B1tta/Drug-ACE huggingface dataset:
[Title]: Intrapatient comparison of treatment with chlorthalidone, spironolactone and propranolol in normoreninemic essential hypertension.
[Abstract]: The effects of chlorthalidone, spironolactone and propranolol in reducing blood pressure were compared in the same 11 normoreninemic hypertensive patients. All three drugs decreased the blood pressure significantly and no agent had a superior blood pressure-lowering effect. The blood pressure did not normalize. The data suggest that no one variable--volume factors, relative hyperactivity of the renin-aldosterone system or beta-adrenergic hyperactivity--is the prime mover in normoreninemic hypertension. Long-term treatment with chlorthalidone resulted in slight hyperreninism (26.3 +/- 4.9 ng-ml-1-3 hours-1) (mean +/- standard error) with concomitant changes in plasma aldosterone (23.0 +/- 3.2 ng-100 ml-1). The body weight decreased significantly (--1.8 kg, P less than 0.005). Plasma potassium concentrations were low (3.2 +/- 0.1 mEq-liter -1). Creatinine clearance was unimpaired (117 +/- 6 ml-min-1). Treatment with spironolactone resulted in more marked hyperreninism (47.0 +/- 14.3 ng-ml-1-3 hours-1) and hyperaldosteronism (61.9 +/-11.8 ng-100 ml-1). The body weight decreased significantly (--1.9 kg, P less than 0.004). Significant hyperkalemia occurred (4.4 +/- 0.1 mEq-liter-1). The glomerular filtration rate decreased significantly to 93 +/- 3 ml-min-1 (P less than 0.004). Treatment with propranolol resulted in marked suppression of the plasma renin activity (1.8 +/- 0.2 ng-ml-1-3 hours-1) and plasma aldosterone levels (8.9 +/- 1.3 ng-100 ml-1). A significant increase in body weight occurred (+2.3 kg, P less than 0.013). The plasma potassium concentration increased to a level not significantly different from the value found after treatment with spironolactone (4.2 +/- 0.1 mEq-liter-1). The creatinine clearance decreased significantly to 99 +/- 5 ml-min-1 (P less than 0.008). Hyperreninemia (by spironolactone and chlorthalidone), effective hyperaldosteronism (by chlorthalidone) and volume retention (by propranolol) are considered to represent expressions of mechanisms counteracting the depressor effects of these different pharmacologic maneuvers, leading to the maintenance of supranormal blood pressure.
[Drug-Disease]: chlorthalidone - normoreninemic hypertension
[Title]: Intrapatient comparison of treatment with chlorthalidone, spironolactone and propranolol in normoreninemic essential hypertension.
[Abstract]: The effects of chlorthalidone, spironolactone and propranolol in reducing blood pressure were compared in the same 11 normoreninemic hypertensive patients. All three drugs decreased the blood pressure significantly and no agent had a superior blood pressure-lowering effect. The blood pressure did not normalize. The data suggest that no one variable--volume factors, relative hyperactivity of the renin-aldosterone system or beta-adrenergic hyperactivity--is the prime mover in normoreninemic hypertension. Long-term treatment with chlorthalidone resulted in slight hyperreninism (26.3 +/- 4.9 ng-ml-1-3 hours-1) (mean +/- standard error) with concomitant changes in plasma aldosterone (23.0 +/- 3.2 ng-100 ml-1). The body weight decreased significantly (--1.8 kg, P less than 0.005). Plasma potassium concentrations were low (3.2 +/- 0.1 mEq-liter -1). Creatinine clearance was unimpaired (117 +/- 6 ml-min-1). Treatment with spironolactone resulted in more marked hyperreninism (47.0 +/- 14.3 ng-ml-1-3 hours-1) and hyperaldosteronism (61.9 +/-11.8 ng-100 ml-1). The body weight decreased significantly (--1.9 kg, P less than 0.004). Significant hyperkalemia occurred (4.4 +/- 0.1 mEq-liter-1). The glomerular filtration rate decreased significantly to 93 +/- 3 ml-min-1 (P less than 0.004). Treatment with propranolol resulted in marked suppression of the plasma renin activity (1.8 +/- 0.2 ng-ml-1-3 hours-1) and plasma aldosterone levels (8.9 +/- 1.3 ng-100 ml-1). A significant increase in body weight occurred (+2.3 kg, P less than 0.013). The plasma potassium concentration increased to a level not significantly different from the value found after treatment with spironolactone (4.2 +/- 0.1 mEq-liter-1). The creatinine clearance decreased significantly to 99 +/- 5 ml-min-1 (P less than 0.008). Hyperreninemia (by spironolactone and chlorthalidone), effective hyperaldosteronism (by chlorthalidone) and volume retention (by propranolol) are considered to represent expressions of mechanisms counteracting the depressor effects of these different pharmacologic maneuvers, leading to the maintenance of supranormal blood pressure.
