Hepatocellular carcinoma (HCC) makes up 75%-85% of all primary liver cancers and is the fourth most common cause of cancer related death worldwide. Chronic liver disease is the most significant risk factor for HCC with 80%-90% of new cases occurring in the background of cirrhosis. Studies have shown that early diagnosis of HCC through surveillance programs improve prognosis and availability of curative therapies. All patients with cirrhosis and high-risk hepatitis B patients are at risk for HCC and should undergo surveillance. The recommended surveillance modality is abdominal ultrasound (US) given that it is cost effective and noninvasive with good sensitivity. However, US is limited in obese patients and those with non-alcoholic fatty liver disease (NAFLD). With the current obesity epidemic and rise in the prevalence of NAFLD, abdominal computed tomography or magnetic resonance imaging may be indicated as the primary screening modality in these patients. The addition of alpha-fetoprotein to a surveillance regimen is thought to improve the sensitivity of HCC detection. Further investigation of serum biomarkers is needed. Semiannual screening is the suggested surveillance interval. Surveillance for HCC is underutilized and low adherence disproportionately affects certain demographics such as non-Caucasian race and low socioeconomic status.
In spite of significant advancement in HCC management, its incidence continues to rise. There remains an urgent need to continue refining understanding of HCC and develop strategies to increase utilization of the available preventive measures and curative treatment modalities for HCC.
Summary Alcoholic cirrhotics evaluated for liver transplantation are frequently malnourished or obese. We analyzed alcoholic cirrhotics undergoing transplantation to examine time trends of nutrition/weight, transplant outcome, and effects of concomitant hepatitis C virus (HCV) and/or hepatocellular carcinoma (HCC). Nutrition and transplant outcomes were reviewed for alcoholic cirrhosis with/without HCV/HCC. Malnutrition was defined by subjective global assessment. Body mass index (BMI) classified obesity. A total of 261 patients receiving transplants were separated (1988–2000, 2001–2006, and 2007–2011) to generate similar size cohorts. Mean BMI for the whole cohort was 28 ± 6 with 68% classified as overweight/obese. Mean BMI did not vary among cohorts and was not affected by HCV/HCC. While prevalence of malnutrition did not vary among cohorts, it was lower in patients with HCV/HCC (P < 0.01). One-year graft/patient survival was 90% and not impacted by time period, HCV/HCC, or malnutrition after adjusting for demographics and model end-stage liver disease (MELD). Alcoholic cirrhotics undergoing transplantation are malnourished yet frequently overweight/obese. Among patients selected for transplantation, 1-year post-transplant graft/patient survival is excellent, have not changed over time, and do not vary by nutrition/BMI. Our findings support feasibility of liver transplantation for alcoholic cirrhotics with obesity and malnutrition.
Background and Aim Auto-immune (AI) markers are reported in patients with steatohepatitis liver disease. However, their clinical significance is unclear. Methods Charts of patients due to alcohol (ALD) or non-alcoholic fatty liver disease (NAFLD) were stratified for anti-nuclear antigen (ANA>1:80), anti-smooth muscle antibody (ASMA>1:40), or anti-mitochondrial antibody (AMA>1:20). Study outcomes were patient survival and complications of liver disease. Results Of 607 patients (401 NAFLD), AI markers were available in 398 (mean age 50 ±15 y; 52% males; median body mass index (BMI) 38; 44% diabetic; 62% Nonalcoholic steatohepatitis (NASH) as type of Steatohepatitis; median MELD score 9). A total of 78 (19.6%) patients were positive for AI markers without differences for ALD vs. NAFLD, cirrhosis vs. no cirrhosis, and NASH vs. no NASH. There were no differences for age; gender; BMI; cirrhosis at presentation; MELD score; endoscopic findings; and histology based on AI markers. Serum ALT was higher among patients with AI markers (65±46 vs. 59±66 IU/l; P=0.048). Data remained unchanged on analyzing NAFLD patients. None of the 11 ANA positive patients (1:640 in 4) showed findings of AI hepatitis. Biopsy in 3 AMA positive patients showed mild bile duct damage in one patient. On median follow-up of about 3 years, there were no differences on liver disease outcomes (ascites, encephalopathy, variceal bleeding), Hepatocellular carcinoma transplantation, and survival. Conclusions Auto-immune markers are frequently present in steatohepatitis liver disease patients. Their presence is an epiphenomenon without histological changes of autoimmune hepatitis. Further, their presence does not impact clinical presentation and follow-up outcomes.
Hepatitis C virus (HCV) infection and alcohol abuse are two most important causes of chronic liver disease in the United States. Alcoholic hepatitis is a unique clinical syndrome among patients with chronic and active alcohol abuse with a potential for high short-term mortality. About 20% of patients presenting with alcoholic hepatitis have concomitant HCV infection. Mortality from alcoholic hepatitis is increased in the presence of concomitant hepatitis C due to synergistic interaction between HCV and alcohol in causing hepatocellular damage. Large prospective randomized studies are needed to develop guidelines on the use of corticosteroids among patients with alcoholic hepatitis and concomitant HCV infection. The impact of antiviral therapy on mortality and outcome in the setting of alcoholic hepatitis remains a novel area for future research.
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