SUN-690 - Metabolic Mimicry: Severe Hypocupremia as A Reversible Cause of Neuromuscular Decline in Hypothyroidism vs. Incidental Anti-Cn1A Positivity

Introduction:
Post-bariatric patients are vulnerable to overlapping endocrine and nutritional deficits. This case highlights how severe hypothyroidism can mask a concurrent copper deficiency polyneuropathy, stressing the importance of micronutrient evaluation and cautious interpretation of autoimmune markers in complex metabolic contexts.

Case Presentation: A 59-year-old man with a history of bariatric surgery (Gastric Bypass) presented with periorbital edema, cold intolerance, and muscle weakness. Labs revealed TSH 372 mIU/mL, free T4 0.37 ng/dL, and elevated CK (518 U/L), consistent with thyroid myopathy. Levothyroxine therapy normalized thyroid and CK levels, yet weakness and gait disturbances persisted. Neurological exam revealed ataxia, and EMG confirmed large-fiber polyneuropathy without myopathic findings. Skin and muscle biopsies ruled out small-fiber involvement and no findings suggestive of inclussion bodies myositis were found. Lab work showed normal B12 but copper deficiency. (64.5 µg/dL) and low vitamin A. Rheumatologic workup revealed isolated anti-cN1A positivity, raising concern for inclusion body myositis (IBM). However, aggressive copper and vitamin repletion led to significant neurological recovery, effectively excluding IBM and reclassifying anti-cN1A as incidental. Spine MRI did not have findings of demyelination, however brain MRI revealed a 1.6 cm pituitary macroadenoma. Endocrine evaluation confirmed it as a nonfunctioning incidentaloma, unrelated to the initial thyroid failure.

Discussion: Severe hypothyroidism may obscure coexisting metabolic neuropathies, especially in post-bariatric patients. The persistence of ataxia despite thyroid normalization prompted further evaluation, revealing hypocupremia. Copper plays dual roles: supporting myelination and acting as a cofactor for thyroid peroxidase. This convergence likely amplified both neuromuscular and endocrine dysfunction. Furthermore, anti-cN1A positivity—though specific for IBM—proved misleading, as symptom resolution with micronutrient correction argued against autoimmune etiology. This underscores the need to treat reversible metabolic causes.

Conclusion: Copper deficiency neuropathy may mimic refractory hypothyroid symptoms. In post-bariatric settings, clinicians must broaden differentials beyond thyroid dysfunction. Early identification and correction of copper deficiency can prevent misdiagnosis and irreversible neurologic damage.

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