Barrett’s Esophagus

Columnar metaplasia

REF: Robbin’s pathology 7^th edition page 804 Repeat from June 2008 (surgery)

Barrett esophagus:

• Barrett esophagus is a complication of long standing gastroesophageal reflux, occurring over time in up to 10% of patients with symptomatic GERD.
• It is single most important risk factor of esophageal adenocarcinoma

In Barrett esophagus distal squamous mucosa is replaced by metaplastic columnar epithelium as a response to prolonged

injury (columnar metaplasia)

Two criteria are required for the diagnosis of Barrett esophagus:

1. Endoscopic evidence of columnar epithelium lining above the gastroesophageal junction
2. Histological evidence of intes
3. epithelium

Schwartz writes – “The definition of Barrett’s esophagus (BE), has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus. It is now recognized that the specialized intestinal type epithelium found in the Barrett’s mucosa is the only tissue predisposed to malignant degeneration. Consequently, the diagnosis of Barrett’s esophagus is presently made given any length of endoscopically identifiable columnar mucosa that proves on biopsy to show intestinal metaplasia. While long segments of columnar mucosa without metaplasia do occur, they are uncommon and are probably congenital in origin. The hallmark of intestinal metaplasia is the presence of intestinal goblet cells.”

Barrett esophagus is well recognized as a complication of gastroesophageal reflux disease (GERD).

Prolonged exposure of the esophagus to the refluxate of GERD can erode the esophageal mucosa, promote inflammatory cell infiltrate, and ultimately cause epithelial necrosis.

This chronic damage is believed to promote the replacement of healthy esophageal epithelium with the metaplastic columnar cells of Barrett esophagus.

The condition occurs in a 2:1 male-to-female ratio.

The most significant morbidity associated with Barrett esophagus is the development of adenocarcinoma in the esophagus.

Frequent esophagoscopy is needed in people with Barrett’s esophagus as it doesn’t regress.

Barrett’s esophagus refers to the metaplastic change of distal esophageal mucosa from normal squamous epithelium to columnar epithelium, in response to chronic gastroesophageal reflux.

The most common type of metaplasia is intestinal type of metaplasia and presence of intestinal goblet cell is the hallmark of intestinal metaplasia.

Stricture formation and peptic ulceration of columnar lined epithelium of esophagus is common complication of barrett’s esophagus.

Barrett’s esophagus can be classified into long segment( involvement of >3 cm of esophagus) and short segment disease ( involvement of < 3 cm of esophagus).

Long segment disease carries more risk for adenocarcinoma.

Barrett’s esophagus is associated with sliding hernia not with paraesophageal hernia.
 

Ref: Robbins 8/e, Page 770; Bailey & Love 25/e, Page 1022.

Odynophagia means painful swallowing, it is seen in inflammatory lesions of food passages (i.e oral cavity, pharynx and esophagus).

Barrett’s esophagus is specialized columnar metaplasia that replaces the normal squamous mucosa of the distal esophagus in some persons with GERD.

Barrett’s epithelium is a major risk factor for adenocarcinoma of the esophagus and is readily detected endoscopically, due to proximal displacement of the squamocolumnar junction.

Methylene blue dye is taken up by the cytoplasm or absorptive cells such as the normal epithelial cells of the colon and small intestine and goblet cells, which are present in Barrett’s epithelium.

Chromoendoscopy is considered by some as a tool for recognizing high-risk lesions within Barrett’s esophagus and for facilitating definitive therapy.

The most commonly used dye is methylene blue.

It will not stain nonabsorptive normal epithelium of the stomach as is found in the cardia and fundus, or normal squamous mucosa of the esophagus.

Barrett’s esophagus is a condition in which squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium containing goblet and columnar cells in some patients with GERD.

Barrett’s Esophagus:

The Prague Criteria for grading of Barrett’s esophagus was named because it was first presented by the IWGCO at the 2004 United European Gastroenterology Week meeting in Prague.

• Identify the gastroesophageal junction as at the tops of the gastric mucosal folds
• For circumferential columnar-appearing mucosa above the gastroesophageal junction define this extent in centimetres above the gastroesophageal junction: – report as the C value
• For any tongue-like areas of columnar-appearing mucosa, measure the Maximum extent in centimetres above the gastroesophageal junction: – report as the M value

Barrett esophagus is a metaplasia of the esophageal mucosa caused by the replacement of the squamous epithelium with columnar epithelium.

