A Study of chronic Hepatitis in northern India
Singh, D.S., Lecturer in Medicine, Jawaharlal Institute of Post-graduate Medical Education and Research, Pondicherry. Sama, S.K., Consultant Gastroenterologist, Sir Ganga Ram Hospital, New Delhi. and Singh, G., Senior Technician, Department of Gastroenterology, All-India Institute of Medical Sciences, New Delhi, India.
| Follow-up study showed that all the four cases (25 per cent) with persistent hepatitis recovered completely within one to one and half years. While 6 patients (37.5 per cent) with chronic aggressive hepatitis, chronic hepatitis of undetermined type and active cirrhosis of the liver ended fatally. Three of them died within six months of their illness. The remaining 6 cases (37.5 per cent) who survived had good response to steroid therapy. In 3 cases azathioprine in dosage of 100 mg per day was used in addition to steroid and supportive measures. Of the two hepatitis B antigen and antibody negative cases, one had chronic persistent hepatitis and recovered within 9 months whereas the other one developed active cirrhosis of the liver within two and half years. | Fig. 1:Liver from a case of chronic persistent hepatitisshowing mild degenerative changes, hypercellularity ofportal tract with mononuclear cells and well preservedlimiting plates x 10 |
Fig. 2:Liver histology from a patient of HBAg positivechronic aggressive hepatitis showing lobular andperiportal hepatitis, mononuclear cells infiltration of theportal tracts, disruption of limiting plates andpiecemeal necrosis of the hepatocytes x 200. |
DISCUSSION
The relationship between acute viral hepatitis, chronic hepatitis and cirrhosis liver has always been a controversial subject. Serial liver biopsy and autopsy data have shown progression from acute viral hepatitis to cirrhosis (Sherlock, 1948; Krarup and Roholm, 1941; Schaffer et al., 1967; Kunkel and Labby, 1950; and Sherlock, 1970). The main argument against such a possibility is the reports of follow-up studies of epidemic hepatitis and acute infectious hepatitis, which fail to show progression to chronic liver disease (Zieve et al., 1955; Neefe and Stokes, 1945; Chuttani et al., 1966). Past history of jaundice in patients of cirrhosis liver suggested the role of antecedent acute viral hepatitis in the aetiology of chronic liver disease. However, in the absence of definite serological and virological studies, it was not possible to document that the hepatitis was viral in aetiology. |
| Study of Australia antigen, an immunological marker of virus B antigen (HBAg), is a distinct advancement in the field of hepatology. The association of hepatitis B antigen with chronic hepatitis in ¾ cases observed in this study, very strongly suggests that majority of the cases of chronic active liver disease in India are due to virus B hepatitis. Past history suggestive of viral hepatitis in 50 per cent cases, history of injections or inoculations in 68.7 per cent and blood transfusion in 25 per cent in this study also support the etiological relationship between virus B hepatitis and chronic liver disease in tropics. Moreover, liver biopsy showed changes of hepatitis in all the patients. In the present series, serial liver biopsies showed progression from acute viral B hepatitis to active cirrhosis of the liver within four months to one and half years after the initial observation in 3 cases (Plate CXXXIX, Fig. 3). |
Fig. 3:Second liver biopsy 4 months after the first biopsyfrom a patient of HBAg positive chronic aggressivehepatitis showing well formed pseudolobules, thickfibrous band with active liver cell necrosis anddegeneration. These findings are typical of cirrhosis ofliver with chronic hepatitis x 100. |
There are some differences between HBAg positive chronic hepatitis seen in the present study in Delhi and autoimmune chronic active hepatitis reported from the West. Hepatitis B antigen (HBAg) positive chronic liver disease is common in males of older age group, often have acute onset like viral hepatitis, and the systemic manifestations, auto-antibodies and extreme hypergamma-globulinaemia are rare. Similar observations have been made by Sherlock (1972); Wright (1970), Hadziyannis (1970); Bulkley (1970); Finalyson et al. (1972); Vischer (1970) and Grob et al. (1971). However, Bianchi et al. (1972) from Italy observed no significant difference between HBAg positive and negative chronic active hepatitis.
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