Gastritis, Treatment and Classification

What is Gastritis

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

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
2. Endoscopic
A. Endoscopic forms of gastritis:

• eritematous exudative
• maculo-erosive
• papulo-erosive
• atrophic
• hypertrophic
• hemorrhagic 

B. Classification by extension:

• antral-type B-produced by H. Pylori infection
• fundic-Type A-autoimmune (generating Biermer anemia)
• pangastritis.

3. Histologic

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

4.Etiology. The classification of gastritis includes the following possible etiologies:

A. Infectious:

• 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

Administration of:

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

The duration of antisecretory therapy will be for 6-8 weeks.

B) Gastric mucosal protectives

-sucralfate 4g/day (qid)might be associated.

C) Antacids

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.

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Functional Dyspepsia Diagnosis and Treatment

Definition

Functional dyspepsia is a functional disease(without organic reason), characterized by a symptomatology located in the upper abdomen, its manifestation are epigastric pain, satiety, flatulence or discomfort.

Etiopathogenesis of functional dyspepsia

In cases with quasiulcerous symptomp the role of Helicobacter Pylori or hypersecretory status may be incriminated; in those with flatulence, a disorder in gastric emptying(dismotility)or even disorders of the sensorial digestive perception(the patient perceives as abnormal a usual quantity of gas located in the digestive tube).

Classification of functional dyspepsia

It is done in accordance with the dominant symptoms:

• functional dyspepsia ”ulcer-like”;
• functional dyspepsia type dismotility “dismotility dyspepsia”;
• essential  functional dyspepsia.

In the ulcer-like dyspepsia:

• epigastric pain,
• discomfort,
• frequently painful hungers are prevalent, but the superior digestive endoscopy reveals the absence of ulcer.

In dismotility dyspepsia, the patient complains of  epigastric satiety, a sensation of epigastric “load”, flatulence, eructations, but the digestive investigations will reveal the absence of lesion. Essential functional dyspepsia will contain a mixture of the symptoms above.

Diagnosis

Clinical diagnosis consists of an epigastric symtomatology more or less noisy,but in which loss, digestive hemorrhage or anemia are absent. The prevalent type of symptoms will allow the “framing” into one of dyspepsia forms.

Paraclinic diagnosis consists into a series of explorations, which will demonstrate the absence of organic lesions. Firstly, the abdominal ultrasonography will show a gallbladder without calculi, a normal pancreas, and a liver without changes. The superior digestive endoscopy will show a normal esophagus, stomach and duoden. The barium enemaor colonoscopy will be proved by the absence of organic lesions.

Differential diagnosis in functional dyspepsia must be done with all the organic lesions of the upper abdomen (reflux esophagitis, esophageal neoplasia, achalasia, gastro-duodenal ulcer, gastric neoplasm, gastric lymphoma, acute or chronic pancreatitis, gallstones etc.).

-the irritable colon (characterized by disorders of transit, flatulence, sensation of incomplete  stool, discomfort in the lower abdomen etc.).

Evolution is favorable, with more or less in time, generally according to alimentation, stress etc. The prognosis is favorable.


Treatment of functional dyspepsia

It addresses mainly to the symptoms and it will be administered at their apparition.

Treatment of “ulcer-like” dyspepsia

Antisecretory drugs of the class H2 histaminic blockers:

• Ranitidine 300mg/day
• Famotidine 20-40mg/day,
• or PPI given during the symptomatic periods or PPI (20-40mg)

Eradication of Helicobacter Pylori

In  approximately a half of patients in which the triple the therapy Helicobacter Pylori is eradicated, the symptoms may disappear or reduce, but in the others, the symptoms persist.

Treatment of “dismotility” functional dyspepsia consists generally in prokinetics.

• Metoclopramide(1 tb 30 minutes before principal meals)
• Domperidone(Motilium 1 tb 30 minutes before principal meals)
• Cisaprid(Coordxinax, Prepulsid 5-10 mg 30 minutes before principal meals). Digestive ferments at meals(Digestal, Mezym, Festal, Kreon etc.) or intestinal gas absorbents, such as dimeticon(Sab-simplex) may also be administered.

Treatment of essential functional dyspepsia, disease with symptoms of the two entities above,will be made with medication addressed to the dominant manifestations(pain or satiety).

In all forms of dyspepsia,if stress plays a role in the apparition of symptoms,an easy sedative treatment should be administered or even psychotherapy(often when the patient find out he has no organic lesions,the psychic effect is positive).

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