Viral hepatitis pathophysiology

H., Shorey, J., Combes, B. Viral hepatitis complicating the Dubin-Johnson syndrome. Gastroenterolcw 1972 63 331-339 Wolkoff, A.W., Wolpert, E., Pascasio, F.N., Arias, I.M. Rotor s syndrome. A distinct inheritable pathophysiologic entity. Amer. J. Med. 1976 60 173-179... 

HAV is primarily responsible for acute hepatitis. It is most often linked to sporadic events of contaminated food in the United States and to international travel, and is usually a self-limited disease. HBV and HCV are primarily responsible for the development of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Immunomodulatory therapy and direct antiviral agents have been developed for both HBV and HCV. These therapeutic modalities require long courses of therapy and are associated with limited success. This chapter will focus on the pathophysiology, clinical course, and management of these three primary causes of viral hepatitis, namely HAV, HBV, and HCV. 

Although there are no data about the serum concentrations of protein Fv in different pathophysiological conditions, it is not inconceivable that this protein synthesized by the liver in patients with acute and chronic viral hepatitis infections can contribute, through the release of mediators from cardiac mast cells, to some of the cardiovascular manifestations observed in some of these patients [45—48]. 

Molecular tests consist of numerous molecular methods. They are collected under two groups of tests the first category of tests have been designed to detect viral replication (qnantitative or quahtative) in peripheral blood or the liver and the second have been designed to identify genotype specific sequence or sequence variation of clinical or pathophysiological importance in the hepatitis virus genome. 

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