Adinolfi L E, Giordano M G, Andreana A, Tripodi M F, Utili R, Cesaro G, Ragone E, Durante Mangoni E, Ruggiero G
Institute of Medical Therapy, Second University of Naples, Naples, Italy.
Br J Haematol. 2001 Jun;113(3):590-5. doi: 10.1046/j.1365-2141.2001.02824.x.
The pathogenesis of thrombocytopenia in chronic hepatitis is not well known. This study evaluated the relationship between liver injury, serum thrombopoietin, splenomegaly and thrombocytopenia in chronic viral hepatitis. Two hundred and nine patients were enrolled, 85 with splenomegaly and 124 without. Thrombocytopenia was present in 71% and 23% of patients with or without splenomegaly respectively. In subjects with low platelet count, those with splenomegaly showed significantly lower platelet numbers than those without splenomegaly. The spleen size correlated with portal hypertension. An inverse correlation between spleen size and platelet count was observed (r = -0.54; P < 0.0001). In patients without splenomegaly, thrombocytopenia was associated with the grade of fibrosis; platelet counts were the highest in patients with fibrosis 0-2, lower in those with grade 3 (P < 0.008) and lowest in those with grade 4 (P < 0.05). These findings were independent of demographic and biochemical characteristics, hepatic necroinflammatory activity, portal hypertension and splenomegaly. Patients with normal platelet counts showed higher thrombopoietin levels than those with low platelet counts (P < 0.0001). An inverse correlation between thrombopoietin levels and fibrosis grade was observed (r = - 0.50; P < 0.0001). Median thrombopoietin levels were 58 and 27 pg/ml for fibrosis grade 0-1 and grade 4 respectively (P < 0.001). These data indicate that advanced hepatic fibrosis, causing an altered production of thrombopoietin and portal hypertension, plays the central role in the pathogenesis of thrombocytopenia in chronic viral hepatitis.
慢性肝炎中血小板减少症的发病机制尚不清楚。本研究评估了慢性病毒性肝炎中肝损伤、血清血小板生成素、脾肿大与血小板减少症之间的关系。共纳入209例患者，其中85例有脾肿大，124例无脾肿大。有或无脾肿大的患者中血小板减少症的发生率分别为71%和23%。在血小板计数低的患者中，有脾肿大的患者血小板数量明显低于无脾肿大的患者。脾脏大小与门静脉高压相关。观察到脾脏大小与血小板计数呈负相关（r = -0.54；P < 0.0001）。在无脾肿大的患者中，血小板减少症与纤维化程度相关；纤维化0-2级的患者血小板计数最高，3级患者较低（P < 0.008），4级患者最低（P < 0.05）。这些发现与人口统计学和生化特征、肝脏坏死性炎症活动、门静脉高压和脾肿大无关。血小板计数正常的患者血小板生成素水平高于血小板计数低的患者（P < 0.0001）。观察到血小板生成素水平与纤维化程度呈负相关（r = -0.50；P < 0.0001）。纤维化0-1级和4级患者的血小板生成素水平中位数分别为58和27 pg/ml（P < 0.001）。这些数据表明，导致血小板生成素产生改变和门静脉高压的晚期肝纤维化在慢性病毒性肝炎血小板减少症的发病机制中起核心作用。
