Can Gastritis Be Brought On By Acid Rebound?

Acid rebound occurs when the body produces too much acid after stopping an acid-suppressing medication, leading to GERD symptoms. This excess stomach acid can be similar to or worse than the original symptoms. PPI use is known to cause acid rebound, which is related to PPI-induced gastrin secretion and gastrin’s effect. Hypergastrinemia is believed to play a role in rebound hyperacidity when PPIs are abruptly discontinued.

RAHS is the recurrence of symptoms due to an increase in gastric acid secretion above pre-treatment levels after stopping PPI therapy. This trophism is caused by the marked hypergastrinaemia that occurs secondary to the profound acid suppression during proton pump inhibitor treatment. If you have taken PPIs for several months or more, it is possible that you may experience rebound acid secretion and your symptoms may be worse.

Acid rebound can cause gastritis, as too much acid at once can irritate the stomach lining. It is found in Helicobacter pylori-negative, but not positive, subjects, possibly due to the enhanced oxyntic gastritis that occurs during treatment. Some conditions that can cause high stomach acid levels include ZES, H. pylori infection, and rebound acid hypersecretion from PPI use.

Does too much stomach acid cause gastritis?

What is gastritis?. Gastritis is when your stomach lining gets red and swollen (inflamed).

Your stomach lining is strong. In most cases, acid does not hurt it. But it can get inflamed and irritated if you drink too much alcohol, have damage from pain relievers called NSAIDs, or smoke.

What causes gastritis?. Gastritis may be caused by many things. It can be caused by diet and lifestyle habits, such as:

• Drinking too much alcohol
• Smoking
• Extreme stress. This can be from serious or life-threatening health problems.
• Long-term use of aspirin and over-the-counter pain and fever medicines

What is the longest gastritis can last?

Gastritis may last for only a short time (acute gastritis) or it may linger for months to years (chronic gastritis).

The esophagus, stomach, large and small intestine, aided by the liver, gallbladder and pancreas convert the nutritive components of food into energy and break down the non-nutritive components into waste to be excreted.

The stomach connects the esophagus to the small intestines and is where the majority of food digestion takes place.

What can be mistaken for gastritis?

Many other health conditions can cause symptoms similar to those found with gastritis, including:Gastroesophageal reflux disease (GERD)Peptic ulcer disease (which may also be a complication of gastritis)Gastroparesis. Gallbladder disease. Inflammatory bowel disease (IBD)Pancreatitis.

Gastritis symptoms can include upper abdominal pain, and sometimes nausea, vomiting, and/or a feeling of fullness soon after eating. The condition is characterized by inflammation of the stomach lining. This inflammation can be erosive, causing sores in the stomach lining, or non-erosive, which doesn’t wear away the lining.

There are many causes of gastritis, with the bacterial infection Helicobacter pylori ( H. pylori ) among the most common. Excessive use of nonsteroidal anti-inflammatory medication ( NSAIDs ) or alcohol are additional common causes of gastritis.

This article discusses gastritis symptoms, potential causes of gastritis, and how the condition is diagnosed and treated with gastritis medication and other interventions.

How bad is acid rebound?

Proton pump inhibitors (PPIs) are commonly used for the long-term treatment of gastroesophageal reflux disease (GERD) and other upper gastrointestinal disorders, such as healing peptic ulcers and prophylactic treatment of peptic ulcers. They are also used as symptomatic treatment in patients with functional dyspepsia. However, the long-term use of PPIs can lead to rebound acid hypersecretion (RAHS), which can occur after the withdrawal of therapy due to a compensatory increase in gastric acid production. Studies have shown that pentagastrin-stimulated acid secretion after discontinuation of PPIs increased significantly compared to before treatment. In healthy volunteers treated with PPIs, the latter induced gastrointestinal symptoms in 40-50% of subjects after discontinuation of PPI therapy but after stopping the placebo. It is crucial for practicing physicians to be aware of the underlying mechanisms and inform patients about potential RAHS before discontinuing PPIs to avoid unnecessary therapy. RAHS may lead patients to reuptake PPIs, as symptoms are incorrectly thought to originate from underlying conditions like GERD. Further research is needed to facilitate appropriate management of RAHS in the future.

