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Potent Oral Hypoglycemic Agents for Microvascular Complication: Sodium-Glucose Cotransporter 2 Inhibitors for

Eun Hyung Cho1, Se-Jun Park2, Seongwook Han3

  • 1Kong Eye Hospital, Seoul, Republic of Korea.

Journal of Diabetes Research
|January 10, 2019
PubMed

Insights

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) significantly slowed diabetic retinopathy (DR) progression in type 2 diabetes patients compared to sulfonylurea. This protective effect on DR progression was observed independently of glycemic control improvements.

Area of Science:

  • Endocrinology
  • Ophthalmology
  • Pharmacology

Background:

  • Diabetic retinopathy (DR) is a leading cause of vision loss in type 2 diabetes.
  • Understanding treatments that mitigate DR progression is crucial for patient outcomes.

Purpose of the Study:

  • To investigate the impact of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on diabetic retinopathy (DR) progression.
  • To compare the effects of SGLT2i versus sulfonylurea on DR in type 2 diabetes patients.

Main Methods:

  • Retrospective review of medical records for 21 type 2 diabetes patients on SGLT2i and 71 on sulfonylurea.
  • Diabetic retinopathy severity assessed using the Early Treatment Diabetic Retinopathy Study (ETDRS) scale.
  • Propensity score matching used to adjust for confounding factors like age, diabetes duration, initial DR grade, and HbA1c.

Main Results:

  • Fewer patients on SGLT2i showed DR progression compared to sulfonylurea users (14% vs. 44%, P=0.014).
  • SGLT2i treatment was associated with a significantly lower risk of DR progression (P=0.021).
  • This protective effect remained significant after propensity score matching (P=0.013), independent of glycemic control.

Conclusions:

  • Sodium-glucose cotransporter 2 inhibitors (SGLT2i) demonstrate a potential to slow diabetic retinopathy progression in type 2 diabetes.
  • The observed benefit of SGLT2i on DR progression appears independent of their glucose-lowering effects.
  • Further research is warranted to confirm and elucidate the mechanisms behind SGLT2i's effect on DR progression.

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