Epithelial damage, mucosal inflammation and epithelial cell regeneration represent the histologi-cal response of the stomach to injury. The term 'gastritis' implies the microscopic evidence of inflammation, in which all processes of mucosal response to injury are present, whereas the term 'gastropathy' is used for conditions in which epithelial injury is associated with cellular regeneration and the inflammation is not the prominent feature.1 The definite diagnosis of gastritis is thus exclusively based on histological assessment of biopsy specimens, whereas gastropathies are occasionally diagnosed on endoscopic appearance. For this reason, great confusion has been generated by the inappropriate use of the term gastritis.
Gastritis and gastropathy were previously classified either as primary (idiopathic) or secondary on the basis of the underlying etiology.2 It is now clear that most cases of unexplained gastritis are caused by previously unrecognized Helicobacter pylori (H. pylori) infection. Recently, an endoscopic classification of gastritis and gastropathy, has been proposed, that differentiates between erosive and/or hemorrhagic gastritis or gastropathy and non-erosive gastritis or gastropathy.3 The confounding aspect lies in the fact that some disorders can be either erosive or non-erosive. The most common causes of gastritis are summarized in Table 7.1.
Infectious gastritides Bacterial gastritides Helicobacter heilmannii
Although H. pylori is by far the most common agent in bacterial gastritides (discussed in detail in
Chapter 6), a spirochete-like organism, Helicobacter heilmannii (formerly Gastrospirillum hominis), has been found to infect the human stomach. H. heilmannii is closely related to Helicobacter types found in dogs and cats, such as Helicobacter felis. In a pediatric population, Oliva et al found a prevalence of infection of 0.3%, whereas in domestic cats and dogs the frequency of infection was up to 100%.4,5 H. heilmannii infection is thought to be a zoonosis, and a fecal-oral route of transmission is suggested. Recently, van Loon et al found an identical H. heilmannii strain in a 5-year-old boy and his cats.6
Histology shows a typical chronic inflammation, milder than H. pylori gastritis, and the presence of a spiral organism with four to six coils per cell and up to 12 flagella at each pole. The bacterium is usually recognized focally and in small groups in the foveola, maintaining a large distance from the surface epithelium. Endoscopic features such as erosions, peptic ulcerations and antral nodularity have rarely been reported. Eradication treatment, as with H. pylori infection, should be considered in both humans and animals.
Tuberculosis infection of the stomach is very rare and usually occurs in patients with immune deficiency or after transplantation.7 In adults, gastric tuberculosis typically involves the antrum and extends to the lesser curvature, although in patients with AIDS it may also involve the esoph-agogastric junction. Endoscopic features include hypertrophic nodular lesions and multiple ulcers, whereas outlet obstruction, caused by prepyloric narrowing or mass effect, has rarely been described. Histology can show both caseous and non-caseous granulomas. Culture of biopsy specimens is essential to establish the diagnosis,
Table 7.1 Common causes of gastritis and gastropathy
Bacteria Helicobacter pylori
Helicobacter heilmannii Mycobacterium tuberculosis, Mycobacterium avium-intracellulare
Fungi - Protozoa Candida albicans
Histoplasma, Mucormycosis Anisakis simplex Giardia lamblia Cryptosporidium
Drugs and other agents
Aspirin and other non-steroidal anti-inflammatory drugs
Potassium chloride, calcium
Chemotherapeutic agents, antibiotics, prostaglandin E-| Ethanol, cocaine, methamphetamines Gastrostomy tubes Endoscopic procedures Foreign-body ingestion Stress
Portal hypertensive gastropathy
Zollinger-Ellison and pseudo-Zollinger-Ellison syndrome Lymphocytic gastritis
Chronic varioliform gastritis Celiac gastritis
Helicobacter pylori lymphocytic gastritis Crohn's disease
Gastritis associated with other autoimmune diseases Graft-versus-host disease
Gastropathies due to drugs 97
because the organism may not be seen microscopically.
Organisms of the Mycobacterium avzum-intracel-lular complex are common pathogens in immuno-suppressed patients, and mainly occur in the small and large intestines. However, the stomach may occasionally be involved, with refractory gastric ulcerations.8
Viral infections of the stomach typically affect immunocompromised or severely debilitated children. Their frequency substantially increases in such children, whereas they are quite rare in healthy subjects. Rare cases of gastric involvement by herpes simplex virus (HSV) or disseminated varicella zoster virus (VZV) infections have been reported.9,10 Bleeding from hemorrhagic gastropa-thy has been described in children with influenza A infection.11 Cytomegalovirus (CMV) is the main recognizable viral agent, occurring in both healthy and immunodeficient children, and has been involved as an etiologic agent in Ménétrier's disease.
Fungal infections, such as Candida albicans, histo-plasmosis and mucormycosis, rarely affect the stomach, although bleeding, gastric ulcers and perforation during disseminated infections have been described in preterm or sick neonates, as well as in malnourished or immunodeficient children.
In adults, acute gastric anisakiasis frequently occurs in countries where the consumption of raw or undercooked fish is high. It is caused by ingesting the organism's larvae. Because humans represent an aberrant host, it is a dead-end infection characterized by an intense acute eosinophilic inflammation. Acute gastrointestinal symptoms, such as upper abdominal pain, nausea and vomiting occur within a few hours, and acute anaphy-lactic reactions have been described in patients previously exposed to the organism.12 Endoscopic findings include multiple erosions, edema and single or multiple worms, while histology shows an acute eosinophilic inflammation. The removal of worms with endoscopic forceps induces rapidly symptomatic relief.
Gastric colonization of Giardia lamblia has been reported in 0.3% of adults undergoing upper gastrointestinal endoscopy.13 Because giardiasis is associated with intestinal metaplasia of the stomach, some authors suggest that this organism is not a gastric pathogen.
Gastric outlet obstruction due to enteric cryp-tosporidiosis has been reported in immunocompromised patients.14
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