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Determination of levels of leucotrienes in patients with hepatitis B
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摘要: 通过观察与Ⅰ型超敏反应相关的乙型肝炎患者血清中LTD4水平及其与肝细胞损害相关性的研究,进一步论证Ⅰ型超敏反应与乙型肝炎发病机制的关系。应用ELISA和全自动生化分析仪,检测42例急、慢性乙型肝炎患者及35例正常对照组血清中LTD4、ALT和AST水平,并观察三者间的相关性。结果显示,急性组血清中LTD4含量明显高于对照组和慢性组;慢性组血清LTD4含量也明显高于对照组,慢性轻度组、中度组及重度组之间无显著性差异;LTD4水平与ALT、AST含量呈显著的正相关关系。提示,乙型肝炎患者血清LTD4水平可反映肝损害程度,而且对病情和预后的判定有一定的参考价值;作为Ⅰ型超敏反应性炎症的重要指标,LTD4可能参与了乙型肝炎的发病和肝细胞的免疫损伤过程。Abstract: To investigate the relationship between type Ⅰ hypersensitivity and pathogenesis of hepatitis B by observation of serum level of leucotrienes (LTD4) and liver damage in patients with hepatitis B.The serum from 42 cases with acute or chronic hepatitis B and 35 control subjects were analyzed.The level of serum LTD4 was determined by sandwich ELISA.And the levels of serum ALT and AST were measured using omni automatic biochemistry analyzer.The levels of serum LTD4 in patient group was higher than those in control group.Furthermore, the correlation between the level of LTD4 and the level of ALT and AST was also observed.The level of serum LTD4 reflects the liver damage in the patients with acute or chronic hepatitis B.It indicated that LTD4 might play some role in the pathogenesis of hepatitis B.
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Key words:
- hepatitis B /
- pathogenesis /
- type Ⅰ hypersensitivity /
- LTD4
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[1]Samuelsson B, Hammarstrom S.Leukotrienes:a novel group of bio-logically active compounds[J].Vitam Horm, 1982, 39∶1. [2]Samuelsson B. Leukotrienes: mediators of immediate hypersensitivity reactions and inflammation[J]. Science, 1983, 220 (4597) ∶568. [3]Borgeat P, Samuelsson B.Arachidonic acid metabolism in polymor-phonuclear leukocytes:[J]effects of ionophore A23187.Proc NatlAcad Sci USA, 1979, 76 (5) ∶2148. [4] Weller PF, Lee CW, Foster DW, [J]. Generation and metabolism of 5-lipoxygenase pathway leukotrienes by human eosinophils: [J]predominant production of leukotriene C4. Proc Natl Acad Sci USA, 1983, 80 (24) ∶7626. [5]Wendel A, Tiegs G.Leukotriene D4 mediates galactosamine/endo-toxin-induced hepatitis in mice[J].Biochem Pharmacol, 1987, 36 (12) 1867. -
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