AUTOIMMUNE MARKERS FOR PROGRESSION OF LIBBY AMPHIBOLE LAMELLAR PLEURAL THICKENING

Abstract

SESSION TITLE: Occupational and Environmental Lung Disease SESSION TYPE: Original Investigation Posters PRESENTED ON: October 18-21, 2020 PURPOSE: The Libby Epidemiological Research Program, funded by the Agency for Toxic Substances and Disease Registry, found that autoimmune outcomes were associated with exposure to Libby Asbestiform Amphibole (LAA). THis has been previously published. In addition to the cancers and pulmonary fibrosis typically found with chrysotile asbestos, a highly inflammatory and progressive pleural fibrosis (LPT – lamellar pleural thickening) is frequently found in people exposed to LAA. Progressive LPT can lead to severe pleural pain and/or rapidly worsening pulmonary function. Autoantibodies have been shown to occur in mice and humans exposed to LAA. The purpose of this study was to determine which specific autoantibodies, if any, were related to progressive LPT and to perform sensitivity and specificity testing to determine their usefulness as potential screening markers for progressive disease. METHODS: After IRB approval, a selection of adult patients from the Center for Asbestos Related Diseases (CARD) database was stratified into groups as Progressive LPT, Stable LPT, and no LPT. Participants were required to have had a CT scan of the chest without contrast within the past 2 years as well as a serum sample drawn within 2 years of their CT scan. Two patients each were selected from the Stable LPT and No LPT groups and matched as close as possible to the 19 participants in the Progressive LPT group. Samples were analyzed for ANA (anti-nuclear antibody), MCAA (mesothelial cell autoantibodies), (PLG) Antiplasminogen, Cytokines IL-1beta and IL-17. Afterwards, statistical analysis was applied to determine sensitivity and specificity. RESULTS: ANA was found more frequently in the Progressor group than the Stable or No groups. Positive MCAA was more frequent in the Progressor group, but only statistically greater than the No group. Positive PLG was more frequent in the Progressor group than both the Stable and No groups. IL-1beta and IL-17 had no significant differences between groups. All three antibodies, ANA, MCAA, and PLG, had higher specificity than sensitivity. The most specific test with the strongest predictive values was PLG. When the Stable group was included, none of the three tests had predictive value as a screening test. CONCLUSIONS: Screening for autoimmune markers associated with Progressive PLT might allow early detection and also suggest new therapeutic strategies. The data cited in this study support the association of ANA, MCAA, and PLG with progressive LPT but not stable LPT. CLINICAL IMPLICATIONS: ANA may have some role as a screening tool for risk of severe clinical disease with LPT progression. PLG or MCAA may have some role in predicting progressive LPT, especially when combined with ANA, but while there may be high specificity, sensitivity remains low. Further studies need to validate this finding in women. None of these markers had value in predicting Stable PT. DISCLOSURES: no disclosure on file for Charles Black; No relevant relationships by Tracy McNew, source=Web Response No relevant relationships by Karen Lee Morrissette, source=Web Response No relevant relationships by Jean Pfau, source=Web Response