Ans. is ‘a i.e., Lower esophagus lined by columnar ephithelium

 Barrett’s esophagus

• Is metaplastic change ,of gastro esophageal mucosa from normal squamous epithelium to columanar epithelium, in response to chronic gastro -esophageal reflux.

o The function between squamous esophageal mucosa and gastric mucosa moves proximally . o Three types of columnar epithelium have been described in Barrett’s esophagus :

(i)    Intetinal type -the most common type

(ii)  The junctional type and

(iii)The gastiric fundic type

o Barrett’s esophagus is a premalignant codition for adenocarcinoma esophagus o The hallmark of inestinal metaplasia is the presence of intestinal goblet cells.

Ans. is ‘a’ ie More incidence of sq.cell ca

There is increased incidence of adenocarcinoma in Barret’s esophagus.

o Barrett’s esophagus is a premalignant condition with increased incidence of adenocarcinoma of esophagus. o Also remember

Barrett’s esophgus is the single most important risk factor for adenocarcinoma of esophagus .

The adenocarcinoma develops at the squamo -Columnamr junction (-85%) or within 2cm of the junction.

Ans. is ‘b’ i.e., Columnar metaplasia

Ans. is ‘a’ i.e., Lower esophagus lined by columnar ephithelium

Barrett’s esophagus

• Is metaplastic change of distal esophageal mucosa from normal squamous epithelium to columnar epithelium, in response to chronic gastro-esophageal reflux.
• The junction between squamous esophageal mucosa and gastric mucosa moves proximally.
• Three types of columnar epithelium have been described in Barrett’s esophagus:

i)        intestinal type – the most common type

ii)      the junctional type and

iii)    the gastric fundic type

• Barrett’s esophagus is a premalignant condition for adenocarcinoma esophagus
• “The definition of Barrett’s esophagus (BE) has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus. It is now recognized that the specialized intestinal type epithelium found in the Barrett’s mucosa is the only tissue predisposed to malignant degeneration. Consequently, the diagnosis of BE is presently made given any length of endoscopically indentifiable columnar mucosa that proves on biopsy to show intestinal metaplasia.” – Schwartz 9/e p831 (8/e, p868)

Also remember

The hallmark of intestinal metaplasia is the presence of intestinal goblet cells.

Ans. is ‘b’ i.e. Intestinal metaplasia 

Schwartz writes – “The definition of Barrett’s esophagus (BE), has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus. It is now recognized that the specialized intestinal type epithelium found in the Barrett’s mucosa is the only tissue predisposed to malignant degeneration. Consequently, the diagnosis of Barrett’s esophagus is presently made given any length of endoscopically identifiable columnar mucosa that proves on biopsy to show intestinal metaplasia. While long segments of columnar mucosa without metaplasia do occur, they are uncommon and are probably congenital in origin. The hallmark of intestinal metaplasia is the presence of intestinal goblet cells.”

Ans is ‘a’ ie More incidence of sq. cell ca 

There is increased incidence of adenocarcinoma in Barret’s esophagus.

• Barrett’s esophagus is a premalignant condition with increased incidence of adenocarcinoma of esophagus. The risk of adenocarcinoma increases with increasing length of columnar-lined epithelium
• Also remember
• Barrett’s esophagus is the single most important risk factor for adenocarcinoma of esophagus.
• The adenocarcinoma develops at the squamo-columnar junction (-85%) or within 2 cm iof the junction.

Ans is ‘a’ i.e. Stricture & ‘c’ i.e. peptic ulcer 

• The typical complications of Barrets esophagus include peptic ulcers in the colummar lined segment of esophagus high and long strictures and a dysplasia – cancer sequence.

Ans. is ‘a’ i.e. Sequence of prolonged GE reflux; ‘b’ i.e. It is premalignant; ‘c’ i.e. Lower esophageal mucosa is replaced by intestinal type 

Ans is ‘a’ i.e. Premalignant; ‘c’ i.e. Can be diagnosed by seeing under endoscope

• Diagnosis of Barrett’s esophagus

The diagnosis of Barrett’s esophagus is suspected on endoscopy when there is difficulty in visualizing the squamo-columnar junction at its normal location and by the appearance of pink, more luxuriant columnar mucosa in the lower esophagus instead of gray-pink squamous mucosa.

