Stomach Diseases

Stomach Diseases

Helicobacter Pylori colonizes the gastric mucosa and continues to live in the mucus, protected from the acid environment.

The pathogenesis of Helicobacter Pylori-related gastroduodenal diseases is not fully known, but it is thought that many factors play a role.

  • Virulence factors of the bacteria
  • Adhesion to gastric epithelium,
  • Loss of microvilli,
  • Luminal border irregularity,
  • Edema, endoxin-like secretions,
  • Motility,
  • Urease enzyme activity,
  • Proteolytic enzyme activity are among the virulence factors.
In people colonized with HP (helicobacter pylori) CR. Active Gastritis => P. Ulcer => Atrophic Gastric, Gastric Denocarcinoma and Malt Lymphoma can lead to.

WHO IS PERFORMING THE TEST AND TREAT APPROACH?

The American GE Association’s recommendation is as follows.

  • If the clinician decides to treat when HP is detected,
  • If acute P. Ulcer or P. Ulcer is detected before,
  • If there is P. Ulcer bleeding,
  • If there is a family history of stomach Ca,
  • If there is early stomach cancer,
  • If there is gastric malt lymphoma,

OTHER INDICATIONS

If there are alarm symptoms in people under 60 years of age with unexplained dyspepsia,

  • In patients who will receive long-term PPI treatment,
  • In patients who will receive long-term NSAID treatment,
  • In the presence of unexplained B12 and Fe deficiencies,
  • In people with immune thrombocytopenia, HP treatment should be performed.

HAS THE RELATIONSHIP BETWEEN HP (HELICOBACTER PYLORI) AND STOMACH DISEASES DECREASED IN RECENT YEARS?

In recent years, prevalence studies have found that the frequency of H. Pylori has decreased significantly all over the world. With the decrease in prevalence, the prevalence of duodenal and gastric ulcers has also decreased. This situation can be explained by the improvement in economic and hygienic conditions.

A study conducted in Asian countries between 2003 and 2012 (covering 134,800 people) found that the prevalence of H. Pyolori decreased by 2% annually. (While it was 42% in 2003, it was found to be 24% in 2012)
D. Ulcer decreased from 12.5% ​​to =>% 6.5.
Gastric Ulcer decreased from 7.5% to =>% 3.7.
No decrease was found in gastric cancer in the same years. (3.7% and 2.3%)
In addition, in the same study, the frequency of R. Esophagitis increased from 6% to 12.8%.
The relationship between H. Pylori and gastric cancer, the cascade that starts with H. Pylori infection is as follows.

Cr. Superficial Gastritis => Cr. Atrophic Gastritis => IM => Dysplasia => Gastric Cancer
Here, IM is accompanied by intestinal type gastric carcinoma in particular.
The role of H. Pylori eradication in the gastric carcinogenesis cascade is whether it reverses Atrophy and Metaplasia in particular. Studies have shown that eradication improves gastric atrophy, but has no effect on IM.

TREATMENT

There is still no optimal treatment regimen for H. Pylori. Due to the development of resistance to clarithromycin and metronidazole, the 2017 H. Pylori cancer? Report (Maastricht V.) recommended that all treatment regimens be applied for 14 days. If clarithromycin and metronidazole resistance is over 15%, Bismuth quadruple treatment should be the first choice. If 2 resistance is 15%, the effectiveness of the Bismuth quadruple treatment regimen will decrease. The success of sequential treatment decreases in the presence of clarithromycin resistance alone, metronidazole resistance alone, or resistance to both.