Alcoholic liver disease.

These recommendations provide a data-supported approach. They are based on the following: (i) a formal review and analysis of the recently published world literature on the topic (Medline search); (ii) American College of Physicians Manual for Assessing Health Practices and Designing Practice Guidelines (1); (iii) guideline policies, including the American Association for the Study of Liver Diseases (AASLD) Policy on the development and use of practice guidelines and the AGA Policy Statement on Guidelines (2); and (iv) the experience of the authors in the specified topic. Intended for use by physicians, these recommendations suggest preferred approaches to the diagnostic, therapeutic, and preventive aspects of care. They are intended to be flexible, in contrast to the standards of care, which are inflexible policies to be followed in every case. Specific recommendations are based on relevant published information. To more fully characterize the quality of evidence supporting the recommendations, the Practice Guideline Committee of the AASLD requires a Class (reflecting the benefit vs. risk) and Level (assessing the strength or certainty) of Evidence to be assigned and reported with each recommendation (Table 1, adapted from the American College of Cardiology and the American Heart Association Practice Guidelines) (3,4).

Treatment of alcoholic hepatitis.

Cirrhosis and its sequelae are responsible for close to 2% of all causes of death in the United States. Some studies have suggested that the costs of liver disease may account for as much as 1% of all health care spending, with alcohol-related liver disease (ALD) representing a major portion. It accounts for between 40% to 50% of all deaths due to cirrhosis, with an accompanying rate of progression of up to 60% in patients with pure alcoholic fatty liver over 10 years, and a 5-year survival rate as low as 35% if patients continue to drink. A subset of patients with ALD will develop an acute, virulent form of injury, acute alcoholic hepatitis, which has a substantially worse prognosis. Despite enormous progress in understanding the physiology of this disease, much remains unknown, and therefore, a consensus regarding effective therapy for ALD is lacking. Conventional therapy is still based largely on abstinence from alcohol, as well as general supportive and symptomatic care. Unfortunately, hepatocellular damage may progress despite these measures. Multiple treatment interventions for both the short- and long-term morbidity and mortality of this disease have been proposed, but strong disagreement exists among experts regarding the value of any of the proposed specific therapeutic interventions.

Management and outcome in hepatorenal syndrome: need for renal replacement therapy in non-transplanted patients.

PURPOSE: Hepatorenal syndrome (HRS) type I is a devastating complication of decompensated cirrhosis. Liver transplantation (LT) offers an excellent survival, and renal replacement therapy (RRT) may be useful until transplantation is available. The survival benefit of RRT in the absence of LT is thought to be short and its benefit in these patients is unknown. To investigate this, we studied the outcome of different therapies (pharmacological, RRT, and LT) in patients with type 1 HRS. METHODS: Medical records (2005-2009) of all cirrhotic patients admitted to our facility with abnormal renal function were reviewed. Patients with preexisting renal disease, diagnosis other than type I HRS, or those without long-term follow-up were excluded. RESULTS: Of 380 patients reviewed, 30 were studied. Nineteen (63.3 %) patients underwent liver transplantation. No difference in baseline liver or renal parameters was noted between those who were or were not transplanted. A decreased mortality was noted (5.3 vs. 64.6 %; p = 0.0005) compared to patients who were not transplanted during the study follow-up median period of 7.8 [CI 1.9-34] months. Among non-transplanted patients, no differences in median survival (8.8 vs. 6.5 months; p = 0.62) or in other parameters studied were found in those patients who received RRT compared to those who did not. Similarly, no survival difference was found comparing those who did or did not receive pharmacological therapy without transplant. CONCLUSION: In type I HRS, LT offers better survival. Among patients who do not receive LT, RRT does not provide an improved survival benefit.

High prevalence of normal serum albumin in NASH patients with ascites: a retrospective analysis.

BACKGROUND: Ascites usually occurs in the setting of end-stage liver disease and low serum albumin and is associated with increased mortality. However, some patients develop ascites despite normal serum albumin (NSA), when a higher portal pressure and/or enhanced renal sodium retention would be expected. This study investigated the relationship between the hepatic venous pressure gradient (HVPG) and serum albumin in ascitic patients with different etiologies of cirrhosis and mortality. METHODS: Records of all patients with non-malignant ascites who underwent HVPG measurement from 2005 to 2009 were reviewed. RESULTS: One hundred and thirty-eight 138 patients met inclusion criteria; 18.8% had NSA. No difference in sodium excretion or diuretic use was noted in patients with and without NSA. NASH patients were more likely to have a NSA (34.2% vs 12.4%; P=0.001) as well as lower HVPG (15 vs 17.9 mmHg; P=0.009) compared to other etiologies. MELD and HVPG predicted overall survival. However, mortality did not differ by disease etiology, though NASH patients had lower CTP (7.6 vs 8.5; P<0.001) and MELD (15.6 vs 18.1; P=0.09) scores, particularly among patients who died. CONCLUSIONS: In patients with ascites and NSA, there were no increase in HVPG or urinary sodium retention. NASH patients with ascites had lower HVPG and a higher prevalence of NSA. They also had a higher mortality relative to MELD and CTP scores in other patients. In these patients, mechanisms other than portal and oncotic pressures and sodium retention play a role in ascites development, and increase mortality rate when complicated by low albumin.

Diagnosis and management of alcoholic liver disease.

Alcohol is the most commonly used hepatotoxin worldwide. About 90% of heavy drinkers (more than 60 g/day of alcohol) show evidence of fatty livers, while only 10-35% develop alcoholic hepatitis and 5-15% developed cirrhosis. The daily intake of alcohol that results in liver injury varies and depends on a number of risk factors. Alcoholic disease developes at lower doses in females, Hispanic, obese objects, and patients with hepatitis C. Insights into the pathogenesis of alcohol-induced liver injury has improved significantly but the translation into clinical benefit has been slow. The importance of continued abstinence and correction of nutritional deficiencies are major components in the long-term management of liver disease. Alcohol hepatitis has a variable mortality and the prognosis is determined most commonly by the modified discriminant function. The mocel of end-stage liver disease (MELD) is being increasingly used to predict outcome in alcoholic hepatitis even though standard cut offs are not available. Anti-inflammatory therapy with corticosteroids and anticytokine therapy with corticosteroids and pentoxifylline are effective for patients with severe alcoholic hepatitis. Patients with endstage liver disease should be considered for liver transplantation. Six months of abstinence is considered to be a requirement prior to transplant, but this length of time may be adjusted in individual bases.