–        the diagnosis is confirmed by biopsy.

• Strictures in Barrett’s esophagus occur at the squamo-columnar junction and move high up as the squamo­columnar junction moves up with progressive injury.

Ans. is `b’ i.e., Premalignant condition 

• About option (a)

– Barrett’s esophagus is more common in men than in women (3 : 1 ratio)

• About option (c)

Schwartz surgery and CSDT writes that Barrett’s esophagus can be reversed but only with antireflux surgery (response to medications is not good). Read below lines from CSDT (13/e p438) Schwartz (9/e p841): CSDT writes-“A fundoplication may promote regression of the columnar epithelium. Many studies have shown that regression occurs in 15-50% of patients when the length of the Barrett segment is less than 3 cm.”

Schwartz writes- “The common belief that Barrett’s epithelium cannot be reversed is likely false. DeMeester and associates reported that, after antireflux surgery, loss of IM (intestinal metaplasia) in patients with visible BE was rare, but occurred in73% of patients with inapparent IM of the cardia. This suggests that the metaplastic process may indeed be reversible if reflux is eliminated early in its process, that cardiac mucosa is dynamic, and that, as opposed to IM extending several centimeters into the esophagus, IM of the cardia is more likely to regress following antireflux surgery.

Gurski and colleagues reviewed pre- and posttreatment endoscopic biopsies from 77 Barrett’s patients treated surgically and 14 treated with PPIs. Histopathologic regression occurred in 28 of 77 patients (36.4%) following antireflux surgery, and in one of 14 (7.1%) patients treated with PPlsalone (P 3 cm) BE.

Although these studies do not conclusively prove the ability of antireflux surgery to reverse the changes of early BE, they do provide encouragement that, given early changes, the process may indeed be reversible.”

• More about the t/t of Barret’s oesophagus
• First, the natural course of Barrett’s oesophagus.

–  Barrett’s esophagus develops during healing of erosive esophagitis with continued acid reflux and the Barrett’s esophagus progresses through a dysplastic stage before developing into adenocarcinoma. The stages are.

– Erosive esophagitis —> Metaplasia (Barrett’s esophagus)  Low grade dysplasia —> high grade dysplaisa —> Adenocarcinoma

• Treatment of Barrett’s esophagus is same as for reflux esophagitis — Conservative (antacids, H2 blocking agents, elevation of the head of bed, and avoidance of smoking and alcohol etc.) and Anti-reflux surgery (Nissen’s fundoplication is anti-reflux procedure of choice)
• As there is substantial increased risk of cancer with Barrett’s esophagus, a regular follow-up with endoscopy and biopsy is done. This allows detection of cancer at an early stage with improved long-term survival after resection

In the absence of dysplasia —> Surveillance endoscopy every 12-24 months.

• In the presence of low-grade dysplasia —->

Patients with low grade dysplasia should be treated for 12 weeks with high-dose acid suppression therapy and then biopsy repeated. (the rationale for this approach is to decrease the mucosal inflammation by blocking acid secretion, allowing the pathologist a more accurate reading).If the repeated biopsy show metaplasia or high-grade dysplasia, the patient should be managed accordingly.

If repeated low-grade dysplasia is seen- surveillance endoscopy is done every 6-12 months.

• If high grade dysplasia is detected (the diagnosis must be confirmed by two experienced pathologist) —> esophagectomy with removal of all columnar lined epithelium

Or

if resection is not done, then the patient should be strictly followed at 3 monthly interval. If cancer is detected resection is done.

Rationale for esophagectomy in high grade dysplasia is based on the following considerations- (a) cancer ” 

is already present in about 30 to 50% of patients operated for high grade dysplasia. (b) cancer develops in about 50% fo patients during follow up.)

• 19. Ans is ‘b’ ie Premalignant condition [Ref CSDT 13/e p438 (11/e, p488); Bailey & Love 25/e p1023 (24/e p 1007)]
• As already explained Barrett’s esophagus is an Intestinal metaplasia (not squamous metaplasia) which follows the metaplasia – dysplasia – cancer course (a premalignant condition for adenocarcinoma of esophagus)
• Now about the medical tit [option (d)]
• Though medical treatment does not revert back the metaplastic changes, it can be used to treat the underlying reflux disorder and prevent further damage.

