Prakash V. A. K. Ramdass

Background: Irritable bowel syndrome (IBS) and gallbladder disease share overlapping symptoms that may contribute to diagnostic uncertainty and unnecessary cholecystectomy. This systematic review and meta-analysis evaluated whether patients with IBS are more likely to undergo cholecystectomy than those without IBS. Methods: A systematic search of PubMed, Embase, Web of Science, and Google Scholar was conducted through June 3, 2026. Observational studies comparing cholecystectomy among adults with and without IBS were included. Random-effects meta-analysis was performed to calculate pooled odds ratios (ORs) with 95% confidence intervals (CIs). Subgroup analyses, sensitivity analyses, influence diagnostics, meta-regression, publication bias assessment, and risk-of-bias evaluation were conducted. Results: Ten studies met the inclusion criteria for the systematic review, and nine studies comprising 181,848 participants and 6,249 cholecystectomy events were included in the meta-analysis. Patients with IBS had significantly higher odds of undergoing cholecystectomy than controls (OR = 2.57, 95% CI 1.36–4.85; p = 0.009). Between-study heterogeneity was substantial (I ² = 98.1%), but the association remained robust across leave-one-out sensitivity analyses. Subgroup analyses and meta-regression demonstrated that study design, geographic region, IBS diagnostic criteria, study quality, and sample size did not significantly influence the pooled effect estimate. No evidence of publication bias was detected, and the included studies were generally of good methodological quality. Conclusions: Patients with IBS have significantly higher odds of undergoing cholecystectomy than individuals without IBS. These findings support careful evaluation of biliary symptoms in patients with IBS to improve diagnostic accuracy, optimize patient selection for surgery, and reduce unnecessary cholecystectomy. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420261412571 , identifier CRD420261412571.

Background: Fusobacterium nucleatum , an oral-associated bacterium implicated in several extraoral diseases, has recently been proposed as a potential contributor to endometriosis through microbial translocation, inflammation, and fibrosis. However, the consistency and clinical significance of this association remain uncertain. This systematic review evaluated the human and experimental evidence linking F. nucleatum with endometriosis and assessed the plausibility of a proposed oral microbe-host axis. Methods: PubMed/MEDLINE, Embase, Web of Science, and Google Scholar were searched from inception through August 31, 2026, following PRISMA 2020 guidelines. Human and animal studies reporting F. nucleatum or historically related F. nucleatum -complex taxa in relation to endometriosis were included. Risk of bias was assessed using a prespecified adapted ROBINS-I framework for human observational studies and SYRCLE for animal studies. Owing to substantial heterogeneity in anatomical compartments, detection methods, and outcomes, meta-analysis was not appropriate and findings were synthesized qualitatively. Results: Four human studies encompassing 384 participants at the study level were included, although analysis-specific denominators varied. Direct tissue evidence came from two studies and was conflicting: Muraoka et al. reported Fusobacterium positivity in 64.3% of endometrial samples from women with endometriosis versus 7.1% of controls in a 42-versus-42 tissue subset, whereas Graciano-España et al. found no significant case-control difference in F. nucleatum abundance among 55 cases and 37 controls. Indirect microbiome studies reported oral Fusobacterium enrichment in moderate/severe endometriosis and vaginal F. animalis depletion in chronic pelvic pain with endometriosis. All human studies were judged at serious overall risk of bias, and certainty of evidence was very low. Experimental evidence suggesting TGF-β-mediated lesion growth and fibrosis derived principally from one translational study and lacked independent replication. Conclusions: Current evidence supports biological plausibility but not a consistent or causal association between F. nucleatum and endometriosis. Direct tissue evidence is limited to two conflicting studies, while non-tissue microbiome findings are indirect. Standardized contamination-controlled sampling, paired anatomical-site sampling, strain-level analyses, and longitudinal studies are required before microbial translocation, temporality, causality, or antimicrobial treatment can be established. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420261337885 .

