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肝硬化患者凝血功能障碍与门静脉高压程度的关系

[Blood coagulation disorders in liver cirrhosis in relation to the degree of portal hypertension].

作者信息

Klingemann H G, Schmidt U, Brunswig D, Egbring R, Kaffarnik H

出版信息

Fortschr Med. 1980 Oct 23;98(40):1561-66.

PMID:6970156
Abstract

Investigated were the haemostasis of 45 patients with histologically confirmed liver cirrhosis. The patients were subdivided into three groups according to the extent of their porto caval collateral circulation as proved by laparoscopy, gastroscopy and radiology: I = no porto caval shunts (n = 10); II = moderate porto caval shunts (n = 13); III = distinct porto caval shunts (n = 14). A 4th group consisted of 8 patients with bleeding from oesophageal varices. The results indicated a significant decrease in the stages I-III of the coagulation factors produced in the liver (incl. factor XIII and AT III) and the thrombocytes. Unchanged remained the concentration of factor VIII, whereas the factor VIII associated antigen showed an increased activity depending on the severity of the disease (stages I-III). In patients with bleeding from oesophageal varices, values of about 300% of normal could be demonstrated. Depending on the stage of the porto caval collateral circulation, the concentration of fibrin(ogen) split products were also increased. For comparison, patients with pre- and posthepatic blockage were investigated, whose portal hypertension was not caused by liver cirrhosis. Besides a mild thrombopenia they only showed a secondary hyperfibrinolysis. The results, above all in the cases of liver cirrhosis, can be explained by pathophysiological mechanism: a decreased synthesis of clotting factors-a disturbed portal microcirculation with fibrin deposition-an impaired function of the liver RES.

摘要

对45例经组织学确诊为肝硬化的患者的止血情况进行了研究。根据腹腔镜检查、胃镜检查和放射学检查所证实的门静脉腔静脉侧支循环程度,将患者分为三组:I组 = 无门静脉腔静脉分流(n = 10);II组 = 中度门静脉腔静脉分流(n = 13);III组 = 明显门静脉腔静脉分流(n = 14)。第4组由8例食管静脉曲张出血患者组成。结果表明,肝脏产生的凝血因子(包括因子XIII和抗凝血酶III)以及血小板在I - III期显著减少。因子VIII的浓度保持不变,而因子VIII相关抗原的活性则根据疾病严重程度(I - III期)而增加。在食管静脉曲张出血的患者中,可显示出大约为正常数值300%的值。根据门静脉腔静脉侧支循环的阶段,纤维蛋白(原)降解产物的浓度也会增加。作为对照,对肝前和肝后阻塞的患者进行了研究,他们的门静脉高压并非由肝硬化引起。除了轻度血小板减少外,他们仅表现为继发性纤维蛋白溶解。上述结果,尤其是在肝硬化病例中,可通过病理生理机制来解释:凝血因子合成减少 - 伴有纤维蛋白沉积的门静脉微循环紊乱 - 肝脏网状内皮系统功能受损。

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