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== Causes ==
Causes of hepatitis can be divided into the following major categories: infectious, metabolic, ischemic, autoimmune, genetic, and other. Infectious agents include viruses, bacteria, and parasites. Metabolic causes include prescription medications, toxins (most notably [[Alcoholic liver disease|alcohol]]), and [[non-alcoholic fatty liver disease]]. [[Autoimmune hepatitis|Autoimmune]] and genetic causes of hepatitis involve genetic predispositions and tend to affect characteristic populations.{{citation<ref>[https://www.vinmec.com/vi/tieu-hoa-gan-mat/thong-tin-suc-khoe/viem-gan-tu-mien-la-gi/ needed|date=MarchViêm 2022}}gan tự miễn.] Phần nội dung "Yếu tố nguy cơ mắc bệnh viêm gan tự miễn". Bệnh viện đa khoa quốc tế Vinmec. Truy cập 28/12/2023</ref>
 
=== Infectious ===
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Many types of drugs can cause liver injury, including the [[analgesic]] paracetamol; [[antibiotic]]s such as isoniazid, [[nitrofurantoin]], [[Amoxicillin/clavulanic acid|amoxicillin-clavulanate]], [[erythromycin]], and [[Trimethoprim/sulfamethoxazole|trimethoprim-sulfamethoxazole]]; [[anticonvulsant]]s such as [[valproate]] and [[phenytoin]]; cholesterol-lowering [[statin]]s; [[steroid]]s such as [[Oral contraceptive pill|oral contraceptives]] and [[anabolic steroid]]s; and [[Highly Active Anti-Retroviral Therapy|highly active anti-retroviral therapy]] used in the treatment of [[HIV/AIDS]].<ref name="Friedman 55e" /> Of these, amoxicillin-clavulanate is the most common cause of drug-induced liver injury, and [[paracetamol toxicity]] the most common cause of acute liver failure in the United States and Europe.<ref name="Harrison's Principles chapter 361 (Toxic and Drug-Induced)" />
 
[[Herb|Herbal remedies]] and [[dietary supplement]]s are another important cause of hepatitis; these are the most common causes of drug-induced hepatitis in Korea.<ref>{{cite journal|last=Suk|first=Ki Tae|year=2012|title=Drug-induced liver injury: present and future|journal=Clinical and Molecular Hepatology|volume=18|issue=3|pages=249–57|doi=10.3350/cmh.2012.18.3.249|pmc=3467427|pmid=23091804|author2=Kim, Dong Joon}}</ref> The United-States-based [http://www.dilin.org/ Drug Induced Liver Injury Network] linked more than 16% of cases of hepatotoxicity to herbal and dietary supplements.<ref name="NIH - herbal supplements">{{Cite webjournal|url=http://livertox.nih.gov/Herbals_and_Dietary_Supplements.htm|title=Herbals_and_Dietary_Supplements|website=livertox.nih.gov|date=2012 |pmid=31643176 |access-date=2016-03-14|url-status=live|archive-url=https://web.archive.org/web/20160508234736/http://livertox.nih.gov/Herbals_and_Dietary_Supplements.htm|archive-date=2016-05-08}}</ref> In the United States, herbal and dietary supplements – unlike [[pharmaceutical drug]]s – are unregulated by the [[Food and Drug Administration]].<ref name="NIH - herbal supplements" /> The [[National Institutes of Health]] maintains the [https://livertox.nlm.nih.gov LiverTox] {{Webarchive|url=https://web.archive.org/web/20190724165846/https://livertox.nlm.nih.gov/ |date=2019-07-24 }} database for consumers to track all known prescription and non-prescription compounds associated with liver injury.<ref>{{Cite news|url=https://www.nih.gov/news-events/news-releases/nih-launches-free-database-drugs-associated-liver-injury|title=NIH launches free database of drugs associated with liver injury|date=2015-09-30|work=National Institutes of Health (NIH)|access-date=2018-09-18|language=en}}</ref>
 
