IMMUNOSTAINING FOR MEMBRANE ATTACK COMPLEX OF COMPLEMENT IS RELATED TO CELL NECROSIS IN FULMINANT AND ACUTE HEPATITIS

Background/Aims: Complement activation is one of the mechanisms involv ed in inflammatory lesions. Initiation of the complement terminal path way at a cell surface leads to the formation of a cytolytic membrane a ttack complex. Our study assesses whether a membrane attack complex-as sociated mechanism is involved in liver cell necrosis of fulminant and subfulminant hepatitis. Methods: Immunostaining for membrane attack c omplex was compared with immuno-staining for cytokeratin and complemen t inhibitory proteins such as membrane cofactor protein, decay-acceler ating factor, and homologous restriction factor in 15 patients with fu lminant hepatitis and 5 patients with nonfulminant acute hepatitis. Re sults: In all patients, hepatocytes surrounding necrotic areas, but no t those at a distance, were stained for membrane attack complex, where as the opposite staining pattern for membrane cofactor protein was obs erved. In controls, no hepatocyte staining for membrane attack complex was observed, whereas membrane cofactor protein, but not decay-accele rating factor or homologous restriction factor, was detected on hepato cytes. Conclusions: Complement activation by antibody-dependent or non -antibody-dependent mechanisms might be involved in the pathogenesis o f either fulminant or acute hepatitis. Modulation of membrane cofactor protein expression on hepatocytes might contribute to the sensitivity of hepatocytes to membrane attack complex and subsequent cell lysis.