Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have encountered five hemodialysis patients who had received enteral nutrition and recovered from erythropoietin-resistant anemia with neutropenia after the correction of copper deficiency. We reduced the required doses of recombinant human erythropoietin (rHuEPO) to maintain the target hematocrit levels and three patients were finally weaned from the rHuEPO therapy. Thus, copper deficiency is involved in erythropoietin-resistant anemia in hemodialysis patients.
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PMID:Correction of copper deficiency improves erythropoietin unresponsiveness in hemodialysis patients with anemia. 1659 92

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

The hematologic manifestations of copper deficiency are well known and include anemia and neutropenia. In the past few years, the neurological manifestations of acquired copper deficiency in humans has been recognized, the most common being a myelopathy presenting with a spastic gait and prominent sensory ataxia. The known causes of acquired copper deficiency include prior gastric surgery, excessive zinc ingestion, and malabsorption; however, often the cause is unclear. Hyperzincemia may be present even in the absence of exogenous zinc ingestion. The clinical features and neuroimaging findings are similar to the subacute combined degeneration seen in patients with vitamin B12 deficiency. Copper and vitamin B12 deficiency may coexist. The neurological syndrome may be present without the hematologic manifestations. Copper supplementation resolves the anemia and neutropenia promptly and completely and may prevent the neurological deterioration. Improvement, when it occurs, is often subjective and preferentially involves sensory symptoms. This article describes patients with copper deficiency myelopathy seen at the Mayo Clinic in Rochester, Minn, and reviews the literature on neurological manifestations of acquired copper deficiency in humans.
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PMID:Copper deficiency myelopathy (human swayback). 1703 63

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

A 48-year-old man was referred to our hospital in December, 2005 because of general fatigue, gait disturbance and bradycardia. He had a history of polysurgery due to recurrent ileus and had been treated with home total parenteral nutrition for the short-bowel syndrome since 2003. Clinical findings on admission included marked emaciation and severe weakness of the extremities. Pancytopenia was noted in the peripheral blood. The serum levels of copper and ceruloplasmin were 3 microg/dl and 3 mg/dl, respectively, while Vit. B12 and folate were within the normal range. The bone marrow demonstrated cytoplasmic vacuolation in the myeloid and megakaryocytic series, and sideroblastic changes. No evidence of hematologic malignancies was presented. The diagnosis was copper deficiency and the patient was treated with copper supplementation. Four weeks after copper therapy, the serum level of copper rose to 50 microg/dl and ceruloplasmin to 14 mg/dl. Significant improvements in the hematologic profile, ECG findings and weakness of extremities were noted. Although bicytopenia (anemia and neutropenia) is considered to be a feature of hematologic disorders caused by copper deficiency, the present case showed pancytopenia. The exact mechanism of the unusual association of thrombocytopenia and other abnormalities with copper deficiency remains to be elucidated.
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PMID:[Copper deficiency with pancytopenia, bradycardia and neurologic symptoms]. 1744 78

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

Tetrathiomolybdate (TTM) is a copper chelator that has also demonstrated antiangiogenic, antifibrogenic and anti-inflammatory actions in preclinical studies. The drug, from the University of Michigan was licensed to Pipex Pharmaceuticals Inc for development for several indications; development of the drug for cancer was later licensed to Attenuon LLC. In a phase III clinical trial, TTM stabilized neurological function in patients with Wilson disease, causing significant recovery in 81% of patients at 3 years post initiation of therapy; a second phase III trial was ongoing at the time of publication. A phase I/II clinical trial demonstrated the efficacy of TTM in patients with idiopathic pulmonary fibrosis, and led the FDA to grant TTM Orphan Drug status for this disease. Several phase II clinical trials had also been completed in patients with various cancers, and revealed mixed efficacy. TTM was also assessed in a phase I clinical trial for age-related macular degeneration, but the results reported from the trial were negative; no further development has occurred for this indication. TTM was assessed for the treatment of psoriasis in a phase II clinical trial, but no data have been reported. At the time of publication, phase II and phase III clinical trials were ongoing in patients with Alzheimer's disease and primary biliary cirrhosis, respectively. The most common clinical side effects observed for TTM over the range of indications have been anemia, neutropenia, leukopenia and transaminase elevations. These side effects were generally resolved with either a dose adjustment or temporary suspension of the dosing regimen. TTM is predicted to most likely find a niche in the therapy of Wilson disease, for which current treatment options are limited.
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PMID:Tetrathiomolybdate, a copper chelator for the treatment of Wilson disease, pulmonary fibrosis and other indications. 1868 94


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