Serrated polyposis syndrome

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Serrated polyposis syndrome
Other namesHyperplastic polyposis syndrome (former)
Hyperplastic Polyp of the Rectum (14060044206).jpg
Hyperplastic polyp seen under microscopy with H&E stain
Specialty Gastroenterology
Symptoms Asymptomatic
Complications Colorectal cancer (~20%) [1]
Usual onset55 years of age (average) [2]
TypesDistal and proximal
CausesEnvironmental and genetic factors
Risk factors Smoking, Lymphoma [3]
Diagnostic method Colonoscopy
TreatmentSurveillance colonoscopy
Polypectomy
Surgery
Frequency0.03–0.5%. [4]

Serrated polyposis syndrome (SPS), previously known as hyperplastic polyposis syndrome, is a disorder characterized by the appearance of serrated polyps in the colon. While serrated polyposis syndrome does not cause symptoms, the condition is associated with a higher risk of colorectal cancer (CRC). The lifelong risk of CRC is between 25 and 40%. SPS is the most common polyposis syndrome affecting the colon, but is under recognized due to a lack of systemic long term monitoring. [5] Diagnosis requires colonoscopy, and is defined by the presence of either of two criteria: ≥5 serrated lesions/polyps proximal to the rectum (all ≥ 5 mm in size, with two lesions ≥10 mm), or >20 serrated lesions/polyps of any size distributed throughout the colon with 5 proximal to the rectum. [6]

Contents

A family history of SPS and smoking tobacco are associated with a higher risk of serrated polyposis syndrome, whereas the use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with a lower risk. While the only validated genetic cause of SPS is RNF43, [7] additional important genetic abnormalities include BRAF mutations, abnormal CpG island methylator phenotype, and microsatellite instability. However, most individuals with the syndrome do not have an associated germline mutation. The types of polyps found in SPS include sessile serrated adenomas/polyps, traditional serrated adenomas, and hyperplastic polyps. SPS occurs in 2 phenotypes: proximal and distal. Proximal SPS has a greater risk of CRC than distal SPS.

The vast majority of cases may be managed with colonoscopy with removal polyps (polypectomy). Polyp removal is recommended to decrease the risk of colorectal cancer. Repeat colonoscopy should be performed every 1–2 years. If polyps are very large, numerous, or increase in number rapidly, then surgery may be necessary. Surgery may also be warranted if CRC is suspected or confirmed. First-degree relatives of people with SPS have an increased risk of CRC, and should undergo early screening with colonoscopy.

Types

Traditional serrated adenoma seen under microscopy with H&E stain, showing serrated crypts Traditional serrated adenoma intermed mag.jpg
Traditional serrated adenoma seen under microscopy with H&E stain, showing serrated crypts

SPS may occur with one of two phenotypes: distal or proximal. [6] The distal phenotype may demonstrate numerous small polyps in the distal colon (sigmoid) and rectum, whereas the proximal phenotype may be characterized by relatively fewer, but larger polyps in the proximal colon (cecum, ascending colon, etc.). [6] Individuals meeting only criterion 3 from 2010 criteria, or only criterion 2 from the 2019 classification, have a distal phenotype have a lower risk of CRC compared with the proximal phenotype. [6]

Signs and symptoms

Sessile serrated adenoma seen under microscopy with H&E stain Sessile serrated adenoma 3 very high mag.jpg
Sessile serrated adenoma seen under microscopy with H&E stain

Serrated polyposis syndrome often does not cause symptoms. The risk of colon cancer is between 25 and 40%. [8]

Sessile serrated polyps, as seen during endoscopy or colonoscopy, are flat (rather than raised) and are easily overlooked. Serrated lesions range in size from small (<5 mm) to large, and often have a "mucous cap" overlying the polyp. Serrated lesions are frequently located on the folds of the colon (haustral folds).[ citation needed ]

