I Recently Did a Colonoscopy on a Patient With Rectal Bleeding. The Patient Had Inflammation in the Rectosigmoid and Also in the Cecal Area. Is This Crohn’s Disease?
Colonoscopy plays an essential role in the evaluation of patients with rectal bleeding. In patients found to have colitis on colonoscopy, the distribution and appearance of the inflammatory process and the presence of “skip” lesions can help the endoscopist distinguish ulcerative colitis (UC) from Crohn’s disease (CD). Mucosal biopsies can confirm a diagnosis of chronic inflammatory bowel disease (IBD), exclude other causes of colitis, and differentiate between UC and CD. However, as there can be overlap in the endoscopic and histologic appearance of UC and CD, the clinician often relies on the presence or absence of terminal ileal and/or upper gastrointestinal (GI) involvement to help distinguish CD from UC. Increasingly, serological testing including anti-Saccharomyces cerevisiae (ASCA), anti-nuclear cytoplasmic antibodies (ANCA), outer membrane porin protein C (ompC), and CBir1 (flagellin) have been used to distinguish CD from UC. Although medical therapy is often similar for patients with either UC or Crohn’s colitis, the long-term prognosis and surgical management vary considerably between these 2 disorders. Therefore, making the correct diagnosis is vital with regard to making management decisions.
The traditional teaching is that the inflammation in UC involves the rectum and progresses proximally in a continuous fashion.1 In contrast, CD often spares the rectum and can have “skip lesions.” Skip lesions are areas of uninvolved mucosa both endoscopically and microscopically interspersed between inflamed tissue in the GI tract. However, several exceptions to the traditional teaching for differentiating between these 2 phenotypes of IBD have been described in recent years. As they relate to the patient described above, these include the presence of periappendiceal inflammation in patients with left-sided UC, a patchy disease that develops in patients with UC as a result of medical therapy (“cecal patch”), and patchy disease that develops in patients with UC as a result of medical therapy (Figure 1-1).
Figure 1-1. Periappendiceal inflammation (A, B). Normal transverse colon (C). Rectal inflammation (D).
Several studies have evaluated patchy cecal and periappendiceal inflammation in patients with limited left-sided UC. D’Haens originally described this phenomenon in 1997.2 D’Haens et al coined the term “cecal patch” to describe a subset of UC patients with left-sided colitis associated with cecal inflammation and who also had endoscopic and histologic sparing of the transverse colon. In their prospective study, 20 consecutive patients with established left-sided UC were followed for approximately 9 years. Fifteen patients (75%) were found to have periappendiceal inflammation that was separated from distally inflamed segments of the colon by areas of uninvolved mucosa. None of the patients developed features of CD.
In another prospective endoscopic and biopsy study by Yang et al, appendiceal orifice inflammation (AOI), as determined concomitantly by endoscopy and histology, was seen in 26% of 94 patients who had UC that did not extend proximally to the hepatic flexure.3 There was no statistically significant difference in the prevalence of appendiceal orifice involvement between previously medically treated and newly diagnosed cases of UC, and thus, these authors concluded that appendiceal involvement was not due to the effects of medical therapy. In 2002, Matsumoto et al examined 40 patients with distal UC (including 10 patients who were presenting with their initial flare of UC) and found periappendiceal involvement in 23 (57%) of them.4 In 2004, Mutinga et al compared clinical and pathologic features, as well as the natural history of disease, in a cohort of 12 patients with left-sided UC combined with patchy right colonic inflammation to a control group of 35 patients with isolated left-sided UC who were followed for almost 9 years. They found no differences between the two groups with regard to the severity of the disease, the prevalence of extraintestinal manifestations, a family history of colitis, or gender distribution. The only statistically significant difference between the groups was age. The subject group with patchy right colonic inflammation was noted to be about 10 years older. None of the subjects with patchy right-sided disease had disease progression to pancolitis, development of high-grade dysplasia (HGD), or clinical or pathologic features consistent with CD.5
Apparent skip lesions in UC may also develop in patients with UC over time or as a result of medical therapy. Kim et al studied 32 UC subjects on medical therapy who underwent serial colonoscopies for a period of up to 13 years. Patchy disease, rectal sparing, or both were found on follow-up colonoscopy in 59% of the patients.6 In a 1995 study, Bernstein et al prospectively examined 39 UC subjects on medical therapy, and described endoscopic evidence of discontinuous patchiness in 44% of them.7 Odze et al performed a prospective randomized study and found that 64% of the patients treated with 5-aminosalicyclic acid (5-ASA) enemas showed reversion of previously inflamed rectal mucosa to a completely normal state (without chronic or active inflammation) in at least one of the patients’ rectal biopsies. Patients treated with 5-ASA enemas also showed a statistically higher percentage of normal biopsies (36%) per patient compared with the placebo-treated group (12%).8 These studies suggest that skip lesions, including rectal sparing and patchiness of disease, may occur over time in patients with UC, and may be associated with medical therapy.
In summary, UC patients with inflammation in the distal colon and cecum, as well as with endoscopic and histologic sparing of the remainder of the colon, should not be considered as having CD unless there are other features to suggest CD, such as deep fissuring ulcerations, evidence of fistula, or granulomas on histopathology. Assuming that there are no features to suggest small bowel involvement on imaging, the patient described above should be classified as having UC with a cecal patch.
1. Yantiss RK, Odze RD. Pitfalls in the interpretation of non-neoplastic mucosal biopsies in inflammatory bowel disease. Am J Gastroenterol. 2007;102(4):890-904.
2. D’Haens G, Geboes K, Peeters M, Baert F, Ectors N, Rutgeerts P. Patchy cecal inflammation associated with distal ulcerative colitis: a prospective endoscopic study. Am J Gastroenterol. 1997;92(8):1275-1279.
3. Yang SK, Jung HY, Kang GH, et al. Appendiceal orifice inflammation as a skip lesion in ulcerative colitis: an analysis in relation to medical therapy and disease extent. Gastrointest Endosc. 1999;49(6):743-747.
4. Matsumoto T, Nakamura S, Shimizu M, et al. Significance of appendiceal involvement in patients with ulcerative colitis. Gastrointest Endosc. 2002;55(2):180-185.
5. Mutinga ML, Odze RD, Wang HH, et al. The clinical significance of right-sided colonic inflammation in patients with left-sided chronic ulcerative colitis. Inflamm Bowel Dis. 2004;10(3):215-219.
6. Kim B, Barnett JL, Kleer CG, Appelman HD. Patchiness in treated ulcerative colitis. Am J Gastroenterol. 1999;94(11):3258-3262.
7. Bernstein CN, Shanahan F, Anton PA, Weinstein WM. Patchiness of mucosal inflammation in treated ulcerative colitis: a prospective study. Gastrointest Endosc. 1995;42(3):232-237.
8. Odze R, Antonioli D, Peppercorn M, Goldman H. Effect of topical 5-aminosalicylic acid (5-ASA) therapy on rectal mucosal biopsy morphology in chronic ulcerative colitis. Am J Surg Pathol. 1993;17(9):869-875.