Abstract
Crohn disease (CD) is a chronic inflammatory disease which progressively affects the digestive tract with unknown etiology. During the disease course, intestinal fibrosis will gradually develop in many CD patients and results in irreversible fibrosis stricture, causing refractory abdominal pain and even intestinal obstruction, and necessitating one or more surgical interventions. Thus far the exact etiology of CD remains unknown. It is believed that genetic, environmental and immunologic factors are involved, which may also predict the development of intestinal fibrosis. Recent studies have found the association of mutations in genes, such as NOD2, ATG16L1, CX3CR1, IL-23R and MMP3 with the fibrogenic phenotype of CD. In addition, serum extracellular matrix molecules, growth factors, miRNAs and microbial antibodies have also been linked to the fibrogenesis in CD patients, however the results of researches were divergent. Therefore it is of significance to explore noninvasive markers of intestinal fibrosis with high sensitivity and specificity, and the high-throughput proteomic technique may be an approach that deserves further investigation. Screening the high-risk patients for the fibrostenotic phenotype of CD by susceptibility genes, and early detection of intestinal fibrosis using noninvasive serum markers, will help improve the treatment outcomes and reduce the surgical rates. The article aims at summarizing the current susceptibility genes and serum markers of intestinal fibrosis in CD.
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