P52 Vitamin D deficiency is associated with adverse survival in patients with idiopathic pulmonary fibrosis. (12th November 2019)

• Record Type: Journal Article
• Authors: Kumar, R; Mann, J; Chua, F; Maher, T; Renzoni, E; Kokosi, M; Kouranos, V; Molyneaux, P; Wells, A; Mackintosh, J; George, P
• Is Part Of: Thorax. Volume 74(2019)Supplement 2
• Page Start: A117
• Page End: A118
• Publication Date: 2019-11-12
• Subjects: Chest -- Diseases -- Periodicals; Thorax; Chest -- Diseases; Periodicals; Periodicals; 617.54
• DOI: 10.1136/thorax-2019-BTSabstracts2019.195
• Languages: English
• ISSNs: 0040-6376

Abstract

Abstract : Background: Vitamin D (VitD) has been shown to have anti-fibrotic properties in the bleomycin mouse model of pulmonary fibrosis. This study aimed to establish whether an association exists between VitD deficiency and outcomes in patients with idiopathic pulmonary fibrosis (IPF). Methods: The VitD status of an anti-fibrotic treated IPF patient cohort at a single UK tertiary centre was retrospectively analysed. Clinical deficiency was defined as VitD<25 nmol/L as per NICE guidelines. Serial lung function was determined in the 12 months (or as close as possible) after the VitD test. Frequency of infections and acute exacerbation events were recorded, and transplant-free survival was calculated from the earliest patient contact. Results: Of 300 IPF patients, 92 (30.6%) had documented VitD results (78.3% male, mean age 72±8 years). Sixteen (17.4%) patients were clinically deficient. Baseline FVC and DLco were 70.3%±11.9% and 39.1%±12.9% in the non-deficient and 68.4%±10.7% and 39.8%±8.8% in the deficient groups respectively (p=0.55, p=0.85 respectively). There was no significant difference in the prevalence of VitD deficiency between patients taking Pirfenidone (11/66 (17%)) and Nintedanib (5/26 (19%))(p=0.77). Median transplant-free survival was 1128 days in the non-deficient group and 532 days in the deficient group (p=0.0079)(Figure 1). Following adjustment for age, gender and baseline composite physiologic index (CPI), the Cox proportional hazard ratio for VitD deficiency and transplant-free survival was 2.36 (95% CI 1.128–4.942, p=0.023). There was no difference in mean annual relative change in FVC between deficient (-8.0%±8.9%) and non-deficient patients (-9.1% ±12.9%)(p=0.79). The incidence of infections and acute exacerbations did not significantly differ between groups. Conclusions: In this cohort of antifibrotic treated IPF patients, there is an association between VitD deficiency and adverse outcomes. Whether VitD deficiency is associated with a poorer prognosis as a surrogate for a co-morbid state or is relevant to IPF disease pathogenesis remains unclear. Although limited by cohort size, it is curious that reduced survival appears to be independent of lung function decline and further analyses with regard aetiology of mortality is required. Prospective studies of VitD supplementation in antifibrotic treated IPF patients may be indicated to explore a potential therapeutic role.