Erosive Gastritis

Patients with erosive gastritis may be initially asymptomatic, but most common symptoms include dyspepsia, nausea, vomiting and heartburn [1] [8]. The first sign, however, may be bleeding from the upper (hematemesis) and lower (melena) gastrointestinal tract and ranges from mild to severe. Symptoms usually develop within 12 hours after injury, whereas bleeding is seen after 2-5 days [1]. Acute stress gastritis is a severe form of erosive gastritis and is characterized by severe bleeding and is primarily encountered in critically ill patients as a result of hypoperfusion of the gastrointestinal tract [1].

The diagnostic workup should start with a detailed patient history that may reveal the causative agent of erosive gastritis. Previous use of NSAIDs, alcohol or history of gastritis can suggest erosive gastritis in patients having GI symptoms and the diagnosis is confirmed by endoscopy [6]. Through this procedure, a direct view into the gastric mucosa can be obtained and the site of erosion can be identified. Additional studies may include H. pylori testing, either by serology, urea breath test, fecal antigen test or microscopic identification after obtaining a biopsy of the gastric mucosa.

Treatment principles may vary depending on the severity of symptoms and the extent of erosion. In general, first-line therapy includes administration of proton-pump inhibitors (PPIs) such as omeprazole or pantoprazole and H2-receptor blockers such as cimetidine or ranitidine [1]. Misoprostol, a prostaglandin E1 agonist, has shown to be effective in reducing the extent of symptoms [11]. Antimicrobial therapy, as well as administration of PPIs are sometimes necessary if H. pylori is the causative agent. Gefarnate is a drug that disrupts prostaglandin E2 and prostacyclin synthesis and has shown significant results in alleviating chronic erosive gastritis [12], while octreotide, a somatostatin analog, has been used in the setting of erosive gastritis associated with pancreatitis [13]. In the case of bleeding that does not respond to therapy, of if significant amounts of blood are lost, endoscopic hemostasis is necessary to stop further blood loss and several techniques are described, including adrenaline injection, thermal coagulation and band ligation procedures [14].

The prognosis is generally good, as treatment provides good results. When severe bleeding occurs, however, which may be the case in acute stress gastritis, it may cause significant morbidity, since the majority of patients are in intensive care and are critically ill [1].

Although Helicobacter pylori infection is known to be the most common cause of gastritis and peptic ulcer disease, chronic use of NSAIDs are more commonly associated with erosive gastritis, as they reduce mucosal defense by inhibiting synthesis of prostaglandins [2]. Alcohol consumption, stress, radiation therapy, gastric hypoperfusion in the setting of trauma and instrumentation are also known causes of this form of gastric injury [1]. In most cases, especially if H. pylori is the cause, erosions are more frequently seen in the gastric antrum [7].

Data regarding the presence of erosive gastritis is scarce and the majority of information is turned to peptic ulcer disease and gastroesophageal reflux disease (GERD). Previous studies have shown that erosive findings were found in 0.5-11% of patients who underwent endoscopic examination [8]. A multicenter study from China that included almost 9000 patients showed that more than 40% of patients who report gastrointestinal symptoms were found to have erosive changes in the gastric mucosa [6]. Diabetes mellitus is considered to be a risk factor for this condition [5]., as is high body mass index and obesity, whereas fast eating speed has also been implicated as a harmful factor [4]. An increased rate of this condition is observed in patients with cardiovascular and other somatic diseases and their correlation remains to be elucidated [9].

Under physiological conditions, hydrochloric and various digestive enzymes are secreted in the stomach for proper food digestion and create a highly acidic environment (pH in the stomach is around 1) [2]. To protect the gastric mucosa from these vigorous conditions, mucosal cells secrete a thick layer of mucin and a layer of pH-neutral fluid containing bicarbonate [13]. Normally, this balance is constantly maintained, but in the presence of some stimuli that either enhance gastric acid secretion or reduce synthesis of protective mucosal layers, erosion occurs. Alcohol directly stimulates gastrin and hydrochloric acid secretion [10]., and Helicobacter pylori causes similar effects through its ability to survive in acidic conditions. NSAIDs are the most common iatrogenic factor that contributes to erosive gastritis, presumably due to inhibition of prostaglandins that are normally synthesized in order to repel gastric acid [2].

