Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

This review summarizes 169 cerebral vascular accidents in women taking oral contraceptives: 94 arterial (including 13 of the authors' cases), 20 venous, 37 neuroophthalmologic (5 of the authors'), and 18 undetermined diagnoses. The arterial accidents involved the carotid in 56, the vertebrobasilar in 27. Few were fatal; most were considered thromboses; none were due to hemorrhage; few could have been due to emboli or dissecting aneurisms. Aggravation or appearance of migraine was noted in 34 and transient focal cerebral ischemia in 28 cases before arterial accident. No definite time span was obvious, but many occurred 1-6 months or over 2 years after starting pills. Venous accidents were usually fatal, often extended thromboses of the superior longitudinal sinus. Clinically there was severe headache (85%), vomiting, fever without rapid pulse, alteration of consciousness, papillary edema, focal cerebral signs. Ophthalmologic accidents included retinal, arterial, and venous occlusion; paralysis of oculomotor nerve; optic neuritis; and pseudo-tumor-cerebri. The authors recommended caution with oral contraceptives in case of cerebral vascular episodes, migraine, visual disturbances, chorea, hyperlipidemia, and hypertension.
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PMID:[Cerebrovacular accidents and oral contraceptives]. 443 14

Prospective longitudinal cerebral blood flow values were serially plotted over a four-year interval against the course of cerebral ischemia before, during, and after onset of clinical symptoms. Of 161 normal subjects (mean age, 62 years), 86 were risk free and 75 had hypertension, heart disease, diabetes mellitus, and/or hyperlipidemia. Twenty-one subjects developed cerebrovascular symptoms during the prospective trial. Mean hemispheric cerebral blood flow values were significantly lower for at risk than for risk-free subjects. Symptomatic subjects showed lower values than those in either of the two asymptomatic groups at every session. Statistical analysis of cerebral blood flow values for symptomatic patients compared one and two years prior to onset of symptoms, at the onset of symptoms, and 1 year later showed reductions compared to asymptomatic risk-factored subjects tested in a similar prospective manner. Measurable declines in cerebral perfusion accompany development and progression of aortocerebral atherosclerosis prior to clinical appearance of signs and symptoms of cerebrovascular disease. If confirmed, these observations should permit the institution of preventive medical and/or surgical interventive measures and an evaluation of their outcome.
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PMID:Progressive cerebral ischemia antedates cerebrovascular symptoms by two years. 648 37

30 patients aged between 45 and 78 years and who had suffered from transient global amnesia (TGA), were seen at the Department of Neurology, Pordenone Public Hospital, in the period 1978 to 1982. 25 patients had one or more risk factors for cerebrovascular disease, such as hypertension, cardiac abnormalities, diabetes and hyperlipidemia. EEG examination revealed abnormal activity only in 7 patients. Brain Computed Tomography showed cerebral atrophy in 10 and hypodense lesions in 3 patients. 16 patients had been followed up for a mean interval of 20 months. During the follow-up period, 4 patients had recurrent TGA and one had a transient ischemic attack in the vertebrobasilar arterial system. In the follow-up group, 15 patients showed permanent memory impairment. The high incidence of risk factors for cerebrovascular disease seems to confirm that TGA is probably due to transient cerebral ischemia. The high rate of permanent memory impairment, almost always connected with the coexistence of cerebrovascular risk factors, is not in agreement with the postulated good prognosis of TGA.
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PMID:Transient global amnesia. 651 86

The present study has been devoted to the analysis of 120 patients presenting with reversible focal cerebral ischemia without conventional signs of cardiopathy and/or relevant atherosclerotic disease. In 77% of the patients vascular risk factors, such as hypertension or hyperlipemia, were present. In 23% of the patients, no abnormal finding was discovered at clinical, hematochemical and cardiological examinations. In these patients a further cardiological evaluation was performed with echocardiography. Dynamic electrocardiography was performed in 52 patients. Echocardiography and dynamic electrocardiography revealed the occurrence of 6 cases of mitral valve prolapse (MVP), 2 cases of frequent premature ventricular beats, and 1 proximal atrial arrhythmia. All 6 cases of MVP were detected in the subgroups of patients without vascular risk factors. In our patients younger than 45 years, the relative frequency of MVP attains 21.5%. This study confirms that MVP has to be regarded as a risk factor for focal cerebral ischemia in young patients.
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PMID:Mitral valve prolapse as a risk factor for TIA. A study with echocardiography and dynamic ECG. 688 93

One hundred and one patients below 45 years and showing objective signs of cerebral ischemia were studied retrospectively for pathogenic factors. Twelve were below 15 years; the male to female ratio was 1:1. Factors known as predisposing (heart disease, hypertension, hyperlipemia, diabetes mellitus or infectious diseases) and other possible factors (e.g. trauma, abuse) were found in 41 patients. Among women using contraceptive pills there might be an increased risk of development of cerebral thrombosis, but the material was not large enough to warrant statistical analysis. In 64 patients one or more abnormal coagulation values were found, the most frequent being a deficient vessel wall fibrinolysis, which was noted in 38%. We therefore consider it worthwhile to investigate the fibrinolytic defence mechanism of the vessel wall in patients with cerebral thrombosis, since it is possible to treat this condition with specific fibrinolytic stimulating agents.
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PMID:Coagulation studies in children and young adults with cerebral ischemic episodes. 732 67

