One previous study reported that although the levels of MPs in pSS patients with high or low disease severity were higher than health controls, those in pSS patients with high disease severity were lower than those in patients with low disease severity(Table 1) [22].The potential explanations include consumption or confinement of MPs by adhesion in the tissue target of pSS, MPs sequestered in leukocyte-platelet complexes, and MPs destruction induced by phospholipases, especially secretory phospholipase A2, in active disease [22–27]. This evidence concerns the gene PLA2G2D and peeling skin syndrome.