Conclusion
In conclusion, evidence exists that cellular and humoral immune-mediated processes result in hepatic necrosis in FH. Activation of the immune coagulation system appears to be an integral part of the inflammatory process resulting in fibrin thrombi which have been demonstrated in the liver, kidneys and lungs of patients with FH. A beneficial role of PG in the treatment of FH has been demonstrated, but controlled trials are required to firmly establish the efficacy of these agents. At present liver transplantation remains the treatment of choice in selected patients with FH. Further studies of the role of the immune system in the pathogenesis of this disease are required to devise more effective therapeutic strategies.
Keywords: Hepatitis, Internal Medicine, Immune System, Liver Transplantation, Therapeutic Strategy
Abbreviations
- DIC
disseminated intravascular coagulation
- dmPGE2
dimethyl prostaglandin E2
- ELAM
endothelial-leukocyte adhesion molecule
- FH
fulminant hepatitis
- HBV
hepatitis B virus
- HBcAg
hepatitis B core antigen
- HBsAg
hepatitis B surface antigen
- HE
hepatic encephalopathy
- IFN
interferon
- MHC
major histocompatibility complex
- MHV
murine hepatitis virus
- PCA
procoagulant activity
- PG
prostaglandins
- TNF
tumor necrosis factor
- 2-5 AS
oligoadenylate synthetase
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