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Search Results: 1 - 10 of 4471 matches for " Alcoholic hepatitis "
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Corticosteroids and pentoxifylline for the treatment of alcoholic hepatitis: Current status
Ashwani K Singal,Ishmeet Walia,Anjna Singal,Roger D Soloway
World Journal of Hepatology , 2011, DOI: 10.4254/wjh.v3.i8.205
Abstract: The treatment of choice for patients with severe alcoholic hepatitis (AH) is use of corticosteroids. Many randomized well designed studies have been reported from all over the world on the use of corticosteroids in the treatment of AH. However, the data on the efficacy of corticosteroids in these patients have been conflicting. Initial meta-analyses also failed to show beneficial effects of corticosteroids. Based on individual data meta-analysis showing clear benefit of corticosteroids amongst patients with severe AH (modified discriminant function of 32 or more), led American College of Gastroenterology to recommend use of corticosteroids as the first line treatment option amongst patients with severe AH. However, corticosteroids are relatively contraindicated amongst patients with severe AH and coexistent sepsis, gastrointestinal bleeding, and acute pancreatitis. These patients may be candidates for second line treatment with pentoxifylline. Further, specific treatment of AH with corticosteroids far from satisfactory with as many as 40%-50% of patients failing to respond to steroids, thus classified as non-responsive to steroids. The management of these patients is a continuing challenge for physicians. Better treatment modalities need to be developed for this group of patients in order to improve the outcome of patients with severe AH. This article describes at length the available trials on use of corticosteroids and pentoxifylline with their current status. Route of administration, dosage, adverse effects, and mechanisms of action of these two drugs are also discussed. Finally, an algorithm with clinical approach to management of patients who present with clinical syndrome of AH is described.
Severe alcoholic hepatitis: Glucocorticoid saves lives and transplantation is promising
Alain Braillon
World Journal of Gastroenterology , 2011, DOI: 10.3748/wjg.v17.i19.2454
Abstract: Glucocorticosteroids have been used as the only treatment for a long time which significantly reduced the mortality of the patients with severe alcoholic hepatitis. The efficacy of transplantation has been recently addressed in a pilot study. The result seems promising but needs larger multicenter trials.
Early mortality of alcoholic hepatitis: A review of data from placebo-controlled clinical trials
Chao-Hui Yu, Cheng-Fu Xu, Hua Ye, Lan Li, You-Ming Li
World Journal of Gastroenterology , 2010,
Abstract: AIM: To investigate the early mortality of placebo-treated alcoholic hepatitis patients.METHODS: Mortality data about alcoholic hepatitis patients who participated in randomized placebo-controlled trials were searched from PubMed, EMBASE, and Cochrane Library, extracted and analyzed.RESULTS: A total of 661 placebo-treated patients in 19 trials were included. The overall mortality rate was 34.19% with a median observation time of 160 d (range 21-720 d). Hepatic failure, gastrointestinal bleeding and infection were the three main causes of death, accounting for 55.47%, 21.17% and 7.30% of all deaths, respectively. One-month mortality data about 324 placebo-treated alcoholic hepatitis patients in 10 trials were reported with a pooled mortality rate of 20.37%. The one-month mortality rate of patients with moderate to severe alcoholic hepatitis tended to be higher than that of general patients (22.69% vs 10.93%, P < 0.05), whereas no significant difference was observed between the patients from North America or Europe (22.43% vs 18.45%, P > 0.05), neither any difference was found between the studies published before and after 1990 (18.18% vs 21.88%, P > 0.05).CONCLUSION: Alcoholic hepatitis is a severe liver disease with a high mortality rate, and hepatic failure, gastrointestinal bleeding and infection are the three main causes of death.
