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The prevailing theory for the development of autoimmune hepatitis is thought to be the interplay of genetic predisposition, an environmental trigger (virus, drugs, herbs, immunizations), and failure of the native immune system resulting in chronic inflammation of hepatocytes and subsequent fibrosis of the liver. [7] [8] [9]
This manifests as lipid peroxidation, mitochondrial damage, and glutathione (an endogenous antioxidant) depletion. [7] Damaged hepatocytes release Danger associated molecular patterns (DAMPs) which are molecules that lead to further activation of the immune system's inflammatory response and further hepatocyte damage. [7]
[17] [59] Rather, infection of liver cells activates the innate and adaptive arms of the immune system leading to an inflammatory response which causes cellular damage and death, including viral-induced apoptosis via the induction of the death receptor-mediated signaling pathway.
Risk factors known as of 2010 are: Quantity of alcohol taken: Consumption of 60–80 g per day (14 g is considered one standard drink in the US, e.g. 1 + 1 ⁄ 2 US fl oz or 44 mL hard liquor, 5 US fl oz or 150 mL wine, 12 US fl oz or 350 mL beer; drinking a six-pack of 5% ABV beer daily would be 84 g and just over the upper limit) for 20 years or more in men, or 20 g/day for women ...
Cirrhosis associated immune dysfunction is caused by reduced complement component synthesis in the liver including C3, C4 and reduced total complement activity . [130] The complement system is a part of the innate immune system and assists immune cells and antibodies in destroying pathogens. The liver produces compliment factors, but this may ...
Histopathology of shock liver, showing its hallmark [1] pathologic finding centrilobular necrosis but viable periportal hepatocytes. H&E stain. The necrotic hepatocytes have barely discernible nuclei. Symptoms: Mental confusion [2] Causes: Heart failure, Infection [3] Diagnostic method: Doppler ultrasound, Blood test [3] Treatment
The complications are hepatic encephalopathy and impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood). The 1993 classification defines hyperacute as within 1 week, acute as 8–28 days, and subacute as 4–12 weeks; [ 1 ] both the speed with which the disease develops and the underlying ...
Water-soluble fractions of particulate matter are the most important part of translocation to the liver, through extrapulmonary circulation. When particulate matter gets into the bloodstream, it combines with immune cells and stimulates innate immune responses. Pro-inflammatory cytokines are released and cause disease progression. [46]
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