[Drug-Disease]: propranolol - normoreninemic hypertension
[Title]: Intrapatient comparison of treatment with chlorthalidone, spironolactone and propranolol in normoreninemic essential hypertension.
[Abstract]: The effects of chlorthalidone, spironolactone and propranolol in reducing blood pressure were compared in the same 11 normoreninemic hypertensive patients. All three drugs decreased the blood pressure significantly and no agent had a superior blood pressure-lowering effect. The blood pressure did not normalize. The data suggest that no one variable--volume factors, relative hyperactivity of the renin-aldosterone system or beta-adrenergic hyperactivity--is the prime mover in normoreninemic hypertension. Long-term treatment with chlorthalidone resulted in slight hyperreninism (26.3 +/- 4.9 ng-ml-1-3 hours-1) (mean +/- standard error) with concomitant changes in plasma aldosterone (23.0 +/- 3.2 ng-100 ml-1). The body weight decreased significantly (--1.8 kg, P less than 0.005). Plasma potassium concentrations were low (3.2 +/- 0.1 mEq-liter -1). Creatinine clearance was unimpaired (117 +/- 6 ml-min-1). Treatment with spironolactone resulted in more marked hyperreninism (47.0 +/- 14.3 ng-ml-1-3 hours-1) and hyperaldosteronism (61.9 +/-11.8 ng-100 ml-1). The body weight decreased significantly (--1.9 kg, P less than 0.004). Significant hyperkalemia occurred (4.4 +/- 0.1 mEq-liter-1). The glomerular filtration rate decreased significantly to 93 +/- 3 ml-min-1 (P less than 0.004). Treatment with propranolol resulted in marked suppression of the plasma renin activity (1.8 +/- 0.2 ng-ml-1-3 hours-1) and plasma aldosterone levels (8.9 +/- 1.3 ng-100 ml-1). A significant increase in body weight occurred (+2.3 kg, P less than 0.013). The plasma potassium concentration increased to a level not significantly different from the value found after treatment with spironolactone (4.2 +/- 0.1 mEq-liter-1). The creatinine clearance decreased significantly to 99 +/- 5 ml-min-1 (P less than 0.008). Hyperreninemia (by spironolactone and chlorthalidone), effective hyperaldosteronism (by chlorthalidone) and volume retention (by propranolol) are considered to represent expressions of mechanisms counteracting the depressor effects of these different pharmacologic maneuvers, leading to the maintenance of supranormal blood pressure.
[Drug-Disease]: spironolactone - normoreninemic hypertension
[Title]: The effect of phenylephrine on pain and flare intensity in eyes with uveitis.
[Abstract]: PURPOSE: To investigate the influence of protein concentration in the anterior chamber, measured by laser flare meter, on pain sensation after phenylephrine instillation in patients with iridocyclitis. METHODS: Twenty-five consecutive patients with iridocyclitis were included. Patients with cataract, exfoliation syndrome, diabetes mellitus, glaucoma or any other previous ocular diseases or ocular surgery were excluded. Patients were divided into two groups: Group 1--without fibrinoid reaction (FR) in the anterior chamber (18 patients), and Group 2--with FR (7 patients). Protein concentration in the anterior chamber was measured with laser flare meter (FC 500, Kowa Co., Japan). Pupil size was measured by Alcon Tilo Scale, and pain sensation was estimated by Visual Analogue Scale (VAS, Kabi Pharmacia). All measurements were done before and 1 hour after topical instillation of 10% phenylephrine hydrochloride into the subconjunctival sac of the inflamed eyes. RESULTS: Eyes with iridocyclitis and fibrinoid reaction (FR) have a higher flare intensity compared to those without FR (p<0.05). Pupil size was significantly increased after phenylephrine instillation in both study groups (Wilcoxon test, p<0.05). The VAS pain and flare intensity were significantly decreased in group without FR after phenylephrine instillation (Group 1) compared to values before treatment (Wilcoxon test, p<0.05). In eyes with FR (Group 2), no significant influence of phenylephrine instillation was found on VAS pain and flare intensity. CONCLUSIONS: After phenylephrine instillation, flare intensity and pain were significantly decreased only in eyes with iridocyclitis and without FR. The decreasing level of flare intensity, and paralysis of the pupil after phenylephrine instillation seem to alleviate pain in those eyes.
[Drug-Disease]: phenylephrine - pain
[Title]: The effect of phenylephrine on pain and flare intensity in eyes with uveitis.
