Rare causes of gastritis

Rare causes of gastritis

Histologically, gastritis refers to inflammation in the stomach. Endoscopically, gastritis refers to a number of abnormal features such as erythema, erosions, and subepithelial hemorrhages.

Gastritis can also be subdivided into erosive, nonerosive, and specific types of gastritis with distinctive features both endoscopically and histologically.

What are the Rare causes of gastritis?

Acute Neutrophilic Leukocytic Gastritis

• •Acute gastritis, characterized by dense infiltration of the stomach with neutrophilic leukocytes, is rare.
• •This rarity is in distinction to the much more common “active” gastritis, where neutrophils can be present along with chronic inflammatory cells (lymphocytes, plasma cells), as in Helicobacter pylori (Hp) gastritis.

Phlegmonous (Suppurative) Gastritis

• •Phlegmonous (suppurative) gastritis is an infection of the gastric submucosa and muscularis propria, often sparing the mucosa.
• •Many types of invasive microorganisms have been identified, including gram-negative bacteria, anaerobes, gram-positive organisms including group A streptococci, and fungi.
• •The gastric phlegmon may simulate a mass. Infection may spread from the stomach to the liver and spleen, with abscess formation.
• •The esophagus may also be involved in or even be the apparent source of the infection.
• •Acute phlegmonous/necrotizing gastritis has been associated with a variety of conditions including recent large intake of alcohol, upper respiratory tract infection, and AIDS and other immunocompromised states, including liver transplantation.
• •An especially severe form of phlegmonous gastritis is emphysematous gastritis, due to infections with gas-producing organisms. Gas in the wall of the stomach and in the portal venous system is often present. Radiographic studies (plain films, CT) show gas bubbles conforming to the contour of the stomach, often in the form of cystic gas pockets.
• •Although full recovery from phlegmonous or emphysematous gastritis may occur, the condition may progress to gastric (and esophageal) gas gangrene and be fatal. Risk factors for emphysematous gastritis include gastroduodenal surgery, ingestion of corrosive materials, gastroenteritis, or GI infarction. Patients with phlegmonous or emphysematous gastritis typically present with acute upper abdominal pain, peritonitis, purulent ascitic fluid, fever, and hypotension.
• •Preoperative diagnosis is possible with plain film, US, or CT. Gastroscopy with or without biopsy and culture of gastric contents may establish the diagnosis.
• •Grossly, the stomach wall appears thick and edematous with multiple perforations, and the mucosa may demonstrate a granular, green-black exudate. Microscopically, the edematous submucosa reveals an intense polymorphonuclear infiltrate and numerous gram-positive and/or gram-negative organisms, as well as vascular thrombosis. The mucosa may demonstrate extensive areas of necrosis.
• •The mortality rate of phlegmonous gastritis is close to 70%, probably because it is so often misdiagnosed and because treatment is initiated too late. The definitive treatment is either resection or drainage of the stomach, combined initially with large doses of systemic broad-spectrum antibiotics directed against the most common organisms (Escherichia coli and other gram-negative bacilli, anaerobic and group A streptococci, and Staphylococcus aureus).

Environmental Metaplastic Atrophic Gastritis (EMAG)

• •EMAG is characterized by the involvement of both the gastric antrum and corpus with mucosal atrophy and intestinal metaplasia.
• •Gastroscopy may show a pale mucosa, shiny surface, and prominent submucosal vessels. However, endoscopy is neither sensitive nor specific in diagnosing chronic atrophic gastritis, especially in patients younger than age 50. Magnifying endoscopy and auto fluorescence imaging video endoscopy may be more sensitive in detecting atrophy. 
• •The pathogenesis of EMAG is multifactorial, but Hp infection plays the most important role and has been incriminated in about 85% of patients. 

Autoimmune Metaplastic Atrophic Gastritis (AMAG)

• •AMAG, also called diffuse corporal atrophic gastritis, is an autoimmune destruction of glands in the corpus of the stomach. AMAG is the pathologic process in patients with pernicious anemia, an autoimmune disorder often occurring in patients of northern European or Scandinavian background and in African Americans.
• •Patients with AMAG exhibit achlorhydria or hypochlorhydria, hypergastrinemia secondary to low or absent gastric acid with antral G-cell hyperplasia, and low serum PGI concentrations and low ratios of serum PGI/PGII. They often have circulating antibodies to parietal cell antigens and to intrinsic factor (IF). Antibodies to IF are less sensitive but more specific for AMAG, whereas antibodies to parietal cells are more sensitive but less specific. These antibodies can apparently cross from the maternal circulation to the fetus to cause neonatal vitamin B₁₂ deficiency with methylmalonic aciduria. Autoreactive T cells against the H⁺,K⁺-ATPase are also thought to play a role in the pathogenesis of AMAG.

