Lo Iacono O, García-Monzón C, Almasio P, García-Buey L, Craxí A, Moreno-Otero R
Liver Unit, Hospital de la Princesa, Universidad Autónoma de Madrid, Spain.
Aliment Pharmacol Ther. 1998 Nov;12(11):1091-9. doi: 10.1046/j.1365-2036.1998.00412.x.
In chronic hepatitis C the relation of circulating adhesion molecules to disease features before, during and after therapy has not been completely established.
To analyse the basal levels of circulating adhesins and the changes induced by interferon in these patients.
We studied, using ELISA assays, the serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in 52 patients with chronic hepatitis C on entry, prior to finalizing a 6-month course of interferon-alpha therapy and at the end of the follow-up. Correlations with clinical, virological and histological features, including inflammation and fibrosis, were calculated by Pearson's r-test.
Liver necroinflammation was more closely related to sICAM-1 (r = 0.54, P = 0.0000) than to sVCAM-1 (r = 0.32, P = 0.02). Fibrosis, both as serum pIIIP and histological scoring, was, however, clearly related to sVCAM-1 (1071+/-291 in patients who scored 0-2 vs. 1870+/-458 in patients who scored 3-4; P = 0.0000). Severe fibrosis was never found below a sVCAM-1 cut-off threshold of 1300 ng/mL. Levels of both adhesins did not correlate with viraemia and were comparable among 1b and non-1b genotypes. Sustained response to interferon was significantly related to low viraemia (P = 0.03), non-lb type (P = 0.04) and low sICAM-1 (P = 0.04), but not to sVCAM-1. On finalizing therapy, patients with normal transaminases had reduced sICAM-1 (P = 0.0005), but not sVCAM-1 levels.
In chronic hepatitis C, sICAM-1 was a marker of liver necroinflammation while sVCAM-1 reflected fibrosis. Both low sVCAM-1 and pIIIP serum concentrations were strictly linked, suggesting that measuring sVCAM-1 could give information on the degree of liver fibroplasia.
在慢性丙型肝炎中，循环黏附分子与治疗前、治疗期间及治疗后的疾病特征之间的关系尚未完全明确。
分析这些患者循环黏附素的基础水平以及干扰素诱导的变化。
我们采用酶联免疫吸附测定法（ELISA），对52例慢性丙型肝炎患者在开始为期6个月的α干扰素治疗前、治疗结束时及随访结束时的血清可溶性细胞间黏附分子-1（sICAM-1）和血管细胞黏附分子-1（sVCAM-1）水平进行了研究。通过Pearson相关系数r检验计算其与临床、病毒学及组织学特征（包括炎症和纤维化）的相关性。
肝脏坏死性炎症与sICAM-1的相关性（r = 0.54，P = 0.0000）比与sVCAM-1的相关性（r = 0.32，P = 0.02）更为密切。然而，无论是血清Ⅲ型前胶原肽（pIIIP）还是组织学评分，纤维化均与sVCAM-1明显相关（评分为0 - 2分的患者sVCAM-1为1071±291，评分为3 - 4分的患者为1870±458；P = 0.0000）。在sVCAM-1截止阈值低于1300 ng/mL时，从未发现严重纤维化。两种黏附素的水平均与病毒血症无关，且在1b型和非1b型基因型之间相当。对干扰素的持续应答与低病毒血症（P = 0.03）、非1b型（P = 0.04）及低sICAM-1（P = 0.04）显著相关，但与sVCAM-1无关。治疗结束时，转氨酶正常的患者sICAM-1水平降低（P = 0.0005），但sVCAM-1水平未降低。
在慢性丙型肝炎中，sICAM-1是肝脏坏死性炎症的标志物，而sVCAM-1反映纤维化。低sVCAM-1和血清pIIIP浓度密切相关，提示检测sVCAM-1可提供有关肝脏纤维增生程度的信息。
