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DIFFERENTIAL DIAGNOSIS OF GASTROINTESTINAL POLYPS

Robert D. Odze, M.D., F.R.C.P.C.

GASTROINTESTINAL POLYPS

A polyp is a circumscribed nodular lesion or tumor that protrudes above the level of the surrounding mucosal
surface. Pathologists usually receive material in the form of biopsies or endoscopic polypectomy specimens. The role
of the pathologist is to establish a diagnosis or at least to be able to put it into one of the general polyp categories, and to
determine whether the lesion has been adequately excised. The clinical management will often depend on the specifics
in the pathology report. It is important to realize that a biopsy of a polypoid lesion is like examining the “tip of the
iceberg”. Thus, it is important to know the endoscopic appearance of the polyp before making any final decision
regarding the nature of the lesion.

ESOPHAGEAL POLYPS

Most symptomatic polyps of the esophagus are malignant. Most benign polyps of the esophagus are
mesenchymal. In order of decreasing frequency, the most common benign polypoid lesions of the esophagus are:
inflammatory polyps, esophageal cysts – webs, heterotopias, and benign leiomyomas. Squamous papillomas are
increasing in frequency as clinicians become more aware of this entity.

1. Esophageal Squamous Papilloma

General Features:

 Single or multiple
 Prevalence – 0.1-0.4% [autopsy studies]
 Pathogenesis – probably related to chronic mucosal irritation and human papilloma virus [up to 50%]
 Males = females [average age 50, range 2:86]
 Benign [little or no malignant potential]

Pathologic Features:

 Average size 0.5 cm. Distal esophagus > mid- > upper esophagus
 Three morphologic types: exophytic, endophytic, spiked
 Exophytic type [50%] = finger-like papillary configuration
 Endophytic type [37%] = round smooth surface contour, inverted papillomatous proliferation
 Spiked-type [13%] = verrucoid proliferation of squamous epithelium with spiked surface, prominent granular layer,
and hyperkeratosis
 All have branched fibrovascular core covered by benign acanthotic squamous epithelium with prominent basal zone
and complete surface maturation
 Koilocytosis, parakeratosis, and binucleated cells often present
 Inflammation [neutrophilic and mononuclear] usually present
 Rarely show dysplastic changes [less than 3 cases reported in literature]

Differential diagnosis:

 Pseudoepitheliomatous hyperplasia, mucosal fold, verrucous carcinoma

 Endoscopic observation of a polyp important for the diagnosis
 Verrucous carcinoma shows minimal, primarily basal layer dysplastic features and single-cell keratinization,
broader acanthotic pegs, +/- central areas of degenerated keratin, pushing margins

2. Inflammatory Polyp

 Most common polyp of the esophagus

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 Usually occur at esophagogastric junction, associated with gastroesophageal reflux
 May be composed entirely of granulation tissue [pyogenic granuloma]

3. Cysts

 Retention cyst formed by dilation of esophageal gland ducts

 Submucosal, often in the lower esophagus
 Rule out duplication cyst [lined by esophageal, bronchial, or gastric epithelium]

4. Heterotopia

 Gastric most common, thyroid, parathyroid and sebaceous heterotopia less common
 Usually upper to mid esophagus
 Ectopic sebaceous glands appear as small macules, often multiple, may be intraepithelial or located in the lamina
propria. May be associated with hyper-and parakeratosis

5. Adenoma

• May arise from submucosal gland/duct, salivary gland-like morphology, two-layered epithelium
• Most arise in Barrett’s esophagus and form a polypoid area of dysplasia. Therefore, not a true
adenoma
- natural history similar to flat dysplasia, high association with carcinoma
- microscopic appearance similar to flat dysplasia

6. Polypoid Carcinosarcoma

• Biphasic tumor composed of squamous cell carcinoma admixed with spindle cell component
• Most located in the mid to lower esophagus, cause obstruction
• Often associated with squamous dysplasia
• Spindle cell component varies from undifferentiated spindle cells to large pleomorphic bizarre giant
cells, rarely smooth muscle, skeletal muscle, bone or cartilage differentiation
• Prognosis similar to squamous cell carcinoma

7. Lymphoid Polyp

• Benign reactive lymphoid hyperplasia more common than lymphoma

• Hodgkin’s disease > non-Hodgkin’s lymphoma

8. Mesenchymal Polyps

• Benign leiomyoma and granular cell tumors most common, fibrovascular polyps extremely rare
• GIST rare in esophagus
Leiomyoma
 All benign, arise from inner layer of muscularis propria
 Most incidental finding, usually less than 2 cm and limited to the wall
 Bland hypocellular spindle cell population arranged in fascicles and whorls +/- epithelioid
differentiation and hyalinization
 No necrosis, no mitoses
 Leiomyomatosis = series of nodular thickenings of he muscularis that involves the entire
esophagus
 Seedling leiomyomas [distal esophagus and GE junction]

Granular cell tumor

 Benign neoplasm of schwann cell origin
 Distal esophagus most common site, single or multiple
 Sheets of uniform histiocyte-like cells with finely granular eosinophilic cytoplasm and small vesicular
nuclei
 Positive PASD, positive S-100, autophagic lysosomes filled with myelin-like membranous debris by EM
 Overlying pseudoepitheliomatous hyperplasia common, may mimic carcinoma
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Fibrovascular Polyp
 Benign pedunculated mesenchymal tumor of unknown etiology
 Upper third of esophagus [cricopharyngeal muscle], may be large [17 cm], long pdicle
 Composed of mature mesenchymal tissues covered by normal squamous epithelium, inflammation may be
prominent, +/- ulceration
 Slow growing lesion, no malignant potential
 Main differential diagnosis with other benign mesenchymal tumors and sarcoma

GASTRIC POLYPS

Clincal-pathologic correlation important for evaluation of gastric polyps. The endoscopist has to make the decision as
to whether a polyp is present for the pathologist to accurately interpret the findings. Biopsies taken near ulcers and other
inflamed sites, such as gastroenterostomy stomas, may have an expanded inflamed lamina propria, hyperplastic pits and
marked regenerative features, all of which may mimic hyperplastic polyps or even adenomas. There is an increased
incidence of polyps in pernicious anemia, chronic atrophic gastritis, and in gastric mucosa after partial gastrectomy.
Endoscopic prevalence of 3% - 5%. 75% of gastric polyps are hyperplastic/inflammatory polyps. Other frequently
encountered polyps of the stomach include fundic gland polyps, adenomas, leiomyomas, and heterotopic tissues. Many
classifications of gastric polyps exits [Ming, Elster, Cong et al, Snover]. This discussion will be based on the Ming
classification.

