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.
ABSTRACT
Clinical, biochemical, immunological and morphological features of 16 patients of chronic hepatitis are reported. All the patients presented with persistent/progressive or recurrent hyperbilirubinaemia of more than 12 weeks. Hepatocellular failure with or without signs of portal hypertension, bleeding tendency and hepatic encephalopathy were other important clinical presentations. Serum alkaline phosphatase over 30 KAU was present in about one third of the patients. Study for hepatitis B antigen (HBAg) was positive in three fourth of the cases. Differences between HBAg positive chronic hepatitis observed in the present study and chronic active hepatitis described from the West have been highlighted. On the basis of morphological findings patients were categorised into portal and lobular hepatitis (4 cases), periportal and lobular (3 cases), chronic hepatitis undetermined type (2 cases) and cirrhosis of the liver with activity (7 cases). Progression from chronic hepatitis to cirrhosis of liver was documented by serial liver biopsies in 3 cases within 4 months to one and a half year after initial illness. The disease had an overall mortality of 37.5 per cent with poor response to steroid therapy.
INTRODUCTION
Chronic hepatitis is defined as persistent or progressive liver disease characterised by clinical, biochemical and morphological evidences of hepatic dysfunction of more than three months duration (Mistilis and Blackburn, 1967; Sherlock, 1972; Murray Lyon et al., 1973). Chronic hepatitis is of two types: chronic persistent hepatitis and chronic aggressive (active) hepatitis. Chronic persistent hepatitis is a benign condition characterised by malaise, fluctuating transaminase levels and portal hepatitis on histology. Chronic aggressive hepatitis, on the other hand, is a more serious disease with progression to cirrhosis liver in more than 50 per cent cases within 5 years. There is marked derangement of liver functions and periportal hepatitis with or without lobular hepatitis on histology. When systemic manifestations like acne, skin rashes, ulcerative colitis and Sjogren syndrome are present the term ‘chronic active hepatitis’ is used. In the absence of such manifestations the condition is called chronic persistent hepatitis. The object of the present study was to characterise the clinical, biochemical, immunological, morphologic features and natural history of chronic hepatitis as seen in northern India and to study its association with hepatitis B antigen.
MATERIAL AND METHODS
Sixteen patients presenting with persistent/progressive hepatocellular (non-surgical) jaundice of more than 12 weeks were taken up for the present study. All the cases were admitted to All-India Institute of Medical Sciences (A.I.I.M.S.) Hospital during July 1971 to December, 1973. Detailed clinical, biochemical and immunological study was done and recorded on a pre-planned proforma. Follow-up record was maintained in the liver clinic of the Department of Gastroenterology.
Standard techniques were used for routine haematological and biochemical tests. Serum transaminases were estimated by the method of Reitman and Frankel (1957).
Australia antigen and antibody were studied by agar gel diffusion (AGD) counterelectrophoresis (CEP) and sandwich solid phase radio immunoassay (RIA), employing the techniques described by Blumberg et al. (1970); Pesendorfer et al. (1970); and Walsh et al. (1970) respectively. Test for LE cell was done in all the cases. Antinuclear factor was tested by immunofluorescence technique (Holborrow, 1970). Aspiration liver biopsy was carried out using Klatskin aspiration needle. Haematoxylin, eosin and reticulin staining were used for detailed morphological study. The histological criteria described by Degroote et al. (1968) were employed for the diagnosis of chronic hepatitis.
Age and sex distribution: There were 12 males and 4 females. Age at the onset of the disease varied from 28 years to 73 years. The disease was observed after the age of 50 in 8 cases. The onset of illness was abrupt resembling acute viral hepatitis in 6 cases, while in the remaining 10 cases the onset was insidious.
