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)

Generalized or localized itch without primary skin manifestations may be the presenting symptom of serious internal diseases. Five characteristic cases of pruritus are discussed: Hodgkin's disease, primary sclerosing cholangitis, polycythemia vera, iron deficiency (with pica), and uremia. Other important causes must be considered; all forms of cholestasis, including primary biliary cirrhosis, drug-induced, pregnancy-related, and extrahepatic cholestasis; other hematologic and malignant disorders such as non-Hodgkin's lymphoma, leukemia, multiple myeloma, solid tumors, and myelodysplastic syndromes; metabolic and endocrine diseases, most notably diabetes mellitus, hyperthyroidism, hypothyroidism, and carcinoid syndrome; focal neurologic diseases such as brain tumors, cerebral infarctions and multiple sclerosis; adverse drug reactions without rash; infectious diseases, especially parasitic and HIV infections. A diagnostic laboratory screening for pruritus of undetermined origin is suggested.
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PMID:[Pruritus--also a challenge in internal medicine]. 852 44

Anaemia is a common manifestation of juvenile rheumatoid arthritis (JCA). We have evaluated 26 JCA patients with anaemia and compared their laboratory parameters to those without anaemia. In the patients with anaemia, activation criteria such as erythrocyte sedimentation rate (ESR) and CRP were significantly higher than in those without anaemia. Anaemia was present in all systemic JCA patients and was present in 42% and 78% of the oligoarticular and polyarticular types, respectively. Serum iron levels and transferrin saturations were low in all, whereas serum iron-binding capacities of the patients were normal. Mean ferritin level was 249pg/l (range 8.46-1000pg/l). There was a significant correlation between ferritin levels and CRP and ESR (r = 0.48 and r = 0.55 respectively) (both p < 0.05). Epo levels were normal. Twelve (60%) of the bone marrow aspiration specimens stained positive for iron whereas 40% stained negative; there were also changes suggestive of myelodysplasia. Sideroblasts were also decreased in number. Thus, in these patients iron is not sufficiently transferred to the erythroid series and/or cannot be used by erythroblasts, accompanied by a possible absolute iron deficiency. Thus we suggest that the iron in JCA tends to be stored in the form of ferritin, not in an accessible form and impaired metabolism along with other factors are effective in the anaemia of JCA.
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PMID:Anaemia in juvenile chronic arthritis. 879 53

In this study the analytical performances of two recently introduced assays for soluble transferrin receptors in serum were tested. The Ramco transferrin assay was compared with the Eurogenetics assay. In a small clinical study serum samples from patients with anaemia of chronic disease, iron deficiency and myelodysplastic syndrome were analysed, as well as sera from healthy volunteers. The analytical performances of the Ramco assay were found to be acceptable. In the Eurogenetics test however, inter-assay imprecision and the end of run drift were unacceptably high. We were able to confirm that in patients with uncomplicated iron deficiency the concentration of soluble transferrin receptors is higher than in healthy volunteers. In cases of anaemia of chronic and inflammatory disease, the levels of soluble transferrin receptors in serum are slightly, but not significantly, higher than in normal subjects. Measurement of soluble transferrin receptors in serum provides a good differentiation between anaemia of chronic disease and iron deficiency.
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PMID:Analytical and clinical implications of soluble transferrin receptors in serum. 936 99

Serum levels of M-CSF were determined by an ELISA method in 29 and 34 patients with HbH disease (alpha 1/alpha 2 or alpha 2/HbCS) or beta zero-thal/HbE, respectively, in 28 haematologically normal subjects and in five patients with anaemia due to iron deficiency or myelodysplasia. In HbH disease and beta zero-thal/HbE, M-CSF concentrations were significantly higher than those in the normal subjects [986 +/- 138 and 1385 +/- 133, respectively, vs. 500 +/- 33 pg/ml (mean +/- SEM); p < 0.01, and p < 0.001, respectively]. By contrast, in patients with anaemia due to iron deficiency, M-CSF levels were within the normal range. In HbH disease and in beta zero-thal/HbE, M-CSF levels correlated inversely with mean basal Hb values (r = -0.39, p = 0.05 and r = -0.60, p < 0.001, respectively). In addition, in some of the HbH and beta zero-thal/HbE patients, monocyte ADCC activities towards red cells were tested and found to be approximately twice as high as those in normal controls [38.3 +/- 5.7 and 30.7 +/- 4.6 vs. 17.8 +/- 1.8% specific lysis (mean +/- SEM), respectively; p < 0.01 and p < 0.02, respectively]. When thalassaemic patients and normal controls were considered together there was a significant correlation between M-CSF levels and monocyte ADCC activities (r = 0.51, p < 0.02). The results suggest that in HbH disease and in beta zero-thal/HbE, raised serum M-CSF contributes to the anaemia by enhancing the effector function of mononuclear phagocytes towards red cells.
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PMID:Increased serum levels of macrophage colony-stimulating factor (M-CSF) in alpha- and beta-thalassaemia syndromes: correlation with anaemia and monocyte activation. 900 77

