Intentional L-Thyroxine Overdose: A Case Overview

Abstract

Thyroid hormone production begins in the hypothalamus, where thyrotropin-releasing hormone (TRH) stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH). TSH binds to receptors on thyroid follicular cells, activating pathways that drive thyroid hormone synthesis. Within thyrocytes, iodinated thyroglobulin is processed to release T3 (20%) and T4 (80%) into the bloodstream. These hormones influence nearly every organ system by increasing metabolic rate and energy consumption. In the heart, they enhance catecholamine effects, increasing heart rate and cardiac output; in the lungs, they improve oxygenation by stimulating respiratory center. They support muscle development, boost basal metabolic rate, regulate metabolism, and play a critical role in growth and brain maturation in children.

Objectives: The progression of the condition and thyroid hormone levels during recovery following thyroxine poisoning were evaluated and analysed.

Methods: a case analysis and summary.

Results: During the recovery period, thyroid hormone levels gradually increased; however, the patient remained largely asymptomatic. This suggests that the presentation of the condition varies and is not uniform across all age groups.

Conclusions: It remains unclear how thyroxine overdose impacts individuals of different ages with varying presentations. However, it is understood that T3 may act as a competitive inhibitor at receptor sites, mitigating L-thyroxine toxicity and potentially leading to a benign response to overdose.