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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 11-year-old girl presented with a refractory hypochromic microcytic anemia, hypoferremia, normoblastic hyperplastic bone marrow, hypergammaglobulinemia, and growth retardation. Many varied treatments failed to produce any improvement. Ferrokinetic studies revealed rapid plasma clearance and increased plasma iron turnover, but impaired incorporation of 59Fe. Excretion of 57Co after an oral dose indicated an increased iron absorption. A (99M)Tc-sulfur colloid scintigram of the abdomen failed to demonstrate abnormal uptake. A nodal mass showing the plasma-cell variant of angiofollicular hyperplasia was removed from the gastrolienal ligament. Follow-up studies at 3 and 6 months revealed complete correction of the anemia, a 4.8-cm increase in height, and normal serum gamma-globulin levels. Serum obtained before operation inhibited the incorporation of 59Fe that was induced by a standard dose of erthyropoietin in the exhypoxic mouse system, and this inhibition persisted in serum obtained 3 days after surgery but disappeared by 6 days. The data suggest that the hyperplastic angiofollicular lymph node (plasma-cell variant) secreted a substance the inhibited erythropoiesis.
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PMID:Intra-abdominal, angiofollicular lymph node hyperplasia (plasma-cell variant) with an antierythropoietic factor. 5 Nov 37

Exfoliative cytology smears from the buccal mucosa of patients with sickle-cell anemia, selected controls, and patients with other diagnosed anemias were studied for nuclear aberrations. A filar micrometer eyepiece was used to count the number of nuclei larger than 14 microns in mean diameter in a 500 cell count on each slide. Use of the Scheffe method of paired comparisons, disclosed that the number of cells larger than 14 microns in mean diameter, was significantly smaller in the control subjects, patients with microcytic anemia, and subjects with sickle-cell anemia than in the patients with megaloblastic anemia. Serum folate-deficient subjects had significantly more nuclei, per 500 cells, larger than 14 microns than control subjects or subjects on folate therapy. An explanation for the enlarged nuclei in smears from sickle-cell anemia patients is given. The possible use of this counting procedure to evaluate tissue folate status is suggested.
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PMID:Nuclear characteristics of buccal mucosa cells in sickle-cell anemia. 26 83

The duodenal mucosa of genotypically normal iron replete and iron deficient mice and mice with sex-linked (sla) and microcytic anemias (mk) was examined for the presence of iron-binding proteins. Following continuous, 15 or 120 minute, in vivo intraenteric exposure of a closed duodenal loop to 59Fe, a high speed supernatant of homogenized mucosal tissue was chromatographed on G-200 Sephadex. Two major peaks of 59Fe activity were observed. The molecular weight, and immunological properties of peak I were similar to ferritin whilst those of peak II were similar to transferrin. The distribution of 59Fe between peaks I and II in mk/mk animals was similar to that in genotypically normal iron deficient animals indicating that the intramucosal mechanisms for iron transport were reacting appropriately to the iron deficient state of mice with microcytic anemia. In contrast, the distribution of 59Fe between peaks I and II in sla/Y animals was the reverse of that found in genotypically normal iron deficient animals suggesting the possibility of an intramucosal iron binding protein defect in sex-linked anemia.
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PMID:Mucosal iron binding proteins in sex-linked anemia and microcytic anemia of the mouse. 28 79

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.
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PMID:Ochratoxin A-induced iron deficiency anemia. 45 31

Study of 36 cases of thyrotoxicosis demonstrated the prevalence of anaemia (17 cases) and of microcytosis (26 cases). In patients with a microcytosis, serum iron was measured in 9, being found to be low in 5 of them, whilst amongst twelve 10 had anti-thyroid antibodies and anti-gastric antibodies. Atrophic gastritis was seen in the 5 patients who underwent endoscopy. Four biopsies revealed 3 cases of atrophic gastritis and one of simple gastritis. The types of anaemia seen and their mechanisms are discussed: microcytic anaemia related to disturbed iron metabolism or to its impaired intestinal absorption; normocytic anaemia; macrocytic anaemia possibly preceding pernicious anaemia. It would seem to be possible to distinguish two pathogenic categories: thyrotoxicosis reversible changes in iron metabolism, and atrophic gastritis associated with hyperthyroidis in an "auto-immune context" and which has led to the concept of "thyro-gastric" disease.
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PMID:[Anaemia and microcytosis during thyrotoxicosis. Physiopathological discussion. 36 cases (author's transl)]. 58 36

