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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this review is to examine current research on the iron status of the elderly and factors that influence the body burden of iron. Studies of noninstitutionalized elderly individuals report mean iron intakes that meet current Recommended Dietary Allowances for iron. Dietary practices that may decrease iron bioavailability, and hence iron stores in the body, include low intakes of ascorbic acid or high intakes of calcium, and decreased consumption of highly available iron from meat, fish, and poultry. Although not well documented, the effect of age on iron absorption and iron excretion appears to be small, and body stores of iron increase with age. It is difficult to estimate the prevalence of iron deficiency in elderly persons, because impaired iron status can be the result of iron deficiency or chronic disease. Further study is necessary to determine whether red blood cell ferritin and serum transferrin receptors may be useful biochemical markers to differentiate the anemia of chronic disease from iron deficiency anemia. Hereditary hemochromatosis is a genetic disease that greatly increases the body burden of iron and the risk of hepatic disease among homozygotes. Because iron deficiency or iron excess may impair health, the role of iron in diseases associated with aging such as depressed immune response, neurological dysfunction, cancer, and heart disease is discussed.
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PMID:Iron nutriture in elderly individuals. 800 89

Decreased arterial oxygen saturation in cyanotic congenital heart disease causes a compensatory rise in haemoglobin and haematocrit levels. There is an inverse correlation between arterial oxygen saturation and haemoglobin/haematocrit. This holds true as long as the erythropoiesis is not restricted by other factors. The haematological values and arterial oxygen saturations of three children with cyanotic congenital heart disease are presented. They illustrate how iron deficiency causes discrepant values for arterial oxygen saturation and haemoglobin/haematocrit and that "normal" haemoglobin/haematocrit levels in such children may constitute anaemia. Measurements of MCV, MCH and serum ferritin reveal the existence of iron deficiency anaemia. Low grade iron medication is recommended for children with cyanotic congenital heart disease.
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PMID:[Normal hemoglobin levels in children with cyanotic heart disease. Is it iron deficiency anemia?]. 832 97

A recent prospective three-year follow-up study of 1931 men in Finland demonstrated a significant 2.2-fold greater risk of acute myocardial infarct in 42- to 60-year-old men who had serum ferritin concentrations above 200 micrograms/dL. However, the mean plasma ferritin concentration in this population was high and the prevalence of hemochromatosis was unknown; these issues mitigate the suggestion that high-normal iron stores leads to heart disease.
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PMID:Are we at risk for heart disease because of normal iron status? 851 89

A group of 67 children with cyanotic congenital heart disease (CCHD) were studied, and 35 were given iron treatment according to a regimen that gives iron to patients with a hematocrit (Hct) below 60%. The patients were categorized as iron-deficient and iron-sufficient according to their transferrin saturation and ferritin values. The pretreatment hemoglobin (Hb) and Hct values of the groups were similar. The mean Hct was nearly three times as much as the mean Hb in the iron-sufficient group and more than three times as much as the Hb in the iron-deficient group. Excessive erythrocytosis in the iron-deficient group was impressive. Mean corpuscular volume (MCV) values were below 72.7 fl in all of the iron-deficient patients. After treatment the Hb, Hct, transferrin saturation, and ferritin increased significantly in both groups, with the increments greater in the iron-deficient group. Increments in the erythrocyte (RBC) count were significant in the iron-sufficient group but insignificant in the iron-deficient one. Increments of MCV in the iron-deficient group were significant but insignificant in the iron-sufficient group. Our study demonstrated that prediction of Hb, RBC count, and MCV, measurements of which are easy and inexpensive and require little blood, can suffice for the diagnosis of iron deficiency in patients with CCHD without altering systemic perfusion.
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PMID:Parameters of iron deficiency in children with cyanotic congenital heart disease. 866 27

There has developed a general theory of chronic and degenerative disease causation--the Oxidative Stress Theory. This theory states that the production of tissue-damaging free radicals is an essential component in the pathogenesis of chronic diseases and that iron may help to catalyze the reactions producing free radicals. As a result, it has been suggested that the risk of coronary heart disease increases with increasing body iron stores. In support of that hypothesis, a prospective epidemiologic study of heart disease in Finnish men found that the risk of heart attack increased with increasing levels of serum ferritin. However, the vast majority of the epidemiologic data, including results from prospective, cross-sectional, and case-control and autopsy studies, published since that initial study have failed to support the original hypothesis that high body iron stores increase the risk of coronary heart disease.
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PMID:Iron and heart disease: the epidemiologic data. 893 17

