Alkaline Gastritis - Features, Diagnosis, and Treatment

Introduction:

Alkaline reflux gastritis is most common after surgery that disturbs the pylorus' protective sphincteric function, most often after distal gastrectomy (Billroth I or Billroth II), but it can also happen after simple gastrojejunostomy or pyloroplasty. The syndrome has also been identified following cholecystectomy and ampullary sphincteroplasty without surgical changes to the stomach or pylorus. It is believed that pancreatic and biliary secretions enter the duodenum on a continuous basis instead of being stored in the gallbladder and duct reservoirs until elicited by the presence of food. Under such conditions, the contents of the duodenum are not absorbed by food and are available in excess to reflux into the stomach.

What Are the Clinical Features of Alkaline Gastritis?

• Epigastric pain is a major presenting complaint in bile gastritis patients. The pain is normally a burning sensation, aggravated by eating, and is continuous.

• The second most common symptom is occasional nausea and bilious vomiting, which occurs in about half of all patients and almost always in conjunction with pain.

• Weight loss due to anorexia (eating disorder) and a fear of causing pain and vomiting, iron deficiency anemia, and achlorhydria (absence of hydrochloric acid) are less reliable features.

• Even though chronic blood loss occurs in patients with bile gastritis, iron-deficiency anemia is usually a result of inadequate iron absorption due to decreased or lacking gastric acidity.

• Because the symptoms are nonspecific, after ruling out a recurrent peptic ulcer, stomal obstruction, afferent loop obstruction, small gastric pouch, esophagitis, motility disorders, gallstones, pancreatitis, and giardiasis, the diagnosis of alkaline gastritis is one of exclusion.

What Are the Endoscopic Features?

• Redness, swelling, friability, granularity, erosions, adherent mucus, and atrophy of the mucosa are all common endoscopic findings. These alterations are most noticeable in the peristomal region.

• They typically terminate suddenly at the gastrojejunal junction, but in more severe cases, they may extend proximally, even to the lower esophagus.

• It is not uncommon to observe superficial gastric mucosal ulceration and also spontaneous bleeding of the mucosa.

• Because of the constant regurgitation of bile-stained duodenal contents into the stomach, there is always an abundance of bile in the gastric remnant.

• However, gastritis, especially peristomal gastritis, occurs in 80 to 100 percent of distal gastrectomy patients, usually without symptoms.

What Are the Laboratory Features?

Normal serum chemistry values exist. Iron deficiency anemia affects 20 to 50 percent of patients. The presence of hypochlorhydria (lack of stomach acids) in the majority of patients is most likely the result of chronic enterogastric reflux, which results in atrophic gastritis and acid suppression.

What Are the Histological Findings?

• Histologic findings showed varying degrees of inflammation superficially; in less severe cases, there is a loss of mucosal cells and metaplasia and internalization in advanced cases.

• There may be areas of focal mucosal hemorrhage, superficial ulceration, a decrease in the height of the mucosal column, and a chronic inflammatory infiltrate.

• Even though all four morphologic types of gastritis-superficial, erosive, atrophic, and hypertrophic-have been shown in bile gastritis patients, as many other types may be observed in the same patient, atrophic gastritis is the most common feature, with a decrease in the number of chief and parietal cells.

What Is the Pathophysiology of Alkaline Gastritis?

Pathogenesis of the disease has been studied in three areas: enhanced enterogastric reflux, adverse effects of bile, alkali, and pancreatic enzymes on susceptible mucosa, and host defense deficiencies.

How to Diagnose Alkaline Gastritis?

• The challenges in precisely arriving at this diagnosis are certainly at least partially responsible for the lack of consistent good treatment results and have disappointed some investigators to the point of questioning its existence as a valid clinical entity.

• Since clinical and endoscopic aspects have been so unreliable, novel diagnostic tests for alkaline reflux gastritis attempt to quantify reflux, define a complex mixture of the refluxate in symptomatic patients, and reproduce the disorder's typical symptoms through gastric lavage with various fluids.

• Direct measurement of bile acid reflux in gastric aspirates has been used in semiquantitative efforts to find patients with alkaline gastritis.

