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)

Anaemia is common in renal insufficiency and has various causes: 1) depressed marrow production of red cells, probably due to reduced production of erythropoietin, though the possibility of direct marrow inhibition on the part of uraemic toxins cannot be ruled out, together with iron deficiency, as occurs in prolonged dialysis management; 2) greater red cell destruction attributable to extraglobular factors and other mechanisms (microangiopathy, drugs, etc.); 3) greater blood loss following thrombocytopenia, reduced platelet adhesivity and agglutinability, dialysis. The main premisses on which the treatment of anaemia of uraemic patients is based are discussed.
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PMID:[Anemia in chronic renal insufficiency]. 73 54

The natural history and haematological features of 18 patients with a chronic form of myelomonocytic leukaemia are described. The majority were elderly and, in this series, females predominated. Haematological prodomata, such as unexplained monocytosis, leucopenia, or thrombocytopenia were common, and the clinical onset was insidious. Splenomegaly was variable but tended to increase as the disease progressed. Anaemia was usually less than in the acute disease, unless compounded by iron deficiency. The blood film typically showed a mixed monocytosis and granulocytosis, cells in both lines showing abnormalities. 'Paramyeloid' cells, appearing in Romanowsky stained films intermediate between myelocytes and monocytes, were characteristic, although cytochemical and electron microscopical analysis suggests that these cells may be allotted to one or other cell line. The marrow aspirate was characteristically hypercellular, showed granulocytic hyperplasia, and, in contrast to the well-differentiated blood picture, the proportion of poorly differentiated cells, including blasts, was high. Serum lysozyme levels were usually raised. Five of the 18 cases survived more than 5 years, while 10 lived 2 years or longer. The morphological and clinical features form part of a spectrum including acute myelomonocytic leukaemia, into which several of the patients transformed. Recognition of the syndrome is important because the patients are probably best managed without intensive chemotherapy.
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PMID:Chronic myelomonocytic leukaemia. 105 74

The onset of postpolycythemic myeoloid metaplasia or spent polycythemia has been recognized for many years. As the result of many different series, the development of postpolycythemic myeolid metaplasia might be expected in from 15%-20% of patients with postpolycythemia vera. It appears that an etiologic role for sodium phosphate 32P may exist in this evolutionary pattern. About 70% of patients with PPMM will have symptoms with the onset of the syndrome. The major mechanisms producing symptoms result from (1) anemia, (2) pressure from massive splenomegaly, and (3) bleeding problems. Iron deficiency is a frequent cause of anemia in patients with PPMM. The major mechanism of anemia in these patients, however, relates to ineffective erythropoiesis and shortened red cell survival. Androgen trials for ineffective erythropoiesis seem worthwhile, although data on this point is too limited to draw any firm conclusions. A steroid trial for those patients with major hemolytic episodes is indicated. In those patients in whom adrenal steroid therapy fails to control major hemolysis, a consideration for splenectomy exists. Pressure-related manifestations secondary to massive splenomegaly have been treated with radiation therapy and oral alkylators. Although there is data to document amelioration of painful symptoms with associated shrinking of the spleen, long-term control of this problem has not been forthcoming. Again, patients who are medical failures in control of pressure-related manifestations may be considered for splenectomy. Bleeding problems may arise with PPMM secondary to thrombocytopenia, thrombocythemia, or qualitative platelet dysfunction. Adrenal steroids have met with some success in improving platelet counts in patients with life-threatening thrombocytopenia. Those patients who are medical failures with adrenal steroids in terms of thrombocytopenia might be candidates for splenectomy. Control of thrombocythemia has been observed with oral alkylator therapy and chlorambucil may have a special role in managing this complication. Qualitative platelet defects leading to severe bleeding are best managed with fresh platelet transfusions. Patients with PPMM in contrast to patients with agnogenic myeoloid metaplasia have a more lethal syndrome and shortened survivorship. Causes of death in patients with PPMM include cardiac problems, transition to acute leukemia, hemorrhage, and infection.
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PMID:The evolution into and the treatment of late stage polycythemia vera. 125 Dec 24

