Nutrients, Vol. 17, Pages 3698: High Prevalence and Clinical Associations of Vitamin D Deficiency in Inflammatory Bowel Disease: Evidence from a Tertiary Center Cohort
Nutrients doi: 10.3390/nu17233698
Authors:
Theodora Kafentzi
Ploutarchos Pastras
Ioanna Aggeletopoulou
Efthymios P. Tsounis
Georgios Geramoutsos
Nikitas Kimiskidis
Maria Bali
Konstantinos Thomopoulos
Georgia Diamantopoulou
Georgios Theocharis
Christos Triantos
Background/Objectives: Vitamin D in its active form, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], plays a critical role in immune regulation, gut barrier function, and systemic inflammation. Its deficiency is frequent in Inflammatory Bowel Disease (IBD), but the clinical implications remain uncertain. The aim of the study is to assess the prevalence of vitamin D deficiency in a well-characterized IBD cohort in Western Greece, and explore its associations with clinical features, laboratory biomarkers, and treatment intensity. Methods: In this cross-sectional study, 184 consecutive, well-characterized IBD outpatients followed at a tertiary referral center in Western Greece underwent clinical evaluation and laboratory testing between January 2023 and December 2024. Vitamin D is determined by measuring 25-hydroxyvitamin D [25(OH)D], which reflects the body’s vitamin D stores due to its longer half-life compared with the biologically active form. Deficiency was defined as serum 25(OH)D < 20 ng/mL. Associations with disease type, clinical and laboratory biomarkers, severity indices, and treatment were analyzed using multivariate logistic regression. Results: Vitamin D deficiency was identified in 67 patients (36.4%). Although unrelated to disease type, hospitalization, surgery, or disease activity indices, deficiency correlated with systemic inflammation, nutrition/metabolic markers, and treatment intensity. More specifically, vitamin D-deficient patients exhibited higher platelet counts (p = 0.005) and erythrocyte sedimentation rate (ESR) (p = 0.014), lower hemoglobin (p = 0.005), albumin (p = 0.011), and serum glutamic-oxaloacetic transaminase (SGOT) (p = 0.009) levels and more frequent use of biologic therapy (p = 0.009). In multivariate analysis, vitamin D deficiency remained independently associated with biologic therapy (aOR = 0.374; 95% CI: 0.148–0.946), platelet count (aOR = 0.996, 95% CI: 0.992–0.999), and SGOT (aOR = 1.05, 95% CI: 1.00–1.10), indicating consistent links between vitamin D deficiency and treatment intensity, systemic inflammation, and nutritional or metabolic status. Conclusions: Vitamin D deficiency is common among IBD patients and independently associates with systemic inflammation, metabolic impairment, and intensified treatment requirement, supporting its potential role as a marker of disease burden.
Background/Objectives: Vitamin D in its active form, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], plays a critical role in immune regulation, gut barrier function, and systemic inflammation. Its deficiency is frequent in Inflammatory Bowel Disease (IBD), but the clinical implications remain uncertain. The aim of the study is to assess the prevalence of vitamin D deficiency in a well-characterized IBD cohort in Western Greece, and explore its associations with clinical features, laboratory biomarkers, and treatment intensity. Methods: In this cross-sectional study, 184 consecutive, well-characterized IBD outpatients followed at a tertiary referral center in Western Greece underwent clinical evaluation and laboratory testing between January 2023 and December 2024. Vitamin D is determined by measuring 25-hydroxyvitamin D [25(OH)D], which reflects the body’s vitamin D stores due to its longer half-life compared with the biologically active form. Deficiency was defined as serum 25(OH)D < 20 ng/mL. Associations with disease type, clinical and laboratory biomarkers, severity indices, and treatment were analyzed using multivariate logistic regression. Results: Vitamin D deficiency was identified in 67 patients (36.4%). Although unrelated to disease type, hospitalization, surgery, or disease activity indices, deficiency correlated with systemic inflammation, nutrition/metabolic markers, and treatment intensity. More specifically, vitamin D-deficient patients exhibited higher platelet counts (p = 0.005) and erythrocyte sedimentation rate (ESR) (p = 0.014), lower hemoglobin (p = 0.005), albumin (p = 0.011), and serum glutamic-oxaloacetic transaminase (SGOT) (p = 0.009) levels and more frequent use of biologic therapy (p = 0.009). In multivariate analysis, vitamin D deficiency remained independently associated with biologic therapy (aOR = 0.374; 95% CI: 0.148–0.946), platelet count (aOR = 0.996, 95% CI: 0.992–0.999), and SGOT (aOR = 1.05, 95% CI: 1.00–1.10), indicating consistent links between vitamin D deficiency and treatment intensity, systemic inflammation, and nutritional or metabolic status. Conclusions: Vitamin D deficiency is common among IBD patients and independently associates with systemic inflammation, metabolic impairment, and intensified treatment requirement, supporting its potential role as a marker of disease burden. Read More