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The association between obesity and peptic ulcer disease (PUD) is inconclusive. To evaluate the association of obesity and metabolically healthy obesity (MHO) with PUD risk, we performed a retrospective cohort study of 32,472 subjects without PUD at baseline who underwent repeated health examinations. Participants were stratified by body mass index (BMI) and metabolically healthy state. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazard modelling. During the follow-up period, 1940 PUD cases occurred. PUD, particularly gastric ulcer (GU), had significantly higher cumulative incidence in obese subjects compared to non-obese subjects (p value < 0.001). The HR for developing GU was 1.32 (95% CI, 1.16–1.49; p value <0.001); after adjusting for confounding factors (lifestyle, metabolic, and Helicobacter pylori status), the association was no more significant (p value = 0.789). For duodenal ulcer (DU), cumulative incidence between obese and non-obese groups was not significantly different (p value = 0.464). The risk of developing DU in the obese group was not significantly different from the non-obese group (HR 0.95; 95% CI, 0.83–1.09; p value = 0.469) and consistently showed no association after adjusting for metabolic parameters (p value = 0.199). Furthermore, MHO subjects had no increase in GU or DU risks. In this large cohort study, PUD risk was not associated with obesity or MHO.

A wound is damage of a tissue usually caused by laceration of a membrane, generally the skin. Wound healing is accomplished in three stages in healthy individuals, including inflammatory, proliferative, and remodeling stages. Healing of wounds normally starts from the inflammatory phase and ends up in the remodeling phase, but chronic wounds remain in an inflammatory stage and do not show progression due to some specific reasons. Chronic wounds are classified in different categories, such as diabetic foot ulcer (DFU), venous leg ulcers (VLU) and pressure ulcer (PU), surgical site infection (SSI), abscess, or trauma ulcers. Globally, the incidence rate of DFU is 1–4 % and prevalence rate is 5.3–10.5 %. However, colonization of pathogenic bacteria at the wound site is associated with wound chronicity. Most chronic wounds contain more than one bacterial species and produce a synergetic effect that results in previously non-virulent bacterial species becoming virulent and causing damage to the host. While investigating bacterial diversity in chronic wounds, Staphylococcus, Pseudomonas, Peptoniphilus, Enterobacter, Stenotrophomonas, Finegoldia, and Serratia were found most frequently in chronic wounds. Recently, it has been observed that bacteria in chronic wounds develop biofilms that contribute to a delay in healing. In a mature biofilm, bacteria grow slowly due to deficiency of nutrients that results in the resistance of bacteria to antibiotics. The present review reflects the reasons why acute wounds become chronic. Interesting findings include the bacterial load, which forms biofilms and shows high-level resistance toward antibiotics, which is a threat to human health in general and particularly to some patients who have acute wounds.

Although Helicobacter pylori infection is typically acquired in childhood, the role of H. pylori infection in gastroduodenal diseases in childhood remains to be defined. The purpose of this study was to evaluate the prevalence of H. pylori infection in children with gastritis, duodenal ulcer, and gastric ulcer. This was a retrospective analysis of 283 Japanese children (mean age, 11.5 years) with non-nodular gastritis ( n = 73), nodular gastritis ( n = 67), duodenal ulcer ( n = 100), and gastric ulcer ( n = 43). H. pylori status was based on biopsy tests. Clinical symptoms at the time of endoscopy were analyzed with regard to a possible association with the infection. The prevalence of H. pylori in non-nodular gastritis, nodular gastritis, duodenal ulcer, and gastric ulcer was 28.8%, 98.5%, 83.0%, and 44.2%, respectively. H. pylori was significantly linked to duodenal ulcer and gastric ulcers in the age group of 10-16 years, but not in the age group of 9 years and under. In children with H. pylori infection, nodular gastritis was observed in 26.3% of gastric ulcer patients and in 74.7% of duodenal ulcer patients ( P < 0.001). H. pylori infection was significantly associated with the prevalence of anemia ( P < 0.05). H. pylori is the most important causal factor for the development of duodenal ulcer in childhood. While H. pylori infection appears to be a risk factor in gastric ulcer, other causes are responsible for most cases. Nodular gastritis is the most common type of H. pylori gastritis in childhood. Chronic infection with H. pylori is associated with anemia.