[Abstract]: PURPOSE: To investigate the influence of protein concentration in the anterior chamber, measured by laser flare meter, on pain sensation after phenylephrine instillation in patients with iridocyclitis. METHODS: Twenty-five consecutive patients with iridocyclitis were included. Patients with cataract, exfoliation syndrome, diabetes mellitus, glaucoma or any other previous ocular diseases or ocular surgery were excluded. Patients were divided into two groups: Group 1--without fibrinoid reaction (FR) in the anterior chamber (18 patients), and Group 2--with FR (7 patients). Protein concentration in the anterior chamber was measured with laser flare meter (FC 500, Kowa Co., Japan). Pupil size was measured by Alcon Tilo Scale, and pain sensation was estimated by Visual Analogue Scale (VAS, Kabi Pharmacia). All measurements were done before and 1 hour after topical instillation of 10% phenylephrine hydrochloride into the subconjunctival sac of the inflamed eyes. RESULTS: Eyes with iridocyclitis and fibrinoid reaction (FR) have a higher flare intensity compared to those without FR (p<0.05). Pupil size was significantly increased after phenylephrine instillation in both study groups (Wilcoxon test, p<0.05). The VAS pain and flare intensity were significantly decreased in group without FR after phenylephrine instillation (Group 1) compared to values before treatment (Wilcoxon test, p<0.05). In eyes with FR (Group 2), no significant influence of phenylephrine instillation was found on VAS pain and flare intensity. CONCLUSIONS: After phenylephrine instillation, flare intensity and pain were significantly decreased only in eyes with iridocyclitis and without FR. The decreasing level of flare intensity, and paralysis of the pupil after phenylephrine instillation seem to alleviate pain in those eyes.
[Drug-Disease]: phenylephrine - iridocyclitis
[Title]: Prilocaine versus lignocaine for minor lid procedures.
[Abstract]: PURPOSE: To determine whether prilocaine is a more comfortable local infiltration anaesthetic agent than the more widely used lignocaine for minor eyelid procedures. METHODS: A prospective randomised study was undertaken to compare the discomfort between local infiltration of plain 2% prilocaine versus its equivalent, plain 2% lignocaine. One hundred and twenty-five patients were recruited. Pain was assessed subjectively using a visual analogue pain score, graded from 0 to 10. RESULTS: The mean pain score for the prilocaine group was 1.82 compared with 3.19 for the lignocaine group. Using the Mann-Whitney U-test for significance, U = 1236.5; p < 0.001. CONCLUSION: Prilocaine is a more comfortable local infiltration anaesthetic agent than lignocaine when used for minor eyelid procedures.
[Drug-Disease]: Prilocaine - pain
[Title]: Enalapril and prednisone in children with nephrotic-range proteinuria.
[Abstract]: The effect of enalapril and low prednisone doses on the urinary protein electrophoretic pattern was studied in 13 pediatric patients with glomerular diseases and steroid-resistant nephrotic syndrome. Enalapril was administered at doses of 0.2-0.6 mg/kg per day for 24-84 months, and prednisone was introduced 2 months later in 11 patients at doses of 30 mg/m2 on alternate days. The urine protein electrophoretic pattern showed a reduction of 80% and 70% in the total protein and albumin, respectively, after enalapril. Total urinary protein decreased from 5.46 to 1.1 g/m2 per day (P<0.001). A marked change from a pattern of non-selective urinary protein loss to an albumin-selective proteinuria was observed. Mean total plasma proteins increased from 4.7 to 5.43 g/dl (P<0.001). Four patients became free of proteinuria 24 months after enalapril was started, but only 2 remained free of proteinuria at 48 months of follow-up. The other 11 patients had persistent albuminuria of between 0.5 and 2.6 g/m2 per day with a selective urinary electrophoretic pattern. No additional decrease was observed after steroids were introduced. A clinical improvement in edema was observed in all children. Three patients developed transient acute renal failure, during the course of an infectious disease; 2 developed peritonitis and 1 pneumopathy. In these patients withdrawal of enalapril was necessary until a complete recovery of renal function was observed. Four patients were hypertensive on admission, achieving normal blood pressure 1 month after enalapril was started. No episodes of systemic arterial hypotension were seen. Creatinine clearance and serum potassium showed no statistically significant change.
[Drug-Disease]: enalapril - albuminuria
[Title]: Enalapril and prednisone in children with nephrotic-range proteinuria.
