Hypoglycaemia and counterregulatory hormone responses in severe falciparum malaria: Treatment with Sandostatin

The 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...

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Main Authors: R. E. Phillips, C. Hatz, D. A. Warrell, S. Looareesuwan, M. E. Molyneux
Other Authors: University of Oxford
Format: Article
Published: 2018
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Online Access:https://repository.li.mahidol.ac.th/handle/123456789/22794
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Institution: Mahidol University
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Summary:The 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.