Macular edema constitutes a serious pathologic entity of ophthalmology
resulting in vision loss with a remarkable impact on the quality of life
of patients. It is the final common pathway of various systemic diseases
and underlying intraocular conditions, with diabetes mellitus being the
most frequent cause. Other causes include venous occlusive disease,
intraocular surgery, and inflammatory conditions of the posterior
segment of the eye. Macular edema is a recognized side effect of various
systemic and local medications and requires special consideration among
ophthalmologists and other clinicians. Recently, antidiabetic
thiazolidinediones have been implicated in the development of macular
edema, and a review of the English literature revealed that other
systemically administered drugs like fingolimod, recently approved for
relapsing forms of multiple sclerosis, the anticancer agents tamoxifen
and the taxanes, as well as niacin and interferons have been reported to
cause macular edema. Ophthalmologic pharmaceutical agents, like
prostaglandin analogs, epinephrine, timolol, and ophthalmic preparation
preservatives have also been reported to cause macular edema as an
adverse event. The purpose of this article is to provide a short,
balanced overview of the available evidence in this regard. The
available data and the possible pathophysiologic mechanisms leading to
the development of macular edema are discussed. Possible therapeutic
strategies for drug-induced macular edema are also proposed