[Abstract]: The effect of enalapril and low prednisone doses on the urinary protein electrophoretic pattern was studied in 13 pediatric patients with glomerular diseases and steroid-resistant nephrotic syndrome. Enalapril was administered at doses of 0.2-0.6 mg/kg per day for 24-84 months, and prednisone was introduced 2 months later in 11 patients at doses of 30 mg/m2 on alternate days. The urine protein electrophoretic pattern showed a reduction of 80% and 70% in the total protein and albumin, respectively, after enalapril. Total urinary protein decreased from 5.46 to 1.1 g/m2 per day (P<0.001). A marked change from a pattern of non-selective urinary protein loss to an albumin-selective proteinuria was observed. Mean total plasma proteins increased from 4.7 to 5.43 g/dl (P<0.001). Four patients became free of proteinuria 24 months after enalapril was started, but only 2 remained free of proteinuria at 48 months of follow-up. The other 11 patients had persistent albuminuria of between 0.5 and 2.6 g/m2 per day with a selective urinary electrophoretic pattern. No additional decrease was observed after steroids were introduced. A clinical improvement in edema was observed in all children. Three patients developed transient acute renal failure, during the course of an infectious disease; 2 developed peritonitis and 1 pneumopathy. In these patients withdrawal of enalapril was necessary until a complete recovery of renal function was observed. Four patients were hypertensive on admission, achieving normal blood pressure 1 month after enalapril was started. No episodes of systemic arterial hypotension were seen. Creatinine clearance and serum potassium showed no statistically significant change.
[Drug-Disease]: enalapril - edema
[Title]: Enalapril and prednisone in children with nephrotic-range proteinuria.
[Abstract]: The effect of enalapril and low prednisone doses on the urinary protein electrophoretic pattern was studied in 13 pediatric patients with glomerular diseases and steroid-resistant nephrotic syndrome. Enalapril was administered at doses of 0.2-0.6 mg/kg per day for 24-84 months, and prednisone was introduced 2 months later in 11 patients at doses of 30 mg/m2 on alternate days. The urine protein electrophoretic pattern showed a reduction of 80% and 70% in the total protein and albumin, respectively, after enalapril. Total urinary protein decreased from 5.46 to 1.1 g/m2 per day (P<0.001). A marked change from a pattern of non-selective urinary protein loss to an albumin-selective proteinuria was observed. Mean total plasma proteins increased from 4.7 to 5.43 g/dl (P<0.001). Four patients became free of proteinuria 24 months after enalapril was started, but only 2 remained free of proteinuria at 48 months of follow-up. The other 11 patients had persistent albuminuria of between 0.5 and 2.6 g/m2 per day with a selective urinary electrophoretic pattern. No additional decrease was observed after steroids were introduced. A clinical improvement in edema was observed in all children. Three patients developed transient acute renal failure, during the course of an infectious disease; 2 developed peritonitis and 1 pneumopathy. In these patients withdrawal of enalapril was necessary until a complete recovery of renal function was observed. Four patients were hypertensive on admission, achieving normal blood pressure 1 month after enalapril was started. No episodes of systemic arterial hypotension were seen. Creatinine clearance and serum potassium showed no statistically significant change.
[Drug-Disease]: enalapril - hypertensive
[Title]: Enalapril and prednisone in children with nephrotic-range proteinuria.
[Abstract]: The effect of enalapril and low prednisone doses on the urinary protein electrophoretic pattern was studied in 13 pediatric patients with glomerular diseases and steroid-resistant nephrotic syndrome. Enalapril was administered at doses of 0.2-0.6 mg/kg per day for 24-84 months, and prednisone was introduced 2 months later in 11 patients at doses of 30 mg/m2 on alternate days. The urine protein electrophoretic pattern showed a reduction of 80% and 70% in the total protein and albumin, respectively, after enalapril. Total urinary protein decreased from 5.46 to 1.1 g/m2 per day (P<0.001). A marked change from a pattern of non-selective urinary protein loss to an albumin-selective proteinuria was observed. Mean total plasma proteins increased from 4.7 to 5.43 g/dl (P<0.001). Four patients became free of proteinuria 24 months after enalapril was started, but only 2 remained free of proteinuria at 48 months of follow-up. The other 11 patients had persistent albuminuria of between 0.5 and 2.6 g/m2 per day with a selective urinary electrophoretic pattern. No additional decrease was observed after steroids were introduced. A clinical improvement in edema was observed in all children. Three patients developed transient acute renal failure, during the course of an infectious disease; 2 developed peritonitis and 1 pneumopathy. In these patients withdrawal of enalapril was necessary until a complete recovery of renal function was observed. Four patients were hypertensive on admission, achieving normal blood pressure 1 month after enalapril was started. No episodes of systemic arterial hypotension were seen. Creatinine clearance and serum potassium showed no statistically significant change.