Alcoholic hepatitis 2010: A clinician’s guide to diagnosis and therapy
Maziyar Amini, Bruce A Runyon
World Journal of Gastroenterology , 2010,
Abstract: Alcoholic hepatitis (AH) remains a common and life threatening cause of liver failure, especially when it is severe. Although the adjective “acute” is frequently used to describe this form of liver injury, it is usually subacute and has been developing for weeks to months before it becomes clinically apparent. Patients with this form of alcoholic liver disease usually have a history of drinking heavily for many years. While certain aspects of therapy, mainly nutritional support and abstinence are well established, significant debate has surrounded the pharmacologic treatment of AH, and many institutions practice widely varying treatment protocols. In recent years a significant amount of literature has helped focus on the details of treatment, and more data have accumulated regarding risks and benefits of pharmacologic treatment. In particular, the efficacy of pentoxifylline has become increasingly apparent, and when compared with the risks associated with prednisolone, has brought this drug to the forefront of therapy for severe AH. This review will focus on the clinical and laboratory diagnosis and pharmacologic therapies that should be applied during hospitalization and continued into outpatient management. We conclude that the routine use of glucocorticoids for severe AH poses significant risk with equivocal benefit, and that pentoxifylline is a better, safer and cheaper alternative. While the full details of nutritional support lie beyond the scope of this article, nutrition is a cornerstone of therapy and must be addressed in every patient diagnosed with AH. Finally, while traditional psychosocial techniques play a major role in post-hospitalization care of alcoholics, we hope to make the medical clinician realize his or her role in reducing recidivism rates with early and frequent outpatient visits and with the use of baclofen to reduce alcohol craving.
Infección diseminada y severa por citomegalovirus en paciente inmunocompetente
Izquierdo Rubio,S.; Taxonera Samsó,C.; Ladero Quesada,J. M.; Almansa Menchero,C.; Díaz-Rubio,M.;
Anales de Medicina Interna , 2002, DOI: 10.4321/S0212-71992002000500005
Abstract: usually, cytomegalovirus infection dosen?t cause symtons in immunocompetents patients although sometimes can. in alcoholic and cirrhotic subjects can cause several and fatal infections. we describe a case of disseminated cytomegalovirus infection in an alcoholic patient with excellent response to ganciclovir.
New data on alcoholic liver disease
A.A. Antonyan,E.I. Kashkina,R.V. Lyakisheva
Saratov Journal of Medical Scientific Research , 2010,
Abstract: The review of recent data is presented in the article. it concerns pathogenesis, course, progressing of pathologic process in liver, methods of treatment of patients with alcoholic liver disease
Definition, epidemiology and magnitude of alcoholic hepatitis
Sarpreet Basra,Bhupinderjit S Anand
World Journal of Hepatology , 2011, DOI: 10.4254/wjh.v3.i5.108
Abstract: Alcoholic liver disease (ALD) is a major cause of alcohol-related morbidity and mortality. Its presentation ranges from fatty liver to alcoholic hepatitis (AH), cirrhosis, and hepatocellular carcinoma. Although the amount and pattern of alcohol consumption is a well recognized predisposing factor for the development of serious liver pathology, environmental factors and the host’s genetic make-up may also play significant roles that have not yet been entirely explored. Continuing alcohol consumption is a major factor that influences the survival of patients with AH. The presence of cirrhosis at presentation or its development on follow up is a major factor determining the outcome in the long run. This chapter deals with the epidemiology and magnitude of ALD in general and AH in particular.
Symptoms and signs of acute alcoholic hepatitis
Gurjot Basra,Sarpreet Basra,Sreeram Parupudi
World Journal of Hepatology , 2011, DOI: 10.4254/wjh.v3.i5.118
Abstract: Although there is not one specific sign or symptom related to alcoholic hepatitis (AH), a constellation of symptoms and signs can help make the diagnosis of AH with reasonable accuracy. Documentation of chronic and active alcohol abuse is paramount in making a diagnosis of AH. Clinical presentation after abstinence for more than 3 m should raise doubts about the diagnosis of AH and dictate the need for considering other causes of liver disease, decompensation of alcoholic cirrhosis, sepsis and malignancy as the cause of patient’s clinical profile.
