Upper Gastrointestinal Tract Involvement in Inflammatory Bowel Diseases: Histologic Clues and Pitfalls

Abstract

The upper gastrointestinal (UGI) manifestations of inflammatory bowel diseases (IBDs) are frequently obscured by classic ileal and colonic symptoms and are reported to involve only 0.5% to 4% of adult patients. However, because of the improvement of endoscopic techniques and the growing use of esophagogastroduodenososcopy with biopsy, both asymptomatic and clinically significant esophageal, gastric, and duodenal manifestations are increasingly recognized. The UGI involvement in IBD was historically synonymous with Crohn’s disease (CD), but the doctrine of ulcerative colitis (UC) being limited to the colon has been challenged, and UC-related gastroduodenal lesions have been reported. The diagnosis of UGI IBD should ideally rely on a combination of the clinical history, endoscopic picture, and histologic features. Although endoscopic changes such as aphthoid or longitudinal ulcers and bamboo-joint-like pattern are suggestive of CD, histologic evaluation increases the sensitivity of the IBD diagnosis since histologic alterations may be present in endoscopically unremarkable mucosa. Conversely, in many cases, the histologic findings are nonspecific, and the knowledge of clinical history is vital for reaching an accurate diagnosis. The presence of epithelioid granuloma is highly suggestive of CD but is present in a minority of CD cases; thus, pathologists should be aware of how to diagnose UGI IBD in the absence of granulomata. This article reviews the most important clinical, endoscopic, and histologic features of IBD-associated esophagitis, gastritis, and duodenitis, as well as the IBD-related manifestations in the biliary tract and the postcolectomy setting.

Application of a pattern‐based approach to histological diagnosis in very early onset IBD (VEO‐IBD) in a multicentric cohort of children with emphasis on monogenic disease with IBD‐like morphology

“…Of note, a poorly defined IBD‐U pattern of injury in our cohort was statistically correlated with MD, meaning that ill‐defined aspects of IBD‐like damage should prompt suspicion. Furthermore, while upper GI findings are often normal, some features such as focally enhanced gastritis 17 and the aforementioned villous blunting/atrophy should again be looked for and mentioned in the pathology report.…”

Series of clinical observations of Crohn’s disease of the upper gastrointestinal tract

“…При этом заболевании может поражаться любой отдел ЖКТ, однако, наиболее часто определяются воспалительные изменения в терминальном отделе подвздошной кишки и/ или толстой кишке [1]. Частота поражения верхних отделов ЖКТ, по данным разных авторов [2,3] колеблется от 0,5-34%. Такой разброс данных в эпидемиологических исследованиях вызван отсутствием стандартизированных методов диагностики и лечения пациентов с указанной локализацией БК.…”

“…Чаще всего поражение верхних отделов ЖКТ сочетается с воспалением в терминальном отделе подвздошной кишки и толстой кишки [3] и встречается в детском возрасте, а также у пациентов молодой возрастной группы. К эндоскопическим признакам БК верхних отделов относят афты, линейные эрозии или язвы и поражения по типу «бамбуковых стеблей» [2]. Между тем, стоит учитывать, что ряд эндоскопических изменений при БК верхних отделов ЖКТ может напоминать картину таких заболеваний, как язвенная болезнь желудка или двенадцатиперстной кишки, рефлюкс-эзофагит при гастроэзофагеальном рефлюксе, хронический гастрит.…”

Colitis-Induced Small Intestinal Hypomotility Is Dependent on Enteroendocrine Cell Loss in Mice

“…The symptoms experienced by patients with inflammatory bowel disease, especially ulcerative colitis, may include those that are colonic in nature, such as bloody stools, abdominal pain, and weight loss, as well as those that are more general in nature, such as severe nausea and abdominal bloating. 1 , 2 , 3 Although the first set of symptoms may be attributable to the effects of colonic inflammation itself, those that are more vague seem to overlap with the symptoms that patients with small intestinal dysmotility experience, 4 such as occur in response to medications, 5 , 6 or diabetes. 7 In support of this possibility, several investigators have described the development of intestinal dysmotility in experimental colitis, 8 , 9 , 10 , 11 which has been attributed to impaired enteric nervous function.…”