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.