Armour® Thyroid Rage - A Dangerous Mixture.

Armour® Thyroid (Forest Pharmaceuticals, LLC; affiliate of Allergan, Dublin, Ireland) is a natural porcine derivative thyroid supplement that is frequently used without physician monitoring by health enthusiasts as a weight loss supplement. Although there are no publications associating Armour Thyroid and major coronary events, significant drug interactions may exist. A 32-year-old male with a history of hypothyroidism, cystic acne, and solitary congenital kidney presented to the emergency room after experiencing crushing substernal chest pain radiating to his left shoulder, accompanied by diaphoresis and shortness of breath. The patient denied any tobacco use or family history of heart disease. He was self-administering 120 mg of Armour Thyroid daily.   On examination, the patient was well-developed with cystic acne and a flushed appearance. His vital signs on admission were a blood pressure of 171/106 mmHg, heart rate of 88 beats per minute (bpm), and respiratory rate of 16 breaths/min. The electrocardiogram revealed marked ST-segment elevation in the anterior chest leads. Laboratory studies revealed elevated troponins. Urine drug screen was negative. The patient underwent an emergent coronary angiogram, which confirmed an occluded left anterior descending artery. He was treated successfully by thrombectomy and stenting of his left anterior descending artery. Evaluation for other causes of thrombosis was negative: glycosylated hemoglobin (HbA1C) 5.5%, low-density lipoprotein (LDL) 127 mg/dL, high-density lipoprotein (HDL) 33 mg/dL, hypercoagulable evaluation negative, and hemoglobin (Hgb) 17.1 gm/dL. Luteinizing hormone (LH) and follicle stimulating hormone (FSH) were < 0.20 miu/mL. Thyroid profile results were thyroid-stimulating hormone (TSH) 0.20 miu/mL (low), T3 free 4.08 pg/mL (high), and T4 total 1.2 mcg/dL (low), which were consistent with exogenous thyroid hormone administration. Focused questioning triggered by his cystic acne led to the discovery that the patient was self-administering exogenous testosterone replacement therapy. The patient declined to share specifics with the healthcare team. This was confirmed by a high testosterone level of 1,311 ng/dL. Hyperthyroidism increases the risk of cardiovascular events two to three times through the propagation of a hypercoagulable, hypofibrinolytic state possibly via an increase in clotting factors, a decrease in fibrinolytic enzymes, and an increased inhibition of the protein C pathway. The effect of androgens on cardiovascular mortality is uncertain. Androgens stimulate the hemostatic system, increase adverse lipid profile, and erythropoiesis. The combined therapy likely resulted in a synergistic potentiation of hypercoagulable, hypofibrinolytic effects of both agents. Given the absence of other cardiovascular risk factors, the cause of the myocardial infarction in our patient was likely due to drug interaction between Armour Thyroid and exogenous testosterone therapy. Due to the potential drug interaction between both natural and prescribed thyroid hormone and testosterone supplements, patients should be discouraged from self-administration of thyroid or anabolic steroids. Due to the lack of standardization in the T3 content, the use of Armour Thyroid should be avoided.