アルコール性肝炎
WordNet
- characteristic of or containing alcohol; "alcoholic drinks"
- a person who drinks alcohol to excess habitually (同)alky, dipsomaniac, boozer, lush, soaker, souse
- addicted to alcohol; "alcoholic expatriates in Paris"- Carl Van Doren (同)alcohol-dependent
- any of a series of volatile hydroxyl compounds that are made from hydrocarbons by distillation
- a liquor or brew containing alcohol as the active agent; "alcohol (or drink) ruined him" (同)alcoholic drink, alcoholic_beverage, intoxicant, inebriant
- inflammation of the liver caused by a virus or a toxin
PrepTutorEJDIC
- アルコールの,アルコール性の / アルコールのはいった;アルコール漬けの / アルコール中毒の / アルコール中毒[患]者
- 『アルコール』,酒精 / 『アルコール飲料』,酒
- 肝[臓]炎
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/03/22 01:16:52」(JST)
[Wiki en表示]
Alcoholic hepatitis |
Micrograph showing a Mallory body, a histopathologic finding associated with alcoholic hepatitis. H&E stain.
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Classification and external resources |
Specialty |
gastroenterology |
ICD-10 |
K70.1 |
ICD-9-CM |
571.1 |
MedlinePlus |
000281 |
MeSH |
D006519 |
[edit on Wikidata]
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Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake of alcohol. It is usually found in association with fatty liver, an early stage of alcoholic liver disease, and may contribute to the progression of fibrosis, leading to cirrhosis. Signs and symptoms of alcoholic hepatitis include jaundice, ascites (fluid accumulation in the abdominal cavity), fatigue and hepatic encephalopathy (brain dysfunction due to liver failure). Mild cases are self-limiting, but severe cases have a high risk of death. Severe cases may be treated with glucocorticoids.
Contents
- 1 Signs and symptoms
- 2 Diagnosis
- 3 Pathophysiology
- 4 Treatment and management
- 5 See also
- 6 References
Signs and symptoms
Alcoholic hepatitis is characterized by a myriad of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen (ascites), and modest elevation of liver enzyme levels (as determined by liver function tests). Alcoholic hepatitis can vary from mild with only liver enzyme elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and even liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both severe categories is 50% within 30 days of onset.
Alcoholic hepatitis is distinct from cirrhosis caused by long-term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Some alcoholics develop acute hepatitis as an inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.
Diagnosis
The diagnosis is made in a patient with history of significant alcohol intake who develops worsening liver function tests, including elevated bilirubin and aminotransferases. The ratio of aspartate aminotransferase to alanine aminotransferase is usually 2 or more.[1] In most cases, the liver enzymes do not exceed 500. The changes on liver biopsy are important in confirming a clinical diagnosis.
Pathophysiology
Some signs and pathological changes in liver histology include:
- Mallory's hyaline body - a condition where pre-keratin filaments accumulate in hepatocytes. This sign is not limited to alcoholic liver disease, but is often characteristic.[2]
- Ballooning degeneration - hepatocytes in the setting of alcoholic change often swell up with excess fat, water and protein; normally these proteins are exported into the bloodstream. Accompanied with ballooning, there is necrotic damage. The swelling is capable of blocking nearby biliary ducts, leading to diffuse cholestasis.[2]
- Inflammation - neutrophilic invasion is triggered by the necrotic changes and presence of cellular debris within the lobules. Ordinarily the amount of debris is removed by Kupffer cells, although in the setting of inflammation they become overloaded, allowing other white cells to spill into the parenchyma. These cells to hepatocytes with Mallory bodies.[2]
If chronic liver disease is also present:
- Fibrosis
- Cirrhosis - a progressive and permanent type of fibrotic degeneration of liver tissue.
Treatment and management
Clinical practice guidelines by the American College of Gastroenterology have recommended corticosteroid treatment.[3] Patients should be risk stratified using a MELD Score or Child-Pugh score.
