Intest Res.  2019 Jan;17(1):36-44. 10.5217/ir.2018.00126.

Current new challenges in the management of ulcerative colitis

• Fukuda T
• Naganuma M
• Kanai T

• KMID: 2438441
• DOI: http://doi.org/10.5217/ir.2018.00126

Abstract

Ulcerative colitis (UC) is a chronic inflammatory condition of the gastrointestinal tract. Although the cause of UC is postulated to be multifactorial in nature, including genetic predisposition, epithelial barrier defects, dysregulation of immune responses, and environmental factors, the specific pathogenesis of UC is still incompletely understood. In the treatment of UC so far, a method of suppressing immunity and treating it has been mainstream. Immunosuppressant drugs, including thiopurines (azathioprine or 6-mercaptopurine), anti-tumor necrosis factor-α (anti-TNF-α) antibody (infliximab and adalimumab), and calcineurin inhibitor, can be used in treat patients with corticosteroid-dependent and/or corticosteroid-refractory moderate-to-severe UC. Recently, in addition to such a conventional therapeutic agent, golimumab, which is the first transgenic human monoclonal anti-TNF-α antibody to be fabricated, anti α-4/β-7 integrin antibody, and Janus kinase inhibitor have been reported to novel immunosuppressant therapy. Furthermore, other treatments with unique mechanisms different from immunosuppression, have also been suggested, including fecal microbiota transplantation and Indigo naturalis, which is a Chinese herbal medicine. We compared the features and efficacy of these new treatments. In this issue, the features and treatment options for these new treatments is reviewed.

Keyword

Colitis, ulcerative; Vedolizumab; Tofacitinib; Indigo naturalis; Fecal microbiota transplantation

MeSH Terms

Asian Continental Ancestry Group
Calcineurin
Colitis, Ulcerative*
Fecal Microbiota Transplantation
Gastrointestinal Tract
Genetic Predisposition to Disease
Herbal Medicine
Humans
Immunosuppression
Indigo Carmine
Methods
Necrosis
Phosphotransferases
Ulcer*
Calcineurin
Indigo Carmine
Phosphotransferases

Figure

• 

  Fig. 1. Administration route of Indigo naturalis. (A) This is a hypothesis of the mechanism of pulmonary artery hypertension (PAH) onset by Indigo naturalis administration. Administration of Indigo naturalis increases the concentration of Indigo in the blood. Indigo acts as an aryl hydrocarbon receptor (AhR) ligand, resulting in an increase in serotonin concentration, a metabolite of tryptophan. Serotonin causes PAH. (B, C) shows an ingenuity of administration method to reduce side effects of Indigo naturalis. (B) The capsules that collapse in the large intestine decrease absorption of Indigo naturalis in the small intestine. (C) Suppository is administered without going through the small intestine.

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