Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six black infants and young children with high titers of milk precipitins were identified by screening the sera of 160 children with idiopathic chronic lung disease. None of the six had immunoglobulin deficiency, elevation of sweat chlorides, SS hemoglobin, or recurrent aspiration. All six children had typical manifestations of milk-induced pulmonary hemosiderosis: recurrent pulmonary infiltrates (6/6), hemosiderin-laden pulmonary macrophages (5/6), intermittent wheezing (5/6), eosinophilia (4/6), anemia (4/6), iron deficiency (4/4), failure to thrive (4/6), and elevated levels of serum IgE (4/4). Three children also had chronic rhinitis and eventually developed large adenoids, hypercapnia and acidosis during sleep, and right heart failure. Elimination of cow milk from the diet, symptomatic therapy, and adenoidectomy when indicated resulted in improvement of all six patients. Pulmonary hemosiderosis and some cases of upper airway obstruction with pulmonary hypertension appear to be two stages, early and delayed, of the same immunophysiologic process. Early dietary intervention may prevent the cardiovascular complications of this process.
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PMID:Hyperreactivity to cow milk in young children with pulmonary hemosiderosis and cor pulmonale secondary to nasopharyngeal obstruction. 117 19

n vitro, rheological studies establish that whole blood viscosity and yield stress are high in patients with an erythrocytosis. However, a number of factors ensure that these patients, under physiological conditions, do not show the clinical features observed in other hyperviscosity states. These include red cell axial migration in flowing blood and "plug flow" in the largest vessels. In addition, a small increase in vessel diameter leads to large increases in blood flow, and generally high blood flows produce the lowest blood viscosity values. The increased hemoglobin levels and the increase in oxygen-carrying capacity at high hematocrit values compensate for the tissue hypoxia. In the "non-hypoxemic" erythrocytoses (polycythemia vera, idiopathic and apparent erythrocytosis), there is an increased incidence of vascular occlusion in untreated patients. The reasons for this include reduced peripheral blood flow, increased platelet-vessel wall interactions, and the demonstrated in vitro hyperviscosity which comes into play with abnormally low flow, seen in vivo under pathological conditions. In the erythrocytosis of hypoxemic lung disease and its associated hypoxemia, pulmonary vasoconstriction enhances susceptibility to hyperviscosity effects in particular. Moreover, the vasoconstriction caused by the hypoxemia prevents the normal adaptive changes of increased vessel diameter. Microcytic hypochromic red cell changes of iron deficiency do not cause a higher viscosity value at any given hematocrit value compared with normal red cells. However, in hypoxemic states oxygen-carrying capacity should be maximized, since the hemoglobin value is disproportionately lower at any given hematocrit in the presence of microcytic hypochromic cells compared with normal red cells.
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PMID:Hemorheology in the erythrocytoses. 1137 90

Restless leg syndrome (RLS) and periodic limb movement disorder (PLMD) are considered to be a continuum of a neurological sleep disorder associated with abnormal iron metabolism or deficiency. I describe a case of RLS and PLMD in a cystic fibrosis patient with iron deficiency from chronic hemoptysis. This is the first case that reports RLS and PLMD manifesting from iron deficiency caused by chronic hemoptysis in advanced cystic fibrosis lung disease.
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PMID:Restless leg syndrome manifested by iron deficiency from chronic hemoptysis in cystic fibrosis. 1698 19

In adult CF patients iron deficiency (ID) is common and primarily functional due to chronic inflammation. No recent data are available on the cause of ID and iron deficiency anemia (IDA) in children with CF. Over the last decades onset of inflammation and pulmonary disease in children with CF is delayed by improved nutritional status. We questioned whether ID occurs in the same extent among children with CF as in adult CF patients. We therefore conducted a study to investigate the iron status of children with CF and to determine whether ID and IDA are associated with dietary iron intake, lung disease severity and Pseudomonas aeruginosa (PA) infection. Clinical charts of 53 children with CF aged 0-16 were reviewed. Follow-up varied from 1 to 14 years with 343 annual observations in total. Thirty-two children (60.4%) were iron deficient in at least 1 year and ID was present in 84 of 343 observations (24.5%). In 2011 ID was present in 9 children (17.0%). Ten children (18.9%) were anemic in at least 1 year and anemia was present in 13 of 328 observations (4.0%). IDA was present in at least 1 year in 6 children (11.3%). Ferritin (Fer) was positively associated with age. Higher Fer values found in older children represent an increased state of inflammation, rather than an improved iron status, and might increase the relative contribution of functional ID. This study shows that ID is common in relatively healthy, well-nourished children with CF. The mechanism of ID in children with CF is currently unknown. A prospective study using both soluble transferrin receptor and Fer as indicators for ID will provide more insight in the incidence and causes of ID in children with CF.
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PMID:Iron deficiency occurs frequently in children with cystic fibrosis. 2400 Jan 93