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.