[The significance of anti-HBc and occult hepatitis B virus infection in the occurrence of hepatocellular carcinoma in patients with HBsAg and anti-HCV negative alcoholic cirrhosis].

BACKGROUND/AIMS: Alcohol and the hepatitis B virus (HBV) exert synergistic effects in hepatocelluar carcinogenesis. We aimed to elucidate the clinical significance of the antibody to hepatitis B core antigen (anti-HBc) and occult HBV infection on the development of hepatocellular carcinoma (HCC) in patients with alcoholic liver cirrhosis (LC). METHODS: Patients with alcoholic LC alone (n=193) or combined with HCC (n=36), who did not have HBsAg or antibody to hepatitis C virus were enrolled. Clinical data and laboratory data including anti-HBc were investigated at enrollment. The polymerase chain reaction was applied to HBV DNA using sera of patients with HCC or LC after age and sex matching. RESULTS: Patients with HCC were older (60+/-11 years vs. 53+/-10 years, mean+/-SD, P<0.001), more likely to be male (100% vs. 89%, P=0.03), and had a higher positive rate of anti-HBc (91.2% vs. 77.3%, P=0.067), and a higher alcohol intake (739+/-448 kg vs. 603+/-409 kg, P=0.076) than those with LC. Age was the only significant risk factor for HCC revealed by multiple logistic regression analysis (odds ratio, 1.056; P=0.003). The positive rate of anti-HBc and alcohol intake did not differ in age- and sex-matched subjects between the LC (n=32) and HCC (n=31) groups. However, the detection rate of serum HBV DNA was higher in the HCC group (48.4%) than in the LC group (0%, P<0.001). CONCLUSIONS: Anti-HBc positivity is not a risk factor for HCC. However, occult HBV infection may be a risk factor for HCC in patients with alcoholic LC.

[A comparative cross-sectional study of the development of hepatocellular carcinoma in patients with liver cirrhosis caused by hepatitis B virus, alcohol, or combination of hepatitis b virus and alcohol].

BACKGROUND/AIMS: Alcohol may be a cocarcinogen in patients with chronic viral hepatitis. We investigated the effect of alcohol on the development of hepatocellular carcinoma (HCC) in liver cirrhosis (LC) caused by hepatitis B virus (HBV). METHODS: All patients with LC or HCC associated with HBV or alcohol, admitted between March 2001 and June 2005, were included. Patients were divided into three groups according to the etiology of LC: Alcohol (AL), HBV, or HBV alcohol (HBV AL). Age and laboratory data at the enrollment of study were analyzed. The logistic regression coefficiency for the prevalence of HCC was calculated by using variables such as age, gender, serologic markers, and etiology of LC. RESULTS: In LC patients (n=342), the proportions of AL, HBV, and HBV AL groups were 44%, 39%, and 17%, respectively. The proportions of HCC in AL, HBV and HBV AL groups were 17%, 55%, and 76%, respectively. Age at the diagnosis of HCC was younger in HBV AL than in AL group (p=0.036). In logistic regression analysis for the risk factor of HCC, odds ratio of age was 1.056 (p0.001). Odds ratios of HBV and HBV AL group comparing AL were 8.449 (p0.001) and 17.609 (p0.001), respectively. Therefore, old age and chronic alcohol intake in patients with HBsAg were the risk factors of HCC. CONCLUSIONS: Chronic alcohol intake may be an additive factor for the development of HCC in patient with LC caused by HBV. However, a prospective cohort study is needed to confirm these findings.

[A case of colon obstruction developed during the recovery period of acute pancreatitis].

Complications of acute pancreatitis usually occur in pancreas and its contiguous organs. The prevalence of colonic invasion is rare, however, the consequence is fatal, with mortality above 50%. The initial symptoms and onset times are variable and major affected sites are transverse colon and splenic flexure. The spread of inflammatory exudates into the colon is the main mechanism of colonic invasion. If the colonic stenosis develops, it is necessary to manage it surgically. We report a case who arrived at the hospital with watery diarrhea and abdominal distension in the recovery period of acute alcoholic pancreatitis and was diagnosed as a colonic obstruction in the splenic flexure. The patient underwent loop ileostomy instead of the resection of the lesion because of severe adhesion around the splenic flexure. The patient died due to sepsis 5 days after the operation.