Pathophysiology

SPS is not caused by a single gene mutation. Several genetic abnormalities are associated with the condition, and a familial or inherited pattern may occur. Key genetic abnormalities include mutations in BRAF, abnormal CpG island methylator phenotype, and microsatellite instability. Additional implicated genes include: SMAD4, BMPR1A, PTEN, GREM1, and MUTYH. The only validated genetic cause of SPS is RNF43. [7] However, most individuals with SPS do not have a germline mutation in any of the associated genes, including RNF43. [4] As the underlying genetic risks for SPS are not fully understood, genetic testing is not recommended. Both autosomal dominant and autosomal recessive patterns of inheritance have been reported, [8] as well as sporadic. Individuals with SPS have serrated polyps, which include hyperplastic polyps, traditional serrated adenomas, and sessile serrated polyps. [5] In addition to serrated polyps, adenomas are often identified. [5]

Diagnosis

The diagnosis of serrated polyposis syndrome is achieved when either one of two criteria are met: ≥5 serrated lesions/polyps proximal to the rectum (all ≥ 5 mm in size, with two lesions ≥10 mm), or >20 serrated lesions/polyps of any size distributed throughout the large bowel with 5 proximal to the rectum. [6] Any serrated polyp is counted towards the diagnosis, including sessile serrated lesions, hyperplastic polyps, and traditional serrated adenomas. [4] In addition, the cumulative number of serrated lesions is cumulative over time and includes multiple colonoscopies. [4] The diagnosis of SPS is often overlooked, [9] and requires lifelong tracking of cumulative serrated polyps. [5]

Treatment

Colonoscopy is the mainstay of treatment for SPS, which allows for the identification of polyps and removal. [5] Polyp removal is recommended to prevent the development of colorectal cancer. If polyps are relatively few, then removal may be achieved with colonoscopy. After polyps are removed, repeat colonoscopy is recommended in 1 to 3 year intervals. [10] [5] On average, about 2.8 colonscopies are necessary to achieve control of disease. [11] The majority of cases may be managed with colonoscopy alone. [11] Narrow-band imaging, an imaging technique used to enhance features of mucosa seen during colonoscopy, may improve detection of serrated lesions; [12] however, one multicenter trial did not show improved detection. [13]

If polyps are very numerous, very large, or their growth cannot be controlled with colonoscopy, then surgery may be necessary. [14] When surgery is necessary, a total abdominal colectomy with ileorectal anastomosis should be considered to minimize the risk of colon cancer. [15] If surgery is necessary and involvement of polyps is focal or largely confined to a particular section of bowel, then segmental resection may be considered. [15] Segmental resection is also recommended for cancer. [16] In most cases, the rectum is left in place. Any remaining segments of colon or rectum require annual surveillance with colonoscopy. [16]

First degree relatives of people with SPS are at a higher risk of colorectal cancer [5] [17] [18] and SPS. [19] As such, these individuals should undergo screening with colonoscopy [20] beginning at the earliest of the following: 40 years of age, the age of the youngest diagnosis of SPS in the family, or 10 years younger than the earliest CRC related to SPS. [5] Repeat colonoscopy should be performed at 5 year intervals. [6]

Prognosis

The overall risk of colorectal cancer is about 19.9%. [1] However, the risk of cancer varies widely and depends on age, polyp burden, phenotype and the presence of dysplasia on histology. [4] Endoscopic surveillance can decrease the risk of progression to cancer. [4]

History

The condition was originally known as hyperplastic polyposis syndrome. [14] When the syndrome was first recognized, only hyperplastic polyps were included in its definition, [14] and the syndrome was believed to not be associated with a higher risk of colorectal cancer. [21] In 1996, a case series revealed an association of the syndrome with cancer and serrated adenomas. [22] Subsequently, other types of serrated polyps were found to occur in this condition, so the name was adjusted to the present "serrated polyposis syndrome." [14]

