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|Title:||Hypoglycaemia and antimalarial drugs: Quinidine and release of insulin|
|Authors:||R. E. Phillips|
N. J. White
R. C. Turner
D. A. Warrell
Nuffield Department of Clinical Medicine
|Citation:||British Medical Journal (Clinical research ed.). Vol.292, No.6531 (1986), 1319-1321|
|Abstract:||Life threatening hypoglycaemia has been closely associated with the use of quinine, but the effect of quinidine and the synthetic antimalarials on the homoeostasis of glucose has not been investigated. In volunteers given a fixed dose of 500 mg base and patients with malaria given a quinidine loading dose (15 mg base/kg) mean (SEM) plasma insulin concentrations rose from 6.1 (1.5) mU/1 to 10.9 (4–4) mU/1 (p < 0.02) and 10.4 (2.0) mU/1 to 18.5 (5.3) mU/l(p < 0.04), respectively. Plasma glucose concentrations fell from 4.5 (1.1) mmol/1 (81 (20) mg/100 ml) to 4.0 (0–3) mmol/1 (72 (5) mg/100 ml) in volunteers (p < 0.04) and from 5–7 (1.3) mmol/1 (102 (23) mg/100 ml) to 4.8 (1–6) mmol/1 (86 (29) mg/100 ml) in patients (p < 0.05). One of two patients with cerebral malaria and acute renal failure became profoundly hypoglycaemic (plasma glucose concentration 1.4 mmol/1 (25 mg/100 ml), plasma insulin concentration 3.1 mU/1). Hypoglycaemia may occur in any severely ill fasting patient given parenteral quinidine. The other antimalarials tested, chloroquine, amodiaquine, mefloquine, and halofantrine, did not stimulate the release of insulin, an important advantage that should be taken into account when treatment is chosen for Plasmodium falciparum malaria. © 1986, British Medical Journal Publishing Group. All rights reserved.|
|Appears in Collections:||Scopus 1969-1990|
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