Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current medical practice recommends the use of alternatives to estrogen-replacement therapy for the treatment of menopausal sequelae in younger women with breast cancer, although this clinical recommendation is undergoing reappraisal. Until prospective randomized studies addressing hormone use in this population are available, estrogen use in breast cancer patients will remain controversial. Because estrogen-replacement therapy is not the standard of practice and there is limited information available on nonestrogen therapies, women with breast cancer who are menopausal may not be prescribed or counseled about nonestrogen options. The efficacy, safety, and extent of use of most nonestrogen treatment modalities (other hormonal preparations, nonhormonal drugs, homeopathic preparations, and non-drug treatments) are not well documented and, unlike estrogen, many are selective in their benefit and do not share estrogen's universal impact. The use of several nonestrogen approaches for the prevention and treatment of osteoporosis has been promising. Traditional recommendations to maintain skeletal integrity, such as weight-bearing exercise; a diet rich in calcium and limited in caffeine, alcohol, and protein; avoidance of smoking; and measures to minimize trauma have been expanded to include the use or investigation of drugs (either alone or in combination). These drugs include progestins, vitamin D metabolites, injectable and intranasal synthetic salmon calcitonin, bisphosphonates, sodium fluoride, parathyroid hormone, growth factors, tamoxifen, etc. Strict control of the known risk factors, such as smoking, dyslipidemia, and hypertension as well as exercise, weight control, and the use of tamoxifen, are employed for the prevention and treatment of cardiovascular complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonhormonal alternatives for the management of early menopause in younger women with breast cancer. 799 60

Persons with chronic SCI have several metabolic disturbances. As a consequence of inactivity and the body compositional changes of decreased skeletal muscle with a relative increase in adiposity, a state of insulin resistance and hyperinsulinemia has been demonstrated to exist, associated with abnormalities in oral carbohydrate handling. Elevated plasma insulin levels in persons with SCI probably contribute to the cause of frequent dyslipidemia and hypertension. This constellation of metabolic changes represents an atherogenic pattern of CHD risk factors with many of the distinctive features of a cardiovascular dysmetabolic syndrome that is called syndrome X. Reduction in modifiable risk factors for CHD should decrease the occurrence of catastrophic cardiovascular events. There is evidence to suggest that endogenous anabolic hormone levels are depressed in a proportion of individuals with SCI. Depression of serum testosterone and growth hormone/IGF-I levels may exacerbate the adverse lipid and body compositional changes, reduce exercise tolerance, and have deleterious effects on quality of life. Because of immobilization, individuals with paraplegia have osteoporosis of the pelvis and lower extremities, and those with tetraplegia also have osteoporosis of the upper extremities. In addition, there is evidence to suggest that bone loss progresses with time in persons with chronic SCI. This may be caused by chronic immobilization per se or may be a consequence of adverse hormonal changes, including deficiency of anabolic hormones or deficiency of vitamin D and calcium with secondary hyperparathyroidism. Serum thyroid function abnormalities resembling the euthyroid sick "low T3 syndrome" have been reported in those with acute and chronic spinal cord injury. Depressed serum T3 and elevated rT3 in chronic SCI may be caused by associated illness. Current practice has been hesitant to treat abnormal serum thyroid chemistries associated with nonthyroidal illness. Recognition of metabolic abnormalities in individuals with SCI is vital as a first step in improving clinical care. The application of appropriate interventions to correct or ameliorate these abnormalities promises to improve longevity and quality of life in persons with SCI.
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PMID:Metabolic changes in persons after spinal cord injury. 1068 Jan 61

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
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PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

Vascular calcification is a frequent complication of uremic patients. In addition to classical risk factors such as age, male gender, smoking, inflammation, hypertension, dyslipidemia, and diabetes, which also exist in the general population, patients with chronic renal failure have other risk factors such as oxidative stress, inflammation, hyperparathyroidism, hypoparathyroidism, hypercalcemia, hyperphosphatemia, and overtreatment with calcium and vitamin D. These latter risk factors may even have a better predictive value than classical risk factors for coronary heart disease in uremic patients.
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PMID:Advanced oxidation protein products, parathyroid hormone and vascular calcification in uremia. 1220 1