Endometriosis and irritable bowel syndrome (IBS) are chronic pain disorders that frequently coexist and share key pathophysiological features, including neuroinflammation, visceral hypersensitivity, peripheral sensitization, and central sensitization. Emerging evidence suggests that extracellular adenosine triphosphate (ATP)-mediated activation of the P2X3 receptor is a common mechanism driving persistent nociceptive signaling in both conditions. This narrative review examines the role of ATP–P2X3 signaling in the pathogenesis of endometriosis and IBS, highlighting its involvement in neuroimmune crosstalk, dorsal root ganglion plasticity, and cross-organ sensitization. We summarize experimental and clinical evidence supporting P2X3 as a therapeutic target and discuss the development of selective P2X3 antagonists, including gefapixant, eliapixant, sivopixant, and camlipixant. Although these agents have shown clinical benefit in refractory chronic cough, their application to endometriosis and IBS remains largely unexplored. Current evidence is predominantly preclinical, underscoring the need for biomarker-driven translational studies and clinical trials. Overall, ATP–P2X3 signaling represents a promising shared mechanistic pathway linking endometriosis and IBS and a potential target for the development of precision, nonopioid therapies for chronic pelvic and visceral pain.

Background: Irritable bowel syndrome (IBS) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are chronic, debilitating disorders characterized by substantial symptom burden, impaired quality of life, and high healthcare utilization. IBS is a disorder of gut–brain interaction with a global prevalence ranging from 3.8% to 9.2%, while ME/CFS is defined by persistent, exertion-intolerant fatigue and multisystem dysfunction. Growing evidence suggests frequent co-occurrence of these conditions, implicating shared mechanisms such as immune dysregulation, autonomic imbalance, and altered gut–brain signaling. However, the magnitude of their association has not been comprehensively quantified. Methods: We conducted a systematic review and meta-analysis by searching Embase, PubMed, Scopus, and Google Scholar databases from inception through February 2026. Eligible observational studies reporting associations or prevalence between IBS and ME/CFS were included. Random-effects meta-analyses were performed to pool odds ratios (ORs) and prevalence estimates. Heterogeneity was assessed using I ² statistics. We evaluated for publication bias and assessed for risk of bias. Results: Twenty-two studies were included in the systematic review and 18 in the meta-analysis. Individuals with ME/CFS had significantly higher odds of IBS compared with controls (OR = 7.20; 95% CI: 2.77–18.76; I ² = 72.1%). The pooled prevalence of IBS among individuals with ME/CFS was 37% (95% CI: 23–54%), with substantial heterogeneity (I ² = 99.5%). Subgroup analysis revealed that diagnostic criteria significantly influenced prevalence ( p < 0.0001), while meta-regression identified ME/CFS diagnostic criteria as a significant moderator. Conclusion: IBS and ME/CFS are strongly associated, suggesting shared underlying mechanisms. These findings support integrated screening approaches and coordinated, multidisciplinary management to improve outcomes in affected patients. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251006255 .

Objectives: Medical errors are a leading cause of preventable harm worldwide and disproportionately affect women and racial minorities. However, evidence regarding racial disparities in medical errors among women remains inconsistent, and it is unclear whether disparities reflect differences in overall error rates or differences in specific types of errors. This study aimed to quantify racial disparities in medical errors among Black and White women receiving medical care. Methods: A systematic review and meta-analysis was conducted following PRISMA guidelines. EMBASE, PubMed, Google Scholar, ScienceDirect, and Web of Science were searched for peer-reviewed studies examining racial disparities in medical errors among women. Random-effects meta-analyses were performed in RStudio to calculate pooled odds ratios (ORs) and 95% CIs. Results: Thirteen studies involving 3,608,296 women were included in the systematic review, and 11 studies were included in the meta-analysis. Overall, Black women had higher odds of experiencing medical errors compared with White women; however, the association was not statistically significant (OR=1.18, 95% CI: 0.68-2.06). Subgroup analyses demonstrated that patient safety events were significantly more common among Black women (OR=1.19, 95% CI: 1.02-1.39), whereas diagnostic and human errors showed no significant racial differences. Further analysis revealed a significant difference between underdiagnosis in Black women and overdiagnosis in White women. Conclusions: Although overall medical error rates did not differ significantly between Black and White women, Black women were more likely to experience underdiagnosis and patient safety events, whereas overdiagnosis was more frequently observed among White women.

