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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maria Daria Haust, MD, has made many significant contributions to our understanding of atherogenesis in children, particularly in associating the earliest lesions (fatty spots and streaks) with the normal growth and remodeling of arteries. It is my privilege to link her early work to more recent findings which show that the early lesions seen in the arteries of children before puberty bear no relationship to the risk of atherosclerosis in later life. Furthermore, present evidence supports the view that intervening in childhood (2-15 years) with low-fat low-cholesterol diets or even worse, lipid-lowering drugs to prevent atheroslerotic plaques in adulthood is wasted effort. Overzealous parents may unwittingly induce malnutrition in their children and many children with restricted access to palatable foods, will yearn for them even more as they become older leading to over weightness. Pediatricians from various scientific bodies around the world vary in their advice to mothers regarding diets for children. The program adopted by Health Canada on the advice of pediatricians in that country, which is also supported by the European Society of Pediatrics, Gastroenterology and Nutrition, recommends that the fat content of diets for children should be tapered gradually from 40% of energy at 2 years of age to 30% of energy at the conclusion of linear growth (late adolescence).
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PMID:The role of dietary and plasma lipids in childhood atherogenesis. 1194 33

Oxidative stress results from an imbalance between oxidant production, including reactive oxygen species (ROS), reactive nitrogen species (RNS), chlorinated compounds, and antioxidant defense mechanisms. Most reports prove that oxidative stress is present in ESRD patients. Several studies tend to accreditate the hypothesis by which oxidative stress is a strong co-factor for the development of complications related to long-term HD such as atherosclerosis, amyloidosis, malnutrition, anemia, and infection. In order to evaluate the rationale for curative action against oxidative damage in chronic renal failure patients, we reviewed the putative factors involved in this process. Antioxidant systems are severely impaired in uremic patients and gradually altered with the degree of renal failure. Moreover, the inflammatory state caused by the hemoincompatibility of the dialysis system plays a critical role in the activation of NADPH oxidase, aggravating the pro-oxidant status of uremic patients. Prevention of ROS overproduction by improvement of dialysis biocompatibility, an important component of adequate dialysis, might be completed by antioxidant supplementation.
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PMID:Oxidative stress in hemodialysis patients: is NADPH oxidase complex the culprit? 1198 24

End-stage renal disease (ESRD) is characterized by a high mortality rate, derived largely from cardiovascular disease (CVD). In patients with ESRD, high levels of pro-inflammatory cytokines and increased oxidative stress are common features that may contribute to malnutrition, anaemia, recombinant human erythropoietin (rHuEPO) resistance, and atherosclerosis. Inflammation predicts poor outcome in ESRD. It is multifactorial in cause and, while it may reflect the underlying CVD, the acute-phase response may also contribute to both oxidative stress and progressive vascular injury. In patients with ESRD, the acute-phase response may be influenced by a number of factors unrelated to dialysis and perhaps by the dialysis procedure itself. Inflammation and the acute-phase response interact with the haematopoietic system at several levels resulting in reduced erythropoiesis, accelerated destruction of erythrocytes, and blunting of the reactive increase in erythropoietin in response to reduced haemoglobin levels. In patients with ESRD, rHuEPO resistance has been linked with inflammation, the latter of which is often associated with a state of functional iron deficiency. Patients with ESRD are thought to have a reduced capacity to handle oxidative stress. There is recent evidence that a relationship may exist between inflammation and oxidative stress and treatment of anaemia with rHuEPO. However, iron may also generate oxidative stress. Controlled trials are needed before evidence-based recommendations for the management of inflammation-induced anaemia and resistance to rHuEPO can be defined.
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PMID:Anaemia, rHuEPO resistance, and cardiovascular disease in end-stage renal failure; links to inflammation and oxidative stress. 1209 5

