Gastritis

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Inleiding

Gastritis is een inflammatoire afwijking van de maagmucosa veroorzaakt door een tal van factoren zoals i)infectie (H. pylori), medicijngebruik (NSAID's, alcohol), stress en auto-immuun fenomenen (atrofische gastritis). Vaak betreft het asymptmatische gevallen, maar soms betreft het dyspepsie of een GI-bloeding. Endoscopie is vereist voor een adequate diagnose. Behandeling is gericht op de onderliggende oorzaak.

Gastritis wordt obderverdeeld in i) erosieve en ii) niet-erosieve gastritis, gebasseerd op de ernst van de mucosale schade. Tevens kan ze onderverdeeld al naar gelang haar lokalisatie ie. cardia, antrum, body. Hstologisch kan ze onderverdeeld worden in i) acuut en ii) chronisch. Dit is gebaseerd op basis van het type inflammatoire cellen.

 

1. EROSIVE GASTRITIS

Erosive gastritis is gastric mucosal erosion caused by damage to mucosal defenses. It is typically acute, presenting with bleeding, but may be subacute or chronic with few or no symptoms. Diagnosis is by endoscopy. Treatment is supportive, with removal of the inciting cause. Certain ICU patients (eg, ventilator-bound, head trauma, burn, multisystem trauma) benefit from prophylaxis with acid suppressants. Causes of erosive gastritis include NSAIDs, alcohol, stress, and less commonly radiation, viral infection (eg, cytomegalovirus), vascular injury, and direct trauma (eg, nasogastric tubes). Superficial erosions and punctate mucosal lesions occur. These may develop as soon as 12 h after the initial insult. Deep erosions, ulcers, and sometimes perforation may occur in severe or untreated cases. Lesions typically occur in the body, but the antrum may also be involved.

Acute stress gastritis, a form of erosive gastritis, occurs in about 5% of critically ill patients. The incidence increases with duration of ICU stay and length of time the patient is not receiving enteral feeding. Pathogenesis likely involves hypoperfusion of the GI mucosa, resulting in impaired mucosal defenses. Patients with head injury or burns may also have increased secretion of acid.

Symptoms and Diagnosis

Patients with mild erosive gastritis are often asymptomatic, although some complain of dyspepsia, nausea, or vomiting. Often, the first sign is hematemesis, melena, or blood in the nasogastric aspirate, usually within 2 to 5 days of the inciting event. Bleeding is usually mild to moderate, although it can be massive if deep ulceration is present, particularly in acute stress gastritis. Acute and chronic erosive gastritis are diagnosed endoscopically.

Treatment

In severe gastritis, bleeding is managed with IV fluids and blood transfusion as needed. Endoscopic hemostasis should be attempted, with surgery (total gastrectomy) a fallback procedure. Angiography is unlikely to stop severe gastric bleeding because of the many collateral vessels supplying the stomach. Acid suppression should be started if the patient is not already receiving it.

For milder gastritis, removing the offending agent and using drugs to reduce gastric acidity (see Gastritis and Peptic Ulcer Disease) may be all that is required.

Prevention

Prophylaxis with acid-suppressive drugs can reduce the incidence of acute stress gastritis. However, it mainly benefits certain high-risk ICU patients, including those with severe burns, CNS trauma, coagulopathy, sepsis, shock, multiple trauma, mechanical ventilation for > 48 h, hepatic or renal failure, multiorgan dysfunction, and history of peptic ulcer or GI bleeding. Prophylaxis consists of IV H2 blockers, proton pump inhibitors, or oral antacids to raise intragastric pH > 4.0. Repeated pH measurement and titration of therapy are not required. Early enteral feeding also can decrease the incidence of bleeding. Acid suppression is not recommended for patients simply taking NSAIDs unless they have previously had an ulcer.

 

NON-EROSIEVE GASTRITIS

Nonerosive gastritis refers to a variety of histologic abnormalities that are mainly the result of H. pylori infection. Most patients are asymptomatic. Diagnosis is by endoscopy. Treatment is eradication of H. pylori and sometimes acid suppression.

