title: Alpha-1 antitrypsin deficiency in patients with chronic hepatitis.
abstract: OBJECTIVE
  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.
  
  
  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.
authors.affiliation: Department of Internal Medicine, Hacettepe University School of Medicine, Ankara, Turkey.
authors.forename: Halis
authors.initials: H
authors.lastname: Şımşek
authors.forename: Aslı
authors.initials: A
authors.lastname: Pinar
authors.forename: Akif
authors.initials: A
authors.lastname: Altinbaş
authors.forename: Alparslan
authors.initials: A
authors.lastname: Alp
authors.forename: Yasemin H
authors.initials: YH
authors.lastname: Balaban
authors.forename: Yahya
authors.initials: Y
authors.lastname: Büyükaşik
authors.forename: Osman
authors.initials: O
authors.lastname: Özcebe
authors.forename: Gülşen
authors.initials: G
authors.lastname: Hasçelık
authors.forename: Gökhan
authors.initials: G
authors.lastname: Gedıkoğlu
authors.forename: Gonca
authors.initials: G
authors.lastname: Tatar
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001706:Biopsy; D005260:Female; D006521:Hepatitis, Chronic / Q000097:blood / Q000150:complications* / Q000235:genetics; D006801:Humans; D008099:Liver / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D010641:Phenotype; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D055815:Young Adult; D000515:alpha 1-Antitrypsin / Q000235:genetics*; D019896:alpha 1-Antitrypsin Deficiency / Q000097:blood / Q000209:etiology* / Q000235:genetics
chemical_list: D000515:alpha 1-Antitrypsin