This report suggests modest changes in the criteria used for the diagnosis of ET and allows tentative recommendations concerning therapy. As outlined in Table I, we believe that absent stainable marrow iron does not necessarily indicate iron deficiency in these patients and that the serum ferritin and RBC mean corpuscular volume should be incorporated in this assessment. Normal values speak strongly against iron-deficient erythropoiesis. A search for the bcr/abl gene rearrangement should be included with the marrow karyotype to exclude CML. Finally, cytogenetic data and morphologic study of the marrow should be used to be certain that a MDS should not be considered. It may be that measurements of serum thrombopoietin levels may be useful in the future. Nonetheless, in principle, ET remains a diagnosis of exclusion as we have originally suggested. For therapy, HU remains an excellent choice for the older patient at risk for thrombosis. Nonetheless, no myelosuppressive therapy remains a perfectly viable option, particularly for the young patient and the older with low thrombotic risk. The roles of anagrelide and alpha interferon in this setting have not been fully defined. Experience with both has still been relatively short. It would be ideal if prospective, randomized trials could be mounted to address these questions. We conclude with confidence that return to older approaches such as 32P and AA in patients who fail on HU is to be discouraged. The use of anagrelide or interferon alfa seems to be a much more appropriate approach. We have not investigated the role of antithrombotic agents such as aspirin in ET. In PV, the combination of aspirin, 300 mg three times daily, and dipyridamole, 75 mg three times daily, failed to reduce the rate of thrombosis and was associated with an increased rate of hemorrhage. It is rational to suggest that lower doses of aspirin (ie, < 325 mg daily) might be associated with less hemorrhage and, perhaps, a beneficial effect on thrombosis. This remains to be shown.
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PMID:Experience of the Polycythemia Vera Study Group with essential thrombocythemia: a final report on diagnostic criteria, survival, and leukemic transition by treatment. 902 60

The presence of transferrin receptors on erythroblasts in patients with iron deficiency, anaemia of chronic disease (ACD) and myelodysplastic syndrome (MDS) was studied by two-colour analysis on a flow cytometer. CD 71 was used to quantify the number of transferrin receptors and GLY-A to identify erythroblasts. In cases of iron deficiency, the number of transferrin receptors was increased on part of the erythroblasts thus facilitating iron uptake by the cells. In patients with ACD or MDS, a decrease of the number of transferrin receptors on erythroblasts was found. This leads to the conclusion that the ineffective response to iron therapy in cases of ACD and MSD can be explained by a decline of transferrin receptors on the red cells.
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PMID:The expression of transferrin receptors on erythroblasts in anaemia of chronic disease, myelodysplastic syndromes and iron deficiency. 906 6

The expression of transferrin receptors on the cell membrane of erythroblasts was analysed with flow cytometry in patients with different forms of anaemia. At the same time the concentration of soluble transferrin receptors (sTfRs) was analysed in serum. It was shown that only in iron deficiency a high concentration of sTfRs in serum could be explained with an increased expression of transferrin receptors on the erythroblastic membrane. In anaemia of chronic disease and myelodysplasia a discrepancy between a low expression on the cell membrane and normal or elevated serum values was seen. From this study we conclude that the concentration of sTfRs in serum does not only depend on the expression of transferrin receptors on the erythroblasts but also on the erythroid activity.
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PMID:Relationship between soluble transferrin receptors in serum and membrane-bound transferrin receptors. 949 May 71

In iron deficiency, zinc protoporphyrin (ZPP) is produced instead of heme, and the ZPP concentration in erythrocytes increased (normal value < 2.3 micrograms ZPP/g Hb). The ZPP level and comparison with the other normally used tests in iron deficiency in the group of the patients with iron deficiency, ACD, MDS, AML, plasmocytoma was investigated. The ZPP level was determined by hematofluorometry in samples from 96 patients. Thirty five patients with iron depletion showed decreased both serum ferritin (median 5.9 ng/ml), and hemoglobin level (median 9.8 g/dl) with significantly increased ZPP level (median 8.5 micrograms/gHb). An increased level of ZPP (median 3.95 micrograms/gHb) with normal level of ferritin (median 24 ng/ml) and iron (median 50 (g/dl) in the serum of patients with ACD was determined. Measurement of ZPP level in the combination with ferritin and peripheral blood morphology allows to classify the degree of iron deficiency. The ZPP levels higher than 4.55 micrograms/gHb confirms iron deficiency in the group of anaemic patients.
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PMID:[Zinc protoporphyrin (ZPP) in diagnosis of anemia]. 964 80

