[HLA and acute pericarditis].
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Biomedical subjects
Publications and source records attributed to R Bartram.
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Nine patients (median age 78 years, range 62-92) treated with a constant oral dosage of digoxin were evaluated for the effect of trimethoprim on serum digoxin values. Serum digoxin increased by 22% during trimethoprim treatment (p less than 0.05). Subsequently, 6 healthy subjects (median age 29 years, range 24-31) were evaluated for the effect of trimethoprim on digoxin pharmacokinetics after an i.v. dose. Trimethoprim administration did not affect total body clearance of digoxin and the glomerular filtration rate. The renal clearance of digoxin decreased by 17% (p less than 0.05) and the extrarenal clearance of digoxin increased by 14% (N.S.). Biological half-life of digoxin and apparent volumes of central and peripheral compartments were unchanged during the study. It is suggested that the increase in serum digoxin in the elderly patients is due to decreased renal tubular secretion of digoxin and not to disturbance of the extrarenal clearance.
The influence of trimethoprim on renal function has been investigated in two groups of volunteers, both without a history of either acute or chronic urinary tract disease. All had normal serum creatinine. They were treated with trimethoprim 200 mg bd for 14 days. In group A (median age 78 years), serum creatinine increased significantly from median 89 to 134 mumol/l (P less than 0.01) during the first week and returned to normal 1 week after termination of treatment to median 90 mumol/l (P less than 0.02). After 1 week's treatment in group B (median age 29 years), serum creatinine had increased significantly from median 87 to 107 mumol/l (P less than 0.05), remained stable in the second week and returned to the pre-treatment level 1 week after cessation of treatment: 87 mumol/l (P less than 0.05). The glomerular filtration rate determined by 51Cr-EDTA clearance did not change. There was a significant decrease in the 24-h endogenous creatinine clearance after 14 days' treatment from 111 to 87 ml/min/1.73 m2 (P less than 0.05). Our results are consistent with an age-independent reversible trimethoprim-induced inhibition of the tubular secretion of creatinine.
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