Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We here present a Japanese family with type I hereditary heparin cofactor II (HC II) deficiency. The propositus (a 61-year-old man) suffered from angina pectoris and coronary artery disease was confirmed by coronary angiography. He underwent percutaneous transluminal coronary angioplasty (PTCA) four times in one year. Combined use of heparin, aspirin, and nitrates could not prevent the return of his symptoms and restenosis of segment 6 of the left anterior descending artery. His HC II activity and antigen levels were 49% and 50%, respectively, and his daughter also showed similar low levels. Cerebral infarction had occurred in two family members. Argatroban, a selective potent thrombin inhibitor, was administered after the fourth PTCA for the purpose of preventing reocclusion and achieved a successful outcome. A relationship between HC II deficiency and thrombosis has not yet been established. Our case suggests that standard heparin therapy is not effective in preventing restenosis in such individuals, in whom the process is accelerated by thrombin generation at the site where PTCA produces rupture of the atherosclerotic plaque. Argatroban may be more effective under low HC II conditions because of its potent inhibition of thrombin activity at sites of vascular wall damage.
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PMID:Hereditary heparin cofactor II deficiency and coronary artery disease. 161 93

A 13-year-old boy was admitted to this hospital for evaluation of pitting edema of both legs. Three years ago, he had been diagnosed to have nephrotic syndrome. Two and half years ago, because of persistent heavy proteinuria, poor response to steroids and frequent relapse of disease, a renal biopsy was done; characteristics of IgM nephropathy was shown. About a year previously, the patient felt dizziness and weakness of the left side of his body upon awakening one morning. Neurologic examination showed loss of muscle tone, muscle power and deep tendon reflexes. Sensory and cranial nerve function were intact. Blood pressure was normal. The CT scan of brain showed a patch of low attenuation area in the right temporal region, obliteration of the right cortical sulci and mild compression of right lateral ventricle. A diagnosis of nephrotic syndrome with right cerebral infarction was made. The patient's condition became stable two days later after mannitol infusion, correction of electrolytes, and supportive therapy. According to literature, most cases of nephrotic syndrome complicate with renal thrombosis, pulmonary emboli, and deep vein thrombosis. Few cases complicate with cerebral thrombosis and infarction. If patient have low plasma albumin and anti-thrombin III level, hyperfunction of platelet aggregability and use long-term diuretic therapy, they may be at higher risk of thromboembolic complications. If thromboembolic complications exist, anticoagulation treatment should be instituted. Prophylactic therapy with aspirin or dicumarol is not currently recommended.
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PMID:[Nephrotic syndrome complicated with cerebral infarction: report of one case]. 182 17

To evaluate the clinical usefulness of D-dimer, various effects on the measurement of D-dimer were examined. Although both fibrinolytic and fibrinogenolytic products were detected by the measurement of FDP, only fibrinolytic products were detected by the measurement of D-dimer. In patients with DIC and other thrombo-embolic diseases, plasma D-dimer levels were significantly higher than in normal persons. A significant positive correlation between plasma D-dimer and serum FDP was found in DIC patients. In patients with DIC associated with acute promyelocytic leukemia, which is thought to be an increased fibrinogenolysis state, serum FDP was higher than the plasma D-dimer which suggests that increased fibrinogenolysis affects the result of serum FDP measurement. Plasma D-dimer significantly increased 5 minutes after endoscopic embolization with thrombin in the patients with esophageal varices. However serum FDP increased 30 minutes after the treatment, which suggests that the D-dimer is more useful for rapid detection of coagulo-fibrinolytic change than serum FDP. Plasma D-dimer was significantly higher in patients with cerebral infarction and increased with age. These finding suggest the usefulness of plasma D-dimer measurement for the specific and rapid evaluation of coagulo-fibrinolytic activation and thrombo-embolic state.
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PMID:[Clinical usefulness of the measurement of plasma D-dimer levels]. 192 Aug 61

Plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PAP), von Willebrand factor antigen (vWF:Ag) plasminogen activator antigen (PA) and plasminogen activator inhibitor-1 antigen (PAI-1), were determined in 110 patients with arterial thromboembolic diseases within 4 weeks after attack (Th; 41 cases with myocardial infarction and 69 with cerebral infarction), 67 patients with various types of carcinoma (Ca; 31 cases without metastasis and 36 with metastasis) and 50 age-matched healthy individuals (Co). The following results were obtained: 1) Mean plasma levels of TAT, PAP, vWF:Ag, PA and PAI-1 were significantly higher in Th than Co. 2) Mean plasma levels of TAT, PA and PAI-1 were significantly higher in Ca than Co regardless of metastasis but those of PAP and vWF:Ag were significantly higher only in Ca with metastasis than Co. 3) Significant relationship was observed between plasma levels of TAT and PAP both in Th and Ca. 4) Significant relationship was also observed between plasma levels of TAT and vWF:Ag, PA or PAI-1 in Th, but not in Ca. It is suggested from these results that the coagulopathies observed in these patients result from the activation of intravascular blood coagulation and fibrinolysis, and that vascular endothelial cell damage may play an important role in the activation in Th.
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PMID:Studies on the pathogenesis of coagulopathy in patients with arterial thromboembolism and malignancy. 214 28

The mean levels of fibrinopeptide A (FPA), thrombin-antithrombin complex (TAT), and soluble fibrin (tPA method) in cancer patients (n = 32) were intermediate between those of patients with cerebral infarction and pancreatitis who had the most abnormal results and patients with myocardial infarction and pneumonia who had the least abnormal results. Patients with disseminated malignancies (n = 16) had significantly higher mean levels of FPA (10.6 vs. 5.3 nmol/l) and TAT (11.0 vs. 4.4 pmol/l) than patients with limited malignancies (n = 16). The difference in soluble fibrin (fibrin monomer, FM; 22.1 vs. 18.0 nmol/l) was not significant. The values of FPA, FM, and TAT in the patient population correlated significantly. There was a negative correlation between the level of antithrombin and test results for FPA (-0.69), FM (-0.48), and TAT (-0.38) in the cancer patients. Even cancer patients with locally limited disease may have elevated FPA, FM, and TAT test results, indicating a state of definite hypercoagulation.
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PMID:Indices of hypercoagulation in cancer as compared with those in acute inflammation and acute infarction. 228 6

To determine the prevalence of the factor V Leiden gene mutation in relation to the phenotypes of cerebral infarction and cerebral hemorrhage, we studied 386 randomly selected cases of acute stroke and 247 control subjects. Factor V genotype was determined by amplification of a 267-bp sequence of exon/intron 10 of the factor V gene. Levels of prothrombin fragment F(1 + 2), a marker of thrombin generation, were determined in both acute and convalescent stroke and related to factor V genotype. Prothrombin fragment F(1 + 2) was assessed by using an enzyme-linked immunosorbent assay. Sixteen stroke cases (4.1%) were identified as having the mutation compared with 14 (5.6%) control subjects. Prothrombin fragment F(1 + 2) levels were estimated in 191 cases and found to be elevated both acutely and after 3 months, but they were not related to factor V genotype. Prothrombin fragment F(1 + 2) is elevated in acute stroke and requires further evaluation in relation to cerebrovascular disease. These results suggest that the factor V Leiden gene mutation is not a risk factor for arterial thrombosis causing stroke.
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PMID:Factor V Leiden gene mutation and thrombin generation in relation to the development of acute stroke. 777 34

