notes by dott. Claudio Italiano
Gastritis is a term that was once used improperly by ordinary people to indicate "heartburn", and, therefore, a dyspeptic syndrome (from the Greek, poor digestion); today it takes on new significance based on the recent acquisition that antral gastritis is attributable to Helicobacter pylori (H.P.) infection and is associated with duodenal ulcer. In general all gastritis have an inflammatory condition but different etiopathogenetic mechanisms. The various classifications of gastritis previously in use are those of Sidney which divides it into a) acute gastritis and b) chronic gastritis c) special gastritis.
Types:
Helicobacter pylori gastritis
Acute infections from infectious causes: bacterial, e.g. from Helicobacter
heimmanii, phlegmon, mycobacterial infection, from treponema pallidum in
syphilis, from parasites, from fungi
Acute gastritis stress from the critical patient
Type A: predominant in the gastric body, on autoimmune genesis
Type B: predomixant in the gastric antrum, associated with Helicobacter pylori,
environmental
Type AB:Indefinite type
Special forms of gastritis:
Lymphocytic gastritis
Eosinophilic gastritis
Crohn's disease
Sarcoidosis
Granulomatous gastritis isolated
Acute gastritis may be associated with Helicobacter pylori infection,
responsible for increased acidity and subsequently hypochlorhydria when the
infection proceeds, with signs also lasting annually. Generally the Helicobacter
pylori infection can be chronic and be recognized through the biopsy and urease
tests, of which the bacterium is equipped and which make viral from yellow to
magenta the test liquid in which the frustules of gastric mucosa taken during
endoscopy, is often the result of toxic and pharmacological damage. Still in the
field of "acute gastritis" some authors include acute lesions of the gastric
mucosa, which are determined by the use or abuse of anti-inflammatory drugs,
including aspirin, ie acetylsalicylic acid or other NSAIDs (indomethacin,
ibuprofen, naproxen, tolmetin, sulindac, piroxicam, fenoprofen). In these cases
in the patient, since the drug is absorbed through backscatter in the gastric
mucosa, surface antral erosions with micro bleeding are determined. The patient
most of the time comes to our attention because he complains of fatigue and
aggravating gastric pyrosis or because he has noticed feces, such as black ink
and the doctor has performed a blood count with anemia of acute loss (hemorrhage).
Haemorrhage is usually not massive but can be relevant and put the patient's
life at risk. Other times, gastritis occurs in the alcoholic patient, due to
direct damage to alcohol on the gastric mucosa, alcohol gastritis. Stress ulcers
are manifested by acute ischemia of the mucosa (Cushing ulcers) or respiratory
failure, in burns and generally occur in the antrum; it frequently occurs in
patients in severe conditions admitted to intensive care.
Their most severe manifestation is gastrointestinal haemorrhage; the endoscopic aspect will be of gastric erosions associated with punctiform hemorrhagic lesions or frankly hemorrhagic gastritis, with acute erosion in the 2/3 of the residual mucosa. It must be said that acute gastritis by anti-inflammatory drugs recognize as factors of increased risk, the use of coffee, alcohol, Helicobacter infection, smoke.
Atrophic gastritis is a histopathological entity characterized by chronic
inflammation of the gastric mucosa with loss of gastricglandular cells and
replacement by intestinal-type epithelium,pyloric-type glands, and fibrous
tissue. Atrophy of the gastricmucosa is the endpoint of chronic processes, such
as chronicgastritis associated with Helicobacter pylori infection,
otherunidentified environmental factors, and autoimmunity directedagainst
gastric glandular cells.
Atrophic gastritis represents the end stage of chronic gastritis, both infectious
and autoimmune. In both cases, the clinica manifestations of atrophic gastritis
are those of chronic gastritis,but pernicious anemia is observed specifically in
patients withautoimmune gastritis and not in those with H. pylori–
associatedatrophic gastritis.
