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)

Programming is an epigenetic phenomenon by which nutrition, environment and stress acting in a critical period earlier in life change the organism's development. This process was evolutionarily selected as an adaptive tool for the survival of organisms living in nutritionally deficient areas and submitted to stressful conditions. Thus, perinatal malnutrition turns on different genes that provide the organism with a thrifty phenotype. In conditions of abundant supply of nutrients, those programmed organisms can be at risk of developing metabolic diseases (obesity, dyslipidemia, diabetes and hypertension). How nutrition or neonatal stress can program the immune system is less well known. Here, we discuss some of the hormonal and metabolic changes that occur in mothers and neonates and how those factors can imprint hormonal or metabolic changes that program neuroimmunomodulatory effects. Some of these changes involve thyroid hormones, leptin, insulin, glucocorticoids and prolactin as potential imprinting factors. Most of them can be transferred through the milk and may change with malnutrition or stress. We discuss the programming effects of these hormones upon body weight, body composition, insulin action, thyroid, adrenal and immune and inflammatory responses, with special emphasis on leptin, a cytokine that seems to play a central role in these events.
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PMID:Neonatal programming of neuroimmunomodulation--role of adipocytokines and neuropeptides. 1878 Oct 82

Chronic kidney disease (CKD) is an important risk factor for end-stage renal disease (ESRD) and cardiovascular events as well. Early-onset and progressive atherosclerosis is common in patients with CKD, which is caused by varieties of factors including dyslipidemia. CKD-related dyslipidemia such as increased triglyceride-rich atherogenic lipoproteins such IDL, small dense LDL and low HDL associated with insulin resistance, oxidative stress, inflammation, and malnutrition co-existing dyslipidemia such as high LDL are both causetive for early-onset atherogenesis and, possibly progression of CKD, thus are the therapeutic targets in early intervention of CKD. Life-style modification aimed for both renoprotection and anti-dyslipidemia as well as medications for metabolic disorders in CKD patients such as Ca/P imbalance is crucial for correction of dyslipidemia, and also prevention of cardiovasclular events and ESRD in CKD patients. Among anti-dyslipidemic drugs, statin, so far, is only class of drug proved to be effective for such purpose on evidence-basis.
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PMID:[Dyslipidemia as a therapeutic target for prevention of cardiovascular events and end-stage renal disease]. 1878 7

Metabolic syndrome (MS) is a common condition strongly associated with the development of type 2 diabetes and coronary heart disease (CHD). High triglycerides (TG) and low high density lipoprotein cholesterol (HDL-C) often occur together and represent the fundamental dyslipidemia of patients with MS. This abnormal lipoprotein profile is a major risk factor for premature cardiovascular disease. This review briefly discusses new findings on structure and functions of HDL in the atherogenic dyslipidemic condition known as MS. While the knowledge of the association between HDL-C and CHD began with the observation of an inverse relationship between HDL-C values and CHD risk, information in recent years shows the important role of HDL function in the pathogenesis of atherosclerosis. HDL particles are heterogeneous in structure, intravascular metabolism and antiatherogenic activity. Reductions in HDL-C concentrations, as seen in MS, are frequently associated with an abnormal HDL subclass distribution, altered HDL chemical composition, reduced antiinflamatory and antioxidative properties, and low capacity to promote cholesterol efflux. Deficiency of HDL particle number and attenuated antiaterogenic activity favor accelerated atherosclerosis. These data justify renewed emphasis on low HDL-C as a major risk factor in the prevention and treatment of CHD. Pharmacological interventions that increase HDL-C can also improve the quality and biological activities of HDL particles. Fibrates, nicotinic acid, cholesteryl ester transfer protein inhibitors, and reconstituted HDL are being investigated. Patients with MS constitute a high risk group that would particularly benefit from intervention to rise HDL-C.
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PMID:[Some physiopathologic features of metabolic syndrome]. 1893 96