1. HYPERPLASTIC/INFLAMMATORY POLYPS

A. Polypoid foveolar hyperplasia

 Most common form of localized gastric mucosal expansion
 Commonly related to healing ulcer and gastrojejunostomy stomas
 Also seen at edge of erosions, secondary to NSAID’s, alcohol, or chronic erosive gastritis
 Microscopic Features
- uniformly lengthened pits with corkscrew appearance
- no increase in number of pits
- mild edema and inflammation in lamina propria
- deep glands normal or atrophic
- no architectural distortion characteristic of hyperplastic polyps

B. Hyperplastic Polyp [regenerative, hyperplasiogenesis]

 Most common polyp in the stomach [incidence 1/1000, 75% of gastric polyps]
 Prevalence increases in inflammatory conditions such as chronic atrophic gastritis, pernicious anemia,
chronic antral gastritis, post-gastrectomy gastritis
 Pathogenesis – inflammatory regenerative lesion due to branching and dilatation of hyperplastic foveolae.
Secondary to excessive and unchecked regenerative growth of the normal proliferative zone of the gastric
epithelium. May be clonal in origin.

Pathologic Features:
 Generally small, dome-like or stalk [average size 1.0 cm, up to 12 cm], single or multiple, antrum +/-
fundus, cardia.
 Elongation, dilatation [cystic] and architectural distortion of foveolar epithelium
 Epithelium is mucus-type cells, globoid cells may be present +/- int. metaplasia, deep pyloric-type glands
 Frequent epithelial infoldings produce luminal serration
 Lamina propria shows increased inflammation, mild muscularis hyperplasia, +/- surface ulceration/erosion
 Little or no pseudostratification, mitotic activity low, but may be present at the base or at the surface
 Dysplasia or carcinoma rare

Differential diagnosis:
 Gastric cystica polyposa – usually located near gastric stump
- may be indistinguishable from large hyperplastic polyp or juvenile polyp
- lack of smooth muscle, entrapped epithelium is key to diagnosis
- requires clinical information to establish diagnosis
● Hamartoma [Peutz-Yegher polyp]
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- does not have expanded inflamed lamina propria
- more well-developed muscularis mucosa
- usually multiple
- no association with chronic gastritis
● Menetrier’s disease
- diffuse enlargement of fundic mucosa, spares antrum
- histology may be similar
- surface and foveolar hyperplasia, +/- inflammation, normal or atrophic glands
- different clinical and endoscopic profile

Natural History:
 may regress, remain stable or grow in size
 low malignant potential, both within the polyp and in the adjacent gastric mucosa
 incidence of malignant change; range -.5% - 7.1% [average 2.1%]
 probably develops through dysplasia-carcinoma sequence
 dysplasia and carcinoma elated to polyp size [greater than 2.5 cm] and shape [pedunculated].
 Hyperplastic polyps may contain marked regenerative changes important to distinguish from true dysplasia
 Regeneration = mucous depletion, high NC ratio, large vesicular nuclei, prominent nucleoli, with
inflammation and ulceration. No atypical mitotic activity.

C. Gastritis Cystica Polyposa/Profunda

 Polyp or nodule formed by entrapment of glands in the muscularis or submucosal submucosal space due to
epithelial misplacement and regeneration. Often associated with Billroth II resection, severe chronic and
atrophic gastritis.
 Hyperplasia and cystic changes of the gastric pits associated with acute and chronic inflammation of the
lamina propria, +/- superficial erosion.

Differential Diagnosis:

 Invasive carcinoma
- GCP has little or no atypia, no desmoplasia, and usually surrounded by lamina propria
 Hyperplastic polyp
- may be indistinguishable from GCP
-GCP shows increased submucosal glands
 Pancreatic heterotopia
-GCP has less muscular hypertrophy, more inflammation
 Peutz-Yegher polyp
- GCP has increased inflammation and less structured muscularis hyperplasia

D. Polypoid gastritis
 Enlarged gastric fold/localized expansion of the mucosa due to inflammation
- may be antral, fundic or both
- typical features of gastritis without prominent foveolar hyperplasia or architectural distortion

2. HAMARTOMATOUS POLYPS

A. Fundic Gland Polyp

 Sporadic – incidence 0.8-1.4%, F>M, average age 52, 40% multiple, B-catenin mutations, low risk of
dysplasia
 FAP associated – incidence 20-100%, M=F, average age 40, 90% multiple, somatic APC mutations, high
risk of dysplasia
 Generally asymptomatic, discovered incidentally at endoscopy
 May rarely reach large size, cause obstruction.

