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Tandon BN, Krishnamurthy L, Koshy A, et al. Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. Gastroenterology. 1977;72(3):488-94
Tandon, B. N., Krishnamurthy, L., Koshy, A., Tandon, H. D., Ramalingaswami, V., Bhandari, J. R., Mathur, M. M., & Mathur, P. D. (1977). Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. Gastroenterology, 72(3), 488-94.
Tandon, B N, et al. "Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India." Gastroenterology vol. 72,3 (1977): 488-94.
Tandon BN, Krishnamurthy L, Koshy A, Tandon HD, Ramalingaswami V, Bhandari JR, Mathur MM, Mathur PD. Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India. Gastroenterology. 1977 Mar;72(3):488-94. PMID: 832797.
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Elsevier Science

Gastroenterology. 1977 Mar;72(3):488-94.

Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India.

Gastroenterology

B N Tandon, L Krishnamurthy, A Koshy, H D Tandon, V Ramalingaswami, J R Bhandari, M M Mathur, P D Mathur

PMID: 832797

Abstract

An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.

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