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histotoxic symptoms may be due to these, but the exact mechanism of action of thiocyanates is not known.4 Thiocyanate intoxication with blood concentrations above 200 mg/l may be rapidly corrected by haemodialysis, which reportedly removes several grams of the drug.5 We tried peritoneal dialysis but in the absence of clearance studies, which we could not do, we cannot comment on the procedure for intoxication with this compound. Patients, methods, and resultsThe effects of nifedipine on an oral glucose tolerance test (100 g of glucose)were studied in five women and one man. None had evidence of endocrinopathy or were receiving drugs. Mean Nifedipine induced distinct glucose intolerance (figure). Fasting plasma glucose concentrations showed a significant increase of 10%; basal insulin concentrations were significantly reduced (26%). During the oral glucose tolerance test plasma glucose concentrations were appreciably raised after administration of the drug, and at 60, 90, and 120 minutes values of 9-56, 9-89, and 7-67 mmol/l respectively were observed (172, 178, and 138 mg/ 100 ml). This contrasted with the normal glucose tolerance in all subjects before administration of nifedipine. In five subjects insulin concentrations were reduced at 30 and 60 minutes; in this subgroup the effect was significant. At 30 minutes the mean insulin concentrations were 0-62±0-12 v 0-85 ±0-14 nmol/l (90+ 18 v 123 +20 uU/ml) (p <0 01); and at 60 minutes 0-76±0-17 v 1-13+0-21 nmol/l (110+24 v 164±30 juU/ml) (p<0 05). In the sixth subject plasma insulin concentration was increased twofold and fourfold at 30 and 60 minutes respectively. This subject was the only one whose plasma glucose concentrations remained normal during the second oral glucose tolerance test. Fasting plasma glucagon concentration was measured by radioimmunoassay (Unger's 30 K antiserum) in three subjects and five additional normal subjects. Glucagon concentrations were significantly increased by nifedipine (0 045 0-008 v 0 034 ±0-006 nmol/l (p<005) (153 +27 v 115 +22 pg/ml).
histotoxic symptoms may be due to these, but the exact mechanism of action of thiocyanates is not known.4 Thiocyanate intoxication with blood concentrations above 200 mg/l may be rapidly corrected by haemodialysis, which reportedly removes several grams of the drug.5 We tried peritoneal dialysis but in the absence of clearance studies, which we could not do, we cannot comment on the procedure for intoxication with this compound. Patients, methods, and resultsThe effects of nifedipine on an oral glucose tolerance test (100 g of glucose)were studied in five women and one man. None had evidence of endocrinopathy or were receiving drugs. Mean Nifedipine induced distinct glucose intolerance (figure). Fasting plasma glucose concentrations showed a significant increase of 10%; basal insulin concentrations were significantly reduced (26%). During the oral glucose tolerance test plasma glucose concentrations were appreciably raised after administration of the drug, and at 60, 90, and 120 minutes values of 9-56, 9-89, and 7-67 mmol/l respectively were observed (172, 178, and 138 mg/ 100 ml). This contrasted with the normal glucose tolerance in all subjects before administration of nifedipine. In five subjects insulin concentrations were reduced at 30 and 60 minutes; in this subgroup the effect was significant. At 30 minutes the mean insulin concentrations were 0-62±0-12 v 0-85 ±0-14 nmol/l (90+ 18 v 123 +20 uU/ml) (p <0 01); and at 60 minutes 0-76±0-17 v 1-13+0-21 nmol/l (110+24 v 164±30 juU/ml) (p<0 05). In the sixth subject plasma insulin concentration was increased twofold and fourfold at 30 and 60 minutes respectively. This subject was the only one whose plasma glucose concentrations remained normal during the second oral glucose tolerance test. Fasting plasma glucagon concentration was measured by radioimmunoassay (Unger's 30 K antiserum) in three subjects and five additional normal subjects. Glucagon concentrations were significantly increased by nifedipine (0 045 0-008 v 0 034 ±0-006 nmol/l (p<005) (153 +27 v 115 +22 pg/ml).
carbohydrate impairment. Glucagon concentrations were not investigated. Because of the potential diabetogenic properties of nifedipine plasma glucose concentrations should thus be monitored in patients receiving this drug. We thank Dr J C Henquin for invaluable discussions and critical advice, and Mrs Detaille for secretarial help. I Opie LH. Drugs and the heart. Calcium antagonists. Lancet 1980;i:806-9. 2 Koch G. Plasma renin activity, epinephrine and norepinephrine at rest and during exercise in young adults and boys. ScandJ3 Clin Lab Invest 1977;37, suppl 147:107.
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