Abstract Introduction Thyroid storm (TS) is a life-threatening endocrine emergency marked by extreme adrenergic and hypermetabolic stress. Mortality remains high with clinical manifestations including tachycardia, hypertension, hyperthermia, altered mental status, and cardiac dysfunction. TS is usually precipitated by infection, surgery, or noncompliance with antithyroid medications. However, exogenous substance use, particularly sympathomimetics and anabolic steroids, can also contribute to its onset. Staged therapy includes beta-blockers, thioamides, hormone sequestration, and glucocorticoids. We present a complex presentation of TS precipitated by polypharmacy, highlighting the impact of surreptitious use of exogenous hormones and stimulants in triggering and exacerbating thyrotoxicosis. Description A 52-year-old man with anxiety presented with acute left-sided chest pressure, dyspnea, palpitations, emesis, diarrhea, and 40-pound weight loss over three months. Medications included alprazolam and topical testosterone. On arrival, he was tachycardic at 128 beats per minute and hypertensive at 175/112 mmHg. Labs revealed elevated troponin I 98.2 ng/mL, pro-BNP 549 pg/mL, and creatine kinase 1066 U/L. Thyroid studies showed undetectable thyroid-stimulating hormone 0.01 mIU/mL, markedly elevated triiodothyronine 650 ng/dL, and suppressed thyroxine 0.2 ng/dL, suggestive of thyrotoxicosis. Electrocardiogram showed sinus tachycardia; chest x-ray suggested congestive heart failure; CT angiography was non-contributory. Burch-Wartofsky Point Scale (BWPS) was 65, consistent with TS. Intensive care unit (ICU) management included hydrocortisone, methimazole, propranolol, and cholestyramine. Despite dexmedetomidine infusion and antipsychotics, severe agitation and delirium persisted, necessitating endotracheal intubation and deep sedation. Urine toxicology was positive for benzodiazepines. Ultrasonography noted a mildly hypervascular, homogenous thyroid and a 4 mm nodule. Further investigation revealed use of amphetamine/dextroamphetamine, clenbuterol, triamcinolone, and exogenous testosterone for weight loss. Discussion This case highlights the complex interplay between thyroid function and exogenous substances, particularly sympathomimetics, corticosteroids, and anabolic steroids. Clenbuterol, a beta-2 agonist with potent sympathomimetic effects, is commonly misused for weight loss and muscle growth. Hyperadrenergic agents may induce a hypermetabolic state, both triggering and masking thyrotoxicosis. Initial symptoms mimicked acute coronary syndrome with chest pain and troponemia. Severe agitation refractory to standard sedation required intubation, emphasizing the need for aggressive supportive care. BWPS aided early diagnosis and intervention. Propranolol was essential in mitigating adrenergic overstimulation, methimazole and cholestyramine targeted thyroid hormone synthesis and sequestration, respectively. TS remains a diagnostic and therapeutic challenge, especially when triggered by illicit substances. This case highlights polypharmacy, an uncommon but critical etiology, as a precipitant of TS. Clinical scoring tools can guide early recognition and initiation of staged treatment in the ICU to reduce morbidity and mortality. This abstract is funded by: None
Shahab et al. (2026) studied this question.