Erythrocyte basic ferritin (EF) concentration was determined in 64 normal subjects, 123 patients with anemia and 12 patients with leukopenia and thrombocytopenia. There was a significant difference between males and females. Other iron indices, including plasma iron (PI), total iron binding capacity (TIBC), zinc protoporphyrin (ZnPP) and plasma ferritin (PF) were also determined in all the subjects and bone marrow iron stain was determined in the 135 patients. The lowest EF concentration was seen in patients with iron deficiency anemia, being significantly lower than that in normal subjects. EF concentration in patients with iron deficiency erythropoiesis was also lower than that in normal subjects and at the same time significantly different from that in patients with iron deficiency anemia. EF concentration increased prior to PF concentration in patients with iron deficiency anemia who had been treated for a period of 1-8 weeks. EF concentration in patients with anemia of chronic diseases had a significant difference as compared with that in normal subjects and in patients with iron deficiency anemia, but EF concentration in those patients who were accompanied by iron deficiency was similar to that in patients with simple iron deficiency anemia. EF concentration in some iron overloaded patients (aplastic anemia, megaloblastic anemia, MDS etc.) was significantly higher than that in normal subjects. It was demonstrated that there was a good correlation between EF concentration and bone marrow sideroblastic iron in the rank correlation analysis of the iron indices in 135 patients (rs 0.893, P less than 0.01). PF concentration had the best correlation with marrow iron (rs 0.948, P less than 0.01).
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PMID:[Evaluation of erythrocyte basic ferritin in the diagnosis of anemia]. 208

In the present study the 60 patients with brucellosis and evaluation of bone marrow aspirate seen at the Hospital Base Cayetano Heredia from 1980 to 1986 were included. Iron deficiency was found in the bone marrow in 34.5% of patients, 31% in males and 36% in females. No correlation was found between iron deficiency and severity of the hematological or non-hematological clinical features. Bone marrow cytophagocytosis was found in 28.3% of patients. All had moderate to severe clinical features, and it is postulated that this finding may be helpful as a severity marker in patients with brucellosis. Bone marrow cytophagocytosis was significantly associated with the presence of hematologic abnormalities in general; anemia was the most common of these, followed by thrombocytopenia. This finding suggests that cytophagocytosis is an important mechanism in the pathogenesis of these abnormalities in brucellosis. Bone marrow hypercellularity was present in 70% with normocellularity in 28.3% and one case of pure megakaryocytic aplasia. In thirty-five patients pathological study of bone marrow was carried out 10 of these (28.5%) had granulomas. Their presence was not correlated with the clinical severity. Peripheral blood finding were: anemia in 83.3%, with two cases of hemolytic anemia and positive direct Coombs test, one of them associated with thrombocytopenia (Evans syndrome); leukopenia in 21%, basically due to neutropenia; thrombocytopenia in 33.3%, in one case associated with positive antiplatelet antibodies and with pure megakaryocytic aplasia in others; pancytopenia in 13.5% of cases (8 patients) associated to bone marrow cytophagocytosis in 5 cases (64.5%) and thus suggesting that this might be the major underlying pathogenetic mechanism.
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PMID:[Evaluation of the bone marrow in patients with brucellosis. Clinico-pathological correlation]. 209

Animals with hereditary abnormalities of hematopoiesis are quite useful in the study of regulatory pathways of megakaryocytopoiesis and platelet formation. Seven such animal models are analyzed here. The Wistar Furth rat has been recently discovered to have reduced platelet number, but large mean platelet volume, and is, therefore, a model of hereditary macrothrombocytopenia. Study of the Wistar Furth rat may help to elucidate the process of platelet formation. Two mouse mutants the S1/S1d and W/Wv, have macrocytic anemia with reduced megakaryocyte number, but normal platelet count. In these mice, the platelet count is maintained by increased platelet production per megakaryocyte. These models demonstrate that factors other than platelet level are monitored in the feedback regulation of megakaryocytopoiesis and platelet production, and further study should lead to a better understanding of the regulation of megakaryocyte size. The Belgrade rat has severe microcytic anemia with decreased megakaryocyte number. Megakaryocyte size is increased, but platelet count is moderately reduced and thus the megakaryocyte-platelet picture resembles that of severe iron deficiency anemia. A more in depth examination of this model should delineate the effects of iron deficiency and hypoxia on megakaryocytopoiesis. The grey collie dog has cyclic hematopoiesis with large asynchronous fluctuations in all blood cell counts at approximately 2-week intervals. Megakaryocytes have not been studied. This model should be a tool to define the relationships between hematopoietic growth factors and differentiation of the various hematopoietic cell lineages. The br/br rabbit has a transient disturbance in fetal megakaryocytopoiesis and brachydactyly due to spontaneous amputation. Further study of this model may provide a better understanding of fetal megakaryocyte development and establish whether an association exists between the abnormal megakaryocytes and the limb amputations. The nude mouse with its severe T-lymphocyte deficiency has been studied to ascertain whether T cells play a regulatory role in normal and acute thrombocytopenia-stimulated megakaryocytopoiesis. The question of whether T cells or their products are responsible for reactive thrombocytosis in chronic inflammation could be examined with this model. These animal mutants have provided and should continue to provide important models for understanding the regulation of megakaryocytopoiesis and platelet production.
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PMID:Animal models with inherited hematopoietic abnormalities as tools to study thrombopoiesis. 264 83