- Corticosteroids: These guidelines suggest that patients with a modified Maddrey's discriminant function score > 32 or hepatic encephalopathy should be considered for treatment with prednisolone 40 mg daily for four weeks followed by a taper.[3]
- Pentoxifylline: A randomized controlled trial found that among patients with a discriminant function score > 32 and at least one of the following symptoms (a palpable, tender enlarged liver, fever, high white blood cell count, hepatic encephalopathy, or hepatic systolic bruit), 4.6 patients must be treated with pentoxifylline for 4 weeks to prevent one patient from dying.[4] Subsequent trials have suggested that pentoxifylline may be superior to prednisolone in the management of acute alcoholic hepatitis with discriminant function score >32. Advantage of pentoxifylline over prednisolone was better tolerability, lesser side effects, with decreased occurrence of renal dysfunction in patients receiving pentoxifylline.[5]
- Potential for combined therapy: A large prospective study of over 1000 patients investigated whether prednisolone and pentoxifylline produced benefits when used alone or in combination.[6] Pentoxifylline did not improve survival alone or in combination. Prednisolone gave a small reduction in mortality at 28 days but this did not reach significance, and there were no improvements in outcomes at 90 days or 1 year.
See also
- AST/ALT ratio
- Steatohepatitis
References
Using Wikipedia for research
- ^ Sorbi D, Boynton J, Lindor KD (1999). "The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease". Am. J. Gastroenterol. 94 (4): 1018–22. doi:10.1111/j.1572-0241.1999.01006.x. PMID 10201476.
- ^ a b c Cotran; Kumar, Collins (1998). Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. ISBN 0-7216-7335-X.
- ^ a b McCullough AJ, O'Connor JF (1998). "Alcoholic liver disease: proposed recommendations for the American College of Gastroenterology". Am. J. Gastroenterol. 93 (11): 2022–36. doi:10.1111/j.1572-0241.1998.00587.x. PMID 9820369.
- ^ Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O (2000). "Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial". Gastroenterology 119 (6): 1637–48. doi:10.1053/gast.2000.20189. PMID 11113085. (ACP Journal Club synopsis)
- ^ De BK, Gangopadhyay S, Dutta D, Baksi SD, Pani A, Ghosh P (2009). "Pentoxifylline versus prednisolone for severe alcoholic hepatitis: a randomized controlled trial". World J. Gastroenterol. 15 (13): 1613–9. PMC 2669113. PMID 19340904.
- ^ Thursz MR, Richardson P, Allison M, Austin A, Bowers M, Day CP, Downs N, Gleeson D, MacGilchrist A, Grant A, Hood S, Masson S, McCune A, Mellor J, O'Grady J, Patch D, Ratcliffe I, Roderick P, Stanton L, Vergis N, Wright M, Ryder S, Forrest EH (2015). "Prednisolone or pentoxifylline for alcoholic hepatitis". N. Engl. J. Med. 372 (17): 1619–28. doi:10.1056/NEJMoa1412278. PMID 25901427.
Alcohol and health
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Specific
interactions |
Note: see Template:Psychoactive substance use for diagnoses
- Aging
- Alcohol-induced mood disorders
- Brain
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- Weight
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Substance
abuse
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Sobriety
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- Alcohol detoxification
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Alcohol
limitation
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Addiction medicine
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- Alcoholism
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Religion and alcohol |
- Christian views on alcohol
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Social issues |
- Alcohol advertising
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- Sex
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General |
- Short-term effects of alcohol
- Long-term effects of alcohol
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UpToDate Contents
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English Journal
- Liver cell-targeted delivery of therapeutic molecules.
- Kang JH1, Toita R2, Murata M3,4.
- Critical reviews in biotechnology.Crit Rev Biotechnol.2016 Feb;36(1):132-43. doi: 10.3109/07388551.2014.930017. Epub 2015 Sep 11.
- The liver is the largest internal organ in mammals and is involved in metabolism, detoxification, synthesis of proteins and lipids, secretion of cytokines and growth factors and immune/inflammatory responses. Hepatitis, alcoholic or non-alcoholic liver disease, hepatocellular carcinoma, hepatic veno
- PMID 25025274
- Osteopontin is a proximal effector of leptin-mediated non-alcoholic steatohepatitis (NASH) fibrosis.
- Coombes JD1, Choi SS2, Swiderska-Syn M3, Manka P4, Reid DT5, Palma E6, Briones-Orta MA1, Xie G3, Younis R7, Kitamura N7, Della Peruta M8, Bitencourt S9, Dollé L9, Oo YH10, Mi Z11, Kuo PC11, Williams R1, Chokshi S6, Canbay A12, Claridge LC13, Eksteen B5, Diehl AM3, Syn WK14.
