Akademik Veri Yönetim Sistemi
TURKISH JOURNAL OF GASTROENTEROLOGY, cilt.23, sa.5, ss.569-573, 2012 (SCI-Expanded, Scopus, TRDizin)
Background/aims: Alpha-1 antitrypsin deficiency causes accumulation of mutant alpha-1 antitrypsin molecules in hepatocytes, and is attributed to severe liver injury even in heterozygous state. However, there is a question as to whether alpha-1 antitrypsin deficiency is only a cause of liver injury or has a worsening effect on the underlying liver disease. We aimed to determine the role of alpha-1 antitrypsin deficiency in the ongoing chronic hepatitic process. Materials and Methods: Fifty-four patients with the diagnosis of chronic hepatitis by liver biopsy (36 chronic hepatitis B virus, 8 chronic hepatitis C virus, 7 non-alcoholic steatohepatitis, 2 primary biliary cirrhosis, and 1 autoimmune hepatitis) and 51 age- and sex-matched control subjects chosen from among healthy blood donors were included in the study. Isoelectric focusing for identifying alpha-1 antitrypsin phenotypes was performed in all patients and control subjects, whereas the histopathological examination was done only in patients. Results: Alpha-1 antitrypsin-deficient variant was absent in patients and controls. The mean serum alpha-1 antitrypsin level was significantly lower in patients (157.4 +/- 33 mg/dl) than controls (134.8 +/- 30 mg/dl) (p<0.00). Histological activity index and fibrosis grade in the liver were not related to the serum alpha-1 antitrypsin level (p: 0.276 and 0.902, respectively). Additionally, the serum alpha-1 antitrypsin levels among normal variants of alpha-1 antitrypsin did not differ according to the underlying liver diseases (p: 0.928). Conclusions: This prospective case-control study could not define any additional effect of alpha-1 antitrypsin deficiency on liver histopathology in chronic hepatitis patients.