Acute pancreatitis (AP) presents clinicians with a fundamental challenge: while the majority of patients recover with minimal intervention, a significant minority deteriorate rapidly, developing organ failure and life-threatening complications. Early identification of high-risk patients remains one of the most clinically important and unresolved problems in AP management. This narrative review examines how biomarkers have evolved beyond their traditional diagnostic role to become integral to early risk stratification and therapeutic decision-making in patients with AP. We adopt a time-dependent, clinically integrated perspective to bridge the gap between pathophysiological insights and bedside practice. A structured search of PubMed and Embase databases was conducted covering publications from 1998 to 2025. Approximately 120 articles were screened, and 58 were selected based on relevance, methodological quality, and clinical applicability. Traditional markers (CRP, procalcitonin) retain meaningful prognostic utility but are constrained by delayed rises and limited specificity. Early cytokines — notably IL-6 and IL-15 — offer superior sensitivity within the first 24 h. Emerging biomarkers, including growth differentiation factor-15 (GDF-15) and pentraxin-3 (PTX-3), may outperform conventional scoring systems at admission. Biomarkers also inform therapeutic decisions in hypertriglyceridemia-associated AP, biliary AP requiring ERCP, and suspected infected pancreatic necrosis. A pragmatic, time-dependent integration of molecular biomarkers with clinical scoring systems offers the most realistic pathway toward personalized management of AP. The greatest clinical value of biomarkers lies in refining clinical judgment during the earliest and most critical phases of the disease.
Early detection of hepatocellular injury remains a significant clinical challenge due to the limitations of conventional biomarkers such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), which often rise only after substantial liver damage has occurred. α-Glutathione S-transferase (α-GST), a cytosolic enzyme highly expressed in hepatocytes, has emerged as a promising biomarker due to its rapid release and short plasma half-life, enabling earlier detection of liver injury. This study aimed to systematically review and synthesize clinical evidence on the diagnostic and prognostic utility of α-GST in detecting hepatocellular injury across various clinical contexts. A systematic literature review was conducted using major databases, including PubMed/MEDLINE, Scopus, Web of Science, Embase, and the Cochrane Library, covering studies published from 1988 to 2023. Eligible studies included human subjects with confirmed or suspected hepatocellular injury and reported α-GST measurements in serum or plasma alongside comparator biomarkers such as ALT and AST. Data were extracted and analyzed qualitatively due to heterogeneity in study design and outcomes. Evidence indicates that α-GST demonstrates superior temporal sensitivity compared to conventional aminotransferases, with earlier elevation in acute liver injury, ischemia–reperfusion injury, and drug-induced liver injury. It also detects subclinical hepatocellular damage in chronic liver diseases, including hepatitis C, even when ALT levels remain normal. Reported diagnostic performance shows sensitivity ranging from 78 to 92
Abstract Purpose Extraintestinal manifestations of inflammatory bowel disease (IBD) include anxiety and depression, with estimates varying across IBD types. We conducted a review and meta-analysis to estimate prevalence and incidence of anxiety and depression in IBD, compare psychiatric burden in Crohn’s disease (CD) and ulcerative colitis (UC), and identify heterogeneity. Methods MEDLINE (PubMed) and Embase were searched for anxiety/depression in IBD until May 2026. Random-effects meta-analyses calculated pooled prevalence/risk; heterogeneity was evaluated through Cochran’s Q, I², τ², and meta-regression. PROSPERO ID CRD420261297050. Results Twenty-two studies were included in the analysis. Thirteen studies ( n = 5,616) reported an anxiety prevalence of 24% (95% CI, 19–30%), and 15 studies ( n = 5,956) reported a depression prevalence of 24% (95% CI, 20–28%). Six cohort studies showed that IBD was associated with increased anxiety (HR 1.36, 95% CI, 1.17–1.59) and depression risk (HR 1.44, 95% CI, 1.35–1.54) versus non-IBD controls. No differences were observed between CD and UC for anxiety (OR 1.05, 95% CI, 0.64–1.73) or depression (OR 1.13, 95% CI, 0.86–1.48). Region explained heterogeneity, and instruments did not influence the estimates. The findings were robust, and no publication bias was identified. Conclusions One in four with inflammatory bowel disease (IBD) experiences anxiety or depression, and Crohn’s disease (CD) and ulcerative colitis (UC) burden suggest inflammation underlies this risk. Findings support assessment, clarify gut-brain links, and identify beneficiaries.
