Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases of Blackfan-Diamond hypoplastic anemia are reported. Five were initiated within six months of life. All cases showed intense anemia, severe reticulopenia and hypersideremia. Two of them had associated malformations. Treatment was established with Dexametasone at high doses, followed by a maintenance treatment at lower doses. A partial response was obtained in all cases. Treatment with deforroxiamine was used in order to paliate hemosiderosis. Two cases developped microangiopathic hemolitic anemia; relations with primary disease could not be determined.
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PMID:[Long term evolution in Blackfan-Diamond hypoplastic anemia (author's transl)]. 98

Acute and chronic forms of disease can be distinguished in Trypanosoma vivax infection in the goat. The main difference between the acute and chronic form seems to be the presence of microthrombi in the acute stage of infection; these consist of platelets, trypanosomes, monocytoid cells and some fibrin. This thrombus formation seems directly related to the high parasitaemia in acute trypanosomiasis and may result in ischaemia which could also explain the haemorrhages, the oedema of the lungs and other tissues, and the necrotic changes found in several organs. The anaemia, associated with erythrophagocytosis, haemosiderosis, extramedullary haemopoiesis and hyperactivity of the bone marrow, seemed to be of haemolytic origin. The factors leading to emaciation seemed to be degenerative atrophy of muscular tissue and loss of protein in the urine caused by a possible immune complex glomerulonephritis.
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PMID:The pathology and pathogenesis of Trypanosoma vivax infection in the goat. 102 33

Six black infants and young children with high titers of milk precipitins were identified by screening the sera of 160 children with idiopathic chronic lung disease. None of the six had immunoglobulin deficiency, elevation of sweat chlorides, SS hemoglobin, or recurrent aspiration. All six children had typical manifestations of milk-induced pulmonary hemosiderosis: recurrent pulmonary infiltrates (6/6), hemosiderin-laden pulmonary macrophages (5/6), intermittent wheezing (5/6), eosinophilia (4/6), anemia (4/6), iron deficiency (4/4), failure to thrive (4/6), and elevated levels of serum IgE (4/4). Three children also had chronic rhinitis and eventually developed large adenoids, hypercapnia and acidosis during sleep, and right heart failure. Elimination of cow milk from the diet, symptomatic therapy, and adenoidectomy when indicated resulted in improvement of all six patients. Pulmonary hemosiderosis and some cases of upper airway obstruction with pulmonary hypertension appear to be two stages, early and delayed, of the same immunophysiologic process. Early dietary intervention may prevent the cardiovascular complications of this process.
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PMID:Hyperreactivity to cow milk in young children with pulmonary hemosiderosis and cor pulmonale secondary to nasopharyngeal obstruction. 117 19

Ten infants and children suffering from Thalassaemia major, proven by clinical, hematological and biochemical criteria, were subjected to intestinal biopsy. Specimens were studied for histological and histochemical patterns. The histological picture showed shortening and fusion of villi with cellular infiltration. Reduced mucopolysaccharides and relatively normal alkaline phosphatase activity were demonstrated. The degree of histological and histochemical changes correlates with the degree of anemia. The effects of these changes on the iron absorption and the tissue hemosiderosis are aroused. The possibility of these changes, being non-specific and secondary to anemia and tissue hypoxia is also postulated.
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PMID:Intestinal mucosal changes in thalassaemia major. 123 Mar 51

Heinz body anemia was induced in dogs by consecutive oral administration of 200 mg/kg and 60 mg/kg of aminopyrine, 200 mg/kg of phenacetin and 5 mg/kg of acetylphenylhydrazine, for either 8 or 16 weeks. Biochemical analysis showed a decrease of haptoglobin in plasma and reduced-glutathion in red blood cells in association with anemia. Hematologically, an increase in osmotic fragility and cell volume of erythrocytes were also noted. Pathological examination revealed marked erythrophagia and hemosiderosis in the reticuloendothelial system of treated animals. A new anti-inflammatory analgesic 31252-S (3-(1-hydroxy-2-piperidinoethyl)-5-phenylisoxazole citrate) was also tested for the hemolytic effects in dogs. Blood analyses revealed a slight increase of Heinz bodies and a decrease of reduced-glutathion in red blood cells without anemia. These findings suggest that 31252-S have weaker oxidant properties than those of aminopyrine and phenacetin. The present studies showed that the concentration of reduced-glutathion in red blood cells of non-treated dogs was approximately 50% lower than that of the erythrocytes of normal human beings. This finding appeared to correspond with high susceptibility of red blood cells to hemolytic effects of oxidant-drugs in dogs.
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PMID:[Oxidant-drug induced hemolytic anemia in dogs]. 124 68

Patients with hereditary hemolytic anaemias have been known to have immunoglobulin alterations related to an increased susceptibility to infection. In the present series, immunoglobulins, G, A and M have been estimated in 50 thalassemic children aged 10 months to 13 years. No significant difference was found in any of the immunoglobulins between patients and age-matched controls. No correlation could be shown between immunoglobulin levels and (a) the severity of anaemia, (b) the degree of hemosiderosis, and (c) the frequency of febrile infections per year. Against clinical impressions patients did not shown any increased susceptibility to infections.
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PMID:Immunoglobulin levels in children with homozygous beta-thalassemia. 125 21

