OBJECTIVE: To evaluate whether rosiglitazone maleate, an oral peroxisome-proliferating activated receptor gamma agonist and oral insulin sensitizing agent with potential antiangiogenic activity, delays onset of proliferative diabetic retinopathy (PDR). METHODS: Longitudinal medical record review of all patients treated with rosiglitazone receiving both medical and ophthalmic care at the Joslin Diabetes Center from May 1, 2002, to May 31, 2003 (N = 124), and matched control patients not taking a glitazone drug (N = 158). The mean duration of follow-up was 2.8 years (range, 0.3-9.0 years). RESULTS: Baseline characteristics and final hemoglobin A(1c) values (7.6% and 7.8%, respectively) were similar in the rosiglitazone and control groups (P = .10). In eyes with severe nonproliferative diabetic retinopathy at baseline (rosiglitazone group, 14 eyes; control group, 24 eyes), progression to PDR over 3 years occurred in 19.2% in the rosiglitazone group and 47.4% in the control group, representing a 59% relative risk reduction (Wilcoxon, P = .045; log-rank, P = .059). Fewer eyes in the rosiglitazone group experienced 3 or more lines of visual acuity loss (P = .03). The incidence of diabetic macular edema was similar in both groups. CONCLUSIONS: Rosiglitazone may delay the onset of PDR, possibly because of its antiangiogenic activity. Future clinical investigations should consider analysis of this potential benefit along with ongoing evaluation of potential cardiac risk in studies where the risk-benefit profiles are deemed appropriate.
OBJECTIVE: To evaluate whether rosiglitazone maleate, an oral peroxisome-proliferating activated receptor gamma agonist and oral insulin sensitizing agent with potential antiangiogenic activity, delays onset of proliferative diabetic retinopathy (PDR). METHODS: Longitudinal medical record review of all patients treated with rosiglitazone receiving both medical and ophthalmic care at the Joslin Diabetes Center from May 1, 2002, to May 31, 2003 (N = 124), and matched control patients not taking a glitazone drug (N = 158). The mean duration of follow-up was 2.8 years (range, 0.3-9.0 years). RESULTS: Baseline characteristics and final hemoglobin A(1c) values (7.6% and 7.8%, respectively) were similar in the rosiglitazone and control groups (P = .10). In eyes with severe nonproliferative diabetic retinopathy at baseline (rosiglitazone group, 14 eyes; control group, 24 eyes), progression to PDR over 3 years occurred in 19.2% in the rosiglitazone group and 47.4% in the control group, representing a 59% relative risk reduction (Wilcoxon, P = .045; log-rank, P = .059). Fewer eyes in the rosiglitazone group experienced 3 or more lines of visual acuity loss (P = .03). The incidence of diabetic macular edema was similar in both groups. CONCLUSIONS:Rosiglitazone may delay the onset of PDR, possibly because of its antiangiogenic activity. Future clinical investigations should consider analysis of this potential benefit along with ongoing evaluation of potential cardiac risk in studies where the risk-benefit profiles are deemed appropriate.
Authors: Andreas Stahl; Tim U Krohne; Przemyslaw Sapieha; Jing Chen; Ann Hellstrom; Emily Chew; Frank G Holz; Lois E H Smith Journal: Br J Ophthalmol Date: 2011-03-18 Impact factor: 4.638
Authors: Walter T Ambrosius; Ronald P Danis; David C Goff; Craig M Greven; Hertzel C Gerstein; Robert M Cohen; Matthew C Riddle; Michael E Miller; John B Buse; Denise E Bonds; Kevin A Peterson; Yves D Rosenberg; Letitia H Perdue; Barbara A Esser; Lea A Seaquist; James V Felicetta; Emily Y Chew Journal: Arch Ophthalmol Date: 2010-03
Authors: P J Simpson-Haidaris; S J Pollock; S Ramon; N Guo; C F Woeller; S E Feldon; R P Phipps Journal: PPAR Res Date: 2010-02-28 Impact factor: 4.964