Understanding Barrett’s Esophagus
Gastroesophageal reflux disease (GERD) is the most common digestive affliction in the United States and accounts for over $12 billion in direct costs annually just for the medications used to treat millions of affected individuals. The prevalence of GERD is on the order of 20% of the US population and roughly half the adult population is symptomatic at least monthly according recent data.
[cleeng_content id=”951269877″ price=”1.99″ description=”Purchase the full article.”]The consequences of longstanding GERD can be the development of damage to the junction connecting the esophagus to the stomach (GEJ) because of excessive regurgitation of gastric and duodenal contents into the lower segment of the esophagus. In some of us that damage can lead to a change in the skin lining that is known as Barrett’s esophagus (BE).
The incidence of BE has steadily increased in America since the 1970’s. As the frequency of BE has risen, so has adenocarcinoma of the esophagus. The reason for this is that BE is the precursor tissue for the development of this cancer. The transition to cancer is quite infrequent (about 0.15 to 0.45% per year depending on the study quoted) in America but it is nearly 4% per year in England. It is important to realize, however, that the incidence of adenocarcinoma of the esophagus in the US has increased over 300% since the 1970’s. Additionally, if a patient presents with esophageal adenocarcinoma rather than Barrett’s esophagus, the mortality is very high as few individuals are cured by cancer treatment.
Causes and Risk Factors
Chronic GERD is considered the primary reason some of us will develop BE. The average age of diagnosis of BE is 55-60 years but the disease is seen in children. No case series have been seen in youth younger than age five. Barrett’s esophagus is more common in Caucasian males but as the incidence of this condition is rising in women and in other ethnic groups. History of GERD at a young age, prolonged duration of GERD symptoms, night time reflux and severity of GERD are mentioned in the literature as risk factors associated with the development of BE. Likewise, mounting data show that central obesity (abdominal fat deposition), advanced age and tobacco use place us at increased risk for developing BE.
Patients who suffer from GERD can be plagued with a variety of symptoms such as heartburn, regurgitation, non-cardiac chest pain, wheezing, hoarseness, chronic cough, difficulty swallowing, chronic recurrent nausea/vomiting, dyspeptic abdominal pain, chronic sore throat or painful swallowing but none of these symptoms are predictive of the presence of BE. The majority of people who suffer from GERD never seek medical attention in the present age due to the fact that every major supermarket in America carries half a store aisle of anti-acid medications. We can use these over the counter medications to control our symptoms and never seek medical care. This can delay the diagnosis and appropriate management. An interesting paradox about BE is that some individuals afflicted with BE have a decreased sensitivity to the symptoms of GERD compared to those who have GERD without BE.
As can be seen above symptoms do not predict who has BE. Likewise, risk factors do not establish a diagnosis of Barrett’s esophagus as well. The only way to determine the presence of the change in the skin lining at the GEJ is to look at this area. This is performed by passing an endoscope down through the mouth into the esophagus and visualizing the affected area.
The GEJ will reveal a change in the skin lining in many individuals with BE but visualization of the change alone is not adequate to establish the diagnosis. Biopsies must be obtained to confirm the skin change. Without biopsy confirmation of BE can be problematic as gastroenterologists under and over diagnose the disease frequently.
Once the diagnosis is confirmed by endoscopy and biopsy findings, a repeat endoscopy with more thorough biopsies of the affected area should be performed a year later. If the biopsies do not show any tissue damage suggestive of a high risk for progressing to cancer in the near future (tissue changes called dysplasia much like that seen with a Pap smear of a woman’s cervix) then the patient should be checked with endoscopy and biopsy every three years. The guidelines for endoscopic surveillance of BE have been evolving over the past three decades as we have learned more about the genetics of disease progression.
Natural History of Barrett’s Esophagus
The majority of individuals in the US do not know they even have Barrett’s esophagus. Additionally, the majority of afflicted with this disease will not die from esophageal cancer. A recent study showed that the leading cause of death among those afflicted with BE is heart disease accounting for 35% of deaths followed by pulmonary deaths in 20%. Death from adenocarcinoma of the esophagus associated with BE only accounted for 7% of individuals.
Regardless, progression to cancer is either zero or 100% for an individual. Once you know you are carrying a diagnosis that is a precursor to cancer that has a very high mortality rate, you become engaged in understanding your disease and the appropriate management of the disease.
Barrett’s esophagus can transition into dysplastic tissue. This, in turn can progress to cancer. Fortunately, this process is very slow. If BE tissue does reveal dysplasia a more aggressive endoscopy and biopsy surveillance program is initiated
I am frequently asked if the patient is going to develop cancer. The incidence is low as mentioned above and aggressive medical management or surgery suggests that the transition to dysplasia and cancer can be delayed, if not prevented. A paper published in 2004 showed that treatment with high dose acid suppression reduced the incident development of dysplasia in BE patients by 50% in a 20 year follow-up study of 236 individuals with BE.
With modern interventional endoscopic techniques and medical therapy almost no one needs to progress from dysplasia to cancer. While the incidence of adenocarcinoma for BE continues to rise dramatically (700% since 1970 to 2000) most cases present with cancer rather than developing a malignancy in an individual followed with Barrett’s esophagus. These individuals never sought out medical evaluation of their GERD; rather they presented with cancer at their first evaluation. I follow several thousand patients with BE and none of them have died from esophageal cancer but I diagnose several people with esophageal cancer each year who are presenting for their first evaluation. Most of these individuals are elderly but I have seen esophageal cancer present in people in their 40’s.
