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

Decreased serum albumin levels are commonly observed in patients with carcinoid tumor, who also show several characteristic clinical and biochemical abnormalities. A large comparative study on a group of 96 carcinoid patients was performed with the purpose of identifying some of the mechanisms leading to hypoalbuminemia in patients with this form of cancer, and thereby to shed light on the cause of hypoalbuminemia of cancer in general. Serum albumin values were compared with a number of clinical parameters (including extent of liver metastases, severity of diarrhea, degree of right heart failure, and extent of gastrointestinal surgery) and of laboratory data (prothrombin time, BSP retention, serum transferrin concentration, hematocrit value, and daily urine excretion of 5-hydroxy-indoleacetic acid). In several patients the gastrointestinal protein loss was assessed by the 51Cr-albumin technique, whereas albumin renewal and distribution were evaluated by the use of 125I-albumin. The data obtained showed that the main factors in determining decreased serum albumin levels in patients with carcinoids are both reduced synthesis and increased loss of the protein. The hepatic synthetic defect appears to be related to a progressive decrease in the number of functioning liver cells; the origin of the gastrointestinal protein loss may be related to the obvious tumor involvement of the gut wall, as well as to the pharmacologically-induced diarrhea. Right heart failure occurring as a result of the carcinoid heart disease may be an additional cause for gastrointestinal protein loss in patients with carcinoid tumor.
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PMID:Pathophysiology of hypoalbuminemia associated with carcinoid tumor. 97 3

The nutritional status of nine patients with end-stage heart disease who were supported by a left ventricular assist device (LVAD) for more than 30 days while awaiting cardiac transplantation was evaluated. Nutritional status was indicated by the following scale: 0-2, adequate nourishment; 3-5, moderate malnourishment; greater than 5, severe malnourishment. This scale was based on serial assessments of albumin, transferrin, total lymphocyte count, percentage of ideal body weight, midarm circumference, triceps skinfold, and arm muscle circumference. Each variable was compared with established standards before implantation and before transplantation times and assessed 1 point if less than the normal value and 0 points if within the normal range. At the time of LVAD implantation, 5 patients had a score of 0-2, 3 patients had a score of 3-5, and 1 patient had a score greater than 5. At the time of cardiac transplantation, 7 patients had a score of 0-2, 2 patients had a score of 3-5, and no patients had a score greater than 5. The patients who were able to meet at least 50% of their daily caloric and protein requirements by oral intake alone were noted. At LVAD implantation, only 2 patients (22%) met this requirement; however, 6 patients (67%) met this requirement at the time of cardiac transplantation. All 9 patients underwent cardiac transplantation, and 8 survived. Thus, it appears that extended LVAD support and maintenance of hemodynamic stability allow patients to regain the desire and ability to achieve adequate nutritional status, which may considerably reduce their perioperative transplant risks.
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PMID:Nutritional assessment of patients with extended left ventricular assist device support. 212 42

To test the hypothesis that tissue oxygen delivery would be affected by diminished oxygen stores in cyanotic congenital heart disease, serum ferritin, transferrin saturation, hemoglobin, red cell mean corpuscular volume (MCV), red cell 2,3-diphosphoglycerate (DPG), P50, blood gases, oxygen saturations and systemic oxygen transport were measured in 29 hypoxemic infants and children. For the group, aortic saturation was 81 +/- 9%, PaO2 was 50 +/- 12 mm Hg, hemoglobin 16.2 +/- 2.1 gm/dl and systemic oxygen transport 620 +/- 145 ml/min/m2. P50 was increased above normal values (28.8 +/- 2.3 vs 26.6 +/- 1.1 mm Hg, p less than 0.01), and DPG was 2.35 +/- 0.54 mumol/ml, at the upper limits of normal for this assay. Iron deficiency was present in 8. When patients with P50 greater than or equal to 30 mm Hg and P50 less than 30 mm Hg were compared, iron stores were diminished in the high P50 group: [serum ferritin (19 +/- 8 vs 53 +/- 48 ng/ml, p = 0.0006), transferrin saturation (11 +/- 6 vs 23 +/- 11%, p = 0.003) and MCV (79 +/- 8 vs 86 +/- 4 fl, p = 0.05)]. Hemoglobin, aortic oxygen saturation, PaO2 and systemic oxygen transport were similar in both groups. In children with iron sufficiency, 15 of 21 had MCV greater than 90th percentile for age and sex (p less than 0.001 versus expected distribution). Also, MCV greater than 90th percentile for age and sex had a positive predictive value of 0.88 for iron sufficiency. This study demonstrates that diminished iron stores in cyanotic congenital heart disease are associated with a more right-shifted oxyhemoglobin dissociation curve (increased P50).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of iron deficiency on tissue oxygen delivery in cyanotic congenital heart disease. 334 85

One hundred consecutive adult patients undergoing cardiac operations at a single institution were evaluated preoperatively with regard to their nutritional status. Anthropometric, biochemical, and immunologic characteristics were evaluated in addition to cardiac biopsy specimens to determine right atrial glycogen concentration. Although some positive anthropometric, biochemical, and cell-mediated immunity characteristics were observed to have "statistically significant" correlations with morbidity and mortality for the group as a whole, nearly all of the values remained near or at normal limits. Lighter weight men with a smaller arm muscle circumference and lower concentration of total body fat had more complications than their heavier counterparts. Serum transferrin and cell-mediated immunity also formed weakly positive statistical correlations. Anthropometric correlations in women were of no value. Myocardial glycogen concentrations did not correlate with postoperative morbidity and mortality. Because nearly all of the patients had arteriosclerotic heart disease, the series as a whole may have been skewed toward a group with values too close to normal to differentiate them adequately. It is concluded that routine nutritional assessment is of no value in guiding nutritional management for individual patients, although when patients are analyzed as a group, interesting epidemiologic observations can be made.
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PMID:Should nutritional status be assessed routinely prior to cardiac operation? 684 57

