More research is needed to fully understand probiotics' role in Hp treatment, especially with updated regimens. While they show promise, they are not guaranteed solutions, particularly for children. With rising antibiotic resistance, probiotics may help, but they are only part of the answer.

Probiotics for Hp have limits: they cannot fully eradicate it, effects vary by strain, and benefits are often temporary. Outcomes differ across trials, with rare side effects like sepsis in immunocompromised people. Quality and consistency issues in probiotic products further complicate their use.

Probiotics like Lactobacillus reuteri and Saccharomyces boulardii show promise in improving Hp eradication rates, but they’re not replacements for antibiotics. When combined with antibiotics, they may enhance effectiveness and reduce side effects, offering a more balanced treatment approach.

Saccharomyces boulardii improves Hp eradication rates to 85.4%, compared to 80% without probiotics. Similarly, multistrain probiotics, including Lactobacillus and Bifidobacterium, increase eradication to 93.33%, highlighting their effectiveness in reducing side effects and improving outcomes.

Probiotics like Lactobacillus and Saccharomyces boulardii help combat Hp by producing antimicrobials, lowering acidity, and blocking the bacteria’s adhesion to stomach cells. They also reduce inflammation by lowering interleukin-8 (IL-8), aiding gastric recovery and balancing the microbiota.

Antibiotic therapy for Hp faces rising resistance, especially to clarithromycin (40-50%), causing treatment failures. Side effects like nausea, diarrhoea, and bloating often lead to treatment discontinuation, highlighting the need for alternatives like probiotics to improve treatment outcomes.

For Hp treatment, first-line therapy is a combination of amoxicillin (AMX), a proton pump inhibitor (PPI), and clarithromycin (CLR) in areas with low CLR resistance. In regions with high CLR resistance (>15%), metronidazole, AMX, PPI, and CLR or bismuth quadruple therapy are recommended.

Molecular 16S rRNA analysis of Hp-infected stomachs shows a sharp decline in diversity—33 types compared to 262 in healthy individuals. The loss of beneficial microbes like Streptococcus and the rise of pathogenic bacteria highlights the severity of gastric dysbiosis, driving further complications.

Hp disrupts gastric microbiota via urease, which raises pH and has flagella that penetrate the mucus layer. Adhesins and virulence factors (CagA, VacA) trigger inflammation and cytokine release, damaging the mucosa. This reduces bacterial diversity, creating dysbiosis and favouring Hp dominance.