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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From a clinical standpoint, the search for iron deficiency is based upon serum ferritin. However, serumferritin values may be pathologic in other numerous pathological conditions such as inflammation, liver diseases, malignant hematologic disorders, hemolysis, etc. Proteic profile combines the analyze of proteins variations: protein results are converted in percent of normal values referenced for the technique used. It has been suggested that on the protein profile, an increase in serum transferrin level compared to a normal serum albumin level (DAT: difference albumin-transferrin), appears early in the course of iron deficiency. In order to know the value of a pathologic DAT > or = 28% in the diagnosis of iron deficiency, we prospectively studied 156 patients consecutively hospitalized in an internal medicine department. Iron deficiency was defined by a low serum ferritin level. Diagnosis performance (sensitivity, specificity, positive and negative predictive values) of different biologic markers of iron deficiency (serum iron, saturation of total iron-binding capacity, low mean erythrocyte volume) and DAT was compared to the performance of low serum ferritin values. With the exception of low serum ferritin (which have by definition a specificity and a positive predictive value of 100%), pathologic DAT appeared as the best index of iron deficiency with the highest sensitivity (67.4%), specificity (97.3%), positive predictive value (91.2%), negative predicitive value (87.7%) and diagnosis efficacy (sensitivity x specificity = 0.66). A pathologic DAT associated to a low serum ferritin level increased the diagnosis performance of both tests to 0.72. Diagnosis efficacy of DAT was not changed (0.66) in 83 patients with a confounding factor for serum ferritin analysis (inflammation, liver diseases, malignant hematologic disorders, hemolysis) when diagnosis efficacy of all other tests decreased. There was a negative correlation between serum ferritin level and DAT level (r = 0.55; P < 0.0001). In conclusion, an increase of serum transferrin of more than 28% compared to serum albumin on a proteic profile gives a significant benefit for the diagnosis of iron deficiency. This benefit increases when data of both DAT and serum ferritin are associated.
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PMID:[Protein profile and iron deficiency: value of the study of the albumin-transferrin couple]. 888 Nov 90

Iron deficiency (ID) is the most common nutritional deficiency worldwide especially among young children, women in pregnancy and breastfeeding. This study was undertaken to assess the prevalence of ID in 1288 pupil ranging in age from 11 to 14 years. Haemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular Hb (MCH), serum iron (Fe) serum transferrin (Trf), serum ferritin (Ft) and an inflammtory proteic profil (IPP) were measured. The IPP combines the analysis of protein variations: protein results are converted in percent of normal values referenced for the technique used. It has been suggested that on the protein profile, an increase in serum transferrin level compared to a normal serum albumin level (DAT: difference albumin-transferrin), appears early in the course of ID. Iron deficiency was defined by a low serum ferritin (< 15 ng/mL) and/or a pathologic DAT (> 28%). Approximately, 33.8% of children had Ft < 15 ng/mL and 12,8% had DAT > 28% while ferritin values were in the normal range. Diagnosis performance (sensitivity, specificity and diagnosis efficacy) of ferritin and DAT were compared to the performance of high serum transferrin receptor (sTfR) values in 2 populations presenting or not a biological inflammation. Only the diagnosis efficacy of DAT was constant in both situations. In conclusion, the serum ferritin concentration is the first indicator of body storage iron identifying ID, however normal or elevated values of ferritin may be difficult to interpret particulary in the presence of inflammation. sTfR and DAT values are thus reliable indicators of ID in such circumstances.
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PMID:[Difference albumin-transferrin interest in the iron deficiency detection in a cohort of 1288 schoolchildren in the district of Tunis]. 1716 59

Iron deficiency (ID) disrupts brain dopamine (DA) and norepinephrine (NE) metabolism including functioning of monoamine transporters and receptors. We employed caudate microdialysis and no net flux (NNF) in post-weaning rats to determine if ID decreased the extraction fraction (E(d)). Five micromolar quinpirole, a dopamine D(2) receptor agonist, resulted in 80% decrease in extracellular DA and 45% higher E(d) in control animals. The D(2) agonist had no effect on E(d) in ID animals despite a reduction in basal DA. DAT mRNA levels were reduced by 58% with ID, while DAT protein in ventral midbrain and caudate and membrane associated DAT were also reduced by ID. Carbidopa/l-DOPA was administered to determine if elevated extracellular DA in ID was due to increased release. The DA response to l-DOPA in ID rats was 50% smaller and delayed, whereas the NE response was threefold higher. The caudate concentration of NE was also elevated in ID. Elevated dopamine-beta-hydroxylase activity in ID provides a tentative explanation for the increased NE response to l-DOPA. These experiments provide new evidence that ID results in altered synthesis and functioning of DAT and perhaps suggests some compensatory changes in NE metabolism.
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PMID:Iron deficiency alters dopamine uptake and response to L-DOPA injection in Sprague-Dawley rats. 1836 28

Referral to hematology for anemia is common. In paroxysmal nocturnal hemoglobinuria (PNH), cells deficient in the glycosylphosphatidyl inositol (GPI) anchor are lysed by complement. Eculizumab improves overall survival and quality of life while reducing hemolysis, transfusion requirements, and thrombosis. We evaluated the frequency of screening for PNH in patients with unexplained anemia. Key clinical features, laboratory data, and investigations were recorded for patients referred for anemia since 2010, without a specific cause found. PNH testing was done by flow cytometry. 540 patients had: anemia not yet diagnosed (NYD, n=318 (including unexplained iron deficiency, n=92; DAT-negative hemolysis, n=9)); anemia of chronic disease, n=173; and pancytopenia NYD, n=49. 82.4% had LDH testing done; 85.0% total bilirubin; 78.7% reticulocyte counts; and 40.6% haptoglobin level; 131 (24.2%) had possible hemolysis. PNH testing was done in 56 (10.4%). Those screened for PNH were more likely to have: younger age (P=0.04); a history of thrombosis (P<0.001); undergone a BMBx (P<0.001); received RBC transfusions (P=0.0018); or evidence of DAT-negative hemolysis (P<0.001). In summary, PNH was tested for in a minority of patients with unexplained anemia (10.4%) despite potential indicators of hemolysis in 24.2%. Increased screening could identify patients who would benefit from treatment and should be considered.
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PMID:Frequency of and reasons for paroxysmal nocturnal haemoglobinuria screening in patients with unexplained anaemia. 2913 83