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)

A 33 year-old man with undiagnosed neuropathy showing mental retardation and involuntary movements has been nourished for a long period by total parenteral nutrition (TPN) because of frequent vomiting and repeated aspiration pneumonitis. After ten months' TPN, macrocytic anemia and neutropenia developed and iron preparation was administered without hematological improvement. Bone marrow examination revealed normocellular marrow without features of megaloblastosis and dysplasia. In some erythroblasts and immature myeloid cells, vacuoles were observed and mature granulocytes were reduced in the bone marrow. Both serum copper and ceruloplasmin were very low (12 micrograms/dl and 7mg/dl, respectively). Thus, oral administration of copper sulfate resulted in marked increase of reticulocytes and subsequent improvement of anemia and neutropenia within two months. Copper deficiency is a rare condition, but during an unusual nutrition such as TNP, hematological abnormality due to copper deficiency must be noticed to occur.
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PMID:[Anemia and neutropenia due to copper deficiency during long-term total parenteral nutrition]. 849 15

Deficiency symptoms of trace elements developed in patients receiving long-term total parenteral nutrition (TPN) are as follows. [Zinc deficiency]: moist eczematoid dermatitis and alopetia are occurred in patients receiving TPN which not containing zinc. Plasma zinc level was very low. The response to intravenous zinc therapy is striking. [Copper deficiency]: anemie and neutropenia caused in patients receiving TPN which not containing copper. These abnormalities disappeared after copper therapy. [Manganese deficiency]: bone changes which thought to be due to manganese deficiency was observed in patient receiving TPN. [Selenium deficiency]: dilated cardiomyopathy resembles to Keshan disease was occurred in patients receiving TPN for long term. [Chromium deficiency]: TPN induced chromium deficiency developed characterized by peripheral neuropathy and glucose intolerance. [Molybudenum deficiency]: Amino acid intolerance due to molybudenum deficiency is occurred in patients receiving TPN. Requirement of trace elements for human adults from TPN estimated as follows. zinc: 3-4 mg/day, copper: 0.02-0.05 mg/day, iron: 1-2 mg/day, manganese: 0.15-0.80 mg/day, selenium: 0.02-0.05 mg/day, chromium: 0.01-0.015 mg/day, molybudenum: 0.075-0.250 mg/day and iodine: 0.070-0.140 mg/day.
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PMID:[Trace elements in long-term total parenteral nutrition]. 858 86

Six antineutrophil antibody (ANA)-positive patients with copper deficiency were classified into two groups; those with (group A, n = 3) and those without (group B, n = 3) neutropenia. The percent binding of ANA for normal peripheral neutrophils was similar in both groups (83.5 +/- 7.2 vs. 79.1 +/- 10.5%). The percent binding of sera to cultured promyelocytic leukemia cells (HL-60) was increased in group A (from 3.7 +/- 3.2 to 12.2 +/- 2.3%) but not in group B (from 65.3 +/- 21.7 to 40.7 +/- 6.3%) after stimulation of HL-60 with DMSO. The stimulated HL-60 cells expressed CD 16 and CD 11b antigens. In the presence of monoclonal antibody for CD 16, the titer of ANA was nil in group A and unchanged in group B. Thus, ANA of patients with neutropenia may recognize mainly the CD 16 antigen, the Fc gamma receptor III of neutrophils.
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PMID:Characterization of antineutrophil antibodies in patients with neutropenia associated with nutritional copper deficiency. 861 Apr 76