[Drug-Disease]: enalapril - proteinuria
[Title]: [Amantadine for the treatment of levodopa dyskinesias in Parkinson's disease].
[Abstract]: The development of dyskinesias is a common side effect during chronic levodopa therapy in parkinsonian patients. Recent reports suggest that amantadine, a drug with well known antiparkinsonian activity, is effective in the treatment of this complication. In order to evaluate its usefulness we conducted an open label, prospective and longitudinal study in 26 patients with Parkinson's disease (PD) on chronic levodopa therapy who presented peaks of dose dyskinesias. After 3 weeks' treatment dyskinesia severity was reduced by 70% (p < 0.0001) on the I SAPD scale and by 68.8% (p < 0.0002) on the UPDRS IV subscale. Patients were later evaluated every 45 days showing persistent drug benefit during follow-up ranging from 2 to 11 months (mean 6.5 months). One third of our series presented unwanted effects which were only severe enough in 2 cases to discontinue treatment. In the others, side effects were transient or readily abated with amantadine dose reduction. Our findings support amantadine as a safe and useful drug to treat levodopa-induced dyskinesias which on occasion prove as disabling as PD itself. Treatment with amantadine should routinely be considered before indicating pallidotomy for levodopa-induced dyskinesias.
[Drug-Disease]: amantadine - dyskinesias
[Title]: [Amantadine for the treatment of levodopa dyskinesias in Parkinson's disease].
[Abstract]: The development of dyskinesias is a common side effect during chronic levodopa therapy in parkinsonian patients. Recent reports suggest that amantadine, a drug with well known antiparkinsonian activity, is effective in the treatment of this complication. In order to evaluate its usefulness we conducted an open label, prospective and longitudinal study in 26 patients with Parkinson's disease (PD) on chronic levodopa therapy who presented peaks of dose dyskinesias. After 3 weeks' treatment dyskinesia severity was reduced by 70% (p < 0.0001) on the I SAPD scale and by 68.8% (p < 0.0002) on the UPDRS IV subscale. Patients were later evaluated every 45 days showing persistent drug benefit during follow-up ranging from 2 to 11 months (mean 6.5 months). One third of our series presented unwanted effects which were only severe enough in 2 cases to discontinue treatment. In the others, side effects were transient or readily abated with amantadine dose reduction. Our findings support amantadine as a safe and useful drug to treat levodopa-induced dyskinesias which on occasion prove as disabling as PD itself. Treatment with amantadine should routinely be considered before indicating pallidotomy for levodopa-induced dyskinesias.
[Drug-Disease]: levodopa - PD
[Title]: Haemodynamic and metabolic effects of rilmenidine in hypertensive patients with metabolic syndrome X. A double-blind parallel study versus amlodipine.
[Abstract]: OBJECTIVE: To compare the effects of rilmenidine with those of amlodipine on blood pressure, glucose metabolism, plasma lipid concentration and fibrinolysis parameters. DESIGN: A four-month randomized double-blind, parallel group study. PATIENTS AND METHODS: Obese hypertensive patients with hypertriglyceridaemia (> or = 2.3 mmol/l) and impaired glucose tolerance (OMS-ADA) were included (n = 52). A placebo run-in period of 2 weeks was followed by 4 months of double-blind treatment with either rilmenidine or amlodipine. Blood pressure was recorded using a mercury sphygmomanometer. Glucose metabolism was evaluated by an oral glucose tolerance test RESULTS: Of the 52 patients recruited, 47 (21 rilmenidine and 26 amlodipine) completed the 4-month treatment period. The intention-to-treat analysis showed a comparable reduction in systolic and diastolic blood pressure (SBP, DBP) with the two anti-hypertensive treatments (rilmenidine -13.9/-13.5 mmHg; amlodipine - 17.6/-15.0 mmHg). Insulin concentrations under basal conditions and 2 h after a standard oral glucose load did not change significantly after treatment in both groups. Plasma glucose under basal conditions and 2 h after a standard oral glucose load as well as the area under the plasma glucose concentration curve tended to decrease in the rilmenidine group and to increase in the amlodipine group so that the changes in these parameters were significantly different between the two study groups (P= 0.041, P = 0.042 and P = 0.015, respectively). Plasminogen activator inhibitor type 1 (PAI-1) antigen and PAI-1 activity were only decreased in the rilmenidine group (not statistically significant). CONCLUSION: Our results demonstrate that rilmenidine and amlodipine have a comparable anti-hypertensive effect but only rilmenidine is able to improve glucose metabolism.
[Drug-Disease]: rilmenidine - hypertensive