Cases reported "Anemia, Hypochromic"

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11/19. Unusual cause of short stature.

    A 24-year-old man evaluated for paresthesias and short stature was found to be hypocalcemic on initial presentation. Further evaluation showed that he had a low-normal parathormone level by amino-terminal assay, medullary stenosis of the long bones, and multiple ophthalmologic abnormalities. The remainder of his pituitary function, including growth hormone response to insulin-induced hypoglycemia, was normal. As no family history of similar findings was evident, a sporadic case of Kenny's or Kenny-Caffey syndrome was diagnosed. He became normocalcemic in response to vitamin d and calcium carbonate therapy. The results of testing in this patient and the findings in other patients previously described with the Kenny-Caffey syndrome are reviewed.
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12/19. Intra-abdominal, angiofollicular lymph node hyperplasia (plasma-cell variant) with an antierythropoietic factor.

    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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13/19. Acquired iron-deficiency anaemia due to impaired iron transport.

    A previously healthy 39-year-old woman presented with severe iron-deficiency anaemia, but she had lost no blood and her serum iron level was high. Her bone marrow was hypercellular with a predominance of erythroid elements and had no stainable iron deposits, but it also showed dyserythropoiesis and an excess of apparently normal plasma cells. IgM was demonstrated on her bone-marrow erythrocytes and their precursors. On azathioprine and prednisone therapy she had a complete clinical and haematological remission. The impaired iron transport and the associated dyserythropoiesis were probably due to an IgM-mediated autoimmune process. diabetes mellitus, which first appeared during her anaemic illness, could also have been due to an autoimmune process. This is the first report of an iron-deficiency anaemia caused by a naturally acquired impairment of iron transport.
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14/19. iron deficiency and sickle cell anemia.

    In a patient with sickle cell anemia, iron deficiency was accompanied by hypochromic, microcytic RBCs, absence of bone marrow iron, and a low serum ferritin level. The mean corpuscular hemoglobin concentration (MCHC) was decreased (27.6 g/dL) and was associated with an extreme scarcity of sickled erythrocytes in blood smears. iron therapy resulted in reticulocytosis and an increase in sickled erythrocytes. in vitro studies demonstrated a decrease in sickling of erythrocytes as a function of oxygen saturation of the blood when the patient was iron deficient. The whole blood oxygen dissociation curve showed a substantial decrease in oxygen pressure necessary to produce 50% saturation of hemoglobin at pH 7.4 and 37 degrees C (P50), indicating an increased oxygen affinity. These data suggest that a reduction of the MCHC induced by iron deficiency may ameliorate sickling.
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15/19. giant lymph node hyperplasia (Castleman's disease) of the mesentery. Observations on the associated anemia.

    A mesenteric mass, histologically characterized as giant lymph node hyperplasia was found in an 18-yr-old man with at least 11 yr of growth retardation and anemia. The anemia was characterized by iron deficiency from selective malabsorption of iron, and by features of the anemia of chronic disorders. In contrast with a previous report, no inhibitor of erythropoietin was found and there was no abnormality of erythropoietin secretion. Resection of the mass was followed by rapid correction of the anemia and catch-up growth. The mass had histologic features of the hyaline vascular and plasma cell types of Castleman's disease with multinucleate giant cells probably of macrophage origin. Immunologic studies of the mass showed that the B lymphocytes were polyclonal and the T lymphocyte helper/suppressor cell ratio was normal, suggesting that giant lymph node hyperplasia is a local inflammatory reaction.
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keywords = macrophage
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16/19. Use of sodium chromate Cr51 in diagnosing childhood idiopathic pulmonary hemosiderosis.

    The diagnosis of idiopathic pulmonary hemosiderosis (IPH) may be elusive. A 6-year-old boy had microcytic hypochromic anemia and a hemolytic component. hemosiderin-laden macrophages were not found in the gastric aspirate. He had no pulmonary signs or symptoms. Extensive hematologic and roentgenologic investigations failed to reveal the cause of the anemia. Quantitative serial scintigraphic scanning showed significant (35%) pulmonary sequestration of autologous erythrocytes labeled with sodium chromate Cr51. The half-life of the RBCs was moderately decreased (half-life, 15 days; normal, 25 to 35 days). An open-lung biopsy specimen confirmed the diagnosis of IPH. A diagnosis of IPH should be considered when children have iron deficiency anemia and pulmonary signs or symptoms. Organ sequestration studies may be helpful in equivocal cases.
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keywords = macrophage
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17/19. Pulmonary hemosiderosis and immune thrombocytopenia. Initial manifestations of collagen-vascular disease.

    Severe iron deficiency anemia, pulmonary infiltrates, and cutaneous hemorrhage associated with thrombocytopenia developed in a 7-year-old girl. A typical clinical course and the presence of abundant hemosiderinladen macrophages in the gastric juice and alveoli suggested a diagnosis of idiopathic pulmonary hemosiderosis (PH). Investigation of the marked thrombocytopenia, not previously reported as a finding in IPH, resulted in the demonstration of antiplatelet antibody in the patient's serum and on her platelets. Response to corticosteroid administration and splenectomy was consistent with idiopathic thrombocytopenic purpura (ITP). The IPH and ITP may have occurred coincidentally in this patient, but certain pathophysiological similarities between these two disorders and ultimate development of a poorly defined fatal diffuse connective tissue disorder suggest that thrombocytopenia and intrapulmonary hemorrhage were related.
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ranking = 477.3639002657
keywords = macrophage
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18/19. iron deficiency anemia. Every case is instructive.

    awareness of subtle symptoms of mild iron deficiency is increasing, but unsuspected iron deficiency is a persistent problem, especially among certain groups, such as menstruating women and milk-fed infants. The diagnosis must be clearly established through appropriate testing, and an underlying cause should always be sought. Useful tests include determination of serum ferritin and iron levels and of iron-binding capacity. A nomogram is available that correlates the serum ferritin value with the degree of inflammation present, but in some patients, bone marrow aspiration and iron staining is still required. When oral iron therapy is undertaken, an appropriate non-enteric-coated, non-sustained-release preparation should be chosen. Gradually increasing the amount of iron supplementation and taking the tablets with meals help limit side effects and ensure patient compliance. iron therapy should be continued for 6 months after the hemoglobin level returns to normal so that total iron stores are replaced. Follow-up to ensure that iron deficiency anemia has not recurred and that the diagnosis was correct is required.
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19/19. Idiopathic pulmonary hemosiderosis: ultrastructural studies and responses to azathioprine.

    Two boys are presented who fulfilled criteria for a diagnosis of idiopathic pulmonary hemosiderosis. A lung biopsy specimen from the first patient showed alveolar-capillary basement membrane abnormalities, together with abnormalities of capillary endothelial cells and hemosiderin-laden macrophages. A lung biopsy specimen from the second patient showed mainly capillary endothelial abnnormalities and interestitial fibrosis. Both patients had a noticeable improvement in symptoms and relative stabilization of their roentgenographic and pulmonary function abnormalities following azathioprine therapy.
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ranking = 477.3639002657
keywords = macrophage
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