Selenium
Congestive cardiomyopathy and the selenium content of serum
Oster O, Prellwitz W, Kasper W, Meinertz T.A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. Therefore the serum selenium content of 20 patients with proven congestive cardiomyopathy was measured and compared to that of a healthy control group. The serum selenium content of the patients with cardiomyopathy was found to be different from that of the healthy control group. The mean value of selenium in serum for the control group was 80.1 micrograms Se/1 (SD +/- 13.2) within a range of 53 and 117 micrograms Se/1. From the 20 patients with congestive cardiomyopathy six patients showed selenium concentrations in the normal value range of the control group; in the serum of 14 patients a distinct lower selenium content was found (mean value 47.8 micrograms Se/1 (SD +/- 16.2)) within a range of 23 and 70 micrograms Se/1. A positive correlation was found between serum selenium content and the left ventricular ejection fraction. Our results suggest that a deficiency of selenium may be present in a number of patients with congestive cardiomyopathy.
Selenium deficiency and fatal cardiomyopathy in a patient receiving long-term home parenteral nutrition
Quercia RA, Korn S, O'Neill D, Dougherty JE, Ludwig M, Schweizer R, Sigman R.Fatal cardiomyopathy in a patient who received home parenteral nutrition (HPN) for eight years is reported, and the relationship of selenium deficiency to cardiomyopathy and other adverse effects is discussed. A 42-year-old white man with Crohn's disease who was receiving HPN was admitted to the hospital with severe chest pain and dyspnea. During the three days following admission, his symptoms of congestive heart failure and compensated metabolic acidosis persisted despite treatment. On hospital day 6, the patient developed increased ventricular irritability and refractory ventricular fibrillation and died. At autopsy, the heart weighted 500 g, all chambers were dilated, and the myocardium was grossly flabby. Extremely low concentrations of selenium (5-12% of normal) were found in plasma, heart, liver, and kidney tissue samples. The pathological findings in this patient were similar to those in two previously reported cases and strongly suggest that the fatal cardiomyopathy was secondary to selenium deficiency. Selenium is an integral part of the enzyme glutathione peroxidase, which plays an important role in the metabolism of tissues and organs. For metabolically stable patients receiving total parenteral nutrition, the suggested selenious acid dosage is 25-60 micrograms/day for adults and 1.4-30 micrograms/kg/day for pediatric patients. In selenium-depleted adults, a dosage of 100 micrograms/day administered intravenously for 21-31 days has been recommended to reverse symptoms. All HPN patients and hospitalized patients receiving extended parenteral nutrition should be monitored for selenium deficiency and given supplements if necessary.
Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure
de Lorgeril M, Salen P, Accominotti M, Cadau M, Steghens JP, Boucher F, de Leiris J. Laboratoire du Stress Cardiovasculaire et Pathologies Associees, UFR de Medecine et Pharmacie, Universite Joseph Fourier de Grenoble, Domaine de la Merci, 38706 La Tronche, Grenoble, France. michel.delorgeril@ujf-grenoble.frBACKGROUND: Chronic heart failure (CHF) seems to be associated with increased oxidative stress. However, the hypothesis that antioxidant nutrients may contribute to the clinical severity of the disease has never been investigated. AIMS: To examine whether antioxidant nutrients influence the exercise capacity and left ventricular function in patients with CHF. METHODS: Dietary intake and blood levels of major antioxidant nutrients were evaluated in 21 consecutive CHF patients and in healthy age- and sex-matched controls. Two indexes of the severity of CHF, peak exercise oxygen consumption (peak VO2) and left ventricular ejection fraction (LVEF), were measured and their relations with antioxidants were analysed. RESULTS: Whereas plasma alpha-tocopherol and retinol were in the normal range, vitamin C (P=0.005) and beta-carotene (P=0.01) were lower in CHF. However, there was no significant association between vitamins and either peak VO2 or LVEF. Dietary intake (P<0.05) and blood levels of selenium (P<0.0005) were lower in CHF. Peak VO2 (but not LVEF) was strongly correlated with blood selenium: r=0.76 by univariate analysis (polynomial regression) and r=0.87 (P<0.0005) after adjustment for age, sex and LVEF. CONCLUSIONS: Antioxidant defences are altered in patients with CHF. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction. Further studies are warranted to confirm the data in a large sample size and to investigate the mechanisms by which selenium and other antioxidant nutrients are involved in CHF.
Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure
de Lorgeril M, Salen P, Accominotti M, Cadau M, Steghens JP, Boucher F, de Leiris J. Laboratoire du Stress Cardiovasculaire et Pathologies Associees, UFR de Medecine et Pharmacie, Universite Joseph Fourier de Grenoble, Domaine de la Merci, 38706 La Tronche, Grenoble, France. michel.delorgeril@ujf-grenoble.frBACKGROUND: Chronic heart failure (CHF) seems to be associated with increased oxidative stress. However, the hypothesis that antioxidant nutrients may contribute to the clinical severity of the disease has never been investigated. AIMS: To examine whether antioxidant nutrients influence the exercise capacity and left ventricular function in patients with CHF. METHODS: Dietary intake and blood levels of major antioxidant nutrients were evaluated in 21 consecutive CHF patients and in healthy age- and sex-matched controls. Two indexes of the severity of CHF, peak exercise oxygen consumption (peak VO2) and left ventricular ejection fraction (LVEF), were measured and their relations with antioxidants were analysed. RESULTS: Whereas plasma alpha-tocopherol and retinol were in the normal range, vitamin C (P=0.005) and beta-carotene (P=0.01) were lower in CHF. However, there was no significant association between vitamins and either peak VO2 or LVEF. Dietary intake (P<0.05) and blood levels of selenium (P<0.0005) were lower in CHF. Peak VO2 (but not LVEF) was strongly correlated with blood selenium: r=0.76 by univariate analysis (polynomial regression) and r=0.87 (P<0.0005) after adjustment for age, sex and LVEF. CONCLUSIONS: Antioxidant defences are altered in patients with CHF. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction. Further studies are warranted to confirm the data in a large sample size and to investigate the mechanisms by which selenium and other antioxidant nutrients are involved in CHF.
Fulminant heart failure due to selenium deficiency cardiomyopathy (Keshan disease)
Burke MP, Opeskin K. Victorian Institute of Forensic Medicine, Department of Forensic Medicine, Monash University, Southbank, Australia.Selenium deficiency is a rare cause of cardiomyopathy that may be encountered by the forensic pathologist. Selenium deficiency is associated with a cardiomyopathy, myopathy and osteoarthropathy. In Asia and Africa, dietary selenium deficiency is associated with a cardiomyopathy known as Keshan disease and an osteoarthropathy called Kashin-Beck disease. Chronic selenium deficiency may also occur in individuals with malabsorption and long term selenium-deficient parenteral nutrition. Selenium deficiency causes myopathy as a result of the depletion of selenium-associated enzymes which protect cell membranes from damage by free radicals. We present a case of fulminant heart failure in a middle aged woman with a complex medical and surgical history including documented malabsorption and selenium deficiency. Pathological examination of the heart showed features consistent with Keshan disease.
Selenium status, kwashiorkor and congestive heart failure
Manar MJ, MacPherson GD, Mcardle F, Jackson MJ, Hart CA. College of Medicine, University of Malawi, Blanthre. manary@kids.wustl.eduSelenium deficiency is associated with congestive heart failure (CHF) in geographic areas where dietary selenium intake is low and in individuals receiving total parenteral nutrition. Among 66 children with kwashiorkor (including marasmic-kwashiorkor), those who developed CHF had lower serum selenium concentrations than those who did not (32.9 +/- 8.3 vs 41.1 +/- 11.9 microg/L, mean +/- SD, p = 0.03). This association was independent of serum albumin and selenium status was not associated with severity of symptoms, anthropometric indices or HIV infection. CONCLUSION: This association raises the possibility that selenium may contribute to CHF in washiorkor.
