Abstract

PurposeChronic spontaneous urticaria (CSU) is a disease that is primarily seen in adults and is comparatively rare in children. Consequently, only a few studies have focused on the pathogenesis of the disease in children. This study investigated the possible role of metalloproteinase-9 (MMP-9) in the pathogenesis of CSU in children.MethodsThe study group was composed of 54 children with CSU; 34 healthy children comprised the control group. The demographic and clinical features of the study group were extensively evaluated, and laboratory assessments were also performed. An enzyme-linked immunosorbent assay was used to evaluate levels of plasma MMP-9. Disease activity was quantified using the urticaria activity score (UAS).ResultsThe median value of plasma MMP-9 was 108.9 ng/mL (interquartile range, 93.3-124.1) in the CSU group and 87.8 ng/mL (69.4-103.0) in the control group. The difference between the 2 groups was statistically significant (P<0.001). Also, MMP-9 levels showed a significant positive correlation with UAS (rho=0.57, P<0.001). Twenty-six percent of patients had positive autologous serum skin test (ASST) results. Neither UAS nor plasma MMP-9 levels were significantly different between ASST-positive and -negative patients (P>0.05).ConclusionsPlasma MMP-9 levels were elevated in children with CSU and were positively correlated with disease activity. MMP-9 may be both a good biomarker of disease activity and a potential therapeutic target in CSU.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.