Copper and Magnesium Deficiencies in Patients With Short Bowel Syndrome Receiving Parenteral Nutrition or Oral Feeding

Braga, Cristiane Giffoni; Ferreira, Iahel Manon de Lima; Marchini, Júlio Sérgio; Cunha, Selma Freire de Carvalho da

doi:10.1590/s0004-28032015000200004

Cited by 13 publications

(11 citation statements)

References 39 publications

(49 reference statements)

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“…Mg intakes have decreased bỹ 50% in the American diet over the past century (17). It is estimated that only~40% of the US population consumes the recommended daily intake of Mg (19), and the elderly, those (4,20,25,29,45,63). Using LLC-PK 1 cells, a porcine renal tubular epithelial cell line used most commonly to study nephrotoxic drugs and mechanisms to block drug-induced nephrotoxicity (24), we showed that exposure to Mg deficiency in vitro promoted cisplatin-mediated cytotoxicity and inflammation, and Mg supplementation blocked this effect (Fig.…”

Section: F345mentioning

confidence: 99%

Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity

Kumar

Solanki

Xue

et al. 2017

American Journal of Physiology-Renal Physiology

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Approximately 30% of all cancer patients treated with cisplatin, a widely used broad-spectrum chemotherapeutic agent, experience acute kidney injury (AKI). Almost all patients receiving cisplatin have magnesium (Mg) losses, which are proposed to aggravate AKI. Currently, there are no methods to successfully treat or prevent cisplatin-AKI. Whereas Mg supplementation has been shown to reduce AKI in experimental models and several small clinical trials, the effects of Mg status on tumor outcomes in immunocompetent tumor-bearing mice and humans have not been investigated. The purpose of this study was to further examine the effects of Mg deficiency (±Mg supplementation) on cisplatin-mediated AKI and tumor killing in immunocompetent mice bearing CT26 colon tumors. Using a model where cisplatin alone (20 mg/kg cumulative dose) produced minimal kidney injury, Mg deficiency significantly worsened cisplatin-mediated AKI, as determined by biochemical markers (blood urea nitrogen and plasma creatinine) and histological renal changes, as well as markers of renal oxidative stress, inflammation, and apoptosis. By contrast, Mg supplementation blocked cisplatin-induced kidney injury. Using LLC-PK renal epithelial cells, we observed that Mg deficiency or inhibition of Mg uptake significantly enhanced cisplatin-induced cytotoxicity, whereas Mg supplementation protected against cytotoxicity. However, neither Mg deficiency nor inhibition of Mg uptake impaired cisplatin-mediated killing of CT26 tumor cells in vitro. Mg deficiency was associated with significantly larger CT26 tumors in BALB/c mice when compared with normal-fed control mice, and Mg deficiency significantly reduced cisplatin-mediated tumor killing in vivo. Finally, Mg supplementation did not compromise cisplatin's anti-tumor efficacy in vivo.

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Section: F345mentioning

confidence: 99%

Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity

Kumar

Solanki

Xue

et al. 2017

American Journal of Physiology-Renal Physiology

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“…Chronic diarrhea, celiac disease, Crohn's disease, foregut surgery, and short‐bowel syndrome might lead to copper deficiency through decreased global intestinal absorption . Exudative enteropathies cause malabsorption of multiple nutrients, including copper .…”

Section: Causesmentioning

confidence: 99%

Copper Deficiency: Causes, Manifestations, and Treatment

et al. 2019

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Background: The metabolism of the essential trace element copper remains incompletely understood and, until recently, nearly ignored in acute medicine. Menkes disease was for long the only known copper deficiency condition, but several case reports and investigations conducted over the last 2 decades have shown that deficiency is more frequent than previously suspected, with devastating individual consequences and potential public health consequences. The copper needs in healthy individuals are 0.9 mg/d, which translates to 0.3 mg/d intravenously in parenteral nutrition; the present review aims at gathering actual knowledge. Method and results: A review of literature was conducted in PubMed and Cochrane systematic reviews to identify the most recent information about copper deficiency and generate a narrative review. Copper deficiency has hereditary and acquired origins, the latter being the most frequent. Clinical manifestations are nonspecific but affect all organs and systems, particularly the hematologic (anemia) and the neurologic (myeloneuropathy) systems. Deficiency also affects the cardiovascular, cutaneous, and immune systems. Severe copper deficiency due to reduced absorption after bariatric bypass surgery has become frequent. Conclusion: Deficiency is more frequent than previously recognized, probably because of changing nutrition patterns but also because of some treatments that have become very common such as bypass bariatric surgery and, in acute medicine, prolonged continuous renal replacement therapy. The patients may present with severe hematologic and neurologic complications that go untreated because copper deficiency was not considered in the differential diagnosis: These complications often need active intravenous repletion with doses 4-8 times the usual nutrition recommendations. (Nutr Clin Pract. 2019;34:504-513)