The principal causes of morbidity and mortality in children with chronic renal failure on maintenance hemodialysis are cardiovascular complications. Recently, it has been suggested that oxidative stress, chronic inflammation and malnutrition are risk factors for cardiovascular disease. However, to date, biomarkers of oxidative stress have not been well studied in children. The aim of this study was to investigate the relationship between oxidative stress and cardiovascular risk factors in children on hemodialysis therapy. Twenty-eight hemodialysis patients (13 females, 15 males; mean age 15.1 +/- 2.5 years) and 20 healthy children (13 females, seven males; mean age 14.3 +/- 2.7 years) were included in the study. Levels of antibodies to oxidized low-density lipoprotein (oLABs), high sensitivity C-reactive protein (hs-CRP), albumin, prealbumin, transferrin, and ferritin were measured. Antibodies to oxidized low-density lipoprotein (LDL) in hemodialysis patients were lower than those in the controls (P < 0.05). The patients with lower oLAB titers had higher levels of hs-CRP and ratio of erythropoietin to hematocrit (EPO/Htc), and lower levels of albumin, prealbumin, apolipoprotein A-1 (ApoA(1)), and high-density lipoprotein (P < 0.05). Antibodies to oxidized LDL in hemodialysis patients with dyslipidemia were lower than those of patients with normal lipid profile (P < 0,05). This study showed that children treated by hemodialysis are exposed to oxidative stress and chronic inflammation. We suggest that oLAB levels are decreased in children on hemodialysis as a result of severe oxidative stress and that these antibodies are related to inflammation, anemia, malnutrition and dyslipidemia.
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PMID:Oxidative stress in children on hemodialysis: value of autoantibodies against oxidized low-density lipoprotein. 1895 4

Successful kidney transplantation leads to restoration of renal function. Some metabolic disorders from chronic renal failure may persist and new metabolic abnormalities can develop (obesity, diabetes, hypertension, bone disease, and anemia). Additionally, influence of immunosuppressive drugs (corticosteroids, cyclosporine A, tacrolimus, and rapamycin) may aggravate the course of diabetes, hypertension, and dyslipidemia. Nutritional management of renal transplantation is divided into the pretransplant period, transplant surgery, and early and late posttransplant period. Patients in the pretransplant period in dialysis treatment may develop protein-energy malnutrition and negative nitrogen balance, with loss of lean body mass and fat deposits. Nutritional management in the early posttransplant period with a functioning kidney graft necessitates fluid and electrolyte balance control with protein intake of 1,2/kg BW/day and 30-35 kcal/kg BW/day. In a nonfunctioning kidney graft, dialysis treatment continues and the therapeutic dose of immunosuppressive drugs must be reduced. The principal objective in the late posttransplant period is the maintenance of optimal nutritional status. Nutrition is important in managing obesity, insulin resistance, diabetes, hyperlipidemia, and hypertension. Other posttransplant conditions for which diet and/or nutritional supplements may be beneficial include hypomagnesemia, hypophosphatemia, hyperuricemia, hyperkalemia, hyperhomocysteinemia, chronic renal allograft failure, renal anemia, and renal bone disease.
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PMID:Nutritional consequences of renal transplantation. 1912 81

Patients on peritoneal dialysis (PD) are at high cardiovascular (C-V) risk, and dyslipidemia, one of the major traditional C-V risk factors, is a common complication in chronic kidney disease. PD treatment may worsen lipid profile, because it confers a more atherogenic state than hemodialysis. There is evidence that in the general population, lipid-lowering therapy reduces C-V mortality, both in terms of primary and secondary prevention. The association between dyslipidemia and C-V mortality in dialysis patients is not well defined, and hypocholesterolemia, related to malnutrition/inflammation, is a confounding factor. However, despite the unfavorable lipid profile in PD patients and their high C-V mortality rate, until now we have had no conclusive data that the treatment of dyslipidemia in PD patients might contribute to reducing C-V mortality. At the moment, following the ATPIII and K-DOQI recommendations in considering dialysis patients as high C-V risk patients seems a reasonable approach, awaiting new large trials in PD patients. The present therapeutic tools to treat dyslipidemia in PD patients, such as diet, fibrates, omega-3, statins, carnitine, phosphate binders and use of glucose-free dialysis bags, are considered, with attention to high-risk diabetic patients, with the possible use of intraperitoneal insulin. The data indicate a correctable nihilism in treating dyslipidemia in the general population, probably even exacerbated in PD patients. However, it will only be with the correction of all of the C-V risk factors, traditional and uremia-related ones, that in future we shall hope to observe the reduction of C-V death in PD patients.
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PMID:Therapeutic tools for dyslipidemia in peritoneal dialysis patients. 1922 18

