What is armour thyroid

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Oxford Academic. Google Scholar. Rachael Proumen, DO. Runa Acharya, MD. Amy Patel, MD. Select Format Select format. Permissions Icon Permissions. Abstract Treatment of hypothyroidism is predominantly with levothyroxine due to its ability to generate stable T3 levels and its long half-life.

For commercial re-use, please contact journals. Issue Section:. Download all slides. View Metrics. Email alerts Article activity alert. Advance article alerts. On examination, the patient was well-developed with cystic acne and a flushed appearance.

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. Thyroid profile results were thyroid-stimulating hormone TSH 0. 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.

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. An increased incidence of myocardial infarction has been reported in patients suffering from hyperthyroidism due to the pro-coagulant effects of thyroid hormone [ 1 ].

On the other hand, levothyroxine supplementation based upon physiological requirements under medical supervision has been demonstrated to be safe with no increase in cardiac events [ 2 ]. There are no reports of Armour Thyroid causing cardiovascular events. There is conflicting evidence about the effect of testosterone hormone supplementation on myocardial infarction with some studies suggesting a cardioprotective effect of testosterone supplementation [ 3 ].

On the other hand, case reports have been published that describe sudden death in athletes using androgenic steroids [ 4 ]. A year-old male presented to the emergency department with 20 mins of cramping retrosternal chest pain radiating to his left shoulder accompanied by sweating and shortness of breath.

He did not have a history of any cardiovascular risk factors, such as a history of smoking, diabetes, or hypertension. He did not have any family history of cardiac events in family members at an early age. He had a self-reported diagnosis of hypothyroidism for which he was self-administering mg of Armour Thyroid daily. Physical exam was notable for well-developed musculature and cystic acne.

Other physical examination findings were unremarkable. Initial lab work reported markedly increased levels of cardiac troponin. Urine drug screen was negative, eliminating cocaine as a potential etiology. Emergent left heart catheterization was performed via the right radial artery using the Seldinger technique.

The remainder of the coronary arteries were patent without evidence of atherosclerotic changes. The patient was started on dual antiplatelet therapy with aspirin and clopidogrel, in addition to heparin and eptifibatide infusions.

Focused questioning to elicit the potential cause of the myocardial infarction led to the revelation that the patient participated in recreational bodybuilding for which he self-administered exogenous testosterone therapy and was using Armour Thyroid as a weight loss supplement. Free triiodothyronine T3 was high at 4.

Prior studies of testosterone supplementation have reported conflicting data [ 3 - 4 ]. Some studies have reported worsening of the lipid profile, while others reported improvement. Similarly, some studies have reported improvement in angina symptoms, while others did not report any effect. Testosterone supplementation may lead to increased activation of the hemostatic system with elevations in prothrombin, antithrombin III, and protein S, and a decrease in the tissue plasminogen activator and its inhibitor.

Exogenous testosterone replacement therapy has been associated with the development of venous emboli through directly induced polycythemia, hypertension, and hyperlipidemia but a causation for cardiovascular events has not been established [ 5 ].

Hyperthyroidism has been associated with a higher incidence of coronary artery disease and acute cardiovascular events [ 6 ]. Increased levels of free thyroxine hormone lead to increased concentrations of clotting factors and fibrinogen with a decrease in tissue plasminogen activator leading to a hypercoagulable, hypofibrinolytic environment [ 1 ].

Levothyroxine supplementation in hypothyroidism has not been associated with an increased risk of acute cardiovascular events [ 2 ]. Testosterone affects thyroid hormone carrier proteins causing a decrease in thyroxine-binding globulin, thyroid stimulating hormone, and total T4 but an increase in free T4 and T3 [ 7 ].

The patient demonstrated a similar pattern for his thyroid hormone tests. Armour Thyroid is a porcine desiccated thyroid-derived supplement that was being used by the patient for weight loss.

Due to the lack of standardization, there might have been significant batch-to-batch variation in the number of active ingredients being consumed by the patient. The co-self-administration of Armour Thyroid and testosterone in this patient possibly led to the development of a hypercoagulable, hypofibrinolytic milieu with alterations in the clotting factors and polycythemia.

This would have accelerated the development of a thrombus in his LAD in the absence of underlying atherosclerosis in his coronary arteries. Coadministration of Armour Thyroid and testosterone may cause thromboembolic events.