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Trace Mineral Deficiencies – Diagnosis and Treatment
Published in Jennifer Doley, Mary J. Marian, Adult Malnutrition, 2023
Kavitha Krishnan, Julianne Werner
Risk factors for copper deficiency include dietary deficiency, PN without copper, burns, losses from fistulas and ostomies, and malabsorption states such as SBS, celiac disease, and gastric surgery (e.g. gastric bypass and total or subtotal gastrectomy).2,4,66 Prolonged zinc supplementation of 25–150 mg/d and high vitamin C intake greater than 1500 mg/d can impair copper absorption.2,18,67,68 Copper absorption occurs in the small intestine and varies depending on serum copper levels. During lower dietary intake, copper is actively transported to aid in absorption, while during higher copper intake, passive diffusion is activated.2 Copper deficiency is uncommon, but can result from decreased absorption or intake, or increased GI losses.
A Brief History of Nutritional Medicine and the Emergence of Nutrition as a Medical Subspecialty
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Recognition of the importance of trace elements dates to the late 1920s with discoveries on the inorganic constituents of milk (Wright and Papish 1929). Copper was shown to be a requirement for the synthesis of hemoglobin by Edwin B. Hart (1874–1953) in 1928 (Kresge, Simoni, and Hill 2008). Copper deficiency is quite rare in humans, mostly seen in premature infants and patients on total parenteral nutrition (TPN) without copper supplementation. The anemia it causes is generally described as normocytic and hypochromic (Shils and Shike 2006). Copper’s main role in hemoglobin synthesis has to do with the ability of copper-containing enzymes to convert ferrous iron into ferric so that it can be loaded onto transferrin (Vashchenko and MacGillivray 2013).
Trace Minerals
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Clinical symptoms of copper deficiency (sideroblastic anemia, bone demineralization) appear after a long-term, chronic deficit of copper has been maintained. Of course, perhaps the simplest and least expensive means of assessing copper status is to administer a copper supplement and monitor copper status, both biochemically and clinically. Unfortunately, this method is retrospective, but does combine diagnosis and treatment at one time.
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.
Copper deficiency myeloneuropathy with a history of malabsorption: a tale of two cases
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Anum Qureshi, Emily Bergbower, Janki Patel
Copper’s primary absorption site is in the small intestine from where it is distributed to the rest of the body (Figure 1). Acquired copper deficiency is rare but often seen among patients with malabsorption syndromes, such as celiac disease, or a history of gastric bypass surgery, small bowel obstruction (SBO), and small intestinal bacterial overgrowth (SIBO). It has been a known cause of anemia for decades but has only been identified as a cause of reversible myelopathy since approximately 2000 with more than 50 cases reported in the literature [1–6]. In fact, copper deficiency is the second most common etiology after B12 deficiency for myeloneuropathy in patients with malabsorption syndromes [2,4]. In cases of subacute combined degeneration, the two deficiencies are often indistinguishable clinically and can even coexist. Treatment of copper deficiency comprises copper supplementation. With appropriate supplementation, many symptoms, such as myeloneuropathy, can be reversed entirely [2]. We are presenting two cases of copper deficiency secondary to malabsorption syndromes leading to myeloneuropathy (Table 1).