Once an individual is diagnosed with Barrett’s esophagus, aggressive steps should be taken to control the GERD. These are called step one therapeutic maneuvers. These include the following:
- Reduce central obesity, if present
- No late evening snacking; give yourself a four hour window before lying down
- Smaller meal size
- Avoid carbonated beverages; one 12 ounce soda induces reflux for 4 hours
- Stop caffeine intake by 2 pm; caffeine relaxes the GEJ
- Stop smoking
- Stop ingesting all Trans fats (partially or completely hydrogenated fats)
See my book: 42 Days to a New Life for an in depth discussion about this
- Include a multivitamin, calcium, vitamin D & omega-3 fatty acids in your daily routine
- Avoid fatty meals late in the day
- Elevation of the head of the bed in some individuals
- Avoid aggravating foods (spicy foods, acidic foods/beverages)
- Avoid excessive carbohydrate intake (they make you reflux grow belly fat)
See my book: Fructose Exposed for more information on this subject
While all of these help reduce GERD, you usually need some form of medication to heal inflammation in the esophagus. Many medications have been developed for that purpose. It is easy to control GERD-related symptoms in the majority of patients with a regimen customized to the individual.
Gaviscon with alginate: the alginate forms a foam barrier on top of the gastric contents and provides quick relief but it only lasts about two hours before its effectiveness is lost. Additionally, Gaviscon does not provide lasting healing to the esophagus.
Histamine type 2 receptor antagonists were the mainstay of treatment during the late 1970’s until the late 1980’s. These medications include Tagamet, Zantac, Pepcid and Axid. These medications provide symptom reduction within 30-60 minutes after ingestion. While studies suggest that they lose their potency with prolonged use, my experience with their use since they came to market has not typically borne that out in clinical practice. Many patients use them to control symptoms very effectively, especially with night time GERD breakthrough symptoms.
Proton pump inhibitors came on the medical scene in the late 1980’s with the Food and Drug Administration (FDA) allowing the release of Prilosec. This immediately became one of the most in demand medications for the next decade. Other medications in this drug class followed including Prevacid, Aciphex, Protonix, Nexium, Zegerid and Dexilant. These medications have become the mainstay of long term therapy for GERD and Barrett’s esophagus for many patients. The market place and insurance plans drive quite a bit in the specific choice of treatment of these diseases as several of these medications are now generic or are able to be purchased over the counter without prescription.
Promotility medications in various forms have been around for a long time. This class of medication stimulates the stomach to empty quicker than normal; some tighten the GEJ muscle and improve muscle contraction of both the esophagus and stomach. These medications have had their problems because of side effects, lack of FDA approval for GERD use and medication withdrawal by the FDA precluding routine use in many patients with BE. These medications include metoclopramide, cisapride, erythromycin, domperidone and tegaserod.
One of the unfortunate aspects of BE management is that symptom relief does not necessarily guarantee healing of damaged tissue at the GEJ. One of the reasons for this is that bile and neutralized acid contents refluxing into the esophagus can cause ongoing damage as well as lack of symptom relief. Additionally, some individuals suffer from systemic diseases, infections or trauma to the esophagus that may not allow symptom control or healing of the GEJ.
Sometimes the only way to control symptoms of GERD and BE is surgery. While surgical repair of a hiatal hernia dramatically reduces reflux into the distal esophagus and routinely decreases the need for the use of medications, up to 15% of individuals will slowly return to medical therapy due to surgical failure. At the same time, surgery is no guarantee that your Barrett’s esophagus will not progress to cancer. My clinical experience and prospective monitoring of hundreds of patients with BE who have undergone surgery support several issues. First, surgery does fail over time in about 15% of patients. Second, most individuals feel that surgery is clearly beneficial for them if there is no complication. Third, I have only seen two individual who progressed to high grade dysplasia after surgery. One of these individuals was nearly 20 years out from his surgery. The other had gained 40 pounds and tore out his surgical repair about a decade after surgery.
Appropriate preoperative evaluation is critical if you are going to proceed with surgery as there are a number of issues that can confound the outcome of hiatal hernia surgery. Underlying gallbladder disease, loss of function of the esophagus due to systemic disease or primary esophageal dysfunction, loss of normal gastric emptying (gastroparesis) of past trauma to the esophagus can prevent a good surgical outcome in some patients if not appropriately addressed. Your gastroenterologist and/or surgeon need/s to investigate these issues before surgery is contemplated.
If an individual develops dysplasia, various approaches to management have evolved. Aggressive endoscopic surveillance with frequent biopsying is presently recommended for most patients. New endoscopic techniques are now available to destroy the dysplastic tissue and these include: cryotherapy (freezing the tissue), heating the tissue to kill the cells, photodynamic therapy and resection of the tissue. The heating techniques include: laser, argon plasma coagulation, heater probe, multipolar electrocoagulation and radiofrequency ablation. Resection of the dysplastic tissue can be done by way of endoscopic mucosal resection if it involves only a small area. If there is a large amount of BE, surgical resection of the top of the stomach and bottom of the esophagus with reconstruction can be performed. Each of these techniques has advantages and disadvantages as well as differing applicability, depending on the individual situation.
Aggressive management of dysplasia associated with Barrett’s esophagus is very important as the 5 year survival for patients with esophageal cancer is less than 20%. As I mentioned earlier however, most individuals in surveillance programs never get to cancer as appropriate intervention prevents this from occurring. Likewise, most people with BE die from another cause.
Barrett’s esophagus is the precursor change to the bottom of the esophagus from long standing GERD that can lead to esophageal adenocarcinoma. The annual incidence of cancer is low but carries a high mortality if the cancer is the initial presentation. The majority of individuals with BE in America are undiagnosed. The only way to establish the diagnosis is by endoscopy with biopsy. No symptom or risk factor diagnoses the disease. Medical and surgical therapy is tailored to the individual depending on numerous factors. Many options are now available in the management of BE. Thorough preoperative evaluation is critical for a good surgical outcome.[/cleeng_content]