S4875 Copper Collapse: A Case of Zinc-Induced Copper Deficiency in Ulcerative Colitis With ATP7B Heterozygosity

Introduction: Micronutrient deficiencies are increasingly recognized in patients with inflammatory bowel disease (IBD). Copper deficiency is an under-recognized yet clinically significant cause of anemia and neurologic dysfunction. Excess zinc intake is a well-known but often overlooked cause of acquired copper deficiency. Genetic factors such as heterozygous ATP7B mutations may further modulate copper homeostasis. We report a case of such a patient who presented with low copper levels. Case Description/Methods: A 41-year-old White man with a history of ulcerative colitis and prostate cancer presented with progressive fatigue and blurry vision. Imaging of the head was normal. He was found to have diplopia and was diagnosed with abducens nerve palsy. He endorsed to taking long-term zinc supplementation, which he thought would help with Ulcerative colitis flares. Laboratory workup revealed severe copper deficiency (serum copper 37 µg/dL, ceruloplasmin 11.4 mg/dL). Upper endoscopy revealed only mild gastritis, ruling out significant malabsorption. He was sent to a hematology clinic where genetic testing revealed a heterozygous ATP7B mutation. The copper deficiency was attributed to zinc-induced malabsorption compounded by active colitis and genetic predisposition. His copper levels slightly improved but did not normalize, even with intravenous (IV) copper infusion; however, he experienced slight relief from his symptoms. Discussion: This case emphasizes a rare but clinically important association of IBD with mineral deficiencies augmented by genetic predisposition. Copper deficiency should be considered in IBD patients presenting with anemia, cytopenias, or neuropathy, especially if zinc supplementation is involved. Excessive zinc supplementation as well as presence of underlying IBD can interfere with copper absorption. In our patient presence of heterozygous ATP7B mutation does not cause clinical Wilson’s disease, but it has been known to predispose patient to alter copper homeostasis by lowering ceruloplasmin levels and thus worsening copper deficiency. As in our case, patient was started on IV copper infusions considering his IBD to be a cause of malabsorption of oral copper. Clinicians should consider genetic analysis in complicated cases of copper deficiency who do not respond drastically to IV copper. Close follow up and adequate supplementation can prevent irreversible complications. More research is needed in this area to determine the long term outcome of patients who receive copper supplementation.