Volume 18, Issue 6
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645



Infection with is characterized by severe weakness, hypotension, vomiting, diarrhea, hyponatremia, and other clinical findings compatible with adrenal insufficiency. Previous investigators have correlated morphologic adrenocortical abnormalities in fatal cases with the clinical syndrome and suggested acute adrenal insufficiency as the mechanism of death. Standard methods were used to assess pituitary and adrenal function in 29 nonimmune patients with naturally acquired falciparum malaria. Symptoms and signs compatible with adrenal insufficiency were present in all patients during the acute illness. Levels of plasma 17-hydroxycorticosteroid (17-OHCS) were increased in all patients, and 12 of 14 patients tested had diurnal variation of abnormalities. In contrast to the increased plasma 17-OHCS, the urinary 17-OHCS and 17-ketosteroids were at the lower limit of normal in all patients. Administration of Metopirone® to 14 patients elicited a normal response. Excretion of urinary aldosterone, measured in 15 patients, was normal or increased. It is assumed that the observed depression of urinary-steroid excretion in association with increased plasma 17-OHCS levels reflects decreased hepatic conjugation during the acute illness, since hepatomegaly and increased serum glutamic oxalacetic transaminase levels were frequent and creatinine clearance was normal. We conclude that pituitary and adrenal function are normal during acute falciparum malaria despite clinical findings suggestive of adrenal insufficiency.


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