Predictive Value of Serum Markers SFRP1 and CC16 in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

Abstract

Background. Chronic obstructive pulmonary disease (COPD) patients are particularly vulnerable to acute exacerbation, resulting in a huge socioeconomic burden. Objective. In this study, we evaluated the value of serum secreted frizzled-related protein 1 (SFRP1) and Clara cell-secreted protein (CC16) in predicting the risk of acute exacerbations in patients with COPD. Methods. The study included 123 COPD patients admitted to our hospital from May 2020 to June 2021, including 65 patients in stable stage (STCOPD group), 58 patients in acute exacerbation stage (AECOPD group), and 60 healthy volunteers (control group). Serum SFRP1 and CC16 levels were detected by enzyme-linked immunosorbent assay (ELISA). The receiver operating characteristics curve (ROC) analysis was performed to evaluate the sensitivity and specificity of serum SFRP1 and CC16 for predicting the risk of acute exacerbation in COPD patients. Results. The age among groups is significantly different, but there is no difference in the gender and body mass index (BMI). The level of serum SFRP1 in the AECOPD group was significantly higher than that in the STCOPD group and the control group, and the level of serum CC16 was lower than that in the STCOPD group and the control group. Serum SFRP1 was negatively correlated with forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) (r = −0.473, P < 0.001 ). Serum CC16 was positively correlated with FEV1/FVC (r = 0.457, P < 0.001 ). The area under the curve (AUC), sensitivity, and specificity of SFRP1 for predicting the risk of exacerbation was 0.847 (95% CI: 0.775 to 0.920), 86.20%, and 80.00%. The AUC, sensitivity, and specificity of CC16 for predicting the risk of exacerbation were 0.795 (95% CI: 0.711 to 0.879), 74.10%, and 86.20%. Conclusions. These findings suggest that SFRP1 and CC16 may be useful serum markers for predicting the risk of exacerbation in COPD patients.

Correlation of Serum Clara Cell Secretory Protein 16, Plasma Fibrinogen and Serum Amyloid A with the Severity of Acute Exacerbated COPD and Their Combination in Prognosis Assessment

“…14 Another biomarker focused in our study is Clara cell secretory protein-16 (CC16), a major functional protein secreted by Clara cells. 15 In COPD, inflammation, oxidative stress and increased alveolar-capillary permeability significantly enhance the expression of CC16. CC16 can inhibit phospholipase A2 activity and reduce cell membrane phospholipid catabolism, and also directly inhibit the expression of various inflammatory factors and their biological activities, which play an important role in the development mechanism of asthma, COPD, and acute lung injury.…”

Mechanistic Regulation of Wnt Pathway-Related Progression of Chronic Obstructive Pulmonary Disease Airway Lesions

“…It is suggested that SFRP1, as a member of the largest family of Wnt signaling pathway inhibitors, is involved in the occurrence and development of COPD by competitively binding to Frizzled receptor on the cell membrane to inhibit the Wnt pathway. 10,61 By analyzing the transcriptome of wild-type and mutant lungs, Wnt/RYK signaling was observed to regulate chronic obstructive pulmonary disease by up-regulating inflammatory genes in vitro. 62 These data suggest that Wnt signaling is important to avoid an overwhelming and harmful inflammatory response during acute infection.…”

Retracted: Predictive Value of Serum Markers SFRP1 and CC16 in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…Tis article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. Tis investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”