Large Hyperplastic Polyps Research Articles

Distribution and prevalence of colorectal hyperplastic polyps using magnifying pan‐mucosal chromoendoscopy and its relationship with synchronous colorectal cancer: Prospective study

Patients with multiple (hyperplastic polyposis) or large hyperplastic polyps (HPs) predominantly in the right-sided colon, have been reported to have an increased risk of colorectal cancer (CRC). This prospective study was conducted to clarify the distribution of various sized HPs using magnifying pan-mucosal chromoendoscopy and its relationship with synchronous CRC. Patients eligible for this study had an initial total colonoscopy. Indigo carmine dye was sprayed throughout the whole colon and rectum, and diagnoses were made using magnifying colonoscopy. A total of 263 patients were enrolled, and a total of 3060 HPs were observed in 226 (86%) patients. The prevalence of patients with intermediate size (> or = 6 mm) HPs was 8.7% (n = 23) and that of patients with large HPs (> or = 10 mm) was 0.8% (n = 2). Of 3060 HPs, the numbers of diminutive (< 6 mm), intermediate size and large HPs were 3020, 38 and two, respectively, and 5.0%, 42.1% and 100% of these were located in the right-sided colon, respectively. Synchronous CRC was observed in 64 (24%) of 263 patients. Compared to patients without HPs, patients with intermediate size HPs showed a significant increase in odds ratio (OR) for synchronous CRC (OR = 4.9: 95% CI [1.3-18.2]), but there was no significant association between synchronous CRC and patients with diminutive or large HPs. Compared to diminutive HPs, intermediate size and large HPs were predominantly located in the right-side colon. Moreover, intermediate size HPs were significantly correlated with synchronous CRC.

Angiogenesis in colon hyperplastic polyp

Despite the significance of tumor angiogenesis and the extensive knowledge on the molecular basis of blood vessel formation in carcinoma of colorectum, no data exist in hyperplastic polyp. This prompted us to examine angiogenesis in hyperplastic polyp. Eleven small hyperplastic polyps, 13 large hyperplastic polyps and their adjacent normal mucosas were included in this study. Angiogenesis was assessed by immunohistochemistry using monoclonal antibody against CD34. Angiogenic factor, thymidine phosphorylase was also examined by immunohistochemistry. Intra-tumoral microvessel density (IMD) in large hyperplastic polyp was significantly higher than that in small hyperplastic polyp ( P<0.01) and that in normal mucosa ( P<0.01). DAD in small hyperplastic polyp was also significantly higher than that in normal mucosa ( P<0.01). Expression of dThdPase was almost observed in stromal cells in normal, small and large hyperplastic polyp. In addition, the proportion of the stromal cells expressing dThdPase in large hyperplastic polyp was significantly higher than that in small hyperplastic polyp and normal tissue ( P<0.01, respectively). The proportion of the stromal cells expressing dThdPase in small hyperplastic polyp was significantly higher than that in normal tissue ( P<0.01). The present study provides that angiogenesis may have an important role(s) in the development of hyperplastic polyp and dThdPase in stromal cells may support angiogenesis in hyperplastic polyp. Anti-angiogenic therapy might be available for suppression of hyperplastic polyp.

Phenotypic characteristics and risk of cancer development in hyperplastic polyposis: case series and literature review.

Hyperplastic polyposis (HP) is a poorly understood condition. The aim of this study is to describe the phenotype and the risk of cancer in HP. Patients with HP, as defined by the WHO International Classification, were identified through the University of Utah and the Huntsman Cancer Institute databases. Family history was retrieved when possible. Fifteen patients were identified (10 M, 5 F) with a mean age at diagnosis of 52.6 +/- 16.4 yr (18-71). Sixty-five colonoscopies were performed (2-11 per person). A median of 90 polyps (16-210) per person and 15 polyps (range, 0-100) per procedure were reported. The median follow-up was 33 months (3-133); no cancer occurred during this period. Polyps were more frequent in the distal than the proximal colon (74%vs 26%; p < 0.001). The median polyp size was 4 mm (1-40 mm). Fifty-one hyperplastic polyps >10 mm were identified in 10 patients (38 proximal, 13 distal; p= 0.089). Forty-eight adenomas were found in 11 patients and were uniformly distributed. Serrated adenomas (n = 3) were found in one patient. A unique patient had 20 large hyperplastic polyps, 24 adenomas, 3 serrated adenomas, and 118 hyperplastic polyps. None of the patients had a first-degree relative with colon cancer. In HP, hyperplastic polyps are more frequently distal colonic, and vary greatly in size and number. Most patients also develop adenomas that are distributed throughout the colon. No cancers developed within 3 yr of follow-up. Colonoscopic surveillance at intervals of 1-3 yr, depending upon the number and size of both adenomatous and hyperplastic polyps, appears prudent.

