Implication of pharmacogenetic polymorphism in the development of bilateral acute iris illumination syndrome (BAIT) in a cohort of Colombian patients.

Bilateral acute iridious transillumination syndrome (BAIT) is a relatively new clinical entity, first described in 2004 as an adverse effect related to Moxifloxacin.

Over the years, different hypotheses have emerged as possible reasons why this disease may occur, however, the most accepted hypothesis in the literature proposes that the drug, due to its high affinity to melanin-rich tissues, may cause toxic effects, such as the release of iridiated pigments into the aqueous humor.

It is also important to highlight that this disease causes a high impact on the quality of life of the patients, since many of the manifestations that occur are irreversible; for example, these patients present permanent mydriasis media due to a damage of the pupillary sphincter, causing severe photophobia that prevents them from performing an important number of daily activities.

The present study aims to contribute to the analysis of the involvement of pharmacogenes in the etiology and BAIT syndrome. The results obtained from this study could lead to the identification of pharmacogenetic markers that allow us to predict this adverse reaction to moxifloxacin.

In this way, we could be able to prevent the disease and also make a timely diagnosis of it, taking into account the model of personalized medicine.

Pharmacogenetics, Ophthalmology, Adverse reaction.