Colonoscopy is an essential diagnostic and therapeutic tool in gastroenterology, significantly impacting colorectal cancer (CRC) detection and management. Effective bowel preparation is critical for optimal visualization, directly influencing colonoscopy accuracy and patient outcomes. However, diabetic patients frequently encounter challenges achieving adequate bowel preparation, primarily due to gastroparesis, autonomic neuropathy, altered colonic motility, fluid–electrolyte imbalances, and complexities related to antihyperglycemic medication adjustments. This review aims to evaluate the current literature on bowel preparation efficacy in diabetic patients undergoing colonoscopy, assess existing guidelines from leading gastroenterological societies, and highlight the necessity for detailed, diabetes-specific recommendations. We conducted a comprehensive PubMed search identifying 20 pertinent studies, including randomized controlled trials, meta-analyses, multicenter studies, cohort studies, and reviews. The findings consistently indicate diabetes as an independent predictor of inadequate bowel preparation. Furthermore, an evaluation of guidelines from the European Society of Gastrointestinal Endoscopy (ESGE), the US Multi-Society Task Force, and the Canadian Association of Gastroenterology revealed either absent or insufficiently detailed diabetes-specific recommendations. Given the rising global prevalence of diabetes and CRC, inadequate bowel preparation significantly impacts the quality of colonoscopy, adenoma detection rates, patient safety, and healthcare costs. This review underscores the urgent need for additional research focusing on tailored bowel preparation strategies for diabetic patients. Ultimately, the implementation of standardized, evidence-based protocols designed explicitly for this high-risk group is essential to enhance diagnostic efficacy, improve patient outcomes, and reduce CRC-related morbidity and mortality.

Background: Thrombosis is a detrimental sequala of COVID-19 infection; thus, prophylactic anti-coagulant therapy has been deemed mandatory in treatment unless serious contraindications are present. Susceptibility to thromboembolic events in COVID-19, or following COVID-19 vaccination, is likely attributable to an interplay of factors, including a patient’s baseline clinical status and comorbidities, alongside genetic risk factors. In Europe, 8–20% of the population are homozygous for the MTHFR (methylene tetrahydrofolate reductase) variant, which compromises folate metabolism and elevates homocysteine levels. While heightened homocysteine levels are considered a risk factor for thromboembolic events, the precise clinical significance remains a contentious issue. However, recent research suggests elevated homocysteine levels may predict the course and severity of COVID-19 infection. Given the lack of reliable biomarkers predictive of COVID-19 thrombotic risk existing in practice, and the accessibility of MTHFR screening, we established two main outcomes for this study: (1) to determine the association between hereditary MTHFR mutations and COVID-19 severity and thromboembolic events and (2) to determine the link between MTHFR variants and adverse thrombotic events following COVID-19 vaccination. Methods: The review was conducted in accordance with PRISMA guidelines. Medline, Scopus, and Web of Science databases were searched from pandemic inception (11 March 2020) to 30 October 2023. Eligibility criteria were applied, and data extraction performed. Results: From 63 citations identified, a total of 14 articles met the full inclusion criteria (8 of which were cross-sectional or observational studies, and 6 were case studies or reports). Among the eight observational and cross-sectional studies evaluating the relationship between MTHFR variants (C667T; A1298C) and thromboembolic events in COVID-19 infection, four studies established a connection (n = 2200), while the remaining four studies failed to demonstrate any significant association (n = 38). Conclusions: This systematic review demonstrated a possible association between the MTHFR gene variants and COVID-19 severity, thromboembolic events, and adverse events following vaccination. However, the paucity of robust data precluded any firm conclusions being drawn. Further prospective trials are required to determine the connection between the MTHFR gene variant and COVID-19 infection and vaccination outcomes.

Background/Objectives: Nicotine-free electronic cigarettes (NFECs) are becoming increasingly popular, especially among youth and non-smokers, yet their effects on the gastrointestinal tract (GIT) remain poorly understood. This systematic review synthesizes available in vitro, in vivo, and limited human evidence on NFEC-associated changes in gastrointestinal health and function. Methods: Literature searches were conducted in Medline, Web of Science, Cochrane, and Scopus in July 2025, following PRISMA guidelines. Eligible studies examined NFEC effects on any GIT segment, including the oral cavity, liver, intestines, and microbiome. Data on study design, exposure characteristics, and main outcomes were extracted and narratively synthesized. Results: Of 111 identified records, 94 full-text articles were retrieved, and 21 studies met the inclusion criteria. Most were preclinical, with only one human pilot study. Evidence from oral cell and microbial models suggests that NFEC aerosols can induce pro-inflammatory cytokine production, impair cell viability, and disrupt microbial metabolism through their base constituents (propylene glycol, vegetable glycerine, and flavourings). Animal studies indicate possible hepatic oxidative stress, altered lipid metabolism, and gut barrier dysfunction, with some data suggesting more pronounced steatosis in nicotine-free exposures compared to nicotine-containing counterparts. Microbiome studies report reduced tight junction expression and altered neutrophil function. Conclusions: Current evidence is limited and predominantly preclinical but indicates that NFEC exposure can affect multiple aspects of gastrointestinal health. Robust longitudinal and interventional human studies are urgently needed to determine the clinical relevance of these findings and to inform regulation and public health policy.

