Introduction
Tyrosine kinase inhibitors (TKIs) are highly efficient in the treatment of Chronic Myeloid Leukemia (CML). However, this is usually a lifelong therapy for a great number of patients (only approximately 20% are able to stop this medication safely and permanently). Therefore, adverse events of TKIs are a matter of debate (usually infrequent, manageable and different according to the TKI in use; the most common are muscular pain, fatigue, arthritis, pleural effusions, cardiac toxicity and diarrhea) [1, 2].
Ocular toxicity is classified as a rare adverse event, but also assumed to be underestimated and under-reported [2]. In general, the most common ocular events are periorbital and eyelid edema, erosion of the epithelial surface (keratitis), corneal opacity, blurred vision, periocular pain and conjunctivitis, serous retinal detachment (a rare event; fluid accumulates under the layers of the retina and symptoms include blurred vision, often in both eyes) [3-5]. These events are usually seen in the initial phases of treatment. The decision to reduce dose, hold or discontinue a TKI is complex and should be made after a risk–benefit analysis [2]. The mechanism underlying seems to be connected to the platelet-derived growth factor receptor (PDGFR) and the c-kit marker in mast cells [2]. It was found that the PDGFR is responsible for maintaining the interstitial pressure in the dermis, also expressed in the periocular tissue (as c-kit). TKIs can inhibit these receptors and increased capillary permeability and fluid extravasation [6-7]. The targeting of c-kit–positive mast cells on the conjunctiva can also cause subconjunctival hemorrhage, an event described with Imatinib [6].
The authors report here a case of progressive ocular impairment in a CML patient treated with three different TKIs, raising the issue of ocular toxicity caused by these drugs.