SAT-179 Methylphenidate and Hypogonadism- An Interesting Case

Abstract Disclosure: S. Sivakumar: None. O. Jafery: None. S. Chandrasekar: None. Introduction: Methylphenidate is the first-line drug used in the comprehensive treatment program for ADHD. The use of psychotropic medications including Methylphenidate has surged in the past decade, especially in young children. However, the side effect profile of this drug remains under-evaluated. Hypogonadism has been increasingly reported in the pre-pubertal age group with escalating use of this drug. Cardiovascular problems, and behavioural and mood problems are the commonest known side effects of methylphenidate. However, how this drug affects the human reproductive system and causes gonadotrophic side effects is not studied much. It has previously been shown to cause hypogonadism in non-human primates and reduce testosterone concentration in mice. Case: A 16-year-old boy was seen in Endocrinology clinic who had been suffering from gynaecomastia. He was diagnosed with ADHD 4 years ago and started on methylphenidate. He developed gynaecomastia significant enough to affect him psychologically leading to reduced social interactions. Hormone panel showed low FSH, LH and testosterone. Later Methylphenidate was stopped by psychiatrist as part of his ADHD treatment for 4 months. On examination at this time, he had normal secondary sexual characteristics. Gynaecomastia was evident with areolar enlargement with a slight increase in breast tissue. Surprisingly, a repeat hormone panel after stopping this drug for around a year revealed normal LH, FSH, and testosterone levels. An ultrasound scan of the breasts showed increased adipose tissue in the subareolar region without any increase in fibro glandular tissue (pseudo gynaecomastia). DEXA scan showed reduced bone mineral density, MRI showed normal pituitary gland, Ultrasound scan showed normal sized testes with mild varicocele. Discussion: Methylphenidate blocks the reuptake of dopamine and noradrenaline in presynaptic neurons and inhibits their transport thereby increasing the dopamine concentration which creates a stimulant effect. The exact mechanism by which this drug causes hypogonadism is unclear, but it is speculated that methylphenidate acts on alpha and beta receptors in testes. The possibility of pre-testicular azoospermia due to stimulant medication-induced pituitary failure and dopamine excess is another proposal. Though there is ambiguity in the pathophysiologic connection, studies have shown that long-term use of ADHD medications could increase the risk of hypogonadism in post-pubertal males. Conclusion: Long-term use of methylphenidate has been shown to cause hypogonadism in animals however research in human samples is limited. The medication is very effective in the treatment of ADHD and with current escalating trends in the use of methylphenidate, strict guidelines should be there to monitor gonadal function, especially in children which can help them attain healthy puberty. Presentation: Saturday, July 12, 2025