Familial adenomatous polyposis (FAP) is an inherited autosomal dominant syndrome caused by germ-line mutations of the adenomatous polyposis coli (APC) gene. Clinical diagnosis of familial adenomatous polyposis is usually based on the presence of >100 colonic adenomas, which, if left untreated, progress to colorectal cancer, typically at age under 40 years. Attenuated adenomatous polyposis coli is a variant of familial adenomatous polyposis and also has been described as "hereditary flat adenoma syndrome". Attenuated adenomatous polyposis coli is recognized by the occurrence of <100 (> or =5 or > or =10) colonic adenomas. It is tend to be located proximal to splenic flexure and a later onset of colorectal carcinoma than familial adenomatous polyposis. PURPOSE: This study was performed to analyze the clinicopathologic features of suspicious attenuated adenomatous polyposis coli, to document the occurrence of colorectal carcinoma, and to assess the definition of attenuated adenomatous polyposis coli. METHODS: From June 1989 to June 1998, we reviewed 773 cases of colonic adenomas and compared with three groups (Group I, II, III) at Asan Medical Center. Median follow-up period was 16.4 months (range, 1 to 102 months). RESULTS: The incidence of suspicious attenuated adenomatous polyposis coli (Group II) was 4.9%. The most common symptom was anal bleeding (36.9%). Median size and number of adenomas were 1.0 cm (0.2 to 7.5 cm), 2 (1 to 43), respectively.Location of adenoma was prevalent at right colon in Group II (P<0.05). In respect to the occurrence of carcinoma in situ (CIS), it was more frequently presented in Group II (13.5%) and Group III (13.6%) whereas 4.1% in Group I (P<0.05). Recurrence rates within 12 months after polypectomy or surgery in Group II was 13.5% whereas 5.6% in Group I (P<0.05). CONCLUSIONS: Histopathology revealed suspicious attenuated adenomatous polyposis coli with villous component to be relatively correlated with occurrence of colorectal carcinoma. In suspicious attenuated adenomatous polyposis coli (Group II), the interval of the recurrence of the polyps was shorter than the control group with right colonic predominancy. These findings might be associated with genetic codominance of APC gene or other mutator genes.