The effect of NAFLD (non-alcoholic fatty liver disease) on long-term outcome of chronic hepatitis B in Iranian patients  [PDF]
Arezoo Estakhri, Ali Akbari Sari, Sahar Naz Nedjat, Marym Rohban, Naser Rakhshani, Seyed Mohammad Tavangar, Reza Malekzadeh, Ghodrat Montazeri
Open Journal of Gastroenterology (OJGas) , 2012, DOI: 10.4236/ojgas.2012.21004
Abstract: Background: The influence of Non-Alcoholic Fatty Liver Disease on the outcome of chronic hepatitis B disease, including viral, biochemical and histologic characteristics, in Iranian patients is not yet fully un- derstood. Aim: To evaluate the effect of Non-Alcoholic Fatty Liver Disease (NAFLD) on long-term histology- cal, biochemical and viral outcome of chronic he- pa-tictis B in Iranian patients. Methods: We retro- spec-tively evaluated 94 “e Ag” negative chronic hepatitis B patients (with NAFLD: 44, without NAFLD: 50). Non-Alcoholic Fatty Liver Disease was diagnosed based on liver biopsy according to Kleiner classifica-tion. Liver biopsy was done for all patients. Serologi-cal and biochemical variables were evaluated with repeated measure analysis. Results: Non-Alcoholic Fat- ty Liver Disease (NAFLD) was present in 47% of the patients (44 out of 94 patients). In the NAFLD group, increase in AST, ALT, stage (P = 0.002), grade, and total score of liver biopsy were independently related to non-alcoholic fatty liver disease, while HBV-DNA viral load did not correlate with the presence of a fatty liver. Conclusion: Abnormalities of liver enzymes and liver histopathology are more prevalent in concurrent chronic hepatitis B and Non-Alcoholic Fatty Liver Disease (NAFLD).
Alteraciones gasométricas en pacientes cirróticos hospitalizados
Lorenzo-Zú?iga,V.; álvares,M.A.; Planas,R.; Morillas,R.; Domènech,E.; Cabré,E.; Gassul,M. A.;
Anales de Medicina Interna , 2005, DOI: 10.4321/S0212-71992005000500002
Abstract: background and objectives: gas exchange alterations have been described in cirrhotic patients; but by the moment, a few prospective studies have focused in them. the aim of this study was to describe the frequency and severity of gasometric alterations in hospitalized cirrhotic patients, a their correlationwith hepatocellular disfunction. patients and methods: 50 consecutive cirrhotic patients (41 males) admited for liver decompensation (ascites, liver encephalopathy, alcoholic hepatitis and upper gastrointestinal bleeding) without acute or chronic cardiopulmonary disfunction were included in the study. patients were classificated according with child-pugh score (a, n = 13; b, n = 21; c, n = 16). severe alcoholic hepatitis (sah) was confirmed in 7 patients. arterial gasometry was performed in all patients before discharge. contrast echocardiography was performed in any case of suspicion of hepatopulmonary syndrome (hps). results: light hypoxemia was observed (80.9 mmhg), without differences with child-pugh. hypocapnia was significantly more evident in child c than in a and b (31.2 ± 3.1 vs. 38.1 ± 4.3 y 36.3 ± 5 mmhg; p < 0,05), respectively. cirrhotic patients with sah showed a significantly higher hypocapnia by comparison with others (31.2 ± 3.1 vs. a 36.3±5 mmhg; p < 0.05). in multivariate analysis, independent prognostic variables for hypocapnica were plasmatic levels of protrombin time, albumin and sodium. hps was confirmed in 8 patients (16%). conclusions: the most prevalent gas exchange abnormality in cirrhosis was the alteration of alveolar-arterial oxygen tension gradient, directly correlated with hepatocellur disfunction. hypocapnia could be a compensatory mechanism or the result of the activation of central respiratory centres by non-depurated substances by the liver.
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