Abstract

We report the case of a 39-year-old West African man in whom high-density lipoprotein cholesterol (HDL-C) was identified as undetectable at <0.08 mmol/L. Total cholesterol in the same sample was 2.85 mmol/L; triglycerides were only mildly elevated at 2.32 mmol/L. He was admitted with a 2-week history of polydipsia, polyuria, weight loss and hyperpyrexia. Dual malarial infection with Plasmodium ovale and falciparum was identified and attributed to a recent trip to Nigeria without chemoprophylaxis. Also, he was diagnosed with diabetes mellitus with random hyperglycemia of 39 mmol/L but no ketonemia. Subsequent investigation revealed a low apolipoprotein A1 of 0.38 g/L (1.04–2.02), confirming a true HDL-C deficit. On clinical examination, he had neither orange tonsils consistent with Tangier disease nor corneal opacification consistent with lecithin-cholesterol acyltransferase deficiency. The patient was an avid gym goer but denied anabolic steroid abuse, a fact supported by a transient primary testosterone deficiency at presentation (testosterone 6.56 nmol/L, RR 8.6–29; follicle-stimulating hormone high at 9.2 mU/L, luteinising hormone high at 11.9 mU/L). He was treated for malaria and started on metformin for diabetes. At 8-week follow-up, his HDL-C was entirely normal at 1.38 mmol/L. We believe this severe drop in HDL-C level to be due to acute inflammation caused by malaria. As extreme drops in HDL-C have been found to be associated with the poorest prognosis, prospective identification of HDL-C and prompt clinical liaison may be of benefit.

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