INDOMETHACIN STIMULATES GLUCOSE-PRODUCTION IN ADULTS WITH UNCOMPLICATED FALCIPARUM-MALARIA

In healthy subjects, basal hepatic glucose production is (partly) regu lated by paracrine intrahepatic factors. It is unknown if these paracr ine factors also influence basal glucose production in infectious dise ases with increased glucose production. We compared the effects of 150 mg indomethacin (n = 9), a nonendocrine stimulator of glucose product ion in healthy adults, and placebo (n = 7) on hepatic glucose producti on in Vietnamese adults with uncomplicated falciparum malaria. Glucose production was measured by primed, continuous infusion of [6,6-H-2(2) ]glucose. After indomethacin, the plasma glucose concentration and glu cose production increased in all subjects from 5.3 +/- 0.1 mmol/L to a maximum of 7.1 +/- 0.3 mmol/L (P < .05) and from 17.6 +/- 0.8 mu mol. kg(-1).min(-1) to a maximum of 26.2 +/- 2.5 mu mol.kg(-1).min(-1) (P < .05), respectively. In the control group, the plasma glucose concentr ation and glucose production declined gradually during 4 hours from 5. 4 +/- 0.2 mmol/L to 5.1 +/- 0.1 mmol/L (P < .05) and from 17.1 +/- 0.8 mu mol.kg(-1).min(-1) to 15.1 +/- 1.0 mu mol.kg(-1).min(-1) (P < .05) , respectively. There were no differences in plasma concentrations of insulin, counterregulatory hormones, or cytokines between the groups. We conclude that indomethacin administration results in a transient in crease in glucose production in patients with uncomplicated falciparum malaria in the absence of changes in plasma concentrations of glucore gulatory hormones or cytokines. Thus, this study indicates that in unc omplicated falciparum malaria, the rate of basal hepatic glucose produ ction is also regulated by paracrine intrahepatic factors. Copyright ( C) 1998 by W.B. Saunders Company.