Refractive changes after pharmacologic resolution of diabetic macular edema.
OBJECTIVE
To determine precisely the mean change in refractive power induced by treatment in patients with diabetic macular edema (DME).


METHODS
Prospective, randomized study.


METHODS
Fifty eyes of 50 consecutive patients with clinically significant macular edema receiving all 3 types of current state-of-the-art treatment with intravitreal antiedematous substances (ranibizumab, bevacizumab, or triamcinolone).


METHODS
Patients were followed up at monthly intervals and were treated following a standardized pro re nata regimen according to protocol. Best-corrected visual acuity (BCVA) was determined by certified visual acuity examiners. The refractive power of the treated eyes was determined using a push-plus technique. The change in refraction between baseline and the visit when the macula was completely dry or when the central subfield thickness (CST) measured by optical coherence tomography had reached the thinnest level was analyzed.


METHODS
Spherical equivalent refraction (SER) and CST.


RESULTS
Fifty eyes of 50 patients received intravitreal therapy using ranibizumab (n = 11), bevacizumab (n = 20), or triamcinolone (n = 19). Mean BCVA was 0.33±0.23 logarithm of the minimum angle of resolution (logMAR) and mean CST was 492±130 μm. The mean SER was 0.41±2.06 diopters (D) at baseline. The BCVA at the time of optimal retinal morphologic features was 0.24±0.2 logMAR, mean CST was 300±78 μm, and mean change in SER was -0.01±0.46 D. Changes is BCVA and CST were statistically significant (P < 0.0001), but the SER change was not (P = 0.824).


CONCLUSIONS
Appropriate spectacle correction can be prescribed to patients with DME any time during ongoing therapy using antiedematous substances because resolution of retinal thickening is not associated with an increased risk of a myopic shift.
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
Gábor G
GG
Deák
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
Jan
J
Lammer
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
Sonja
S
Prager
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
Georgios
G
Mylonas
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria.
Matthias
M
Bolz
Department of Ophthalmology, Medical University of Vienna, Vienna, Austria. Electronic address: ursula.schmidt-erfurth@meduniwien.ac.at.
Ursula
U
Schmidt-Erfurth
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000068258:Bevacizumab; D003930:Diabetic Retinopathy / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D005451:Fluorescein Angiography; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D058449:Intravitreal Injections; D008269:Macular Edema / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000069579:Ranibizumab; D012029:Refraction, Ocular / Q000502:physiology*; D012030:Refractive Errors / Q000503:physiopathology*; D041623:Tomography, Optical Coherence; D014222:Triamcinolone Acetonide / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014792:Visual Acuity / Q000502:physiology
D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D005938:Glucocorticoids; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D014222:Triamcinolone Acetonide; D000069579:Ranibizumab