Immunosuppressive treatment is a critical procedure in dialysis patients, in whom an increased risk of infection is already present. Haemodialytic treatment increases the patient's susceptibility to bacterial infection, mainly by impairing polymorphonuclear leukocyte phagocytosis, but it can also restore the patient's immunological defences by improving the T-cell function, which is reduced by pre-dialysis uraemia. Patients on dialysis usually continue the immunosuppressive treatment that had been established for the illness that caused their renal failure [e.g. systemic lupus erythematosus (SLE) or renal vasculitis]. Less frequently, patients on dialysis need immunosuppression for immunological or inflammatory diseases that appear 'de novo' after initiation of dialysis. SLE and antineutrophil cytoplasmic antibody (ANCA)-related vasculitides are immunological illnesses that frequently cause end-stage renal failure (ESRF). A reduction in serological and/or clinical activity is usually observed in SLE patients after they reach ESRF, but a similar or increased frequency of extrarenal relapse episodes in lupus patients after the beginning of the dialysis, compared with the pre-dialysis period, has also been described. Frequency of relapse episodes in patients on dialysis treatment for ANCA-related vasculitides varies from 10 to 30% per patient/year in different reports, and it is higher than the frequency of relapses after renal transplantation; anti-rejection therapy seems to be the most likely protective factor in these conditions. The treatment of relapse episodes in SLE or ANCA vasculitis in dialysis-dependent patients is usually not different from treatment of relapses in patients with dialysis-independent renal function. However, the risk of severe infection caused by immunosuppressive treatment is relevantly higher in dialysis patients. Furthermore, there is a lack of prospective controlled studies indicating the optimal management of immunosuppressive protocols in dialysis patients. A particularly careful assessment of the patient's risks and benefits is necessary in deciding how long immunosuppressive treatment should last after acute or rapidly progressive renal damage, that should require dialysis treatment, in patients with SLE or ANCA vasculitis. In the above conditions, the risks of prolonging immunosuppressive treatment must be balanced against the relatively good prognosis offered to these patients by dialysis and renal transplantation. In a retrospective review of 24 patients receiving long-term steroid therapy (>3 months) in our dialysis unit in the past 5 years, we found relevant clinical differences in the patients receiving steroid treatment compared with 24 controls. Steroid-treated patients showed less favourable nutritional conditions, with lower serum albumin and body mass index vs non-steroid-treated patients; moreover, C-reactive protein values were persistently higher in the steroid-treated group. Steroid treatment in these patients was usually performed at the beginning of regular dialysis, as a continuation of the treatment that started before the initiation of dialysis. Only two patients, who needed a prolonged low-dose steroidal treatment to control a malnutrition-inflammation-atherosclerosis (MIA) syndrome, started steroids many years after beginning dialysis. Steroid treatment was effective in improving the nutritional condition and inflammatory symptoms in these two patients after all conventional measures had failed.
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PMID:Immunosuppressive treatment in dialysis patients. 1214 70

End-stage renal disease (ESRD) is characterized by an exceptional mortality rate, much of which is the result of cardiovascular disease (CVD). Although traditional risk factors are common in ESRD patients, they may not be sufficient alone to account for the high prevalence of CVD in this condition. Recent evidence demonstrates that chronic inflammation, a non-traditional risk factor which is observed commonly in ESRD patients, may cause malnutrition and progressive atherosclerotic CVD by several pathogenetic mechanisms. The causes of inflammation in ESRD are multifactorial and, while it may reflect underlying CVD, an acute-phase reaction may also be a direct cause of vascular injury by several pathogenetic mechanisms. Available data suggest that pro-inflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation and atherosclerosis (MIA) would improve survival in dialysis patients. Recent evidence has demonstrated strong associations between inflammation and both increased oxidative stress and endothelial dysfunction in ESRD patients. As there is as yet no recognized, or even proposed, treatment for ESRD patients with chronic inflammation, it would be of obvious interest to study the long-term effect of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as the outcome in these patients.
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PMID:Inflammation in end-stage renal failure: could it be treated? 1254 10

End-stage renal disease (ESRD) is characterized by an exceptional cardiovascular mortality rate. Although traditional risk factors are common in ESRD patients, they alone may not be sufficient to account for the high prevalence of cardiovascular disease (CVD). Recent evidence demonstrated that chronic inflammation, a non-traditional risk factor which is commonly observed in ESRD patients, may cause malnutrition and progressive atherosclerotic CVD by several pathogenetic mechanisms. Although both malnutrition and inflammation have been shown to be strong predictors of cardiovascular mortality in ESRD patients, it must be remembered that the majority of studies describing the presence of inflammation and malnutrition have been performed in Western and Asian industrialized countries. As it is evident that the prevalence of malnutrition and inflammation may differ markedly between different regions of the world and developing countries face a much higher prevalence of chronic infectious diseases, comparative inter-regional studies focusing on the etiology and prevalence of the malnutrition, inflammation and atherosclerosis syndrome are warranted.
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PMID:Inflammation, malnutrition and atherosclerosis in end-stage renal disease: a global perspective. 1220 91

Oxidative stress which results from an imbalance between oxidant production and antioxidant defense mechanisms is now a well recognized pathogenesis factor that could be implicated in the hemodialysis (HD)-related pathology. This review focuses on: 1) factors that may be responsible for oxidative stress in HD patients (hemoincompatibility of the dialysis system--hemoreactivity of the membrane and trace amounts of endotoxins- and uremia per se); 2) implication of such phenomenon in long term complications including anemia, amyloidosis, accelerated atherosclerosis and malnutrition and finally and 3) prevention ways consisting in improving the hemocompatibility of the dialysis system and supplementing the deficiency patients with antioxidants.
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PMID:[Oxidative stress, hemo-incompatibility and complications of long-term dialysis]. 1222 52

