[A Case of Colorectal Carcinoma with Subserosal Fibrosis in the Absence of Tumor Invasion].

BACKGROUND: Chronic inflammatory conditions, such as obstructive colitis and inflammatory bowel disease(IBD), are representative causes of colonic fibrosis. In addition, there have been reports that endoscopic interventions, including biopsies and local therapies, may induce submucosal fibrosis.

CASE PRESENTATION: A 50‒year‒old woman presented to our hospital with abdominal pain and fever that had developed the day before presentation. She reported chronic constipation for several years and had not had a bowel movement for several days. Abdominal computed tomography revealed bowel wall thickening from the lower rectum(RS)to the upper rectum(Ra), along with enlargement of the regional lymph nodes. Colonoscopy revealed a lesion located approximately 12 cm from the anal verge in the rectum, presenting as a type 2 advanced carcinoma involving one‒third of the circumference. Histopathological examination of the biopsy specimen revealed well‒differentiated tubular adenocarcinoma(tub1), and positron emission tomography‒computed tomography(PET‒CT)showed no evidence of distant metastasis. Based on these findings, the clinical diagnosis was rectal cancer, cT3N2aM0, Stage Ⅲb. The patient underwent laparoscopic low anterior resection. Intraoperative findings revealed rectal distension with a tumor appearing to reach the subserosal layer, raising suspicion of subserosal invasion. D3 lymph node dissection was performed, and the rectum was resected with anastomosis using the double stapling technique. The postoperative course was uneventful: the patient resumed oral intake on postoperative day 6 and was discharged on day 11. Histopathological examination of the resected specimen revealed pT2N0M0, Stage Ⅰ disease. Notably, subserosal fibrosis accompanied by lymphoid follicular hyperplasia was observed, without any continuity between the tumor and the fibrotic area. The patient has remained recurrence‒free during the 3‒year follow‒up period after surgery.

DISCUSSION: In this case, subserosal fibrosis was observed without histological evidence of tumor invasion into the subserosal layer. Moreover, no common causes of colonic fibrosis were identified. A possible mechanism for the fibrosis is chronic mechanical traction at the tumor base, resulting in reactive changes in the subserosa.

CONCLUSION: We report a rare case of colorectal carcinoma associated with subserosal fibrosis in the absence of tumor invasion. A brief review of the relevant literature is also presented.