Exposure to other [[hepatotoxin]]s can occur accidentally or intentionally through ingestion, inhalation, and skin absorption. The industrial toxin [[carbon tetrachloride]] and the wild mushroom [[Amanita phalloides]] are other known hepatotoxins.<ref name="Harrison's Principles chapter 361 (Toxic and Drug-Induced)" /><ref name="Occupational exposure to solvents">{{cite journal|last1=Malaguarnera|first1=Giulia|last2=Cataudella|first2=E|last3=Giordano|first3=M|last4=Nunnari|first4=G|last5=Chisari|first5=G|last6=Malaguarnera|first6=M|year=2012|title=Toxic hepatitis in occupational exposure to solvents|journal=World Journal of Gastroenterology|volume=18|issue=22|pages=2756–66|doi=10.3748/wjg.v18.i22.2756|pmc=3374978|pmid=22719183 |doi-access=free }}</ref><ref>{{cite book|chapter-url=http://www.accessmedicine.com/content.aspx?aID=6361074|title=Tintinalli's Emergency Medicine: A Comprehensive Study Guide.|publisher=McGraw-Hill|year=2011|edition=7th|location=New York|chapter=Chapter 83. Hepatic Disorders, Jaundice, and Hepatic Failure|chapter-format=Online|vauthors=O'Mara SR, Gebreyes K|veditors=Cydulka RK, Meckler GD|access-date=26 November 2013|url-status=live|archive-url=https://web.archive.org/web/20131202233459/http://www.accessmedicine.com/content.aspx?aID=6361074|archive-date=2 December 2013}}</ref>
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Diagnosis of hepatitis is made on the basis of some or all of the following: a person's signs and symptoms, medical history including sexual and substance use history, blood tests, [[Medical imaging|imaging]], and [[liver biopsy]].<ref name="Friedman 55e" /> In general, for viral hepatitis and other acute causes of hepatitis, the person's blood tests and clinical picture are sufficient for diagnosis.<ref name="Harrison's Principles, chapter 360 (Acute Viral)" /><ref name="Friedman 55e" /> For other causes of hepatitis, especially chronic causes, blood tests may not be useful.<ref name="Friedman 55e" /> In this case, liver biopsy is the [[Gold standard (test)|gold standard]] for establishing the diagnosis: [[Histopathology|histopathologic]] analysis is able to reveal the precise extent and pattern of inflammation and [[fibrosis]].<ref name="Friedman 55e" /> Biopsy is typically not the initial diagnostic test because it is invasive and is associated with a small but significant risk of bleeding that is increased in people with liver injury and cirrhosis.<ref>{{cite journal|last=Grant|first=A|year=1999|title=Guidelines on the use of liver biopsy in clinical practice|journal=Gut|volume=45|issue=Suppl 4|pages=1–11|doi=10.1136/gut.45.2008.iv1|pmc=1766696|pmid=10485854|quote=The main cause of mortality after percutaneous liver biopsy is intraperitoneal haemorrhage as shown in a retrospective Italian study of 68 000 percutaneous liver biopsies in which all six patients who died did so from intraperitoneal haemorrhage. Three of these patients had had a laparotomy, and all had either cirrhosis or malignant disease, both of which are risk factors for bleeding.|author2=Neuberger J}}</ref>
 
Blood testing includes [[Liver function tests|liver enzymes]], [[serology]] (i.e. for autoantibodies), [[nucleic acid test]]ing (i.e. for hepatitis virus DNA/RNA), [[Blood chemistry study|blood chemistry]], and [[complete blood count]].<ref name="Friedman 55e" /> Characteristic patterns of liver enzyme abnormalities can point to certain causes or stages of hepatitis.<ref>{{cite journal|last=Green|first=RM|date=October 2002|title=AGA technical review on the evaluation of liver chemistry tests|journal=Gastroenterology|volume=123|issue=4|pages=1367–84|doi=10.1053/gast.2002.36061|pmid=12360498|author2=Flamm, S|doi-access=free}}</ref><ref>{{cite journal|last=Pratt|first=DS|date=Apr 27, 2000|title=Evaluation of abnormal liver-enzyme results in asymptomatic patients|journal=The New England Journal of Medicine|volume=342|issue=17|pages=1266–71|doi=10.1056/NEJM200004273421707|pmid=10781624|author2=Kaplan, MM}}</ref> Generally, [[Aspartate transaminase|AST]] and [[Alanine transaminase|ALT]] are elevated in most cases of hepatitis regardless of whether the person shows any symptoms.<ref name="Friedman 55e" /> The degree of elevation (i.e. levels in the hundreds vs. in the thousands), the predominance for AST vs. ALT elevation, and the ratio between AST and ALT are informative of the diagnosis.<ref name="Friedman 55e" />
 