Pathology

Superficial gastritis: Lymphocytes and plasma cells mixed with neutrophils are the predominant infiltrating inflammatory cells. Inflammation is superficial and may involve the antrum, body, or both. It is usually not accompanied by atrophy or metaplasia. Prevalence increases with age.

• Deep gastritis: Deep gastritis is more likely to be symptomatic (eg, vague dyspepsia). Mononuclear cells and neutrophils infiltrate the entire mucosa to the level of the muscularis, but exudate or crypt abscesses seldom result, as might be expected by such infiltration. Distribution may be patchy. Superficial gastritis may be present, as may partial gland atrophy and metaplasia.
• Gastric atrophy: Atrophy of gastric glands may follow in gastritis, most often long-standing antral (sometimes referred to as type B) gastritis. Some patients with gastric atrophy have autoantibodies to parietal cells, usually in association with corpus (type A) gastritis and pernicious anemia. Atrophy may occur without specific symptoms. Endoscopically, the mucosa may appear normal until atrophy is advanced, when submucosal vascularity may be visible. As atrophy becomes complete, secretion of acid and pepsin diminishes and intrinsic factor may be lost, resulting in vitamin B12 malabsorption.
• Metaplasia: Two types of metaplasia are common in chronic nonerosive gastritis: mucous gland and intestinal. Mucous gland metaplasia (pseudopyloric metaplasia) occurs in the setting of severe atrophy of the gastric glands, which are progressively replaced by mucous glands (antral mucosa), especially along the lesser curve. Gastric ulcers may be present (typically at the junction of antral and corpus mucosa), but whether they are the cause or consequence of these metaplastic changes is not clear. Intestinal metaplasia typically begins in the antrum in response to chronic mucosal injury and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa—with goblet cells, endocrine (enterochromaffin or enterochromaffin-like) cells, and rudimentary villi—and may even assume functional (absorptive) characteristics. Intestinal metaplasia is classified histologically as complete (most common) or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia. Intestinal metaplasia may lead to stomach cancer.

 

Symptoms and diagnosis

Most patients with H. pylori–associated gastritis are asymptomatic, although some have mild dyspepsia or other vague symptoms. Often the condition is discovered during endoscopy performed for other purposes. Testing of asymptomatic patients is not indicated. Once gastritis is identified, testing for H. pylori is appropriate.

Treatment

Treatment of chronic nonerosive gastritis is H. pylori eradication. Treatment of asymptomatic patients is somewhat controversial given the high prevalence of H. pylori–associated superficial gastritis and the relatively low incidence of clinical sequelae (ie, peptic ulcer disease). However, H. pylori is a class J carcinogen; eradication removes the cancer risk. In H. pylori–negative patients, treatment is directed at symptoms using acid-suppressive drugs (eg, H2 blockers, proton pump inhibitors) or antacids.

 

POSTGASTRECTOMY GASTRITIS

Postgastrectomy gastritis is gastric atrophy developing after partial or subtotal gastrectomy (except in cases of gastrinoma). Metaplasia of the remaining corpus mucosa is common. The degree of gastritis is usually greatest at the lines of anastomosis. Several mechanisms are responsible: bile reflux, which is common after such surgery, damages the gastric mucosa; loss of antral gastrin decreases stimulation of parietal and peptic cells, causing atrophy; and vagotomy may result in a loss of vagal trophic action.

There are no specific symptoms of gastritis. Postgastrectomy gastritis often progresses to severe atrophy and achlorhydria. Production of intrinsic factor may cease with resultant vitamin B12 deficiency (which may be worsened by bacterial overgrowth in the afferent loop). The relative risk of gastric adenocarcinoma seems to increase 15 to 20 yr after partial gastrectomy; however, given the low absolute incidence of postgastrectomy cancer, routine endoscopic surveillance is probably not cost effective, but upper GI symptoms or anemia in such patients should prompt endoscopy.

