MON-377 - When Fatigue Becomes Fatal: Severe Hypothyroidism Presenting as Hypertensive Urgency

Background:

Hypothyroidism is often dismissed as a low-energy, low-output state. Yet in extreme cases, severe thyroid hormone depletion can paradoxically trigger dangerous elevations in blood pressure through marked increases in systemic vascular resistance. Hypertensive urgency as a presenting feature of hypothyroidism remains underrecognized and frequently misattributed to essential hypertension.

Case Presentation:
A 40-year-old man with no prior antihypertensive treatment presented with escalating headaches, blurry vision, and atypical chest pain. Home and clinical blood pressure readings were persistently in the 170s/120s mmHg, prompting evaluation for hypertensive urgency. Over the preceding year, he reported progressive fatigue, cold intolerance, constipation, weight gain, hyperlipidemia, and declining functional capacity. Six months earlier, laboratory testing had revealed severe hypothyroidism (TSH 64.8 µIU/mL, free T4 0.49 ng/dL), yet treatment was deferred and follow-up was lost.

On admission, blood pressure measured 178/121 mmHg with preserved heart rate. Examination was notable for myxedematous facies and periorbital edema. Thyroid studies demonstrated profound peripheral thyroid hormone depletion with TSH 84.0 µIU/mL, free T4 < 0.3 ng/dL, total T3 63 ng/dL, and free T3 1.9 pg/mL. Thyroid peroxidase antibodies were markedly elevated (262 IU/mL), confirming autoimmune thyroiditis. Cardiac biomarkers, electrocardiography, chest imaging, head CT, and toxicology screening were unrevealing, excluding alternative causes of secondary hypertension.

Endocrinology consultation identified severe T3 deficiency with unopposed alpha-adrenergic tone as the principal driver of the patient’s marked diastolic hypertension. Levothyroxine was initiated at 1.6 µg/kg/day (150 µg daily). Targeted antihypertensive therapy with nifedipine and prazosin was employed to reduce vascular resistance. Blood pressure improved during hospitalization and continued to normalize following discharge as thyroid hormone replacement progressed.

Conclusion:
This case exposes an interesting paradox: profound hypothyroidism presenting as hypertensive urgency. Severe T3 depletion can present as primary hypertension and drive life-threatening blood pressure elevations. Recognition of hypothyroidism as a reversible cause of secondary hypertension is critical, as thyroid hormone replacement alone may substantially normalize blood pressure and prevent unnecessary long-term antihypertensive therapy.

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