Cytomegalovirus Gastritis

• •Cytomegalovirus (CMV) is a human herpesvirus (HHV5) that may infect the stomach. Although gastric CMV infection may occur in an immunocompetent host, infection usually occurs in the immunocompromised. Patients with transplants, AIDS, or cancer, or who are taking immunosuppressive drugs (especially glucocorticoids), are at increased risk.
• •Patients with CMV infection of the stomach may experience epigastric pain that may be postural, with fever and atypical lymphocytosis. Upper GI (UGI) tract radiographic studies, if performed, may reveal a rigid and narrowed gastric antrum suggestive of an infiltrating antral neoplasm.
• •Gastroscopy may reveal a congested and edematous antral mucosa, covered with multiple ulcerations, suggestive of gastric malignancy, submucosal antral mass, or gastric ulcer.
• •A hypertrophic and/or polypoid type of gastritis resembling Ménétrier disease with a similar type of protein-losing gastropathy has been described, especially in children, including one case with CMV/Hp coinfection. 

HSV Gastritis

• •Gastritis from HSV-1 (HHV1) or varicella-zoster virus (VZV; HHV3) is rare. Infected individuals typically experience the initial infection at an early age, and the virus then remains dormant until reactivation.
• •Reactivation has been related to radiation therapy, cancer chemotherapy, lymphoma, and cancer. The typical immunocompromised patient with these viral gastritides may experience nausea, vomiting, abdominal pain, fever, chills, fatigue, and weight loss.

Mycobacterial Gastritis

Gastric infection with Mycobacterium tuberculosis is a rare entity. Patients typically present with abdominal pain, nausea and vomiting, GI bleeding, anemia, fever, and weight loss. Gastric TB may be associated with gastric outlet obstruction or with hemorrhage from a tuberculous gastric ulcer.

Actinomycosis Gastritis

Primary gastric actinomycosis is a rare, chronic, progressive, suppurative disease characterized by formation of multiple abscesses, draining sinuses, abundant granulation, and dense fibrous tissue.

Other Bacterial Gastritis

• •Helicobacter heilmannii spiral bacteria are an infrequent cause of chronic active gastritis and may be a risk factor for gastric MALT lymphoma.
• •These organisms, originally known as Gastrospirillum hominis, are longer than Hp and have multiple spirals. One of these H. heilmannii species, Helicobacter bizzozeronii, has been isolated from human gastric mucosa.
• •Another organism that, like Hp, can stain with the Giemsa reagent is Campylobacter hypointestinalis. The clinical significance of these non-Hp curved bacilli remains to be established.

Mucormycosis Gastritis

• •Gastric mucormycosis (also called zygomycosis or phycomycosis) is a rare and highly lethal fungal infection.
• •Risk factors include malnutrition, immunosuppression, antibiotic therapy, and metabolic acidosis, usually diabetic ketoacidosis.
• •Most patients present with UGI bleeding or gastric ulcers. Gastric mucormycosis can be classified as invasive or noninvasive (colonization). The former is characterized by deep invasion of the stomach wall and by blood vessel involvement with the fungus.
• •Abdominal pain is the most frequent presenting complaint. In the noninvasive type, the fungus colonizes the superficial mucosa without causing an inflammatory response.

Other Fungal Gastritis (Aspergillosis, Cryptococcosis Monascus ruber)

• •Acute Aspergillus gastritis is rare and can be highly invasive.
• •The stomach and duodenum may be involved in immunocompromised hosts in conjunction with cryptococcal meningitis.
• •Monascus ruber gastritis, acquired by eating dried, salted fish, can result in invasive infection.

Parasitic Gastritis

• •Invasive anisakidosais (formerly, anisakiasis) may occur after the ingestion of raw marine fish containing nematode larvae of the genus Anisakis. Most cases of anisakidosis have been diagnosed in Japan.
• •The parasite may migrate into the wall of the stomach, small intestine, or colon. Typically, patients present with sporadic epigastric pain or have no symptoms at all. Gastric perforation due to chronic gastric anisakidosis may occur.
• •Some patients exhibit a mild peripheral eosinophilia. Endoscopy may show firm, yellowish submucosal masses with erosions. Radiographic studies may reveal notched-shadow defects suggestive of a gastric tumor.

Granulomatous gastritis

• •A variety of granulomatous diseases can affect the stomach. Crohn disease is the most common of them in children. Sarcoidosis and Crohn disease are the most common in adults.
• •Infection with spirochetes, mycobacteria, fungi, parasites, and the Whipple’s bacillus can also cause granulomatous gastritis, as can foreign bodies, lymphoma, Langerhans cell histiocytosis (gastric eosinophilic granuloma), eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), and chronic granulomatous disease of childhood.