The Use of Indigocarmine Spray Increases the Colonoscopic Detection Rate of Flat Adenomas and Large Sessile Hyperplastic Polyps

Background: In Western populations, it is not clear whether indigocarmine (IC) spray during colonoscopy increases the detection of colorectal polyps. Methods: 500 patients were prospectively entered into this study. FAP and IBD patients were excluded. The patients were randomly allocated into 3 groups; A (n=200): A Japanese colonoscopist with expertise in IC spray performed chromo-colonoscopy with 0.2% IC solution sprayed onto the entire colon during scope withdrawal; B (n=200): Initial 100 patients (B-1), a Western colonoscopist with no previous experience of IC spray performed conventional colonoscopy, but with at least 10 minutes observation during colonoscopy withdrawal. In the next 100 patients (B-2), he performed chromo-colonoscopy with IC spray; C (n=100): Historical controls performed by the Western colonoscopist consecutively performed prior to the study. In all groups, all lesions were resected using standard techniques. Polyps were classified as pedunculated, sessile and flat. Histology was assessed by a single, blinded pathologist. Sex, age, indication, family history of colorectal cancer and past history of colorectal cancer were investigated as candidate confounding factors. Results: Mean numbers of all polyps (AP), neoplastic polyps (NP), flat neoplastic polyps (FNP) and large sessile hyperplastic polyps (LSHP) are shown in the table. In all types of polyps, there were significant differences between A and B-1, A and C, but there was no significant difference between A and B-2. Sex, age and indication were confounding factors in AP, NP and FNP. Family history was a confounding factor in NP, and past history in FNP. The negative binomial regression model was applied, because this model is a much better fit for the observed proportion rather than a Poisson regression model. Adjusting for confounding factors did not change the results Conclusion: IC spray significantly increases the detection rates of AP, NP, FNP and LSHP in a western population. Gastroenterologists can rapidly learn the technique.

Prevalence of significant proximal colorectal neoplasia in patients with large proximal hyperplastic polyps

Prevalence of significant proximal colorectal neoplasia in patients with large proximal hyperplastic polyps

The significance of large hyperplastic polyps

The significance of large hyperplastic polyps

Aberrant DNA Methylation: Have We Entered the Era of More Than One Type of Colorectal Cancer?

It has been known for over two decades that DNA from colorectal cancer (CRC) is hypomethylated compared to that from normal colonic epithelia. 1,2 More recently it has also been recognized that specific CpG dinucleotide islands are often hypermethylated in this tumor type, 3 giving rise to the term CpG island methylator phenotype, or CIMP+. 4 Hypomethylation may contribute to the activation of oncogenes, whereas CpG-island specific hypermethylation has been linked to the transcriptional silencing of tumor suppressor genes. The relationship between these two epigenetic phenomena has not been examined, however, in CRC. Intuitively one might expect that tumors with severe global DNA hypomethylation might also show a lower frequency of CpG island hypermethylation due to a lower overall content of methyl groups. The meticulous study by Bariol et al 5 in this issue of The American Journal of Pathology reveals this not to be the case. No association was apparent between global 5-methyl cytosine content and the number of methylated CpG sites in a relatively large and representative series of 97 premalignant and malignant lesions. With only one exception, all of the 22 CRCs investigated showed a lower 5-methyl cytosine content compared to normal mucosa from the same patient. Moreover, approximately 30 to 40% of hyperplastic polyps, adenomas, and CRCs showed no methylation at any of the five CpG sites examined. This most recent study by the Ward laboratory follows on from their previous work in characterizing CIMP+ CRCs. 6 It is also relevant to the notion put forward by these and other workers that CIMP+ and the closely related tumor subgroup with microsatellite instability (MSI+) originate in large hyperplastic polyps and serrated adenomas. 7,8 Increasingly, it is becoming recognized that tumors with widespread DNA hypermethylation have distinctive clinicopathological and molecular features. 4,6,9 Although the study by Bariol et al 5 emphasizes and probably serves to justify the current interest in hypermethylation as opposed to hypomethylation, there is clearly much more to be learned about the general role of aberrant DNA methylation in the development and progression of CRC.

A resected large tubular adenomatous polyp regrowing as a large hyperplastic polyp

A resected large tubular adenomatous polyp regrowing as a large hyperplastic polyp

Hyperplastic polyposis of the colon and rectum.