- Biochimica et biophysica acta.Biochim Biophys Acta.2016 Jan;1862(1):135-44. doi: 10.1016/j.bbadis.2015.10.028. Epub 2015 Oct 31.
- INTRODUCTION: Liver fibrosis develops when hepatic stellate cells (HSC) are activated into collagen-producing myofibroblasts. In non-alcoholic steatohepatitis (NASH), the adipokine leptin is upregulated, and promotes liver fibrosis by directly activating HSC via the hedgehog pathway. We reported tha
- PMID 26529285
- MicroRNA Cargo of Extracellular Vesicles from Alcohol-exposed Monocytes Signals Naive Monocytes to Differentiate into M2 Macrophages.
- Saha B1, Momen-Heravi F1, Kodys K1, Szabo G2.
- The Journal of biological chemistry.J Biol Chem.2016 Jan 1;291(1):149-59. doi: 10.1074/jbc.M115.694133. Epub 2015 Nov 2.
- Membrane-coated extracellular vesicles (EVs) released by cells can serve as vehicles for delivery of biological materials and signals. Recently, we demonstrated that alcohol-treated hepatocytes cross-talk with immune cells via exosomes containing microRNA (miRNAs). Here, we hypothesized that alcohol
- PMID 26527689
Japanese Journal
- アルコール性肝炎重症度スコアの有用性の検証と治療介入による予後への影響についての検討
- アルコール性肝炎重症度スコアの有用性の検証と治療介入による予後への影響についての検討
- 堀江 義則,山岸 由幸,海老沼 浩利,金井 隆典
- 肝臓 55(1), 22-32, 2014
- … アルコール性肝炎のうち,重症度スコア(Japan Alcoholic Hepatitis Score, JAS)で中等症・重症例では,禁酒しても肝腫大が持続する例があり予後不良である.2011年度の中等症・重症アルコール性肝炎の全国調査を行い,中等症26例(死亡4例:死亡率15%),重症33例(死亡17例:52%)の報告があった.JASとMELDスコアに相関を認めた.重症の死亡例でCr, PT(INR)が高く,消化管出血,腎不全,DICの合併率が高か …
- NAID 130003393953
- A liposomal delivery system that targets liver endothelial cells based on a new peptide motif present in the ApoB-100 sequence
- Akhter Afsana,Hayashi Yasuhiro,Sakurai Yu,Ohga Noritaka,Hida Kyoko,Harashima Hideyoshi
- International journal of pharmaceutics 456(1), 195-201, 2013-11-01
- … Liver dysfunction is associated with a variety of liver diseases, including viral or alcoholic hepatitis, fibrosis, cirrhosis, and portal hypertension. …
- NAID 120005394547
Related Links
- Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake of alcohol. It is usually found in association with hepatosteatosis, an early stage of alcoholic liver disease, and may contribute to the progression of fibrosis, ...
Related Pictures
★リンクテーブル★
[★]
- 英
- alcoholic hepatitis
- 関
- アルコール性肝障害。肝障害
概念
- アルコールの過飲により生じた肝炎。
- 経過中に脂肪肝や肝硬変に至り、また肝細胞癌も発症し、最後には肝機能を失い(非代償性肝硬変)に至り死亡する
血液検査
- 典型的にはAST,ALTは300-500IU/L程度。
- AST優位:AST:ALT=2:1
重症度
- 血小板減少、鉄飽和度上昇、T-Bil上昇、PT-INR上昇は重症肝炎を示唆する。
- Maddrey discriminant function (DF, also known as the Maddrey score)
- DF = (4.6 x [prothrombin time (sec) - control prothrombin time (sec)]) + (serum bilirubin(mg/dl))
- DF value ≥32 or 脳症があるときはステロイド治療の適応。禁忌:慢性B型肝炎、敗血症、消化管出血
治療
[★]
急性アルコール性肝炎
[★]
- holic …中毒の人
- アルコールの。アルコール性の。アルコール含有の。アルコール漬けの。アルコール腫による。アルコール中毒の
- 関
- alcohol、alcoholics、alcoholism
[★]
- 関
- alcoholic
- 関
- also Fetal alcohol syndrome
[★]
アルコール
- 関
- ethanol