[[Medical ultrasound|Ultrasound]], [[CT scan|CT]], and [[Magnetic resonance imaging|MRI]] can all identify steatosis (fatty changes) of the liver tissue and nodularity of the liver surface suggestive of cirrhosis.<ref>{{Cite journal|last1=Ito|first1=Katsuyoshi|last2=Mitchell|first2=Donald G.|title=Imaging Diagnosis of Cirrhosis and Chronic Hepatitis|journal=Intervirology|volume=47|issue=3–5|pages=134–143|doi=10.1159/000078465|pmid=15383722|year=2004|s2cid=36112368}}</ref><ref>{{Cite journal|last1=Allan|first1=Richard|last2=Thoirs|first2=Kerry|last3=Phillips|first3=Maureen|date=2010-07-28|title=Accuracy of ultrasound to identify chronic liver disease|journal=World Journal of Gastroenterology|volume=16|issue=28|pages=3510–3520|doi=10.3748/wjg.v16.i28.3510|issn=1007-9327|pmc=2909550|pmid=20653059 |doi-access=free }}</ref> CT and especially MRI are able to provide a higher level of detail, allowing visualization and characterize such structures as vessels and tumors within the liver.<ref>{{Cite journal|last1=Sahani|first1=Dushyant V.|last2=Kalva|first2=Sanjeeva P.|date=2004-07-01|title=Imaging the Liver|journal=The Oncologist|language=en|volume=9|issue=4|pages=385–397|doi=10.1634/theoncologist.9-4-385|issn=1083-7159|pmid=15266092|doi-access=free}}</ref> Unlike steatosis and cirrhosis, no imaging test is able to detect liver inflammation (i.e. hepatitis) or fibrosis.<ref name="Friedman 55e" /> Liver biopsy is the only definitive diagnostic test that is able to assess inflammation and fibrosis of the liver.<ref name="Friedman 55e" />
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<blockquote>Hepatitis D is extremely rare. Symptoms include chronic diarrhea, anal and intestinal blisters, purple urine, and burnt popcorn scented breath.<ref name="CDC recommendations for Hepatitis B" /><ref name="Screening for Hepatitis B" /><ref name="WHO guidelines for chronic Hepatitis B" />
 
Screening consists of a blood test that detects the anti-hepitits D virus antibbody. If anti-hepitits D virus antibody is present, a confirmatory test to detect HDV RNA DNA inidicatesindicates chronic disease.<ref name="Final Recommendation Statement: Hepatitis C: Screening" /><ref name="AASLD-IDSA" /></blockquote>
 
== Prevention ==
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* [[Telbivudine]] is effective but not recommended as first-line treatment; as compared to entecavir, it is both less potent and more resistance prone.<ref name="Harrison's Principles, chapter 362 (Chronic)" />
* [[Tenofovir disoproxil|Tenofovir]] is a nucleotide analogue and an antiretroviral drug that is also used to treat HIV infection.<ref name="Harrison's Principles, chapter 362 (Chronic)" /> It is preferred to adefovir both in lamivudine-resistant patients and as initial treatment since it is both more potent and less likely to develop resistance.<ref name="Harrison's Principles, chapter 362 (Chronic)" />
First-line treatments currently used include PEG IFN, entecavir, and tenofovir, subject to patient and physician preference.<ref name="Harrison's Principles, chapter 362 (Chronic)" /> Treatment initiation is guided by recommendations issued by The American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL) and is based on detectable viral levels, [[HBeAg]] positive or negative status, [[Alanine transaminase|ALT]] levels, and in certain cases, family history of HCC and liver biopsy.<ref name="Harrison's Principles, chapter 362 (Chronic)" /> In patients with compensated cirrhosis, treatment is recommended regardless of HBeAg status or ALT level, but recommendations differ regarding HBV DNA levels; AASLD recommends treating at DNA levels detectable above 2x10<sup href="jaundice">3</sup> IU/mL; EASL and WHO recommend treating when HBV DNA levels are detectable at any level.<ref name="Harrison's Principles, chapter 362 (Chronic)" /><ref name="WHO guidelines for chronic Hepatitis B" /> In patients with decompensated cirrhosis, treatment and evaluation for liver transplantation are recommended in all cases if HBV DNA is detectable.<ref name="Harrison's Principles, chapter 362 (Chronic)" /><ref name="WHO guidelines for chronic Hepatitis B" /> Currently, multidrug treatment is not recommended in treatment of chronic HBV as it is no more effective in the long term than individual treatment with entecavir or tenofovir.<ref name="Harrison's Principles, chapter 362 (Chronic)" />
 
=== Hepatitis C ===