Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
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Low fibrinolytic activity may increase the risk of thrombosis. Plasminogen activator inhibitor-1 (PAI-1) is an inhibitor of the fibrinolytic system. We examined the PAI-1 levels in patients with ischemic stroke. Plasma levels of PAI-1 were measured using enzyme-linked immunosorbent assay (ELISA) in 55 consecutive patients (age 60.2 +/- 11.4, 40 males and 15 females) with ischemic stroke. The PAI-1 assessments as well as neurological examinations using validated stroke scales were conducted at admission and 1 week, 1 month, and 3 months after stroke. Sex- and age-matched controls (+/- 4 years) underwent plasma PAI-1 measurement once. Etiology of the stroke was classified using the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. All pertinent stroke risk factors were recorded. All patients were contacted 3 years after stroke for recurrent vascular thrombotic disease. The plasma PAI-1 levels were 17.2 +/- 7.8 IU at admission, 11.2 +/- 9.2 IU at 1 week, 14.4 +/- 7.9 IU at 1 month, and 17.8 +/- 7.8 IU at 3 months among patients and 11.8 +/- 9.5 IU among controls (p values are < .002, .7, .12, and < .0005, respectively). As a rule, the neurological scores did not show a correlation to the PAI-1 levels. Presence of diabetes, hypertension, obesity, smoking, anticoagulant treatment, and sleep apnea did not affect the PAI-1 levels at any time point. Females had slightly higher PAI-1 levels. Age was a strong determinant for PAI-1 levels being higher in younger patients at every sampling time point (p values .02, .02, .02, and .03 respectively). The etiology of the ischemic stroke did not have an impact on PAI-1 levels. In 16 patients recurrent thrombosis had occurred. The high PAI-1 levels at admittance may reflect either an acute phase response or a chronic state. Normalized levels at 1 week and 1 month may be due to hospital diet, antithrombotic medication, weight loss, active physical therapy, and better care for diabetes. PAI-1 levels at 3 months after stroke did not predict recurrent thrombosis.
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PMID:Plasminogen activator inhibitor-1 in patients with ischemic stroke. 1145 24

Obesity is an epidemic disease that threatens to inundate health care resources by increasing the incidence of diabetes, heart disease, hypertension, and cancer. These effects of obesity result from two factors: the increased mass of adipose tissue and the increased secretion of pathogenetic products from enlarged fat cells. This concept of the pathogenesis of obesity as a disease allows an easy division of disadvantages of obesity into those produced by the mass of fat and those produced by the metabolic effects of fat cells. In the former category are the social disabilities resulting from the stigma associated with obesity, sleep apnea that results in part from increased parapharyngeal fat deposits, and osteoarthritis resulting from the wear and tear on joints from carrying an increased mass of fat. The second category includes the metabolic factors associated with distant effects of products released from enlarged fat cells. The insulin-resistant state that is so common in obesity probably reflects the effects of increased release of fatty acids from fat cells that are then stored in the liver or muscle. When the secretory capacity of the pancreas is overwhelmed by battling insulin resistance, diabetes develops. The strong association of increased fat, especially visceral fat, with diabetes makes this consequence particularly ominous for health care costs. The release of cytokines, particularly IL-6, from the fat cell may stimulate the proinflammatory state that characterizes obesity. The increased secretion of prothrombin activator inhibitor-1 from fat cells may play a role in the procoagulant state of obesity and, along with changes in endothelial function, may be responsible for the increased risk of cardiovascular disease and hypertension. For cancer, the production of estrogens by the enlarged stromal mass plays a role in the risk for breast cancer. Increased cytokine release may play a role in other forms of proliferative growth. The combined effect of these pathogenetic consequences of increased fat stores is an increased risk of shortened life expectancy.
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PMID:Medical consequences of obesity. 1518 Oct 27