Pathologic Features:
 Average size 0.4 cm, hyperemic, sessile, flat nodular, smooth surface, no ulcer
 Composed of normal gastric fundic epithelium arranged in a disorderly and/or microcystic configuration
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 Glandular compartment shows distorted architecture with irregular gland buds, tortuous glands or irregular
stellate glandular configurations
 Cysts lined by fundic gland cells, mucous cells, or mixture of both, +/0 edema, inflammation
 Focal intramucosal muscularis hyperplasia in a pericystic configuration

Differential Diagnosis:
 Normal or regenerating gastric epithelium
- normal gastric mucosa may show occasional small cysts, particularly if regenerating
- however, no glandular architecture distortion, cysts are small and regular, and
infrequent
 Hyperplastic polyp

Natural History:
- little or no malignant potential
- may develop dysplasia, particularly in FAP

B. Familial Hamartomas

 Juvenile Polyposis
- May occur in generalized gastrointestinal polyposis or as a very rare isolated form of gastric
juvenile polyposis
- Grossly and microscopically almost identical to typical hyperplastic polyps, except show less
muscularis
- May develop dysplasia or carcinoma rarely

 Peutz-Yegher Syndrome
- clinical history is usually diagnostic
- polyps are similar to hyperplastic polyps but show less inflammation, and a more well-developed
muscularis in a tree-like network, and are composed of normal gastric epithelial cell-types
- may show extension of mature glands into underlying submucosa or muscularis propria. R/O
gastritis cystica polyposa and invasive adenocarcinoma

 Cronkhite-Canada Syndrome
- sessile lesion containing hyperplastic, often cystically dilated, pits in an edematous lamina propria
+/- inflammation
- surrounding stomach may have giant folds
- adjacent mucosa shows alternating areas of atrophy and polyp formation
- shares features of juvenile polyps, hyperplastic polyps, and Menetrier’s disease
- up to 20% develop malignant transformation [mostly stomach and colon]
- diagnosis established in conjunction with clinical history

C. Heterotopia

 Pancreatic heterotopia
- most occur in antrum pre-pyloric region, submucosal lesion
- Dome shaped mass [1-3 cm] with typical entral umbilicated or dimpled center [exocrine secretions
exit into lumen]
- Histologically composed of a mixture of exocrine glands and ducts, +/- islet cells
- Often admixed with thick bundles of smooth muscle
- Differential Diagnosis – invasive adenocarcinoma, GCP

3. EPITHELIAL NEOPLASTIC POLYPS

A. Adenoma
 Incidence: 8%-105 of polyps with age, chronic gastritis, FAP
 Pathologic Features:
- most occur in antrum [flat, papillary], flat more common
- flat adenomas are usually tubular microscopically, similar to colon morphologically
- papillary adenomas are usually tubular/villous or villous
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- papillary [villous]adenoma usually sessile or stalk, may reach large size [15 cm], formed of
columnar cells with striated borders, may see goblet cells, Paneth cells or parietal cells
- often associated with intestinal metaplasia in adjacent mucosa
- rarely may be composed entirely of gastric-type epithelial cells [4%], few composed of a
mixture of gastric and intestinal-type cells [2%] and the most common form has exclusively
intestinal-type dysplastic cells
 Natural History
- high incidence of malignant transformation, particularly in the papillary [villous] adenoma
[40%- 75%].
- lower incidence in flat adenoma
- presence of a cancer correlates with size, papillary contour, and grade of dysplasia
 Principles of managemnt similar to colonic adenomas

B. Carcinoma
 Polypoid or papillary adenocarcinoma may present as a polypoid lesion
 Distinction from benign adenoma may be difficult
 Diagnosis based on presence of lamina propria or stalk invasion combined with cytologic
features of adenocarcinoma

4. NON-EPITHELIAL POLYPS
 Includes lamina propria infiltrates such as xanthoma and histiocytosis-X, lymphoid polyps
[benign and neoplastic], and a variety fo mesenchymal tumors which are common to the
stomach such as inflammatory fibroid polyp, GIST’s, and neurofibromas [see below]

SMALL INTESTINAL POLYPS

Most small intestinal polyps are benign. Malignant tumors of the small intestine are rare [approximate 1% - 2% of all
gastrointestinal tumors] and the majority occur in the distal portion of the small intestine. In these regions, polypoid
carcinoids, lymphomas and tumors of mesenchymal origin are the most common. Benign tumors most often occur in the
duodenum and form approximately 40% - 50% of all polypoid lesions in the small intestine. In that region, the most
common polypoid lesions are Brunner’s gland hyperplasia/hamartoma, reactive lymphoid hyperplasia, nodular
duodenitis, heterotopia, and adenomas. In the distal small intestine, lipomas and benign stromal tumors make up a larger
majority of the benign polyps.

1 . Hyperplastic Polyps

 Brunner’s gland hyperplasia is the most common duodenal polyp or nodule.

 May be single, more often multiple, mainly proximal duodenum.

2. Inflammatory Polyps

A. Nodular duodenitis:
 Persistent cases of chronic peptic duodenitis may develop increased amounts of lymphoid tissue and cause
numerous small nodules.
 Microscopic features include prominent mucous cell metaplasia, Brunner’s gland hyperplasia, reactive lymphoid
follicular hyperplasia, and a variable amount of villous shortening, and neutrophilic mononuclear inflammation.

B. Inflammatory polyp:
 Secondary to mucosal injury similar to the pathogenesis in the colon
 Pyogenic granulomas have been described in duodenum

3. Hamartoma

 Most hamartomatous polyps of the small intestine are syndromic [Peutz-Yagher, Juvenile Polyposis, Cronkhite-
Canada syndrome, Cowden’s syndrome].
 Brunner’s gland hamartoma may occur sporadically.
- consists of mucosal/submucosal Brunner’s glands in a lobular configuration admixed with adipose tissue
and smooth muscle [3-5 mm size].
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- Paneth cell may be prominent.
- probably not neoplasms [not adenomas].
- presence of adipose tissue and smooth muscle form the basis of the diagnosis of hamartoma vs hyperplasia.

4. Heterotopia

A. Gastric heterotopia.

 Small nodules associated with inflammation, erosion or ulceration in proximal duodenum.

