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H. pylori (Heliobacter pylori, is a type of a gram-negative bacterium found
on the luminal surface of the gastric epithelium, was first isolated by Warren
and Marshall in 1983.It can damage the tissue in your stomach and the first
part of your small intestine (the duodenum). This can cause redness and
soreness. In some cases it can also cause painful sores called peptic ulcers in
your upper digestive tract .

These bacteria, however, were thought to be contaminants from digested

food rather than true gastric colonizers. About 20 years ago, researches
showed that gastric colonization with H. pylori can lead to variety of upper
gastrointestinal disorders, such as chronic gastritis, peptic ulcer disease,
gastric mucosa associated lymphoid tissue

Infection with H. pylori is a cofactor in the development of three important

upper gastrointestinal diseases:

 Duodenal or gastric ulcers (reported to develop in 1 to 10% of infected

patients), gastric cancer (in 0.1 to 3%), and gastric mucosa-associated
lymphoid-tissue (MALT) lymphoma (in <0.01%).

The risk of these disease outcomes in infected patients varies widely

among populations.

The susceptibility of an individual to these clinical outcomes is multifactorial

and depends on H. pylori virulence, environmental factors, the genetic
susceptibility of the host and the reactivity of the host immune system.
Despite the host immune response, H. pylori infection can be difficult to
eradicate. H. pylori is categorized as a group I carcinogen since this
bacterium is responsible for the highest rate of cancer-related deaths
worldwide. Early detection of cancer can be life saving.

The 5-year survival rate for gastric cancer patients diagnosed in the early
stages is nearly 90%. Gastric cancer is asymptomatic in the early stages but
always progresses over time and begins to cause symptoms when untreated.
In 97% of stomach cancer cases, cancer cells metastasize to other organs. H.
pylori infection is responsible for nearly 60% of the intestinal-type gastric
cancer cases but also influences the development of diffuse gastric cancer.
The host genetic susceptibility depends on polymorphisms of genes involved
in H. pylori-related inflammation and the cytokine response of gastric
epithelial and immune cells. H. pylori strains differ in their ability to induce a
deleterious inflammatory response. H. pylori-driven cytokines accelerate the
inflammatory response and promote malignancy. Chronic H. pylori infection
induces genetic instability in gastric epithelial cells and affects the DNA
damage repair systems. Therefore, H. pylori infection should always be
considered a pro-cancerous factor.

A. Colonize mucosal lining of stomach & duodenum in man & animals

• Adherent to gastric surface epithelium or pit epithelial cells deep

within the mucosal crypts adjacent to gastric mucosal cells

• Mucosa protects the stomach wall from its own gastric milleu of
digestive enzymes and hydrochloric acid

• Mucosa also protects Helicobacter from immune

B. response most gastric adenocarcinomas and lymphomas are concurrent

with or preceded by an infection with H. pylori.
1. Urease: The enzyme urease is a very important factor forcolonization of
H. pylori in the gastric mucosa. The enzyme pro-duces ammonia from
urea, which in turn increases the pH of the gastric mucosa in the
immediate vicinity of the bacterial cell. It helps, therefore, to neutralize
gastric acidity and also in colonization of the organism in gastric mucosa.
The enzyme also stimulates monocytes and neutrophil chemotaxis and
stimulates production of cytokines.

2. Flagella: Flagella are also very important for colonizationof H. pylori.

These help the organism to penetrate into gastric mucous layer; hence, it is
protected from acidic environment of the stomach.
3. Adhesins: These include hemagglutinin, sialic acid-bindingadhesins, and
Lewis blood group adhesins. All these factors facilitate binding of H. pylori
to gastric mucosa.

4. Enzymes: H. pyloriproduces many enzymes, such as muci-nase,

phospholipases, superoxide dismutase, and catalase. Both mucinase and
phospholipase break down gastric mucus, while superoxide dismutase
and catalase prevent phagocytic killing of the bacteria.

5. Heat shock protein (Hsp-B): The heat shock protein facili-tates expression
of the enzyme urease .

6. Acid inhibitory protein: This protein causes hypochlorhy-dria by blocking

secretions of acid from parietal cells.

7. Cytotoxin: This causes vacuolation in epithelial cells of the host.

 yytnbEyhtntyni yrtnE
 H. pylori enters via the mouth.
 yetyni yontnaviyhnyvatytt Eyoobchc yitbyayoitbnynhn r itb yhnyho
killed by the acid .
 The presence of the enzyme urease on its surface protects it for
sufficient time before penetrate the mucus layer.
  The spiral shape, motility, and the production of phospholipase
and the ammonium ion (which affects the tertiary structure of the
mucus making it thin and watery) allow the Helicobacter to
penetrate the mucus layer very quickly.
y
 yydb anythnihtyni yrtnE
 enynt oyttnyttbna Eyd t nban yni yeaonbhvy dhni honyatny
tn byni yoornovtoa y aE boyatnyni b itb yb nahtoyb onbhvn ny
y.otn tonntyni yontnaviyatnyn
 Spread from person to person.
 Spread is via the fecal-oral route or oral-oral route.
 H. pylori can only adhere to gastric epithelial tissue, which is
found in the stomach and in the first part of the duodenum.
 The organism is found mainly in the antrum of the stomach
but can also be found in all parts of the stomach and
duodenum.

