Gastritis (гастрит)

Contents

1 Causes and Treatment

1.1 Acute

1.2 Chronic

1.2.1 Metaplasia

1.2.2 Helicobacter pylori

1.3 Treatment

2 Symptoms

3 Diagnosis

4 References

5 See also

Gastritis is an inflammation of the lining of the stomach, and has many
possible causes.[1] The main acute causes are excessive alcohol
consumption or prolonged use of nonsteroidal anti-inflammatory drugs
(also known as NSAIDs) such as aspirin or ibuprofen. Sometimes gastritis
develops after major surgery, traumatic injury, burns, or severe
infections. Gastritis may also occur in those who have had weight loss
surgery resulting in the banding or reconstruction of the digestive
tract. Chronic causes are infection with bacteria, primarily
Helicobacter pylori. Certain diseases, such as pernicious anemia,
chronic bile reflux, and certain autoimmune disorders can cause
gastritis as well. The most common symptom is abdominal upset or pain.
Other symptoms are indigestion, abdominal bloating, nausea, and
vomiting. Some may have a feeling of fullness or burning in the upper
abdomen.[2][3] A gastroscopy, blood test, complete blood count test, or
a stool test may be used to diagnose gastritis.[4] Treatment includes
taking antacids or other medicines, such as proton pump inhibitors or
antibiotics, or avoiding hot or spicy foods. For those with pernicious
anemia, B12 injections are given.[5]

Acute

Erosive gastritis is gastric mucosal erosion caused by damage to mucosal
defenses.[2] Alcohol consumption does not cause chronic gastritis. It
does, however, erode the mucosal lining of the stomach; low doses of
alcohol stimulate hydrochloric acid secretion. High doses of alcohol do
not stimulate secretion of acid.[6] NSAIDs inhibit cyclooxygenase-1, or
COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the
stomach, which increases the possibility of peptic ulcers to form.[7]
Also, NSAIDs, such as aspirin, reduce a substance that protects the
stomach called prostaglandin. These drugs used in a short period of time
are not typically dangerous. However, regular use can lead to
gastritis.[8]

Chronic

If the cardiac sphincter fails to do its job properly, some stomach acid
can escape up the esophagus. This causes very painful «heartburn» or
«gastritis» in the chest as the esophageal walls are eroded by the
hydrochloric acid. Chronic gastritis refers to a wide range of problems
of the gastric tissues that are mainly the result of H. pylori
infection.[2] The immune system makes proteins and antibodies that fight
infections in the body to maintain a homeostatic condition. In some
disorders, the body accidentally targets the stomach, believing it is a
foreign protein or pathogen. It makes antibodies against, severely
damages, and may even destroy the stomach and/or its lining.[8] In some
cases, bile, normally used to aid digestion in the small intestine, will
enter through the pyloric valve of the stomach, because it had been
removed during surgery or may not work properly. This also leads to
gastritis. Gastritis may also be caused by other medical conditions,
including HIV/AIDS, Crohn’s disease, certain connective tissue
disorders, or liver/kidney failure.[9]

Metaplasia

Mucous gland metaplasia, the reversible replacement of differentiated
cells, occurs in the setting of severe damage of the gastric glands,
which then waste away (atrophic gastritis), which are progressively
replaced by mucous glands. Gastric ulcers may develop; it is unclear if
they are the causes or the consequences. Intestinal metaplasia typically
begins in response to chronic mucosal injury in the antrum, and may
extend to the body. Gastric mucosa cells change to resemble intestinal
mucosa and may even assume absorptive characteristics. Intestinal
metaplasia is classified histologically as complete or incomplete. With
complete metaplasia, gastric mucosa is completely transformed into
small-bowel mucosa, both histologically and functionally, with the
ability to absorb nutrients and secrete peptides. In incomplete
metaplasia, the epithelium assumes a histologic appearance closer to
that of the large intestine and frequently exhibits dysplasia.[2]

Helicobacter pylori

Helicobacter pylori colonizes the stomach of more than half of the
world’s population, and the infection continues to play a key role in
the pathogenesis of a number of gastroduodenal diseases. Colonization of
the gastric mucosa with Helicobacter pylori results in the development
of chronic gastritis in all infected individuals and in a subset of
patients chronic gastritis progresses to complications (i.e. ulcer
disease, gastric neoplasias, some distinct extra gastric disorders).[10]
However, gastritis has no adverse consequences for most hosts and
emerging evidence suggests that H. pylori prevalence is inversely
related to gastroesophageal reflux disease and allergic disorders. These
observations indicate that eradication may not be appropriate for
certain populations due to the potentially beneficial effects conferred
by persistent gastric inflammation.[11]