 Well developed surface and foveolar-type epithelium with underlying pyloric-type glands admixed with
specialized cells [parietal and chief-cells].
 Architecture usually well maintained
 Differential diagnosis includes mucous cell metaplasia and/or pyloric metaplasia secondary to chronic
duodenitis
 Presence of parietal and chief cells and preserved architecture helps establish the diagnosis.

B. Pancreatic heterotopia [ myoepithelial hamartoma, adenomyoma].

 Similar to gastric pancreatic heterotopia
 Islets found in two-thirds of cases.
 Myoepithelial hamartoma = ductal tissue with surrounding smooth muscle, without islets.
 May develop acute and chronic pancreatitis, pseudocyst formation, or rarely, adenocarcinoma.

5. Epithelial Neoplastic Polyps

 Most are either adenomas or carcinoid tumors.

 Polypoid adenocarcinoma of the small bowel extremely rare.

A. Adenoma
 May be sporadic or FAP associated, are uncommon [less than 10% of duodenal polyps], most
occur in the periampullary region, multiple lesions usually secondary to FAP.
Pathologic Features:
• Similar to typical colonic adenomas, more often papillary
• Paneth cells and edocrine cells are common, particularly in the upper portions of the
adenomatous epithelium [opposite to reactive epithelium].
• Ampullary adenomas often associated with underlying carcinoma.
Natural History:
• Similar to colon adenomas
• Large size, high grade dysplasia, and villous contour more likely to contain, or develop,
malignancy

B. Carcinoid tumor
 See lecture on neuroendocrine tumors

6. Non-Epithelial Polyps

 In the proximal small intestine, lymphoid hyperplasia/neoplasia and GIST’s most common
 Distal small intestine, benign mesenchymal tumors [lipoma, hemangioma] and inflammatory fibroid polyps
occur most often.

A. Inflammatory fibroid polyp [eosinophilic granuloma, submucosal fibroma]

 Defined as a primarily submucosal tumor, benign, that consists of proliferating fibroblast-like stromal cells,
small blood vessels and inflammatory cells, particularly eosinphils.
 Represent reactive lesions that contain polyclonal cell populations, diploid DNA content and increased
proliferative activity in the stromal cells and vascular cells.
 All age groups, males and female, symptoms related to location: stomach: obstruction, small intestine:
intussusception.

Pathologic Features:
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 Occur in two main sites: distal stomach [pylorus] and distal ileum.
 Rarely occur in esophagus, colon and proximal small intestine.
 Gastric tumors show small size [less than 3 cm], may be associated with atrophic gastritis, may ulcerate, and
fill the superficial submucosal with a sharp lower border at the upper level of the muscularis propria,
mucosal involvement common.
 The small intestinal tumor, usually larger [>3 cm], often pedunculated, often extensively ulcerated, are
transmural tumors involving submucosal and muscularis propria and may extend into the subserosa as well,
no mucosal involvement is typical.
 Variably cellular and haphazard proliferation of spindle-shaped stromal cells, granulation tissue-like
vascularity, polymorphic chronic inflammatory cell infiltrate often with prominent osinophils, and an
edematous or myxoid stroma.
- spindle cells and eosinphils tend to form concentric layers around small thin walled
blood vessels.
- small intestinal polyps show increased edematous stroma, longer elongated vascular
channels, predominantly stellate-shaped stromal cells, a more mixed inflammatory cell
population including plasma cells and lymphocytes and alack of a prominent
perivascular aggregation of spindle cells and inflammatory cells.
- stromal cells contain a mixture of fibroblast, myofibroblast and histiocytes.
- typically CD34 positive, CD117 negative

Differential Diagnosis:
 Malignant mesenchymal tumor
- mesenchymal tumors have a more uniform cell population, increased mitotic activity and
atypia, lack of perivascular lamination, less inflammatory cells, and a pushing infiltrative
margin
- inflammatory fibroid polyps have characteristic histology with splitting or splaying of
muscle wall fibers, mitotic activity limited to vascular endothelial cells and fibroblasts.
 Fibromatosis
- more uniform cell population, lack of inflammation, typical infiltration pattern in muscle
and fat.
 Inflammatory pseudotumor
- different location, more diffuse appearance, more striking plasma cell population.
 Marked granulation tissue reaction around an ulcer
- no well-developed polypoid lesion, lack of vascular lamination, primarily mucosal
involvement

Natural History:
 Benign lesions with no malignant potential

B. Gangliocytic paraganglioma
 Rare, benign tumor of uncertain histogenesis located exclusively in the second portion of the duodenum.
 Unencapsulated tumor that infiltrates the submucosal, muscularis propria, and lamina propria, +/-
ulceration.
 Composed of a mixture of epithelioid polygonal-shaped cells, spindle cells, and larger
ganglion cells, +/- typical carcinoid-type cells
 Immunohistochemistry positive for chromogranin and other hormonal peptides in the epithelioid cell
population. Spindle cell population positive for neural markers [S-100, GFAP].
 Are low-grade malignant tumors, can be locally infiltrative, and rarely metastasize to regional lymph nodes.
 Differential diagnosis includes typical carcinoids tumor [no ganglion cells, no neural spindle cell
population], neurofibroma [no epithelioid cells], and GIST [uniform spindle cell population with myoid
features].

