Thyrotoxicosis factitia: a rare cause of junctional rhythm and cardiac arrest

Abstract

Thyrotoxicosis factitia is a hyperthyroid state due to the accidental or deliberate thyroxine ingestion. It can have many complications depending upon the organ involved. We present a case of a heavy built athlete presenting with cardiac arrest, who was found to be abused the thyroxine hormone for bodybuilding. Electrocardiogram (EKG) was significant for junctional arrhythmias along with interval supraventricular tachycardia (SVT) and bradycardia. The patient ultimately expired due to a failed resuscitation. To our knowledge, this is the first reported case of junctional arrhythmias caused by exogenous thyroxine.

Efficacy of I-131 Treatment Dosage for Hyperthyroidism With Current Institution Formula

“…Sahmaran et al studied the minimally significant changes and reproducibility of 131 I uptake. Gultekin utilized the following formula: Dose = k (MBq/g) × thyroid weight (g)/24-h RAIU; this study has statistically non-significant differences between RAIU measurements; this study has age and remeasurement-related geometric limitations [4]. After reviewing these calculations and formulas, we chose our institute's formula because we believe it is more precise, accurate, and yields better results than other studies.…”

“…The excessive production of thyroid hormone triggers the progression of hyperthyroidism that eventually results in thyrotoxicosis [1]. The predominant causes of hyperthyroidism include toxic multinodular goiter, Graves' disease, thyrotoxicosis factitial (or factitious thyroiditis), postpartum thyroiditis, subacute (or de Quervain) thyroiditis, and Jod-Basedow phenomenon (or iodine-induced hyperthyroidism) [2][3][4][5][6][7]. The excessive intake of pharmaceutical thyroid hormone or thyroxine abuse in weight loss candidates also triggers hyperthyroidism due to factitious thyroiditis [8,9].…”

From hormone replacement therapy to regenerative scaffolds: A review of current and novel primary hypothyroidism therapeutics

“…If too little L-T4 is administered, serum TSH levels remain high and symptoms of hypothyroidism persist, whilst if the dosage is too high, serum TSH levels may decrease excessively, and symptoms of thyrotoxicosis may be encountered. This includes parlous cardiac issues such as tachycardia, arrhythmias, palpitations ( 72 ). Overtreatment with L-T4, which leads to TSH levels below 0.1 mlU/L, has also been shown to be associated with adverse skeletal health, in the form of bone mineral density loss increasing risk for fractures and osteoporosis, especially in elderly patients ( 73 , 74 ).…”

“…Whilst it has been proposed that weekly and intermittent administrations of L-T4 could prevent these issues, a dose sevenfold higher would be required. High doses of L-T4 may lead to a condition known as iatrogenic thyrotoxicosis factitia, when tissue is exposed to high levels of circulating thyroid hormone, causing the patient to experience symptoms of thyrotoxicosis such as palpitations, sweating and anxiety ( 72 ).…”