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17

A microcomputer program (BCDE) has been developed to analyze automated blood cell counts and differentials' similarity to normal values or to 36 disease categories. In 50 normal subjects, the analytic program listed the correct diagnosis as the first diagnosis in 49 cases (the only diagnosis in 44) and second of two diagnoses in one case. In 182 subjects with known hematologic disorders, the correct diagnosis was listed first in 134 and second or third in an additional 40. Subjects with iron deficiency, heterozygous thalassemia, immune thrombocytopenia, anemia of chronic disease, reactive thrombocytosis, acute infection, and chronic leukemia had the disorder identified as the most likely one by the analytic program with both sensitivity greater than 80% and specificity greater than 98%. Subjects with acute leukemia, folate deficiency, sickle cell anemia, cytotoxic chemotherapy, and chronic liver disease had the disorder identified as most likely by the program with a sensitivity less than 80%. In a different 11 cases with known hematologic status, a panel of 37 physicians identified the disorder(s) or normality only 72% of the time, whereas the analytic program listed the correct diagnosis first in 10 of 11 (91%). The analytic program appears useful for both triage of normal from abnormal data and for the initial differential analysis of abnormal data.
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PMID:Evaluation of BCDE, a microcomputer program to analyze automated blood counts and differentials. 330 76

Two patients with iron deficiency experienced rapid decreases in their platelet levels following initiation of replacement therapy with oral ferrous sulfate or ferrous gluconate. The first patient, whose pretreatment platelet count was 168,000 per mm3, developed marked thrombocytopenia (platelet count, 21,000 per mm3) on the sixth day of iron repletion. The second patient's platelet level fell from 725,000 to 105,000 per mm3 on the tenth day of therapy. In both instances, platelet levels gradually returned to normal levels. The data suggest that the administration of oral iron resulted in an acute reduction in platelet production. The mechanism(s), prevalence, and clinical significance of thrombocytopenia following iron repletion in patients with iron deficiency anemia remain unknown.
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PMID:Thrombocytopenia associated with repletion of iron in iron-deficiency anemia. 333 37

Mild leukopenia and thrombocytopenia are common in multitransfused hemophiliacs. Because little attention has previously been directed to measurements of erythropoiesis in these patients, we prospectively examined hemoglobin concentration and RBC indices in 94 children and young adults with hemophilia during comprehensive clinic visits. Additional studies performed in many included serum transferrin saturation, ferritin, haptoglobin, and free erythrocyte protoporphyrin measurements. Hemoglobin concentrations were recorded as age-related percentile values. Hemophiliacs of all ages and degrees of severity often had lower than average values for hemoglobin; 31% had values less than the third percentile, 46% less than the tenth percentile, and 83% less than the mean value. Reduced hemoglobin percentile values were unrelated to age, severity of disease, or human immunodeficiency virus antibody status. Only five patients had an obvious cause for anemia. Serum ferritin, transferrin saturation, and erythrocyte protoporphyrin values were usually normal, indicating that iron deficiency and anemia of chronic disease were uncommon. Although serum haptoglobin was reduced in 44% of the patients, reticulocyte count was infrequently increased. We conclude that hemoglobin values are frequently less than the mean normal values for age in hemophiliacs. Although frank anemia is common, it is usually mild and without obvious cause. Hemophiliac individuals with slightly reduced hemoglobin values probably do not routinely require detailed investigation for occult blood loss, iron deficiency, or inflammation.
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PMID:Reduced hemoglobin values in children and young adults with hemophilia. 336 83


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