Prognosis and Prognostic Scoring Models for Alcoholic Liver Disease and Acute Alcoholic Hepatitis

2016 ◽  
Vol 20 (3) ◽  
pp. 491-497 ◽  
Author(s):  
Pierre M. Gholam
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Acute Alcoholic Hepatitis

Falling Rates of Hospital Admissions for Alcoholic Liver Disease in Northeast Italy: A Retrospective Study on a Large Database

2019 ◽  
Vol 54 (6) ◽  
pp. 662-666
Author(s):  
Diego Caroli ◽  
Erik Rosa-Rizzotto ◽  
Claudio Pilerci ◽  
Salvatore Lobello ◽  
Franca De Lazzari ◽  
...  
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Hospital Admissions ◽  
Age Groups ◽  
Veneto Region ◽  
Admission Rates ◽  
Hospitalization Rates ◽  
Acute Alcoholic Hepatitis ◽  
Regional Population

Abstract Aim To describe recent trends in hospital admission rates for alcoholic liver disease (ALD) in the Veneto region of Italy. Methods This retrospective cohort study is based on anonymous hospital discharge records (HDRs) for 2000–2017 from all public and accredited private hospitals operating within the context of the Regional (Veneto) Health Services that are conserved in National/Regional database. It examined the HDR’s of all the hospitalizations of the residents of the Veneto region that were registered under an ALD diagnosis. These were classified under three subheadings: acute alcoholic hepatitis Alcoholic liver cirrhosis and ‘other ALD’. Results During 2000–2017, 30,089 hospital admissions (out of a total regional population of 4,900,000) were registered for ALD. Hospitalization stratified by age showed that the percentage attributable to acute alcoholic hepatitis is higher in younger age groups: 42% in 15–24-year-old (odds ratios (ORs): 14.74; CI95%: 7–30.86; P < 0.000) and 15% in the 25–44-year-old (OR: 3.51; CI95%: 3.12–3.94; P < 0.000). A longitudinal analysis of hospitalization patterns showed a 7% increase in average age in both sexes (from 58.8 ± 9.2 to 62.4 ± 9.7) and a substantial decrease (63.5%) in standardized hospitalization rates (HRs, χ2 trend: 4099.827; P < 0.000) and a smaller decrease (47%) in standardized mortality rates (χ2 trend: 89.563; P < 0.000). Conclusions The fall in the overall ALD-related HR in the Veneto region can be explained by a decrease in population alcohol consumption. Increase in the HRs for acute alcoholic hepatitis in the age group 15–44 suggests an ongoing need for strategies to prevent alcohol abuse by young people.

Monocytosis Correlated With Acute Alcoholic Hepatitis: A Case Report and Literature Review

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4725-4725 ◽  
Author(s):  
Qi Shi ◽  
Lisa Thomas
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Conflicts Of Interest ◽  
Laboratory Finding ◽  
Fatty Infiltration ◽  
Clinical Feature ◽  
Total Serum ◽  
Wall Thickening ◽  
Acute Alcoholic Hepatitis

