Temel Tuncer, Cansu Dondu Uskudar, Temel Halide Edip, Ozakyol Aysegul Harmanc
Department of Internal Medicine, Division of Gastroenterology, Faculty of Medicine, Eskisehir Osmangazi University, Eskisehir, Turkey.
Department of Internal Medicine, Division of Rheumotology, Faculty of Medicine, Eskişehir Osmangazi University, Eskisehir, Turkey.
Hepat Mon. 2014 May 5;14(5):e18556. doi: 10.5812/hepatmon.18556. eCollection 2014 May.
Patients with cirrhosis usually have thrombocytopenia in discrete levels. The mechanism of thrombocytopenia is thought as splenic sequestration and destruction of platelets, impaired bone marrow generation and diminished hepatic thrombopoietin synthesis.
The aim of this study was to evaluate serum thrombopoietin levels and its relationship with thrombocytopenia at patients with cirrhosis.
Ninety-two cirrhotic patients and 45 healthy controls without history or findings of pathologies that can effect thrombopoietin levels were enrolled by simple random sampling to patient and control groups of this case control study performed at Eskisehir-Turkey. Thrombopoietin was measured in serum samples with a solid phase enzyme-linked immune absorbent assay. Additionally, spleen size and volume index were determined.
Platelet counts were lower in patients with cirrhosis (97000 ± 8000/mm(3)) than in healthy subjects (240000 ± 51000/mm(3), P < 0.001). Significant difference was determined for platelet counts among child A, B and C stages (Child A vs. Child B P < 0.05 Child A vs. Child C P < 0.001-Child B vs. Child C P < 0.05). Serum TPO concentration was higher (69 ± 12 pg/mL) in cirrhotic group than healthy controls (49 ± 9 pg/ml) (P < 0.05). No significant difference in TPO levels were found among the Child A, B and C stages (64 ± 11 pg/mL, 75 ± 13 pg/mL and 68 ± 10 pg/mL, respectively). Spleen size and SVI was significantly higher in the cirrhotic patients than healthy controls (148 ± 14 mm vs. 98 ± 11 mm, P < 0.001-9167 ± 287 cm(2) vs. 4118 ± 123 cm(2)). Significant difference was determined for spleen size and spleen index among child A, B and C stages (Child A vs. Child B P < 0.05 Child A vs. Child C P < 0.001-Child B vs. Child C P < 0.05). TPO levels were significantly different between cirrhotic patients with platelet levels below 50.000/mm(3) (n = 16, plt-count: 41000 ± 8300/mm(3), TPO levels: 73 ± 7 pg/mL) and above 50.000/mm(3) (n = 76, plt-count: 105000 ± 9500/mm(3), TPO levels: 65 ± 10 pg/mL) (P < 0.01). In correlation analysis, there was a strong negative correlation between platelet count-spleen size (P < 0.001, r = -0.74) and platelet count-serum TPO levels (P < 0.001, r = -0.71).
Our results suggest that liver cirrhosis does not cause impaired thrombopoietin production even in the late stage of disease. Thrombopoietin has no contribution for the occurrence of thrombocytopenia in cirrhosis; splenic sequestration seems to be the main factor.
肝硬化患者通常有不同程度的血小板减少。血小板减少的机制被认为是脾脏对血小板的扣押和破坏、骨髓生成受损以及肝脏血小板生成素合成减少。
本研究旨在评估肝硬化患者的血清血小板生成素水平及其与血小板减少的关系。
通过简单随机抽样，将92例肝硬化患者和45例无影响血小板生成素水平的病史或病理检查结果的健康对照纳入在土耳其埃斯基谢希尔进行的本病例对照研究的患者组和对照组。采用固相酶联免疫吸附测定法检测血清样本中的血小板生成素。此外，测定脾脏大小和体积指数。
肝硬化患者的血小板计数（97000±8000/mm³）低于健康受试者（240000±51000/mm³，P<0.001）。在Child A、B和C期之间，血小板计数存在显著差异（Child A与Child B相比，P<0.05；Child A与Child C相比，P<0.001；Child B与Child C相比，P<0.05）。肝硬化组血清TPO浓度（69±12 pg/mL）高于健康对照组（49±9 pg/ml）（P<0.05）。在Child A、B和C期之间，TPO水平未发现显著差异（分别为64±11 pg/mL、75±13 pg/mL和68±10 pg/mL）。肝硬化患者的脾脏大小和脾脏体积指数显著高于健康对照组（148±14 mm对98±11 mm，P<0.001；9167±287 cm²对4118±123 cm²）。在Child A、B和C期之间，脾脏大小和脾脏指数存在显著差异（Child A与Child B相比，P<0.05；Child A与Child C相比，P<0.001；Child B与Child C相比，P<0.05）。血小板水平低于50000/mm³（n = 16，血小板计数：41000±8300/mm³，TPO水平：73±7 pg/mL）和高于50000/mm³（n = 76，血小板计数：105000±9500/mm³，TPO水平：65±10 pg/mL）的肝硬化患者之间，TPO水平存在显著差异（P<0.01）。在相关性分析中，血小板计数与脾脏大小（P<0.001，r = -0.74）以及血小板计数与血清TPO水平（P<0.001，r = -0.71）之间存在强负相关。
我们的结果表明，即使在疾病晚期，肝硬化也不会导致血小板生成素产生受损。血小板生成素对肝硬化中血小板减少的发生没有作用；脾脏扣押似乎是主要因素。
