Is There An Association Between Masculinizing Hormone Therapy And Cataract Development?

To report a unique case of a young transgender man who presented with bilateral mature cataracts following masculinizing hormone therapy, with subsequent literature review

Tennent Institute of Ophthalmology, Gartnavel General Hospital, Glasgow, United Kingdom.

A 27-year-old transgender man (female-to-male) presented with bilateral gradual visual deterioration over 6 months (Hand Movements Right and 6/60 Left initially; Left reduced to counting fingers at time of surgery).  Mature white cataracts were diagnosed, and successfully treated with phacoemulsification, resulting in 6/6 vision. No cataractogenic risk factors were identified except patient’s father had cataracts aged 45. The patient reported receiving 12-weekly intramuscular testosterone undecanoate over the previous 5 years as transitioning masculinizing hormone therapy and questioned if it could have accelerated cataract development.

Our literature review revealed a paucity of data on the relationship between androgens and cataract. One animal study suggested that chick lenses become opaque in the presence of exogenous testosterone, but in a human study no association was seen between blood testosterone levels and cataract. Higher levels of dehydroepiandrosterone sulfate (DHEAS), a biologically active androgen, has been associated with reduced cataract risk in postmenopausal women. However, studies have not shown exogenous testosterone consistently raises DHEAS levels in transgender men. Data surrounding parity, menarche, menopause and hormone replacement therapy in women generally supports a protective role of endogenous and exogenous oestrogen on the crystalline lens.

No conclusive evidence exists regarding any link between masculinizing hormone therapy and cataractogenesis. Our patient may have genetic predisposition for pre-senile cataract given their family history. We hypothesise such significant cataractogenesis may have been accelerated by rapid oestrogen suppression secondary to exogenous testosterone administration in this patient, rather than as a direct effect. More research is needed, as this clinical scenario has not been previously reported.