Gastritis can be an acute or chronic gastric disease, characterized by inflammatory lesions produced by various etiologic and pathogenic factors. They may be asymptomatic or with unspecific clinical expression.
Gastropathies represent a group of gastric mucosal lesions, predominant epithelial and/or vascular (by stasis or ischemia) but without or minimal inflammatory component, unlike gastritis.
Gastritis classification is as follows:
1. Clinical evolution
A. Acute. Evolves towards healing or chronicity most of them are self-limited and spontaneously recover.
B. Chronic. They are long-term inflammations that may heal after therapy or evolve no matter of the therapy. Read More
A. Endoscopic forms of gastritis:
- eritematous exudative
B. Classification by extension:
- antral-type B-produced by H. Pylori infection
- fundic-Type A-autoimmune (generating Biermer anemia)
A. Acute gastritis - numerous neutrophiles localized intraepithelial, in the lamina propria or aggregated in the glandular lumens (cryptic abcesses).
B. Chronic gastritis - immuno-competent lymphocytes and plasmocytes. It evolves in some decades to atrophic gastritis. The activity degrees depend on the presence of neutrophiles and the degree of infiltration in the profound layers. Low activity is characterized by presence of neutrophiles only in the lamina propria. In the moderate activity, the neutrophiles are present in high density in the gastric foveoles. The degree of activity is severe when the neutrophiles are present intraepithelial. Chronic gastritis is inactive when neutrophiles are absent.
C. Atrophic gastritis represents the final stage of chronic gastritis evolution, and is characterized by the disappearance of the oxintic glandular structure,with a distortion of the reticulin net. The inflammatory process invades the whole wall thickness; the histopathologic examination should mention the presence or absence of intestinal metaplasia.
The System includes an endoscopic section, with three subdivisions: topography, lesion type, endoscopic category of gastritis, and a histological section, including, the etiology, topography and gastritis forms.
The grading of histological lesions of gastritis in the Sydney System refers to the next six histological characteristics; for each of them there is a grading in moderate, mild and severe:
- acute inflammation-neutrophiles
- chronic inflammation-limphoplasmocytes
- activity-polimorphonuclear infiltrate
- atrophy-loss of specialized glands
- intestinal metaplasia
- Helicobacter Pylori
- Bacterial: H. Pylori (mostly), Helicobacter Heilmannii, alpha hemolytic Streptococcus, Staphylococcus etc.
- Viral: Cytomegalovirus, Herpes-virus
- Fungal: Candida
- Parasites: Strongiloides, Toxoplasma.
B. Autoimmune: Atrophic gastritis with Biermer anemia.
C. Drug-induced: NSAIDS(nonsteroid anti-inflammatory)
D. Specific: Crohn’s disease, eosinophilic gastritis, lymphocytar gastritis.
Chronic Gastritis H. Pylori Positive
It is type B gastritis, defined by the inflammation of the gastric mucosa principally antral, induced by Helicobacter pylori.
The pathogenetic mechanism of inducing gastric lesions is related to the peculiarities of the bacteria and to its enzymatic equipment, having a result an immune response of the host (local and systemic) against different proteic structures of the bacteria. The antibodies against the proteins secreted by Helicobacter Pylori with protective role seem to be involved in the gastritis pathogenesis.
The macroscopic aspect is of diffuse or patchy congestion, mostly antral with acute or chronic erosions. In 25% of cases a nodular gastritis appears.
Microscopically, a palimorphonuclear infiltrate may be noticed, together with the gastric cryptic affecting, the apparition of some aggregates of lymphoid follicles, and the reduction of mucus in the epithelial cells. Concerning the evolution, an active chronic gastritis is described(with a rich polimorphonuclear infiltrate), and an inactive chronic gastritis(with prevalence of mononuclear cells).
The clinical features are unspecific and overlap those of the non-ulcer dyspepsia. Epigastric pain, nausea, vomiting may appear. These symptoms disappears only after eradication treatment.
The B type gastritis diagnosis is done endoscopically, showing the antral lesions and also by taking biopsies, showing the Helicobacter Pylori bacteria by different techniques.
The evolution of gastritis may be towards atrophic chronic gastritis and further to intestinal metaplasia, dysplasia and finally gastric cancer or nonHodgkin lymphoma.
The treatment is the eradication of Helicobacter Pylori infection.
1. The diet. A diet with avoidance of acid, hot or seasoned food might still be recommended. The exclusion of coffee during the acute period may be recommended.
Aspirin intake, as well as NSAIDS and corticoids should be forbidden.
2. Medical therapy
A) Antisecretory drugs
- H2 histaminic receptor blockers:
- Cimetidine 1000mg/day
- Ranitidine 300 mg/day
- Nizatidine(Axid) 300 mg/day
- Famotidine (Quamatel) 40mg/day
Famotidine will be preferred, given once or twice a day and without drug interferences of Cimetidine(cytochrome P450).
- HK ATP-ase pump blockers:
- Esomeprazole (Nexium) 40mg/day
- Omeprazole (Losec, Antra, Ultop) 40 mg/day
- Pantoprazole (Controloc) 40 mg/day
- Lanzoprazole (Lanzap) 30mg/day
- Rabeprazole (Pariet) 20mg/day
B) Gastric mucosal protectives
-sucralfate 4g/day (qid)might be associated.
To neutralize the acid excess and reduce the painful symptoms, symptomatic medication such as Maalox, Almagel, Alfogel etc. are used.
Schemes of treatment in Helicobacter Pylori infection
The schemes including proton pump blockers (zomeprazole, lanzoprazole or pantoprazole), associated with two antibiotics are indicated, triple or even quadruple schemes are used.
The triple therapy includes OAM=Omeprazole(40mg/day)+Amoxicillin(2g/day)+Metronidazole(1500mg/day); or the ideal association is OAC=Omeprazole+Amoxicilline+Claritromicine(macrolide in dose of 1000mg/day).
The quadruple therapy is composed of Omeprazole+Subcitric bismuth (De-Nol)+Tetracycline+Metronidazole.
The anti HP therapy duration is for 7 day.