COLORECTAL POLYPS

Hyperplastic polyps, adenomas, inflammatory polyps and polypoid carcinomas are most common. Polyps less than
0.5 cm in size are considered diminutive

1. Hyperplastic Polyp [metaplastic polyp]

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● Most common polyp of the colon, often multiple
● Etiology unclear, probably related to crypt fusion and defects in apoptosis in combination with hyper-maturation
of the upper crypt and surface epithelium

Pathologic Features:
● All lesions less than 1 cm in size [most less than 0.5 cm], sessile, smooth, no stalk.
● Serrated or saw-tooth surface contour with extensive papillary infolding of the epithelium cells and an
overabundance of mature goblet cells
● Basal portion of crypt may show increased mitotic activity and marked regenerative features [hyperchromaticity,
pseudostratification].
● May see disordered muscularis mucosa, thick subepithelial collage layer, Paneth cells.
● Several recent subtypes described [goblet cell rich type, mucin depleted type, sessile serrated polyp (see below)]

Differential diagnosis:
1. Serrated adenoma; hyperplastic polyps lack cytologic atypia, clumped chromatin, and mature to the surface
with a single cell layere. Serrated adenoma has low-power appearance of a hyperplastic polyp with high-
power cytologic features of neoplasia [lack of maturation to surface].
2. Hyperplastic polyp with focal adenomatous change [mixed polyp]
3. Sessile serrated polyp [“adenoma”}
4. Inflammatory polyp with hyperplastic changes [inflammation, +/- erosion, ulceration]

2. Inflammatory Polyps

A. Inflammatory polyp [generic]

● May be isolated or associated with inflammatory bowel disease, infectious disorders, ischemic colitis,
perianastomotic sites and often found adjacent to ulcers or diverticular openings.
● Etiology due to regeneration and repair post-ulceration.
● Cystically dilated crypts with inflamed stroma, +/- reactive epithelial changes, hyperplastic changes, +/-
erosion or ulceration, usually multiple.
● May reach large sizes [giant inflammatory polyp associated with IBD], may be filliform

Differential diagnosis:
● Juvenile polyp
- usually pedunculated [inflammatory polyps usually sessile], more organized [lamina propria hamartoma].
- clinical history may be informative
● Mucosal prolapse-associated inflammatory polyp
- prominent fibromuscular hyperplasia of lamina propria, epithelial regenerative changes, variable
inflammation
- appropriate clinical setting
● Hyperplastic polyp with inflammation
- hyperplastic changes are diffuse, inflammation is less prominent

B. Inflammatory myoglandular polyp

● Solitary pedunculated polyp consisting of hyperplatic glands with occasional cystic dilatation and
proliferation of smooth muscle in the lamina propria [in a radial fashion] that spreads into inflammatory
granulation tissue
● usually located in sigmoid colon
● May simply represent a Peutz Yegher polyp

C. Inflammatory cap polyp

● descriptive term that describes an inflammatory polyp with cystically dilated crypts, hyperplastic features,
inflammation of lamina propria, variable amount of fibromuscular hyperplasia in lamina propria, and a
prominent granulation or fibrin cap overlying surface erosion.
● Occur predominantly in the rectosigmoid colon in IBD
● Histological features identical to those seen in mucosal prolapse injury [similar etiology]

D. Mucosal prolapse-associated inflammatory polyp

Sub-types:
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● Inflammatory cap polyp
● Inflammatory cloacogenic polyp
● Solitary rectal ulcer syndrome-associated polyp
● Diverticular disease-associated polyp
● Ulcer-associated polyp
● Proplapsing redundant mucosa

Pathologic Features:
● variable size [range 0.5-4 cm], typically sessile, may be stalk, may be a smooth surface or a
papillary/villous surface contour, +/- ulceration.
● Hyperplastic and regenerative crypts, normal architecture or cystically dilated, variable inflammation in the
lamina propria, marked fibromuscular proliferation in the lamina propria
● Surface erosion and granulation tissue may be present [inflammatory cap polyp]. Large polyps often
villiform and may show extension of cystically dilated crypts into the submucosal [localized colitis cystica
polyposa/profunda]. Foci of hemorrhage [recent and remote], necrosis and inflammation may be pesent in
the polyp and in adjacent mucosa.

Differential Diagnosis:
- The clinical and endoscopic features help distinguish specific types of inflammatory polyps related to
mucosal prolapse.
● Solitary rectal ulcer syndrome: diagnosis requires appropriate clinical setting [female, 30’s – 40’s, history
of strining on defecation, constipation, anal, rectal or abdominal pain or bleeding ulceration, +/- polyp,
location in anterior wall of the rectum [up to 18 cm], +/- multiple polyps.
● Inflammatory cloacogenic polyp: typical location [anal/rectal junction, transitional epithelium].
● Diverticular disease-associated inflammatory polyp.
● Inflammatory myoglandular polyp
- usually sigmoid colon, well-developed muscular hyperplasia of lamina propria, less ulceration and
granulation tissue.
- may resemble diverticular disease-associated polyp [may be same condition].
● Inflammatory and juvenile polyps
- less fibromuscular hyperplasia
- otherwise, similar histologic features
● Hyperplastic polyp: lack necrosis, inflammation and fibromuscular proliferation
● Adenoma [without or without misplaced epithelium]: lack of surface maturation, neoplastic epithelium.
● Colitis cystica polyposis/profunda: see below

E. Colitis Cystica Polyposis/Profunda

 Includes any condition in which mature colinic epithelium extends through the muscularis mucosa into
the submucosal or muscularis propria
 May be isolated [solitary rectal ulcer syndrome], or diffuse or multiple [such as inflammatory bowel
disease, radiation injury, schistosomiasis, or in normal colon].
 Due to regeneration and repair after ulceration with resulting entrapment of crypts in the submucosa or
muscularis.
 Differential diagnosis includes
1. Normal lymphoepithelial complex
2. Invasive adenocarcinoma
- presence of dysplastic epithelium, inflammation, desmoplasia, and absence of a rim of lamina
propria around the infiltrating glands indicates malignancy.

3. Hamartoma [See Polyp Syndrome Below].

4. Miscellaneous Polyps

● Appendiceal intussusception, inverted appendiceal stump, retained appendiceal stalk after polypectomy, mucosal
bumps, tags and excrescences, and cholesterol embolus polyp.
● Intestinal pneumatosis and endometriosis rarely present as polypoid lesions.
- reveal characteristic endometrial glands and stroma, foci of fresh and old hemorrhage, variable amounts of
fibrosis and marked smooth muscle hypertrophy.

