Erythematous mucosa in the antrum is a common finding during an upper endoscopy, indicating inflammation in the lower part of the stomach. This descriptive term signifies Antral Gastritis, where the stomach lining appears red due to increased blood flow as the body attempts to heal irritation or damage. Identifying the underlying causes of this inflammation is crucial for effective treatment and preventing potential complications.
Defining Erythematous Mucosa in the Antrum
Erythematous mucosa refers to the inner lining of a digestive organ displaying abnormal redness and swelling, which is the body’s physical response to irritation or injury. The mucosa is the soft, protective layer lining the stomach, and this redness is a direct sign of inflammation, or gastritis, in that specific location.
The “antrum” is the lower, muscular section of the stomach that connects to the duodenum, the first part of the small intestine. This region is responsible for grinding food and regulating the release of stomach acid into the small bowel through the pyloric valve. When inflammation is confined to this lower area, it is specifically called antral gastritis.
Antral gastritis occurs when the protective mucous barrier in this region is weakened, allowing digestive acids and other irritants to damage the underlying tissue. While the visual finding of redness confirms inflammation, a definitive cause requires further investigation, often through a biopsy taken during the endoscopy. The finding of erythematous mucosa in the antrum is therefore a pointer toward a problem, not the final answer to what is causing the patient’s symptoms.
Primary Causes: H. Pylori and NSAIDs
The two most frequent and significant causes of inflammation in the stomach lining globally are infection with the bacterium Helicobacter pylori and the regular use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs). The presence of H. pylori is the most common cause of chronic gastritis, often localizing its effects prominently in the antrum.
This spiral-shaped bacterium colonizes the protective mucus layer of the stomach, producing the enzyme urease, which neutralizes stomach acid locally. This allows the bacteria to survive and triggers a chronic inflammatory response. This continuous inflammation attracts immune cells to the area, resulting in the characteristic redness and swelling of the antral mucosa.
Regular or long-term use of NSAIDs, such as ibuprofen, naproxen, or aspirin, represents the second major cause of antral inflammation. These medications work by blocking the activity of cyclo-oxygenase (COX) enzymes, which stops the production of pain- and inflammation-causing chemicals. Unfortunately, NSAIDs also inhibit the production of protective prostaglandins, which are compounds that help maintain the integrity of the stomach lining and regulate blood flow to the mucosa.
When these protective prostaglandins are reduced, the antral mucosa becomes significantly more vulnerable to damage from its own stomach acid. This pharmacological effect can lead to direct irritation, erosions, and the visible redness seen during an endoscopy. The damage caused by NSAIDs is independent of any bacterial infection and is a direct chemical injury to the mucosal defense system.
Lifestyle and Systemic Triggers
Beyond the primary causes, several other factors related to lifestyle and systemic conditions can irritate the stomach lining and result in erythematous changes in the antrum. One common trigger is bile reflux, which occurs when the pyloric valve separating the stomach from the small intestine fails to close properly. Bile, an alkaline fluid produced by the liver, then backs up from the duodenum into the stomach, where its components directly irritate and damage the antral mucosa.
Excessive or chronic consumption of irritants like alcohol and tobacco also contributes significantly to this inflammation. Alcohol directly damages the stomach’s mucosal cells, increasing their permeability and vulnerability to acid. Smoking compounds this issue by reducing blood flow to the stomach lining, which impairs the tissue’s ability to heal itself.
A less common systemic cause is autoimmune gastritis, where the body’s immune system mistakenly attacks its own stomach cells. While this often affects the upper part of the stomach, it can contribute to overall gastric inflammation. Furthermore, certain rare disorders, such as eosinophilic gastroenteritis, involve the infiltration of specific immune cells into the stomach lining, leading to visually erythematous changes.
Diagnostic Procedures and Treatment Protocols
When erythematous mucosa is observed during an upper endoscopy, the next steps focus on identifying the specific underlying cause to guide treatment. The most important diagnostic step is a biopsy, where small tissue samples are collected from the inflamed antrum for microscopic examination. This histological analysis confirms the presence of gastritis, assesses its severity, and can directly identify the presence of H. pylori bacteria.
If H. pylori infection is suspected, additional non-invasive tests may be used, such as a urea breath test or a stool antigen test, to confirm the active presence of the organism. Once confirmed, the standard treatment is a combination of medications, often referred to as triple therapy, which includes two different antibiotics and a proton pump inhibitor (PPI) to reduce stomach acid production. The goal of this regimen is complete eradication of the bacteria.
Treatment for non-infectious causes is tailored to the trigger. If NSAIDs are the cause, the first action is typically to discontinue the drug or switch to an alternative pain reliever, such as acetaminophen, which does not affect the protective prostaglandins. Medications that reduce stomach acid, like PPIs or H2 blockers, are generally prescribed to allow the inflamed mucosa time to heal. For bile reflux, drugs that bind bile acids may be used, and lifestyle modifications, such as reducing alcohol intake and quitting smoking, are universally recommended to support the healing process and prevent recurrence.