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KHUROO MS, SALEEM M, TELI MR & SOFI MA. FAILURE TO DETECT CHRONIC LIVER DISEASE AFTER EPIDEMIC NON-A, NON-B HEPATITIS. LANCET 1980; ii (8185):97-98.

By : KHUROO MS, SALEEM M, TELI MR & SOFI MA.         Dated : 12/11/2017

KHUROO MS, SALEEM M, TELI MR & SOFI MA. FAILURE TO DETECT CHRONIC LIVER DISEASE AFTER EPIDEMIC NON-A, NON-B HEPATITIS.  LANCET 1980; ii (8185):97-98. PMID: 6105287

A waterborne epidemic of non-A, non-B hepatitis occurred in the Kashmir valley between November, 1978, and April, 1979.1 From January to March, 1980, the cases recorded during this epidemic were assessed for evidence of chronic liver disease. Four villages in which 102 cases of viral hepatitis had been recorded were surveyed. 4 patients died in the first two weeks of their illness with fulminant hepatic failure. None of the others had since died. One patient was positive for HBsAg, and liver biopsy in this patient 7 months after the infection showed features of chronic active hepatitis and cirrhosis. This patient was excluded from the study. 15 patients were not available for assessment at the time of survey.

The remaining 82 patients were interviewed and given a detailed physical examination. Blood was drawn for estimation of serum bilirubin, serum glutamic pyruvic transaminase (SGPT), and HBsAg. The illness in these patients had lasted from 5 days to 3 months (mean 29 days). The present assessment was done 8 to 17 months after the original illness (mean 14.8 months). None of the patients had persistent jaundice, ascites, or hepatic encephalopathy. 16 (19.5%) had recurrent mild abdominal pain, 11 (13.5%) had lost weight; 8 (9.8%) had anorexia, and 6 occasionally had dark urine. 3 patients had had a second distinct episode of jaundice after recovery from the original illness. 6 patients (7%) had soft palpable hepatomegaly, and in 5 (6 %) the spleen was palpable below the costal margin. Serum bilirubin was below 1 mg/dl in all cases. SGPT levels were within normal limits in 78 cases, in 4 cases SGOT levels were above the upper limit of normal (35, 42, 45, and 50 IU/l). Liver biopsy was not done in any of the cases.

In addition, 30 patients who had had acute viral hepatitis from this epidemic were followed up 2 to 6 months from the onset of their disease by serial liver function tests. In all cases serum bilirubin and serum enzymes returned to normal after a variable interval.

Evidence of chronic liver disease was lacking in most of our patients. Various abdominal complaints and palpable liver and spleen can occur after acute viral hepatitis in the presence of normal liver histology and were seen nearly the same percentage in healthy contacts.2 None of the patients in the present study had chronic or recurrent jaundice or raised serum bilirubin in one-year follow-up. 4 had raised SGPT levels and could have developed chronic liver disease.  However, none had symptoms or abnormal physical findings, and in none was SGPT raised to twice the upper limit of normal. We decided not to do liver biopsies in these cases. Liver functions, especially serum hepatic enzymes, can fluctuate in chronic liver disease,3 and a single estimation of liver-function tests could have overlooked chronic liver disease in some of our cases. This possibility was excluded, because 30 patients with acute non-A, non-B hepatitis followed prospectively had no residual abnormality of liver function on repeated testing.

Non-A, non-B hepatitis was first described after blood transfusion,4 and chronic liver disease followed in a high percentage of cases.3,5,6 We, however, failed to detect chronic liver disease after acute non-parentally transmitted non-A, non-B hepatitis. The reason for this is not clear, but possible explanation are the large amount of viral protein administered during transfusion or, perhaps more importantly, the existence of at least two non-A, non-B viral agents, one of which is more commonly associated with post-transfusion hepatitis as well as an unusual tendency to be associated with the development of chronic liver disease.