Background: Helicobacter pylori (H. pylori) is a prevalent bacterial pathogen implicated in different stomach and duodenal diseases, including chronic gastritis, gastric and duodenal ulcer, and stomach cancer. The COVID-19 pandemic has significantly influenced antibiotic prescription practices, potentially exacerbating antibiotic resistance in H. pylori. Objective: This study aims to investigate antibiotic prescription during the COVID-19 pandemic in Croatia and its possible impact on H. pylori antibiotic resistance, with a focus on Croatia. Methods: An extensive literature search was conducted to identify relevant studies from March 2020 to June 2024. The search strategy included terms related to COVID-19, antibiotic prescription, and Croatia. Studies were selected based on predefined eligibility criteria, focusing on observational research addressing antibiotic use during the pandemic. Results: The COVID-19 pandemic has led to significant fluctuations in community antibiotic consumption within the European Union/European Economic Area. In Croatia, antibiotic use in 2022 surpassed 2019 levels, driven by increased consumption of macrolides and other antibiotics. This surge, influenced by early pandemic treatment claims and penicillin shortages, contributed to rising antibiotic resistance in H. pylori. Resistance rates to clarithromycin and levofloxacin were notably high, driven by mutations in the 23S rRNA, gyrA, and gyrB genes. Discussion: The increased antibiotic use during the COVID-19 pandemic has highly likely complicated H. pylori eradication efforts, highlighting the necessity of judicious antibiotic use and robust antimicrobial stewardship. The pandemic underscored the need for new therapeutic strategies, optimized eradication regimens, and advanced diagnostic methods to manage bacterial infections effectively. Conclusions: The COVID-19 pandemic has significantly affected antibiotic use and resistance patterns, posing new challenges for H. pylori eradication. Addressing these challenges requires a multifaceted approach, including the development of new drugs and advanced diagnostics, coupled with sustained efforts in antimicrobial stewardship to combat emerging resistance threats.

Background: Carpal tunnel syndrome (CTS) is the most common peripheral neuropathy caused by compression of the median nerve in the carpal tunnel. The presented study aimed to evaluate clinical outcomes by comparing two techniques of wound closure following carpal tunnel surgery in subjects randomized to the application of tissue adhesive or sutures. Methods: From April 2022 to December 2022, a single-center randomized prospective trial was conducted at the University Hospital of Split in Croatia. The study participants consisted of 100 patients (70 females) aged 61.56 ± 12.03 years, randomly assigned to suture-based wound closure (n = 50) or tissue adhesive-based wound closure (n = 50) with two-component skin adhesive Glubran Tiss 2^®. The outcomes were assessed postoperatively during the follow-up period at intervals of 2, 6, and 12 weeks. A scar assessment was performed using the POSAS (Patient and Observer Scar Assessment Scale) and cosmetic VAS (Visual Analog Scale). The VNRS (Verbal Number Rating Scale) was used to assess pain. Results: There were significant differences between glue-based wound closure and suture-based wound closure at 2-week and 6-week intervals after the surgery on the POSAS and cosmetic-VAS scales (better aesthetic effect with glue-based wound closure technique where noticed), with less postoperative pain at the same intervals. With the 12-week interval, differences in outcomes were insignificant. Conclusions: This trial demonstrated that cyanoacrylate-based adhesion mixtures might be possibly superior in the short term in terms of cosmetic appearance and discomfort compared to conventional skin suturing techniques for the closing of surgical wounds following open CTS decompression, but there was no difference between both procedures in the long term.

Background and Objectives: Cardiometabolic disease, a term encompassing metabolic syndrome (MS) and cardiovascular disease (CVD), represents a major and growing global health burden driven by interconnected metabolic and cardiovascular dysfunction. Emerging evidence suggests that the gut microbiota plays a central role in modulating metabolic, inflammatory, and cardiovascular (CV) pathways, giving rise to the concept of the heart–gut axis. However, human evidence integrating microbiome-mediated mechanisms across the cardiometabolic spectrum remains incompletely synthesized. This focused systematic review aimed to synthesize the current human evidence on microbiome-mediated mechanisms linking metabolic syndrome (MS) and related metabolic phenotypes with cardiovascular risk (CVR) and subclinical cardiovascular (CV) outcomes within the conceptual framework of the heart–gut axis. Materials and Methods: A systematic literature search was conducted in PubMed, Scopus, Web of Science, and the Cochrane Library in accordance with PRISMA 2020 guidelines. Human observational and interventional studies evaluating gut microbiota composition, function, or microbiota-derived metabolites in relation to cardiometabolic, and CV outcomes were included. Risk of bias was assessed using the Cochrane RoB 2 and ROBINS-I tools, and findings were synthesized narratively. Results: Ten human studies published between 2016 and 2025 met the inclusion criteria. Across these studies, gut dysbiosis was consistently associated with adverse cardiometabolic risk profiles and subclinical CV outcomes, including insulin resistance, systemic inflammation, subclinical atherosclerosis, and CV prognosis in high-risk populations. Microbiota-derived metabolites, particularly trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), as well as emerging metabolites such as phenylacetylglutamine (PAGln) and imidazole propionate (ImP), were identified as key mediators linking metabolic syndrome and related metabolic disturbances with CVR and subclinical cardiovascular disease (CVD). Markers of intestinal barrier dysfunction and endotoxemia further supported the role of chronic low-grade inflammation within the heart–gut axis. Conclusions: Current human evidence supports the heart–gut axis as a biologically plausible and clinically relevant contributor to cardiometabolic disease. Gut microbiota-derived metabolites, intestinal barrier dysfunction, and systemic inflammation represent interconnected pathways linking MS with CVR. Advancing our understanding of these mechanisms may inform the development of microbiome-targeted strategies to complement established approaches for cardiometabolic and CV prevention.