Gastropathy: Definition, Prevalence, Characteristics, Associated Comorbidities, Causes and Management

Used in medical terminology, it can refer to any number of medical ailments or diseases that affect the stomach.

There are several related conditions that are distinct diseases. For example, portal hypertensive gastropathy and hyperplastic gastropathy produce different symptoms.

Ménétrier’s disease is a complex disorder that affects the lining of the stomach and can cause debilitating symptoms. Erythematous gastropathy without bleeding is another condition that may require drug treatment.

Stomach disease can present itself in a number of forms, and because of this, any number of chronic stomach-related diseases can be classified as gastropathy.

Indeed, any disease that causes stomach pain, inflammation, bleeding, or other digestive problems can be placed in that category.

For example, patients who have Crohn’s disease or ulcerative colitis may experience gastric symptoms. Some symptoms that can occur may include ulcerations in the stomach lining and recurring nausea.

Stomach bleeding may or may not be directly related to the condition.

Patients suffering from the erythematous form of this condition will normally develop ulcers – such as ulcers and abrasions on the lining of the stomach or intestines. These can become inflamed, causing extreme pain or mild discomfort. In some cases, bleeding can occur.

This can be treated with medicine or surgery if necessary.

Hypertrophic gastropathy can be caused by a number of factors, including genetic disposition and even stress. Inflammation and pain are typical symptoms, as is excess mucus in the stomach lining.

Patients suffering from this condition experience nausea and vomiting more frequently. In cases where an obstruction has occurred, surgical intervention may be necessary.

Something known as diabetic gastropathy can be described as a stomach-related condition that affects diabetics. This disease can produce several symptoms localized in the gastrointestinal tract due to the malabsorption of insulin.

Nausea and vomiting can occur in patients suffering from this stomach-related diabetic problem. Most often, symptoms can be controlled by modifying diet and regulating glucose levels in the body.

Erosive gastropathy is a condition typically caused by medications that destroy the lining of the stomach. This can cause injury or damage to eroded tissue and often a painful burning sensation.

Stomach bleeding is not common with the erosive form of this disorder, although it can occur in more severe cases. For the condition to heal completely, patients must stop using medications that have caused bruising or damage.

NSAID drug-induced gastropathy

NSAID-induced gastropathy can be the result of too high a dose or too frequent intake of NSAID drugs, as well as long-term use.

These drugs are used to decrease pain and inflammation and are often taken when diagnosed with osteoarthritis and rheumatoid arthritis or other musculoskeletal conditions.

Doctors often prescribe this drug for these people and also suggest over-the-counter (OTC) types of NSAIDs.

Due to the easy accessibility of these medications, the incidence rate of NSAID-induced gastropathy is high, especially among people> 60 years of age.

NSAID-induced gastropathy can lead to stomach or duodenal ulcers that can even lead to death. There are thousands of hospitalizations each year just for symptoms resulting from NSAID use.

Although these rates are high, most people are unaware of the risk of these drugs and continue to take them. Furthermore, this induced gastropathy continues asymptomatically until it is too late and has caused further damage to the gastrointestinal tract.

NSAIDs are COX-1 inhibitors that suppress the mucosal barrier of the gastrointestinal system, which can lead to rupture of the gastrointestinal tract and increased acidity of gastric contents.


Rheumatoid arthritis (RA) and osteoarthritis (OA) patients taking NSAIDs have an incidence of ulcers of approximately 15-20%.

Although a 15-25% incidence of gastric and / or duodenal ulcers has been shown in all patients taking NSAIDs, most experts estimate that the bleeding rate is only 2-4%.

In elderly patients taking NSAIDs, the relative risk for gastrointestinal surgery is 10 times, and for gastrointestinal cause of death, approximately 4.5 times higher than in control groups.

Approximately 20 million patients in the US take NSAIDs regularly; the risk of hospitalization for serious gastrointestinal adverse events is 1-2%, resulting in approximately 200,000 to 400,000 hospitalizations per year at an average cost of $ 4,000 per patient, or $ 0.8-1.6 billion annually.