At-risk patients can be prophylactically treated with either PPIs or histamine-receptor antagonists to reduce the incidence of erosive gastritis, in particularly the acute stress form [1]. Use of NSAIDs should be carefully considered, especially if chronic use is necessary, whereas heavy alcohol consumption mandates significant reductions.

Erosive gastritis is a condition in which injury of the mucosal lining of the stomach occurs. Helicobacter pylori (the causative agent of peptic ulcer disease in vast majority of cases), Campylobacter jejuni and cytomegalovirus are recognized as causative agents, but this form is more commonly associated with chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), radiation, alcohol consumption, stress and instrumentation [1]. The pathogenesis model still remains incompletely understood, but an imbalance between protective mucosal defenses and exposure to injurious factors has been proposed as the main disease mechanism [2]. Secretion of hormones such as gastrin, insulin and thyroxine, increased intragastric pressure, presence of Helicobacter pylori and increased concentrations of biliary acids contribute to disruption of the mucosa, resulting in epithelial erosions [3]. High body mass index and high eating speed or overeating are shown to be significant risk factors for all gastrointestinal diseases, including erosive gastritis [4]., as is diabetes mellitus type 2 [5]. The clinical presentation may significantly vary depending on the severity and extent of erosions. In general, erosive gastritis may be divided into acute and chronic. Patients suffering from acute forms may develop dyspepsia, nausea and vomiting, while severe cases present with either upper or lower gastrointestinal bleeding (hematemesis and melena, respectively). Bleeding may be mild or quite severe and can necessitate rapid therapeutic measures. Acute stress gastritis is a specific subtype that occurs in approximately 5% of patients that are critically ill, presumably as a result of diffuse hypoperfusion of the GI tract [1]. Chronic erosive gastritis, on the other hand, is often asymptomatic. Signs and symptoms supported by patient history and evaluation of potential risk factors such as chronic NSAID use, alcohol abuse or previous H. pylori infection, can aid the physician in making a presumptive diagnosis, but endoscopy is considered as the gold standard for diagnosis [6]. Direct visualization of erosions is achieved through this diagnostic method, after which appropriate treatment measures can be taken. Treatment depends on the severity of gastritis. Conservative measures such as fluid administration and use of proton pump inhibitors or histamine (H2)-receptor antagonists may be sufficient in patients who experience mild symptoms, while bleeding, especially in severe cases, requires endoscopic hemostasis that attempts to stop the bleeding from the eroded mucosa.

Erosive gastritis is a form of injury of the stomach lining that can occur due to various reasons. In contrast to classical forms of gastritis, where Helicobacter pylori is by far the most common cause, the use of non-steroidal anti-inflammatory drugs (NSAIDs), alcohol consumption, stress and radiation therapy are shown to be important causes, in addition to infection. To digest food and battle against various threats, the stomach secretes hydrochloric acid and various digestive enzymes that create a highly acidic environment, which poses a major threat to the stomach epithelium. To sustain acid pH, the mucosal lining produces abundant amounts of fluid that are pH-neutral and secretes other compounds that protect the stomach from injury. But in the case of increased gastric acid production or reduced capacity for protective fluid synthesis, which may be induced by any of the mentioned causes, injury of the epithelium occurs and symptoms may appear. In initial stages, patients may not complain of any symptoms, but indigestion, nausea and vomiting are most frequently reported. Bleeding may occur, although it is seen only in severe cases. Blood may be found in vomit or in stool and may require rapid diagnostic and therapeutic measures. To make the diagnosis, initial suspicion can be based on signs and symptoms, but to confirm erosive gastritis, endoscopy is the main diagnostic method. Endoscopy comprises insertion of a tube with a camera through the throat and into the stomach, which can easily identify the site of erosion and bleeding. Therapy depends on the severity of symptoms. Use of drugs that reduce production of gastric acid such as proton pump inhibitors or histamine-receptor antagonists is considered to be first-line therapy, whereas endoscopic management of erosions is recommended in cases of bleeding. The prognosis of erosive gastritis with proper therapy is generally good, but severe bleeding from gastric erosions requires prompt treatment, especially in the setting of acute stress gastritis, a form of erosive gastritis that is seen in patients who are severely ill due to other causes. Fluid administration and blood transfusions may be necessary to restore blood that is lost. High risk patients, such as those who are undergoing radiation therapy or those with a history of gastritis, may benefit from prophylactic use of drugs that reduce gastric acid production.

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