Ans is ‘b’ ie Premalignant condition 

• As already explained Barrett’s esophagus is an Intestinal metaplasia (not squamous metaplasia) which follows the metaplasia – dysplasia – cancer course (a premalignant condition for adenocarcinoma of esophagus)
• Now about the medical tit [option (d)]
• Though medical treatment does not revert back the metaplastic changes, it can be used to treat the underlying reflux disorder and prevent further damage.

Ans. is ‘a’ i.e. Adenocarcinoma 

Ans. is ‘a’ , ‘c’ i.e. Metaplasia, Adenocarcinoma more common 

In barrett’s esophagus red, velvety metaplastic mucosa is seen between the smooth pale pink esophageal squamous mucosa and the lusher lightbrown gastric mucosa. It may present as patches or as a broad irregular circumferential band.

Ans. is ‘a’ & ‘b’ i.e. Metaplasia & Peptic stricture 

Reflux esophagitis & Barrett’s esophagus is associated with sliding hernia not paraesophageal hernias.

Ans. is ‘a’, ‘b’, ‘c’ i.e. Long esophageal segment involved, Metaplasia, Peptic ulcer

• Barrett’s esophagus can be classified into long segment disease (involvement of more than 3 cm of esophagus) and short segment disease ( < 3 cm involvement).
• Long segment disease carries more risk for adenocarcinoma

Ans. is ‘d’ i.e. Reflux esophagitis

Answer is B (Intestinal Metaplasia)

Barret’s esophagus is a metaplasia of the esophageal mucosa caused by replacement of squamous epithelium with columnar epithelium.

Specialized intestinal epitheliutn (intestinal metaplasia) is the most common and most important type of columnar epithelium seen in Barret’s esophagus.

Answer is A (More incidence of squamous carcinoma)

Barret’s oesophagia is associated with an increased incidence of adenocarcinoma and not squamous cell carcinoma. Barret’s esophagus is associated with columnar metaplasia of distal (lower esophagus).

Answer is A & C (Stricture and Peptic ulcer)

Complications of Barret’s Oesophagus

• Peptic Ulcer (Barret’s Ulcer: Chronic Peptic Ulceration in the columnar lined mucosa)
• Strictures
• Adenocarcinoma (Dysplagia — cancer sequence)

Answer is a D (Associated with oesophageal varices)

Barret’s oesophagus is not associated with oesophageal varices.

Barret’s oesophagus is characterized replacement of lower oesophageal mucosa by intestinal (columnar) type of epithelium. It is considered premalignant with increased risk of adenocarcinoma, and is believed to be caused by prolonged gastroesophageal reflux.

Answer is D (None):

All statements about Barret’s Esophagus are true

• Stricture in Barret’s esophagus may present in high oesophagus

Barret’s oesophagus can also lead to chronic peptic ulcers of the esophagus with high and long strictures.

• Barret’s esophagus is premalignant

Barret’s esophagus can progress to adenocarcinoma

• Diagnosis can be suggested by Endoscopy

Endoscopy shows a ‘salmon pink’ epithelium above the gastroesophageal junction which replaces the whitish squamous epithelium.

• Diagnosis is confirmed by biopsy

Diagnosis is confirmed by pathological examination and requires the identification of columnar (intestinal) type epithelium characterized by the presence of goblet cells.

• Metaplasia of esophageal squamous epithelium into columnar in distal oesophagus
• Most common type of columnar epithelium is intestinal epithelium (intestinal metaplasia)U
• Metaplasia characteristically affects the distal (lower) oesophagus
• It is consequence of severe reflex esophagitisU
• More common in men^u (Males > Females)
• More common in whites (Whites > Blacks)
• More common with increasing age (incidence increases with age)
• Considered a premalignant condition
• Type of cancer associated in an adenocarcinoma
• Columnar metaplasia that carries maximum risk of adenocarcinoma is intestinal metaplasia (intestinal epithelium)U
• Can lead to chronic peptic ulceration of esophagus (Barret ulcer)
• Can lead to high (midoesophageal) and long strictures

Answer is B (Premalignant condition)

Barret’s oesophagus is a premalignant condition with increased risk of adenocarcinoma. Barret’s esophagus is more common in males

More common in males (Males > Females)0 More common in White (Whites > Blacks)e More common with increasing ageU

Barret’s metaplasia once established does not respond to conservative management

`Established Metaplasia does not regress with antisecretory treatment’ – Harrison

Although medical treatment does not regress the metaplastic changes, it is still advocated to prevent continued insult.