Animal and human studies have shown that copper is involved in the function of several enzymes. Studies have also shown that copper is required for infant growth, host defense mechanisms, bone strength, red and white cell maturation, iron transport, cholesterol and glucose metabolism, myocardial contractility, and brain development. Copper deficiency can result in the expression of an inherited defect such as Menkes syndrome or in an acquired condition. Acquired deficiency is mainly a pathology of infants; however, it has been diagnosed also in children and adults. Most cases of copper deficiency have been described in malnourished children. The most constant clinical manifestations of acquired copper deficiency are anemia, neutropenia, and bone abnormalities. Other, less frequent manifestations are hypopigmentation of the hair, hypotonia, impaired growth, increased incidence of infections, alterations of phagocytic capacity of the neutrophils, abnormalities of cholesterol and glucose metabolism, and cardiovascular alterations. Measurements of serum copper and ceruloplasmin concentrations are currently used to evaluate copper status. These indexes are diminished in severe to moderate copper deficiency; however, they are less sensitive to marginal copper deficiency. Erythrocyte superoxide dismutase and platelet cytochrome c activities may be more promising indexes for evaluating marginal copper deficiency.
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PMID:Copper as an essential nutrient. 861 66

The biochemical basis for the essentiality of copper, the adequacy of the dietary copper supply, factors that condition deficiency, and the special conditions of copper nutriture in early infancy are reviewed. New biochemical and crystallographic evidence define copper as being necessary for structural and catalytic properties of cuproenzymes. Mechanisms responsible for the control of cuproprotein gene expression are not known in mammals; however, studies using yeast as a eukaryote model support the existence of a copper-dependent gene regulatory element. Diets in Western countries provide copper below or in the low range of the estimated safe and adequate daily dietary intake. Copper deficiency is usually the consequence of decreased copper stores at birth, inadequate dietary copper intake, poor absorption, elevated requirements induced by rapid growth, or increased copper losses. The most frequent clinical manifestations of copper deficiency are anemia, neutropenia, and bone abnormalities. Recommendations for dietary copper intake and total copper exposure, including that from potable water, should consider that copper is an essential nutrient with potential toxicity if the load exceeds tolerance. A range of safe intakes should be defined for the general population, including a lower safe intake and an upper safe intake, to prevent deficiency as well as toxicity for most of the population.
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PMID:Essentiality of copper in humans. 958 35

The objective of this study was to examine the role of copper in neutrophil development and function. Mice were made copper deficient by feeding dams a diet containing 1.05 microg copper starting at parturition. Control mice were fed the same diet containing 6 microg copper. The pups were weaned to the diet and killed when they were 5-6 wk old. Peripheral blood cell counts, margination and cell maturity were measured. The response to an intraperitoneal injection of lipopolysaccharide (LPS) was also determined. Copper deficiency resulted in twice as many neutrophils and fewer than half the number of lymphocytes. Half as many cells in copper-deficient mice expressed Ly-6G, a granulocytic marker of cell maturity. In addition, copper-deficient cells expressed only half the amount of Ly-6G per cell than was expressed by copper-adequate cells. This suggested that the cells were younger, or arrested in their maturation as a result of copper deficiency. An arrest of maturation has been proposed as the cause of neutropenia in human copper deficiency. Injection of LPS in copper-adequate mice resulted in twice as many Ly-6G-expressing cells in the periphery. LPS injection into copper-deficient mice resulted in a severe leukopenia but did not influence Ly-6G expression any more than did copper deficiency alone. LPS treatment caused an increase in myeloperoxidase activity associated with the lungs of copper-deficient mice. The results suggest that although the neutrophils of copper-deficient mice are immature, they can be sequestered by the lung when stimulated to do so.
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PMID:Arrested maturation of granulocytes in copper deficient mice. 980 34

Saudi Rhazya stricta is used in folkloric medicine for the treatment of various disorders. R stricta leaves were fed to male Wistar albino rats at 2%, 10% or 50% of the diet for 6 w. Decreased growth rate, soft feces, dullness, ruffled hair and hepatonephrotoxicity were observed in rats on 10% and 50% Rhazya diet. Fifty percent Rhazya was fatal to rats, and hepatorenal lesions at 3 and 6 w confirmed changes in serum enzyme activity and in total protein, albumin, bilirubin and urea concentrations. Serum copper was decreased and zinc was increased in rats on 50% R stricta at 3 and 6 w, and were accompanied by anemia and neutropenia. Two percent Rhazya diet promoted growth as the plant leaves contained 28.3% crude protein and 16.6% crude fat and were not deficient in copper, zinc or iron.
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PMID:Experimental Rhazya stricta toxicosis in rats. 994 75

