Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron deficiency anaemia was induced in rabbits by repeated bleeding. The leucocyte alkaline phosphatase (LAP) of 26 +/- 28 units was significantly reduced compared with control values of 233 +/- 35 units (P less than 0.001). Leucocyte NBT reduction was also diminished, both in Hanks solution (P less than 0.01) and in autologous serum (P less than 0.001). After administration of iron, these values returned to normal. The results suggest that reduced LAP may reflect a deficiency of iron dependent constituents which are necessary for the integrity of normal granulocyte metabolism.
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PMID:Reduced leucocyte alkaline phosphatase activity and decreased NBT reduction test in induced iron deficiency anaemia in rabbits. 38 63

To determine the quantitative effects of iron deficiency on erythropoiesis and to assess the response of erythroid progenitors to sustained anemia, we developed quantitative assays for various hematopoietic progenitors in the adult, Sprague-Dawley rat including erythroid colony- and burst-forming cells (CFU-E and BFU-E), granulocyte/macrophage colony-forming cells (CFU-GM), and megakaryocytic colony-forming cells (CFU-Meg). CFU-E were cultured in methylcellulose and grew best in the presence of fetal calf serum. CFU-GM, BFU-E, and CFU-Meg grew better in normal rat plasma and required the presence of pokeweed mitogen-stimulated rat spleen cell conditioned medium. The numbers of progenitors and nucleated erythroblasts in total marrow were estimated by the ratios of radioactivity in the humerus to the total skeleton as determined by radioiron dilution. The numbers of progenitors and erythroblasts in the spleen were measured by simple dilution. Sustained anemia was brought about through chronic iron deficiency. The response to iron deficiency anemia (IDA) was monitored by the numbers of the various progenitors and their cell cycle characteristics as measured by the tritiated thymidine suicide technique. With IDA, the number of CFU-F in the body (marrow plus spleen) was increased to 3.5 times control, whereas the numbers of BFU-E and CFU-GM were unchanged. There was no difference in the percentage of CFU-E, BFU-E, and CFU-GM in DNA synthesis (68%, 19.4%, and 18.8%, respectively). With iron therapy of IDA, CFU-E numbers in marrow began to decrease by day 1 and fell in a manner reciprocal to changes in the hematocrit. Marrow and spleen erythroblasts, 1.7 times control in IDA, increased further to 3.9 times control by the fourth day after iron administration. There was no change in BFU-E or CFU-GM numbers in response to iron repletion, although the fraction of progenitors increased in the spleen. Thus, IDA does not limit the increase in CFU-E seen with anemia, but does restrict erythroid maturation. Furthermore, the increase in CFU-E and the state of chronic anemia occur without detectable changes in the number of cell cycle state of the more primitive BFU-E.
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PMID:Hematopoiesis in the rat: quantitation of hematopoietic progenitors and the response to iron deficiency anemia. 394 11

Apoptosis of peripheral leukocytes in 9 patients with myelodysplastic syndromes (MDS) was examined in vitro, using peripheral blood that had been gently incubated at 37 degrees C for 5 hours. The MDS patients included 3 with refractory anemia, 2 with refractory anemia with ringed sideroblasts, and 4 with refractory anemia with excess blasts. Peripheral blood specimens were also obtained from a control group consisting of 10 patients with iron deficiency anemia (IDA), 10 with idiopathic thrombocytopenic purpura (ITP) and 10 healthy individuals. Apoptotic granulocytes (Apo-Gs) were identified by morphological changes, including nuclear fragmentation, and expressed as a percentage of every 300 granulocytes counted. Apo-Gs were counted 1, 2, 3, 4, and 5 hours after incubation. Although the percentage of apo-Gs climbed over time in the MDS patients, a small number of apo-Gs were also observed in the healthy individuals. In the MDS patients, the proportions of apo-Gs 5 hours after incubation (37 degrees C) were significantly higher than those in the IDA and ITP patients and healthy individuals (15.7 +/- 8.0% in MDS patients vs. 2.8 +/- 1.2% in IDA patients, 2.3 +/- 1.7% in ITP patients, and 0.7 +/- 0.6% in healthy individuals; p < 0.005). No significant differences were observed in the proportions of apo-lymphocytes. DNA fragments were observed in blood lymphocyte from an MDS patient examined. Negative correlations between the percentages of granulocytes and Apo-Gs tended to be observed in the MDS patients. These results suggest that a strong susceptibility to peripheral granulocyte apoptosis is one of possible causes of granulocytopenia in MDS patients.
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PMID:[Apoptosis of peripheral leukocytes in patients with myelodysplastic syndromes]. 986 18

MYH-9 related platelet disorders belong to the group of inherited giant platelet disorders. The MYH-9 gene encodes the non-muscular myosin heavy chain IIA (NMMHCIIA), a cytoskeletal contractile protein. Several mutations in the MYH-9 gene lead to macrothrombocytopenia, and cytoplasmic inclusion bodies within leukocytes, while the number of megakaryocytes in the bone marrow is normal. Four overlapping syndromes, known as May-Hegglin anomaly, Epstein syndrome, Fechtner syndrome and Sebastian platelet syndrome, describe different clinical manifestations of MYH9 gene mutations. Macrothrombocytopenia is present in all affected individuals, whereas only some develop additional clinical manifestations such as renal failure, hearing loss and presenile cataracts. The bleeding tendency is usually moderate, with menorrhagia and easy bruising being most frequent. The biggest risk for the individual is inappropriate treatment due to misdiagnosis of chronic autoimmune thrombocytopenia. More than 30 mutations within the 40 exons of the MYH-9 gene leading to macrothrombocytopenia have been identified, of which the upstream mutations up to amino acid ~1400 are more likely associated with syndromic manifestations than the downstream mutations. Diagnosis is based on identification of the granulocyte inclusion bodies using blood smears and immunofluorescence and is finally confirmed by identifying the mutation. Treatment is supportive and should be aimed to prevent iron deficiency anemia. Beside renal failure, the biggest risk for patients affected by a MYH-9 disorder are the adverse effects resulting form treatment based on the misdiagnosis of immune thrombocytopenia.
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PMID:MYH-9 Related Platelet Disorders: Strategies for Management and Diagnosis. 2111 48