만성 B형간염에서 혈청 내 수용성 Fas 및 수용성 Fas ligand의 임상적 의의
Clinical Significances of Serum Soluble Fas and Soluble Fas Ligand in Chronic Hepatitis B
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목적: 만성 B형간염을 포함한 여러 간질환에서 Fas 매개성 세포자멸사가 간세포 사멸 기전의 하나로 알려져 있으며, 만성 C형간염의 경우에 혈청 내 sFas 및 sFasL가 Fas 매개성 세포자멸사를 조절한다고 보고되어 있다. 이에 B형간염바이러스 양성인 만성 간질환 환자의 혈청에서 sFas와 sFasL를 측정하여 혈청 내 ALT 수치, 간조직의 염증 정도, 간내 Fas 및 FasL 표현 정도의 연관성을 조사하였다. 대상과 방법: HBV 양성인 만성 간질환 환자 58명과, 건강검진을 위해 내원한 간질환의 근거가 없는 29명을 대상으로 하였다. HBV 양성인 환자는 ALT 수치 40 IU/L를 기준으로 2군으로 나누었다. ELISA 방법으로 sFas 및 sFasL 수치를 측정하여 혈청 내 ALT, 간의 조직 활성도와 간조직의 Fas 및 FasL 발현의 연관성을 조사하였다. 결과: 혈청 내 ALT가 상승된 환자군의 혈청 내 sFas 수치는 5.34±2.98 ng/mL로 건강 대조군 및 ALT가 정상인 환자군보다 높았다(각각 P<0.01, P<0.05). 혈청 내 ALT가 상승된 환자군의 혈청 내 sFasL 수치는 0.09±0.03 ng/mL로 건강 대조군 및 ALT가 정상인 환자군보다 낮았다(각각 P<0.01, P<0.01). 혈청 내 sFas 수치는 간내 염증 활성도 및 섬유화가 중등도 이상일 때 대조군보다 유의하게 증가하였다(P<0.05). 혈청 내 sFasL 수치는 간내 조직 활성도와는 연관성이 없었다. 혈청 내 sFas 및 sFasL 수치와 간내 Fas 및 FasL 표현 정도와는 유의한 연관성이 없었다. 결론: 혈청 내 sFas 및 sFasL 체계는 B형간염의 병태생리에 관여하는 인자 중 하나이며, 특히 혈청 내 sFas는 간의 염증 정도를 대변해 줄 수 있는 지표로 생각한다.
Abstract
Apoptosis via Fas/FasL system is thought to be involved in the development of hepatocyte death in viral hepatitis B. In chronic hepatitis C, sFas/sFasL system was reported to control liver injury induced by Fas/FasL mediated apoptosis. To determine the role of sFas/sFasL system in chronic hepatitis B, we analyzed serum sFas/sFasL in 58 HBV patients and 29 healthy controls. Methods: HBV patients were categorized into two groups; normal ALT (≤40 IU/L) and elevated ALT (>40 IU/ L). Serum sFas/sFasL levels in HBV patients were measured by ELISA and was compared with those in 29 healthy controls. Serum ALT levels, histological activity, and Fas/FasL expression of liver were compared. Results: Chronic hepatitis B patients with elevated ALT had significantly higher serum sFas levels than those in healthy controls (P<0.01). Serum sFasL levels, however, were significantly lower than those in healthy controls (P<0.01). Patients with moderate to marked degree of inflammation and fibrosis had significantly higher serum sFas levels than those in healthy controls (P<0.05). Serum sFasL levels had no correlation with the hepatic histological activity. Serum sFas/sFasL levels also had no significant correlation with the Fas/FasL expression of liver. Conclusions: Serum sFas/sFasL levels play a possible role in the pathogenesis of chronic hepatitis B. These results suggest that serum sFas levels might serve as a marker for estimating the degree of hepatic histological activity.
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