Alpha-1 antitrypsin deficiency in patients with chronic hepatitis.

Amac: Alfa-1 antitripsin eksiklii, mutant alfa-1 antitripsin molekulunun hepatositte depolanmas› sonucu karacier hasar›na se- bep olmaktad›r. Alfa-1 antitripsin eksikliinin karacier hasar›n›n oluflmas› icin tek bafl›na yeterli olup olmad›¤› bilinmemektedir. Bu cal›flmada, kronik hepatit tan›s› olan hastalardaki alfa-1 antitripsin eksiklii varl›¤›n› tespit etmeyi amaclad›k. Gerec ve Yontem: Cal›flmaya tan›s› karacier biyopsisi ile konan 54 hasta (36 kronik hepatit B, 8 kronik hepatit C, 7 non-alkolik steato- hepatit, 2 primer biliyer siroz ve 1 otoimmun hepatit) ve 51 yafl ve cinsiyet uyumlu gonullu kan donoru dahil edildi. Butun hasta- larda ve kontrol grubunda alfa-1 antitripsin fenotiplendirmesi icin isoelektrik fokuslama yontemi kullan›l›rken hasta grubunda ka- racier biyopsi orneinde histopatolojik inceleme yap›ld›. Bulgular: Hicbir hastada ve kontrol grubunda alfa-1 antitripsin eksik varyant› tespit edilmedi. Ortalama alfa-1 antitripsin serum duzeyi hasta grubunda kontrol grubuna gore anlaml› olarak daha du- fluk idi (s›ras›yla 157.4±33 mg/dL ve 134.8±30 mg/dL, p<0.00). Karacier doku orneindeki histopatolojik aktivite indeksi ve fib- rosis evrelemesi ile alfa-1 antitripsin serum duzeyi aras›nda bir iliflki bulunmad› (s›ras›yla, p:0.276 ve 0.902). Hasta grubundaki serum alfa-1 antitripsin duzeyi, altta yatan hastal›¤a gore bir farkl›l›k gostermemektedir (p: 0. 928). Sonuc: Bu prospektif-vaka kontrol cal›flmas›nda, alfa-1 antitripsin eksikliinin kronik karacier hastal›¤› surecine ek bir katk›s› olup olmad›¤› deerlendiri- lememifltir. Anahtar kelimeler: Alfa-1 antitripsin eksiklii, kronik karacier hastal›¤›, antitripsin fenotiplendirmesi 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 de- ficiency 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 di- agnosis of chronic hepatitis by liver biopsy (36 chronic hepatitis B virus, 8 chronic hepatitis C virus, 7 non-alcoholic steatohepati- tis, 2 primary biliary cirrhosis, and 1 autoimmune hepatitis) and 51 age- and sex-matched control subjects chosen from among he- althy 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 antitry- psin-deficient variant was absent in patients and controls. The mean serum alpha-1 antitrypsin level was significantly lower in pa- tients (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.