Introduction: Copper is an important transition metal that acts as a cofactor for several enzymes that play a role in maintaining normal antioxidant, hematological, skeletal, vascular, and neurological function. Copper deficiency, or hypocupremia, can be a sequela of inherited disorders like Menkes disease and Wilson’s disease. Acquired copper deficiency may result from zinc toxicity, use of total parenteral nutrition and other chronic dietary supplementation, and malabsorptive states including post Roux-en-Y Gastric Bypass (RYGB) surgery and other bariatric procedures. Symptoms of hypocupremia can include cytopenia, myeloneuropathy, hypopigmentation, hypercholesterolemia, thyroid dysfunction among others. Here, we describe a patient with an acquired copper deficiency that was incidentally found 3 years post RYGB surgery with symptoms of cytopenia and thyroid hormone instability.

Case Presentation: A 59 year old Caucasian woman with a history of RYGB surgery presented to an outpatient family medicine clinic for routine follow up for long-standing, uncontrolled hypothyroidism despite reported adherence to taking Levothyroxine as prescribed. She was originally diagnosed with primary hypothyroidism in her 20s when she had a high TSH and a low T4. She presented with cold intolerance, dry skin, chronic fatigue, brittle hair, and cytopenia for several years. Physical exam revealed that her thyroid was not enlarged with an absence of masses or nodules but rather symmetric and nontender. Her hypocupremia was incidentally found while investigating the cause for her abnormal liver enzymes seen on CMP. Her serum ceruloplasmin was 15.7 mg/dL and her serum copper was 40 mcg/dL. Recent CBCs revealed chronic normocytic anemia and neutropenia, which is consistent with symptoms of hypocupremia. Differential diagnosis includes primary hypothyroidism exacerbated by hypocupremia along with primary hypothyroidism exacerbated by medication noncompliance.

Working Diagnosis: Given her reported adherence to Levothyroxine with adjustments of dosage in line with her TSH levels, the working diagnosis is uncontrolled primary hypothyroidism worsened by hypocupremia from her RYGB.

Management: The patient was referred to an endocrinologist and was sent to an infusion center for intravenous copper supplementation and will be monitored for future hematological and thyroid homeostasis.