This bacterium is a spiral-shaped, Gram-negative bacterium with a width of 0.5
microns and a length of 2 and 6.5 microns. It is equipped with a multiple
coating and a unipolar flagella and a powerful urease activity (on which the
urease test is based when a gastric biopsy sample is taken which immerses itself
in the colorimetric reactive system); Both the form and the flagellum allow the
bacterium to detect itself in the gastric mucosa and its urease activity allows
it to create an ammonium and bicarbonate ion barrier, essential for its
colonization. The H.P. has a diffusion correlated with the socio-economic
development, so much so that in underdeveloped countries the infection is
present in 80-90% of the subjects and increases, with us, with the age up to
50-60% after the 70 years. The H.P. it lives in the stomach and binds to gastric
epithelial cell receptors, but sometimes also to receptors of the ectopic
gastric epithelium of the intestinal tract, Barrett's esophagus, Meckel's
diverticula and heterotopic plaques of the gastric mucosa of the rectum. During
the gastroscopic investigation, it can be detected through a) the culture of a
fragment of biopsy gastric tissue; b) urease test on a gastric biopsy;
non-invasive alternating method are c) the serological test which aims to look
for IgG or IgA antibodies directed to the various bacterial antigens by means of
ELISA e) the breath test with marked urea: the patient ingests a tablet of
marked urea and, if the bacterium is present, free marked CO2 which is collected
in a sample of expired air and subsequently analyzed.
Because the H.P. is associated with chronic antral gastritis and, subsequently, those affected by this pathology may have ulcerative relapses; because the H.P. can increase gastrin levels and, therefore, the production of hydrochloric acid, perhaps also through an inhibition of somatostatin produced by the antral D cells that exerts inhibition on G cells that podruno gastrin. Finally, the infection can over time lead to an excessive production of acid and, consequently, to damage to the duodenal mucosa, which ultimately leads to a transformation into intestinal gastric metaplasia (ie islands of gastric mucosa into the duodenum, where there should not be any). Hence duodenitis and a possible duodenal ulcer, which can be treated with classical methods. Furthermore, duodenal ulcer may be due to other causes, for example the use of non-steroidal anti-inflammatory drugs (NSAIDs), of which the progenitor is aspirin, due to their damaging blocking effect on mucosal prostaglandins; it can be determined in Zollinger-Ellison syndrome or in unusual manifestations such as Crohn's disease. All individuals infected with H.P. have a histological picture characteristic of active chronic gastritis, (inflammation in the upper half of the gastric mucosa, with mild atrophy and maximum activity at the antrum where HP is detected) but only a minority of them, however, will develop ulcerative disease, or for immune or genetic predisposition or for more virulent strains of HP The symptoms of gastritis generally are characterized by slow, laborious digestion, pain or epigastric burning, sense of repellence and vomiting and hemorrhage (especially in the acute form); in the case of gastric ulcer pain is exacerbated by ingestion of food; in duodenal ulcer, however, is calmed by the ingestion of food, because the pylorus is closed and no more acid flows into the duodenum.
The eradication therapy. It usually consists of the association of drugs that
regulate acid secretion and the use of 2 antibiotics, but includes several
variants.
In general, therapy is performed with:
a) proton pump inhibitor (omeprazole and substitutes) 20 mg x twice daily +
amoxocillin gx tablets twice daily and / or clarithromycin 250 mg x twice daily
tablets + metronidazole 400 mg x two tablets times a day. This treatment is
continued for 7 days and then continued for 3-5 weeks with the pump inhibitor
alone.
b) pump inhibitor (omeprazole) + amoxocillin tablets 1 g X twice a day or
clarithromycin 500 mg tablets twice a day, all for 15 days, with less efficacy
for eradication which will be 70-80% .
It must be carried out in subjects who have relapses and a pump inhibitor can be
used every other day or at lower doses or the old ranitidine. Other drugs from
which the subject can benefit, especially if the peptic disease is associated
with reflux esophagitis, ie the condition in which the lower esophageal
sphincter (LES) is incontinent or the malposizionate cardias with consequent
ascent of acid in the esophagus and sign of regurgitation and of the "shoelace
of the shoe", will be:
a) antacids, ie preparations based on aluminum and magnesium hydroxide, in
different combinations, to be taken after meals or when needed;
b) more specific for reflux, combinations of alginic acid + aluminum hydroxide +
magnesium trisilicate + sodium bicarbonate that should be taken immediately
after the meal and before going to bed: they form a reaction with gastric acid
and alginic acid precipitates under form of foamy gel, in the presence of CO2
and floating on the gastric juice, so that in case of reflux it constitutes a
mechanical barrier to the action of the acid.
c) the old and always valid antiacid sucralfate which is a basic salt of sucrose sulphate.
d) prostaglandins, misoprostol
e) motor drugs that help the continence of SLE: ex. clebopride, sulpiride; they
increase the tone of SLE and facilitate gastric emptying.