Introduction Alcohol is a most frequent cause of liver disease in western countries. Alcoholic hepatitis is observed in approximately 20% of heavy drinkers. Acute alcoholic hepatitis (AH) is associated with mortality as high as 50%.Up to 40% of patient with severe alcoholic hepatitis die within 6 months after the onset of the clinical syndrome. Identifying individuals with a high mortality risk is crucial in the management of acute alcoholic hepatitis. We observed a patients with acute alcoholic hepatitis tend to have an increased level of monocytes. Case presentation 47-year-old male with a significant history of alcohol abuse for 30 years presented with confusion, generalized shaking, and tremors for 4 days was admitted to the hospital. The patient was hospitalized 6 months ago for acute alcoholic hepatitis. Physical examination: Bp 140/80mmHg, Ultrasound of Abdomen showed hepatomegaly with enlarged liver measuring 19.1 cm in the midclavicular line and hepatic steatosis and gallbladder sludge without evidence of wall thickening or pericystic fluid. CT of abdomen Suspected fatty infiltration of the liver. Patient had ammonia level of 56 -58. His MELD score was between 52 in which the alcoholic hepatitis was diagnosed. The patient was treated with Ativan, Chlordiazepoxide, Thiamine, folic acid, Mulativitamin, and lactulose. After patient was treated for 7 days, Symptoms had been well controlled, and all of tests went to back normal range. Table1 shows clinical data of current and previous admission. Discussion Alcoholics develop acute hepatitis as an inflammatory reaction to the cells affected by fatty change. Diagnosis of alcoholic hepatitis based on clinical symptoms and laboratory finding alone including elevated AST/ALT (but may < 300 IU/mL), AST>ALT of 2, Total serum bilirubin > 5mg/deciliter, elevated INR, thrombocytopenia, and hypoalbuminimia, (cirrhosis). Leukocytosis with neutophilic predominance has been reported to correlates with degree of injury. As a feature of alcoholic liver disease, monocytosis was first reported on 1983, however, the mechanism mediates this clinical feature has been unclear. Recently data has been shown that activated monocytes have been postulated to play an important role in the pathogenesis of alcoholic liver disease (ALD), in which can produce Interleukin-1 (IL-1) induces interleukin-6 (IL-6) production during acute alcoholic liver injury phase reactant. The number of monocytes, one of the most important components of the inflammatory process in ALD maybe as an independent marker that can be utilized to determine the disease severity and predict outcome of the patients. Conclusion Our result suggests that monocytosis is associated with acute alcoholic hepatitis (Table 1). Further research may provide us with a better understanding of the clinical scenario and help elucidate the best prevention and treatment options of alcohol–related liver disease. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Liver Transplantation for Alcoholic Liver Disease among Canadian Transplant Centres: A National Study

2013 ◽  
Vol 27 (11) ◽  
pp. 643-646 ◽  
Author(s):  
Natasha Chandok ◽  
Mohammed Aljawad ◽  
Angela White ◽  
Roberto Hernandez-Alejandro ◽  
Paul Marotta ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Liver Transplant ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Graft Loss ◽  
National Policy ◽  
National Study ◽  
Acute Alcoholic Hepatitis ◽  
Number Of Patients

BACKGROUND/OBJECTIVE: Alcoholic liver disease (ALD) is a controversial yet established indication for liver transplantation (LT), and there is emerging evidence supporting a survival benefit in selected patients with severe acute alcoholic hepatitis. The aim of the present survey was to describe policies among Canadian transplant centres for patients with ALD.METHODS: A survey was distributed to the medical directors of all seven liver transplant centres in Canada.RESULTS: All seven liver transplant programs in Canada participated in the survey. Every centre requires patients to have a minimum of six months of abstinence from alcohol before listing for LT. Completion of a rehabilitation program is only mandatory in one program; the remaining programs do not mandate this if patients have demonstrated prolonged abstinence, and sufficient insight and social supports. No program considers LT for patients with severe acute alcoholic hepatitis, although six of the seven programs are interested in exploring a national policy. Random alcohol checks for waitlisted patients are performed routinely on patients listed for ALD at only one centre; the remaining centres only perform checks if there is clinical suspicion. In the past five years, the mean (± SD) number of patients per centre with graft dysfunction from recidivism was 10±4.36; a mean of 2.5±4.36 patients per centre developed graft failure.CONCLUSIONS: With minor exceptions, LT policies for subjects with ALD are uniform across Canadian transplant programs. Presently, no centres perform LT for acute alcoholic hepatitis, although there is broad interest in exploring a national policy. Recidivism resulting in graft loss is a rare phenomenon.

scholarly journals Urinary acrolein metabolite levels in severe acute alcoholic hepatitis patients

2019 ◽  
Vol 316 (1) ◽  
pp. G115-G122 ◽  
Author(s):  
Vatsalya Vatsalya ◽  
Maiying Kong ◽  
Leila Gobejishvili ◽  
Wei-Yang Chen ◽  
Sanjay Srivastava ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Proinflammatory Cytokines ◽  
Alcoholic Hepatitis ◽  
Pathogenic Role ◽  
Cytokeratin 18 ◽  
Acute Alcoholic Hepatitis ◽  
Noninvasive Biomarker ◽  
Liver Cell Death

