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=== Genetic === Genetic causes of hepatitis include [[Alpha 1-antitrypsin deficiency|alpha-1-antitrypsin deficiency]], [[HFE hereditary haemochromatosis|hemochromatosis]], and [[Wilson's disease]].<ref name="Friedman 55e" /> In alpha-1-antitrypsin deficiency, a [[Co-dominant expression|co-dominant]] mutation in the gene for alpha-1-antitrypsin results in the abnormal accumulation of the mutant AAT protein within liver cells, leading to liver disease.<ref>{{Cite journal|last=Teckman|first=Jeffrey H.|date=2013-03-07|title=Liver Disease in Alpha-1 Antitrypsin Deficiency: Current Understanding and Future Therapy|journal=COPD: Journal of Chronic Obstructive Pulmonary Disease|volume=10|issue=sup1|pages=35β43|doi=10.3109/15412555.2013.765839|pmid=23527737|s2cid=35451941|issn=1541-2555}}</ref> Hemochromatosis and Wilson's disease are both [[autosomal recessive]] diseases involving abnormal storage of minerals.<ref name="Friedman 55e" /> In hemochromatosis, excess amounts of iron accumulate in multiple body sites, including the liver, which can lead to cirrhosis.<ref name="Friedman 55e" /> In Wilson's disease, excess amounts of copper accumulate in the liver and brain, causing cirrhosis and dementia.<ref name="Friedman 55e" /> When the liver is involved, alpha-1-antitrypsin deficiency and Wilson's disease tend to present as hepatitis in the neonatal period or in childhood.<ref name="Friedman 55e" /> Hemochromatosis typically presents in adulthood, with the onset of clinical disease usually after age 50.<ref name="Friedman 55e" />
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