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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postweanling rats maintained on a milk-sugar diet develop a sideropenic anemia, the hemoglobin values falling to less than 30 per cent within 8 to 10 weeks. In that period the heart weight increases by more than 3 times, both ventricles enlarging proportionately. As in other forms of cardiac hypertrophy, a progressive increase in the numbers of connective tissue cells occurs. Ultrastructural and stereologic studies show an appreciable proliferation of the mitochondrial mass in myocardial cells, the mitochondrial fractional volume increasing from a normal of 0.38 to 0.48 per unit cell volume. This quantitative increase is accompanied by a progressive deterioration of the internal cristal structure and the appearance of abnormal, degenerating, and necrotic forms of mitochondria as congestive cardiac failure develops. Myofibrils remain normal. The heart of an anemic rat subjected to an additional workload produced by subdiaphragmatic aortic constriction shows an earlier deterioration of the mitochondrial ultrastructure and stereologic profiles. However, it does not become as large as the heart of the purely anemic animal. In anemic animals with an increased workload, the myofibrillar fractional volume increases from a normal of 0.52 to 0.57 per unit cell volume initially. The active sarcomerogenesis is achieved by Z-band proliferation, which was not observed in the heart of the purely anemic animal. These findings provide a structural basis for the functional and biochemical cardiac deterioration observed in the cardiomegaly induced by chronic anemia.
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PMID:Cardiomegaly in chronic anemia in ratsman experimental study including ultrastructural, histometric, and stereologic observations. 12 72

Severe iron deficiency anemia remains a continuing major health hazard among inner city children in Los Angeles. Over a 24-month period, 60 children in whom hemoglobin values were below 7 grams per dl were admitted to hospital; 11 (18 percent) of them were in overt congestive heart failure. Contrary to the popular conceptions, two thirds of the anemic children were undernourished, approximating the 16th percentile for weight on the Iowa growth chart, and the frequency of premature birth was not greater than in the general population. There were no deaths in this series. A management protocol which included partial exchange transfusion of children in congestive heart failure and supportive transfusion for children with hemoglobin levels below 5 grams per dl was employed.
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PMID:Severe iron deficiency anemia. 61 36

Brunner's gland adenoma in the third portion of the duodenum is rare and only two such cases have been reported previously. A 35-year old man presented with high-output congestive heart failure. Profound iron deficiency anemia was corrected by transfusion, allowing detection of a duodenal tumor, which proved pathologically to be a Brunner's gland adenoma.
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PMID:Brunner's gland adenomas associated with high-output congestive heart failure. 102 Jul 45

Anaerobic threshold (AT) has been advocated as an objective method of evaluating exercise capacity in patients with chronic congestive heart failure. The factors that determine AT, however, remain still unclear. To assess the influence of oxygen transport capacity on AT, patients with iron deficiency anemia were studied before and after treatment with iron. Twenty-nine female subjects were studied. They were divided into the following 3 groups: 1) iron deficiency anemia (group IDA: Hgb less than 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes and 6 non-athletes, 2) latent iron deficiency (group Lat-ID: Hgb greater than or equal to 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes, and normal (group Nor: Hgb greater than or equal to 11 g/dl and ferritin greater than or equal to 10 ng/ml) consisting of 15 athletes and 6 non-athletes. By bicycle ergometer using ramp protocol, peak oxygen uptake (peak VO2) and AT were measured in each group. Following the 1st exercise testing, groups IDA and Lat-ID were treated by oral iron for 1-1.5 months. The 2nd exercise testing was then performed. Furthermore, to investigate whether muscle cell energy metabolism itself is altered by iron deficiency, P magnetic resonance spectroscopy (MRS) was performed in 2 relatively severe anemic patients during forearm exercise while assessing the changes in phosphocreatine and inorganic phosphate. Peak VO2 and AT in non-athletes were significantly lower in IDA group than Nor group (peak VO2 (ml/min/kg): 23.7 +/- 5.1 vs 33.3 +/- 3.8, p less than 0.01, AT (ml/min/kg): 15.9 +/- 3.3 vs 21.3 +/- 1.3, p less than 0.01). After iron administration, Hgb was increased significantly in IDA group (from 9.0 +/- 1.8 to 12.1 +/- 0.8 g/dl, p less than 0.01) accompanied by an improvement in peak VO2 and AT (peak VO2 (ml/min/kg): from 34.2 +/- 12.4 to 40.0 + 13.0, p less than 0.001, AT (ml/min/kg): from 20.9 +/- 6.3 to 25.0 +/- 8.0, p less than 0.001). Lat-ID and Nor groups showed no changes. MRS indices of cell energy metabolism of the 2 severely anemic patients did not differ from those of normal controls, and no changes were observed after iron treatment. It is concluded from these results in iron deficiency anemia that oxygen transport is a determinant of anaerobic threshold.
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PMID:[Effect of blood hemoglobin concentration on anaerobic threshold]. 191 24