The significance of multiple hyperplastic polyps in relation to the risk of colon cancer is unknown although recent investigation suggests a causative link. We have prospectively identified a small but distinct group of patients that also suggests an association. These patients have either numerous (usually more than twenty, in sites other than the rectosigmoid alone) or large (greater than 1 cm) hyperplastic polyps, in association with either adenomatous polyps, polyps of mixed pathology or carcinoma of the colon and rectum. Additionally, there is frequently a first or second degree family history of colorectal carcinoma.

Hyperplastic polyps of the colorectum-innocent or guilty?

Hyperplastic polyps have traditionally been regarded as nonneoplastic polyps lacking malignant potential. The demonstration of genetic alterations within these lesions indicates an underlying neoplastic cause. There is evidence that hyperplastic polyps are heterogeneous. Most are innocuous, but subsets may have malignant potential. Risk factors for neoplastic progression include multiple, large, and proximally located polyps. Aberrant methylation resulting in the silencing of cancer genes may be an important underlying mechanism, particularly in pathways progressing to tumors with DNA microsatellite instability. Lesions intermediate between hyperplastic polyp and cancer include admixed polyps and serrated adenomas. Currently, pathologists have different thresholds for diagnosing serrated adenomas, including the distinction from large hyperplastic polyps. Reasons for over looking this pathway in the past may include rapid tumor progression and the fact that proximally located hyperplastic polyps may be flat and not especially numerous. Management of the serrated pathway of colorectal neoplasia may require novel approaches to screening, early detection, and prevention.

Phenotypic and molecular characteristics of hyperplastic polyposis

Background & Aims: Patients with hyperplastic polyposis are reported to have multiple and/or large hyperplastic polyps (HPs) and an increased risk of colorectal cancer, but the phenotype and genetic alterations in hyperplastic polyposis have not been studied in detail. Methods: We evaluated clinical-pathological and molecular characteristics of 129 HPs, 6 serrated adenomas, and 3 admixed hyperplastic-adenomatous polyps from 13 patients with hyperplastic polyposis (more than 20 HPs), 5 patients with a large HP (≥1 cm in diameter), and 5 patients with multiple HPs (5–10 HPs). Results: HPs in the right colon in contrast to the left colorectum had more frequent topographic dysregulation of p21Waf-1/Cip1 expression (94% vs. 76%, P = 0.03) and of proliferation (92% vs. 53%, P = 0.0001), but less frequent allelic loss of chromosome 1p (4% vs. 17%, P = 0.03). K-ras mutation was present in 8% of HPs, p53 gene product overexpression in none, and microsatellite instability in 3% without relationship to microsatellite instability in synchronous cancer. Patients with a large HP differed from those with multiple HPs in having a high frequency of right-sided HP (63% vs. 22%, P = 0.01) and of right-sided colon cancer (100% vs. 8%, P = 0.003). Hyperplastic polyposis was associated with a family history of colorectal cancer (P = 0.01) and with loss of chromosome 1p in HP (21% vs. 0%, P = 0.001). Conclusions: A hyperplastic polyp/dysplasia–to–adenocarcinoma sequence can be manifested in 3 distinct phenotypes consisting of patients with hyperplastic polyposis and chromosome 1p allelic loss in some HPs, in contrast to patients who have large, right-sided HPs or small numbers of HPs that lack 1p loss.GASTROENTEROLOGY 2000;119:323-332

Colorectal Carcinomas Arising in the Hyperplastic Polyposis Syndrome Progress through the Chromosomal Instability Pathway

The hyperplastic polyposis syndrome is characterized by the presence within the colon of multiple large hyperplastic polyps. We describe a case of hyperplastic polyposis syndrome associated with two synchronous carcinomas, one of which arises within a pre-existing hyperplastic lesion. Comparative genomic hybridization was used to determine genetic changes in both carcinomas and several associated hyperplastic lesions. Microsatellite analysis at five loci was performed on carcinomas and representative hyperplastic polyps, and p53 status was analyzed by immunohistochemistry. Both carcinomas showed multiple genetic aberrations, including high level gains of 8q and 13q, and loss of 5q. These changes were not seen in the hyperplastic polyps. Microsatellite instability was not seen in the carcinomas, four separate hyperplastic polyps, the hyperplastic polyp with mild adenomatous change associated with the carcinoma, or a separate serrated adenoma. Allelic imbalance in the cancers at D5S346 and D17S938 suggested allelic loss of both p53 and APC, as well as at the loci D13S263, D13S174, D13S159, and D18S49. An early invasive carcinoma in one hyperplastic polyp stained for p53 protein, but the associated hyperplastic polyp was negative. In this case, neoplastic progression followed the typical genetic pathway of common colorectal carcinoma and occurred synchronously with mutation of p53.

