Progression of ulcerative colitis following diversion colitis.


Journal

Clinical journal of gastroenterology
ISSN: 1865-7265
Titre abrégé: Clin J Gastroenterol
Pays: Japan
ID NLM: 101477246

Informations de publication

Date de publication:
Dec 2022
Historique:
received: 21 02 2022
accepted: 28 08 2022
pubmed: 7 9 2022
medline: 30 11 2022
entrez: 6 9 2022
Statut: ppublish

Résumé

Diversion colitis and ulcerative colitis (UC) can be caused by different mechanisms; however, several case reports have described the development of typical UC following diversion colitis. A 63-year-old man underwent Hartmann's operation following a diagnosis of perforation of a sigmoid colon diverticulum and peritonitis. Stoma closure was performed 4 months later, and the portion of the sigmoid colon with the diverticulum was unintentionally left as a blind end. Following stoma closure, hematochezia worsened, and he was diagnosed as having developed diversion colitis only in the blind sigmoid colon. Intermittent use of topical mesalazine enemas controlled the bowel symptoms; however, 4 years after the stoma closure, bloody stools were observed again. Colonoscopy revealed coarse and friable granular mucosa with adherent mucopurulent exudate in the rectum, and mucosal erythematous edema with adherent mucopurulent exudate in the blind sigmoid colon. The histological findings indicated basal plasmacytosis, and goblet cell depletion and cryptitis in the lamina propria, which is characteristic of UC. To the best of our knowledge, this is the fourth description of a patient who developed UC following diversion colitis. Local inflammation may have triggered the development of UC through hematogenous or lymphogenous circulation of lymphocytes or autoantibodies.

Identifiants

pubmed: 36068373
doi: 10.1007/s12328-022-01696-4
pii: 10.1007/s12328-022-01696-4
doi:

Substances chimiques

Mesalamine 4Q81I59GXC

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1088-1093

Informations de copyright

© 2022. Japanese Society of Gastroenterology.

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Auteurs

Katsuki Yaguchi (K)

Inflammatory Bowel Disease Center, Yokohama City University Medical Center, 4-57 Urafune-cho Minami-ku, Yokohama, 232-0024, Japan.
Department of Gastroenterology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Yusuke Matsune (Y)

Inflammatory Bowel Disease Center, Yokohama City University Medical Center, 4-57 Urafune-cho Minami-ku, Yokohama, 232-0024, Japan.

Reiko Kunisaki (R)

Inflammatory Bowel Disease Center, Yokohama City University Medical Center, 4-57 Urafune-cho Minami-ku, Yokohama, 232-0024, Japan. reikok@yokohama-cu.ac.jp.
Department of Gastroenterology, Yokohama City University Graduate School of Medicine, Yokohama, Japan. reikok@yokohama-cu.ac.jp.

Kentaro Araki (K)

Inflammatory Bowel Disease Center, Yokohama City University Medical Center, 4-57 Urafune-cho Minami-ku, Yokohama, 232-0024, Japan.

Hideaki Kimura (H)

Inflammatory Bowel Disease Center, Yokohama City University Medical Center, 4-57 Urafune-cho Minami-ku, Yokohama, 232-0024, Japan.

Yoshiaki Inayama (Y)

Department of Diagnostic Pathology, Yokohama City University Medical Center, Yokohama, Japan.

Jiro Kumagai (J)

Department of Pathology, Yokohama City Minato Red Cross Hospital, Yokohama, Japan.

Shin Maeda (S)

Department of Gastroenterology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

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