Barrett's esophagus: treatment

It is known that Barrett's esophagus can occur in patients with the progression of GERD, but its development is also possible in patients who do not suffer from this disease. The basic principles of drug treatment of patients with GERD are known, which, as our experience has shown, can also be used in the treatment of patients with GERD complicated by Barrett's esophagus. The search for the most optimal treatment options for such patients continues, the purpose of which is to eliminate not only the clinical manifestations of GERD, but also the elimination of all morphological signs considered characteristic of Barrett's esophagus, and, accordingly, to improve the quality of life of patients. It is often assumed that the treatment of Barrett's esophagus depends mainly on the presence and degree of dysplasia, but it is not always possible to "stop" the progression of dysplasia, as well as its regression.

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Drug treatment of Barrett's esophagus

The main drug treatment for Barrett's esophagus is aimed at inhibiting acid production in the stomach and eliminating (reducing the frequency and intensity) gastroesophageal reflux. Preference in the treatment of patients is given to proton pump inhibitors (omeprazole, pantoprazole, lansoprazole, rabeprazole or esomeprazole), used in the treatment of patients, most often in standard therapeutic doses (respectively 20 mg, 40 mg, 30 mg, 20 mg and 20 mg 2 times a day). It should be remembered that proton pump inhibitors cannot achieve 100% inhibition of acid in the stomach.

In case of resistance to proton pump inhibitors, which reaches 10% in some populations, the treatment of Barrett's esophagus should use histamine H2-receptor antagonists (ranitidine or famotidine, 150 mg and 20 mg 2 times a day, respectively). In such cases, the use of ranitidine or famotidine in higher doses in the treatment of patients with GERD and Barrett's esophagus is fully justified during the period of significant deterioration of the patient's condition for 1-2 weeks, then the doses of the drugs are gradually reduced as recovery occurs.

Inhibition of acid formation in the stomach leads to a decrease in not only the total volume of acid, but also acidification of the contents of the duodenum, which, in turn, helps to inhibit the secretion of proteases, primarily trypsin. However, the pathological effect of bile acids (salts) on the mucous membrane of the esophagus remains. At the same time, long-term inhibition of acid formation in the stomach by proton pump inhibitors leads to a decrease in the total volume of stomach contents due to a decrease in acid secretion, and, accordingly, a higher concentration of bile acids (due to a decrease in their "dilution" with hydrochloric acid). During this period, bile acids (salts) acquire primary significance in the development of esophageal adenocarcinoma. In such cases, treatment of Barrett's esophagus should use ursodeoxycholic acid (ursosan), which has a positive effect on biliary reflux gastritis and biliary reflux esophagitis (one capsule before bedtime).

For the absorption of bile acids in the treatment of patients, if necessary, it is advisable to additionally use non-absorbable antacid drugs (phosphalugel, almagel Neo, maalox, etc.) 3-4 times a day one hour after meals. This will allow the absorption of bile acids entering the stomach with duodenogastric reflux, and then into the esophagus.

For faster relief of heartburn (burning) and/or pain behind the breastbone and/or in the epigastric region, as well as in the presence of the symptom of rapid satiety, treatment of Barrett's esophagus should include the use of prokinetics (domperiodone or metoclopramide), respectively, 10 mg 3 times a day 15-20 minutes before meals. If patients have symptoms associated with increased sensitivity of the stomach to stretching (the appearance of heaviness, fullness and bloating in the epigastric region that occur during or immediately after eating), it is recommended to additionally include enzyme preparations that do not contain bile acids (pancreatin, penzital, creon, etc.) in the treatment of patients.

The disappearance of clinical symptoms, which is possible in patients with GERD and Barrett's esophagus as a result of treatment, is not an indicator of complete recovery. Therefore, treatment of Barrett's esophagus primarily with proton pump inhibitors should be continued: in order to reduce financial costs in the future - copies (generics) of omeprazole (Pleom-20, Ultop, Romisek, Gastrozol, etc.) or copies of lansoprazole (Lancid, Lanzap, Helicol), as well as copies of pantoprazole (Sanpraz), copies of ranitidine (Ranisan, Zantac, etc.) or famotidine (Famosan, Gastrosidin, Quamatel, etc.).

The use of ranitidine in high doses (600 mg per day) in the treatment of patients with GERD and Barrett's esophagus is justified (due to the high probability of side effects) only in cases of individual intolerance to famotidine (60-80 mg per day) or proton pump inhibitors. The therapy allows eliminating GERD symptoms for a certain period in most patients, and in others - reducing their effectiveness and frequency of occurrence. In some patients, as a result of the treatment (with the disappearance of endoscopic signs of esophagitis, healing of ulcers and erosions of the esophagus), there are no symptoms considered characteristic of GERD, in other patients, due to reduced pain sensitivity of the esophagus, the presence of reflux is not accompanied by pain and heartburn.

Considering the possibility of various factors leading to the appearance of Barrett's esophagus, during long-term treatment of patients it is advisable to periodically alternate drugs that inhibit acid formation in the stomach with drugs that have an enveloping and cytoprotective effect, protecting the mucous membrane of the esophagus from the aggressive effects of bile acids and pancreatic enzymes, for example, the use of sucralfate gel (sukrat gel) 1.0 g one hour before breakfast and in the evening before bedtime for at least 6 weeks. However, the possibilities of such treatment of patients with Barrett's esophagus are still unclear, although the use of this drug in the treatment of some patients with GERD gives a certain positive effect. For now, treatment of Barrett's esophagus with proton pump inhibitors is more often proposed (in some cases in combination with prokinetics). However, the following fact may be an argument against it - esophageal adenocarcinoma appears even after the elimination of gastroesophageal reflux and sufficient inhibition of hydrochloric acid, which is possible, however, only for some time after the discontinuation of medications. Apparently, a sufficiently long-term drug treatment of patients is necessary.