The reduction of cardiovascular disease risk in kidney failure involves treatment of modifiable risk factors and provision of proven interventions to patients with established disease. Volume status management is key to blood pressure control. Statins are the agents of choice for the treatment of dyslipidemia. Target hemoglobin levels should be achieved using intravenous iron and erythropoietic agents. Combinations of calcium and noncalcium-containing phosphorus binders and vitamin D and its analogues should be used to attain target parathyroid hormone, phosphorus, and calcium phosphorus product levels. beta Blockers and aspirin are recommended in patients with ischemic heart disease and angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers), and beta blockers are recommended in patients with heart failure with reduced ejection fraction. In patients who require revascularization, studies suggest a survival benefit of coronary artery bypass graft surgery over percutaneous transluminal coronary angioplasty and coronary artery stenting.
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PMID:Treating the Patient with Kidney Failure to Reduce Cardiovascular Disease Risk. 1521 21

Chronic kidney disease is a progressive condition that results in significant morbidity and mortality. Because of the important role the kidneys play in maintaining homeostasis, chronic kidney disease can affect almost every body system. Early recognition and intervention are essential to slowing disease progression, maintaining quality of life, and improving outcomes. Family physicians have the opportunity to screen at-risk patients, identify affected patients, and ameliorate the impact of chronic kidney disease by initiating early therapy and monitoring disease progression. Aggressive blood pressure control, with a goal of 130/80 mm Hg or less, is recommended in patients with chronic kidney disease. Angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists are most effective because of their unique ability to decrease proteinuria. Hyperglycemia should be treated; the goal is an AIC concentration below 7 percent. In patients with dyslipidemia, statin therapy is appropriate to reduce the risk of cardiovascular disease. Anemia should be treated, with a target hemoglobin concentration of 11 to 12 g per dL (110 to 120 g per L). Hyperparathyroid disease requires dietary phosphate restrictions, antacid use, and vitamin D supplementation; if medical therapy fails, referral for surgery is necessary. Counseling on adequate nutrition should be provided, and smoking cessation must be encouraged at each office visit.
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PMID:Chronic kidney disease: prevention and treatment of common complications. 1557 Oct 58

Vascular calcifications are more frequent in dialysis patients than in the general population or in patients with cardiovascular disease (CVD) and normal renal function. The reasons for this high incidence are multiple; they include traditional factors such as hypertension, diabetes, dyslipidemia, and specific factors such as sodium overload, hyperomocysteinemia, chronic inflammation and oxidative stress, as well as mineral metabolism disturbances. Specifically, hyperphosphatemia and the elevated calcium (Ca) x phosphate product have been associated with an increased risk for the development of vascular calcification and death. Treatment with Ca salts can induce hypercalcemia, increased Ca x phosphate product and Ca overload. Sevelamer substitution for Ca salts has been documented to attenuate the progression of coronary artery and aortic calcification. A possible mechanism explaining this observation could be ongoing Ca loading related to oral Ca ingestion. Treatment with Ca salts could induce Ca overload, particularly in patients dialyzed against a high dialysate Ca (>1.5 mmol/L) solution, which is known to determine a positive dialysis balance. Conversely, an overall negative Ca balance can result from low Ca dialysate use (1.25 mmol/L) when the patients do not receive Ca supplements or vitamin D metabolites. Maintaining normal Ca and phosphate balances remains a primary goal in the management of dialysis patients. Control of hyperphopshataemia should be achieved either using Ca and aluminum-free phosphate binders, such as sevelamer, or Ca salts, alone or in combination, provided that a daily oral elemental Ca intake of 1.5 g is not exceeded.
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PMID:[Control of calcium and phosphate metabolism and prevention of vascular calcifications in uremic patients]. 1578 2