5. Epithelial Neoplastic Polyps [Non-Endocrine].

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A. Adenoma
Sub-types: typical [tubular, tubulovillous, villous], flat and serrated.
 Dysplasia in adenomas graded as low-grade [all adenomas by definition], high-grade
[including carcinoma in-situ], intramucosal carcinoma [adenocarcinoma with invasion
limited to mucosa or muscularis mucosa], and invasive carcinoma
[adenocarcinoma with invasion beyond muscularis mucosa into polyp stalk].
 High grade dysplasia shows true stratification of neoplastic cells towards the luminal half of the epithelium
with a greater degree of cytologic atypia, nuclear pleomorphism, increased mitotic activity and loss of
polarity, associated with minor architectural changes [cribriform glands].
 Intramucosal adenocarcinoma shows all features of adenocarcinoma [irregularity and complexity of glands,
open nuclei, pleomorphism, etc.] limited to mucosa.
 Almost 0% risk of metastasis in patients with adenomas that contain high-grade dysplasia or intramucosal
adenocarcinoma.
Important reporting issues:
 In terms of further therapy, the most important reporting issue, aside from the diagnosis, is the status of the
polyp margins.
 High-grade dysplasia, unless extensive and/or associated with positive margins, is not a necessary reporting
point particularly if clinicians are apt to over-react.
 Intramucosal adenocarcinoma may be reported but always with a statement regarding the absence of invasive
cancer, the status of the margins, and a comment regarding the overall adequacy of resection and need for
further therapy [usually none].
 For equivocal foci of intramucosal carcinoma, probably better not to report since it has no more significance,
in most cases, than high-grade dysplasia.

Adenoma variants:
 Adenoma with misplaced epithelium [avoid term “pseudo-invasion”].
- due to twisting of the polyp with breakdown of the muscularis mucosa and extension [misplacement]
of the adenomatous epithelium into the submucosa
- misplaced epithelium has similar cytologic features as surface epithelium, rim of lamina propria present,
connection to the surface may be present, associated hemorrhage and hemosiderin deposition usually
present, no desmoplasia.
- Invasive adenocarcinoma usually shows increased cytologic atypia, more architectural complexity
[branching glands, irregular glands, single cells or small groups of cells etc.] associated with
desmoplasia of the stoma. Hemorrhage may be present.
 Flat adenoma
- May be particularly aggressive [controversial], higher incidence of high-grade dysplasia, undergo
malignant change at a rapid rage [remains to be confirmed].
- May result in invasive adenocarcinoma with no overlying adenomatous precursor.
 Serrated adenoma
- Low-power appearance of a hyperplastic polyps [serrated surface contour, papillary infolding] with
high-power cytologic features of neoplasia
- Recent report of serrated polyposis syndrome.
- Natural history probably similar to typical adenomas.
- Distinguish from hyperplastic polyps by larger size [usually greater than 1.0 cm], cytologic features of
neoplasia [nuclear hyperchromasia, pseudo-stratification, lack of surface maturation].
 Mixed hyperplastic – adenomatous polyp
- shows combination of hyperplastic epithelium and adenomatous epithelium (usually serrated) in some
polyp
- may represent a sessile serrated polyp with dysplasia
 Sessile serrated polyp [“adenoma”]
- sessile growth pattern, often >0.5 cm in size
- often right sided
- dilated crypts, basally branched crypts, horizontal crypts
- dystrophic goblet cells
- methylation abnormalities common ,↑ risk of microsatellite unstable colorectal cancer.

B. Malignant Polyp
Defiinition: polyp that contains invasive adenocarcinoma [cancer beyond the muscularis mucosa into
submucosal].
 12
Two types:
1. Polypoid adenocarcinoma [polyp head totally replaced by cancer]
2. Adenoma with focal malignant degeneration

Important reporting issues:

 histologic grade of cancer
 status of resection margin
 presence or absence of lymphovascular invasion
● Polypectomy inadequate if unfavorable histology
- cancer <0.1 – 0.2 cm
- cancer is poorly-differentiated
- lymphovascular invasion is present
- any sessile polyp with invasive cancer [any grade]
● Risk of metastasis in patients with an adenoma with unfavorable histology ≈ 20%[range 17%- 40%]

C. Polypoid dysplasia and adenomas in inflammatory bowel disease [Adenoma-like DALM]

● lesions are considered adenomas if they occur proximal to site of chronic disease
● lesions are considered “polypoid dysplasia in IBD” if occur within areas of disease, and are associated with
dysplasia at other sites, or adenocarcinoma
● polypoid dysplasia in IBD occurs more often in patients with longer history of colitis[> 15 years], total or
pancolitis, rectal location of the polyp, and if the polyp shows a mixture of adenomatous and normal epithelium
at the surface, and there is significant inflammation within the lesion
● any polypoid dysplastic lesion in IBD that is associated with a “mass” should be considered cancer and
considered an indication for colectomy
● endoscopic appearance is most important feature to determine outcome [Adenoma-like vs. non-adenoma like]
● Adenoma-like lesions in IBD have similar molecular phenotype as sporadic adenomas and have a similar
natural history. Therefore, if it resembles an adenoma grossly, it usually behaves like one and can be treated
with polypectomy.