Cardiovascular disease (CVD) remains the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Although traditional risk factors are common in ESRD patients, they alone may not be sufficient to account for the high prevalence of CVD in this condition. Recent evidence demonstrates that chronic inflammation, a nontraditional risk factor which is commonly observed in ESRD patients, may cause malnutrition and progressive atherosclerotic CVD by several pathogenetic mechanisms. The causes of inflammation in ESRD are multifactorial and, while it may reflect underlying CVD, an acute-phase reaction may also be a direct cause of vascular injury by several pathogenetic mechanisms. Available data suggest that proinflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. Thus it could be speculated that suppression of the vicious cycle of malnutrition, inflammation, and atherosclerosis (MIA syndrome) would improve survival in dialysis patients. Recent evidence has demonstrated strong associations between inflammation and both increased oxidative stress and endothelial dysfunction in ESRD patients. As there is not yet any recognized, or even proposed, treatment for ESRD patients with chronic inflammation, it would be of obvious interest to study the long-term effect of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as outcome in these patients.
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PMID:Inflammation in end-stage renal disease: sources, consequences, and therapy. 1235 37

Radiation hazards in outer space present an enormous challenge for the biological safety of astronauts. A deleterious effect of radiation is the production of reactive oxygen species, which result in damage to biomolecules (e.g., lipid, protein, amino acids, and DNA). Understanding free radical biology is necessary for designing an optimal nutritional countermeasure against space radiation-induced cytotoxicity. Free radicals (e.g., superoxide, nitric oxide, and hydroxyl radicals) and other reactive species (e.g., hydrogen peroxide, peroxynitrite, and hypochlorous acid) are produced in the body, primarily as a result of aerobic metabolism. Antioxidants (e.g., glutathione, arginine, citrulline, taurine, creatine, selenium, zinc, vitamin E, vitamin C, vitamin A, and tea polyphenols) and antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidases) exert synergistic actions in scavenging free radicals. There has been growing evidence over the past three decades showing that malnutrition (e.g., dietary deficiencies of protein, selenium, and zinc) or excess of certain nutrients (e.g., iron and vitamin C) gives rise to the oxidation of biomolecules and cell injury. A large body of the literature supports the notion that dietary antioxidants are useful radioprotectors and play an important role in preventing many human diseases (e.g., cancer, atherosclerosis, stroke, rheumatoid arthritis, neurodegeneration, and diabetes). The knowledge of enzymatic and non-enzymatic oxidative defense mechanisms will serve as a guiding principle for establishing the most effective nutrition support to ensure the biological safety of manned space missions.
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PMID:Free radicals, antioxidants, and nutrition. 1236 82

Cardiovascular disease is the leading cause of mortality in uremic patients. In large cross-sectional studies of dialysis patients, traditional cardiovascular risk factors such as hypertension and hypercholesterolemia have been found to have low predictive power, while markers of inflammation and malnutrition are highly correlated with cardiovascular mortality. However, the pathophysiology of the disease process that links uremia, inflammation, and malnutrition with increased cardiovascular complications is not well understood. We hereby propose the hypothesis that increased oxidative stress and its sequalae is a major contributor to increased atherosclerosis and cardiovascular morbidity and mortality found in uremia. This hypothesis is based on studies that conclusively demonstrate an increased oxidative burden in uremic patients, before and particularly after renal replacement therapies, as evidenced by higher concentrations of multiple biomarkers of oxidative stress. This hypothesis also provides a framework to explain the link that activated phagocytes provide between oxidative stress and inflammation (from infectious and non-infections causes) and the synergistic role that malnutrition (as reflected by low concentrations of albumin and/or antioxidants) contributes to the increased burden of cardiovascular disease in uremia. We further propose that retained uremic solutes such as beta-2 microglobulin, advanced glycosylated end products (AGE), cysteine, and homocysteine, which are substrates for oxidative injury, further contribute to the pro-atherogenic milieu of uremia. Dialytic therapy, which acts to reduce the concentration of oxidized substrates, improves the redox balance. However, processes related to dialytic therapy, such as the prolonged use of catheters for vascular access and the use of bioincompatible dialysis membranes, can contribute to a pro-inflammatory and pro-oxidative state and thus to a pro-atherogenic state. Anti-oxidative therapeutic strategies for patients with uremia are in their very early stages; nonetheless, early studies demonstrate the potential for significant efficacy in reducing cardiovascular complications.
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PMID:The elephant in uremia: oxidant stress as a unifying concept of cardiovascular disease in uremia. 1237 53


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