The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform
Hayder Saeed - One of the best experts on this subject based on the ideXlab platform.
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Copper deficiency anemia: review article
Annals of Hematology, 2018Co-Authors: Zin W. Myint, Thein Htut Oo, Kyaw Zin Thein, Hayder SaeedAbstract:Copper is a crucial micronutrient needed by animals and humans for proper organ function and metabolic processes such as hemoglobin synthesis, as a neurotransmitter, for iron oxidation, cellular respiration, and antioxidant defense peptide amidation, and in the formation of pigments and connective tissue. Multiple factors, either hereditary or acquired, contribute to the increase in Copper deficiency seen clinically over the past decades. The uptake of dietary Copper into intestinal cells is via the Ctr1 transporter, located at the apical membrane aspect of intestinal cells and in most tissues. Copper is excreted from enterocytes into the blood via the Cu-ATPase, ATP7A, by trafficking the transporter towards the basolateral membrane. Zinc is another important micronutrient in animals and humans. Although zinc absorption may occur by direct interaction with the Ctr1 transporter, its absorption is slightly different. Copper deficiency affects physiologic systems such as bone marrow hematopoiesis, optic nerve function, and the nervous system in general. Detailed pathophysiology and its related diseases are explained in this manuscript. Diagnosis is made by measuring serum Copper, serum ceruloplasmin, and 24-h urine Copper levels. Copper deficiency anemia is treated with oral or intravenous Copper replacement in the form of Copper Gluconate, Copper sulfate, or Copper chloride. Hematological manifestations are fully reversible with Copper supplementation over a 4- to 12-week period. However, neurological manifestations are only partially reversible with Copper supplementation.
Zin W. Myint - One of the best experts on this subject based on the ideXlab platform.
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Copper deficiency anemia: review article
Annals of Hematology, 2018Co-Authors: Zin W. Myint, Thein Htut Oo, Kyaw Zin Thein, Hayder SaeedAbstract:Copper is a crucial micronutrient needed by animals and humans for proper organ function and metabolic processes such as hemoglobin synthesis, as a neurotransmitter, for iron oxidation, cellular respiration, and antioxidant defense peptide amidation, and in the formation of pigments and connective tissue. Multiple factors, either hereditary or acquired, contribute to the increase in Copper deficiency seen clinically over the past decades. The uptake of dietary Copper into intestinal cells is via the Ctr1 transporter, located at the apical membrane aspect of intestinal cells and in most tissues. Copper is excreted from enterocytes into the blood via the Cu-ATPase, ATP7A, by trafficking the transporter towards the basolateral membrane. Zinc is another important micronutrient in animals and humans. Although zinc absorption may occur by direct interaction with the Ctr1 transporter, its absorption is slightly different. Copper deficiency affects physiologic systems such as bone marrow hematopoiesis, optic nerve function, and the nervous system in general. Detailed pathophysiology and its related diseases are explained in this manuscript. Diagnosis is made by measuring serum Copper, serum ceruloplasmin, and 24-h urine Copper levels. Copper deficiency anemia is treated with oral or intravenous Copper replacement in the form of Copper Gluconate, Copper sulfate, or Copper chloride. Hematological manifestations are fully reversible with Copper supplementation over a 4- to 12-week period. However, neurological manifestations are only partially reversible with Copper supplementation.
Thein Htut Oo - One of the best experts on this subject based on the ideXlab platform.