Thrombocytic, haemostatic and fibrinolytic quantities were investigated in 47 patients with cerebral infarction and 34 patients with cerebral haemorrhage. Sixteen of the infarction patients and ten patients of the haemorrhage group were on acetylsalicylic acid medication. Of the remaining 55 patients without acetylsalicylic medication 21/31 = 67.7% of the patients in the infarction group and 9/24 = 37.5% of the patients in the bleeding group had unphysiologically enhanced ADP-induced platelet aggregation. With regard to the coagulation and fibrinolysis markers no significant differences were found between the two groups. In both groups, coagulation activity markers (fibrin monomer and thrombin-antithrombin III), as well as D-dimers were significantly higher than in controls in a high proportion of cases. In 5/47 of the infarction patients and in 3/34 of the haemorrhage patients the fibrin monomer levels were elevated to such an extent, that it can be considered as low grade disseminated intravascular coagulation. In the cerebral haemorrhage group, 80.3% of the patients who subsequently died showed a significantly enhanced fibrin monomer concentration, compared with 28.6% of those who survived. The corresponding frequencies for D-dimer were 100% compared with 66.7%. In the cerebral infarction group, the only analytical quantity showing a significant difference between patients with a fatal outcome and those with a non-fatal outcome was ADP (2 mumol/l) induced platelet aggregation (83.3% in the fatal group, 40.0% in the non-fatal group).
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PMID:On the degree of platelet, coagulation and fibrinolysis activation after cerebral infarction and cerebral haemorrhage and the clinical outcome. 826 May 28

Two girls, 22 months and 12 years of age, presented with repeated cerebral infarctions in association with primary antiphospholipid syndrome. The younger patient also suffered from protein C deficiency, while the other one had protein S and complement C4 deficiencies. All other causes of cerebral infarction were excluded; however, vasculitis remains a possibility in one patient. Both girls developed spastic tetraparesis as a sequela of the previous infarctions. The two patients were treated with aspirin and prednisone, with remission of the infarctions during the next 8 months of observation. A primary deficiency of protein C or S is proposed which would produce cerebral thrombosis with exposure of phospholipids; this thrombosis then, like antigens, would generate antibodies acting on the thrombin-thrombomodulin complex, exacerbating the thrombotic process. The association of complement C4 deficiency is an additional risk factor.
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PMID:Childhood stroke associated with protein C or S deficiency and primary antiphospholipid syndrome. 845 4

Determination of various important parameters of coagulation and fibrinolysis, clinical characteristics, and levels of serum lipid were compared in 193 patients with NIDDM and 50 control subjects. Levels of fibrinogen, tissue factor pathway inhibitor (TFPI), thrombin-anti-thrombin complex, and plasminogen activator inhibitor 1 in plasma increased significantly in the diabetic patients. Levels of TFPI correlated significantly with levels of total cholesterol. In the patients with coronary heart disease or cerebral infarction, levels of lipoprotein(a) increased significantly. From these results, we have concluded that there is a thrombotic tendency or at least an imbalance between the hemostatic and thrombosis-protecting system in diabetic patients, especially in patients with angiopathy.
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PMID:Mechanism on disorders of coagulation and fibrinolysis in diabetes. 867 73

We reported a family with early onset cerebrovascular disease. Patient 1 (a 36-year-old man) demonstrated a combination of livedo reticularis and cerebral infarction as previously described as Sneddon syndrome. He also showed transient focal neurologic symptoms and mild dementia. Patient 2 (an elder sister of Patient 1) was suffering from migraine. Their father and paternal uncle died of cerebral infarction, which had developed in their thirties or forties. Patients 1 and 2 showed MRI findings compatible with encephalopathy with Binswanger-type. Contrary to the previous reports on Binswanger-type encephalopathy, both of these patients demonstrated decreased levels of fibrinogen as well as those of factor V, together with negative antiphospholipid antibody. Thus, juvenile onset, autosomal dominant inheritance, the diversity of clinical findings and the coagulopathy in this family were characteristic features. The level of thrombin-antithrombin III complex (TAT) was markedly increased in Patient 1. Treatment with antithrombin (argatroban 20mg i.v. everyday for 28 days) not only reduced the level of TAT but also improved the livedo reticularis and neurological findings. Although gene analysis has not been performed yet on this family, this condition is similar to cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL), which involve juvenile cerebral infarction and dementia as well as migraine.
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PMID:[Familial Binswanger-type encephalopathy with Sneddon syndrome]. 875 90


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