Ulcerative colitis and adenocarcinoma colon diagnosed simultaneously in an 18-year-old male with four months history of bloody diarrhea

To the Editor: A n 18-year-old male patient presented to us with pain in the lower abdomen, diarrhea, and bleeding per rectum since 4 months previously. A 10 × 6 cm lump was seen in the right iliac fossa. Contrast-Enhanced Computed Tomography Scan (CECT) showed thickened wall of the cecum, ascending and descending colon, and rectum suggestive of inflammatory bowel disease (IBD). Colonoscopy showed a circumferential mass in the ascending colon just distal to the cecum. Colon showed loss of haustera and a diffuse colitis. Multiple biopsies from the colon showed features consistent with ulcerative colitis (UC). Biopsies from the colonic mass showed an adenocarcinoma. A total proctocolectomy with iliostomy was performed. The surgical specimen received showed a 6-cm ulcerated circumferential growth in the proximal colon, 3 cm distal to the cecum, involving full thickness of the colonic wall (Fig. 1A). Mucosa of the entire colon was markedly congested. Normal colonic mucosa was not identified. Appendix was thin walled and dilated. On the serosal aspect of the proximal colon a 6-cm mass was identified, separate from the colon wall. The surface of the mass was gray-white and firm. Sections from the ulceroinfiltrative growth in the colon showed a mucin-secreting adenocarcinoma extending from the surface epithelium to the serosa. The tumor cells were arranged in glandular pattern. At some places the cells were lying in pools of mucin (Fig. 1B). Two out of 31 lymph nodes showed tumor metastasis. Sections from other parts of colon and appendix showed disorganized and disoriented glands with loss of mucin, cryptitis, and crypt abscesses. Lamina propria showed paucity of glands, mucosal gap, fat infiltration, and infiltration by lymphocytes, plasma cells, and neutrophils (Fig. 1B). Sections from the serosal mass showed a lymph node with reactive lymphadenitis. A final diagnosis of poorly differentiated mucin secreting adenocarcinoma colon with UC was given. (A) Resected specimen of total proctocolectomy with terminal ileum. Proximal colon showed a circumferential ulceroinfiltrative growth (small arrow). The mucosa of the rest of the colon was completely ulcerated and markedly congested. Normal mucosa was not identified in any part of the colon. In the proximal colon, on the serosal aspect there was a 6-cm diameter mass (large arrow). Inset shows the gray white cut surface of the mass. (B) Sections from the ulceroinfiltrative growth in the proximal colon showed an adenocarcinoma involving the surface epithelium and extending to the serosa. Few places showed malignant cells lying in pools of mucin. The surface epithelium showed inflammation and congestion (H&E, ×400). Ulcerative colitis is a chronic ulceroinflammatory disorder. It can occur at any age group with peaks at 20–25 years and 70–80 years. In cases of UC colorectal carcinoma is observed in 5.5%–13.5% patients in all age groups combined.1 The time from diagnosis of UC to developing adenocarcinoma is about 10–12 years.2 UC begins in the rectum and may spread proximally to involve the entire colon (pancolitis). The most feared complication of long-standing UC at all ages is carcinoma. Established risk factors for developing carcinoma in UC are: long duration of disease (>10 years), large extent of disease, low disease activity, young age at presentation, inadequate pharmacologic therapy, and folate deficiency.1 UC-associated colorectal cancer can occur in any part of the colon. In a study of 27 patients with UC-associated adenocarcinoma, 86% were located in the left colon and 14% in the right colon. In the left colon rectosigmoid was affected most frequently (54% cases).3 In our case the adenocarcinoma was located in the right colon, which is infrequently involved by carcinoma. Microscopically, most carcinomas are adenocarcinomas with varying degrees of differentiation. Adolescents and young adults with childhood-onset UC are at a greater risk for dysplasia and colon cancer. Dysplasia may be evident as early as 7–10 years after onset of colitis and present in patients as young as 16 years. Therefore, the risk for colon cancer in patients with childhood-onset colitis must be based on the duration of illness and not on their chronological age.4 Our patient presented at 18 years of age with adenocarcinoma with only a 4-month history of UC. In a study by Michener et al5 that included 336 patients less than 21 years of age with UC, 35% of patients had symptoms for less than 6 months. In adenocarcinoma associated with UC the underlying inflammatory disease tends to mask the signs and symptoms of carcinoma so that these cancers are extremely insidious. This makes carcinomas in cases of IBD twice as inoperable as carcinomas not associated with IBD. The most important diagnostic procedure for carcinoma colon is endoscopy of the entire colon. The current recommendations for surveillance include biennial colonoscopy with extensive biopsy after 8–10 years of total colitis and after 10–15 years of left-sided colitis.1 To conclude, adenocarcinoma in UC can develop in a patient regardless of age. The duration of symptoms and not the age of the patient should be the criterion chosen for regular surveillance by endoscopy. Multiple endoscopic directed biopsies will help in predicting the risk of malignancy (presence of dysplasia) or diagnose malignancy developing in the background of UC at a much earlier stage.