Sarcoid Gastritis

• •Sarcoidosis is a systemic granulomatous disease, sometimes involving the GI tract and liver. The stomach (usually the antrum) is the most common portion of the GI tract affected in sarcoidosis, being involved in approximately 10% of cases.
• •A diagnosis of sarcoid gastritis of the stomach cannot be made with confidence in the absence of granulomatous disease in other organs.
• •Affected patients, usually in the third to fifth decades of life, typically present with epigastric pain, nausea, vomiting, and weight loss. Occasionally they present with massive GI hemorrhage. Gastric sarcoidosis may result in pyloric outlet obstruction, achlorhydria, and pernicious anemia. Radiographically, gastric sarcoidosis may mimic the diffuse form of gastric carcinoma (“linitis plastica”) or Ménétrier disease.

Collagenous Gastritis

• •Collagenous gastritis is rare and can be associated with collagenous duodenitis, collagenous colitis, lymphocytic colitis, celiac disease, and/or autoimmune disorders.
• •Two clinical patterns have been identified. In children and young adults, the presenting symptoms are anemia and epigastric pain, whereas in older adults (ages 35 to 77), the presenting symptom is often diarrhea due to coexisting celiac disease or collagenous colitis.
• •Biopsy specimens from the body and antrum of the stomach reveal a patchy, chronic, superficial gastritis, focal atrophy, and focal deposition of collagen in the subepithelial region of the lamina propria.
• •Little is known about the etiology, natural history, and proper treatment of this condition.

Lymphocytic Gastritis

• •Lymphocytic gastritis is characterized by a dense lymphocytic infiltration of surface and pit gastric epithelium.
• •Lymphocytic gastritis is related to an endoscopic form of gastritis known as varioliform gastritis, characterized by nodules, thickened rugal folds, and erosions.
• •Lymphocytic gastritis in adults is typically seen in patients with Hp infection.
• •Hp eradication treatment in patients with lymphocytic gastritis causes significant improvement in the gastric intraepithelial lymphocytic infiltrate, corpus inflammation, and dyspeptic symptoms .
• •Patients with gastric MALT lymphoma have a significantly increased prevalence of lymphocytic gastritis due to Hp infection. Thus lymphocytic gastritis may be a precursor of gastric MALT lymphoma in patients with Hp infection.

Eosinophilic Gastritis

• •Eosinophilic gastroenteritis is a rare condition of unknown etiology characterized by eosinophilic infiltration of the GI tract, peripheral blood eosinophilia, and GI symptomatology in the absence of known causes for eosinophilia (e.g., parasitic infection) or another GI disorder (e.g., IBD).
• •Eosinophilic gastroenteritis is classified according to the layer(s) of GI tract involved (i.e., mucosal layer disease, muscle layer disease, and subserosal disease).
• •In the stomach, mucosal involvement may result in abdominal pain, nausea, vomiting, weight loss, anemia, and protein-losing gastropathy.
• •Patients with muscular layer disease generally have gastric outlet obstructive symptoms, and rare patients with subserosal eosinophilic infiltration may develop eosinophilic ascites.

Gastritis Cystica Profunda (GCP)

• •Gastritis cystica profunda (GCP) is a rare condition that can occur as a complication of partial gastrectomy with gastrojejunostomy for PUD, typically occurring at the site of the gastroenterostomy.
• •GCP may also develop in the unoperated stomach. GCP can be associated with Ménétrier disease and with gastric cancer. GCP may also be iatrogenic after attempted gastric polypectomy.
• •Gastric symptoms in GCP, if present, are nonspecific.

Hyperplastic Gastropathy

• •Hyperplastic gastropathy is a rare condition characterized by giant gastric folds associated with epithelial hyperplasia.
• •Two clinical syndromes have been identified: (1) Ménétrier disease and a variant of it referred to as hyperplastic, hypersecretory gastropathy, and (2) Zollinger-Ellison syndrome, demonstrates enlarged gastric folds in these conditions.
• •The enlarged gastric folds in Ménétrier disease are due to foveolar cell hyperplasia, edema, and variable degrees of inflammation.

What are the Presenting Signs & Symptoms

• •Patients with gastritis may be asymptomatic or may present with nonspecific clinical signs and symptoms (e.g., epigastric pain, abdominal tenderness, bloating, anorexia, nausea [with or without vomiting]). Symptoms may be aggravated by eating.
• •Epigastric tenderness in acute alcoholic gastritis (may be absent in chronic gastritis).
• •Foul-smelling breath.
• •Hematemesis (“coffee grounds” emesis).

How is this diagnosed?

Diagnostic Criteria

• •By definition, gastric biopsies must be obtained to be able to diagnose gastritis.
• •Indications for gastroscopic biopsies may include gastric symptoms, gastric erosion or ulcer, thick gastric fold(s), gastric polyp(s) or mass(es), and for diagnosis of Hp infection.

How is this treated?

Treatment varies with the etiology of the gastritis.

References

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