QJM, Vol 91, Issue 3 191-197, Copyright © 1998 by Oxford University Press
M English, S Wale, G Binns, I Mwangi, H Sauerwein and K Marsh
We investigated the pathophysiology of hypoglycaemia in severe malaria in
African children, especially the potential importance of glycerol as a
substrate for gluconeogenesis, and whether substrate limitation contributes
to hypoglycaemia in severe disease. Of 171 children with moderate or severe
malaria, 16% were hypoglycaemic on admission, while at least 9% of children
with severe malaria treated with quinine and a concurrent 4% dextrose
infusion had a definite episode of hypoglycaemia after admission. Blood
levels of gluconeogenic precursors are as high (alanine and lactate) or
higher (glycerol) in those with either hypoglycaemia on or after admission
as they are in children never having an episode of hypoglycaemia. Among
children with severe malaria, however, those having a definite episode of
hypoglycaemia at some stage are more acidotic and have greater evidence of
renal impairment than those who are never hypoglycaemic (mean base excess
-14.4 vs. -7.2, p < 0.001, mean creatinine 97 vs. 64, p < 0.001 and
mean urea 8.1 vs. 5.8, p = 0.03, respectively). These data do not support a
role for reduced gluconeogenic substrate supply in the pathogenesis of
hypoglycaemia in severe childhood malaria, but do support the hypothesis
that gluconeogenesis is impaired. Commonly-used bedside blood glucose
monitoring devices may overestimate blood glucose measurements in the
normal range, and paradoxically may also seriously overestimate the
frequency of hypoglycaemia.
ORIGINAL PAPERS
Hypoglycaemia on and after admission in Kenyan children with severe malaria
Kenya Medical Research Institute, CRC, Kilifi Unit, Kenya.
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