Systemic factors associated with poor anatomical response to anti-VEGF therapy in patients with diabetic macular edema: evidence from a large clinical cohort - Report - MDSpire
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Systemic Influences Linked to Suboptimal Anatomical Outcomes Following Anti-VEGF Treatment in Diabetic Macular Edema Patients: Insights from a Large Clinical Cohort
Systemic Influences Linked to Suboptimal Anatomical Outcomes Following Anti-VEGF Treatment in Diabetic Macular Edema Patients
Overview
This study investigates systemic factors affecting anatomical responses to anti-VEGF therapy in diabetic macular edema (DME) patients. Key findings indicate that metabolic status, particularly HbA1c and fasting glucose levels, correlate with treatment outcomes.
Background
Diabetic macular edema (DME) is a major cause of vision impairment among working-age individuals globally. Despite the effectiveness of anti-VEGF therapy as a first-line treatment, many patients do not achieve optimal anatomical responses, highlighting the need to understand systemic influences on treatment efficacy.
Data Highlights
Measure
Baseline
3-Month Follow-Up
P-Value
Central Macular Thickness (CMT)
325.00 μm (IQR: 281.00–448.00 μm)
291.00 μm (IQR: 268.00–334.00 μm)
< 0.001
Best-Corrected Visual Acuity (BCVA)
0.30 (IQR: 0.15–0.50)
0.40 (IQR: 0.25–0.50)
< 0.001
Key Findings
Median CMT decreased from 325.00 μm to 291.00 μm after three months of treatment.
Median BCVA improved from 0.30 to 0.40 during the same period.
41.48% of eyes were classified as responders based on a >10% reduction in CMT.
Baseline CMT, BCVA, LDL-C, fasting blood glucose, and HbA1c were independently associated with CMT reduction.
Higher baseline BCVA and elevated fasting blood glucose were linked to poor anatomical response.
Clinical Implications
The findings indicate that systemic metabolic factors, such as HbA1c and fasting glucose levels, are associated with treatment outcomes in DME patients undergoing anti-VEGF therapy.
Conclusion
Systemic metabolic status significantly influences the anatomical response to anti-VEGF treatment in DME patients.