The World Health Organization released diagnostic criteria in 2010, which were updated in 2010 and again in 2019. [6] The 2010 classification defined SPS as meeting any of the following criteria: 1) five or more serrated polyps proximal to the sigmoid colon with 2 larger than 10 mm in size, 2) any serrated polyps found proximal to the sigmoid colon in a person with a first-degree relative with serrated polyposis, or 3) more than 20 serrated colon polyps. The updated 2019 classification revised the first criterion to include lesions in the sigmoid colon, and excluded very small polyps (<5 mm). [6] The updated 2019 classification also removed the criterion that included any serrated lesions proximal to the sigmoid colon in a person with a first degree relative with SPS. [6]

Epidemiology

Data regarding overall prevalence of SPS is lacking, but it is estimated to occur in roughly 1 in 100,000. [14] SPS is equally common among men and women. [2] Most individuals with SPS are diagnosed between 40 and 60 years of age, [4] with an average age of 55 years. [2] Nearly half of individuals with SPS have a family member with colorectal cancer. [16] Most individuals (37–70%) with SPS fulfill criterion 3 of the 2010 criteria (now criteria 2 from the 2019 classification). Of the remaining individuals with SPS, roughly half meet only criterion 1 and half meet both criteria 1 and 3 (2010 classification).

Among individuals undergoing colonoscopy for the evaluation of an abnormal fecal occult blood test, the prevalence of SPS ranges from 0.34 to 0.66%. The overall prevalence of SPS is 0.03–0.5%. [4] The prevalence of SPS is between 1 in 127 and 1 in 242 among individuals undergoing colonoscopy. [5] SPS is associated with tobacco use. [14] Aside from colorectal cancer, the risk of others cancers is not increased in people with SPS. [14] Aspirin and nonsteroidal anti-inflammatory drug (NSAIDs) may be associated with a lower risk of SPS. [8] SPS is the most common polyposis syndrome affecting the colon. [5]

There is no clear association of SPS with any cancers other than colorectal cancer. However, there is mixed evidence regarding a possible association with SPS and pancreatic cancer. [17] [23] Individuals with a history of lymphoma have a higher risk of developing sessile serrated polyposis syndrome. [3]

Related Research Articles

<span class="mw-page-title-main">Large intestine</span> Last part of the digestive system in vertebrates

The large intestine, also known as the large bowel, is the last part of the gastrointestinal tract and of the digestive system in tetrapods. Water is absorbed here and the remaining waste material is stored in the rectum as feces before being removed by defecation. The colon is the longest portion of the large intestine, and the terms are often used interchangeably but most sources define the large intestine as the combination of the cecum, colon, rectum, and anal canal. Some other sources exclude the anal canal.

<span class="mw-page-title-main">Colorectal cancer</span> Cancer of the colon or rectum

Colorectal cancer (CRC), also known as bowel cancer, colon cancer, or rectal cancer, is the development of cancer from the colon or rectum. Signs and symptoms may include blood in the stool, a change in bowel movements, weight loss, and fatigue. Most colorectal cancers are due to old age and lifestyle factors, with only a small number of cases due to underlying genetic disorders. Risk factors include diet, obesity, smoking, and lack of physical activity. Dietary factors that increase the risk include red meat, processed meat, and alcohol. Another risk factor is inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis. Some of the inherited genetic disorders that can cause colorectal cancer include familial adenomatous polyposis and hereditary non-polyposis colon cancer; however, these represent less than 5% of cases. It typically starts as a benign tumor, often in the form of a polyp, which over time becomes cancerous.

<span class="mw-page-title-main">Colonoscopy</span> Endoscopic examination of the bowel

Colonoscopy or coloscopy is the endoscopic examination of the large bowel and the distal part of the small bowel with a CCD camera or a fiber optic camera on a flexible tube passed through the anus. It can provide a visual diagnosis and grants the opportunity for biopsy or removal of suspected colorectal cancer lesions.

<span class="mw-page-title-main">Polyp (medicine)</span> Abnormal growth of tissue projecting from a mucous membrane

In anatomy, a polyp is an abnormal growth of tissue projecting from a mucous membrane. If it is attached to the surface by a narrow elongated stalk, it is said to be pedunculated; if it is attached without a stalk, it is said to be sessile. Polyps are commonly found in the colon, stomach, nose, ear, sinus(es), urinary bladder, and uterus. They may also occur elsewhere in the body where there are mucous membranes, including the cervix, vocal folds, and small intestine. Some polyps are tumors (neoplasms) and others are non-neoplastic, for example hyperplastic or dysplastic, which are benign. The neoplastic ones are usually benign, although some can be pre-malignant, or concurrent with a malignancy.

