May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Rosiglitazone May Delay Progression to Proliferative Diabetic Retinopathy
Author Affiliations & Notes
  • L.Q. Shen
    Harvard Medical School, Boston, MA
    Jules Stein Eye Institute, UCLA, Los Angeles, CA
  • A. Child
    Harvard Medical School, Boston, MA
  • D. Magoon
    Harvard Medical School, Boston, MA
  • G. Beebe
    Joslin Diabetes Center, Boston, MA
  • G. Weber
    Harvard Medical School, Boston, MA
  • J. Folkman
    Harvard Medical School, Boston, MA
    Children's Hospital, Boston, MA
  • L.P. Aiello
    Harvard Medical School, Boston, MA
    Dept of Ophthalmology,
    Joslin Diabetes Center, Boston, MA
  • Footnotes
    Commercial Relationships  L.Q. Shen, None; A. Child, None; D. Magoon, None; G. Beebe, None; G. Weber, None; J. Folkman, None; L.P. Aiello, Eli Lilly and Eyetech, C.
  • Footnotes
    Support  HST Student Research Fund, Harvard Medical School
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2333. doi:
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    • Get Citation

      L.Q. Shen, A. Child, D. Magoon, G. Beebe, G. Weber, J. Folkman, L.P. Aiello; Rosiglitazone May Delay Progression to Proliferative Diabetic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2333.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To investigate whether rosiglitazone, an oral medication for diabetes with reported antiangiogenic properties, may delay the development of proliferative diabetic retinopathy (PDR).

Methods: : A longitudinal chart–review study was initiated at the Joslin Diabetes Center (JDC) in 2003. Patients taking rosiglitazone in May, 2003 were included if they received both medical and ophthalmic care from JDC, and had at least one eye exam in the preceding year. A non–glitazone control group matched for baseline characteristics was also included in the study.

Results: : 124 rosiglitazone (rsg) patients and 158 control (ctl) patients were followed for an average of 2.8 + 1.7 years. The two groups were similar (p>0.1) at baseline in age, gender, type and duration of diabetes, HbA1c, blood pressure control, and visual acuity (VA). Final HbA1c was 7.6 and 7.8 in rsg and ctl groups, respectively (p=NS). In patients with severe nonproliferative diabetic retinopathy (NPDR), progression to PDR was 14.3% (2/14 eyes) and 45.8% (11/24 eyes) in the rsg and ctl groups, respectively. When accounting for follow–up duration and loss, development of PDR in rsg group occurred at a slower rate (p=0.0448, Wilcoxon; p=0.0587, Log–Rank). PDR developed in 25% of ctl group within 1 year (95% confidence interval: 122–518 days), while rsg group had not reached this point after 2.5 years. Average final VA was 20/34 in rsg group and 20/46 in ctl. In patients with moderate NPDR, 11.1% (4/36 eyes) and 12.5% (7/56 eyes) developed PDR in rsg and ctl groups, respectively (p=NS). The rates of developing clinically significant macular edema (CSME) in patients with no edema at baseline were 6.5% (12/184 eyes) and 4.5% (10/222 eyes), respectively (p=NS).

Conclusions: : Previous in vitro and animal studies have identified antiangiogenic activity of rosiglitazone. This preliminary, relatively short–term pilot study suggests that rosiglitazone therapy may delay ocular neovascularization in diabetic patients and supports continued evaluation of this cohort as well as more definitive future investigations.

Keywords: diabetic retinopathy • clinical (human) or epidemiologic studies: treatment/prevention assessment/controlled clinical trials • neovascularization 

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