Key result
GLP-1a therapy preserved endothelial function in multiple sclerosis patients over 12 months (RHI 2.1 vs 2.1), whereas the control group experienced significant worsening (RHI 2.1 vs 1.8; p=0.030).
Why the study?
Patients with multiple sclerosis have increased vascular risk, but the effects of GLP-1 agonists on endothelial function in these patients were unclear.
Does dulaglutide prevent worsening of endothelial function in patients with multiple sclerosis?
Cohort (n=25)
No
Does dulaglutide prevent worsening of endothelial function in patients with multiple sclerosis?
Effect estimate: beta = 0.560
Absolute Event Rate: 2.1% vs 1.8%
p-value: p=0.003
GLP-1a therapy may prevent the worsening of endothelial function and improve antioxidant capacity in patients with multiple sclerosis, potentially mitigating vascular risk.
GLP-1a may stabilize endothelial function and raise antioxidant capacity in active MS; hypothesis-generating for vascular protection, needing RCTs before practice change.
Introduction: Epidemiological studies have suggested an increased vascular risk in patients with multiple sclerosis (MS). There is increasing evidence of the beneficial effects of GLP-1 agonists (GLP-1a) in preventing vascular complications and slowing the progression of neurodegeneration. Our objective was to explore the changes in the endothelial function of MS patients after 12 months of GLP-1a therapy. We also explored the role of lipoprotein subfractions and the antioxidant capacity of plasma. Methods: MS patients were enrolled in a prospective, unicentric study. GLP-1a (dulaglutide) was administered to 13 patients. The control population consisted of 12 subjects. Endothelial function was determined by peripheral arterial tonometry and expressed as reperfusion hyperemia index (RHI). Trolox equivalent antioxidant capacity (TEAC) was used to assess the total antioxidant capacity of the plasma. The levels of lipoprotein subfractions were evaluated. Results: The GLP-1a group did not have a significant change in their RHIs after 12 months (2.1 ± 0.6 vs. 2.1 ± 0.7; p = 0.807). However, a significant increase in their TEACs was observed (4.1 ± 1.4 vs. 5.2 ± 0.5 mmol/L, p = 0.010). On the contrary, the subjects in the control group had a significant worsening of their RHIs (2.1 ± 0.5 vs. 1.8 ± 0.6; p = 0.030), without significant changes in their TEACs. Except for a significant decrease in very-low-density lipoprotein (VLDL) (30.8 ± 10.2 vs. 22.6 ± 8.3 mg/dL, p = 0.043), no other significant changes in the variables were observed in the control group. VLDL levels (beta = −0.637, p = 0.001), the use of GLP-1a therapy (beta = 0.560, p = 0.003), and small LDL (beta = 0.339, p = 0.043) were the only significant variables in the model that predicted the follow-up RHI. Conclusion: Our results suggest that the application of additional GLP-1a therapy may have atheroprotective and antioxidant effects in MS patients with high MS activity and thus may prospectively mitigate their vascular risk. However, the lipoprotein profile may also play an important role in the atherogenic risk of MS subjects.
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Hardoňová et al. (2023) conducted a cohort in Multiple Sclerosis (n=25). GLP-1a (dulaglutide) vs. Control group was evaluated on Reperfusion hyperemia index (RHI) (beta = 0.560, p=0.003). GLP-1a therapy preserved endothelial function in multiple sclerosis patients over 12 months (RHI 2.1 vs 2.1), whereas the control group experienced significant worsening (RHI 2.1 vs 1.8; p=0.030).
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