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Pretreatment vitamin D levels were associated with endoscopic improvement in patients with UC and decreased C-reactive protein levels in patients with CD.
Vitamin D may affect clinical and endoscopic outcomes in patients with inflammatory bowel disease (IBD) treated with vedolizumab, according to findings from a retrospective study.
Greater pretreatment vitamin D levels were associated with an increase in endoscopic improvement among patients with ulcerative colitis (UC) and greater nutritional and supplementation improvements in patients with Crohn disease (CD).1
“Treatment failure may be due to alternate immune pathways not targeted by current mediations, low drug levels, antibody formation to a biologic, or suboptimal nutrition. Ideally, we would be able to personalize the care for our patients by identifying factors that predict response to therapy, thus allowing us to choose the appropriate medication with the best efficacy,” wrote investigators.1
Patients with IBD are at risk for micronutrient deficiencies as a result of active bowel inflammation, food avoidance, and medical or surgical treatments, potentially leading to other health complications and impacting treatment outcomes. Vitamin D plays an important role in modulating the immune system, raising questions regarding its impact on clinical and endoscopic responses to therapy.2
Bincy Abraham, MD, MS, distinguished professor and director of the Fondren Inflammatory Bowel Disease Program at the Underwood Center for Digestive Disorders at Houston Methodist Hospital, and colleagues sought to determine the impact of vitamin D levels on clinical response and endoscopic improvement among patients with IBD treated with vedolizumab. Patients between 18 and 80 years of age with UC or CD who were seen at the Fondren IBD program at Houston Methodist and treated with vedolizumab for at least 6 months from 2018 to 2022 were included in the study. Patients diagnosed with indeterminate colitis or short bowel syndrome, on total parental nutrition, on vedolizumab less than 6 months, or considering discontinuing vedolizumab within the next 4 months were excluded from the study.1
In total, 88 patients were enrolled in the study, half (n = 44) with CD and half (n = 44) with UC. The median age of the cohort was 39.5 (Interquartile range [IQR], 31.0- 53.25) years, 30 (34%) patients were male, and 71 (80.7%) were Caucasian. Investigators noted there were no statistically significant differences in age, gender, race, or number of prior therapies between the CD and UC groups.1
All participants received an induction dose of 300 mg vedolizumab at 0, 2, and 6 weeks, then maintenance dosing as standard of care thereafter. Disease outcome was examined based on clinical, lab, and endoscopic assessments. Investigators assessed factors prior to the initiation of therapy that best predicted treatment response, including clinical information on disease location and severity, nutritional status, prior medications, and levels of vedolizumab therapy.1
Of the 44 patients with UC, 34 had pre-vedolizumab vitamin D levels. In patients with UC with vitamin D ≥ 30 ng/mL at the initiation of vedolizumab therapy, investigators noted UC Endoscopic Index of Severity (UCEIS) scores after 6 months of therapy were significantly decreased compared to those with low pretreatment vitamin D levels (1.5 vs 3.87; P = .037). No statistically significant difference between groups in ESR, clinical scores, CRP, fecal markers, iron, vitamin B12, folate, or zinc was observed prior to vedolizumab therapy or after treatment, regardless of vitamin D status.1
After treatment, statistically significant decreases in the UC Activity Index and UCEIS scores were observed (both P < .001). Vitamin D levels improved significantly from 33.2 (IQR, 25.0-38.8) to 45.0 (IQR, 29.5-60.0) (P = .008) ng/mL after vedolizumab initiation. Of note, improvements in vitamin D levels were more significant in the greater pretreatment vitamin D group compared to the lower pretreatment vitamin D group (P = .007).1
Of the 44 patients with CD, 31 had pre-vedolizumab vitamin D levels. Patients with CD with vitamin D ≥ 30 ng/mL at the initiation of vedolizumab therapy had greater iron saturation (12% vs 25%; P = .008) and vitamin B12 levels (433.5 vs 885 pg/mL; P = .003) than those with vitamin D < 30 ng/mL. After treatment, patients with greater pretreatment vitamin D levels had significantly greater vedolizumab levels (27.35 μg/mL) compared to those with low pretreatment vitamin D (14.35 μg/mL; P = .045).1
Statistically significant improvements in the Harvey–Bradshaw Index (P = .002), SES-CD (P = .002), and ESR (P = .004) were observed. As in the UC group, the vitamin D levels in patients with CD improved after the initiation of vedolizumab, increasing from 23.0 (IQR, 17.0-36.0) to 31.0 (IQR, 24.0-51.7) ng/mL (P = .007). Iron and iron saturation levels also improved significantly with vedolizumab therapy (both P < .001), although iron saturation improved more significantly in the greater vitamin D group (24 vs 35.5 ng/mL; P = .007). Investigators pointed out pre- and post-treatment clinical scores, inflammatory markers, endoscopic scores, and folate and zinc levels were similar regardless of the vitamin D levels.1
Although there was a statistically significant decrease in CRP among patients with CD with baseline CRP > 5 mg/dL who had greater improvements in vitamin D (R2 = 0.3; P = .03), the same was not true among patients with UC (R2 = 0.03; P = .589). No other parameters correlated with changes in vitamin D levels.1
“This study suggests that vitamin D can play a role in clinical and endoscopic outcomes and should be assessed routinely and optimized in patients with IBD in a prospective study,” concluded investigators.1
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