Vitamin D3 is modified by vitamin D3-25-hydroxylase in the liver, and 25-hydroxyvitamin D3-1alpha-hydroxylase in the kidney, to form the active metabolite, 1,25-dihydroxyvitamin D3. Chronic kidney disease (CKD) is characterized by reduced synthesis of 1,25-dibydroxyvitamin D3, inadequate renal phosphate clearance and calcium imbalance, secondary hyperparathyroidism (SHPT) and bone disease. CKD patients encounter a much higher risk of cardiovascular disease (CVD) than the general public. The cardiovascular risk factors for CKD patients include conventional factors such as age, gender, hypertension, diabetes, dyslipidemia and smoking, and non-conventional factors, such as anemia, uremia, reduced vascular compliance, inflammation and various hormonal factors. Several vitamin D analogs are currently available for the treatment of SHPT, and recent clinical data show that these analogs provide survival benefit for CKD patients in the order of paricalcitol > calcitriol > no vitamin D analog, independent of parathyroid hormone and calcium. Moreover, the survival benefit seems to be associated with cardiovascular causes. The observations made from these clinical studies raised intriguing questions about the involvement of the vitamin D receptor locus (VDR) in the cardiovascular system. This review discusses recent data regarding the role of vitamin D and its analogs in the CVD associated with CKD.
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PMID:Cardiovascular disease in chronic kidney failure: is there a role for vitamin D analogs? 1581

According to a k/DOQI work group, chronic kidney disease (CKD) can be present also in subjects with glomerular filtration rate (GFR) >90 mL/min or a serum creatinine (sCr) below 1.3 mg/dL. The aim of this study was to document the prevalence of clinical or biologic abnormalities among 190 cadaveric renal transplant patients with excellent and stable renal function at 6 months after transplantation as well as 5 years later. The recipients were 82 women and 108 men of mean age at transplantation of 44.56 +/- 11.73 years. All patients were on Neoral-based immunosuppression with at least 5-year follow-up. Mean sCr was 1.18 +/- 0.2 mg/dL. Mean GFR was 78.57 +/- 27.06 mL/min. Systolic blood pressure was >130 mm Hg in 56.6%, although 78.3% of patients were on antihypertensive therapy; 34.3% were anemic; 75.4% had serum cholesterol >200 mg/dL; 62.2% had serum triglyceride levels >170 mg/dL. Serum intact parathyroid hormone >100 pg/mL was observed in 38% of patients and 43% were on vitamin D supplementation, and 11.4% had developed posttransplant diabetes mellitus. With respect to controls, von Willebrand factor was higher in 81.2% (P < .0001; RR = 11); serum homocysteine levels in 75% (P < 0.001; RR = 7.61); PAI-1 in 37.5% (P = .0009; RR = 4). At 5 years posttransplantation we observed an overall improvement in these abnormalities. The vast majority of renal transplant patients with excellent graft function belong to stage 1 of CKD being affected by hypertension, dyslipidemia, anemia, and residual hyperparathyroidism. Markers of endothelial dysfunction were largely abnormal, a condition that could predispose to cardiovascular events.
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PMID:Chronic kidney disease is still present after renal transplantation with excellent function. 1675 52

The management and prevention of diabetes through lifestyle modifications and weight loss should be the mainstay of therapy in appropriate candidates. Although the results from the Diabetes Prevention Trial and the Finnish Prevention Study support this approach, over 95% of patients not participating in a prevention research study are unable to achieve and maintain any significant weight loss over time. Bariatric surgery for weight loss is an emerging option for more sustainable weight loss in the severely obese subject, especially when obesity is complicated by diabetes or other co-morbidities. The two most common types of procedures currently used in the United States are adjustable gastric bands and Roux-en-Y gastric bypass. These procedures can be performed laparoscopically, further reducing the perioperative morbidity and mortality associated with the surgery. While the gastric bypass procedure usually results is greater sustained weight loss (40-50%) than adjustable gastric banding (20-30%), it also carries greater morbidity and nutritional/metabolic issues, such as deficiencies in iron, B12, calcium, and vitamin D. Following bariatric surgery most subjects experience improvements in diabetes control, hypertension, dyslipidemia, and other obesity-related conditions. In patients with impaired glucose tolerance most studies report 99-100% prevention of progression to diabetes, while in subjects with diabetes prior to surgery, resolution of the disease is reported in 64-93% of the cases. While improvements in insulin resistance and beta-cell function are related to surgically induced weight loss, the rapid post-operative improvement in glycemia is possibly due to a combination of decreased nutrient intake and changes in gut hormones as a result of the bypassed intestine. Post-prandial hyperinsulinemic hypoglycemia associated with nesidioblastosis has been described in a series of patients following gastric bypass surgery, and may be related to the described changes in GLP-1 and other gut hormones.
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PMID:Impact of bariatric surgery on type 2 diabetes. 1770 79


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