The most severe consequence of iron depletion is iron deficiency anemia (IDA), and it is still considered the most common nutrition deficiency worldwide. Although the etiology of IDA is multifaceted, it generally results when the iron demands by the body are not met by iron absorption, regardless of the reason. Individuals with IDA have inadequate intake, impaired absorption or transport, physiologic losses associated with chronological or reproductive age, or chronic blood loss secondary to disease. In adults, IDA can result in a wide variety of adverse outcomes including diminished work or exercise capacity, impaired thermoregulation, immune dysfunction, GI disturbances, and neurocognitive impairment. In addition, IDA concomitant with chronic kidney disease or congestive heart failure can worsen the outcome of both conditions. In this review, the prevalence of IDA related to confounding medical conditions will be described along with its diverse etiologies. Distinguishing IDA from anemia of chronic disease using hematologic measures is reviewed as well. In addition, current diagnostic strategies that are inclusive of clinical presentation, biochemical tests, and differential diagnosis will be outlined, followed by a discussion of treatment modalities and future research recommendations.
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PMID:Iron deficiency anemia. 1839 Jul 80

Patients with heart failure have elevated levels of circulating inflammatory cytokines and commonly have iron deficiency anemia or anemia of chronic inflammation. Clinical trials in patients with congestive heart failure and iron deficiency have demonstrated that intravenous iron treatment appears to improve subjective and objective outcomes. Most patients in these trials were not anemic or only had mild anemia, and hemoglobin concentration rose only slightly after treatment with iron. Experimental evidence demonstrates that iron is a cofactor for muscle function, which could explain the improvement in clinical outcomes. Many questions remain to be answered to understand the role of iron therapy in patients with congestive heart failure.
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PMID:Iron deficiency and heart disease: ironclad evidence? 2123 17

High prevalence of anemia and its direct relation with morbidity and mortality in congestive heart failure (CHF) has been shown in numerous studies. Among etiology factors of anemia are hemodilution, chronic kidney insufficiency, deficiency of iron, folate, and vitamin 12, high level of inflammatory cytokines. Aims of this study were elucidation of causes of anemia in patients with CHF and assessment of dependence of prognosis of these patients on etiology of anemia. We examined 317 patients hospitalized with diagnosis of NYHA class II-IVCHF and anemia (129, [40.7%] men and 188 [59.3%] women, mean age 74.4+/-1.75 years, duration of CHF 4.4+/-0.2 years; 46, 42, 12% with NYHA class IV, III and II, respectively). Causes of anemia were chronic kidney insufficiency, iron deficiency, vitamin B12-deficiency, hemodilution, and chronic diseases. Glomerular filtration rate (GFR) below 50 ml/min was found in 27 patients (8.5%), deficiency of iron with lowered ferritin concentration and/or saturation of transferrin was revealed in 104 (32.8 %), vitamin B12-deficiency in 4 (1.3%), hemodilution in 40 (12.6%) patients. In 142 patients (44.8%) anemia was associated with chronic diseases. Hospital mortality in the whole group was 18.3%. Death rates in patients with hemodilution, chronic kidney insufficiency, vitamin B12-deficiency, anemia due to chronic diseases, and iron deficiency anemia were 32.5, 25.9, 25, 16.2 and 13.5%.
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PMID:[Analysis of causes of development of anemia in patients with chronic heart failure]. 2164 92

Iron deficiency anemia has been associated with a secondary and potentially reversible cardiomyopathy. The pathophysiologic paradigm has been that the hematologic disease begets cardiac dysfunction. There may be, however, a point at which myocardial injury is irreversible in susceptible individuals. We present the case of a 4-year-old, developmentally normal, child who presented with iron deficiency anemia and a dilated cardiomyopathy with congestive heart failure. Despite appropriate correction of the anemia, the patient developed decompensated heart failure requiring milrinone therapy and eventual heart transplantation. This report will alert clinicians to the potential for irreversible adverse cardiac remodeling and the importance of close pediatric cardiology consultation and serial assessment in order to implement appropriate heart failure therapy.
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PMID:Profound Iron Deficiency Anemia and Irreversible Dilated Cardiomyopathy in a Child. 3168 17