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|Year : 2009 | Volume
| Issue : 3 | Page : 233
Co-existence of viral hepatitis with malaria
SA Zaki, S Asif, D Dadge, P Shanbag
Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Mumbai - 400022, India
|Date of Web Publication||2-Nov-2009|
S A Zaki
Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Mumbai - 400022
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Zaki S A, Asif S, Dadge D, Shanbag P. Co-existence of viral hepatitis with malaria. J Postgrad Med 2009;55:233
Malaria and viral hepatitis are endemic in developing countries like India and may co-exist presenting a diagnostic dilemma to the treating physician.
A two-year-old girl presented with high-grade fever, diarrhea, vomiting, and abdominal pain for seven days and jaundice for four days. There was no history of bleeding from any site. She was conscious, febrile with a heart rate of 140/min, respiratory rate 28/min, and blood pressure 100/78 mmHg. Deep icterus and mild pallor were present. The liver was tender and palpable 6 cm below the costal margin and the spleen palpable 3 cm. Other systems were normal. The hemoglobin concentration was 6.8 gm/dL, total leukocyte count 12,600/mL, and platelet count 19,000/mL. Peripheral blood smear showed ring forms of both Plasmodium falciparum and vivax. The total serum bilirubin concentration was 38 mg/dL with a conjugated fraction of 25.8 mg/dL. The serum concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were 2860 U/L 2225.06 U/L 498 IU/L (N: 225-450 IU/L), respectively. Prothrombin time was 20 sec (control: 12 sec). Serum electrolytes, renal function tests, and random blood sugar were normal. Serological test for viral hepatitis was positive for HAV-IgM: 0.9 (N # 0.4) and negative for hepatitis B, C, and E viruses. Serological tests for dengue and leptospirosis were negative.
Intravenous artesunate was started and a packed cell transfusion given for anemia. The child improved with an increase in appetite and a decrease in the icterus. Fever decreased gradually and the child was completely afebrile on the 10 th hospital day. In addition, the liver function tests and prothrombin time gradually improved and she was discharged on the 12 th hospital day.
The presence of highly elevated liver enzymes and deranged prothrombin time alerted us to the possibility of co-existent viral hepatitis. Fever with jaundice is common in both severe malaria and viral hepatitis. In severe malaria, occurrence of jaundice is related to severe hemolysis, hepatocellular damage, drug toxicity or a combination of above factors.  Presentation of acute viral hepatitis is similar, but with a few differences: Fever usually subsides with the appearance of jaundice and the period between onset of fever and jaundice is usually 1-7 days.  Serum aminotransferase levels are markedly elevated in viral hepatitis (8-10 times normal) as compared to in malarial hepatitis in which they are elevated 2-3 times the normal value and the ratio of AST/LDH is more than 4 in viral hepatitis.  Anemia and thrombocytopenia are more commonly seen in patients with severe malaria.  The coagulation profile is usually normal in malaria, even in patients with marked elevation of enzymes. An abnormal coagulation profile should alert one to an underlying infection with a hepatotropic virus or disseminated intravascular coagulation associated with sepsis.  Normally in cases of severe malaria with the onset of treatment, the fever spikes should come down by day 4-5 of illness. Serum bilirubin levels begin receding by 72 hr of starting treatment; however it may be delayed in patients having co-existing other infections,  as seen in our patient.
Thus, dual infections can present diagnostic dilemmas, severe complications, and prolonged course hence it is important that they are diagnosed early in the course of the disease.
| :: References|| |
|1.||Anand AC, Puri P. Jaundice in Malaria. J Gastroenterol Hepatol 2005;20:1322-32. [PUBMED] [FULLTEXT] |
|2.||Mishra D, Chaturvedi D, Mantan M. Typhoid fever and viral hepatitis. Indian J Pediatr 2008;75:509-10. [PUBMED] [FULLTEXT] |
|3.||Devarbhavi H, Alvares JF, Kumar KS. Severe falciparum malaria simulating fulminant hepatic failure. Mayo Clin Proc 2005;80:355-8. [PUBMED] [FULLTEXT] |
|4.||Bhalla A, Suri V, Singh V. Malarial hepatopathy. J Postgrad Med 2006;52:315-20. [PUBMED] |
|5.||Kochar DK, Agarwal P, Kochar SK, Jain R, Rawat N, Pokharna RK, et al. Hepatocyte dysfunction and hepatic encephalopathy in Plasmodium falciparum malaria. Q J Med 2003;96:505-12. |
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