Hematopoiesis and Storage Iron in Infants
Bo Lönnerdal in Iron Metabolism in Infants, 2020
Copper deficiency may occasionally occur in conditions where copper intake is minimal, for instance after prolonged parenteral nutrition if no copper is given. The question is whether copper deficiency exists in infants after preterm delivery and, if so, whether it has any influence on iron metabolism under these conditions. It has been demonstrated that the serum concentrations of copper are lower in preterm than full-term infants during the first months after birth.16 It is difficult, however, to estimate the significance of this finding. It should be cautioned that any form of copper supplementation in formula-fed infants, if it ever proves to be indicated, leads to another problem since the amount of copper ingested is primarily dependent on the copper concentration of the water that is added to powdered formula. The concentration of copper in water is extremely variable in different areas and even between houses within a city particularly if the water supply comes from a private well. These problems are avoided if copper-supplemented ready-to-feed formulas are used.
The Mottled Locus: Mottled (Mo), Blotchy (Moblo), Brindled (Mobr), Dappled (Modp), Mosaic (Moms), Tortoiseshell (Moto), and Viable Brindled (Movbr) Mutations, Chromosome X
John P. Sundberg in Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Mobr, Brindled —The gross, microscopic, and clinical abnormalities in brindled mice are due to a generalized defect in the function of copper containing enzymes and copper-binding proteins.41,42 Neurological abnormalities are due to inactivity of cytochrome c oxidase31,43,44 and dopamine-β-hydroxylase.45,46 Lysyl oxidase functional impairment results in tortuosity of blood vessels.47 Production of melanin requires the copper-containing enzyme tyrosinase. Without it, the brindled mouse develops depigmented hair.47,48 Other organs in the animal’s body, including the kidney and intestine, accumulate large amounts of copper in the form of metallothionein in cytoplasm of cells.49,50 The accumulation interferes with intestinal absorption of copper, further complicating the condition.35 Fatal copper deficiency results because the brain and skin do not receive adequate amounts of copper.50–53 Heterozygous females have lower levels of norepinephrine and higher levels of dopamine or dopamine metabolites in their brains.48 Serum cholesterol levels are not elevated in brindled mice.54
Postoperative Nutritional Management of the Bariatric-Surgery Patient
Emmanuel C. Opara, Sam Dagogo-Jack in Nutrition and Diabetes, 2019
Although copper deficiency is rare in the general population, anatomic changes from bariatric surgery can lead to copper deficiency in bariatric surgery patients. The reduction in gastric acid from stomach resection and bypassing the duodenum reduces copper bioavailability. Signs of copper deficiency are anemia, leukopenia, neutropenia, thrombocytopenia, and neuropathies affecting muscle weakness, peripheral numbness, and paresthesias. Approximately 20% of RYGB patients were copper deficient at 24 months post-surgery.101 Interestingly, no difference in copper intake was seen between copper-deficient and copper-sufficient patients, suggesting that the reduced bioavailability is the mechanism for compromised copper. Complicating assessment of copper status is that serum copper and ceruloplasmin, both biomarkers for copper status, are elevated with inflammation,102 which may hinder the detection of copper deficiency.
Copper deficiency, a rare but correctable cause of pancytopenia: a review of literature
Published in Expert Review of Hematology, 2022
Nayha Tahir, Aqsa Ashraf, Syed Hamza Bin Waqar, Abdul Rafae, Leela Kantamneni, Taha Sheikh, Rafiullah Khan
Our study focuses on prevalence, etiology, pathophysiology, complications, and treatment of copper deficiency. Copper deficiency is a rare and frequently underrecognized cause of anemia, neutropenia, and bone marrow dysplasia. As it is potentially treatable, it should be always kept in the differentials when patients present with neurological and hematological abnormalities. A thorough history, physical examination, and work up are needed to establish diagnosis. Patients with a suspected copper deficiency should have a complete blood picture along with iron studies, vitamin B12, D, and E. Diagnosis is made by measuring the serum copper, ceruloplasmin, and/or 24-h urine copper levels. Copper deficiency is an uncommon cause of bone marrow dysplasia and can mimic myelodysplastic syndrome such as ringed sideroblastic anemia variety. Ringed sideroblastic anemia with neutropenia can especially be kept under the umbrella of copper deficiency. Oral and intravenous supplementation is required with median time to response being 1–3 months. Copper deficiency due to gastrointestinal disease can be associated with deficiency of other nutrients like vitamins B 12, D, and E, and these should be supplemented concomitantly if needed. The patients who have copper deficiency due to excessive zinc ingestion should suffice from stopping zinc. Research has shown that the neurologic manifestations are only partially reversible while hematological manifestations are largely reversible and return to baseline in 12 weeks. Regular follow-ups are required to ensure resolution of symptoms and correction of blood counts.
Copper and zinc deficiency in an alcoholic patient: a case report of a therapeutic dilemma
Published in Journal of Addictive Diseases, 2022
Hiroshi Ito, Yasuhiro Ogawa, Nobutake Shimojo, Satoru Kawano
Copper is a trace element essential for the function of human cellular enzymes. The recommended dietary allowance for copper is 0.9 mg daily in adults.1 Although relatively rare, copper deficiency usually presents symptoms including anemia and ataxia.2 The risk factors for copper deficiency include gastrointestinal surgery, excessive zinc ingestion, and malabsorptive conditions. Case reports have suggested an association between alcohol consumption and copper deficiency.3 However, little is known still about the relationship between the two states. Here, we describe a case of copper deficiency in a patient with alcohol use disorder who also had zinc deficiency. Patients with alcohol use disorder can present zinc and copper deficiencies at the same time. Because copper and zinc are competitively absorbed from the jejunum, this condition poses a therapeutic dilemma.
Protective and antioxidant effects of copper-nicotinate complex against glycerol-induced nephrotoxicity in rats
Published in Drug and Chemical Toxicology, 2020
Ahmed Medhat Hegazy, Ahmed S. Hafez, Rania M. Eid
Copper (Cu) is required for the function of several co-enzymes essential for different physiological functions and integrated into essential biochemical pathways (Linder 1991, Vančo et al. 2008). Copper complexes can modulate Cu homeostasis in different tissues, resulting in protective effects against several degenerative diseases. Copper-nicotinate complex (CNC) [CuCl (HNA)2] was found to exhibit various bioactivities such as anti-tumour and anti-inflammatory activities (Belicchi et al. 2002). The complex has a cytoprotective effect and superoxide dismutase (SOD)-mimicking activity. It has also been found to prevent gastric congestion, prevent capillary damage, stimulate blood flow and reduce LPO and oxidative stress markers (El-Saadani et al. 1993). Additionally, the complex has significant curative effects in rats with induced rheumatoid arthritis and nonalcoholic fatty liver (Salama et al. 2007). Copper deficiency has emerged as a factor in the development of nonalcoholic fatty-liver disease (Aigner et al. 2010, Lampón and Tutor 2010) and ischaemic heart disease (Jalili et al. 1996).