<span class="mw-page-title-main">Adenoma</span> Type of benign tumor

An adenoma is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both. Adenomas can grow from many glandular organs, including the adrenal glands, pituitary gland, thyroid, prostate, and others. Some adenomas grow from epithelial tissue in nonglandular areas but express glandular tissue structure. Although adenomas are benign, they should be treated as pre-cancerous. Over time adenomas may transform to become malignant, at which point they are called adenocarcinomas. Most adenomas do not transform. However, even though benign, they have the potential to cause serious health complications by compressing other structures and by producing large amounts of hormones in an unregulated, non-feedback-dependent manner. Some adenomas are too small to be seen macroscopically but can still cause clinical symptoms.

<span class="mw-page-title-main">Gardner's syndrome</span> Medical condition

Gardner's syndrome is a subtype of familial adenomatous polyposis (FAP). Gardner syndrome is an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon. The extracolonic tumors may include osteomas of the skull, thyroid cancer, epidermoid cysts, fibromas, as well as the occurrence of desmoid tumors in approximately 15% of affected individuals.

<span class="mw-page-title-main">Familial adenomatous polyposis</span> Medical condition

Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated. Three variants are known to exist, FAP and attenuated FAP are caused by APC gene defects on chromosome 5 while autosomal recessive FAP is caused by defects in the MUTYH gene on chromosome 1. Of the three, FAP itself is the most severe and most common; although for all three, the resulting colonic polyps and cancers are initially confined to the colon wall. Detection and removal before metastasis outside the colon can greatly reduce and in many cases eliminate the spread of cancer.

<span class="mw-page-title-main">Peutz–Jeghers syndrome</span> Medical condition

Peutz–Jeghers syndrome is an autosomal dominant genetic disorder characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis). This syndrome can be classed as one of various hereditary intestinal polyposis syndromes and one of various hamartomatous polyposis syndromes. It has an incidence of approximately 1 in 25,000 to 300,000 births.

<span class="mw-page-title-main">Virtual colonoscopy</span> Medical imaging of the colon

Virtual colonoscopy is the use of CT scanning or magnetic resonance imaging (MRI) to produce two- and three-dimensional images of the colon, from the lowest part, the rectum, to the lower end of the small intestine, and to display the images on an electronic display device. The procedure is used to screen for colon cancer and polyps, and may detect diverticulosis. A virtual colonoscopy can provide 3D reconstructed endoluminal views of the bowel. VC provides a secondary benefit of revealing diseases or abnormalities outside the colon.

<span class="mw-page-title-main">Fundic gland polyposis</span> Medical condition

Fundic gland polyposis is a medical syndrome where the fundus and the body of the stomach develop many fundic gland polyps. The condition has been described both in patients with familial adenomatous polyposis (FAP) and attenuated variants (AFAP), and in patients in whom it occurs sporadically.

<span class="mw-page-title-main">Juvenile polyposis syndrome</span> Medical condition

Juvenile polyposis syndrome is an autosomal dominant genetic condition characterized by the appearance of multiple juvenile polyps in the gastrointestinal tract. Polyps are abnormal growths arising from a mucous membrane. These usually begin appearing before age 20, but the term juvenile refers to the type of polyp, not to the age of the affected person. While the majority of the polyps found in juvenile polyposis syndrome are non-neoplastic, hamartomatous, self-limiting and benign, there is an increased risk of adenocarcinoma.

<span class="mw-page-title-main">Colorectal polyp</span> Growth found in bowel wall

A colorectal polyp is a polyp occurring on the lining of the colon or rectum. Untreated colorectal polyps can develop into colorectal cancer.