Background Previous studies demonstrated that the sensitivity of rapid urease test (RUT) for diagnosis of Helicobacter pylori infection decreased during peptic ulcer bleeding. Aim We designed this study and tried to find a better method to improve the detection rate of H. pylori infection at the same session of endoscopic diagnosis of peptic ulcer bleeding. Methods We prospectively enrolled 116 patients with peptic ulcer bleeding. These patients received intravenous proton pump inhibitor and then received upper gastrointestinal endoscopy within 24 h after arrival. We took one piece of biopsy from gastric antrum (Group 1), four pieces from gastric antrum (Group 2), and one piece from the gastric body (Group 3) for three separate RUTs, respectively. 13 C-urease breath test was used as gold standard for diagnosis of H. pylori infection. Results There were 74 patients (64 %) with positive 13 C-urease breath test. Among these 74 patients, 45 patients had positive RUT (sensitivity: 61 %) in Group 1; 55 patients had positive RUT (sensitivity: 74 %) in Group 2; 54 patients had positive RUT (sensitivity: 73 %) in Group 3. There were significant differences between Group 1 and Group 2 ( p  = 0.02) and between Group 1 and Group 3 ( p  = 0.022). Conclusions The sensitivity of RUT was 61 % during peptic ulcer bleeding. The sensitivity of RUT can be increased significantly by increased biopsy number from gastric antrum or biopsy from gastric body.

Background Helicobacter pylori infection is an important risk factor for gastric cancer. In Japan, national health insurance has covered eradication therapy for H. pylori infection–associated gastritis from 2013. However, gastric cancer was the fourth leading cause of cancer death in 2023. We aimed to investigate differences in gastric cancer risk among patients with gastritis, gastric ulcer, duodenal ulcer, and gastric ulcer and duodenal ulcer after H. pylori eradication. Methods This retrospective cohort study used the JMDC Claims Database from February 21, 2013, to August 31, 2023. Patients who received first-line H. pylori eradication therapy and were diagnosed with H. pylori –associated gastritis, gastric ulcer, or duodenal ulcer in the same month or the month before the first eradication therapy prescription were included. Two antibacterial drugs and an acid secretion inhibitor or triple-drug blister-packaged product were prescribed. The primary outcome was gastric cancer incidence. A Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs). A propensity score approach was used to minimize the effect of confounding measures. Results Of 17,245,330 beneficiaries, 148,489 were included. In the weighted cohort (after propensity matching), statistically significant differences were observed in HRs between H. pylori –associated gastritis and duodenal ulcer (HR using the latter as a reference [95% confidence interval]: 2.03 [1.31–3.13]; p  = 0.001), and between gastric ulcer and duodenal ulcer (2.37 [1.52–3.71]; p  < 0.001). The cumulative probabilities (95% confidence interval) per the median follow-up years (3.8 years for all) were 0.44% (0.39–0.48) for H. pylori –associated gastritis, 0.54% (0.46–0.63) for gastric ulcer, 0.22% (0.10–0.33) for duodenal ulcer, and 0.26% (0.08–0.50) for gastric ulcer and duodenal ulcer. Conclusions Patients with H. pylori –associated gastritis and gastric ulcer had a higher risk of gastric cancer than patients with duodenal ulcer, indicating that gastric atrophy remains a risk factor after H. pylori eradication therapy. Careful monitoring, such as by endoscopic examination, is required after successful eradication of H. pylori in patients at higher risk.

Background The aim of this study was to identify the common H. pylori virulence genes among dyspeptic Southwestern Saudi patients and their association with clinical outcomes and histopathological findings to help practitioners and researchers in the region for better management of infections caused by such bacteria. Methods Four hundred two gastric biopsy specimens were analyzed using histopathological examination and real time-PCR. The positive 187 specimens by RT-PCR were genotyped using PCR targeting cagA , vacA and iceA genes. Results One hundred twenty-eight gastric biopsy specimens were positive in genotyping PCRs. The cagA , vacA , iceA 1 and iceA 2 genes were detected in rates of 49.2% (63/128), 100%(128/128), 42.2% (54/128), 32.8% (42/128), respectively. The vacA s1as1bm2 subtype was the highest 23.4% (30/128), followed by m2 and s1a1b subtypes which were equally detected [16.4% (21/128) for each]. The iceA genes were significantly associated with gastritis and gastric ulcer. Overall, vacA genotypes were significantly associated with gastritis, gastric and duodenal ulcers. The vacA subtypes: s1as1bm2 , s1a1b and s2 m2 showed chronic active gastritis in percentages of 90.0, 81, and 84.2%, respectively. All vacA mixed genotypes showed chronic active gastritis. Conclusions H. pylori virulence genes are highly prevalent and diverse among patients with dyspepsia in Southwestern region of Saudi Arabia. The iceA genes and the different vacA subtypes are significantly associated with the clinical outcomes and histopathological changes especially chronic active gastritis.

