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

Bilateral acute iridium 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 can occur; however, the most accepted hypothesis in the literature proposes that the drug, due to its high affinity to melanin-rich tissues, can cause side effects. toxic, as is the release of iridium pigments into the aqueous humor.

It is also important to highlight that this disease has a high impact on the quality of life of patients, since many of the manifestations that occur are irreversible; For example, these patients present permanent median mydriasis due to damage to the pupillary sphincter, thus causing severe photophobia that prevents them from carrying out a significant number of daily activities.

The present study intends to contribute to the analysis of the involvement of pharmacogenes in the etiology and of the 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, it could prevent the disease and also make a timely diagnosis of it, taking into account the model of personalized medicine.

The information that is obtained.