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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following extensive bowel resection, a young woman experienced severe malnutrition; subsequent administration of parenteral nutrition precipitated the copper deficiency syndrome. This consisted of hypocupremia, subnormal ceruloplasmin levels, anemia, and severe neutropenia. The bone marrow was megaloblastic, vacuolated, and sideroblastic; granulocytic maturation was not observed beyond the myelocyte stage. Copper sulfate therapy was followed by a marked reticulocytosis, increase in hematocrit, and recovery of neutrophils. Additional studies indicated that both serum and urinary erythropoietin values were low; serum activity increased after copper supplementation. Abnormal granulopoiesis was demonstrated using the in vitro granulocyte colony assay. The patient's granulcoytic stem cells were normal on two occasions; however, mixing studies showed that culture of the patient's copper-deficient marrow with her copper-deficient serum yielded significantly reduced numbers of granulocyte colonies. Thus, copper appears to be a necessary element for normal hematopoiesis; lack of this trace element may result in ineffective erythropoiesis and granulopoiesis.
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PMID:Observations on the anemia and neutropenia of human copper deficiency. 30 69

Hypocupremia occurred in an adult with sickle cell anemia who received zinc as an antisickling agent for two years. The hypocupremia was associated with microcytosis and relative neutropenia. Administration of copper resulted in an increase in RBC size and leukocyte counts. We have since observed hypoceruloplasminemia of varying degrees in several other sickle cell anemia patients who were receiving oral zinc therapy. This complication was easily corrected by copper supplementation.
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PMID:Hypocupremia induced by zinc therapy in adults. 35 44

Copper deficiency is reported in an infant of very low birthweight. It was characterised by extensive bone changes, severe neutropenia, and hypocupraemia. These manifestations could have been missed but for an intercurrent pneumonia which led to an x-ray of the chest.
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PMID:Copper deficiency in a low birthweight infant. 48

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

Anemia and neutropenia developed in a man who took pharmacologic doses of supplemental zinc. Laboratory investigation showed high zinc level, hypocupremia, low ceruloplasmin level, and ringed sideroblasts. All resolved after withdrawal of zinc. Self-administered zinc appears to have caused severe copper deficiency, with secondary anemia and neutropenia. Physicians should be aware of this deleterious and completely reversible effect of megadose mineral therapy. Zinc ingestion or exposure should be considered in the differential diagnosis of unexplained anemia, leukopenia, or sideroblastic anemia.
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PMID:Copper deficiency and sideroblastic anemia associated with zinc ingestion. 340 36

Copper uptake during three hours from an oral test dose of copper sulphate solution giving three mg Cu++, close to the recommended daily dietary intake, was significantly reduced in patients with proximal intestinal disease, compared with normal subjects. Three out of ten patients had abnormal and otherwise unexplained blood counts compatible with the known haematological effects of copper deficiency and were restored to normal levels on a gluten-free diet. Copper deficiency and proximal intestinal disease should be suspected in patients with otherwise unexplained anaemia, especially neutropenia.
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PMID:Copper malabsorption in coeliac disease. 401 87

Celiac disease was diagnosed in two unrelated infants aged 7 and 7.5 months with severe malnutrition. They showed typical clinical, biological, and histological signs of the disease. Moreover, accompanying copper deficiency was suggested by severe hypocupremia and persistent neutropenia; bone radiographs were also compatible with this diagnosis. Rapid and complete correction of these anomalies could only be obtained after addition of oral copper sulfate to the gluten-free diet. Mechanisms possibly involved in the development of copper deficiency in young infants with celiac disease are: chronic malabsorption; high copper needs in rapidly growing infants; and possibly increased biliary and digestive losses. It is therefore suggested that young children with severe celiac disease should be monitored for their copper status.
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PMID:Copper deficiency in infants with active celiac disease. 403 83

Copper deficiency anemia occurs in some specific situations if supplemental copper is not given: low birth-weight premature infants fed milk only, protracted total parenteral nutrition, chronic diarrhea with severe malnutrition. Severe neutropenia precedes the onset of sideroblastic anemia. Iron therapy is ineffective. Diagnosis is established by the low serum copper concentrations, the delayed osseous anomalies, and the dramatic response to copper therapy. Low serum vitamin E concentrations may be found in low birth-weight premature infants aged six to ten weeks with hemolytic anemia. In such cases, vitamin E therapy is effective. This condition occurs more often in infants fed milk formulas without supplemental copper and in infants given high doses of iron. Whether vitamin E deficiency causes anemia is still an open question. Preventive vitamin E supplementation is only partly effective.
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PMID:[Rare nutritional deficiency anemia: deficiency of copper and vitamin E]. 630 91

Trace metal deficiencies are now a well-documented complication of total parenteral nutrition (TPN). Zinc deficiency may present in a variety of ways including acrodermatitis skin lesions, impaired immunity, poor growth or impaired wound healing, and mental disturbances. Copper deficiency presents a more uniform picture of hematologic abnormalities, usually anemia with leukopenia and neutropenia. Chromium and selenium deficiencies occur much less frequently, but well-documented cases have been reported. We currently recommended regular monitoring and supplementation of these four trace metals during TPN administration. This article describes the clinical abnormalities that may develop when deficiencies of trace metals occur during TPN administration, and we present recommendations for trace metal supplementation during TPN administration.
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PMID:Trace metal abnormalities in adults during hyperalimentation. 679 17

Copper deficiency has been described in premature infants on hyperalimentation. The bony abnormalities are generalized and are usually associated with anemia and neutropenia. These changes present with normal serum levels of iron, ascorbic acid, calcium, phosphorus, and magnesium, as well as with depressed levels of copper and ceruloplasmin. They appear at about three to nine months of age in infants with a low birth weight who are receiving total parenteral nutrition, but can be prevented by greater than normal maintenance levels of copper supplements. Established bone changes improve rapidly after the administration of therapeutic supplements.
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PMID:Skeletal changes associated with copper deficiency. 680 88


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