Endocrine Abstracts

Background: Cerebral malaria may present with altered cognition, severe hemolysis, renal and metabolic dysfunction. The endocrine abnormalities induced by malaria include: hypoglycemia, hypocalcemia, hypercortisolism and compromised pituitary function due to sequestration of drepanocytes in hypothalamo-pituitary portal microvasculature.

Aim: To raise awareness for the risk of pituitary dysfunction in severe malaria.

Case: A previously healthy 22 years old woman was admitted at the emergency department with fever, rigors, vomiting and altered cognition after a flight from Guinea. Malaria was suspected and P.falciparum parasitemia was of 3% at admission. Anemia, pulmonary edema, acute renal lesion (maximum creatinine 9.2 mg/dl (N:0.5-0.9)), thrombocytopenia, hyperbilirubinemia, hypocalcemia and elevated inflammatory markers were present. She had a normal head CT scan. After quinine and doxiciclin treatment a generalized cognition and hematologic improvement was followed by acute renal lesion KDIGO 3, with oliguria and uremia requiring hemodyalisis. Spontaneous miction was followed by prompt increase in urinary output reaching a maximum of 4.9L without fluids or diuretics. After fluid treatment, negative fluid balance reached -5.5L (urinary output 15.5L), followed by dehydration and sinusal tachycardia. The progression and duration of polyuria raised suspicion of diabetes insipidus (DI). Hypotonic polyuria was confirmed, serum osmolality ranged between 269-277mOsmol/Kg (N: 275-298), and sodium levels between 136-138 mmol/l (N:135-145). Low basal copeptin level (1.14pmol/l) was suggestive of central DI and a therapeutical trial with desmopressin was started and titrated up to 0.6 mg/day with clinical improvement. Pituitary function was assessed and elevated ACTH 135.6 pg/ml (N: 7.2-63.3) and 0800 hours cortisol of 23.2 mg/dl required further study. Lack of suppression in 1mg dexamethasone suppression test (18.4 mg/dl) was documented and a sellar MRI obtained. No pituitary adenomas were present, but a neurohypophysis with right deviation and hypersignal in T2 of ‘imprecise meaning’ was described. The hypercortisolism was admitted as a result of hospitalization and acute disease, and was resumed after hospital discharge. After two weeks, desmopressin was stopped without relapse of polyuria, and normal sodium and osmolality levels were documented in urine and serum evaluation, as previously described in DI due to malaria.

Conclusion: In conclusion, cerebral malaria may present with compromised pituitary function, such as diabetes insipidus, requiring prompt diagnosis and treatment.