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“…Patients with short bowel syndrome (SBS) are at risk of Cu deficiency even after weaning onto oral diet. A recent study investigated 22 adults with SBS following intestinal resection, of whom half had been weaned onto oral diet and half remained dependent on PN 27 . Patients in the PN group had a small intestine with a median length of 25 cm (range, 10–100), and 6 patients had a colon.…”

Section: Cu Deficiencymentioning

confidence: 99%

Review of Copper Provision in the Parenteral Nutrition of Adults

Livingstone

2016

Nut in Clin Prac

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ReviewCopper (Cu) is an essential trace element (TE) required for metabolism in all living cells. It has been known to be an essential component of parenteral nutrition (PN) since 1972.1 Provision of the correct amount of Cu is necessary, not only to avoid deficiency and toxicity, but also to promote optimal recovery.2 This article covers the relevant physiology of Cu. It then discusses Cu deficiency and toxicity and examines the evidence behind the recommendations on Cu provision in PN. It provides practical guidance on assessment of Cu status and Cu requirements. The article focuses on adults because provision of Cu in pediatric PN has recently been covered elsewhere, 3 but pediatric studies have been cited where considered appropriate. PhysiologyCu is among the 3 most abundant transition metals in biological systems, the other 2 being iron (Fe) and zinc (Zn). The human body contains around 100 mg of Cu, more than half of which is in bone and muscle. The highest concentrations are in liver, kidney, and brain, reflecting the high metabolic activity of these organs.2 Only 5% is in blood, about 95% of this being bound to ceruloplasmin (Cp) and the remainder to albumin and amino acids. 4 The serum Cu concentration therefore largely reflects the Cp concentration and is affected by factors influencing Cp. Intracellular Cu is usually bound to chaperones and other proteins because free Cu is potentially harmful to cells.Cu, which functions as a component of cuproproteins, has a variety of physiologic roles. For example, it is required for humoral immunity and production of inflammatory cytokines. 5,6 It was recently suggested that the immune system uses Cu intoxication as a means of intracellular bacterial killing. 7,8 Cu is required for the physiologic response to low Fe stores. It is needed for absorption of dietary Fe, release of Fe from hepatocytes and production of hemoglobin.9 Cp oxidizes Fe from the ferrous to ferric state, enabling its transport by transferrin and subsequent use in erythropoiesis. Superoxide dismutase is an antioxidant cuproenzyme that catalyzes the conversion of superoxide radicals to hydrogen peroxide, which is then reduced to water.10 Cu is also necessary for wound healing because it is required for the synthesis of collagen.The average daily oral intake of Cu is 1.0-1.6 mg, which exceeds the RDA of 0.9 mg.11 Dietary Cu is absorbed mainly in the stomach and upper small intestine.2,12 About 55%-75% of dietary Cu is absorbed, which is a high proportion as compared AbstractThe essential trace element copper (Cu) is required for a range of physiologic processes, including wound healing and functioning of the immune system. The correct amount of Cu must be provided in parenteral nutrition (PN) if deficiency and toxicity are to be avoided. While provision in line with the standard recommendations should suffice for most patients, Cu requirements may be higher in patients with increased gastrointestinal losses and severe burns and lower in those with cholestasis. The tests of Cu status that are c...

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Copper and Magnesium Deficiencies in Patients With Short Bowel Syndrome Receiving Parenteral Nutrition or Oral Feeding

Cited by 13 publications

References 39 publications

Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity

Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity

Copper Deficiency: Causes, Manifestations, and Treatment

Review of Copper Provision in the Parenteral Nutrition of Adults

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