Mtonyvih nb tythniyH.ydE tbhyhti vnhttyntt’nyiac yoEndntno.yOt Ey

about 20% do.
Symptoms and signs, if present, are those that arise from gastritis or
peptic ulcer and include:
 tin tyayi tyitoboyyntb ( o ytbyrobthteydahtyhtyEtobyontnaviy
tobydahtynaEy aonynhton oyntyitoboyy.)ain by anhteyatnyanythein
.atnynaEyvtn yatnyetytc byo c ba ynaEoyntyt no
 .std att nyt heiny tooy
 y.g tanhtey
 Nausea and vomiting (bloody vomit).
  y).nEod doha(etnhe onhtty
 .gobdhte
 y.etooytiyadd nhn
 Dark stools (from blood in your stool).y

1. y:s hthva ynhaettoho

A. Endoscopy: gastritis, ulcers, bleeding ulcer, atrophy.
B. CLO test: Rapid diagnostic test.
C. Carbon urea breath test: 13C-UREA swallowed, 13-CO2
exhaled.

2. y:eartbantbEynhaettoho
A. Microbiology: tissue biopsyculture for isolation of H.
pylori. : Antibiotic sensitivity by Microbroth dilution
method.
B. Serology: detection of anti-Helicobacter antibodies or
Anti-Cag A antibodies in serum.
C. Histology: biopsy tissue prepared for giemsa stain and
silver stain for H. pylori. H&E stain.
eiyEtoyntt’nyiac yoEndntno,yEtoyntt’nyt nyntyr ynb an n.yeiyEto'c yr ty
diagnosed with H. pylori, avoid taking no steroidal anti-inflammatory
drugs. These drugs can increase your risk of developing an ulcer H. pylori
infection is usually treated with at least two different antibiotics
simultaneously. This helps prevent bacteria from becoming resistant to a
particular antibiotic.

Treatment may also include medications that can help heal the stomach,
including:

 Proton pump inhibitors: these drugs prevent acid production in the

stomach. Proton pump inhibitors include omeprazole (Prilosec),
esomeprazole (Nexium), lansoprazole (Prevacid), and pantoprazole
(Protonex).
 Bismuth Substance Salicylate: more commonly known by the brand
name Pepto-Bismol, this medication works by coating ulcers and
protecting them from stomach acid.
 Histamine (H-2) blockers: these medications block a substance called
histamine that stimulates acid production. An example is cimetidine
(Tagamet HB). H-2 blockers are only indicated for H. pylori infection
unless proton pump inhibitors cannot be used.

A repeat H. pylori test may be recommended at least four weeks after your
treatment. And if the tests show that the treatment is not effective in
eliminating the infection, you may need another treatment using a different
group of antibiotics.

Is there a vaccine to prevent H. pylori infection?

Not yet, but there are promising results from a late-stage clinical trial.
In this trial, children given the vaccine were protected against H. pylori
infection for up to three years.
You can lower your risk of H. pylori infection if you:
o Drink clean water and use clean water during food
preparation. (This is especially important if you live in areas of
the world known to have a contaminated water supply(.
o Wash your hands thoroughly (20 seconds) with soap and
water before eating and after using the bathroom.
Refrance +cition:
 Kenneth E.L. McColl, M.D. ;Jagan Kumar Baskaradoss, Eman Behbehani,
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tobta ytiyH bra yy.tc bybatntnhl nyv hthva ynbha -db hnhtabEyvbtoo
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pathogen interactions in Helicobacter pylori related gastric cancer. otb ny y
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 American Academy of Pediatrics. Helicobacter Pylori Infections.
(https://www.healthychildren.org/English/health-
issues/conditions/abdominal/pages/Helicobacter-Pylori-Infections.aspx)
 Ryoko Nagata, Hiroki Sato, Shoji Takenaka, Junji Yokoyama, Shuji Terai,
Hitomi Mimuro, Yuichiro Noiri, Analysis of Genetic Relatedness between
Gastric and Oral Helicobacter pylori in Patients with Early Gastric Cancer
Using Multilocus Sequence Typing, International Journal of Molecular
Sciences, 10.3390/ijms24032211, 24, 3, (2211), (2023).