In our study, serum hepcidin concentration was significantly decreased in IBD children compared with controls. Hepcidin correlated positively with ferritin, but not with any of inflammatory markers. It may suggest that in our cohort, hepcidin was regulated predominantly by iron storage level.
Interleukin 17A (IL-17A) and interleukin 17F (IL-17F) appear to play important role in pathogenesis of some autoimmune diseases. However, their role in inflammatory bowel disease (IBD) has not been yet fully elucidated. We aimed to determine serum IL-17A and IL-17F in children with IBD and to assess their association with IBD activity. Recruited children underwent blood tests including complete blood count, C-reactive protein, erythrocyte sedimentation rate, IL-17A and IL-17F and stool sampling for calprotectin. The study group comprised 68 children with IBD, including 43 with ulcerative colitis and 25 with Crohn’s disease. Control group included 20 healthy children. IL-17A was significantly increased in children with IBD (median: 10.95 pg/ml; range: 0.65–200.54 pg/ml) compared to controls (median: 4.09 pg/ml; range: 0.67–26.20 pg/ml) (p = 0.002). IL-17A was significantly increased in patients with active phase of ulcerative colitis (median: 14.58 pg/ml; range: 0.65–200.54 pg/ml) compared to those in ulcerative colitis remission (median: 8.13 pg/ml; range: 1.61–58.56 pg/ml) (p = 0.04). There were no significant differences in IL-17A among patients with active and inactive Crohn’s disease (p = 0.18). IL-17F did not differ significantly between children with IBD (median: 15.11 pg/ml; range: 0.09–189.84 pg/ml) and controls (median: 11.56 pg/ml; range: 0.19–32.49 pg/ml) (p = 0.33). Our study suggests that interleukin 17A may diverse active phase from remission only in ulcerative colitis but not in Crohn’s disease.
Background: There is no single reliable marker of iron homeostasis in inflammatory bowel disease. Aims: To determine diagnostic usefulness of soluble transferrin receptor and soluble transferrin receptor/log ferritin index in iron deficiency anemia in children with inflammatory bowel disease. Methods: We assessed soluble transferrin receptor in serum and calculated soluble transferrin receptor/log ferritin index in 75 children with inflammatory bowel disease. Diagnostic ability to identify iron deficiency anemia was examined by receiver operating characteristic analysis. Results: Study group comprised 27 cases of iron deficiency anemia, 6 anemia of chronic disease with iron deficiency, 5 anemia of chronic disease. Soluble transferrin receptor was significantly increased in children with iron deficiency anemia (median: 1.63 g/ml) compared to non-anemic children (median: 1.02 g/ml). Soluble transferrin receptor/log ferritin index was significantly higher in iron deficiency anemia (median: 1.76) than in anemia of chronic disease (median: 0.55), anemia of chronic disease with iron deficiency (median: 0.68) or patients without anemia (median: 0.72). Soluble transferrin receptor and its index were not correlated with disease activity or inflammatory markers. Diagnostic power for soluble transferrin receptor/log ferritin index (0.864) was superior to soluble transferrin receptor (0.768) in iron deficiency anemia recognition. Conclusion: Soluble transferrin receptor/log ferritin index has better diagnostic utility than soluble transferrin receptor for iron deficiency anemia detection in pediatric inflammatory bowel disease.
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