Neame P B, Kelton J G, Walker I R, Stewart I O, Nossel H L, Hirsh J
Blood. 1980 Jul;56(1):88-92.
The mechanism of isolated thrombocytopenia in septicemia is unknown, but compensated disseminated intravascular coagulation (DIC) has been suggested as a possible cause. To investigate this possibility, platelet counts and sensitive assays for in vivo thrombin and plasmin generation, including fibrinogen gel chromatography and fibrinopeptide A (FPA) assays, were obtained on 31 septicemic patients. Fifteen of 17 patients with gram-negative septicemia and 8 of 14 patients with gram-positive septicemia had thrombocytopenia. Platelet survival studied demonstrated a decreased platelet survival. In 11 of 12 patients with severe thrombocytopenia (platelet count less than 50,000mul), there was laboratory evidence of intravascular coagulation. In contrast, there was little evidence of intravascular coagulation in 8 of 11 patients with moderate thrombocytopenia (platelet counts 50,000 to less than 150,000/mul) or in 7 of 8 patients with normal platelet counts. This report indicates that while DIC accompanies thrombocytopenia in many patients with severe thrombocytopenia, there is frequently little evidence for intravascular coagulation in patients with moderate thrombocytopenia. It is apparent that factors other than intravascular thrombin must play a role in producing the thrombocytopenia of septicemia.
败血症中孤立性血小板减少症的机制尚不清楚，但有人提出代偿性弥散性血管内凝血（DIC）可能是一个原因。为了研究这种可能性，对31例败血症患者进行了血小板计数以及体内凝血酶和纤溶酶生成的敏感检测，包括纤维蛋白原凝胶色谱法和纤维蛋白肽A（FPA）检测。17例革兰阴性败血症患者中有15例、14例革兰阳性败血症患者中有8例出现血小板减少。对血小板存活情况的研究表明血小板存活期缩短。在12例严重血小板减少（血小板计数低于50,000/μl）的患者中，有11例存在血管内凝血的实验室证据。相比之下，11例中度血小板减少（血小板计数为50,000至低于150,000/μl）的患者中有8例，以及8例血小板计数正常的患者中有7例几乎没有血管内凝血的证据。本报告表明，虽然在许多严重血小板减少的患者中DIC与血小板减少同时存在，但中度血小板减少的患者中血管内凝血的证据往往很少。显然，除血管内凝血酶外，其他因素也必定在败血症患者血小板减少的发生中起作用。
