R. E. PhillipsC. HatzD. A. WarrellR. E. PhillipsS. LooareesuwanD. A. WarrellM. E. MolyneuxUniversity of OxfordMahidol UniversityLiverpool School of Tropical Medicine2018-08-102018-08-101993-01-01QJM. Vol.86, No.4 (1993), 233-24014602393146027252-s2.0-0027295258https://repository.li.mahidol.ac.th/handle/20.500.14594/22794The mechanism and response to treatment of severe life–threatening hypoglycaemia (plasma glucose 1.15±0.73 mM/I [±SD]) was studied in eight Thai patients with falciparum malaria. Plasma insulin concentrations were inappropriately high (range 1.0−21.8 mU/I), lactic acidosis was common (arterial blood lactic acid concentration 1.44—17.8 mM/I), but the glucose counterregulatory response, indicated by plasma cortisol, growth hormone, catecholamines and glucagon concentrations, was intact Hyperinsulinaemia was successfully treated in five patients by a continuous intravenous infusion of the long–acting somatostatin analogue Sandostatin (SMS 201—995), 50 μg/h. In volunteer studies a single intramuscular injection of Sandostatin (100 μg) suppressed quinine–induced hyperinsulinaemia within 15 min; this effect was maintained for 6 h. These results suggest that Sandostatin may be a safe and effective way of correcting the hyperinsulinaemic hypoglycaemia complicating quinine treatment of falciparum malaria. This treatment could be particularly useful in fluid–overloaded patients with recurrent hypoglycaemia despite dextrose infusions. © 1993 Oxford University Press.Mahidol UniversityMedicineArticleSCOPUS10.1093/oxfordjournals.qjmed.a068802