The unusual occurrence of microcytic anemia with hypochromia, high iron blood levels and excess of sideroblasts in the bone marrow, observed during the treatment of tuberculosis with isoniazid and rifampicine is reported. Three particularities were noted. First, in our experience, the occurrence of this type of anemia has never been noted previously as a result of these two drugs. Secondly, the improvement of the blood abnormalities was obtained by the combined use of vitamin B6 and vitamin C. Thirdly, the anemia was associated with neuropathy, characterized by areflexia and dysesthesia, which improved with vitamin B6 therapy (but not with vitamin C). Some mechanisms are discussed as being possibly the origin of this kind of anemia, particularly a lack of vitamin B6 resulting from a massive urinary loss of pyridoxal induced by isoniazid as well as both a tissue depletion and an overconsumption of this vitamin. The anemia may be the consequence of a deficiency of hemoglobin synthesis involving probably the first step of the biosynthesis of heme.
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PMID:[Anemia with hypersideroblastosis during anti-tuberculosis therapy. Cure with vitamin therapy]. 67 33

The reliability of a radioimmunometric assay of serum ferritin concentration by a packaged kit was evaluated. In addition, application of the serum ferritin assay to the clinical evaluation of selected anemias was assessed. When appropriate serum dilutions were utilized, this method was sufficiently reproducible and reliable for application to the clinical laboratory. Serum ferritin was found to be a valuable tool in the differential diagnosis of anemia accompanied by hypoferremia, although iron depletion coexisting with either the anemia of chronic disease or active hepatocellular disease may not be clearly appreciated. The primary advantage of the determination was to help characterize the iron status of the patient with a hypochromic microcytic anemia or hypoferremia who would ordinarly require a bone-marrow examination for iron stores.
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PMID:Evaluation of a packaged kit assay of serum ferritin and application to clinical diagnosis of selected anemias. 69 76

This article on microcytic anemia is the first of several on laboratory investigation of anemia. Microcytic anemia, characterized by a mean corpuscular volume of less than 80 cu mu, is usually due to iron deficiency or chronic disease but may signify thalassemia minor. Exact identification of the cause is important, since inappropriate iron therapy may be useless or even dangerous.
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PMID:Investigation of microcytic anemia. 76 90

Five genetic traits in man and laboratory animals have major effects on iron transport. The heterogeneous condition, hemochromatosis, in some families appears to segregate as a Mendelian trait, and is associated with defective control of intestinal iron absorption. In the very rare human autosomal recessive trait, atransferrinemia, there is an almost total lack of transferrin and gross maldistribution of iron through the body. In mice, sex-linked anemia (an X-linked recessive trait) causes iron deficiency through defective iron absorption, at the "exit" step; a similar defect probably exists in placental iron transfer. In microcytic anemia of mice, an autosomal recessive trait, iron absorption is also impaired because of a defect of iron entry into cells, which is probably generalized. Belgrade rat anemia, less understood at present, also may involve a major disorder of iron metabolism. Study of these mutations has provided new knowledge of iron metabolism and its genetic control Their phenotypic interaction with nutritional factors, especially the form and quantity of iron in the diet, may provide new insights for the study of nutrition.
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PMID:Genetic defects of iron transport. 78 24

Size-frequency distribution curves of erythrocytes were generated with the Coulter Counter in 73 normal subjects and patients. Mean corpuscular volume (MCV) determined by routine calculation and MCV determined by size-frequency distribution were similar in all normal subjects and in patients with a single population of erythrocytes. Some patients with iron-deficiency anemia, folate deficiency, and vitamin B12 deficiency had two discrete erythrocyte populations. Some patients with microcytic anemia were shown to have a population of normocytes in addition to the predominant microcytic population. Reticulocytes and normocytes were identified in two patients recovering from macrocytic anemia. Transfused blood was identified as a separate population in a patient with microcytic anemia. In cases with two erythrocyte populations, the MCV of the principal population, as determined from size-distribution curves, differed from the MCV of the entire erythrocyte pool, as was determined by routine methods. Analysis of sequential erythrocyte size distributions in patients under treatment demonstrated the dynamics of erythrocyte subpopulations. Anisocytosis was quantified and shown to be associated frequently with hospitalized patients.
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PMID:Erythrocyte volume distribution in normal and abnormal subjects. 114 95


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