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

The use of megadoses of vitamin and mineral supplements has become common. The authors describe a 17-year-old boy who presented with fatigue after taking large daily doses of zinc supplements for 6 to 7 months in an attempt to treat his acne. A zinc-induced hypocupremia developed, causing anemia, leukopenia, and neutropenia. Anemia and neutropenia resolved 6 months after he stopped taking the zinc. Excessive zinc intake can have toxic effects, and questions about patients' use of vitamin and mineral supplements should be asked when medication histories are taken.
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PMID:Excessive oral zinc supplementation. 1236 2

Copper deficiency is a rare cause of sideroblastic anemia and neutropenia that often is not suspected clinically. The morphologic findings in bone marrow, while not pathognomonic, are sufficiently characteristic to suggest the diagnosis, leading to further testing to establish the correct diagnosis. Excess zinc ingestion is among the causes of copper deficiency. We present 3 cases of zinc-induced copper deficiency in which the diagnosis first was suggested on the basis of bone marrow examination. The first patient was a 47-year-old man with a debilitating peripheral neuropathy that had progressed during the previous 18 months, mild anemia, and severe neutropenia. The second was a 21-year-old man receiving zinc supplementation for acrodermatitis enteropathica in whom moderate normocytic anemia and neutropenia developed. The third patient was a 42-year-old man with anemia, severe neutropenia, and a peripheral neuropathy that had progressed during 8 months. The bone marrow findings in all cases suggested copper deficiency, which was confirmed by further laboratory testing and determined to be due to zinc excess. The morphologic features, clinical manifestations, differential diagnosis, and pathogenetic mechanisms are discussed.
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PMID:Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination. 1576 88

Copper deficiency is rarely reported as a cause of neutropenia and anemia through mechanisms not clearly understood. Most cases have been found in malnourished infants or persons receiving total parenteral nutrition without adequate copper. We report on two otherwise healthy young adults with severe neutropenia and anemia secondary to copper deficiency of unclear etiology, which quickly resolved after supplementation with copper gluconate. Both women consumed excessive quantities of soft drinks, which may have contributed to the development of their copper deficiency. Two cases of an unexplained copper deficiency anemia and neutropenia in otherwise healthy young adults found at a single institution over a short period of time suggests that this problem may be more widespread than is currently realized.
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PMID:Anemia and neutropenia associated with copper deficiency of unclear etiology. 1732 5

Copper deficiency is a rare complication of enteral nutrition. Haematologic abnormalities such as neutropenia and anaemia, but not pancytopenia, have been described associated to copper deficiency. We report the case of a patient requiring long term enteral nutrition through jejunostomy who developed copper deficiency and pancytopenia. In 1991, a 47-year-old woman was admitted with severe gastroesophageal mucositis after an attempted suicide with caustic intake. Enteral nutrition with a commercial, polymeric, fiber-containing formula was started. Twenty-eight months later, the patient developed anemia and neutropenia that did not respond to combined iron and parenteral vitamin B(12) supplementation. In 1996 the patient showed pancytopenia and low serum levels of copper and ceruloplasmin. Pancytopenia improved after copper supplementation. Possible mechanism causing copper deficiency and pancytopenia are discussed. We conclude that assessment of copper status is advisable in patients receiving long-term enteral nutrition by jejunostomy.
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PMID:Copper deficiency with pancytopenia due to enteral nutrition through jejunostomy. 1684 85

Copper deficiency is a recognized but often overlooked cause of anemia and neutropenia. We began checking serum copper levels on patients referred for evaluation for unexplained anemia and neutropenia or myelodysplasia. Eight patients were identified as copper deficient (serum copper less than 70 microg/dL). The anemia was normochromic and normocytic in seven patients. Neutropenia was present in seven patients. Seven patients had been referred for evaluation of myelodysplasia. Three were seen for consideration for allogenic stem cell transplant. Five patients had concomitant peripheral neurological symptoms. Seven patients were treated with oral copper gluconate. All treated patients demonstrated a hematological response; seven had a complete remission. The improvement in anemia and neutropenia was rapid with normalization of blood counts within three to four weeks. In one patient, normalization of the underlying marrow dysplasia was demonstrated by bone marrow histology eight months after copper replacement. The cause of copper deficiency was felt to be gastrointestinal malabsorption in five of our patients. We conclude that copper deficiency should be considered in all patients with unexplained anemia and neutropenia or myelodysplasia.
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PMID:Copper deficiency causes reversible myelodysplasia. 1772 2