Dilated cardiomyopathy and selenium deficiency in AIDS. Apropos of a case
Constans J, Sire S, Sergeant C, Simonoff M, Ragnaud JM. Clinique de medecine interne et des maladies vasculaires, hopital Saint-Andre, Bordeaux, France.Cardiac-related death of HIV-positive patients is not rare. The etiology of AIDS-associated dilated cardiomyopathies often remains unknown, even at autopsy. We report an observation associated to a severe deficit in selenium. The patient had been diagnosed as HIV-positive 2 years before. He presented Pneumocystis carinii pneumonia then Cryptococcus meningitis. Two months later he was hospitalized for pancreatitis and cachexia. He presented global heart failure that lead to death. No microorganism was found in myocardium at autopsy but plasma selenium was dramatically decreased (24 micrograms/L). The deficit in selenium has been associated to a dilated cardiomyopathy in non-AIDS patients. HIV-positive patients have an early decrease in plasma selenium, this concentration is dramatically decreased in malnourished patients. Selenium deficit might be the cause of some of the AIDS-related dilated cardiomyopathies and selenium supplementation might be useful in these patients.
Selenium deficiency and fatal cardiomyopathy in a patient receiving long-term home parenteral nutrition
Quercia RA, Korn S, O'Neill D, Dougherty JE, Ludwig M, Schweizer R, Sigman R.Fatal cardiomyopathy in a patient who received home parenteral nutrition (HPN) for eight years is reported, and the relationship of selenium deficiency to cardiomyopathy and other adverse effects is discussed. A 42-year-old white man with Crohn's disease who was receiving HPN was admitted to the hospital with severe chest pain and dyspnea. During the three days following admission, his symptoms of congestive heart failure and compensated metabolic acidosis persisted despite treatment. On hospital day 6, the patient developed increased ventricular irritability and refractory ventricular fibrillation and died. At autopsy, the heart weighted 500 g, all chambers were dilated, and the myocardium was grossly flabby. Extremely low concentrations of selenium (5-12% of normal) were found in plasma, heart, liver, and kidney tissue samples. The pathological findings in this patient were similar to those in two previously reported cases and strongly suggest that the fatal cardiomyopathy was secondary to selenium deficiency. Selenium is an integral part of the enzyme glutathione peroxidase, which plays an important role in the metabolism of tissues and organs. For metabolically stable patients receiving total parenteral nutrition, the suggested selenious acid dosage is 25-60 micrograms/day for adults and 1.4-30 micrograms/kg/day for pediatric patients. In selenium-depleted adults, a dosage of 100 micrograms/day administered intravenously for 21-31 days has been recommended to reverse symptoms. All HPN patients and hospitalized patients receiving extended parenteral nutrition should be monitored for selenium deficiency and given supplements if necessary.
An etiologic basis for congestive heart failure on the molecular level
Peterson DA.It is here proposed that disordered redox balance leads to congestive heart failure in a variety of diverse clinical situations. These conditions include those associated with an excess of reducing agents, such as catecholamines and thyroid hormone, or impaired oxidant defenses, such as in selenium deficiency. The clinical situations include hypertension, hyperthyroidism, progressive congestive heart failure, amphetamine overdose and hemochromatosis. The molecular damage to the cardiac muscle is postulated to be mediated via reaction oxygen radicals.
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- Candida: Candida infectie - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Behandeling diabetische complicaties - Neuropathie - Retinopathie - Nefropathie - Bloeduiker stabilisatie - Hart en vaatziekten: Cardiomyopathie en Hartfalen - Cardiomyopathy and Heart Failure - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose) - Spataderen - Levensverlenging: Levensverlenging - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Bot en gewricht aandoeningen: - Artrose - Artritis - Osteoporose - Fibromyalgie: - Fibromyalgie - Urinewegen: - Prostaatklachten - Blaasontsteking - Maag- darm aandoeningen: Prikkelbaar Darm Syndroom - Crohn - Colitus Ulcerosa - Voeding: Voeding wat is er mis mee - Melk - Suiker - Aanvulling onvolwaardige voeding - Vitamine supplementen: Voedingssupplementen - Overgewicht: - Overgewicht - SLIM - Oogaandoeningen: - Staar - Slecht ziendheid - Andere artikelen: - HPU - Astma - Multiple Sclerose - Alzheimer - Psoriasis - Depressie - Premenstrueel Syndroom - Orthomoleculaire Geneeskunde
