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

Copper (Cu) deficiency has been reported both in pediatric and adult patients on total parenteral nutrition (TPN). Manifestations of Cu deficiency are usually hematologic in the adult. A 56-yr-old patient with a history of subtotal gastrectomy underwent massive small bowel resection and partial colectomy in 1977. TPN was initiated. Intravenous (iv) trace mineral supplements were not available in 1977 at our institution. By June 1978, the patient manifested neutropenia with a white blood cell (WBC) count of 2000/mm3 and 39% neutrophils or a total neutrophil count (TNC) of 780/mm3. The serum Cu level at that time was 5 micrograms/dl (normal, 70-140), and the serum zinc (Zn) level was low, although within normal limits. Oral supplementation with Cu and Zn tablets proved ineffective. Twice weekly infusions of fresh frozen plasma were begun in April 1979, and intravenous chromium supplementation started in September 1979, but neither the WBC count nor the TNC improved. Intravenous Cu and Zn were approved in October 1979, and were added to the TPN formula. Within 2 weeks, the WBC count rose to 6300/mm3, and the neutrophils increased to 83% with a TNC of 5229. After 12 weeks, the serum Cu level rose to 80 micrograms/dl. The increase in WBC count and percentage of neutrophils can be attributed to the addition of Cu to the TPN infusate.
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PMID:Neutropenia due to copper deficiency in total parenteral nutrition. 309 12

Serum concentrations of copper and ceruloplasmin were measured in 24 very low birthweight babies. They were high in those weighing less than 1000 g, and critically ill or receiving intravenous nutrition, and normal in those with bone disease, neutropenia, or oedema. Care is needed to maintain adequate concentrations without toxicity.
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PMID:Copper and very low birthweight babies. 312 16

Shwachman's syndrome is, after cystic fibrosis, the most common cause of exocrine pancreatic insufficiency in childhood. The cause of the disorder is not known but we were struck by the fact that the histological appearances of pancreatic atrophy in this condition resemble those seen in experimental copper deficiency, in which the pancreatic acinar damage persists long after the copper deficiency is relieved. Other features of Shwachman's syndrome include neutropenia, anaemia and abnormalities of the ribs and of the metaphyses of long bones. All these findings have also been reported in children with copper deficiency during the 1st year of life. We suggest that some or all cases of Shwachman's syndrome are caused by a period of copper deficiency in early infancy.
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PMID:Hypothesis: Shwachman's syndrome of exocrine pancreatic insufficiency may be caused by neonatal copper deficiency. 319 Jan 62

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

Very few cases of acquired severe copper deficiency have been described. The principal effects are haematological, but the precise abnormalities are uncertain due to the possible association of other deficiencies. A case of isolated severe copper deficiency associated with late onset hypogammaglobulinaemia is reported in which the chief findings were macrocytic anaemia, neutropenia and a decrease in mean platelet volume. All these abnormalities resolved when copper therapy was instituted and recurred when the medication was stopped.
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PMID:Macrocytic anaemia due to copper deficiency in a patient with late onset hypogammaglobulinaemia. 367 Dec 60

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

Four preterm infants of very low birthweight (less than 1500 g) developed signs of copper deficiency between age 8 and 10 weeks. All had required prolonged ventilatory support, parenteral nutrition, and nasojejunal feeding. The clinical features, which included osteoporosis, oedema, anaemia, neutropenia, and late apnoea improved when the oral copper intake was increased. Diagnosis was made more difficult because a suitable reference range for plasma copper was not available. Serial measurements of plasma copper in 39 preterm infants who had no important medical problems were used to produce a reference range for plasma copper from 30 weeks' gestation to term plus seven weeks. This information will aid recognition of hypocupraemia in the very low birthweight infant who is particularly at risk of copper deficiency.
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PMID:Copper deficiency in the preterm infant of very low birthweight. Four cases and a reference range for plasma copper. 402 60

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


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