A controlled study was carried out to evaluate the effects of postoperative iron therapy on iron status in anemic children after cardiopulmonary bypass. The patients were 8 boys and 9 girls (mean age 6.5 years) who underwent elective closure of atrial septal defect, secundum type. On postoperative day 9, patients were randomly assigned to either iron supplementation with iron sulfate 5 mg/kg until day 56 or to a control group. Hemoglobin, reticulocytes, transferrin saturation, free erythrocyte protoporphyrin, and ferritin were measured, the final outcome measure being postoperative iron status on day 56. The treatment group showed higher transferrin saturations (33.5% versus 18.0%), smaller decreases in ferritin level (+3.0 versus--13.7 ng/ml), and a lower incidence of depleted iron stores (0/8 versus 5/9) than the control group (all data: P < 0.05). Anemic children after cardiopulmonary bypass for surgical repair of congenital heart disease thus benefit from iron supplementation within the first postoperative weeks.
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PMID:Iron supplementation in children after cardiopulmonary bypass for surgical repair of congenital heart disease. 799 33

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

Iron is a double-edged sword. In moderate quantities and leashed to protein, it is an essential element in all cell metabolism and growth, but it is toxic when unleashed. Because of its ability to switch back and forth between ferrous and ferric oxidation states, iron is both a strong biological oxidant and reductant. The human diet contains a multitude of natural chemicals which are carcinogens and anticarcinogens, many of which act by generating oxygen radicals, which initiate degenerative processes related to cancer, heart disease and aging (the "oxygen radical hypothesis of aging"). Among these many dietary chemicals are many redox agents, including vitamin C and beta carotene. Free radical damage is produced primarily by the hydroxyl radical (.OH). Most of the .OH generated in vivo comes from iron-dependent reduction of H2O2. Supporting too much iron as a free radical-generating culprit in the risk of cancer, NHANES I data indicated that high body iron stores, manifested by increased transferrin saturation, are associated with an increased cancer risk. Other data shows an increased heart attack risk.
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PMID:Most free-radical injury is iron-related: it is promoted by iron, hemin, holoferritin and vitamin C, and inhibited by desferoxamine and apoferritin. 807 94

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

The aim of this study was to evaluate the prevalence of restless legs syndrome (RLS) in patients with end-stage renal disease (ESRD), and to determine its association with sleep disorders and premature discontinuation of dialysis ("sign-offs"). End-stage renal disease patients (N = 204) and a control group of patients with heart disease (N = 129) completed a self-administered questionnaire regarding symptoms of RLS, sleep habits, pruritus, and adherence to dialysis therapy. Laboratory measures and sensory nerve amplitudes were collected on the ESRD patients. Twenty percent of the ESRD patients and 6% of the cardiac patients reported moderate to severe RLS symptomatology. Sleep onset was delayed and total sleep time was diminished in ESRD patients compared with cardiac patients. Symptoms of RLS were directly correlated with all sleep measures as well as with pruritus. Symptoms of RLS, sleep onset latency, and transferrin saturation were independently associated with premature discontinuation of dialysis. Significantly increased risk for mortality was observed in patients with RLS at the 2.5-year follow-up. Restless legs syndrome is a common finding in patients with ESRD and is associated with substantial morbidity.
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PMID:Restless legs syndrome in end-stage renal disease. 880 35

Hemochromatosis is a recessive disorder of iron metabolism characterized by progressive iron loading of parenchymal organs, which accounts for clinical complications such as cirrhosis, diabetes mellitus, cardiopathy, endocrine dysfunctions and arthropathy. Clinical complications, which usually develop after the third or fourth decade of life, can be fatal but may be prevented by phlebotomy if iron excess is detected at a very early stage. The hemochromatosis gene (HFE), located 4.5 megabases telomeric to the HLA-A locus, encodes an HLA class I like protein and two missense mutations, C282Y and H63D in complete disequilibrium have been identified within this gene. Due to its high frequency in the general population, the involvement of H63D in the pathogenesis of the disease remains controversial, and it might correspond to a minor mutation. Conversely, the C282Y mutation is tightly linked to the disease, as it accounts for 80 to 100% of the hemochromatosis cases in Northern Europe. The lower frequency observed, in the patients, in Italy and South of France led to imagine either the implication of other mutations or of other genes. The C282Y mutation is absent in Asia and Africa and is present in the general population with a decreasing gradient of frequency from Northern to Southern Europe. The prevalence of the disease was usually estimated to be 3% but the observed frequency of the C282Y homozygotes is 5% in our breton population raising the question of the penetrance of the disease, and consequently the use of the genotypic test for its systematic screening. As HFE encodes a membrane protein similar to HLA class I protein, its contribution to iron overload is not obvious. The normal protein is predicted to to be expressed at the cell surface in association with beta 2-microglobulin, a localization for which C282Y is critical as it disrupts this association. This protein has also been shown to form a stable complex with the transferrin receptor leading to a decreased affinity for transferrin. A better knowledge of its function will help to decipher iron and different metal-ions metabolism. Although the exact role of the HFE protein is unknown, the genotypic test allows the clinicians to ascertain their diagnosis and genetic counselling.
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PMID:[Molecular genetics of hemochromatosis]. 1052 Apr 11


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