6. Non-Epithelial Polyps
● Lymphoid hyperplasia and polypoid lymphomas, as well as mesenchymal neoplasms such as neurofibroma,
ganglioneuroma, leiomyoma/gastrointestinal stromal tumor, hemangioma, lipoma and inflammatory fibroid
polyps from the majority of non-epithelial polypoid lesions of the colon
● Xanthoma of rectum rare

7. Polyposis Syndromes [See Attached table]

 13

Syndrome Definition and Sub Types Histologic Features Distribution Cancer Risk Genetics Comments

Familial Adenomatous 1) Greater than 100 [usually 1) Typical adenomas [micro 1) Colon 1) 100% APC gene 1) Sulindac
Polyposis [FAP] thousands] of adenomatous polyps adenomas, flat adenomas, and 2) Small intestine [adenocar- [8.5 kilo- may lead to
In large intestine serrated adenomas. [duodenum, periampullary cinoma] bases on regression
2) Gardner’s syndrome =↑ extra- 2) Lymphoid hyperplasia. Region] with age. 2) increased chromosome of polyps.
Intestinal manifestations [skull 3) Gastric Fundic gland polyps. 3) +/- stomach. Risk duodenal 5Q] Screening
+ long bone osteomas, desmoid [periampullary] Aut should
tumors, epidermoid cysts, seba- adenocarcinoma Dominant
include
ceous cysts, lipomas, fibromas, large and
thyroid and adrenal tumors] small intes-
tine.

Flat adenoma Syndrome Less than 100 flat adenomas Predominantly flat adenomas Mainly proximal colon Nearly 100% APC gene
[Attenuated FAP] in proximal colon chromosome 5Q
Aut Dominant

Tourcotte’s Syndrome Comination of colonic adenomas Adenomas [possibly larger] Colon +/- small 100% ? APC muta- 1) Considered
[less than 100] and malignant intestine tions. A variant of
brain tumor [glioblastoma ? DNA mis- FAP.
Multiforme] match repair 2) ? autosomal
Gene. Recessive.

Peutz-Yegher Syndrome Intestinal hamartomatous polyps 1) Arborizing muscular frame Mainly small (intestine, 1) 2%-3% develop Aut Dominant 1) Large
Associated with mucocutaneous work with mucosa containing also stomach and large carcinoma, Chromosome 19 polyps cause
Pigmentation epithelium indigenous to that intestine predominantly (STK11) obstruction
part of the gastrointestinal small intestine and intus-
tract 2) little inflammation [duodenum], but susception,
3) misplaced glands relatively also colon, +/- +/- bleeding
common [rule-out invasive stomach, pancreas
adenocarcinoma). And gallbladder.
2) Dysplasia and
carcinoma within
polyp range 1-30%
of patients. 3)
increased risk
extra-intestinal
cancers [uterus,
ovary, testes]
gastrointestinal
stromal tumors,
+/- breast.
 14

Syndrome Definition and Sub Types Histologic Features Distribution Cancer Risk Genetics Comments

Juvenile Polyposis More than 10 juvenile polyps 1) Hamartomatous polyps with Colon and rectum always, 1) Increased Aut Dominant 1) Heterogen-
Syndrome [usually dozens to hondruds] widely spaced, variably +/- stomach and small [ill-defined] SMAD4 gene eous syndrome
Sub-type I: Juvenile polyposis cystically dilated glands intestine risk of colo- (DPC4) with multiple
coli [colon and rectal polyps lined by normal or hyperplastic rectal carcinoma phenotypic
only]. Epithelium in an inflamed in familial and expressions.
Sub-tyope II: Generalized edematous stroma 2) little or non-familial 2) sporadic
Juvenile polyposis [colon, no smooth muscle 3) may develop juvenile poly- juvenil
Rectum, small intestine and dysplasia and carcinoma 4) +/- posis polyps may
Stomach]. Adenomas 2) increased have incre-
Sub-type III: Non-familial risk of colon ased risk
Juvenile polyposis [sporadic] cancer in first as well?
[associated with congenital degree relatives 3) Hereditary
abnormalities]. 3) cancer related Mixed Poly-
Sub-type IV: Juvenile polyposis to juvenile polyp posis may be
Of infancy [extremely rare]. with dysplasia or a subtype.
adenoma?.

Cowden’s Disorder of oral cutaneos 1) Variable 2) mucosal harmar- Entire GI tract 1) Increased Aut Dominant 1) Intestinal
Syndrome Lesions [multiple facial trich- tomas resemble juvenile polyps [ill-defined] “PTEN” gene ganglioneuro-
alemomas, oral papillomas, acryl with increased lamina propria risk of gastro- (10q23) matosis may
keratosis, lipomas, hemangiomas, fibrosis, disordered mucosa intestinal car- be a sub-type
skin tags, neuromas] and gastro- with disorganized slaying of cinoma 2) increa- of Cowden’s
intestinal hamartomas [35% of muscularis mucosa 3) lesions sed incidence and/or associ-
cases] are diffuse 4) muscularis breast cancer ated with
mucosa Leiomyomas 5) gastro- 3) increased MEN-syndrome
intestinal lipomas 6) intestinal thyroid adenomas, type 2B.
ganglioneuromas 7) Lymphoid goiter and cancer.
Polyps.

Hereditary 1) Type I: Colorectal cancer 1) adenomatuos polyps with Predominantly proximal Nearly 100% DNA 1) Colonoscopy
Non-polyposis Colo- in at least 3 first degree increased incidence of flat [right colon] Later onset Mismatch recommended
Rectal Cancer relatives; two generations; one adenomas [age 40-60] repair Starting at
Syndrome (HNPCC) effected member with colo- gene muta- age 25.
Rectal cancer before age 50. tions in 2) Muir-Torre
2) Type II = as above + extra chromosomes syndrome,
colonic cancer [breast, stomach, 2 + 3 at variant of
pancreas, ovary, uterus, etc]. the germ- HNPCC [incre-
3) polyps less than 100 in number. Line level. ased skin
tumors].