<span class="mw-page-title-main">Sessile serrated lesion</span> Medical condition

A sessile serrated lesion (SSL) is a premalignant flat lesion of the colon, predominantly seen in the cecum and ascending colon.

<span class="mw-page-title-main">Hyperplastic polyp</span> Type of colorectal polyp

A hyperplastic polyp is a type of colorectal polyp.

<span class="mw-page-title-main">Colorectal adenoma</span> Medical condition

The colorectal adenoma is a benign glandular tumor of the colon and the rectum. It is a precursor lesion of the colorectal adenocarcinoma. They often manifest as colorectal polyps.

MUTYH-associated polyposis is an autosomal recessive polyposis syndrome. The disorder is caused by mutations in both alleles of the DNA repair gene, MUTYH. The MUTYH gene encodes a base excision repair protein, which corrects oxidative damage to DNA. Affected individuals have an increased risk of colorectal cancer, precancerous colon polyps (adenomas) and an increased risk of several additional cancers. About 1–2 percent of the population possess a mutated copy of the MUTYH gene, and less than 1 percent of people have the MUTYH associated polyposis syndrome. The presence of 10 or more colon adenomas should prompt consideration of MUTYH-associated polyposis, familial adenomatous polyposis and similar syndromes.

<span class="mw-page-title-main">Histopathology of colorectal adenocarcinoma</span>

The histopathology of colorectal cancer of the adenocarcinoma type involves analysis of tissue taken from a biopsy or surgery. A pathology report contains a description of the microscopical characteristics of the tumor tissue, including both tumor cells and how the tumor invades into healthy tissues and finally if the tumor appears to be completely removed. The most common form of colon cancer is adenocarcinoma, constituting between 95% and 98% of all cases of colorectal cancer. Other, rarer types include lymphoma, adenosquamous and squamous cell carcinoma. Some subtypes have been found to be more aggressive.

Polymerase proofreading-associated polyposis (PPAP) is an autosomal dominant hereditary cancer syndrome, which is characterized by numerous polyps in the colon and an increased risk of colorectal cancer. It is caused by germline mutations in DNA polymerase ε (POLE) and δ (POLD1). Affected individuals develop numerous polyps called colorectal adenomas. Compared with other polyposis syndromes, Polymerase proofreading-associated polyposis is rare. Genetic testing can help exclude similar syndromes, such as Familial adenomatous polyposis and MUTYH-associated polyposis. Endometrial cancer, duodenal polyps and duodenal cancer may also occur.

<span class="mw-page-title-main">Traditional serrated adenoma</span> Medical condition

Traditional serrated adenoma is a premalignant type of polyp found in the colon, often in the distal colon. Traditional serrated adenomas are a type of serrated polyp, and may occur sporadically or as a part of serrated polyposis syndrome. Traditional serrated adenomas are relatively rare, accounting for less than 1% of all colon polyps. Usually, traditional serrated adenomas are found in the distal colon and are usually less than 10 mm in size.

Juvenile polyps are a type of polyp found in the colon. While juvenile polyps are typically found in children, they may be found in people of any age. Juvenile polyps are a type of hamartomatous polyps, which consist of a disorganized mass of tissue. They occur in about two percent of children. Juvenile polyps often do not cause symptoms (asymptomatic); when present, symptoms usually include gastrointestinal bleeding and prolapse through the rectum. Removal of the polyp (polypectomy) is warranted when symptoms are present, for treatment and definite histopathological diagnosis. In the absence of symptoms, removal is not necessary. Recurrence of polyps following removal is relatively common. Juvenile polyps are usually sporadic, occurring in isolation, although they may occur as a part of juvenile polyposis syndrome. Sporadic juvenile polyps may occur in any part of the colon, but are usually found in the distal colon. In contrast to other types of colon polyps, juvenile polyps are not premalignant and are not usually associated with a higher risk of cancer; however, individuals with juvenile polyposis syndrome are at increased risk of gastric and colorectal cancer., Unlike juvenile polyposis syndrome, solitary juvenile polyps do not require follow up with surveillance colonoscopy.

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