Metabolic syndrome (MetS) is defined as a cluster of risk factors for type 2 diabetes and cardiovascular disease; it is also an independent risk factor for developing chronic kidney disease (CKD) in the general population. Therefore, CKD has many similarities and associations with MetS, and the individual risk factors constituting MetS-especially insulin resistance and glucose intolerance, hypertension, dyslipidemia, and obesity-are also common features of the early stages of CKD. In the later stages of CKD, uremia per se and uremic complications such as fluid retention, protein-energy wasting, inflammation, and oxidative stress further contribute to an increase in the prevalence of MetS in CKD patients. In addition, PD patients exposed to glucose-based PD fluids have an increased risk of developing metabolic complications. The broad use of MetS in clinical research has raised the awareness of the public and of individual patients concerning the value of lifestyle interventions. However, the definition and pathogenesis of MetS are still debated, and no standardized definition nor proven prognostic value has been established for MetS as a cluster of risk factors for diabetes or cardiovascular disease in PD patients. Furthermore, considering the paradoxical associations of some of the risk factors in MetS with decreased mortality, another set of risk factors-those specific to patients with uremia (for example, inflammation and malnutrition)-and the appropriate cut-off levels to individual MetS risk factors should be taken account at the same time. Also, the benefit of interventions targeting these risk factors should be clarified in further clinical studies.
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PMID:Definition of metabolic syndrome in peritoneal dialysis. 1927 Feb 3

Cardiovascular disease (CVD) is the main cause of death in peritoneal dialysis (PD) patients, a situation that can be explained by a combination of traditional and nontraditional risk factors for CVD in these patients. Glucose and insulin homeostasis are altered in chronic kidney disease (CKD) patients even in the early stages of CKD, leading to insulin resistance by various pathways. Several factors have been implicated in the pathogenesis of insulin resistance, including anemia, dyslipidemia, uremia, malnutrition, excess of parathyroid hormone, vitamin D deficiency, metabolic acidosis, and increase in plasma free fatty acids and proinflammatory cytokines. Insulin resistance and dyslipidemia are observed and increase with the progression of CKD, playing an important role in the pathogenesis of hypertension and atherosclerosis. Particularly in PD patients, exposure to glucose from dialysis fluid accentuates the foregoing metabolic abnormalities. In conclusion, insulin resistance and altered glucose metabolism are frequently observed in CKD, and although dialysis partly corrects those disturbances, the use of glucose PD solutions intensifies a series of harmful metabolic consequences. New therapeutic measures aimed at reducing metabolic disorders are urgently needed and perhaps will improve PD patient survival.
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PMID:Insulin resistance and glucose homeostasis in peritoneal dialysis. 1927 Feb 4

Patients with benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTSs) have a considerably higher prevalence of cardiovascular disease (CVD) than the general population in old age. Many hypotheses have been created to explain traditional clinical risk factors of CVD, including age, male gender, cigarette smoking, inheritance, high blood pressure (BP), obesity, elevated fasting plasma glucose, diabetes mellitus, dyslipidemia, decreased physical activity and metabolic syndrome; or nontraditional risk factors such as oxidative stress, inflammation, vascular calcification, malnutrition, homocysteine and genetic variation. Although these risk factors are important in CVD pathophysiology and clinical presentation, there is still no single theory sufficient to provide an adequate explanation for all the properties of CVD. We speculate that by causing nocturia-induced sleep disturbances, BP variability, increased sympathetic activity, non-dipping BP variations; BPH may be an insidious risk factor for CVD. Benign prostate hyperplasia may be related to increased BP, coronary ischemic hearth disease or other cardiovascular pathologic conditions. This attention on BPH may produce a new approach to the diagnosis and treatment of CVD. Although the underlying mechanisms are still exactly unclear, further prospective randomized controlled studies are needed to identify if patients with BPH/LUTS is higher risk for CVD.
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PMID:An insidious risk factor for cardiovascular disease: benign prostatic hyperplasia. 1935 54

Middle molecules can be defined as compounds with a molecular weight (MW) above 500 Da. An even broader definition includes those molecules that do not cross the membranes of standard low-flux dialyzers, not only because of molecular weight, but also because of protein binding and/or multicompartmental behavior. Recently, several of these middle molecules have been linked to the increased tendency of uremic patients to develop inflammation, malnutrition, and atheromatosis. Other toxic actions can also be attributed to the middle molecules. In the present publication we will consider whether improved removal of middle molecules by large pore membranes has an impact on clinical conditions related to the uremic syndrome. The clinical benefits of large pore membranes are reduction of uremia-related amyloidosis; maintenance of residual renal function; and reduction of inflammation, malnutrition, anemia, dyslipidemia, and mortality. It is concluded that middle molecules play a role in uremic toxicity and especially in the processes related to inflammation, atherogenesis, and malnutrition. Their removal seems to be related to a better outcome, although better biocompatibility of membranes might be a confounding factor.
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PMID:Back to the future: middle molecules, high flux membranes, and optimal dialysis. 1937 41


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