Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Premature ovarian failure (POF) and Turner's syndrome patients who are also hypoestrogenomic, like postmenopausal women, are considered to be a high risk group for hyperlipemia. Our long-term study was conducted to evaluate the effect of hormone replacement therapy (HRT) on lipid metabolism in 16 POF and 10 Turner's syndrome women. 1. The initial average total cholesterol (TC) of the untreated and treated POF patients (209, 196mg/dl) and that of untreated and treated Turner's syndrome patients (213, 240mg/dl) were significantly higher than those in the control group (175mg/dl) except treated POF patients. LDL cholesterol (LDL-C) of the untreated and treated POF patients (135, 113mg/dl) and that of untreated and treated Turner's syndrome patients (142, 144mg/dl) were significantly higher than those in the control group (108mg/dl) except treated POF patients. In comparison to healthy women of a similar age, POF and Turner's syndrome patients were at high risk of hyperlipemia because of higher serum TC and LDL-C levels. 2. After HRT for 2 years, LDL-C decreased by 18% and 13%, and HDL cholesterol increased by 38% and 41% in POF and Turner's syndrome patients, respectively. Hence AI decreased by 40% and 50% respectively. The younger the hyperlipemic patients are, the higher the relative risk for atherosclerosis is. The results of this study suggest that, because of the beneficial effects of HRT on serum lipid metabolism, it can help to prevent the development of coronary heart disease.
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PMID:[Effect of hormone replacement therapy on lipid metabolism in patients with premature ovarian failure and Turner's syndrome]. 784 37

Normal menopause is associated with vascular endothelial dysfunction, an early stage of atherosclerosis. The effect of premature ovarian failure (or premature menopause) on endothelial function in young women is unknown. Endothelial function was assessed in 18 women with premature ovarian failure before and after 6 months of hormone therapy and was compared with the endothelial function of 20 age- and body mass index-matched premenopausal women. Brachial artery diameter was measured both during hyperemia (an index of endothelium-dependent vasodilation) and in response to glyceryl trinitrate (an index of endothelium-independent vaso-dilation). Flow-mediated dilation was significantly lower in women with premature ovarian failure at baseline (increase in brachial artery diameter during hyperemia by 3.06 +/- 4.33%) than in control women (increase by 8.84 +/- 2.15%; P < 0.0005). Glyceryl trinitrate-induced vasodilation did not differ between the groups. After hormone therapy for 6 months, flow-mediated dilation was improved in women with premature ovarian failure, increasing by more than 2-fold (7.41 +/- 3.86%; P < 0.005 compared with pretreatment) and reaching normal values (P not significant compared with control women). Glyceryl trinitrate-induced vasodilation did not change after treatment in women with premature ovarian failure. Young women with premature ovarian failure have significant vascular endothelial dysfunction. Early onset of endothelial dysfunction associated with sex steroid deficiency may contribute to the increased risk of cardiovascular disease and mortality in young women with premature ovarian failure. Hormone therapy restores endothelial function within 6 months of treatment.
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PMID:Impaired endothelial function in young women with premature ovarian failure: normalization with hormone therapy. 1529 26

