LAUSR

Non-specific abnormalities could be detected by nailfold videocapillaroscopy (NVC) in subject with primary Raynaud’s Phenomenon (RP) several years before the clinical onset of connective tissue diseases (CTD)s [1]. Previous findings from our group proved that ≤30 μm capillary dilations in RP patients have a negative predictive value for developing the ‘scleroderma pattern’ during follow-up [2].To investigate the role of NVC >30 μm capillary dilations as positive predictive factors of the ‘scleroderma pattern’ in RP patients later developing systemic sclerosis (SSc)-related RP.A 10-year retrospective NVC-based investigation evaluated the dataset of sequential NVCs of 18 RP patients later developing SSc (cases) and 19 sex- and age-matched RP patients later developing other CTDs (controls). Both cases and controls had ≥1 NVC performed before the ‘scleroderma pattern’/CTD diagnosis (basal NVC) showing >30 μm dilated capillaries. Each NVC was qualitatively and semi-quantitatively assessed, recording number of total capillaries, number and average/site-specific diameters (arterial, apical, venous) of >30 μm dilated capillaries [3]. Statistical analysis was performed to stratify the risk of developing the ‘scleroderma pattern’.Significant differences of capillary diameters were observed between cases and controls both at basal NVC and during follow-up (p<0.001). The proportion of >30 μm dilated capillaries in basal NVC was the strongest predictor of ‘scleroderma pattern’ in a median 3-year time, with a 27% cut-off (PPV 0.79, 95%CI 0.54,0.94; p<0.001). Additional “Higher risk” NVC hallmarks for ‘scleroderma pattern’ development were apical diameter >40 μm (p<0.001), venous diameter >25 µm (p<0.05) and average diameter ≥35 µm (p<0.005). Conversely, CTDs patients showed a stable NVC ‘non-scleroderma pattern’ over a median 10-year time.This is the first study to show that NVC-detected homogeneous and progressive capillary loop dilations in RP patients significantly contribute to predict the ‘scleroderma pattern’ evolution within a median 3-year time, possibly providing a “very early” window of opportunity in SSc pre-clinical stages.[1]Cutolo M et al. Expert Rev Clin Immunol. 2019;15(7):753–64. [2] Trombetta AC et al. J Rheumatol 2016;43:599–606. [3] Smith et al. Autoimmun Rev 2020; 19(3):102458.None declared