The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.
HNPCC patients had lower stage disease at diagnosis than the unselected CRC cases, mainly due to rarer distant metastases at diagnosis. They survived longer than unselected CRC patients with tumors of the same stage. The estimated death rate for the HNPCC cases, adjusted for stage and age differences, was at most two-thirds of the rate for the hospital series.
Poor differentiation and Crohn's-like reaction are more common in hereditary nonpolyposis colorectal cancer than colorectal cancers from general population. Poor differentiation and lymph node metastases are more commonly seen in MSH2-associated cancers than MLH1. Evaluation of the natural history, pathogenesis, and prognosis of colorectal cancer in hereditary nonpolyposis colorectal cancer should include consideration of which mismatch repair genes are mutated and what the specific mutations are.
Anal fissure (fissure-in-ano) is a very common anorectal condition. The exact etiology of this condition is debated; however, there is a clear association with elevated internal anal sphincter pressures. Though hard bowel movements are implicated in fissure etiology, they are not universally present in patients with anal fissures. Half of all patients with fissures heal with nonoperative management such as high fiber diet, sitz baths, and pharmacological agents. When nonoperative management fails, surgical treatment with lateral internal sphincterotomy has a high success rate. In this chapter, we will review the symptoms, pathophysiology, and management of anal fissures.
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