Henriette Marstein1,2, Thomas Schwartz1, Trond Mogens Aaløkken3,4, May Britt Lund4,5, Berit Flatø4,6, Ivar Sjaastad1,7, Helga Sanner2,6. 1. Institute for Experimental Medical Research and KG Jebsen Center for Cardiac Research, Oslo University Hospital and University of Oslo, Oslo, Norway. 2. Bjørknes University College, Oslo, Norway. 3. Department of Radiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 4. Institute for Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway. 5. Department of Respiratory Medicine, Oslo, Norway. 6. Department of Rheumatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 7. Department of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.
Abstract
OBJECTIVES: To examine associations between cytokines and pulmonary involvement in patients with medium- to long-term JDM. METHODS: In a cross-sectional study, 58 patients examined median (range) 16.8 (6.6-27.0) years after symptom onset were stratified in inactive (JDM-inactive) and active (JDM-active) disease (updated PRINTO criteria); 56 age/sex matched controls were included. Twenty-nine cytokines (in serum) were analysed (Luminex technology/ELISA). Pulmonary function test included forced vital capacity, total lung capacity (TLC) and diffusing capacity for carbon monoxide reported as % of predicted and low forced vital capacity/TLC/diffusing capacity for carbon monoxide. In patients, the presence of clinical pulmonary damage was assessed and high resolution computed tomography scans were scored for interstitial lung disease, chest wall calcinosis and airways disease. RESULTS: Median age of patients was 21 (7-55) years, 59% were female and 36% inactive. In JDM-active and all patients, higher MCP-1, IP-10 and eotaxin correlated with high-resolution computed tomography findings (rs 0.34-0.61; P < 0.05). MCP-1 and eotaxin correlated with pulmonary damage in JDM-active and all patients (rs 0.41-0.49; P < 0.01). Higher TGF-β1 and PDGF (growth factors) were associated with lower lung volumes (forced vital capacity/TLC measures) in all patients; PDGF in JDM-active and TGF-β1 in JDM-inactive patients. IP-10 correlated with TLC% in JDM-active patients. No associations between cytokines and pulmonary function test were found in controls. CONCLUSIONS: In JDM, we found a novel association (not previously described in myositis) between eotaxin and pulmonary involvement; we have previously shown an association between eotaxin and cardiac dysfunction. The associations between IP-10/growth factors/MCP-1 and pulmonary involvement are novel in JDM and were mostly seen in JDM-active patients.
OBJECTIVES: To examine associations between cytokines and pulmonary involvement in patients with medium- to long-term JDM. METHODS: In a cross-sectional study, 58 patients examined median (range) 16.8 (6.6-27.0) years after symptom onset were stratified in inactive (JDM-inactive) and active (JDM-active) disease (updated PRINTO criteria); 56 age/sex matched controls were included. Twenty-nine cytokines (in serum) were analysed (Luminex technology/ELISA). Pulmonary function test included forced vital capacity, total lung capacity (TLC) and diffusing capacity for carbon monoxide reported as % of predicted and low forced vital capacity/TLC/diffusing capacity for carbon monoxide. In patients, the presence of clinical pulmonary damage was assessed and high resolution computed tomography scans were scored for interstitial lung disease, chest wall calcinosis and airways disease. RESULTS: Median age of patients was 21 (7-55) years, 59% were female and 36% inactive. In JDM-active and all patients, higher MCP-1, IP-10 and eotaxin correlated with high-resolution computed tomography findings (rs 0.34-0.61; P < 0.05). MCP-1 and eotaxin correlated with pulmonary damage in JDM-active and all patients (rs 0.41-0.49; P < 0.01). Higher TGF-β1 and PDGF (growth factors) were associated with lower lung volumes (forced vital capacity/TLC measures) in all patients; PDGF in JDM-active and TGF-β1 in JDM-inactive patients. IP-10 correlated with TLC% in JDM-active patients. No associations between cytokines and pulmonary function test were found in controls. CONCLUSIONS: In JDM, we found a novel association (not previously described in myositis) between eotaxin and pulmonary involvement; we have previously shown an association between eotaxin and cardiac dysfunction. The associations between IP-10/growth factors/MCP-1 and pulmonary involvement are novel in JDM and were mostly seen in JDM-active patients.