Barret’s esophagus is associated with columnar metaplasia and not squamous metaplasia.

Answer is A (Adenocarcinoma)

Barret’s esophagus is a premalignant lesion and predisposes to adenocarcinoma of the lower (distal) esophagus.

Answer is B (Barret’s esophagus)

Adenocarcinoma is seen in Barret’s esophagus

Barret’s esophagus is a metaplastic change in the lining mucosa of oesophagus in response to chronic gastroesophagus reflex.

In Barret’s esophagus the junction between oesophageal mucosa (squammous) and gastric mucosa (columnar) moves proximally such that the lower part of esophagus now becomes lined with different types of gastric mucosa. This part of oesophagus has an increased risk for adenocarcinoma i.e.

Adenocarcinoma is seen in Barrets esophagus.

Ans. A: Hyperplastic change in the lining mucosa of esophagus

There is metaplastic change in the lining mucosa of esophagus.

Usually there are no particular severe symptoms, although they do have the most abnormal pH profiles. Patients with Barrett esophagus are predisposed to the most rapidly increasing cause of cancer.

The diagnosis of Barrett esophagus is made at endoscopy when the normal, whitish-appearing squamous epithelium is found to be replaced by a reddish, velvety-appearing intestinal type of columnar epithelium.

Barrett esophagus is thought to evolve to cancer through various stages of dysplasia.

Initially, no dysplasia is found; subsequently, low-grade dysplasia develops in the mucosa, then high-grade dysplasia, and finally carcinoma. Dysplasia is considered indefinite when histological changes are not definitive for dysplasia. Most of these changes cannot be visualized endoscopically.

The hallmark of specialized Barrett’s epithelium is the presence of mucus-secreting goblet cells (intestinal metaplasia). Patients are usually monitored by a program of periodic surveillance endoscopy during which biopsy specimens are taken in 4 quadrants every 2 cm throughout the Barrett segment.

Treatment is that of the underlying cause of GORD

Ans. D: Metaplastic change in the lining mucosa of the esophagus

Barrett’s esophagus is a metaplastic change in the lining mucosa of the esophagus in response to chronic gastro-esophageal reflux

Esophageal cancer:

Important predisposing factors:

– Excess alcohol

– Smoking

– Chronic achalasia

– Tylosis

–  Barrett’s esophagus

– Plummer Vinson syndrome

Features:

– Progressive dysphagia (MC)

– Weight loss

– Weakness

• Esophagoscopy is diagnostic
• Chemotherapy:

– Limited role

– Cisplatin

– Bleomycin

– 5-Fluorouracil

• MC type: Squamous cell Ca
• MC site: Lower end
• MC site of adenoCa: Lower end.
• MC site of squamous cell Ca: Middle third

Ans. b. Intestinal metaplasia

Diagnosis of Barrett’s esophagus is made by demonstration of columnar mucosa, which on histopathology shows Intestinal metaplasia.

“Barrett esophagus is a complication of chronic GERD that is characterized by intestinal metaplasia within the esophageal squamous mucosa.

Barrett’s Esophagus

• Metaplasia of esophageal squamous epithelium into columnar in distal° esophagus
• It is consequence of severe reflux esophagitis°
• MC type of columnar epithelium is intestinal epithelium (Intestinal metaplasia^Q)
• Barrett’s esophagus requires both endoscopically visible segment of columnar lining of distal esophagus and intestinal metaplasia showing goblet cells on biopsy

Columnar epithelium in Barrett’s esophagus

• Intestinal type^Q: MC type, most commonly associated with dysplasia and carcinoma
• Junctional type
• Fundic type
• Metaplasia characteristically affects distal esophagus
• More common in men, whites and with increasing age^Q
• Premalignant condition for adenocarcinomaQ

Complications of Barrett’s Esophagus

• Can lead to chronic peptic ulceration of esophagus (Barrett’s ulcer)^Q
• Can lead to high (midesophageal) and long strictures^Q.