Barinagarrementeria F, Cantú-Brito C, De La Peña A, Izaguirre R
Stroke Clinic, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico.
Stroke. 1994 Feb;25(2):287-90. doi: 10.1161/01.str.25.2.287.
Although 4% of cerebral infarcts in the young can be attributed to hematologic disturbances that predispose to thrombosis, the frequency of cerebral infarcts caused by prothrombotic states is not known. Recently, the association between cerebral infarction and deficiencies of elements of the natural anticoagulant system has been recognized.
Thirty-six consecutive patients under 40 years of age with cerebral infarction of undetermined cause were prospectively studied. Quantitation of natural anticoagulants was done at least 3 months after the cerebral infarction. The following activity tests were performed, all by the chromogenic method: antithrombin III, protein C, plasminogen, tissue plasminogen activator, and inhibitor of tissue plasminogen activator. Protein S was quantified by the Laurell rocket method. All patients underwent a complete cardiological examination, including two-dimensional echocardiography, as well as four-vessel cerebral angiography. Some patients were also studied by transesophageal echocardiography.
Of 36 patients, 17 were male, with a mean age of 28 years. Mean age for women was 25 years. Nine patients (25%; 5 women, 4 men) had a deficiency of one natural anticoagulant and constituted group I. In these patients, isolated protein S deficiency was detected in five cases (13.8%); in one case, we observed the association between protein S deficiency and antiphospholipid antibodies; and deficiency of protein C was seen in one case (2.7%), of antithrombin III in one case (2.7%), and of plasminogen in one case (2.7%). Instances of cerebral infarction without natural anticoagulant deficiency (group II) included 12 women and 15 men. There were no differences in clinical and radiological findings between the two groups.
Considering the importance of prothrombotic state, especially caused by deficiency of protein S, in the development of cerebral infarcts, we suggest that it should be looked for in every young patient affected by this pathological entity and in whom no etiologic factors can be determined.
尽管年轻人群中4%的脑梗死可归因于易导致血栓形成的血液学紊乱，但由血栓前状态引起的脑梗死发生率尚不清楚。最近，人们已经认识到脑梗死与天然抗凝系统成分缺乏之间的关联。
对36例年龄在40岁以下、病因不明的脑梗死患者进行前瞻性研究。在脑梗死至少3个月后对天然抗凝剂进行定量检测。采用发色底物法进行以下活性检测：抗凝血酶III、蛋白C、纤溶酶原、组织型纤溶酶原激活剂及组织型纤溶酶原激活剂抑制剂。采用Laurell火箭免疫电泳法对蛋白S进行定量检测。所有患者均接受了全面的心脏检查，包括二维超声心动图检查以及四血管脑血管造影。部分患者还接受了经食管超声心动图检查。
36例患者中，男性17例，平均年龄28岁。女性平均年龄25岁。9例患者（25%；女性5例，男性4例）存在一种天然抗凝剂缺乏，构成I组。在这些患者中，5例（13.8%）检测到孤立性蛋白S缺乏；1例中，观察到蛋白S缺乏与抗磷脂抗体之间的关联；1例（2.7%）出现蛋白C缺乏，1例（2.7%）出现抗凝血酶III缺乏，1例（2.7%）出现纤溶酶原缺乏。无天然抗凝剂缺乏的脑梗死患者（II组）包括12名女性和15名男性。两组在临床和影像学表现上无差异。
鉴于血栓前状态，尤其是蛋白S缺乏在脑梗死发生中的重要性，我们建议，对于每一位患有这种病理疾病且病因不明的年轻患者，均应检查是否存在血栓前状态。
