Changes in Serum MMP-9 and TIMP-1 Concentrations in Children with Inflammatory Bowel Disease over a Six-Month Observation Period

Inflammatory bowel disease (IBD) is a chronic condition with a long-term and often unpredictable course. The aim of our study was to evaluate serum levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in children with IBD at diagnosis or disease exacerbation and during follow-up to assess their changes during the course of the disease. Patients were assessed at the time of inclusion (T0), after 3 months (T1), and after 6 months of follow-up (T2). At each time point, clinical disease activity was evaluated, along with routine laboratory tests and measurement of fecal calprotectin (fCal). Serum concentrations of MMP-9 and TIMP-1 were determined using the enzyme-linked immunosorbent assay method. Fifty-nine children with IBD were included in the study (19 with Crohn’s disease and 40 with ulcerative colitis; 39 with newly diagnosed disease and 20 with disease exacerbation). During the six-month follow-up, patients received anti-TNF-α therapy with infliximab or adalimumab; at T1, 8 patients received infliximab and 5 received adalimumab, whereas at T2, 17 patients received infliximab and 7 received adalimumab. At T0, significant differences in MMP-9 and TIMP-1 were observed between IBD patients and controls. In the IBD group, a significant decrease in MMP-9 (p < 0.001), TIMP-1 (p < 0.001), and the MMP-9/TIMP-1 ratio (p = 0.006) was observed over the six-month follow-up. At T1, only TIMP-1 levels differed between groups, while at T2 no significant differences were observed. Patients who achieved clinical remission showed a significant decrease in MMP-9 (p = 0.001) and TIMP-1 (p < 0.001) levels, whereas no significant changes were observed in patients who did not achieve remission. However, the percentage change in MMP-9 did not differ significantly according to clinical remission status (p = 0.50). Similarly, patients who achieved fCal-defined biochemical remission showed significant reductions in MMP-9 (p = 0.005), TIMP-1 (p = 0.003), and the MMP-9/TIMP-1 ratio (p = 0.01) over time. In patients without fCal-defined biochemical remission, MMP-9 (p = 0.04) and TIMP-1 (p = 0.01) also decreased significantly over time, whereas the MMP-9/TIMP-1 ratio did not change significantly. However, direct comparisons showed no significant differences in the percentage changes in MMP-9 (p = 0.28) or TIMP-1 (p = 0.37) according to fCal-defined biochemical remission status. In conclusion, serum MMP-9 and TIMP-1 levels change over six months in children with IBD, reflecting changes in disease activity. Changes in these biomarkers were not significantly associated with fCal-defined biochemical remission. A significant difference in TIMP-1 percentage change was observed according to clinical remission status. However, this finding should be considered exploratory and interpreted with caution.