Malarial Hepatopathy-Experience at Tertiary Care Centre of North India
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BACKGROUND: Jaundice is commonly seen in severe malaria (approx. 2.5% patients) but hepatitis is unusual. Hepatocellular dysfunction varies from mild abnormalities in liver function tests (LFTs) to hepatic failure.
AIMS: To study the clinical, biochemical profile, complications and outcome in confirmed Plasmodium falciparum malaria cases with hepatopathy.
MATERIAL AND METHOD: This retrospective study was carried out in a tertiary care hospital in North India by reviewing slide confirmed case records of P falciparum malaria with biochemical evidence of hepatic dysfunction, admitted between 1/10/2012 and 1/10/ 2013.
RESULTS: A total of 13 patients (all male) with mean age 43.07 years, mean duration of fever prior to hospitalisation 6.5 days, were included. Fever persisted in all the patients after the onset of jaundice. Encephalopathy was present in 38.5% (5) of patients. Hepatosplenomegaly, icterus and anaemia (< 10 gm %) were found in 84.61%, 92.30% and 84.61% respectively. Predominant (> 50%) conjugated hyperbilirubinaemia was found in all the patients, with mean total bilirubin level of 21.06 mg % (1.5-54). Hyper-hyperbilirubinaemia (> 10 mg %) was associated with renal failure (serum creatinine > 2.0 mg/ dl) in 77.8% (7) cases. Mean AST, ALT and ALP levels were 164.84 IU/L (38-665), 75 IU/L (43-160) and 132.46 and > 3 upper limit of normal (ULN) was more common with AST than ALT (53.84% vs. 15.38%). Thrombocytopenia was seen in all the patients with mean platelet count of 43,853 /mm3. Most patients had only mild derangement of PT with mean INR of 1.30 (1-1.74). Main complications seen were acute renal failure (ARF) (88.89%), septicaemia (77.79%), acute respiratory distress syndrome (ARDS - 22.22%). ICU care was required by 69.23% of the patients. Mortality was 38.46% (5) and 53.84% patients (8) recovered.
CONCLUSION: Malarial hepatitis is a serious complication in patients presenting with P. falciparum malaria. Renal dysfunction is more common in those with hyper-hyperbilirubinaemia. Whether this is the cause, or effect, is difficult to hypothesise.
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