Treatment

Over-the-counter antacids in liquid or tablet form are a common
treatment for mild gastritis. Antacids neutralize stomach acid and can
provide fast pain relief. When antacids don’t provide enough relief,
medications such as cimetidine, ranitidine, nizatidine or famotidine
that helps reduce the amount of acid the stomach produces are often
prescribed. An even more effective way to limit stomach acid production
is to shut down the acid «pumps» within acid-secreting stomach cells.
Proton pump inhibitors reduce acid by blocking the action of these small
pumps. This class of medications includes omeprazole, lansoprazole,
rabeprazole, and esomeprazole. Proton pump inhibitors also appear to
inhibit H. pylori activity.[12] Cytoprotective agents are designed to
help protect the tissues that line your stomach and small intestine.
They include the medications sucralfate and misoprostol. If NSAIDs are
being taken regularly, one of these medications to protect the stomach
may also be taken. Another cytoprotective agent is bismuth
subsalicylate. In addition to protecting the lining of stomach and
intestines, bismuth preparations appear to inhibit H. pylori activity as
well. Several regimens are used to treat H. pylori infection. Most use a
combination of two antibiotics and a proton pump inhibitor. Sometimes
bismuth is also added to the regiment. The antibiotic aids in destroying
the bacteria, and the acid blocker or proton pump inhibitor relieves
pain and nausea, heals inflammation, and may increase the antibiotic’s
effectiveness.[13]

Symptoms

Severe gastritis is possible when the stomach is viewed without symptoms
being present and may be present despite only minor changes in the
stomach lining. Seniors have a higher likelihood of developing painless
stomach damage. They may have no symptoms at all, such as an absence of
vomiting or pain, until they are suddenly taken ill with internal
bleeding. Pain in the upper abdomen is the most common symptom. The pain
is usually in the upper central portion of the abdomen, the «pit» of the
stomach. Gastritis pain can occur in the left upper portion of the
abdomen and in the back. The pain seems to travel from the belly to the
back. The pain is typically vague, but can be a sharp pain. Belching
either doesn’t relieve pain or only relieves it for a moment. The vomit
is either clear, green or yellow, has a bloody streak in it, or is
completely bloody, depending on the severity of inflammation. Bloating
and a feeling of fullness or burning in the upper abdomen are also signs
of moderate gastritis. Severe gastritis presents pallor, sweating, rapid
heart beat, feeling faint or short of breath, severe chest or stomach
pain, vomiting large amounts of blood, or bloody or dark, sticky,
foul-smelling bowel movements.[14]

Diagnosis

Typically, a diagnosis is made based on the patients description of his
or her symptoms. If a diagnosis is not possible based on these symptoms,
however, other methods are used. Tests for blood cell count, H. pylori,
and pregnancy; and liver, kidney, gallbladder, and pancreas functions,
may be ordered. Urinalysis may be used, or a stool sample taken, to look
for blood in the stool. X-rays may be ordered, as well as ECGs. If none
of these tests are able to be used for diagnosis, the patient may be
recommended to a gastroenterologist. An endoscopy may be performed,
where a flexible probe with a camera on the end is sent into the stomach
to check for stomach lining inflammation and mucous erosion. At the same
time, a stomach biopsy may be taken to test for gastritis and a variety
of other conditions.[15]

References

«Gastritis». University of Maryland Medical Center (University of
Maryland Medical System). 2002-12-01. Retrieved on 2008-10-07.

a b c d «Gastritis». Merck. January 2007. Retrieved on 2009-01-11.

«Gastritis». National Digestive Diseases Information Clearinghouse
(National Institute of Diabetes and Digestive and Kidney Diseases).
December 2004. Retrieved on 2008-10-06.

«Gastritis: Diagnostic Tests for Gastritis». Wrong Diagnosis. December
30 2008. Retrieved on 2009-01-11.

«What is Gastritis?». Cleveland Clinic (WebMD). Retrieved on 2009-01-11.

Wolff G (1989). «[Effect of alcohol on the stomach]» (in German).
Gastroenterol J 49 (2): 45–9. PMID 2679657.

Dajani EZ, Islam K (August 2008). «Cardiovascular and gastrointestinal
toxicity of selective cyclo-oxygenase-2 inhibitors in man» (PDF). J
Physiol Pharmacol. 59 Suppl 2: 117–33. PMID 18812633.

a b Siegelbaum, Jackson (2006). «Gastritis». Jackson Siegelbaum
Gastroenterolgoy. Retrieved on 2008-11-18.

«Gastritis». MayoClinic. April 13, 2007. Retrieved on 2008-11-18.

«Helicobacter pylori infection: a clinical overview.». Dig Liver Dis..
August 2008. PMID 18396114. Retrieved on 2009-01-12.

??&???¬?fection and disease: from humans to animal models.». Dis Model
Mech.. PMID 19048053. Retrieved on 2009-01-12.

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