Iron overload is the main cause of morbidity and mortality in patients with thalassaemia major. In order to establish if the presence of the mutations recently described in the haemochromatosis gene affects the severity of iron overload in thalassaemia patients, we compared the prevalence of mutations C282Y and H63D in 216 young adults regularly transfused and chelated in North-Eastern Italy with the frequency found in a group of blood donors from the same area. For each patient, mean serum ferritin over the last 3 years, liver iron concentration, and the presence of diabetes, hypogonadism and heart disease, were considered. The frequency of the C282Y allele was 1.9% in patients with thalassaemia major and 2.3% in blood donors (P=ns). The frequency of the H63D allele was 16.2% in patients with thalassaemia major and 15.3% in blood donors (P=ns). When age, liver iron concentration and mean yearly serum ferritin levels were compared in patients with and without mutations C282Y and H63D, no significant differences were found. Also, the prevalence of iron-induced complications was not significantly different between patients carrying or not carrying the mutations. The presence of the HH mutations does not seem to influence the degree of iron overload and its consequences in regularly transfused and chelated patients with thalassaemia major.
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PMID:The haemochromatosis mutations do not modify the clinical picture of thalassaemia major in patients regularly transfused and chelated. 985 37

Genetic hemochromatosis is an autosomal recessive disease, characterized by an increased iron absorption, leading to progressive iron overload. The fully expressed phenotype comprises fatigue, skin pigmentation, liver disease with hepatomegaly, cirrhosis and hepatocellular carcinoma, and diabetes. Arthralgias are frequent, cardiopathy or impotence may occur. This presentation is now unfrequent with earlier diagnosis, and patients are often asymptomatic--with only biochemical expression--or pauci-symptomatic (mild fatigue, arthralgias or increased transaminases). Transferrin saturation is always increased. Serum ferritin is proportional to iron burden. Diagnosis is now easy, since most patients are homozygote for the C282Y mutation of the HFE gene. Liver biopsy can be useful to quantify iron overload and assess liver fibrosis. The disease can be lethal due to liver disease, carcinoma or heart disease, but life expectancy goes to normal if patients are treated before the occurrence of cirrhosis. Treatment relies on regular venesections. Familial screening is essential.
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PMID:[Diagnosis and treatment of genetic hemochromatosis]. 1086 97

More than 20 years ago it was proposed that differences in body iron stores may account for differential heart disease prevalence in men and women. In 1992 Finnish investigators presented intriguing supportive evidence for this proposal by showing that middle-aged men with normal but elevated serum ferritin, a biomarker of body iron stores, were at increased risk for acute myocardial infarction. During the past dozen years many studies have followed leading to intense debate on the role of iron in the development of heart disease. A meta-analysis of prospective studies found, however, no support for the iron-heart disease hypothesis. As new disease associations with iron status continue to be explored, consideration needs to be given to the lessons learned from these studies. Moreover, additional efforts need to be made to find a simple, high throughput and more satisfactory measure of the forms of iron in the body that are liable to do damage.
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PMID:The iron-heart disease connection: is it dead or just hiding? 1523 Dec 42

We describe a case of a female who developed haemosiderosis, in the course of treatment for very severe unstable aplastic anaemia for fourteen years. She was 37 years old at the time of initial diagnosis. Her management consisted of regular blood transfusions aimed at haemoglobin above 8.5 g/dl, antimicrobials, oxymetholone, low dose prednisone and folate. She had received about seventy five units of blood at the start of 2 grams of desferrioxamine with every subsequent blood transfusion. Annual tests of serum ferritin showed progressive increase. She developed skin changes, diabetes mellitus, heart disease, recurrent infections, generalized joint and abdominal pains and liver failure. She died within six weeks of developing congestive heart failure coupled with liver failure due to haemosiderosis despite regular use of desferrioxamine.
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PMID:Transfusion haemosiderosis inspite of regular use of desferrioxamine: case report. 1616 82

The life expectancy of patients with thalassemia major has significantly increased in recent years, as reported by several groups in different countries. However, complications are still frequent and affect the patients' quality of life. In a recent study from the United Kingdom, it was found that 50% of the patients had died before age 35. At that age, 65% of the patients from an Italian long-term study were still alive. Heart disease is responsible for more than half of the deaths. The prevalence of complications in Italian patients born after 1970 includes heart failure in 7%, hypogonadism in 55%, hypothyroidism in 11%, and diabetes in 6%. Similar data were reported in patients from the United States. In the Italian study, lower ferritin levels were associated with a lower probability of experiencing heart failure and with prolonged survival. Osteoporosis and osteopenia are common and affect virtually all patients. Hepatitis C virus antibodies are present in 85% of multitransfused Italian patients, 23% of patients in the United Kingdom, 35% in the United States, 34% in France, and 21% in India. Hepatocellular carcinoma can complicate the course of hepatitis. A survey of Italian centers has identified 23 such cases in patients with a thalassemia syndrome. In conclusion, rates of survival and complication-free survival continue to improve, due to better treatment strategies. New complications are appearing in long-term survivors. Iron overload of the heart remains the main cause of morbidity and mortality.
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PMID:Survival and complications in thalassemia. 1633 50


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