GLUCOSE-METABOLISM IN QUININE-TREATED PATIENTS WITH UNCOMPLICATED FALCIPARUM-MALARIA

To investigate host and drug effects on glucose metabolism in acute falciparum malaria, 10 previously untreated, fasting Thai males with uncomplicated infections were given a 2‐h intravenous glucose infusion (5 mg/kg ideal body weight min) with an infusion of quinine dihydrochloride (10 mg/kg body weight) during the second hour. Eight patients were restudied in convalescence. Fasting plasma glucose (mean ± SD) and insulin (geometric mean (— SD to + SD)) were higher during acute illness (5.5 ± 1.0 mmol/l and 6.2 (5.0–7.7) mU/l) than in convalescence (4.2 ± 0.25 mmol/l and 3.7 (2.1–6.7) mU/l; P <0.001 and P = 0.058 respectively). After 1 h, both plasma glucose (9.3 ± 1.4 vs 7.5 ± 0.8 mmol/l, P < 0.001) and insulin (21.2 (13.8–32.5) vs 15.2 (11.2–20.8) mU/l, P = 0.089) remained higher during acute illness; mathematical model (CIGMA) assessment of these values indicated lower tissue insulin sensitivity on admission (97% (71–134)) than in convalescence (139% (109–178), P < 0.025) but normal beta‐cell function on both occasions. Two‐hour plasma glucose (9.5 ± 2.0 mmol/l) and insulin (81.8 (51.5–129.9) mU/l) concentrations during acute illness were also significantly higher than in convalescence (7.2 ± 1.2 mmol/l and 40.1 (23.5–68.4) mU/l, P ± 0.025) despite similar end‐infusion free plasma quinine concentrations (P> 0.5). Basal plasma free fatty acid concentrations were increased in acute illness (0.68 ±.24 vs 0.21 ± 0.12 mmol/l, P < 0.001) but fell to low levels at 2 h in both studies. These data suggest tissue insulin resistance and augmented quinine‐stimulated insulin secretion in acute falciparum malaria, factors which are likely to influence the clinical situation in which malaria‐associated hypoglycaemia occurs. © 1990 Blackwell Scientific Publications Ltd.