Pituitary-adrenal function in uncomplicated falciparum malaria.

To investigate pituitary-adrenal function in acute uncomplicated falciparum malaria, we performed an overnight dexamethasone suppression test in 13 Vietnamese adults with acute malaria and 6 healthy controls. After blood samples were taken for serum cortisol and plasma ACTH at 23.00 hours on the admission day, 1 mg dexamethasone was given and further samples were taken at 08.00, 16.00 and 23.00 hours the next day. The patients received conventional antimalarial and supportive treatment. Baseline plasma ACTH concentrations in the patients [3.9 (0.2-41.2) pmol/l] and controls [3.4 (1.1-4.3) pmol/l] were similar (p=0.51), and exhibited a similar fall after dexamethasone to 0.6 (0.2-2.5) and 0.9 (0.7-1.6) pmol/l at 08.00 hours respectively (p<0.03 vs 23.00 hour values). Serum cortisol levels before dexamethasone were higher in the patients than in the controls [456 (102-821) vs 145 (64-183) nmol/l respectively; p=0.007] and the overnight fall was less in the patients [208 (26-340) and 23 (15-46) nmol/l at 08.00 hours respectively; p<0.001 vs 23.00 hour values and between groups]. Between 08.00 and 23.00 hours, plasma ACTH and serum cortisol remained suppressed in the controls. In the patients, the serum cortisol continued to fall progressively towards control values. These data suggest that there is a raised set point for cortisol inhibition of ACTH secretion but normal corticotrophin responsiveness to dexamethasone in uncomplicated malaria. A raised serum cortisol after dexamethasone in the patients might reflect the combination of a prolonged cortisol half-life and the stimulatory effects of cytokines on the adrenal cortex, with a consequent protective effect against complications such as hypoglycemia.

Peripheral gangrene in nonfatal pediatric cerebral malaria: a report of two cases.

Two Thai girls aged 10 and 13 years from the same rural area were admitted to Paholpolpayuhasena Hospital, Kanchanaburi, Thailand during the rainy season of 1989 with cerebral malaria. After several days of conventional treatment, both developed gangrene involving the feet and toes, but the lesions healed and no other complications were seen. In the absence of convincing clinical and laboratory evidence of vasculitis or coagulopathy, it seems likely that host factors (dehydration, sluggish peripheral circulation, platelet activation, subclinical intravascular coagulation) combined with strain-specific parasite factors (tissue sequestration of mature forms, rosette formation) may predispose to peripheral microvascular occlusion sufficient to produce infarction of tissue in susceptible children. However, despite the apparently ominous appearance of such lesions in a comatose child, the prognosis seems good.