Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Racial differences in stroke are known to exist with persons in the black race having a higher morbidity, mortality and incidence of stroke compared to whites. We evaluated coagulation factors in black and white stroke patients and compared the results between races. D-dimer was elevated more frequently in blacks than whites to a statistically significant degree. There were non-significant trends for blacks to have a positive lupus anticoagulant, low protein C and protein S, higher platelet factor 4, and hyporesponsive platelets to 10 microM epinephrine. The significance of these findings in understanding racial differences in stroke is discussed.
 ...
PMID:Racial differences in coagulation studies in stroke. 135 61

A 52-year-old Chinese female with recurrent cerebral thrombosis associated with hereditary protein S deficiency is described. The need to consider clotting disorders in young patients with no known risk factors for stroke is emphasized.
 ...
PMID:Recurrent cerebral thrombosis associated with protein S deficiency in a Chinese female. 141 82

The association of ischemic cerebrovascular lesions with livedo reticularis is known as Sneddon syndrome. It affects young subjects, primarily women, and its neurological manifestations are TIAs, ischemic stroke, progressive dementia and epileptic seizures. Its etiopathogenesis has still to be clarified. Some authors have associated it with an antiphospholipid antibody syndrome. Recently it has been assumed that a defect in blood coagulation may be involved in its pathogenesis. Here we report a case in which both an increase in coagulation factor VII activity and a deficiency in free protein S were documented.
 ...
PMID:Cerebral ischemia and livedo reticularis in a patient with impairment of coagulation factor VII and free protein S. 142 96

We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.
 ...
PMID:Protein S deficiency in middle-aged women with stroke. 153 5

Protein S is the cofactor of activated protein C which, together with the antithrombin system, is a major regulator of coagulation. Congenital protein S deficiency is an important risk factor for venous thrombosis. In this study of 105 patients with protein S deficiency, 64 had one of several thromboembolic accidents, including 14 arterial thrombotic accidents involving the central nervous system or the myocardium. These accidents occurred in young subjects (mean age: 25 +/- 13 years) only one-third of whom had another risk factor. This high frequency of arterial thrombosis associated with protein S deficiency calls for a prospective study in young subject with cerebral vascular accident or myocardial infarction.
 ...
PMID:[Influence of protein S deficiency on the arterial thrombosis risk]. 182 20

Protein S is a natural anticoagulant plasma protein; familial deficiency is associated with thrombotic complications. Since smoking carries an increased risk of myocardial infarction and stroke, we investigated the protein S system of men who smoke. In plasma, free protein S is functionally active and protein S bound to C4b binding protein is inactive. Male smokers (n = 24) have lower total protein S than nonsmokers (n = 24) (16.8 +/- 4.3 micrograms/ml versus 19.8 +/- 5.1 micrograms/ml, p less than 0.02). C4b binding protein levels are higher (p less than 0.05) in smokers (212 +/- 47 micrograms/ml versus 186 +/- 52 micrograms/ml). Free protein S is significantly lower in smokers (6.9 +/- 2.3 micrograms/ml versus 8.0 +/- 1.9 micrograms/ml, p = 0.02). These alterations in protein S may contribute to the thrombotic complications associated with smoking.
 ...
PMID:The natural anticoagulant protein S is decreased in male smokers. 849 37

We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event. We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined less than or equal to 7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning less than or equal to 1 month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (5.3 +/- 1.1 versus 4.7 +/- 0.9 log-transformed ng/ml, p less than 0.05) and cardiolipin immunoreactivity, IgG isotype (1.8 +/- 1.3 versus 1.1 +/- 0.9 log-transformed phospholipid units, p less than 0.04), and, when studied less than or equal to 2 days after the stroke, increased fibrinogen levels (459 +/- 126 versus 360 +/- 94 mg/dl, p less than 0.05). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities.
Stroke 1991 Aug
PMID:Immunohematologic characteristics of infection-associated cerebral infarction. 148 66

From 1988 to 1990, we observed five cases of aseptic dural sinus and cerebral venous thrombosis, all in non-smoking women (age 18 to 47 years) receiving low dose oral contraceptives. Treatment consisted of full anticoagulation over 2 to 6 months, over which time the neurologic symptoms disappeared almost completely. Extensive tests of the blood clotting system in 4 patients after 6 to 19 months revealed a reduction of free protein S in 2 patients with a history of contraceptive use over several years, and normal results in 2 patients in which the sinus thrombosis occurred within the first 6 weeks of use of the oral contraceptive. Whether the protein S deficiency was congenital or caused by the oral contraceptive cannot be decided retrospectively. Even modern oral contraceptives seem to lead to an increased incidence of sinus thrombosis. Initial symptoms of sinus thrombosis include headache and somnolence, followed either by focal neurologic deficits (often associated with focal seizures) or by signs of increased intracranial pressure. CT scans show venous infarcts or general brain edema and may specifically show the "empty triangle sign" and "delta sign". The CT scan may also be normal if focal neurologic deficits are absent. MRI is favoured as it can directly show the thrombosed sinus or veins. Differential diagnosis includes arterial stroke, brain tumor, encephalitis or "benign intracranial hypertension", which should only be diagnosed after sinus venous thrombosis has been appropriately ruled out. Recently, full anticoagulation has been recommended as therapy.
 ...
PMID:[Aseptic cerebral sinus thrombosis. 5 cases and a review]. 194 57

A 30-year-old man presented with sagittal sinus thrombosis. He had a history of multiple thrombotic events since adolescence, and his father had had a similar history. Laboratory studies revealed the complete absence of free protein S in his plasma. Protein S deficiency, an autosomal dominant disorder, is an identifiable cause of cerebral thrombosis. The literature and our experience with this case suggest that long-term anticoagulant therapy may prevent thrombotic episodes in patients with this disorder.
Stroke 1990 Apr
PMID:Superior sagittal sinus thrombosis in a patient with protein S deficiency. 213 56

Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.
 ...
PMID:Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. 203 43


1 2 3 4 5 6 7 8 9 10 Next >>