Alcohol-associated liver disease (ALD) remains a major health concern worldwide. Alcohol consumption gives rise to reactive/toxic acrolein, a pathogenic mediator of liver injury in experimental ALD. Elevated acrolein adducts and metabolites are detectable in blood and urine. This study evaluates the major urinary acrolein metabolite, 3-hydroxypropylmercapturic acid (HPMA), in patients with acute alcoholic hepatitis (AAH) and examines its association with disease severity and markers of hepatic inflammation and injury. Urine HPMA was significantly higher in patients with severe [model for end-stage liver disease (MELD) ≥ 20] AAH compared with nonsevere AAH (MELD ≤ 19) or non-alcohol-consuming controls, suggesting that urine HPMA is a novel noninvasive biomarker in severe AAH. The association between HPMA and MELD in patients with AAH was nonlinear. In patients with nonsevere AAH, there was a positive trend, although not significant, whereas in severe AAH the association was negative, indicative of extensive injury and glutathione depletion. Consistent with the multifactorial etiology of ALD, our data identified strong combined effects of HPMA and proinflammatory cytokines on hepatocyte cell death, thereby supporting the pathogenic role of acrolein in liver injury. HPMA, together with IL-1β, showed robust associations with cytokeratin 18 caspase-cleaved fragment (CK18-M30; adjusted R2 = 0.812, P = 0.016) and cytokeratin 18 full-length protein (CK18-M65; adjusted R2 = 0.670, P = 0.048); similarly, HPMA, with IL-8, correlated with CK18-M30 (adjusted R2 = 0.875, P = 0.007) and CK18-M65 (adjusted R2 = 0.831, P = 0.013). The apoptosis index (CK18-M30:CK18-M65 ratio) strongly correlated with HPMA, together with IL-1β (adjusted R2 = 0.777, P = 0.022) or tumor necrosis factor-α (TNFα; adjusted R2 = 0.677, P = 0.046). In patients with severe AAH, IL-1β, IL-8, and TNFα are the predominant proinflammatory cytokines that interact with HPMA and play important mediating roles in influencing the extent/pattern of liver cell death. NEW & NOTEWORTHY This is the first study to examine the urinary acrolein metabolite 3-hydroxypropylmercapturic acid (HPMA) in alcoholic liver disease. HPMA was higher in patients with severe acute alcoholic hepatitis (AAH) compared with controls or nonsevere AAH and may be a novel selective, noninvasive biomarker for severe AAH. Consistent with the multifactorial etiology of alcohol-associated liver disease, we identified strong combined effects of HPMA and proinflammatory cytokines (IL-1β, IL-8, and TNFα) on the extent/pattern of liver cell death, thereby supporting the pathogenic role of acrolein.

scholarly journals Treatment of Decompensated Alcoholic Liver Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
John Menachery ◽  
Ajay Duseja
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Nutritional Therapy ◽  
Decompensated Cirrhosis ◽  
Chimeric Antibody ◽  
Necrosis Factor Alpha ◽  
Therapeutic Goals ◽  
Definitive Therapy ◽  
Severe Alcoholic Hepatitis

Alcoholic liver disease (ALD) is a spectrum ranging from simple hepatic steatosis to alcoholic hepatitis and cirrhosis. Patients with severe alcoholic hepatitis can have clinical presentation almost similar to those with decompensated cirrhosis. Scoring with models like Maddrey discriminant function, a model for end-stage liver disease, Glasgow alcoholic hepatitis score, and Lille model are helpful in prognosticating patients with ALD. One of the first therapeutic goals in ALD is to induce alcohol withdrawal with psychotherapy or drugs. Most studies have shown that nutritional therapy improves liver function and histology in patients with ALD. The rationale for using glucocorticoids is to block cytotoxic and inflammatory pathways in patients with severe alcoholic hepatitis. Pentoxifylline, a tumor necrosis factor alpha (TNFα) suppressor, and infliximab, an anti-TNFαmouse/human chimeric antibody, has been extensively studied in patients with alcoholic hepatitis. Liver transplantation remains the definitive therapy for decompensated cirrhosis/alcoholic hepatitis despite the issues of recidivism, poor compliance with postoperative care, and being a self-inflicted disease.

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