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Background:Copper is a mineral that is absorbed in the stomach, duodenum, and jejunum. Gastric bypass surgery, gastrectomy, and short-bowel syndrome commonly lead to copper malabsorption. Copper deficiency primarily presents with hematological and neurological sequelae, including macrocytic anemia and myelopathy. Although hematological disturbances often correct with copper supplementation, neurological manifestations of copper deficiency may be irreversible. We present the case of copper deficiency secondary to malabsorption and management strategies to prevent irreversible neurological sequelae. Presentation: A 48-year-old female with a history of hypothyroidism, ischemic stroke, and Crohn's disease, complicated by subtotal colectomy and small-bowel resections, was admitted for fatigue and progressive neurological deficiencies. Her vital signs were stable, and physical examination was remarkable for weakness of both upper and lower extremities, ataxia, and upper extremities paresthesia. Computed tomography scan of the head without contrast was unremarkable. Magnetic resonance imaging enterography revealed a focal area of narrowing of the remaining small bowel. Copper level was low at 39 μg/dL. After 5 days of intravenous replacement using trace element within parenteral nutrition, her copper level corrected to 81 μg/dL. Her ataxia improved after intravenous copper supplementation and did not recur. Conclusions: Our patient presented with copper deficiency secondary to malabsoprtion. This case highlights the importance of copper testing in the bariatric surgery population and in patients with short-bowel syndrome. Given the irreversible nature of neurological symptoms when compared with the expense of nutrition supplements, routine copper testing should be considered in patients with malabsorptive states or altered anatomy, regardless of initial presentation.

Background: Limited evidence is available to describe the prevalence, causes, and consequences of zinc and vitamin B 6 deficiencies in those with acutely exacerbated inflammatory bowel disease (IBD). Zinc is important for immune function and wound healing, and B 6 is needed for metabolic and neurological function. Patients with IBD are at risk of micronutrient deficiencies, particularly during flares. Presentations:The cases of 2 patients with IBD exacerbations were reviewed in which deficiencies of both zinc and vitamin B 6 were identified.Conclusions: These cases highlight the need for increased screening for zinc and pyridoxine deficiencies in IBD population, especially during disease exacerbation. Therefore, we recommend a comprehensive nutrition workup with physical exam, diet history, and a complete micronutrient panel while ruling out contributing factors. If patients are susceptible to deficiencies during flares, prophylactic oral zinc and pyridoxine supplementation may be considered, with close monitoring for subsequent iron and copper deficiencies. K E Y W O R D SCrohn's disease, inflammatory bowel disease, nutrient deficiency, pyridoxine, vitamin B 6 deficiency, zinc BACKGROUNDInflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is a risk factor of malnutrition and micronutrient deficiencies due to increased intestinal losses, decreased oral intake, diminished absorptive capacity, hypermetabolism, and use of immunomodulatory drugs. 1 Acute identification and correction of micronutrient deficiencies may be complicated by fluctuant drug shortages, insufficient resources, and