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Profile of hepatocellular carcinoma in India: An insight into the possible etiologic associations
Author(s) -
Sarin Shiv Kumar,
Thakur Varsha,
Guptan Rajkumar C,
Saigal Sanjeev,
Malhotra Veena,
Thyagarajan Sadras P,
Das Bhudev C
Publication year - 2001
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2001.02476.x
Subject(s) - hepatocellular carcinoma , medicine , hbsag , hepatitis b virus , hbeag , cirrhosis , hepatitis b , hepatitis c virus , gastroenterology , virology , virus , immunology
Background: Several etiologic factors including hepatitis viruses, alcohol and aflatoxin have been implicated in the pathogenesis of hepatocellular carcinoma (HCC). There is, however, limited information from the Indian subcontinent. Methods: Seventy‐four consecutive cases of HCC were studied. A detailed history, tests for hepatitis B virus (HBV; HBsAg, HBeAg, anti‐HBe, IgG anti‐HBc, anti‐HBs and HBV‐DNA), hepatitis C virus (HCV; anti‐HCV and HCV‐RNA) infection, liver histopathology and HBV‐DNA integration by using Southern blot hybridization were studied. A p53 gene mutation was also studied by using PCR and single‐strand conformation polymorphism. Results: Hepatocellular carcinoma patients were predominantly males (mean age 49.5 ± 14.0 years). Portal hypertension and cirrhosis were seen in 56 (76%) patients, more often ( P < 0.05) in viral marker positive cases. Forty‐five percent of patients had features of hepatic decompensation at presentation. Evidence of HBV infection was present in 53 (71%) patients. Twenty‐six (49%) of these patients had either HBeAg + ve, HBV‐DNA + ve ( n = 12), or HBsAg – ve, HBV‐DNA + ve ( n = 14) forms of HBV infection. Hepatitis B virus DNA integration in the liver tissue was seen in 10 of 17 (59%) patients. Infection with HCV alone was detected in three (4%) and dual HBV and HCV infection in six (8%) patients. A majority (78.5%) of the chronic alcoholics had associated viral infection. The etiology of HCC remained undetermined in 15 (20%) patients. The p53 gene mutations were detected only in three of 21 (14%) liver tissues. Aflatoxin toxicity, oral contraceptive use or metabolic disorder were not seen. Conclusions: In India: (i) HBV infection is the predominant factor for the development of HCC, often related to mutant forms of HBV; (ii) a majority of the HCC patients have overt cirrhosis of the liver; and (iii) HCV and alcohol per se are uncommonly associated.