Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The level of interleukin-6 (IL-6), a cytokine with prothrombotic properties, and its associations with metabolic, coagulation and fibrinolytic parameters were investigated in 68 young women (23-49 years, mean 40 years old) six months to six years after myocardial infarction (MI, N=22), lacunar cerebral infarction (LACI, N=16) and deep vein thrombosis (VT, N=30); all women were in the reproductive period, aged <45 years at the time of acute thrombotic event. Forty-seven age-matched women comprised a control group. Basic and multivariate analysis disclosed different patterns of IL-6 increase in all three groups of patients. In the MI group IL-6 was significantly elevated independently of factors known to increase IL-6 levels; the increase was most pronounced in patients with high lipoprotein(a). This result suggests a prothrombotic association of lipoprotein(a) with IL-6. In the whole LACI group IL-6 was not significantly increased. However, patients with elevated levels of IL-6 had abdominal obesity and elevated fibrinogen, suggesting the possibility that this combination might represent a specific risk profile. In VT group elevated IL-6 level was found in the group of previous users of oral contraceptives (OC). This might be relevant, since it is known that OC could importantly increase (previously elevated) IL-6 level in selected women. Our results suggest the hypothesis that the role of IL-6 might be vascular-bed-specific and further propose that increased IL-6 level might represent a novel, non-classical risk factor for development of MI, LACI and VT in specific subgroups of young women, which have to be clarified in further studies.
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PMID:Possible vascular-bed-specific role of interleukin-6 in young women with a history of myocardial infarction, lacunar cerebral infarction and deep vein thrombosis. 1503 42

Obesity is widely recognized as a risk factor for coronary artery disease, but opinion is divided regarding whether it is an independent risk factor for cerebrovascular disease; even now there is no common view. In this study, the review sought to focus on a prospective study, but since obesity and non-obesity basically cannot be randomly assigned, randomized controlled trials (RCT) are nonexistent. Accordingly, a cohort study (a method of clinical study in which the obesity group is actively followed up for comparison with the non-obesity group in regard to cerebrovascular disease) was mainly conducted. For reference, retrospective case-control studies are also shown. As a result, most epidemiological surveys on the relation between simple obesity and cerebrovascular disease denied any relation. That is, obesity alone, determined only on the basis of height and weight as shown by BMI (body mass index), etc., cannot be an independent risk factor for cerebrovascular disease; obesity can become a risk factor only when accompanied by hypertension, hyperlipidemia, impaired glucose tolerance, etc. Recently, however, most papers conclude that abdominal obesity is a risk factor for cerebral infarction, provided that there are no data confirming that obesity is a risk factor for hemorrhagic cerebrovascular disease (cerebral hemorrhage and subarachnoid hemorrhage).
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PMID:Obesity as a risk factor for cerebrovascular disease. 1509 22

Metabolic syndrome (MetS) consists of 5 metabolic components, which are recognized as risk factors for cerebral infarction. The present study was to evaluate the relative influence of individual metabolic component on incident cerebral infarction. Using a data of 209,339 Koreans registered in National Health Information Corporation, we evaluated the risk for incident cerebral infarction according to the number of metabolic component and each metabolic component for 4.37 years' follow-up. Cox proportional hazards model was used to calculate hazard ratios (HRs) for cerebral infarction and their confidence interval (CI). The more metabolic components accompanied the worse metabolic profile, leading increased incidence of cerebral infarction. The risk of cerebral infarction increased proportionally to the number of present metabolic components (number 0: reference, number 1: 1.78 [1.42-2.23], number 2: 2.20 [1.76-2.74], number 3: 2.61 [2.09-3.25] and number 4-5: 3.18 [2.54-3.98]). Compared to subjects without metabolic component, the impact of each component on cerebral infarction was relatively higher in elevated fasting glucose (1.56 [1.14-2.13]) and elevated BP (2.13 [1.66-2.73]), indicating no statistical significance in low HDL-cholesterol (1.53 [0.96-2.44]), high triglyceride (1.24 [0.84-1.84]) and abdominal obesity (1.05 [0.63-1.73]). Proportional relationship was found between the number of metabolic component and risk of cerebral infarction. Out of metabolic components, fasting glucose and BP are more powerful predictor for cerebral infarction.
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PMID:Components of metabolic syndrome and their relation to the risk of incident cerebral infarction. 3304 Dec 72