There have been several reports on the use of Minocycline, a common antibiotic used to treat Acne, which might have a beneficial effect in the treatment of certain types of macular degeneration and diabetic macular edema. Please contact the office for a record review to see if you have this type of macular degeneration and if you are a candidate for treatment

ARVO Annual Meeting Abstract | April 2010
Minocycline Protects Retinal Pigment Epithelial Cells From Chronic Oxidative Stress

Abstract
Purpose: Multiple pathologic processes are involved in neovascular age-related macular
degeneration (AMD). Current therapies focus on the control of active neovascularization.
There is increasing interest in incorporating therapies that block other pathophysiologic
processes not directly related to neovascularisation such as inflammation to preserve
long-term vision. Minocycline, a semisynthetic tetracycline has been shown to have
immunomodulatory effects on the infammatory process. Minocycline is proposed as an
anti-inflammatory agent to protect retinal pigment epithelial cells. This study investigated
the effect of Minocycline on oxidative stress-induced RPE cell damage.

Methods:  ARPE-19 cells were maintained in Dulbecco’s modified Eagle medium
supplemented with glutamine, penicillin, streptomycin, amphotericin, and 10% fetal calf
serum. Cells were exposed to hydrogen peroxide as a source of oxidative stress, then
exposed to varying concentrations of Minocycline. Cell counts for viability were performed
after exposure to acute and chronic oxidative stress conditions and Minocycline exposure.

Results:  Comparison of cell count viability data with the Mann Whitney test showed no
difference between acute oxidative stress exposure alone and with Minocycline
(p=0.11)After chronic oxidative stress exposure cell viability counts increased signifcantly
after exposure to Minocycline (p=0.04)

Conclusions: The results suggest minocycline protects retinal pigment epithelial cells
from the effects of chronic oxidative stress in culture and supports the potential role of
Minocycline as an adjuvant treatment for neovascular AMD.

Oral Minocycline for the Treatment of Diabetic Macular Edema (DME): Results of a Phase I/II Clinical Study
Catherine A. Cukras, Philip Petrou, Emily Y. Chew

Division of Epidemiology and Clinical Applications, and the
Unit on Neuron-Glia Interactions in Retinal Disease, National Institutes of Health, Bethesda, Maryland.

Abstract
Purpose.
Inflammation contributes significantly to the pathogenesis of diabetic macular edema (DME). In particular, retinal microglia demonstrate increased activation and aggregation in areas of DME. Study authors investigated the safety and potential efficacy of oral minocycline, a drug capable of inhibiting microglial activation, in the treatment of DME.
Methods.
A single-center, prospective, open-label phase I/II clinical trial enrolled five participants with fovea-involving DME who received oral minocycline 100 mg twice daily for 6 months. Main outcome measurements included best-corrected visual acuity (BCVA), central retinal subfield thickness (CST), and central macular volume using spectral-domain optical coherence tomography (SD-OCT) and late leakage on fluorescein angiography (FA).
Results.
Findings indicated that the study drug was well tolerated and not associated with significant safety issues. In study eyes, mean BCVA improved continuously from baseline at 1, 2, 4, and 6 months by+1.0, +4.0, +4.0, and +5.8 letters, respectively, while mean retinal thickness (CST) on OCT decreased by −2.9%, −5.7%, −13.9, and −8.1% for the same time points. At month 6, the mean area of late leakage on FA decreased by −34.4% in study eyes. Mean changes in contralateral fellow eyes also demonstrated similar trends. Improvements in outcome measures were not correlated with concurrent changes in systemic factors.

Conclusions.
In this pilot proof-of-concept study of DME, minocycline as primary treatment was associated with improved visual function, central macular edema, and vascular leakage, comparing favorably with historical controls from previous studies. Microglial inhibition with oral minocycline may be a promising therapeutic strategy targeting the inflammatory etiology of DME.

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