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Copper deficiency anemia: review article
Annals of Hematology, 2018Co-Authors: Zin W. Myint, Thein Htut Oo, Kyaw Zin Thein, Hayder SaeedAbstract:Copper is a crucial micronutrient needed by animals and humans for proper organ function and metabolic processes such as hemoglobin synthesis, as a neurotransmitter, for iron oxidation, cellular respiration, and antioxidant defense peptide amidation, and in the formation of pigments and connective tissue. Multiple factors, either hereditary or acquired, contribute to the increase in Copper deficiency seen clinically over the past decades. The uptake of dietary Copper into intestinal cells is via the Ctr1 transporter, located at the apical membrane aspect of intestinal cells and in most tissues. Copper is excreted from enterocytes into the blood via the Cu-ATPase, ATP7A, by trafficking the transporter towards the basolateral membrane. Zinc is another important micronutrient in animals and humans. Although zinc absorption may occur by direct interaction with the Ctr1 transporter, its absorption is slightly different. Copper deficiency affects physiologic systems such as bone marrow hematopoiesis, optic nerve function, and the nervous system in general. Detailed pathophysiology and its related diseases are explained in this manuscript. Diagnosis is made by measuring serum Copper, serum ceruloplasmin, and 24-h urine Copper levels. Copper deficiency anemia is treated with oral or intravenous Copper replacement in the form of Copper Gluconate, Copper sulfate, or Copper chloride. Hematological manifestations are fully reversible with Copper supplementation over a 4- to 12-week period. However, neurological manifestations are only partially reversible with Copper supplementation.
Kyaw Zin Thein - One of the best experts on this subject based on the ideXlab platform.
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Copper deficiency anemia: review article
Annals of Hematology, 2018Co-Authors: Zin W. Myint, Thein Htut Oo, Kyaw Zin Thein, Hayder SaeedAbstract:Copper is a crucial micronutrient needed by animals and humans for proper organ function and metabolic processes such as hemoglobin synthesis, as a neurotransmitter, for iron oxidation, cellular respiration, and antioxidant defense peptide amidation, and in the formation of pigments and connective tissue. Multiple factors, either hereditary or acquired, contribute to the increase in Copper deficiency seen clinically over the past decades. The uptake of dietary Copper into intestinal cells is via the Ctr1 transporter, located at the apical membrane aspect of intestinal cells and in most tissues. Copper is excreted from enterocytes into the blood via the Cu-ATPase, ATP7A, by trafficking the transporter towards the basolateral membrane. Zinc is another important micronutrient in animals and humans. Although zinc absorption may occur by direct interaction with the Ctr1 transporter, its absorption is slightly different. Copper deficiency affects physiologic systems such as bone marrow hematopoiesis, optic nerve function, and the nervous system in general. Detailed pathophysiology and its related diseases are explained in this manuscript. Diagnosis is made by measuring serum Copper, serum ceruloplasmin, and 24-h urine Copper levels. Copper deficiency anemia is treated with oral or intravenous Copper replacement in the form of Copper Gluconate, Copper sulfate, or Copper chloride. Hematological manifestations are fully reversible with Copper supplementation over a 4- to 12-week period. However, neurological manifestations are only partially reversible with Copper supplementation.
Jorge L. Rosado - One of the best experts on this subject based on the ideXlab platform.
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Zinc and Copper: Proposed Fortification Levels and Recommended Zinc Compounds
Journal of Nutrition, 2003Co-Authors: Jorge L. RosadoAbstract:Micronutrient fortification of foods is now a highly relevant tool worldwide for overcoming micronutrient deficiency. Recent data show that subclinical zinc deficiency is widespread; in Mexico a national survey showed that 25% of children less than age 11 y had plasma zinc concentrations below 10.0 micromol/L (65 microg/dL). Copper deficiency in populations is unknown but Copper supplementation is recommended to accompany zinc supplementation. Of the foods available for fortification, staple cereals are very good candidates for reducing micronutrient deficiencies. Because of its higher stability and lower cost, we recommend fortification of cereal flours with zinc oxide, which is absorbed as well as the less stable and more expensive forms of zinc. Depending on the amount of the food that is expected to be eaten, zinc fortification of staple foods could be 20-50 mg/kg of flour. For Copper fortification the safer compound is Copper Gluconate. Copper sulfate is significantly less expensive, but an evaluation of potential physicochemical reactions that affect the final food product is recommended. The suggested amount of Copper added to staple foods is 1.2-3.0 mg/kg of flour. For food supplements designed as part of supplementation programs to reduce micronutrient deficiency in children less than age 3 y, a dose of the final product (usually approximately 40-50 g) should contain approximately 4-5 mg of zinc and approximately 0.2-0.4 mg of Copper depending on the habitual diet, magnitude of deficiencies and period of supplementation.