Large hyperplastic polyps of the right colon

The 2-cm right colon polyp described by Rothstein and Kochman 1 Rothstein RD Kochman M Large hyperplastic polyps of the right colon. Gastrointest Endosc. 1998; 47: 211-212 Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar appears to display a finding typical for such hyperplastic polyps, that is, “yellowishness.” In my experience, 2 Langdon DE Pigmentation in hyperplastic right and transverse colon polyps. Am J Gastroenterol. 1996; 91: 1675 Google Scholar at least half of larger, purely hyperplastic polyps of the right and transverse colon (all pathologically confirmed) exhibit some degree of yellow, even a brilliant nonwashable yellow. Such yellowishness can be quite helpful, calling attention to a subset of easily missed, very sessile, flat, spreading, hyperplastic lesions. This color occurs because unlike adenomas, hyperplastic polyps take up pigment, not only yellow but also black as in cases of severe melanosis coli. Carcinoids and lipomas can be yellow, but they present a very different endoscopic appearance and texture. I sense that such larger hyperplastic polyps are found among patients undergoing colonoscopy because of increased risk for neoplasia rather than for other indications. I still sample and ablate these polyps, although none has proved to be adenomatous.

FAMILIAL GIANT HYPERPLASTIC POLYPOSIS PREDISPOSING TO COLORECTAL CANCER: A NEW HEREDITARY BOWEL CANCER SYNDROME

A mother and five of her ten offspring developed colonic cancers, the mother and one of the offspring being younger than 50 years of age at diagnosis. Despite fulfilling the Amsterdam criteria for hereditary non-polyposis colorectal cancer (HNPCC), several features pointed towards the possibility that this represented a different syndrome of familial cancer. Most notable was the presence of large, multiple hyperplastic polyps and mixed polyps in four of the subjects whose pathology was available for review. In addition, three of the four subjects had cancers that were negative for DNA replication errors (RER-). The subject with an RER+ cancer had a second RER+ cancer and three adenomas, one in contiguity with the second cancer. This subject also had multiple, large hyperplastic polyps, thereby combining hyperplastic polyposis and a proneness to multiple RER+ tumours. One of the hyperplastic polyps was also RER+. Two of five young asymptomatic descendants have been found to harbour multiple colorectal polyps. It is suggested that giant hyperplastic polyposis is a new familial syndrome predisposing to colorectal cancer.

Mucosal cell proliferation in patients with hyperplastic colorectal polyps.

Morphologic, histochemical, and cytoproliferative characteristics differentiate hyperplastic polyps from adenomas. Even so, these polyps are indicators of populations with a high colorectal cancer risk. Since changes in mucosal cell proliferation are highly predictive biomarkers of the adenomacarcinoma sequence, this study examined the cytoproliferative profiles of mucosa bearing hyperplastic polyps, in a search for the significance of such lesions in bowel carcinogenesis. Proliferative activity demonstrated by immunohistochemical detection of the in vitro uptake of bromodeoxyuridine was evaluated in the rectal mucosa of 26 patients with hyperplastic polyps, 35 with adenomas < 1 cm, 60 with adenomas > 1 cm, 10 with adenomas + synchronous hyperplastic polyps, and 400 controls. An upward shift of the major DNA synthesis zone to the intermediate and surface crypt compartments was found in all four patients groups. Significant hyperproliferation, on the other hand, was only observed in patients with large adenomas or hyperplastic polyps, or small adenomas and synchronous hyperplastic polyps. These findings suggest that hyperplastic polyps are morphologic indicators of tumor initiation in the rectal mucosa and its ensuing hyperproliferation. Abnormalities in the distribution of proliferation in the mucosa do not appear to be specifically associated with the morphogenesis of hyperplastics polyps.

Giant hyperplastic polyps of the gastric remnant simulating carcinoma

Large hyperplastic polyps of the gastric remnant were detected in 2 male patients who had undergone Billroth II gastrojejunostomy for peptic ulcer disease 13 and 18 years earlier. Both patients presented with iron deficiency anemia due to chronic occult gastrointestinal bleeding. The clinical and radiographic findings were initially suggestive of gastric stump malignancy, and one of the resected hyperplastic polyps contained foci of carcinoma in situ. We illustrate the radiographic and pathologic features of these lesions together with a review of the pertinent literature.

Ultrastructure of the absorptive cell glycocalyx in hyperplastic colonic polyps after staining with Alcian Blue and high iron diamine

The glycocalyx of absorptive cells in large intestinal hyperplastic polyp was characterized histochemically at the electron microscope level by the use of the Alcian Blue pH 2.5 and high iron diamine techniques with the aim of comparing their ability in preserving the fine reticular network of the structure. Both the reagents stained glycocalyx, indicating the presence of sulphated acidic glycoconjugates. However, they showed different degrees of condensation of the reactive sites. Alcian Blue preserved its filamentous appearance better.