in large prospective clinical trials, some of which are now being conducted and seem promising.

This study does not have a target disease

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study has a cohort study or clinical trial

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have any cohorts or clinical trial

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

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

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have any comparison patient group

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study has human subjects

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have human subjects

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study contains population size or sample size information

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not contain population size information

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

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

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have any quantitative outcomes

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study has a target drug

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have a target drug

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study has a target disease

Dopamine transporter polymorphisms are associated with short-term response to smoking cessation treatment.

To examine the association between polymorphisms in the dopamine transporter gene (SLC6A3, DAT1) and treatment outcome in smokers attempting to quit using either nicotine replacement therapy or bupropion. The sample consisted of 583 smokers recruited from a smoking cessation clinic, and followed throughout the 4 weeks of post-cessation treatment with behavioural support and either nicotine replacement therapy or bupropion. At 1 week after smoking cessation, the 3' untranslated region (3'UTR) variable number of tandem repeats (VNTRs) and the 30-bp intron 8 VNTR DAT1 genotypes were associated with the ability to stop smoking (3'UTR VNTR, odds ratio=2.0, 95% confidence interval=1.2-3.5, novel intron 8 VNTR, odds ratio=1.8, 95% confidence interval=1.0-2.9), controlling for potential confounders. The results were weaker and no longer significant at a 4-week follow-up. We find evidence, although modest, of a medium-sized effect of DAT1 genotype on the ability to stop smoking early in a smoking cessation attempt. If the effect is real, and is strongest in the very early stages of smoking cessation, this suggests that the primary utility of DAT1 screening in this field will be in the identification of those most at risk of early relapse after quitting.

This study does not have a target disease

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study has a cohort study or clinical trial

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have any cohorts or clinical trial

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

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

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have any comparison patient group

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study has human subjects

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have human subjects

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study contains population size or sample size information

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not contain population size information

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

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

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have any quantitative outcomes

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study has a target drug

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have a target drug

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study has a target disease

Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder.

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge. Changes in [(11)C]raclopride binding potential (BP(ND)) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kg(-1)) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D2/3 receptor BP(ND) and change in BP(ND) following amphetamine as a measure of dopamine release. Voxel-based analysis revealed significantly decreased baseline [(11)C]raclopride BP(ND) in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP(ND) following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP(ND) changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP(ND). This study provides evidence for decreased striatal D2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.

This study does not have a target disease

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study has a cohort study or clinical trial

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have any cohorts or clinical trial

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

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

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have any comparison patient group

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study has human subjects

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have human subjects

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study contains population size or sample size information

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not contain population size information

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

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

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have any quantitative outcomes

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study has a target drug

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have a target drug

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study has a target disease

Potential role of statins in the treatment of heart failure.

Based on the findings of retrospective studies, there has been growing interest in the potential therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with heart failure. The first published prospective randomized study of statins in heart failure patients did not demonstrate improved clinical outcomes (death and nonfatal myocardial infarction or stroke) after treatment with 10 mg daily of rosuvastatin when compared with placebo. However, use of rosuvastatin was associated with a reduced risk of hospitalization when compared with placebo and was well tolerated. Until further information becomes available, routine use of statins is not recommended in the heart failure population.

This study does not have a target disease

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study has a cohort study or clinical trial

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study does not have any cohorts or clinical trial

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

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

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study does not have any comparison patient group

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study has human subjects

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study does not have human subjects

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study contains population size or sample size information

Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial.

In controlled clinical trials there are usually several prognostic factors known or thought to influence the patient's ability to respond to treatment. Therefore, the method of sequential treatment assignment needs to be designed so that treatment balance is simultaneously achieved across all such patients factor. Traditional methods of restricted randomization such as "permuted blocks within strata" prove inadequate once the number of strata, or combinations of factor levels, approaches the sample size. A new general procedure for treatment assignment is described which concentrates on minimizing imbalance in the distributions of treatment numbers within the levels of each individual prognostic factor. The improved treatment balance obtained by this approach is explored using simulation for a simple model of a clinical trial. Further discussion centers on the selection, predictability and practicability of such a procedure.

This study does not contain population size information