An increased risk of gastrointestinal bleeding has even been observed in patients taking low-dose aspirin for cardiovascular prophylaxis.

Gastric and duodenal lesions were more common in patients taking NSAIDs for <3 months, while patients with a longer duration of therapy tended to have more lesions in the small intestine and colon.

Some recent studies have shown that the incidence of duodenal ulcer is increased in Helicobacter pylori-positive patients taking NSAIDs.

Eradication of H.pylori prior to NSAID therapy has recently been reported to markedly reduce the incidence of ulcer disease in patients treated with naproxen.

Among people with arthritis, nearly 30% report daily use of over-the-counter NSAIDs. Safety is often not considered or well understood among OTC NSAID users until after adverse events such as gastropathy have occurred.

Characteristics / Clinical Presentation

Up to 50% of NSAID-induced gastropathy is asymptomatic.

  • Mild dyspepsia
  • Acidity.
  • Nausea.
  • Abdominal discomfort
  • Erosion.
  • Ulcers.
  • Hemorrhage.
  • Drilling.
  • Obstruction.
  • Hidden bleeding.
  • Acute colitis
  • Exacerbation of existing colon disease.

Associated comorbidities


Prostaglandin E1 analog misoprostol can prevent gastric ulcer and duodenal ulcer.

The proton pump inhibitor (PPI) omeprazole reduces gastric ulcer and prevents duodenal ulcer.

Although PPIs can help with gastric irritation, they may also be found to induce the risk of osteoporosis, which often causes hip fractures in elderly patients, as well as increase cardiovascular risk due to low serum magnesium levels. in the blood.

H2 receptor antagonists are effective in preventing duodenal ulcer but not gastric ulcer.

Studies have shown that antacids and buffered tablets do not protect against NSAID injuries.

Diagnostic tests / Laboratory tests / Laboratory values

An early finding of anemia may warrant more extensive diagnostic tests, such as an endoscopy or X-ray to determine NSAID gastropathy.

Hematocrit and hemoglobin levels can also provide information on the degree of bleeding from perforation or hemorrhage. As NSAID-induced ulcers are often asymptomatic, the patient’s history and diagnostic tests / laboratory values ​​are important in the diagnosis.

Endoscopy has a 90% success rate for the diagnosis of a peptic ulcer, however, it is expensive and the rate of correct diagnosis of gastropathy by NSAIDs is high among physicians.

Barium X-ray can also detect and diagnose peptic ulcers, but it is less common than endoscopy.

Etiology / Causes

NSAIDs inhibit the enzyme cyclooxygenase, which is an enzyme necessary for the synthesis of prostaglandins from arachidonic acid.

While inhibiting COX allows NSAIDs to have their anti-inflammatory and analgesic properties by blocking pro-inflammatory prostaglandins, it also blocks the prostaglandins that protect the gastrointestinal system.

Prostaglandins in the gastric system help maintain gastric blood flow, increase bicarbonate production, and increase mucus that serves as a protective barrier against bacterial colonization and mechanical injury.

Decreased blood flow and decreased mucosa decrease healing ability and leave the stomach more exposed to injury from pepsin and gastric acid.

Furthermore, these decreases lead to “increased diffusion of hydrogen ions into epithelial cells with resulting mucosal resistance to injury.”

The role of cyclooxygenase in this process led to the establishment of two isoforms of COX: COX-1 and COX-2. COX-1 is found in all tissues of the body, while COX-2 is found in the area of ​​inflammation, such as in an area of ​​osteoarthritis that contributes to inflammation.

Earlier NSAIDs included COX-1 and COX-2 inhibitors, however, in the 1990s COX-2 drugs were developed to act on areas of inflammation without causing the mucosal effects on the GI tract by inhibiting COX-1.

COX-2 inhibitors are associated with fewer upper gastrointestinal side effects, however, they are not as symptom-free as expected and still put people at risk for injury to the gastroduodenal mucosa.