The present study describes clinicopathological criteria to distinguish the 5 sequential stages proposed by Wasserman et al in the natural history of newly diagnosed PV patients. The European Working Group on MPD (EWG.MPD) extended and modified the PVSG diagnostic criteria of PV by including bone marrow histopathology. From the results of prospective randomized studies in PV it became evident that new clinical trials in previously untreated PV patients should focus on comparing interferon-alpha, a non-leukemogenic approach, versus a potential leukemogenic myelosuppressive treatment modality. Hydroxyurea appears to be the least leukemogenic myelosuppressive agent in long-term prospective clinical PV-studies extending observation periods of more than 10 years. The rational for using IFN-alpha as a first-line treatment option in newly diagnosed PV-patient include its effectiveness to abate constitutional symptoms and to induce a complete remission thereby avoiding phlebotomy, iron deficiency, and macrocytosis associated with hydroxyurea. Moreover IFN-alpha may prevent or delay the development of postpolycythemic myelofibrosis if used early in the course of the disease. Clinicians will be reluctant to postpone the use of hydroxyurea in early stage PV as long as a conservative approach using phlebotomy aiming at a hematocrit below 0.45, plus low-dose aspirin for the control platelet function or anagrelide for the control platelet number is used to keep the patient healthy. Low-dose aspirin will prevent the microvascular thrombotic complications of thrombocythemia associated with PV in remission after phlebotomy, but lacks myelosuppressive activity. Control of megakaryocyte maturation and reduction of platelet production to normal (<400 x 10(9)/l) by relatively low doses of anagrelide will predict a significant reduction of vascular complications in the early stages of PV, may prevent progression to myelofibrosis during follow-up of PV and very probable will postpone the use of hydroxyurea treatment for controlling the platelet count in PV. Large scale randomized clinical trials in PV are proposed, which should aim not only for clinical and hematological response, safety, efficacy, but should also assess toxicity, the need for phlebotomy and whether the development of progressive disease such as splenomegaly, pruritus, myelofibrotic myeloid metaplasia, spent phase, myelodysplasia and acute leukemia can be delayed or prevented by IFN-alpha as compared to a conservative approach of phlebotomy plus low-dose aspirin or anagrelide followed by hydroxyurea when signs of myeloproliferative activity became evident.
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PMID:Diagnosis and treatment of polycythemia vera and possible future study designs of the PVSG. 1067 96

Effective management of early anaemia in the course of chronic renal insufficiency requires the following: (i) implementing an efficient diagnostic strategy to exclude common contributing factors; (ii) initiating epoetin therapy for the majority of patients; for and (iii) ensuring adequate iron supply erythropoiesis. Diagnostic inquiry is warranted whenever the haemoglobin concentration is below the normal range adjusted for age and gender. The most efficient diagnostic approach is to assume erythropoietin deficiency, exclude iron deficiency, and pursue further diagnostic tests only when red-cell indices are abnormal or when leukopenia or thrombocytopenia are also present. Macrocytosis should prompt an inquiry into alcoholism, B12 deficiency, or folate deficiency. Microcytosis suggests iron deficiency or thalassaemia. Associated cytopenias raise the possibility of alcohol toxicity, pernicious anaemia, malignancy, or myelodysplastic syndrome. Epoetin therapy is warranted whenever the haemoglobin concentration has fallen below 10.0 g/dl. To initiate therapy prior to dialysis, epoetin should be administered at an average dose of 100 IU/kg/week (80-120 IU/kg/week, 50-150 IU/kg/ week) by subcutaneous injection. Haemoglobin concentration should be monitored every 2 weeks and the epoetin dose adjusted by increments or decrements of 25% to maintain a rate of rise of haemoglobin concentration of 0.2-0.6 g/dl (0.3 0.6 g/dl/week, 0.2-0.5 g/dl/week). When the target range is achieved, the dose of epoetin should be continually adjusted to maintain a stable haemoglobin concentration. Transferrin saturation and ferritin concentration should be monitored monthly, and sufficient iron provided to maintain transferrin saturation above 20%. The lower the haemoglobin concentration, the greater the likelihood that future intravenous iron will be required. Oral iron supplements should be avoided, since they are costly, ineffective, and troublesome to patients. Finally, a blunted therapeutic response to epoetin therapy provides important diagnostic information and gnostic inquiry.
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PMID:Management of early renal anaemia: diagnostic work-up, iron therapy, epoetin therapy. 1103 56


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