Emerging studies have shed light on the association between Helicobacter pylori (HP) infection and cardiometabolic risk. However, there is no evidence to support a causal link for the relationship in the general population. Our aim was to determine whether HP infection is associated with the risks of incident type II diabetes mellitus (DM) in a population-based cohort consisting of adults from the general population. A total of 69235 adults enrolled in the study obtained health examinations at the Tri-Service General Hospital in Taiwan from 2010 to 2016. HP infection detection was performed by rapid urease tests (RUTs), and endoscopic examinations were used to diagnose gastroesophageal reflux disease (GERD), gastric ulcers (GUs) and duodenal ulcers (DUs). Cross-sectional and longitudinal analyses were performed to examine the association between HP infection and cardiometabolic diseases using logistic regression and Cox regression in a large population-based study. HP infection was significantly associated with the presence of metabolic syndrome (MetS) (OR = 1.26, 95%CI: 1.00-1.57) and DM (OR = 1.59, 95%CI: 1.17-2.17) only in male subjects, and abnormal endoscopic findings were also correlated with cardiometabolic diseases. Our findings demonstrated that participants with HP infection had an elevated risk of developing incident DM (HR = 1.54, 95%CI: 1.11-2.13). In addition, endoscopic findings of a DU (HR = 1.63, 95%CI: 1.02-2.63), rather than GERD or a GU, were also predictive of incident DM. In this cohort, HP infection was a statistically significant predictor of incident DM among male population.

Background Non-surgical chronic wounds, including diabetes-related foot diseases (DRFD), pressure injuries (PIs) and venous leg ulcers (VLU), are common hard-to-heal wounds. Wound evolution partly depends on microbial colonisation or infection, which is often confused by clinicians, thereby hampering proper management. Current routine microbiology investigation of these wounds is based on in vitro culture, focusing only on a limited panel of the most frequently isolated bacteria, leaving a large part of the wound microbiome undocumented. Methods A literature search was conducted on original studies published through October 2022 reporting metagenomic next generation sequencing (mNGS) of chronic wound samples. Studies were eligible for inclusion if they applied 16 S rRNA metagenomics or shotgun metagenomics for microbiome analysis or diagnosis. Case reports, prospective, or retrospective studies were included. However, review articles, animal studies, in vitro model optimisation, benchmarking, treatment optimisation studies, and non-clinical studies were excluded. Articles were identified in PubMed, Google Scholar, Web of Science, Microsoft Academic, Crossref and Semantic Scholar databases. Results Of the 3,202 articles found in the initial search, 2,336 articles were removed after deduplication and 834 articles following title and abstract screening. A further 14 were removed after full text reading, with 18 articles finally included. Data were provided for 3,628 patients, including 1,535 DRFDs, 956 VLUs, and 791 PIs, with 164 microbial genera and 116 species identified using mNGS approaches. A high microbial diversity was observed depending on the geographical location and wound evolution. Clinically infected wounds were the most diverse, possibly due to a widespread colonisation by pathogenic bacteria from body and environmental microbiota. mNGS data identified the presence of virus (EBV) and fungi ( Candida and Aspergillus species), as well as Staphylococcus and Pseudomonas bacteriophages. Conclusion This study highlighted the benefit of mNGS for time-effective pathogen genome detection. Despite the majority of the included studies investigating only 16 S rDNA, ignoring a part of viral, fungal and parasite colonisation, mNGS detected a large number of bacteria through the included studies. Such technology could be implemented in routine microbiology for hard-to-heal wound microbiota investigation and post-treatment wound colonisation surveillance.

Background and aims: A number of Helicobacter pylori outer membrane proteins (OMPs) undergo phase variations. This study examined the relation between OMP phase variations and clinical outcome. Methods: Expression of H pylori BabA, BabB, SabA, and OipA proteins was determined by immunoblot. Multiple regression analysis was performed to determine the relation among OMP expression, clinical outcome, and mucosal histology. Results:H pylori were cultured from 200 patients (80 with gastritis, 80 with duodenal ulcer (DU), and 40 with gastric cancer). The most reliable results were obtained using cultures from single colonies of low passage number. Stability of expression with passage varied with OipA > BabA > BabB > SabA. OipA positive status was significantly associated with the presence of DU and gastric cancer, high H pylori density, and severe neutrophil infiltration. SabA positive status was associated with gastric cancer, intestinal metaplasia, and corpus atrophy, and negatively associated with DU and neutrophil infiltration. The Sydney system underestimated the prevalence of intestinal metaplasia/atrophy compared with systems using proximal and distal corpus biopsies. SabA expression dramatically decreased following exposure of H pylori to pH 5.0 for two hours. Conclusions: SabA expression frequently switched on or off, suggesting that SabA expression can rapidly respond to changing conditions in the stomach or in different regions of the stomach. SabA positive status was inversely related to the ability of the stomach to secrete acid, suggesting that its expression may be regulated by changes in acid secretion and/or in antigens expressed by the atrophic mucosa.