A 32-year-old man with active Crohn's disease and recurrent small bowel strictures underwent abdominal surgery and was subsequently given total parenteral nutrition (TPN). Severe cholestasis developed and copper was removed from the TPN. Although serum ceruloplasmin levels were within normal limits, 8 weeks after copper removal, he developed pancytopenia. Serum copper levels were severely depressed. Bone marrow biopsy was consistent with copper deficiency; cytoplasmic vacuolization of both myeloid and erythroid precursors, megaloblastic erthropoiesis, and marked hypocellularity were observed. IV replacement with copper sulfate resulted in improvement in the patient's anemia, neutropenia, and thrombocytopenia, but the patient died suddenly from cardiac tamponade. Postmortem examination revealed fibrinous and hemorrhagic pericarditis. Despite the rare occurrence of overt copper deficiency, this case emphasizes the need to recognize copper deficiency as an important etiology of iron-resistant anemia in patients receiving TPN. Furthermore, the relative rapidity with which our patient developed pancytopenia suggests that, in view of the established recommendation that copper be removed from TPN in cholestatic conditions, serum copper levels must be measured periodically.
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PMID:Rapid development of severe copper deficiency in a patient with Crohn's disease receiving parenteral nutrition. 1033 25

We report a case of copper deficiency with anemia and neutropenia due to dumping syndrome after total gastrectomy. Parenteral nutrition containing cupric sulfate promptly improved the dumping syndrome, anemia and neutropenia. This case suggests that total gastrectomy with dumping syndrome can cause copper deficiency, and that copper deficiency should be considered when encountering similar patients with severe anemia and neutropenia.
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PMID:[Copper deficiency anemia and neutropenia secondary to total gastrectomy]. 1087 8

Copper deficiency (normal serum copper level: 78-136 micrograms/dl) has been reported in patients with long-term enteral nutrition, caused by a copper deficit in enteral nutrition. Occasionally, this leads to anemia and leukopenia. We used Hershey's pure cocoa that is rich in copper (content 3.8 mg/cocoa 100 g) for copper deficiency. A total of 86 (40 men and 46 women, mean age 69 years) patients on enteral nutrition were studied. The primary diseases were cerebral vascular disease in 71 patients, neurological disease in 5 and others in 10. Those who showed serum copper levels of 20 micrograms/dl or less (N = 8) were given 30-45 g of cocoa (copper content 1.14-1.71 mg) per day for about 40 days. Among them, two patients could not continue because of vomiting and diarrhea and were excluded from this study. Mean serum copper levels increased from 8.7 +/- 6.2 to 99.0 +/- 25.4 micrograms/dl (N = 6). Those who showed serum copper levels 20-77 mg/dl (N = 31) were given 10 g of cocoa (copper content 0.38 mg) per day for about 40 days. When mean serum copper levels increased from 50.5 +/- 19.3 to 89.0 +/- 12.9 micrograms/dl with cocoa administration, anemia and neutropenia caused by copper deficiency showed a tendency to improve. After completing the study period, cocoa was reduced to 5 g (copper content 0.19 mg) per day in 23 patients. The mean serum copper levels increased from 90.7 +/- 10.4 to 100.6 +/- 17.1 micrograms/dl for about 100 days. Recently, the amount of daily copper requirement for adults has been reported to be 1.28-2.5 mg per day. We showed that 10 g of cocoa (0.6 mg total copper: 0.38 mg in cocoa and 0.22 mg in other nutrients) is sufficient to treat copper deficiency, and 5 g of cocoa (0.37 mg total copper: 0.19 mg in cocoa and 0.18 mg in other nutrients) is enough to maintain the normal level of serum copper in patients with long-term enteral nutrition.
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PMID:[Copper supplement with cocoa for copper deficiency in patients with long-term enteral nutrition]. 1091 28


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