DISCUSSION
Abiraterone  is an androgen synthesis inhibitor, and its use is to treat metastatic castration-resistant prostate cancer. The drug works by inhibiting the enzyme CYP17A1, which produces androgens such as testosterone. The medication lowers androgen levels, which can inhibit the growth of prostate cancer. While Abiraterone is generally well-tolerated, it has been associated with cardiovascular toxicity. One study found that treatment with Abiraterone has been related to a more significant risk of cardiovascular events, including hypertension, atrial fibrillation, and heart fai lure (13,14).
QT interval extending has been linked to Abiraterone, and this could increase the risk of potentially fatal arrhythmias such as TdP. Bicalutamide  is a medication that is primarily used to treat prostate cancer. Although it is generally well-tolerated, bicalutamide can have some side effects, including cardiovascular effects. Abiraterone is this patient’s primary cause of torsade, although bicalutamide has a synergistic effect by prolonging the QT interval. Abiraterone inhibits the CYP17A1 enzyme, which produces androgen and cortisol hormones. By blocking this enzyme, Abiraterone reduces the synthesis of these hormones while allowing the production of mineralocorticoids to continue. This results in a decrease in the production of glucocorticoids, which generally provide negative feedback on the hormone ACTH. When the enzyme is inhibited, corticosteroid precursors are redirected toward producing mineralocorticoids, increasing their levels. This increase causes hypokalemia (low potassium levels), fluid retention, and swelling in the body. The current collection of literature regarding the pathophysiological mechanisms of hypogonadism in LQTS is quite limited.
Nevertheless, specific research proposes that a potential outcome of the genetic defects responsible for LQTS could be a shortage in testosterone. The study found that males diagnosed with LQTS demonstrated reduced levels of testosterone compared to individuals without the condition. Additionally, there was an observed negative relationship between testosterone levels and the duration of the QT interval. According to the authors, the genetic anomalies responsible for LQTS may potentially impact the synthesis and control of testosterone, hence resulting in the development of hypogonadism. The administration of testosterone replacement treatment resulted in a notable decrease in the duration of the QT interval in males diagnosed with hypogonadism. This finding implies that insufficient levels of testosterone may play a role in the onset and advancement of LQTS. The hERG channel, a distinct type of ion channel, plays a critical role in maintaining regular cardiac activity (15).
In summary, while the exact mechanism of hypogonadism in long QT syndrome is not yet fully understood, there is evidence to suggest that testosterone deficiency may be a consequence of the genetic abnormalities that cause LQTS. Further research is needed to elucidate the relationship between LQTS and hypogonadism fully and to identify potential treatment strategies. In addition, it is necessary to carry out more studies on the risk factors of abiraterone arrhythmogenesis, and patients with a higher risk should be regularly checked for electrolyte disturbances and EKG status after taking workup.
Statement of CONSENT The patient’s family has consented to the participation of this case report. The patient’s next of kin (according to our hospital policy, the eldest male child) has consented to the publication of this case report.