Copper deficiency is an etiology of anemia, neutropenia, and bone marrow dysplasia that may be under-recognized. We report 5 patients with clinical presentation consistent with MDS who were found to be deficient in copper and whose hematologic abnormalities resolved with copper supplementation. We recommend copper level assessment in patients suspected of having low-risk MDS, especially those with gastrointestinal disorders and neuropathy.
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PMID:Copper deficiency: an important consideration in the differential diagnosis of myelodysplastic syndrome. 1802 79

Copper deficiency is an established cause of hematological abnormalities but is frequently misdiagnosed. Copper deficiency can present as a combination of hematological and neurological abnormalities and it may masquerade as a myelodysplastic syndrome. We reviewed the records of patients with hypocupremia and hematologic abnormalities identified between 1970 and 2005. Patients with hypocupremia unrelated to copper deficiency (e.g. Wilson's disease) were excluded. Forty patients with copper deficiency and hematological abnormalities were identified. Ten patients (25%) had undergone bariatric (weight reduction) surgery and an additional 14 patients (35%) had undergone surgery on the gastrointestinal tract, most commonly gastric resection. In 12 cases, no cause for copper deficiency was identified. Anemia and neutropenia were the most common hematologic abnormalities identified and the majority of the patients also had neurologic findings, most commonly due to myeloneuropathy. Abnormalities observed on bone marrow examination including vacuoles in myeloid precursors, iron-containing plasma cells, a decrease in granulocyte precursors and ring sideroblasts may be valuable clues to the diagnosis. Copper deficiency is an uncommon but very treatable cause of hematologic abnormalities.
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PMID:Hematological manifestations of copper deficiency: a retrospective review. 1828 30

We present a case of pancytopenia in a 9-month-old infant with total parenteral nutrition (TPN) dependence due to short bowel syndrome. Bone marrow examination revealed left-shifted myeloid maturation, erythroid and myeloid dysplasia with normal iron stores. Serum copper level was 2 microm/dl (normal range 90-190 mcg/dl). After supplementation, copper levels normalized at 143 mcg/dl, and the macrocytic anemia, neutropenia, and thrombocytopenia resolved. Copper deficiency should be considered in the differential diagnosis of cytopenias and myelodsyplasia, particularly in the growing number of pediatric patients with TPN dependency or malabsorption.
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PMID:Pancytopenia with myelodysplasia due to copper deficiency. 1862 12

Copper is an essential cofactor in many enzymatic reactions vital to the normal function of the hematologic, vascular, skeletal, antioxidant, and neurologic systems. Copper deficiency in the United States is believed to be relatively rare but has been described in the setting of zinc supplementation, myelodysplastic syndrome, use of parenteral nutrition and chronic tube feeding, and in various malabsorptive syndromes, including following gastrectomy and gastric bypass surgery. Features of copper deficiency include hematologic abnormalities (anemia, neutropenia, and leukopenia) and myeloneuropathy; the latter is a rarer and often unrecognized complication of copper deficiency. We here describe two patients who presented with severe gait abnormalities and anemia combined with neutropenia several years after roux-en-Y gastric bypass (RYGB) surgery for obesity who were found to be severely copper deficient. Intravenous copper repletion resulted in the rapid correction of hematologic indices; combined intravenous and oral copper supplementation and eventual oral copper supplements alone normalized serum copper levels in each patient, but resulted in only partial resolution of the neurologic deficits. This report serves to alert physicians of the association between RYGB procedures and subsequent copper deficiency in order to avoid diagnostic delays and to improve treatment outcomes.
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PMID:Acquired copper deficiency: a potentially serious and preventable complication following gastric bypass surgery. 1985 58

Copper deficiency is likely an underrecognized cause of anemia and neutropenia and may masquerade as a myelodysplastic syndrome (MDS). We report 2 cases of copper deficiency in which the diagnosis was suggested based on the characteristic morphologic findings, such as cytoplasmic vacuolization of erythroid and myeloid precursors and iron-containing plasma cells. It is interesting that both patients had hematogone hyperplasia. This phenomenon, largely absent in MDS, may aid in distinguishing nonclonal causes of cytopenias, such as copper deficiency, from MDS. It is of crucial importance to identify treatable causes of cytopenias when MDS is suspected. We recommend copper level assessment in patients suspected of having low-grade MDS, especially patients with neuropathy and normal results of cytogenetic studies.
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PMID:Hematogone hyperplasia in copper deficiency. 1960 13


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