KL-6 is a 200kDa high-molecule weight glycosidoprotein that was identified and named by Kohno in 1985(6). Researches discovered that KL-6 might be employed as a serological biomarker of ILD. Recent studies have demonstrated that KL-6 can be utilized to diagnose myositis, systemic sclerosis, and rheumatoid arthritis in conjunction with ILD(7–9). However, the clinical importance of serological KL-6 in individuals with pSS-ILD has yet to be determined. We discovered that pSS sufferers with ILD had substantially greater blood KL-6 contents vs sufferers with no ILD, and the threshold for confirming ILD in pSS sufferers was 276.5U/ml, which was lower than studies finished in the past. Hu et al discovered a cut-off value of 461.5U/ml for diagnosing ILD in IIM patients (10).Benyamine et al previously showed that the cutoff threshold for baseline serum KL-6 levels to distinguish SScILD and SSc nonILD was 872 U/ml (11). This might be connected to various CTD. Patients with IIM and SSc tend to have severer lung involvement, and previous studies have shown that serological KL-6 contents represent the seriousness of ILD related to CTD, hence the level of KL-6 was higher than that of the current study, i.e., the results of this study are lower than previous studies. Furthermore, our study is the first to confirm this finding in a Chinese patient population. It is critical to determine the thresholds of KL-6 for identifying ILD sufferers in different races, because those thresholds can be influenced by the different features of diverse races.
PFT is commonly used method to assess and forecast the prognosis of ILD. Our findings revealed that serological KL-6 contents exhibited a moderate negative association with VC percent, FVC percent, FEV1 percent, and DLco percent, which was consistent with earlier findings (2, 10). Salazar et al. demonstrated that serological KL-6 contents were a predictor of early SSc-ILD progression. Furthermore, they discovered that high serological KL-6 contents (1273 U/ml) were related to inferior prognoses in individuals with SSc-ILD (13). Yosuke Kamiya et al. demonstrated that utilizing an appropriate KL-6 threshold (800 U/mL), pSS-ILD sufferers who had increased serological KL-6 contents (> 800 U/mL) exhibited a substantially greater death rate vs sufferers who did not have excessive serum KL-6 levels (14). This shows that detecting and monitoring KL-6 concentrations may be effective as an ILD screening technique.
The current study revealed that only increased KL-6 was an independent risky factor for ILD in pSS patients after multivariable analysis. ILD is produced by the destruction and generation of alveolus type II epitheliums, which manifests as extensive alveolus inflammatory events and lung interstitial fibrotic events. Impaired alveolus epitheliums release substantial KL-6, which can repress fibroblastic aggregation and death. When alveoli were wounded, the permeability of the blood exchange barrier was elevated, and KL-6 swarmed into the blood, which induced elevated serological KL-6 contents (15). Because KL-6 is not an alveolus surfactant, its overproduction may interfere with the expressing of the initial surfactant, alveolus expansion, and pulmonary compliance, resulting in ventilation issues.
There are some limitations to our research. To begin with, the present research was finished retrospectively with an insufficient sample size, which might contribute to selection bias, hence more researches with bigger sample sizes are required. Second, it must be demonstrated that KL-6 can be used to diagnose disease and forecast the occurrence of ILD in pSS patients.
In conclusion,serum KL-6 is an important serologic biomarker for diagnosing pSS- ILD and its remarkably related to the seriousness of lung illnesses.Clinically, prospective researches are warranted to reveal if KL-6 contents can forecast the development of ILD.