Clinical features: Varying degree of clinical icterus was present in all the cases. Other important clinical features were hepatomegaly, splenomegaly, ascites, bleeding tendency spider angiomas and encephalopathy (Table I).
| Table I: Clinical features at the onset and during the course of illness > | ||||||
|
Clinical features* |
Percentage |
||||
Jaundice |
Persistent |
11 |
70 |
|||
Recurrent |
5 |
30 |
||||
Palpable liver |
11 |
66.6 |
||||
Splenomegaly |
12 |
63.3 |
||||
Ascites |
8 |
56.6 |
||||
Bleeding tendency |
7 |
36.6 |
||||
Hepatic coma |
6 |
40.0 |
||||
Spider angioma |
4 |
33.3 |
||||
Palmar erythema |
3 |
30.0 |
||||
Fever |
3 |
40.0 |
||||
Chronic diarrhoea |
2 |
16.6 |
||||
* Total No. of cases = 16 |
||||||
Past history of jaundice was recorded in 8 patients, history of injections in 11, blood transfusion in 4 and surgical interference in two cases. Hepatitis B antigen was positive in 6 cases who had past history of jaundice, 7 with history of injections and two each with history of blood transfusions and surgical interference.
History of Diabetes Mellitus was present in 2 patients and pulmonary tuberculosis in one case. Both the diabetic patients gave history of having taken oral hypoglycaemic drugs. The case of pulmonary tuberculosis was on anti-tubercular treatment viz. streptomycin and isonicotinic acid hydrazide. Hepatitis B antigen was positive in one of the patients of Diabetes Mellitus and also in the patient of pulmonary tuberculosis.
The biochemical profile is presented in Table II, which shows the mean value at the onset as well as the highest and lowest values during the course of the disease. Varying degree of hyperbilirubinaemia was noted in all the cases (over 20 mg. per cent during the peak period in 3 cases), Hypoalbuminaemia of less than 2.7 g per cent was noted during the course of the illness in 4 cases only. Serum globulin of more than 3.1 g per cent was observed in three fourth of the cases, but extreme degree of hyperglobulinaemia (serum globulin over 6.0 g per cent) was not seen in any of the patients. Serum transaminases were significantly elevated in all the cases at the onset of the illness which persisted in two thirds of them during the course of the disease. Mean highest value of alkaline phosphatase during the course of the illness was 31.85 KAU, being more than 30 KAU, in 6 patients.
Table II: Results of conventional liver function tests |
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|
At onset |
During course of disease |
|||||||
No. of patients |
Mean value |
No. of patients |
Mean highest figure |
Mean lowestfigure |
|||||
Total serum bilirubin (mg%) |
16 |
6.35 |
16 |
8.75 |
2.46 |
||||
Serum albumin (g%) |
16 |
3.13 |
16 |
4.17 |
3.95 |
||||
Serum globulin (g%) |
16 |
3.58 |
16 |
3.62 |
3.16 |
||||
Serum alkaline phosphatase (KAU) |
16 |
22.26 |
16 |
31.85 |
15.81 |
||||
Results of Australia antigen study are shown in Table III. Persistent antigenaemia (HBAg beyond 14 weeks) was present in 10 cases and transient antigenaemia in 2 patients. Two cases were positive for antibody to HBAg. Hepatitis antigen was negative by the most sensitive techniques in the remaining four cases. Results of subtyping of antigen showed ayw subtype in 6 cases and adw in the remaining 3 cases. Antinuclear factor was positive in only 2 cases. Of which one was positive for HBAg as well. Test for LE cell was negative in all the cases. Histology of the liver showed features of chronic portal and lobular hepatitis (Plate CXXXVII, Fig. 1) in 4 cases; chronic periportal and lobular hepatitis (Plate CXXXVIII, Fig. 2) in 3 cases and active cirrhosis of the liver (Plate CXXXIX, Fig. 3) in 7 cases. In 2 cases it was difficult to categorise the hepatic lesions to any definite group (Table IV).
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Refference: http://www.himalayahealthcare.com/pdf_files/liv228.pdf
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