Zöhrens G, Armbrust T, Pirzer U, Meyer zum Büschenfelde K H, Ramadori G
Department of Internal Medicine, University of Göttingen, Germany.
Hepatology. 1993 Oct;18(4):798-802. doi: 10.1002/hep.1840180408.
To study the influence of chronic hepatitis on intercellular adhesion molecule-1 serum concentration, we measured intercellular adhesion molecule-1 in the serum of 84 patients with chronic liver disease (17 chronic persistent hepatitis, 42 chronic active hepatitis and 25 active cirrhosis) caused by hepatitis B virus (n = 46), hepatitis C virus (n = 10) and autoimmunity (n = 28). Furthermore, 20 patients with acute viral hepatitis (16 hepatitis B virus and 4 hepatitis A virus) and 6 patients with acute drug-induced hepatitis were included. Sera from 20 healthy persons were used as control. Follow-up examinations were performed during immunosuppressive therapy in 20 patients with autoimmune chronic liver disease (13 chronic active hepatitis and 7 active cirrhosis). Intercellular adhesion molecule-1 serum concentration was significantly increased in patients with acute viral hepatitis, drug-induced hepatitis, chronic active hepatitis and active cirrhosis compared with healthy controls and with patients with chronic persistent hepatitis. Intercellular adhesion molecule-1 was also significantly increased in severe chronic active hepatitis and active cirrhosis compared with moderate chronic active hepatitis and moderate active cirrhosis. Serum concentration of intercellular adhesion molecule-1 decreased significantly in patients with autoimmune chronic liver disease after 2 mo of immunosuppression when remission was present. A close correlation between aspartate aminotransferase and intercellular adhesion molecule-1 serum levels was found. We conclude the following: (a) in chronic liver disease intercellular adhesion molecule-1 serum concentration may represent, at least in part, hepatocellular damage; and (b) intercellular adhesion molecule-1 serum level does not differentiate between chronic autoimmune and chronic viral hepatitis.
为研究慢性肝炎对细胞间黏附分子-1血清浓度的影响，我们检测了84例慢性肝病患者血清中的细胞间黏附分子-1，这些患者包括由乙型肝炎病毒（n = 46）、丙型肝炎病毒（n = 10）和自身免疫（n = 28）引起的17例慢性持续性肝炎、42例慢性活动性肝炎和25例活动性肝硬化患者。此外，还纳入了20例急性病毒性肝炎患者（16例乙型肝炎病毒感染和4例甲型肝炎病毒感染）以及6例急性药物性肝炎患者。选取20名健康人的血清作为对照。对20例自身免疫性慢性肝病患者（13例慢性活动性肝炎和7例活动性肝硬化）进行免疫抑制治疗期间进行了随访检查。与健康对照以及慢性持续性肝炎患者相比，急性病毒性肝炎、药物性肝炎、慢性活动性肝炎和活动性肝硬化患者的细胞间黏附分子-1血清浓度显著升高。与中度慢性活动性肝炎和中度活动性肝硬化相比，重度慢性活动性肝炎和活动性肝硬化患者的细胞间黏附分子-1也显著升高。自身免疫性慢性肝病患者在免疫抑制2个月且病情缓解后，细胞间黏附分子-1的血清浓度显著下降。发现天冬氨酸转氨酶与细胞间黏附分子-1血清水平之间存在密切相关性。我们得出以下结论：（a）在慢性肝病中，细胞间黏附分子-1血清浓度至少部分可代表肝细胞损伤；（b）细胞间黏附分子-1血清水平无法区分慢性自身免疫性肝炎和慢性病毒性肝炎。
