define: hyperplastic
What is a hyperplastic colon polyp?
hyperplastic colon polyps~~~~~~~~~~~~~~~~~~~~~~~~~~
Phenotype and Polyp Landscape in Serrated Polyposis Syndrome: A Series of 100 Patients From Genetics Clinics
Abstract
Serrated polyposis syndrome (SPS), also known as
hyperplastic polyposis, is a syndrome of unknown genetic basis defined
by the occurrence of multiple serrated polyps in the large intestine and
associated with an increased risk of colorectal cancer (CRC). There are
a variety of SPS presentations, which may encompass a continuum of
phenotypes modified by environmental and genetic factors. To explore the
phenotype of SPS, we recorded the histologic and molecular
characteristics of multiple colorectal polyps in patients with SPS
recruited between 2000 and 2010 from genetics clinics in Australia, New
Zealand, Canada, and the United States. Three specialist
gastrointestinal pathologists reviewed the polyps, which they classified
into conventional adenomas or serrated polyps, with various subtypes,
according to the current World Health Organization criteria. Mutations
in BRAF and KRAS and mismatch repair protein
expression were determined in a subset of polyps. A total of 100
patients were selected for the study, of whom 58 were female and 42 were
male. The total polyp count per patient ranged from 6 to 150 (median
30). The vast majority of patients (89%) had polyposis affecting the
entire large intestine. From this cohort, 406 polyps were reviewed. Most
of the polyps (83%) were serrated polyps: microvesicular hyperplastic
polyps (HP) (n=156), goblet cell HP (n=25), sessile serrated
adenoma/polyps (SSA/P) (n=110), SSA/P with cytologic dysplasia (n=28),
and traditional serrated adenomas (n=18). A further 69 polyps were
conventional adenomas. BRAF mutation was mainly detected in
SSA/P with dysplasia (95%), SSA/P (85%), microvesicular HP (76%), and
traditional serrated adenoma (54%), whereas KRAS mutation was
present mainly in goblet cell HP (50%) and in tubulovillous adenoma
(45%). Four of 6 SSA/Ps with high-grade dysplasia showed loss of
MLH1/PMS2 expression. CRC was diagnosed in 39 patients who were more
often found to have a conventional adenoma compared with patients
without CRC (P=0.003). Patients with SPS referred to genetics clinics had a pancolonic disease with a high polyp burden and a high rate of BRAF mutation. The occurrence of CRC was associated with the presence of conventional adenoma.