 

UNCOMMON GASTRITIS SYNDROMES

• Ménétrier's disease
  

  This rare idiopathic disorder affects adults aged 30 to 60 and is more common among men. It manifests as a significant thickening of the gastric folds of the gastric body but not the antrum. Gland atrophy and marked foveolar pit hyperplasia occur, often accompanied by mucous gland metaplasia and increased mucosal thickness with little inflammation. Hypoalbuminemia (the most consistent laboratory abnormality) caused by GI protein loss may be present (protein-losing gastropathy). As the disease progresses, the secretion of acid and pepsin decreases, producing hypochlorhydria.
  
  Symptoms are nonspecific and commonly include epigastric pain, nausea, weight loss, edema, and diarrhea. Differential diagnosis includes (1) lymphoma, in which multiple gastric ulcers may occur; (2) mucosa-associated lymphoid tissue (MALT) lymphoma, with extensive infiltration of monoclonal B lymphocytes; (3) Zollinger-Ellison syndrome with associated gastric fold hypertrophy; and (4) Cronkhite-Canada syndrome, a mucosal polypoid protein-losing syndrome associated with diarrhea. Diagnosis is made by endoscopy with deep mucosal biopsy or full-thickness laparoscopic gastric biopsy.
  
  Various treatments have been used, including anticholinergics, antisecretory drugs, and corticosteroids, but none have proven fully effective. Partial or complete gastric resection may be necessary in cases of severe hypoalbuminemia.
  
  

• Eosinophilic gastritis

  Extensive infiltration of the mucosa, submucosa, and muscle layers with eosinophils often occurs in the antrum. It is usually idiopathic but may result from nematode infestation. Symptoms include nausea, vomiting, and early satiety. Diagnosis is by endoscopic biopsy of involved areas. Corticosteroids can be successful in idiopathic cases; however, if pyloric obstruction develops, surgery may be required.
  
  

• Mucosa-associated lymphoid tissue (MALT) lymphoma:

  This rare condition is characterized by massive lymphoid infiltration of the gastric mucosa, which can resemble Ménétrier's disease.
  
  

• Gastritis caused by systemic disorders:

  Sarcoidosis, TB, amyloidosis, and other granulomatous diseases can cause gastritis, which is seldom of primary importance.
  
  

• Gastritis caused by physical agents:

  Radiation and ingestion of corrosives (especially acidic compounds) can cause gastritis. Exposure to > 16 Gy of radiation produces marked deep gastritis, usually involving the antrum more than the corpus. Pyloric stenosis and perforation are possible complications of radiation-induced gastritis.
  
  

• Infectious (septic) gastritis:

  Except for H. pylori infection, bacterial invasion of the stomach is rare and mainly occurs following ischemia, ingestion of corrosives, or exposure to radiation. On x‑ray, gas outlines the mucosa. The condition can present as an acute surgical abdomen and has a very high mortality rate. Surgery is often necessary.

 

Debilitated or immunocompromised patients may develop viral or fungal gastritis with cytomegalovirus, Candida, histoplasmosis, or mucormycosis; these diagnoses should be considered in patients with exudative gastritis, esophagitis, or duodenitis.

Bron

1. T. Yamada, D.H. Alpers,L. Laine, C. Owyang & D.W. Powell. Textbook of Gastroenterology 4th Ed. 2003. Lippincott Williams & Wilkins.
2. A. Fauci, E. Braunwald, D. Kasper, S. Hauser, D. Longo, J.L. Jameson & J. Loscalzo. Harrison's Principle of Internal Medicine 17th Ed. 2008. McGraw-Hill.
3. A. Avunduk. Manual of Gastroenterology: Diagnosis and Therapy 4th Ed. 2008. Lippincott Williams & Wilkins.
4. E. Kuntz & H.D. Kuntz. Hepatology. Principles and Practice 2nd Ed. 2006. Springer Science & Business Media.

Laatste update: 15-12-2016