Chronic Active Hepatitis
Dasgupta, M., M.D. (Cal.), Hon. Deputy Visiting Physician, Dept. of Medicine and Prof. Mukerjee, A.B., M.D. (Cal.), F.R.C.P. (Lond.), Head of the Department of Medicine R.K. Mission Seva Pratisthan, Calcutta, India.
HISTOLOGICAL RESULTS
The diagnosis was confirmed in each case by needle biopsy of the liver. The essential features noted at the time of diagnosis were chronic inflammatory infiltration into the portal tracts extending to the parenchyma with piecemeal necrosis of liver cells and early formation of inter-lobular septa, best observed by reticulin preparations. Architectural distortion and necrosis of liver cells were not associated with nodular regeneration of liver cells - a distinctive feature that isolates this condition histologically, from cirrhosis. Liver cells were swollen and pale stained, and were arranged in small cylindrical groups some of which surrounded a lumen in rosette formation. There were many plasma cells in some of the sections heavily infiltrated with mononuclear cells. Bile ductules were also proliferated (atypical) at places. The combination of piecemeal necrosis, inflammatory infiltration and reactive proliferation of bile ductules constituted the histological evidence of ‘activity’. Histological evidences of acute icteric hepatitis were also present on top of the above changes described in three of the cases
In the control group the post-treatment biopsies showed progress of liver cell damage and destruction of architecture with progress towards florid cirrhosis In cases treated with the drug, post-treatment biopsies taken at the end of one-and-a-half to two years showed disappearance of piecemeal necrosis of liver cells, evidence of hepatic cell regeneration and arrest of progressive hepatic architectural collapse
DISCUSSION
The syndrome of Active Chronic Hepatitis can occur at any age and sex as will be evident from the report. Previously it was believed that such disorders were preponderant amongst young females (Read et al 1963); but, other reports support our view (Mackay et al 1961, Ichida et al 1965). There was no definite etiological factor observed in our cases. But acute icteric hepatitis has been noticed to initiate the process in three of our cases. Similar occurrence has been pointed out by Schaffner et al 1967. Recent history of operative procedures under general anaesthesia was present in two of our cases and probably presents in two of our cases and probably presents a mode of initiation of hepato-cellular injury by anaesthetic agents. Some others presented with ascites or GIT haemorrhage, etc. No definite mode of presentation was found to be common. Intermittent pyrexia was an important feature in all the cases beside other clinical features of hepatocellular dysfunctions like jaundice, ascites, splenomegaly, GIT haemorrhage, etc. Positive LE cell phenomenon, joint pain, plasma cell infiltration suggested an immunological background in four other cases. This has also been detected by other workers like Mackay (1961) and Scheuer (1968).
Low albumin levels, elevated Y (gamma) globulin and SGOT and BSP values presented an overall picture of a severe degree of hepatocellular dysfunction in all the cases and served as a good diagnostic index in conjunction with the clinical features. Significant improvement of albumin, SGOT, BSP, globulin values occurred at the end of about two years in the seven cases with drug treatment. Deterioration of these functions was observed in the three cases of the control group with death within one year in all three of them.
The liver function tests, therefore, were a good index of the histological picture. Piecemeal necros’s of the liver cells without any nodular regeneration served as one of the main histological features which determines the clinical course. It also leads to lobular distortion, sometimes not evident in H + E preparation but is clear in Reticulin preparation . Distortion of such architecture leads to cirrhosis in the end stage, which is also evident in the three control cases.
Measure of the rate of progress of the lesion known as ‘activity’ is determined histologically by a combination of piecemeal necrosis, inflammatory infiltration and other reactive proliferation of bile ductules (Popper et al 1965).
The overall prognosis is bad. Corticosteroids have been tried and a recent clinical report from London by Cook et al (1970) showed good response with steroids in 22 out of 49 patients followed up for a six year period. 15 among the 27 in the control group died in the same period. Overall significant improvement was noticed in two-three years. The results of Liv.52 treatment in seven treated cases out of the 10 cases observed, showed significant improvement.
Another recent report from MAYO Clinic, (1970) showed the clinical response to with steroids, azothioprine and placebo varying period of three months to three years. Among 15 prednisolone-treated cases there were no deaths. Of the 13 cases treated with azothioprine, four died and amongst 14 control-patients, one died. They focused attention on the prednisolone-treated cases with significant advantages and improvement of liver function tests but the therapeutic efficacy of azothioprine alone in this disorder was evidently suspect.
CONCLUSIONS
Treatment with Liv.52 in our series of Chronic Active Hepatitis cases had good clinical response with improvement of liver function tests done at the end of one and a half years to two years. Histological evidence of improved piecemeal necrosis and arrest of progress of lobular distortion was also evident in these cases.
Evidently, the indigenous drug Liv.52 can produce an identically favourable response as obtained with the conventional steroids minus the attendant hazards and disadvantages of steroid therapy.
The response to Liv.52 was uniformly good as judged by clinical, biochemical and histological criteria; most noticeable was the arrest of the progress of the activity of Chronic Active Hepatitis towards cirrhosis observed during the two-year period of treatment and investigations. A further study of this promising drug in Chronic Active Hepatitis is, therefore, suggested.
SUMMARY
A total number of 10 cases of Chronic Active Hepatitis have been observed for a period varying from 10 months to two years. From clinical biochemical and histological standpoints two of the cases progressed to cirrhosis and died within one year after receiving conventional treatment but the 7 cases which were put on Liv.52 alone (2 tablets t.i.d.) survived with better clinical, biochemical and histological improvement of liver functions.
ACKNOWLEDGEMENT
We are grateful to Swami Gahananandaji, Secretary, R.K. Mission Seva Pratisthan for his kind permission to utilise the hospital records and to M/s. The Himalaya Drug Co., Bombay, for their generous help in the study of the cases by supplying drugs and B.S.P. dyes.
REFERENCES
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Refference: http://www.himalayahealthcare.com/pdf_files/liv208.pdf
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