Relatively rarely, even if there is constant treatment of Barrett's esophagus with proton pump inhibitors (with dynamic observation), during histological examination of biopsy material it is possible to identify areas of "overlapping" of multilayer squamous epithelium of the esophagus on the single-layer columnar epithelium of the stomach or intestine in the terminal section of the esophagus, which to a certain extent indicates the effectiveness of the treatment. Unfortunately, "antireflux" therapy does not affect the more or less significant extent of areas of metaplastic columnar epithelium in the esophagus, detected during endoscopic examinations (with targeted biopsies), and therefore, the risk of esophageal adenocarcinoma does not decrease.

Esophageal adenocarcinoma may also appear after the elimination of pathological changes in the esophageal mucosa visible through a conventional endofibroscope. It is important to periodically conduct dynamic examinations of patients with Barrett's esophagus. There are various proposals for the timing of control examinations of such patients with mandatory esophagoscopy with targeted biopsy and subsequent histological examination of biopsy material obtained from the terminal section of the esophagus - respectively, regularly after 1-2-3-6 months or one year. In our opinion, such observation should be quite active on the part of the physician: some patients who have been successfully treated for GERD (with identified Barrett's esophagus), during subsequent follow-up examinations, while feeling well (in the absence of clinical signs of reflux esophagitis), are reluctant to agree (or even refuse) to come for a repeat clinical endoscopic examination, especially in cases where patients have decreased pain sensitivity (the presence of gastroesophageal reflux is rarely accompanied by the appearance of pain and heartburn behind the breastbone and/or in the epigastric region) or this examination is performed more often than twice a year.

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Surgical treatment of Barrett's esophagus

Periodically, in the literature, in connection with the increase in the frequency of precancerous and malignant changes in the foci of intestinal metaplasia of Barrett's esophagus, the issue of possible options for surgical treatment of patients is discussed. When surgical treatment of Barrett's esophagus is appropriate:

• the likelihood of developing esophageal adenocarcinoma, in some patients with the appearance of distant metastases;
• difficulties in early diagnosis of esophageal adenocarcinoma, including the use of radiological, endoscopic and histological methods of examining materials from targeted esophagobiopsy, especially in the case of invasive cancer; in addition, dysplasia may not be detected due to insufficient accuracy of the biopsy and the small volume of material obtained for histological examination;
• the need for periodic control endoscopic examination with multiple targeted biopsies;
• known difficulties in the morphological interpretation of the obtained data.

When surgical treatment of Barrett's esophagus is not appropriate:

1. it is possible that the morphological changes in the mucous membrane may initially be misinterpreted as dysplasia, and later as a consequence of reactive changes that regress under the influence of “antireflux” therapy;
2. the possibility of regression of epithelial dysplasia of the esophageal mucosa is known in the treatment of patients with Barrett's esophagus under the influence of "antireflux" therapy;
3. the likelihood of developing esophageal adenocarcinoma is not observed in all patients;
4. the occurrence of esophageal adenocarcinoma is possible only 17-20 years after its initial detection;
5. in some patients, even with a high degree of dysplasia, adenocarcinoma of the esophagus does not develop;
6. there is no tendency towards an increase in the extent of metaplasia foci in some patients, despite the progression of GERD;
7. the question of the most rational surgical treatment of patients with Barrett's esophagus has not yet been finally resolved;
8. there is a risk of developing surgical and post-surgical complications, including fatal ones (up to 4-10%);
9. some patients have contraindications to surgical treatment associated with concomitant diseases; some patients refuse surgical treatment.

Considering Barrett's esophagus as one of the complications of GERD, it should be noted that Nissen fundoplication remains the most common operation in the treatment of such patients. Carrying out Nissen fundoplication allows most patients to eliminate such symptoms of GERD as belching and heartburn (at least in the immediate postoperative period), but it is unlikely that this operation can prevent the occurrence of Barrett's esophagus.

There are attempts to repeatedly perform laser photocoagulation (an argon laser is usually used for this purpose) and electrocoagulation using high-frequency currents of foci of metaplastic epithelium, the terminal section of the esophagus (including in the treatment of patients in combination with antisecretory therapy). However, the effectiveness of this method and whether such treatment can prevent the development of esophageal adenocarcinoma are still unclear. The appearance of a corrosive scar after laser therapy is a risk factor for the development of esophageal adenocarcinoma. Neither electrocoagulation nor photodynamic therapy have proven effective in the metaplastic epithelium of the esophageal mucosa.

In recent years, the issue of performing endoscopic resection of small pathological foci of Barrett's esophagus has sometimes been considered, including in combination with photodynamic therapy.

There is no consensus on the treatment of patients with high-grade dysplasia. There is also no consensus on the surgical treatment of patients with Barrett's esophagus with high-grade dysplasia, which is considered the most dangerous in terms of transformation into cancer.

Resection of the distal esophagus and gastric cardia remains a radical operation in patients with diagnosed Barrett's esophagus. However, how expedient is it to conduct this operation widely? This issue also requires clarification.

Taking into account the age and condition of specific patients, treatment of Barrett's esophagus in each specific case is carried out individually, including taking into account the data of dynamic monitoring of their condition.

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