Women with Turner syndrome (TS) have increased risks of atherosclerosis, diabetes mellitus, and obesity. We hypothesized that women with TS have adverse metabolic or inflammatory markers for cardiovascular disease compared with normal women and estrogen-deficient controls. This was a cross-sectional study conducted at University College London Hospitals, UK. One hundred seventeen estrogen-treated women with TS and normal fasting blood glucose were compared with 30 age-matched normal controls and 31 estrogen-treated women with 46,XX premature ovarian failure (POF). The main outcome measures were markers of the metabolic syndrome, including the adipokines IL-6 and leptin, and C-reactive protein (CRP). TS women were more obese than controls (waist circumference, 79.9 +/- 12.4, 73.5 +/- 6.9, and 74.7 +/- 8.6 cm in TS, normal subjects, and POF controls, respectively; P = 0.005; body mass index, 26.8 +/- 5.8, 23.7 +/- 3.2, and 22.9 +/- 3.4 kg/m2; P < 0.001). This obesity was associated with increased CRP (2.9 +/- 1.5, 0.8 +/- 1.0, and 1.2 +/- 0.9 mg/liter; P < 0.001) and IL-6 concentrations (1.5 +/- 0.7, 1.0 +/- 1.5, and 1.2 +/- 0.5 pg/ml; P = 0.014), but lower fasting serum insulin (4.7 +/- 2.3, 6.3 +/- 3.0, and 6.9 +/- 2.9 mIU/ml; P = 0.004), glucose (83 +/- 11, 90 +/- 7, and 90 +/- 7 mg/dl; P < 0.001), and leptin (10.2 +/- 6.3, 14.4 +/- 7.6, and 14.8 +/- 8.1 ng/ml; P = 0.048). Triglyceride concentrations were similar in TS and POF women and were greater than in normal controls (97 +/- 53, 97 +/- 53, and 71 +/- 27 mg/dl; P = 0.024). We conclude that women with TS have various physical and biochemical features suggestive of the metabolic/insulin resistance syndrome, but there is a discrepancy among CRP, IL-6, and leptin, with leptin and fasting insulin concentrations being lower than expected for the degree of obesity. Obesity and estrogen therapy do not fully explain these findings. Women with TS may have specific metabolic defects contributing to cardiovascular risk.
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PMID:Adipokine dysregulation in turner syndrome: comparison of circulating interleukin-6 and leptin concentrations with measures of adiposity and C-reactive protein. 1572 8

New brief reports this month describe five timely topics: IDO inhibitors have demonstrated antitumor properties by increasing immune response to tumors and improving chemotherapy effectiveness. One of the current therapeutic efforts for Alzheimer's disease is directed towards blocking the gamma-secretase activity, thus reducing amyloid-beta production. Patients with premature ovarian failure (POF), at present mainly treated with hormone replacement therapy, are belated for novel treatment options. Selective ERbeta agonists are anticipated to emerge as therapeutics for the treatment of various diseases including inflammatory bowel syndrome, endometriosis, dementia and cognitive disorders. Phospholipase A2 inhibitors specific for enzyme isoforms are actively studied as potential antiallergic/antiasthmatic drugs, antiarthritic agents and therapeutics for atherosclerosis.
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PMID:Chronicles in drug discovery. 1603 84

Cardiovascular disease, including coronary artery disease, stroke and peripheral vascular disease, is the leading cause of death among women. Vascular endothelial dysfunction is an early marker of atherosclerosis. Women with premature ovarian failure (or premature menopause) present an increased risk for cardiovascular disease, which might be attributed to the early onset of vascular endothelial dysfunction, associated with sex steroid deficiency. Cyclical estrogen and progestogen therapy has been shown to restore endothelial function in these young women. Further research is required to assess primarily the long-term effects of hormone replacement therapy on cardiovascular and overall prognosis in young women with premature ovarian failure, as well as the effects of different doses, duration and routes of hormone administration in these women.
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PMID:Premature ovarian failure, endothelial dysfunction and estrogen-progestogen replacement. 1651 63

Premature ovarian failure (POF) appears to be a complex disease entity with several underlying etiopathogenic contributions including the possibility of multiple distinctly different autoimmune mechanisms, in which inflammatory autoimmunity targeted to ovarian-specific germline antigens (e.g., zona pellucida proteins or Mater) or differentiation/regulatory factors (e.g. inhibin-alpha) were regarded as one of the most crucial factors. Platelet-activating factor (PAF) and PAF class oxidized phospholipids stimulate the occurrence and development of inflammation and atherosclerosis. PAF acetylhydrolase (PAF-AH) can hydrolyze PAF and PAF class oxidized phospholipids and eventually prevent the body from the damage of these inflammatory mediators. These findings indicate a potential relationship between PAF-AH and POF thus have major implications for the future health of women who suffer with premature ovarian failure.
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PMID:Platelet-activating factor acetylhydrolase and premature ovarian failure. 2555 49