The Vasospastic Thyroid: Bilateral Leg Pain as a Vascular Manifestation of Hypothyroidism

Hypothyroidism is an endocrine disorder that causes widespread systemic effects, but its impact on vascular tone is often under-recognized. We present a case of severe, longstanding hypothyroidism leading to bilateral lower extremity vasospasm and failure to thrive in a complex patient with significant psychiatric and medical comorbidities. A 46-year-old male with a history of type 2 diabetes, chronic DVT, bipolar disorder, and recent untreated hypothyroidism presented with progressive bilateral leg pain, weakness, and inability to ambulate. He had been discharged a week prior with a TSH of 101 mIU/L and newly initiated levothyroxine 50 mcg. On return, symptoms had worsened, and his mother reported cognitive slowing. Workup revealed stable chronic DVT and new arterial duplex findings showing diffuse high-resistance waveforms consistent with vasoconstrictive physiology in both lower extremities, without stenosis. Creatinine was elevated, likely due to vasomotor nephropathy. Neurological and rheumatological causes were previously excluded. Severe hypothyroidism is known to increase systemic vascular resistance and reduce endothelial-mediated vasodilation, potentially contributing to vasospastic phenomena. In this patient, no other etiology for bilateral vasoconstriction was found. With no history of Raynaud's, vasoactive drug use, or active thrombosis, hypothyroidism remained the most plausible cause. Although rare, such vascular manifestations can lead to functional decline, especially in vulnerable patients. This case highlights the importance of considering hypothyroidism in the differential diagnosis of unexplained vasospasm and functional decline. Timely thyroid hormone replacement may reverse vascular dysfunction and prevent further complications.