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National Medical Journal of India

Malarial hepatitis: a heterogeneous syndrome?

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
A C Anand
C Ramji
A S Narula
W Singh

Atslēgvārdi

Abstrakts

BACKGROUND

The incidence of malarial hepatitis in patients with Plasmodium falciparum infection and jaundice is not known and it is not clear whether the condition is a single entity or a heterogeneous syndrome.

METHODS

We prospectively studied the natural history of all patients with falciparum malaria and jaundice admitted to military hospitals in Northeast India from 1988 to 1991. A possible drug or viral cause for the hepatitis was excluded by the history, serological tests and liver histology.

RESULTS

Of the 732 patients admitted with falciparum malaria, 39 had jaundice but only 18 had malarial hepatitis indicated by a rise in their serum glutamate pyruvate transaminase levels to more than three times the upper limit of normal and an absence of clinical or serological evidence to suggest drug or viral hepatitis. The liver in these patients was always enlarged. Their mean age was 27.6 years and 85% were males. The mean serum bilirubin was 12.7 +/- 10.3 mg/dl, serum glutamate oxaloacetate transaminase was 212.8 +/- 144.9 IU, serum glutamate pyruvate transaminase was 287.1 +/- 206.2 IU and the serum alkaline phosphatase was 20.4 +/- 10.1 KA. Clinically, 2 groups of patients were seen. Thirteen patients who presented with a severe form of disease had coma, deep jaundice and renal failure. The other 5 patients had a relatively mild illness with only fever, headache and vomiting for 2 days. Four patients with severe disease died. Liver histology (studied in 5 patients) showed Kupffer cell hyperplasia and deposition of malarial pigment. Plasmodium falciparum was demonstrated in sinusoidal red blood cells in only 2 cases.

CONCLUSIONS

Malarial hepatitis occurred in 18 out of 39 patients with jaundice and falciparum malaria. It is a heterogeneous syndrome with at least two clinical subsets and the severe disease should not be mistaken for fulminant hepatic failure as there is a better response to therapy.

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