Background/Objectives: Cholecystectomy, the surgical removal of the gallbladder, is one of the most commonly performed abdominal surgical procedures worldwide. Emerging evidence suggests that cholecystectomy may contribute to the development of irritable bowel syndrome (IBS). However, the association remains incompletely understood. This systematic review and meta-analysis aimed to evaluate the relationship between cholecystectomy and IBS. Methods: A systematic search of PubMed, Embase, Scopus, and Web of Science was conducted from database inception to March 2026. Meta-analyses were performed to pool odds ratios (ORs) and prevalence estimates. Heterogeneity, publication bias, and sensitivity analyses were assessed. Results: Seventeen studies involving 3,511,681 participants were included in the systematic review. Eight studies were eligible for the meta-analysis of the association between cholecystectomy and IBS, while twelve studies contributed to the prevalence analysis. No statistically significant difference in the odds of IBS was observed between patients who underwent cholecystectomy and controls (OR = 2.46, 95% CI: 0.97–6.22; p = 0.056; I² = 91.7%). The pooled prevalence of IBS in post-cholecystectomy patients was 21.0% (95% CI: 9.0–42.0), with high heterogeneity (I² ≈ 99%). Sensitivity analyses did not alter the direction of the pooled estimates following sequential omission of individual studies, and no significant publication bias was detected. Conclusions: No statistically significant difference in the pooled odds of IBS was observed between groups, while the pooled prevalence among cholecystectomy patients was approximately 21%, although heterogeneity was substantial. Further research is needed on heterogeneity.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide and is linked to dyslipidemia and cardiometabolic dysfunction. The non-HDL cholesterol to HDL cholesterol ratio (NHHR) has emerged as a composite lipid biomarker that reflects the balance between atherogenic and anti-atherogenic lipoproteins and may have utility in MASLD risk stratification. However, the strength and consistency of the association between NHHR and MASLD remain uncertain. This systematic review and meta-analysis aimed to synthesize the available evidence regarding the association between NHHR and MASLD and evaluate its diagnostic performance. A systematic search of PubMed, Embase, and Google Scholar was conducted from database inception through January 2026 in accordance with PRISMA guidelines. Original human studies evaluating the relationship between NHHR and MASLD were included. Random-effects meta-analyses were performed to calculate pooled standardized mean differences (SMDs) in NHHR between individuals with and without MASLD, pooled odds ratios (ORs) for MASLD according to NHHR levels, and pooled area under the receiver operating characteristic curve (AUC) to evaluate diagnostic performance. Study quality was assessed using the Newcastle-Ottawa Scale. Twenty-four studies were included in the systematic review, and 19 studies comprising 120,985 participants were included in the quantitative synthesis. Individuals with MASLD had significantly higher NHHR values than controls (pooled SMD = 1.01, 95% CI: 0.17-1.84; p = 0.018). Higher NHHR levels were associated with increased odds of MASLD (pooled OR = 1.56, 95% CI: 1.25-1.96; p < 0.001). A clear dose-response relationship was observed, with progressively greater odds of MASLD across increasing NHHR categories: OR = 1.60 (95% CI: 1.21-2.13) for Q2/T2 versus Q1/T1, OR = 1.87 (95% CI: 1.67-2.09) for Q3 versus Q1, and OR = 2.19 (95% CI: 1.77-2.70) for Q4/T3 versus Q1/T1. Twelve studies evaluating diagnostic accuracy demonstrated a pooled AUC of 0.73 (95% CI: 0.70-0.75), indicating moderate discriminatory ability of NHHR for identifying MASLD. NHHR is significantly associated with MASLD and demonstrates a graded relationship with disease association, whereby higher NHHR levels correspond to progressively greater odds of MASLD. Furthermore, NHHR exhibits moderate diagnostic accuracy for identifying MASLD. As a simple, inexpensive, and widely available metric derived from routine lipid testing, NHHR may serve as a practical adjunctive biomarker for MASLD risk stratification and may help identify individuals who could benefit from further evaluation.