The view that only COX-1 affects gastrointestinal problems is simplistic and not the whole story. These medications are discussed below in the medical management section.

Systemic participation

The effects of NSAIDs can occur throughout the gastrointestinal tract from the esophagus to the colon.

A possible complication of ulcers that are not treated is that the ulcer can perforate through the stomach lining and cause the infection to spread, or the ulcer can erode the stomach arteries and create life-threatening bleeding.

In addition to the effects on the GI system, NSAIDs also affect the renal and cardiovascular systems. For more information on the systemic involvement of NSAIDs,

Medical management (current best evidence)

One of the difficulties of NSAID gastropathy is that its course is asymptomatic 50% of the time.

Therefore, it is essential that health professionals evaluate the risk factors of each patient and recommend the discontinued use of an NSAID or the inclusion of an accompanying cytoprotective agent in those patients considered to be at high risk.

A preventive approach to discontinuous use of NSAIDs is recommended rather than treating gastropathy.

However, if NSAIDs cannot be stopped, PPIs or H2 receptor antagonists may be prescribed to reduce gastric effects.

The use of a PPI in conjunction with NSAIDs has been shown to decrease the risk of NSAID-related ulcers and adverse drug events compared to H2 receptor antagonists.

A COX-2 selective NSAID in conjunction with a PPI has shown the best results in reducing the risk of gastropathy in those who must continue to take NSAIDs.

Other treatment options include misoprostol, which is a synthetic prostaglandin designed to replace these losses by NSAIDs.

However, misoprotol has many difficult side effects, such as abdominal pain, nausea, and diarrhea.

Therapy management

Many of the patients seen in physical therapy will take NSAIDs for their disorder.

PTs should take into account risk factors, signs, and clinical systems (and take into account that the patient may be asymptomatic but still have NSAID-induced gastropathy).

In addition, they must take a detailed history of the patient, including medication questions regarding multiple NSAIDs, prescription drugs combined with NSAIDs, and drug changes.

Clinical signs and systems associated with NSAID-induced impairment

  • Asymptomatic
  • Upset stomach (nausea) and stomach pain.
  • Indigestion, heartburn.
  • Skin reactions (itching, rash, acne).
  • Tinnitus.
  • CNS changes (headache, depression, confusion (older adult), memory loss (older adult), mood swings).
  • Renal compromise (muscle weakness, unusual fatigue, restless legs, polyuria, nocturia, itching, increased blood pressure).
  • New onset of back (chest) or shoulder pain
  • Pain relief after eating.
  • Mane.

Risk factors for NSAID-induced gastropathy are listed below. Any recognized risk factor should serve as a red flag.

The incidence of mortality and morbidity from the use of NSAIDs is high among the aging population and it is essential to take a detailed medical history of the patient.

  • Age> 65 years.
  • History of peptic ulcer or gastrointestinal disease.
  • Smoking, use of alcohol.
  • Oral use of corticosteroids.
  • Anticoagulation from the use of other anticoagulants (even when used for cardiac patients in a lower dose.

Kidney complications in clients with hypertension or congestive heart failure or using diuretics or ACE inhibitors

Use of acid suppressants (H2 receptor antagonists, antacids); These agents can mask the warning symptoms of more serious gastrointestinal complications, leaving the client unaware of ongoing damage.

Differential diagnosis

Peptic ulcers are usually caused by H. pylori infection or acid-related consumption and are commonly in young men.

Crohn’s disease is a type of inflammatory bowel disease that causes the gastrointestinal tract to become chronically inflamed.

Common symptoms of this disease include abdominal pain, diarrhea, blood in the stool, and vomiting and can even cause rectal or gastrointestinal bleeding, loss of appetite, and inflammation of the liver.

Gastroesophageal reflux disease (GERD) is caused by acid from the stomach backing up into the esophagus. The most common symptom is heartburn, but people with GERD may also have a dry cough, asthma-like symptoms, and trouble swallowing.