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Infection with cagA-positive Helicobacter pylori lowers risk of gastric adenocarcinoma
Infection with Helicobacter pylori has been linked to a decreased risk of gastric adenocarcia. Helicobacter pylori is a bacterium that causes gastric ulcers and is also responsible for the development of gastric cancer. About half the world’s population is, infected with this bacterium. Infection with this bacterium can cause a variety of gastric disorders and can lead to preneoplastic lesions in up to 20% of cases. However, the outcome of this infection depends on the genetics of the person and the type of strain of Helicobacter pylori that is causing the infection.
While some studies have found an inverse correlation between H. pylori and gastric adenocarcinoma, more research is, needed to fully understand the mechanism behind this association. Researchers in China, the United States, and Europe have been working on ways to reduce the risk of gastric cancer.
Gastric adenocarcinoma is a result of cellular changes, caused by H. pylori infection. Helicobacter pylori induces changes in the host’s cellular growth and expression of tumor suppressor genes. CagA phosphorylates epithelial cells and translocates through the type IV secretion apparatus.
Although no studies have found a direct correlation between H. pylori infection and gastric cancer, it is, linked to decreased risk of gastric adenocarcia in patients with pernicious anemia.
Combined analysis of twelve case-control studies showed that H. pylori infection was, associated with an increased risk of noncardia gastric cancer. However, this association was, not observed in people who have no H. pylori infection.
One study found a relationship between the presence of cagA in the gastric crypts and the risk of gastric cancer. This association was, found in 92% of cancer strains and 81% of control strains. However, no association was found between cagA and vacA alleles. This finding is encouraging and warrants further studies.
This study studied 61 patients with gastric squamous-cell carcinoma. Serum antibodies to HP-CSAs and cagA were, associated with a lower risk of gastric adenocarcomatosis. The association between cagA-positive Helicobacter Pylei and gastric cancer was similar, with ORs of 2.0 and 3.9 (95% CI).
The study involved a cohort of patients with esophageal squamous-cell carcinoma, gastric adenocarcinomi, and gastric squamous-cell carcinoma. Researchers compared the cases and controls by age, gender, and sex.
Treatment
Treatment of peptic ulcer disease caused by Helicobacter pylori (H. pylori) involves using antibiotics to eliminate the pathogen from the stomach. The infection is a common cause of gastritis, peptic ulcer, gastric cancer, and nonulcer dyspepsia. Eradication of the bacteria improves gastric mucosa inflammation and promotes ulcer healing. This treatment also reduces the risk of gastric cancer mortality.
Antibiotic resistance has also been a major challenge in treating H. pylori infections. As a result, new antibiotics targeting H. pylori are being, tested for their efficacy. However, despite these advances, antibiotic stewardship guidelines should still apply when choosing an H pylori treatment regimen. As with any medical problem, multiple factors need to consider when selecting a treatment regimen. The most important factor is a high cure rate.
Treatment of Helicobacter pylori involves the use of antibiotics and other drugs to reduce gastric acidity. While antibiotics can help reduce gastric acidity, they can also affect the gut microbiota, a microbial community that plays a vital role in the human body. This bacteria contributes to energy metabolism, immune modulation, and host defense.
Probiotics have been studied as adjuncts to antibiotics for H. pylori eradication. There is a high risk of adverse effects from antibiotics, so a probiotic-based regimen can be a useful alternative. Probiotics have anti-inflammatory and anti-oxidative effects, which may enhance the efficacy of standard H pylori treatments. However, the added side effects of probiotics should not be underestimated.
In the past, triple-therapy was the gold standard for treating Helicobacter pylori infection. This treatment was accompanied by good safety profile and high eradication rates. Unfortunately, the efficacy of triple therapy has declined in recent years due to the development of antibiotic resistance.
The ACG and the Toronto Consensus agree that empiric triple therapy may not be effective. It recommends longer durations of treatment (14 days) and restricts clarithromycin-based antibiotics. Additionally, bismuth-quadruple therapy should be used as a first-line therapy. There are many other alternative strategies for treating H. pylori, including the use of probiotics and increased awareness of the role of acid suppression.
Generally, patients with refractory H. pylori infection should undergo susceptibility testing. This testing helps to detect the exact strain of the organism in the gastrointestinal tract. However, the process of susceptibility testing is expensive and time-consuming, and the success rate varies from seventy to ninety percent. This treatment regimen should only be used if eradication therapies fail to provide results.
Although vonoprazan-based triple therapy and nonbismuth quadruple therapy are effective, these methods have limitations. The most significant problem with these two methods of treatment is the increase of antimicrobial-resistant strains of H. pylori. This is primarily due to the widespread use of antibiotics in many countries. As a result, the efficacy of these treatments is, reduced.
Dual therapy with vonoprazan and amoxicillin may improve eradication rates for H. pylori in the GI tract while minimizing the adverse effects on the gut microbiota. It may also improve safety.
