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Egeberg and his coauthors reported that HS and inflammatory bowel disease similarities suggest a shared pathogenesis, including the worsening effect of smoking on both conditions; the appearance of scarring and sinus tract formation; the apparent involvement of T-helper 17 cells, interleukin-23, and tumor necrosis factor; and the coinvolvement of genes such as SULT1B1 and SULT1 E1 "Finally, an increased prevalence of spondylarthropathy
has been reported in patients with IBD as well as in those with HS, raising the hypothesis that genetic, epigenetic, and/or environmental factors cooperate to lead to dysregulated inflammatory pathways across these immune-mediated diseases," they wrote.
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