We have reviewed 15 cases of carotid artery stenosis in the neck, consisting of 11 patients with cerebral ischemia and 4 asymptomatic patients, in relation to associated coronary heart disease. The 15 patients had systemic complications, including hypertension in 87%, diabetes mellitus in 40% and hyperlipidemia in 57%. Systemic vascular complications other than coronary heart disease were present in 27% of the patients. Three of the 15 patients had a history of ischemic heart disease and had been treated by cardiologists. One patient developed angina pectoris on the second day of a cerebral ischemic attack. Coronary angiography (CAG) and simultaneous cerebral angiography following carotid endartectomy (CEA) were performed 4 of the remaining 12 patients, who had symptoms or history of ischemic heart attacks. Three of these four patients had stenotic lesions in their coronary arteries. Another one patient among the remaining 8 developed angina pectoris one year after undergoing CEA. This patient had 3-vessel coronary artery disease. These findings suggest that a strong correlation between stenotic lesions of the carotid arteries in the neck and coronary heart disease, with or without episodes of ischemic heart disease. CAG should be strongly recommended in such patients to assess the severity of complicating ischemic heart disease and to improve the prognosis following CEA.
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PMID:[Severe carotid artery stenosis in the neck is frequently associated with coronary heart disease]. 812 3

The factor II G20210A mutation is a recently identified congenital risk factor for venous thrombosis. Its role in artery disease is still undefined. We investigated 72 patients (35 male and 37 female) with documented ischemic stroke occurred before 50 years of age and without risk factors such as diabetes, hypertension, and hyperlipidemia; 198 thrombosis-free individuals were investigated as the control group. We found 7 heterozygotes (9.7%) and 2 homozygotes (2.7%) for the mutant factor II allele among the patients and 5 heterozygotes (2.5%) among the controls; the mutant factor II allele frequency in the patient group (7.6%, 95% confidence interval [CI], 3.3 to 11.9) was significantly higher than in the controls (1.2%; 95% CI, 0.1 to 2.3; P = .0001). The prevalence of other investigated mutant alleles (factor V G1691A, methylenetetrahydrofolate reductase C677T) did not significantly differ between the two groups. The odds ratio for ischemic stroke associated with the carriership of the mutant factor II allele (both heterozygous and homozygous genotypes) was 5.1 (95% CI, 1.6 to 16.3). Heterozygous genotype was associated with a 3.8-fold increased risk for cerebral ischemia (95% CI, 1.1 to 13.1); in particular, assuming an expected prevalence of homozygotes in the general population of 1.6 to 10,000 according to the Hardy-Weinberg equilibrium, the risk associated with the homozygous genotype was estimated exceedingly high, being increased 208-fold.
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PMID:Prothrombin G20210A mutant genotype is a risk factor for cerebrovascular ischemic disease in young patients. 957 89

Mutations such as factor V Leiden G1691A (FVL), prothrombin G20210A (FIIM), methylenetetrahydrofolate reductase (MTHFR) C677T, cystathionine beta-synthase (CBS) 844ins68 and endothelial cell protein C receptor (EPCR) 4031ins23 are risk factors for thromboembolism. To assess the role of these mutations in young adults with cerebral ischemia of otherwise undetermined etiology, 93 patients younger than 50 years old with thromboembolic strokes or transient ischemic attacks were studied. One hundred and eighty-six healthy age-matched and sex-matched blood donors served as controls. The FVL mutation was detected in 15/93 patients and 13/186 controls. After adjustment for smoking, arterial hypertension, and hyperlipidemia, the association of the FVL mutation with cerebral ischemia [odds ratio (OR), 3.19; 95% confidence interval (CI), 1.38-7.39] remained significant. One of 93 patients and 6/186 controls were carriers of FIIM (OR, 0.33; 95% CI, 0.04-2.75). We detected the MTHFR TT677 genotype in 9/93 patients and 26/186 controls (OR, 0.66; 95% CI, 0.30-1.47), a CBS 844ins68 mutation in 12/93 patients and 19/186 controls (OR, 1.30; 95% CI, 0.60-2.81), and an EPCR 4031ins23 mutation in 1/93 patients and in no control individual (P = 0.33). In conclusion, in younger adults the FVL mutation is a risk factor for cerebrovascular disease. FIIM, the MTHFR TT677 genotype and the CBS 844ins68 mutation did not contribute to the risk in this group of patients. The EPCR 4031ins23 mutation is very rare, its possible role needs further investigation.
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PMID:Genetic risk factors in young adults with 'cryptogenic' ischemic cerebrovascular disease. 1243 43


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