Can PPIs make gastritis worse?

The long-term use of Prophylactic Prophylactic Acids (PPIs) has been linked to various complications, including small intestinal bacterial overgrowth, enterochromaffin-like cell hyperplasia, and gastrin-cell tumors. Atrophic gastritis, a risk factor for gastric cancer, remains the most serious complication. Current evidence regarding this complication is contradictory, with studies showing an accelerated onset of atrophic gastritis in some studies and no effect of acid suppression therapy on gastric atrophy in others.

This study aimed to determine the effect of PPI exposure on the diagnosis of gastritis type, H. pylori density, and intestinal metaplasia in patients with gastritis documented by gastroscopic biopsy. Social habits were also evaluated. Three hundred and eleven patients with a pathologic diagnosis of gastritis were identified in the archives of a Medical Center in Beirut, Lebanon, and stratified based on PPI exposure. Demographic data, clinical presentation, and pathologic findings were collected using appropriated data collection sheets. The type of gastritis, intestinal metaplasia, and H. pylori density were correlated with PPI use. To avoid confounders, all gastritis cases associated with specific etiologies other than H. pylori were excluded.

300 cases of either H. pylori gastritis or non-H. pylori gastritis were included, with all cases of non-H. pylori gastritis showing inactive chronic gastritis. Long-term PPI therapy is the mainstay treatment for GERD patients and is often justifiable, so analysis was performed on a subgroup of patients after excluding those with GERD to control for possible bias.

What is rebound gastritis?

Rebound acid hypersecretion. RAHS is the recurrence of symptoms due to an increase in gastric acid secretion above pre-treatment levels after stopping PPI therapy 3. Symptoms of RAHS may include heartburn, regurgitation or dyspepsia.

According to the proposed RAHS mechanism, reduced gastric acidity caused by PPIs induces hypergastrinemia and growth of histamine-releasing enterochromaffin-like cells, which leads to an increased acid secretory capacity once the PPI therapy is discontinued 3.

Concerns have been raised that RAHS may contribute to the increasing long-term use of PPIs 3. The symptoms of RAHS are similar to the underlying condition for which the PPI was used. Therefore, a reinforcing loop can develop where initial treatment creates the need for further treatment 4.

How long does it take to recover from acid rebound?

When counseling about discontinuing a PPI, let patients know that they will likely have symptoms of reflux for about 2 weeks after they stop the medication. Fortunately, there are strategies to help calm reflux symptoms until rebound hyperacidity resolves.

The following therapies will not only increase success for discontinuing a PPI but also are therapeutic for gastroesophageal reflux disease (GERD).

• Deglycyrrhizinated licorice (DGL), 2-4 380 mg tablets before meals or sucralfate (Carafate) 1 gm before meals
• Slippery elm, 1-2 tbsp of powdered root in water or 400-500 mg capsules or 5 mL of a tincture three to four times daily.
• A combination botanical product, Iberogast 1 ml three times daily.

How long does it take for acid rebound to go away?

When counseling about discontinuing a PPI, let patients know that they will likely have symptoms of reflux for about 2 weeks after they stop the medication. Fortunately, there are strategies to help calm reflux symptoms until rebound hyperacidity resolves.

The following therapies will not only increase success for discontinuing a PPI but also are therapeutic for gastroesophageal reflux disease (GERD).

• Deglycyrrhizinated licorice (DGL), 2-4 380 mg tablets before meals or sucralfate (Carafate) 1 gm before meals
• Slippery elm, 1-2 tbsp of powdered root in water or 400-500 mg capsules or 5 mL of a tincture three to four times daily.
• A combination botanical product, Iberogast 1 ml three times daily.

