| Cerebrovascular disease, cancer, heart disease is three fatal human disease.Cerebral infarction with a high incidence of disability is high and the characteristics of high recurrence rate. Thus, finding sensitive laboratory index, reducing the morbidity and mortality have important clinical significance. In recent years, early diagnosis and treatment of cerebral infarction has made significant progress, but still early to judge the lack of a reliable treatment of cerebral infarction, and laboratory parameters. Atherosclerotic plaque rupture, vascular endothelial cell injury, leading to the formation of micro-emboli.Leading to symptoms of brain ischemia and the pathophysiology of acute cerebral infarction mechanism.The greatly increased rate of cerebral infarction.The pathological process of the body a series of physiological responses, including calcium overload, release of oxygen free radicals, enzyme activation, inflammatory cytokine release, etc.In the early diagnosis of these cascades in its course, prognosis, prevention and treatment as early as possible has significant clinical significance.in the early diagnosis of these cascades in its course, prognosis, prevention and treatment as soon as possible have significant clinical significance.Hossmann and Hideo patients with cerebral infarction was found that AT-Ⅲwas significantly lower in the acute phase, with the condition of the links gradually restored to normal levels, they believe this change reflects the plasma AT-Ⅲin acute cerebral infarction was significantly consumed. Now that this is in the process of the formation of cerebral infarction caused by large consumption. Studies indicate the acute stage, there may be the activation of coagulation factors, and thus make a large number of thrombin activation, resulting in coagulation of hyperthyroidism, in the process a large number of AT-Ⅲwas consumed, but also associated with vascular endothelial cells Damage, reduced synthesis of anti-clotting factors, leading to reduced activity of AT-Ⅲ。AT-Ⅲin plasma decreased significantly after cerebral infarction, cerebral infarction which is the body which may lead to damage of vascular endothelial cells prompted the risk factors, and vascular endothelial cell injury leads to exposure of subendothelial adhesive, causing platelet And the activation of coagulation factors, causing the activation of the endogenous coagulation system, and further lead to the activation of extrinsic coagulation system, leading to thrombus formation. After the endothelial cells to the blood in hypercoagulable state, mainly due to AT-III anticoagulant such as reduced platelet adhesion, aggregation effect of greatly enhanced, resulting in thrombosis. Studies have shown that plasma D-dimer is to determine the direct and practical infarction indicator for thrombotic disease monitoring of thrombolytic therapy has some significance. The pathological basis of cerebral infarction is the body of secondary hypercoagulable state and increased fibrinolytic activity. Suehiro reported that endoscopic sclerotherapy of esophageal varices in the last 5 minutes, plasma D-dimer level is elevated. In present the D-dimer plasma levels measured value is higher level。The study results also suggest Suehiro, D-dimer may be the early diagnosis of cerebral infarction as a sensitive and specific indicators, and other than the CT imaging of the morphological changes of time, much earlier, in acute cerebral infarction can be and enhance its therapeutic effect.Studies have shown that patients with acute cerebral activation of coagulation system, blood is hypercoagulable state, contrary fibrinolytic system is weak. D dimer levels in disseminated intravascular coagulation (DIC), thrombotic disease, severe sepsis, pregnancy, liver disease, surgery, trauma and early stage solid tumors and other diseases more than higher, but more than 6 in the disease Hours later. D dimer in patients with solid tumors as a major violation of the lymphatic vascular laboratory parameters. Also elevated D dimer may also be micro-circulation thrombosis or fibrin remodeling the extracellular tips. Also elevated D dimer may also be micro-circulation thrombosis or fibrin remodeling the extracellular tips. Also elevated D dimer may also be micro-circulation thrombosis or fibrin remodeling the extracellular tips. Therefore, D dimer concentration change in the acute stage of cerebral infarction and its clinical significance. In addition, cerebral ischemia and necrosis, the body can activate the inflammatory system, activation of inflammatory system of the body, and hs-CRP as acute phase protein, when its concentration and its concentration changes and pathological changes Closely related, but the change in hs-CRP levels is caused by damaged tissue cells of the non-specific reactions, such as the need to rule out infection, trauma, cardiovascular diseases caused by changes in hs-CRP can not make a right reason to judge. Has been reported:hs-CRP as a cardiovascular disease morbidity and mortality independent predictor of forecast, while the concentration of cerebral infarction in the clinically significant change in the same.In this paper, our hospital in January 2010—Dec.89 cases of acute cerebral infarction sensitivity C-reactive protein (hs-CRP), antithrombin (AT-Ⅲ), D dimer (D-D) change Depth research, clinical observation, and to explore its clinical significance... |
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