SUN-317 - Refractory Hypothyroidism as A Paraneoplastic Syndrome: A Rare Adult Case of Consumptive Hypothyroidism.

Introduction
Consumptive hypothyroidism (CH) is a rare paraneoplastic syndrome caused by aberrant expression of type 3 deiodinase (D3) in tumor tissue, leading to excessive degradation of thyroid hormones. It is mostly reported in infantile hepatic hemangiomas and is rarely described in adults with large mesenchymal tumors such as solitary fibrous tumors (SFTs). We report a case of severe CH in an adult male with a large abdominal SFT complicated by heart failure with preserved ejection fraction (HFpEF).

Case
A 71-year-old man with hypertension and HFpEF presented with acute decompensated heart failure requiring diuresis. He had recently started levothyroxine (LT) 50 mcg daily for newly diagnosed hypothyroidism with reported adherence. On admission Lab work showed severe hypothyroidism: TSH 115 µIU/mL, free T4 0.034 ng/dL, and total T3 38.3 ng/dL with negative anti-TPO antibodies. Imaging revealed a large heterogeneous mass in abdomen with calcifications causing vascular compression and varicosities. Biopsy demonstrated spindle cells positive for STAT6 and CD34, consistent with SFT. Due to anasarca and concern for malabsorption, intravenous levothyroxine 75 mcg daily was started. After 3 days, TSH remained elevated at 98.8 µIU/mL. Reverse T3(rT3) was obtained, which was also elevated at 167.3 ng/dL, confirming CH. LT was cautiously increased to 175 mcg daily but TSH remained 88.4 µIU/mL. Patient developed hyperthyroid symptoms, prompting surgical resection at maximum tolerated dose. Following tumor resection, thyroid function rapidly improved: free T4 normalized, rT3 decreased to 44.4 ng/dL, and TSH decreased to 54 µIU/mL. LT requirements decreased to 100 mcg daily with plans for further tapering

Discussion
CH results from tumor-associated D3 activity driven by sonic hedgehog and MAPK/ERK pathways. Biochemical hallmark is markedly elevated rT3 with suppressed T3 despite supraphysiologic LT administration, distinguishing it from common causes of refractory hypothyroidism. While SFTs typically cause paraneoplastic hypoglycemia (Doege-Potter syndrome), thyroid hormone consumption is rare. Our patient's underlying HFpEF prevented dose escalation beyond 175 mcg daily. Since medical therapy rarely achieves euthyroidism, surgical resection remains the definitive treatment. The rapid normalization of thyroid function following tumor removal confirms the diagnosis and demonstrates that D3 activity ceases once the tumor is removed.

Conclusion
Consumptive hypothyroidism should be suspected in refractory hypothyroidism with large tumors. Markedly elevated rT3 is diagnostic. While supraphysiologic levothyroxine may be attempted, definitive treatment requires surgical resection. In patients with cardiovascular comorbidities, clinicians must balance hypothyroid risks against complications of aggressive thyroid hormone replacement and surgical intervention.

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