Vitamin D and RNFL Thickness in MS Patients without a History of Optic Neuritis

Background: Vitamin D deficiency has been associated with increased risk for developing Multiple Sclerosis (MS) as well as increased disease severity. Appropriate Vitamin D levels may have a modulating effect on inflammation/demyelination and axonal damage. Thinning of Retinal Nerve Fiber (RNFL) layer has been documented in MS patients with and without a history of optic neuritis (ON). Optical Coherence Tomography (OCT) offers a quick, reliable and non-invasive way to assess the RNFL. 

Objectives: To determine the association of Vitamin D and the RNFL in MS patients without a history of ON.  The objective of this cross-sectional study is to compare RNFL thickness in patients that are Vitamin D insufficient to that of those with normal serum levels.  Our hypothesis is that individuals that have insufficient Vitamin D levels will show a decrease of the RNFL thickness –independent form inflammation- compared to the sufficient group. 

Methods: The study cohort included 55 patients diagnosed with MS that had OCT testing to assess RNFL and macular thickness.  Vitamin D level (25(OH)D) was evaluated at the same time. Vitamin D insufficiency was defined as <30 ng/mL and sufficiency defined as ≥30 ng/mL.  Outcome measures of OCT were compared between the Vitamin D insufficient group and the Vitamin D sufficient group.

Results: :This study included 37 patients (mean 44.5 years old) that were Vitamin D insufficient (mean 18 ng/mL), and 18 patients (mean 51 years old) that were Vitamin D sufficient (mean 46 ng/mL).  Vitamin D insufficiency (seen in 67% of patients) was associated with thicker measures of Inferior quadrant (116 vs 103 µm, p=0.045) and average macular thickness (274 vs 261 µm, p=0.031). All the other OCT measures were also thicker in the Vitamin D insufficient group compared to that of the sufficient group, but did not reach significance. 

Conclusions: MS individuals without a history of ON and with vitamin D insufficiency have less thinning of the RNFL than those with normal Vitamin D levels.  RNFL volume loss in MS patients without history of ON is presumably due to a neurodegenerative process and not to an inflammatory/demyelinating event. Given that the group with insufficient vitamin D did not have more retinal axonal loss, the role of Vitamin D in reducing MS disease severity is probably related to anti-inflammatory activity. Further longitudinal studies are warranted to see if vitamin D ultimately impacts the degree of axonal loss measured by OCT.