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.

A clinical syndrome of chronic hepatocellular dysfunction has been recognised recently by the term ‘Chronic Active Hepatitis’. The clinical picture consists of progressive liver cell failure with high serum transaminase levels, raised serum gamma globulin and sometimes a positive LE cell phenomenon. Clinical features might also include arthralgia and amenorrhoea, in addition to features of liver-cell dysfunction. Sometimes the picture resembles the state of acute or recurrent icteric hepatitis. The patients are often young women but the condition can occur at all ages and immunological components like Hashimoto’s disease or ulcerative colitis may be associated.

Clinical reports of such cases have been published as early as 1948 from Australia in the name of ‘Lupoid Hepatitis’ and subsequently from various parts of the globe in different confusing names like ‘Cholangiotic Hepatitis’, ‘Juvenile Cirrhosis’, etc., all signifying a state of chronic hepatitis. There was great confusion amongst clinical and pathological descriptions of such varied entities of chronic hepatitis.

In order to avoid the unqualified term ‘chronic hepatitis’ a more precise and histopathological classification of such disorders had been agreed upon in the meeting of the European Association for the Study of Liver held in Zurich in 1968; and two histological types namely ‘Chronic Persistent Hepatitis’ and ‘Chronic Aggressive Hepatitis’ have been described.

The details of this classification are described by De Groote et al (1968). However it has been pointed out clearly that the cases of the former group have a good prognosis and the latter group remains active (Chronic Active Hepatitis) with a bad prognosis and inevitably leads to cirrhosis.

Our present report deals with 10 such cases of ‘Chronic Active Hepatitis’ diagnosed, investigated, and followed up in our liver clinic during the last two years. Three of these cases on conventional therapy including steroids died within a year and are taken as controls, the remaining seven were treated with Liv.52, an indigenous drug containing Capparis spinosa, Cichorium intybus, Solanum nigrum, Cassia occidentalis, Terminalia arjuna, Achillea millefolium, Tamarix gallica.

OBSERVATIONS

A total of 10 cases of both sexes were diagnosed. The clinical picture was not identical and varied presentations were noted but all had histopathological picture of chronic aggressive hepatitis.

It will be noted from Table 1 that some had presentation like acute icteric hepatitis; others had vague complaints or gross manifestation of hepatocellular dysfunction like ascites, gastro-intestinal tract haemorrhage, etc. In some other cases immediate operative procedures under general anaesthesia have been found to present the clinical state.

Table 1: Summary of Clinical Observations
Case No.			Age Sex	Onset	Progress		Duration of treatment	Biopsy Findings		Results
A At the beginning of treatment											B At the end of treatment
A. CONTROL GROUP :
1.	A.N.		18 M	With jaundice and fever	Remission and relapses of jaundice — 3 times in 13 months. Finally hepatic coma.		13 months	Picture of icteric hepatitis superimposed on Aggressive Hepatitis	Icteric hepatitis + septal formation and cirrhotic changes.	Expired
2.	T.S.		42 M	Flatulent dyspepsia followed by oedema of leg and pyreixa.	Ascites - Massive G.I.T Hge. and death at the end of 10 months.		10 months	Picture of chronic Aggressive Hepatitis.	Picture of hepatic cirrhosis.	Expired
3.	B.D.		38 F	Following Hysterectomy she developed ascites after 2 months.	Later got joint pain, gum bleeding and ascites became refractory to treatment. Finally expired after1 year following hepatic coma.		1 year	Picture of chronic Aggressive Hepatitis.	Picture of hepatic cirrhosis.	Expired.
B. DRUG TREATED GROUP:
4.		S.M.	42 M	Intermittent pyrexia and vague abdominal pain, following appendicetomy 1 year back.	Later developed ascites, spiers and joint pain.		2 years	Picture of chronic Aggressive Hepatitis	Improved	Improved No ascites at present
5.		J.G.	46 M	Vague abdominal pain and an occasional pyrexia.	Later developed ascites and jaundice		2 years	Picture of chronic Aggressive Hepatitis	Improved	No jaundice
6.		P.S.	38 F	— do —	Later developed jaundice and gum bleeding and occasional pyrexia.		2 years	— do —	— do —	Improved No jaundice No fever
7.		I.S.	52 F	Int. pyrexia and joint pain.	Later developed ascites		18 months	— do —	— do —	Improved No fever No ascites
8.		M.P.	36 M	Vague abdominal pain and pyrexia and joint pain	Later developed gum bleeding epigastric pain.		18 months	— do —	— do —	Improved No pain No fever & joint pain.
9.		B.D.	28 F	Jaundice 2 months with fever	Jaundice disappeared. Vague abdominal pain – later developed ascites, shoulder + joint pain.		2 years	Picture of chronic Aggressive Hepatitis superimposed on acute icteric hepatitis	— do —	Improved No jaundice No ascites Pain less.
10.		S.M.	40 F	Jaundice 3 months with int. pyrexia.	Jaundice relieved but abdominal pain remained. Later developed joint pain, oedema feet and int. pyrexia reappeared.		18 months	— do —	— do —	Improved No jaundice No joint pain and fever.

The activity of the disease was diagnosed clinically by the presence of intermittent pyrexia, joint pains, ascites, jaundice, etc.

As our experience with such chronic hepatocellular disorders without an obvious histological picture of cirrhosis was limited, the scope of therapy was unpredictable. Three of these cases, treated with various drugs including steroids, died within one year of diagnosis by developing florid features of hepatic cirrhosis confirmed histologically. We treated the remaining seven cases with an Indian indigenous drug Liv.52 (2 tablets t.i.d.) noted for its effect on preventing damage of liver cells and helping in hepatic regeneration. In these seven cases the disease seemed to be arrested and death has been averted, as far as the results of a two-year follow-up show. Further, there is definite evidence of biochemical and histological improvement of liver function as will be presented. The previous three cases which resulted in death are taken as the ‘control’ group and are compared with the seven cases treated with Liv.52 as the ‘drug-treated’ group.

BIOCHEMICAL RESULTS

Various liver function tests like serum bilirubin, serum protein electrophoresis, alkaline phosphatase, SGOT and Standard BSP (45 mt) tests were performed in all the cases at the time of diagnosis and then at six months’ interval during the follow-up period or as often as possible. Serum bilirubin levels were not always found to be raised in all cases except in cases presenting a picture of acute icteric hepatitis or in those three with progressing damage of liver cells. Details are shown in Fig. 2.

Serum albumin level was low in all cases and persistently low in cases with a bad prognosis. Albumin level increased with improvement of the clinical condition (Fig.3). Of the different fractions of globulin, Y (gamma) globulin showed elevation in all the cases and remained elevated for a long time with the activity of the disease. Gradual decrease of Y (gamma) globulin was noted in one case with good clinical response (Fig.4). Other fractions like (alpha one), (alpha two) and (Beta) globulins had no overall alteration from normal values. The details of each fraction determined at different intervals of the diseases in each patient have been shown in Table II. Y (gamma) globulin results are also represented graphically in Fig. 5. Alkaline phosphatase values were insufficient and details of BSP are shown in Fig.6.

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