Cronkhite-Canada 1) generalized hamartomatous 1) similar to juvenile polyps Entire gastrointestinal 1) Increased Unknown 1) Lesions in
Syndrome polypoid lesions associated with [usually more diffuse] tract [ill-defined] stomach histo-
Cutaneous abnormalities [hair 2) increased cystically dilated risk of colo- logically resem-
Loss, nail dystrophy, skin crypts with inspissated mucus. rectal cancer` ble Menetrier’s
Hyperpigmentation] 3) cystic dilation of crypts disease and hyper-
occurs in interpolypoid mucosa plastic polyps
as well. 4) may develop adeno- 2) In colon, lesions
matous changes. Resemble diffuse
juvenile polyps.
 15

CLASSIFICATION OF
GASTROINTESTINAL POLYPS

Epithelial Non-Neoplastic

Hyperplastic
Inflammatory
Hamartoma [sporadic, familial]
Cysts/Duplications
Heterotopia [embryonic rests]
Miscellaneous [tags, stumps, stalks]

Epithelial Neoplastic

Adenoma[sporadic, familial]
typical, flat, serrated
Polypoid dysplasia in IBD
Carcinoma
Neuroendocrine tumors
Metastasis [epithelial/non-epithelial]

Non-Epithelial

Lamina propria infiltrates [pneumatosis, xanthoma,

Endometiosis, etc.
Mesenchymal [benign, malignant]
Neural, adipose, vascular, smooth muscle derived
Inflammatory fibroid polyp
 16

ESOPHAGEAL POLYPS
[Generic]

Epithelial Non-Neoplastic

Hyperplastic squamous papilloma

Acanthosis/pseudoepitheliomatous hyperplasia
Webs
Glycogenic acanthosis

Inflammatory typical
Pyogenic granuloma

Cysts esophageal glands cysts

Heterotopia gastric, thyroid, parathyroid, sebaceous, pancreas, other

Epithelial Neoplastic

Adenoma Barrett’s-associated, submucosal gland duct

Carcinoma Polypoid carcinosarcoma, other

Metastasis lung, breast, stomach, melanoma, other

Non-Epithelial

Lymphoid hyperplasia, neoplasia

Mesenchymal fibrovascular polyp, inflammatory fibroid polyp, leiomyoma,

granular cell tumor, GIST, GANT
 17

GASTRIC POLYPS
[Generic]

Epithelial Non-Neoplastic

Hyperplastic/inflammatory Hyperplastic [regenerative =/- dysplasia

Polypoid foveolar hyperplasia
Inflammatory [retention] polyp
Gastritis Cystica Polyposa/Profunda
Polypoid gastritis

Hamartoma Fundic gland polyp

Peutz-Yegher polyp
Juvenile polyp
Cronkhite-Canada syndrome polyp

Heterotopia/Ebryonic rests Pancreatic [adenomyoma]

Brunner’s gland
Pancreatic acinar “metaplasia”

Miscellaneous Menetrier’s disease

Prominent folds [rugae]
Mucosal bump, nodules

Epithelial Neoplastic

Adenoma Sporadic/familial

Carcinoma Polypoid or papillary carcinoma

Other Carcinoid tumors

Metastasis

Non-Epithelial

Lymphoid Xanthoma
Histiocytosis X

Lympoid Lympoid hyperplasia

Maltoma

Mesenchymal Inflammatory fibroid polyp

GIST
Neurofibroma [sporadic, von Recklinghausen]
 18

SMALL INTESTINE POLYPS

[Generic]

Epithelial Non-Neoplastic

Hyperplastic Brunner’s gland hyperplasia

Inflammatory Inflammatory polyp [sporadic, IBD]

Pyogenic granuloma
Nodular duodenitis

Hamartoma Peutz-Yegher [sporadic, syndromeic]

Juvenile polyposis
Cronkhite-Canada syndrome polyp
Cowden’s disease
Brunner’s gland hamartoma

Heterotopia/Embryonic rests Gastric, pancreatic [myoepithelial hamartoma]

Miscellaneous Endometriosis

Epithelial Neoplastic

Adenoma Sporadic/FAP

Carcinoma Polypoid carcinoma

Other Carcinoid

Non-Epithelial

Lamina Propria Infiltrates Pneumatosis, MAI, Whipple’s

Lymphoid Hyperplasia/lymphoma

Mesenchymal GIST
Lipoma/lipohyperplaisa of ileocecal valve
Hemangioma
Gangliocytic paraganglioma
Inflammatory fibroid polyp
 19

LARGE INTESTINE POLYPS

[Generic]

Epithelial Non-Neoplastic

Hyperplastic hyperplastic [metaplastic]

Inflammatory Inflammatory [pseudo] polyp

Isolated, IBD-related
Inflamamtory myoglandular
Inflammatory “CAP” polyp
Mucosal prolapse-related polyp
Colitis cystica polyposa/Profunda

Hamartoma Juvenile [sporadic, syndromic]

Peutz-Yegher [sporadic, syndromic]
Cronkhite-Canada syndrome
Cowden’s syndrome

Heterotopia Gastric, salivary, other

Miscellaneous Pneumatosis
Endometriosis
Appendix intussusception/Inverted stump
Mucosal bumps/tags/excrescences
Dermoid cyst

Epithelial Neoplastic

Adenoma Typical/flat/serrated [sporadic/familial]

Adenoma with carcinoma
Polypoid dysplasia in IBD

Carcinoma Polypoid carcinoma

Carcinoid
Metastasis [breast, melanoma]

Non-Epithelial

Lamina Propria Infiltrates Pneumatosis, xanthomam endometriosis

Muciphages

Lymphoid Hyperplasia/neoplasia

Mesenchymal Neurofibroma [sporadic, syndromic]

Ganglioneuroma [sporadic, syndromic]
Leiomayoma/GIST
Hemangioma/AV malformation
Lipoma/lipohyperplasia
Inflamamtory firbroid polyps
Teratoma
 20
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