• Since the mid-1960s, radionuclide studies with gamma emitters such as technetium and indium have been widely used in gastroesophageal reflux analyses. Enterogastric reflux can be studied using these techniques in conjunction with hepatobiliary scanning agents.

• A prospective study of patients with Billroth II anastomosis using Tc-HIDA (technetium(99m) hepatobiliary iminodiacetic acid) scintigraphy discovered that asymptomatic postgastrectomy patients had considerably more reflux than non-operated normals, and patients with symptomatic alkaline reflux gastritis had three times more reflux than asymptomatic postgastrectomy patients.

• This test has yet to be substantiated by studying patients with suspected alkaline reflux gastritis and predicting which patients will respond to surgical diversion of intestinal contents. The test could also be utilized to evaluate the efficacy of bile-diverting surgery, particularly in patients who continue to have symptoms after surgery.

What Is the Treatment for Alkaline Gastritis?

Even though there have been isolated claims that participants or small groups of patients react favorably to one of the medications, there has been no drug proven to be clearly helpful in alleviating symptoms. Patients who have been misdiagnosed with acid hypersecretion or gastric stasis may respond favorably. Some patients with mild bile gastritis illnesses may improve on their own, particularly if the symptoms have only been present for a few months.

Before proceeding with a patient to surgery for emotional and psychiatric disturbance, the doctor is given time to more accurately evaluate the connection of symptoms to the patient's personality.

1. Antacids: Antacids have long been used to treat acid reflux. Aluminum hydroxide is the most efficient bile salt absorbent, comparable to cholestyramine, and superior to aluminum-magnesium hydroxide combinations for gastritis. The maximum recommended dose is 30 cc every two hours.

2. Cytoprotective Agents: Sucralfate, a nonabsorbable basic aluminum salt of sulfated sucrose, becomes viscous in an acid medium and adheres to exposed proteins in damaged mucosa, thereby creating a protective barrier. One gram twice a day is the recommended dose. Prostaglandin E2 analogs appear to be far more appealing and have remarkable cytoprotective properties for gastric mucosa exposed to irritants such as Aspirin and alcohol, as well as bile acids, entirely irrelevant to their antisecretory effects.

3. H2 Antagonists: Cimetidine (300 mg twice a day) and Ranitidine (150 mg twice a day) reduce the secretion of acid and may thus protect the mucosal injury caused by acid back diffusion through tight intercellular junctions destroyed by bile salt exposure.

4. Bile Sale Absorbents: Cholestyramine, the most often used absorbent of bile salt, is a basic anion exchange resin. Constipation and the unpleasant taste of the drug may restrict the tolerance of the patient, but a short duration of treatment is beneficial. The recommended dose is 1 gram twice a day.

5. Agents That Affect Motility: Metoclopramide promotes rapid emptying of the stomach, thereby enhancing the force of antral contraction. It also raises the lower esophageal sphincter's resting tone. It has a minimal effect on the post-partial gastrectomy gastric remnant. Moreover, the drug is successful in the treatment of reflux esophagitis. The recommended daily dose is 10 to 20 mg twice a day. Loperamide, a new Benzimidazole, improves the frequency and amplitude of duodenal and antral contractions and may be useful in controlling enterogastric reflux.

6. Ursodeoxycholic Acid: Ursodeoxycholic acid administration dramatically improved the symptoms of bile gastritis.

7. Antibiotics: Some researchers are using antibiotics to treat bacterial overgrowth in patients with bile gastritis based on the hypothesis that high bacteria counts increase the conversion of conjugated bile salts to the more toxic unconjugated form.

If the patient fails a treatment trial of these various agents, each administered individually or in combination over several weeks, surgical intervention should be considered.

Surgical Treatment: The objective of surgery is to completely divert the contents of the duodenum away from the stomach. This goal is easily achieved after distal gastrectomy by inserting a 40 to 50-cm segment of jejunum between the stomach and the jejunum beyond the Treitz ligament (Roux-en-Y) or a 20-cm segment between the stomach and the duodenum (Henley loop).

Conclusion:

Efforts to understand and manage alkaline reflux gastritis and esophagitis are concentrating on exact diagnostic methods in the expectation of estimating which patients will respond to surgery. Furthermore, new therapeutic modalities are being investigated in an attempt to increase mucosal resistance to potentially toxic substances.