Hantaviruses are emerging rodent-borne pathogens that pose increasing global public health concerns due to their association with hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), both of which can result in substantial morbidity and mortality. Environmental change, climate variability, urbanization, and land-use transformation are increasingly recognized as critical drivers of hantavirus emergence and transmission. This review summarizes current evidence regarding hantavirus virology, epidemiology, pathogenesis, clinical manifestations, diagnostics, surveillance systems, prevention strategies, and One Health preparedness approaches. Emphasis is placed on the influence of climate change and ecological disruption on rodent reservoir dynamics and spillover risk, as well as major surveillance and diagnostic gaps in tropical and Caribbean regions where hantavirus circulation may be underrecognized. Advances in molecular diagnostics, genomic surveillance, vaccine development, monoclonal antibody therapies, and climate-based early warning systems are also discussed. Existing evidence highlights the importance of integrated One Health surveillance systems that combine human, animal, and environmental monitoring to improve early detection and outbreak preparedness. Strengthening laboratory capacity, ecological surveillance, regional collaboration, and public health infrastructure will be essential for reducing the global burden of hantavirus infections and improving preparedness for future zoonotic disease threats.

Hantaviruses are emerging rodent-borne pathogens that pose increasing global public health concerns due to their association with hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), both of which can result in substantial morbidity and mortality. Environmental change, climate variability, urbanization, and land-use transformation are increasingly recognized as critical drivers of hantavirus emergence and transmission. This review summarizes current evidence regarding hantavirus virology, epidemiology, pathogenesis, clinical manifestations, diagnostics, surveillance systems, prevention strategies, and One Health preparedness approaches. Emphasis is placed on the influence of climate change and ecological disruption on rodent reservoir dynamics and spillover risk, as well as major surveillance and diagnostic gaps in tropical and Caribbean regions where hantavirus circulation may be underrecognized. Advances in molecular diagnostics, genomic surveillance, vaccine development, monoclonal antibody therapies, and climate-based early warning systems are also discussed. Existing evidence highlights the importance of integrated One Health surveillance systems that combine human, animal, and environmental monitoring to improve early detection and outbreak preparedness. Strengthening laboratory capacity, ecological surveillance, regional collaboration, and public health infrastructure will be essential for reducing the global burden of hantavirus infections and improving preparedness for future zoonotic disease threats.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine–metabolic disorder affecting 5.5–11.5% of women of reproductive age. While reduced adiponectin levels have been consistently demonstrated in adult women with PCOS, findings in adolescents remain less clearly defined. A systematic review and meta-analysis was conducted in accordance with PRISMA guidelines. PubMed, Embase, Scopus, and Google Scholar were searched from inception to 31 October 2025. Observational studies comparing adiponectin levels in post-pubertal adolescents with PCOS and controls were included. Data were pooled using random-effects meta-analysis in RStudio, with subgroup, sensitivity, heterogeneity, and publication bias analyses conducted. Eighteen studies comprising 1590 participants were analyzed. The pooled analysis demonstrated significantly lower adiponectin levels in adolescents with PCOS compared to controls (mean difference [MD]: −3.19 µg/mL; 95% CI: −4.90 to −1.49; p = 0.0010), with substantial heterogeneity (I² > 90%). Subgroup analyses by diagnostic criteria, geographic region, study design, and weight status consistently showed reduced adiponectin levels in PCOS, with no significant subgroup differences. In conclusion, adolescents with PCOS exhibit significantly lower adiponectin levels, consistent with findings in adult populations. These results support an early association between adiponectin dysregulation and PCOS, although further longitudinal studies are needed to clarify clinical utility.