Does stomach acid return to normal after stopping PPI?

Advise patients about the possibility of rebound acid secretion. Rebound acid secretion can occur when PPIs are withdrawn; one study found that more than 40% of asymptomatic patients experienced dyspepsia one week after completing a four week treatment course of pantoprazole. 12 Serum markers suggest that acid secretion one week following cessation of PPI treatment can be significantly increased above pre-treatment levels. This should return to normal within two weeks. 12.

The symptoms caused by rebound acid secretion, e. g. gastro-oesophageal reflux, are the same as those that would be an indication for PPI treatment, therefore a reinforcing loop can be formed where initial treatment creates the need for further treatment. The possibility of rebound acid secretion should be discussed with patients so they can be prepared for this when withdrawing from PPI treatment.

Medicines that contain both an antacid and an anti-foaming agent, e. g. Mylanta P oral liquid, Acidex oral liquid, Gaviscon Double Strength tablets are likely to be the most effective treatment for rebound acid secretion. Aluminium hydroxide tablets can also be effective. Any of these products can be prescribed as “rescue” medication and provide reassurance to patients if symptoms return.

Can PPI withdrawal cause gastritis?

Inform patients about possible rebound symptoms. Stopping PPI treatment can cause rebound acid hypersecretion, leading to the transient appearance of symptoms such as indigestion, heartburn or regurgitation. 31 The low-acid environment induced by PPI treatment increases gastrin production (hypergastrinaemia) in order to stimulate gastric acid secretion and decrease the gastric pH. 31 When the PPI is withdrawn, there is no longer a mechanism to suppress gastric acid secretion and this increase in acidity causes rebound symptoms which are often indistinguishable from the symptoms of GORD. 31 The process of stepping down should help to minimise these symptoms, particularly if used alongside lifestyle modifications (see: “Lifestyle strategies for managing GORD symptoms”). Other treatments may also be used in the short-term to help manage these rebound symptoms, e. g. a histamine H 2 receptor antagonist or an antacid/alginate (see: ” Stepping down protocol “). 10.

It is difficult to predict how long the acid rebound effects might last and it likely relates to the length of time the patient was taking a PPI. 32 Data from a small study carried out in the United States found that gastrin levels normalised within the first month of discontinuing PPI treatment in patients who had been taking a PPI for four or eight weeks. 24.

A stepping down protocol. There are several approaches to stepping down PPI treatment and there is no evidence that one protocol is superior to another. 10 The process of withdrawing a PPI should be individualised to the patient and guided by the presence or absence of symptoms at each step. Some patients may only require one step down before they can stop their PPI, others may require several steps down and the use of other treatments to manage rebound symptoms. Some patients may continue to use a PPI as needed for the occasional symptoms of GORD. 10, 13.

How to stop acid rebound?

Slowly taper off the PPI over 2-4 weeks (the higher the dose, the longer the taper). While the taper is being completed, use the following for bridge therapy to reduce the symptoms of rebound hyperacidity. Encourage regular aerobic exercise. Encourage a relaxation technique such as deep breathing.

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For patients who have made positive lifestyle changes and are less likely to need continued chronic acid suppression, it can still be difficult to come off PPIs. They often cause rebound hyperacidity, even if the underlying condition has resolved. This occurs due to the lower stomach acidity increasing gastrin secretion, which causes the enterochromaffin cells to hypertrophy. When the PPI is suddenly discontinued, these larger cells have an increased capacity for acid secretion. Figure 1 shows symptoms scores for dyspepsia in asymptomatic people given 40 milligrams of pantoprazole for 6 weeks versus controls. Despite being initially asymptomatic, they experienced rebound dyspepsia that lasted 10-14 days.

When counseling about discontinuing a PPI, let patients know that they will likely have symptoms of reflux for about 2 weeks after they stop the medication. Fortunately, there are strategies to help calm reflux symptoms until rebound hyperacidity resolves.