Published online Jul 28, 2020. doi: 10.3748/wjg.v26.i28.3998
Peer-review started: April 8, 2020
First decision: April 30, 2020
Revised: May 15, 2020
Accepted: July 16, 2020
Article in press: July 16, 2020
Published online: July 28, 2020
Processing time: 110 Days and 22 Hours
Inflammatory bowel diseases (IBD), conventionally consist of Crohn’s disease (CD) and ulcerative colitis. They occur in individuals with high risk genotype for the disease in the setting of appropriate environmental factors. The pathogenesis of IBD involves a dysregulated autoimmune response to gut dysbiosis, which in turn is triggered due to exposure to various inciting environmental factors. But there is no clearly defined etiology of IBD and this type of disease is termed as “idiopathic IBD”, “classic IBD”, or “primary IBD”. We reviewed the current medical literature and found that certain etiological factors may be responsible for the development of IBD or IBD-like conditions, and we consider this form of de novo IBD as “secondary IBD”. Currently known factors that are potentially responsible for giving rise to secondary IBD are medications; bowel altering surgeries and transplantation of organs, stem cells or fecal microbiome. Medications associated with the development of secondary IBD include; immunomodulators, anti-tumor necrosis factor alpha agents, anti-interleukin agents, interferons, immune stimulating agents and checkpoint inhibitors. Colectomy can in some cases give rise to de novo CD, pouchitis of the ileal pouch, or postcolectomy enteritis syndrome. After solid organ transplantation or hematopoietic stem cell transplantation, the recipient may develop de novo IBD or IBD flare. Fecal microbiota transplantation has been widely used to treat patients suffering from recurrent Clostridium difficile infection but can also causes IBD flares.
Core tip: Inflammatory bowel diseases (IBD) are chronic illnesses of the gastrointestinal tract with no clearly defined etiology and are traditionally termed as primary IBD. It is generally believed that IBD results from abnormal immune response to dysbiosis of gut microbiota in a genetically susceptible individual. IBD or IBD-like conditions may also be caused by well-defined etiologies; such as medical, surgical, and organ transplantation. These conditions are coined as secondary IBD. In this review we attempted to highlight some etiological factors, pathogenetic pathways, and clinical features of secondary IBD.