In haematological diseases, insufficient data has been accumulated to evaluate the efficacy of immunosuppressive drug treatment in patients with erythroid aplasia or sideroblastic anaemia. Cyclophosphamide may be efficacious in inhibiting circulating anticoagulants in patients who need continued replacement of clotting factors. Azathioprine, 6-mercaptopurine, cyclophosphamide and vincristine have been used successfully in treating patients with idiopathic thrombocytopenic purpura, and some patients with auto-immune haemolytic anaemia may benefit from the addition of purine analogues. However, the use of immunosuppressive therapy seems to accelerate the presence of haematological malignancies in patients with macroglobulinaemia. In gastro-intestinal diseases, uncontrolled studies have shown nitrogen mustard, 6-mercaptopurine and azathioprine to be of modest benefit to patients with ulcerative colitis and Crohn's disease. In a controlled trial azathioprine plus prednisone proved more effective than prednisone alone in sustaining remission in patients with Crohn's disease. In patients with either chronic active hepatitis or primary biliary cirrhosis, however, there seems to be no benefit from immunosuppressive therapy for primary treatment of these diseases. Cyclophosphamide, azathioprine and methotrexate have all been used with some success in treating patient with uveitis, and in a controlled trial cytarabine has been shown to be beneficial to patients with herpes ophthalmicus. However, no benefit has been shown to patients with the eye changes of Graves' disease with either azathioprine or methotrexate. Patients with Paget's disease appear to be helped by mithramycin. Cyclophosphamide, chlorambucil and azathioprine are ineffective in treating patients with multiple sclerosis. 6-Mercaptopurine, azathioprine, methotrexate and cyclophosphamide have all produced some benefit in patients with myasthenia gravis, and some patients with idiopathic pulmonary haemosiderosis have responded to azathioprine, 6-mercaptopurine and cyclophosphamide. Alkylating agents have proved useful in treating some patients with asthma and in treating frequent relapsers among children with the nephrotic syndrome. In adults with membrano-proliferative glomerulonephritis some patients have responded to combination therapy with cyclophosphamide, azathioprine and corticosteroids. Immunosuppressive therapy is also indicated in prolonging graft survivals in patients receiving organ transplants. Drug toxicities of immunosuppressive agents are discussed. Their long-term effects, including mutagenic potential, have as yet not been fully elucidated.
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PMID:Clinical use of immunosuppressive drugs: part II. 127 59

Pulmonary hemosiderosis (PH), a rare pathology, usually occurring during infancy and childhood, is characterized by numerous and repeated intra-alveolar bleedings, interstitial iron build-up with consequent progressive fibrosis and severe anemia. PH can be basically divided into 3 different categories: Primitive or idiopathic, involving a primitive deficit of antioxidizing enzymes in the erythrocytes in genetically predisposed subjects; Secondary, subsequent to chronic pneumopathy or cardiopathy; Associated with various pathologies including collagenopathies, glomerulonephritis, myocardiopathies, diabetes, steatorrhea, tireotossicosis. A particular type of Pulmonary Hemosiderosis, associated with allergy to cow's milk, has been described for the first time by Heiner. We present in this paper our personal experience of a young patient suffering from pulmonary hemosiderosis induced by cow's milk protein.
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PMID:[Pulmonary hemosiderosis induced by cow's milk proteins: a discussion of a clinical case]. 150 57

The author submits the history and classification criteria of congenital dyserythropoietic anaemia and presents at the same time an observation of one of his female patients who was originally dispensarized as hereditary spherocytosis. Failure of splenectomy led to revision of the finding in bone marrow and a change of diagnosis to congenital dyserythropoietic anaemia type II. The patient died at the age of 27 years from hepatic failure as a result of haemosiderosis.
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PMID:[Congenital dyserythropoietic anemia]. 202 Oct 78

Itai-itai disease is thought to be the result of chronic cadmium (Cd) intoxication. We examined 23 autopsy cases of itai-itai disease and 18 cases of sudden death as controls. Urine and blood samples from 10 patients were collected before they died and revealed the presence of severe anemia and renal tubular injuries. Undecalcified sections of iliac bone were stained with Aluminon reagent, and ammonium salt of aurintricarboxylic acid, and Prussian blue reagent in all cases of itai-itai disease. These two reagents reacted at the same mineralization fronts. X-ray microanalysis revealed the presence of iron at mineralization fronts in itai-itai disease. Five patients showed evidence of hemosiderosis in the liver, spleen, and pancreas, probably as a result of post transfusion iron overload. Renal calculi and calcified aortic walls were also stained with Prussian blue reagent in several patients. Neither ferritin nor transferrin were visualized at mineralization fronts in itai-itai disease by immunohistochemical staining. These results suggest that iron is bound to calcium or to calcium phosphate by a physicochemical reaction. A marked osteomalacia was observed in 10 cases of itai-itai disease by histomorphometry. Regression analyses of data from cases of itai-itai disease suggested that an Aluminon-positive metal inhibited mineralization and that renal tubules were injured. Since bone Cd levels were increased in itai-itai disease, it is likely that renal tubules were injured by exposure to Cd. Therefore, stainable bone iron is another possible aggravating factor for osteopathy in itai-itai disease, and a synergistic effect between iron and Cd on mineralization is proposed.
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PMID:Iron as a possible aggravating factor for osteopathy in itai-itai disease, a disease associated with chronic cadmium intoxication. 203 51


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