Nutrients, Vol. 17, Pages 3291: Can Vitamin D Reduce Glucocorticoid-Induced Adverse Effects in Patients with Giant Cell Arteritis? Results from 1568 Patients in the Spanish ARTESER Registry

Nutrients, Vol. 17, Pages 3291: Can Vitamin D Reduce Glucocorticoid-Induced Adverse Effects in Patients with Giant Cell Arteritis? Results from 1568 Patients in the Spanish ARTESER Registry

Nutrients doi: 10.3390/nu17203291

Authors:
Gastón A. Ghio
Marta Domínguez-Álvaro
Iñigo Hernández Rodríguez
Elisa Fernández-Fernández
Maite Silva-Díaz
Joaquín M. Belzunegui
Clara Moriano
Julio Sánchez Martín
Javier Narváez
Eva Galíndez Agirregoikoa
Anne Riveros Frutos
Francisco Ortiz Sanjuán
Tarek C. Salman Monte
Margarida Vasques Rocha
Carlota L. Iñiguez
Alicia García Dorta
Clara Molina Almela
María Alcalde Villar
José L. Hernández
Santos Castañeda
Ricardo Blanco

Objective: To determine whether oral vitamin D supplementation reduces the risk of glucocorticoid (GC)-associated severe adverse events (SAEs) in patients with giant cell arteritis (GCA) included in the Spanish ARTESER registry. Methods: The ARTESER registry collected data from patients diagnosed with GCA across 26 Spanish public hospitals between June 2013 and March 2019. SAEs were defined as fatal, life-threatening, or requiring hospitalization. Patients were categorized according to the use or non-use of oral vitamin D supplements. Incidence rates (IRs) of SAEs were expressed per person-year with 95% confidence intervals (CIs). Cox proportional hazards models assessed vitamin D supplementation and its interaction with cumulative glucocorticoid dose. Results: Of 1568 patients (mean age 76.9 ± 8.1 years; 70.1% women) receiving GC, 120 (7.6%) experienced SAEs (IR 0.039; 95% CI 0.033–0.047). Vitamin D supplementation was documented in 1186 (75.6%) compared with 382 (24.4%) non-supplemented patients. SAE incidence was similar in supplemented (n = 89; 7.5%; IR 0.038, 95% CI 0.030–0.046) and non-supplemented patients (n = 31; 8.1%; IR 0.045, 95% CI 0.031–0.064) (p = 0.387). Multivariable Cox regression showed a significant interaction between vitamin D supplementation and cumulative glucocorticoid dose (interaction term HR 0.90; p = 0.033), consistent with a dose-dependent protective effect. Conclusions: Vitamin D supplementation was not independently associated with a lower incidence of GC-related SAEs, likely due to residual confounding factors. However, the interaction with cumulative GC exposure suggests a modulatory effect. Prospective studies incorporating stratified baseline vitamin D assessments are warranted.

​Objective: To determine whether oral vitamin D supplementation reduces the risk of glucocorticoid (GC)-associated severe adverse events (SAEs) in patients with giant cell arteritis (GCA) included in the Spanish ARTESER registry. Methods: The ARTESER registry collected data from patients diagnosed with GCA across 26 Spanish public hospitals between June 2013 and March 2019. SAEs were defined as fatal, life-threatening, or requiring hospitalization. Patients were categorized according to the use or non-use of oral vitamin D supplements. Incidence rates (IRs) of SAEs were expressed per person-year with 95% confidence intervals (CIs). Cox proportional hazards models assessed vitamin D supplementation and its interaction with cumulative glucocorticoid dose. Results: Of 1568 patients (mean age 76.9 ± 8.1 years; 70.1% women) receiving GC, 120 (7.6%) experienced SAEs (IR 0.039; 95% CI 0.033–0.047). Vitamin D supplementation was documented in 1186 (75.6%) compared with 382 (24.4%) non-supplemented patients. SAE incidence was similar in supplemented (n = 89; 7.5%; IR 0.038, 95% CI 0.030–0.046) and non-supplemented patients (n = 31; 8.1%; IR 0.045, 95% CI 0.031–0.064) (p = 0.387). Multivariable Cox regression showed a significant interaction between vitamin D supplementation and cumulative glucocorticoid dose (interaction term HR 0.90; p = 0.033), consistent with a dose-dependent protective effect. Conclusions: Vitamin D supplementation was not independently associated with a lower incidence of GC-related SAEs, likely due to residual confounding factors. However, the interaction with cumulative GC exposure suggests a modulatory effect. Prospective studies incorporating stratified baseline vitamin D assessments are warranted. Read More

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