Pain in older adults is highly prevalent and persistently undertreated, and its management becomes substantially more hazardous when renal, hepatic, or respiratory failure co-exists. Age-related pharmacokinetic changes — reduced hepatic blood flow and cytochrome P450 activity, declining glomerular filtration, and altered body composition — are compounded by pharmacodynamic changes, including heightened central nervous system sensitivity and reduced homeostatic reserve. This narrative review synthesises contemporary evidence and current prescribing frameworks into an organ-failure-stratified approach to analgesic selection. Paracetamol and topical agents remain the safest first-line options across all three organ failure states. Non-steroidal anti-inflammatory drugs should be avoided when the estimated glomerular filtration rate falls below 30 mL/min and are contraindicated in cirrhosis. Opioids remain indispensable for moderate-to-severe pain but require dose reduction, interval extension, and close monitoring: fentanyl and buprenorphine are preferred in renal failure, whereas morphine, codeine, and meperidine should be avoided; all opioid doses must be reduced in hepatic failure; and in respiratory failure or chronic obstructive pulmonary disease opioids should be given at the lowest effective dose and never combined with other central nervous system depressants. Adjuvant analgesics carry agent-specific organ restrictions. Frailty, cognitive impairment, and polypharmacy further modify risk. ‘Start low, go slow’ must be calibrated individually to the type and severity of organ dysfunction present.
Inflammatory bowel disease (IBD) is a chronic, immune-mediated condition characterized by inherent immune dysregulation, which is further compounded by immunosuppressive therapies. Patients with IBD face a 1.5- to 1.7-fold elevated risk of herpes zoster (HZ), often at a younger age, with immunosuppression as the primary driver. Beyond increasing clinical burden, HZ leads to debilitating complications such as postherpetic neuralgia, profoundly diminishing quality of life. While anti-tumor necrosis factor (TNF) and Janus kinase (JAK) inhibitors are effective in controlling IBD inflammation, they concurrently elevate HZ risk—with JAK inhibitors exhibiting a dose-dependent effect via disruption of interferon signaling. Despite the availability of the recombinant zoster vaccine (RZV), which demonstrates robust immunogenicity and a favorable safety profile even in immunocompromised patients, vaccination uptake remains suboptimal. This narrative review examines the epidemiological characteristics, immunological pathogenesis, and therapy-specific risk factors of HZ in IBD. We analyze the differential impact of immunosuppressive therapies, evaluate RZV immunogenicity and safety, and synthesize current preventive strategies. Our aim is to provide a practical clinical framework to guide prevention and management of HZ in patients with IBD.
Lupus nephritis (LN) complicated by thrombotic microangiopathy (TMA) represents a severe renal phenotype characterized by immune-mediated inflammation and microvascular injury. S100 calcium-binding protein P (S100P) participates in inflammatory and stress-related signaling, providing a biological rationale for evaluating its potential as a circulating biomarker in LN-TMA. In this single-center longitudinal biomarker study nested within an observational cohort, 100 patients with systemic lupus erythematosus (SLE) and biopsy-confirmed proliferative LN (ISN/RPS class III or IV) with concomitant TMA were evaluated together with 50 age- and sex-matched healthy participants included for baseline biomarker comparison. Serum S100P was measured at baseline and at 6 and 12 months, and longitudinal changes were examined in relation to renal response, conventional laboratory parameters, SLEDAI-2 K, and renal histopathological indices. Baseline serum S100P was markedly higher in patients with LN-TMA than in healthy participants [median 21.3 (IQR 19.1–24.0) versus 0.1 (0.1–1.0) ng/mL; P < 0.001]. Baseline S100P was not significantly associated with SLEDAI-2 K or renal biopsy activity and chronicity indices. At 6 months, partial responders had lower S100P concentrations than nonresponders [8.5 (7.6–9.2) versus 12.4 (8.6–23.2) ng/mL; P = 0.004; AUC = 0.811]. At 12 months, complete responders had substantially lower concentrations than nonresponders [7.5 (6.7–8.4) versus 27.3 (24.3–29.3) ng/mL; P < 0.001; AUC = 0.967]. Longitudinal S100P changes were associated with changes in creatinine, lactate dehydrogenase, C3, and C4. In this single-center LN-TMA cohort, serum S100P was markedly elevated compared with healthy participants and declined substantially among patients achieving renal response. These findings support an association between longitudinal S100P changes and treatment response but do not establish disease specificity or pretreatment predictive value. S100P should therefore be considered a candidate complementary monitoring biomarker requiring validation in larger multicenter cohorts with appropriate disease-control groups.
A narrative review was presented, synthesizing existing literature on the historical understanding, neurobiological mechanisms, diagnostic approaches, and treatment modalities related to delirium. The purpose of this narrative review is to provide an updated overview of delirium, emphasizing its complex pathophysiology, clinical characteristics, risk factors, diagnostic challenges, and management strategies, particularly in patients with neurological disorders. Delirium predominantly occurs in hospitalized patients, especially those with pre-existing neurological conditions. Its pathogenesis is multifactorial, involving neuroinflammatory processes, neurotransmitter imbalances, and disruptions in neural connectivity. Clinically, it presents with acute onset of altered mental status, inattention, disorganized thinking, and fluctuating consciousness. Crucial risk factors include advanced age, cognitive impairment, polypharmacy, metabolic disturbances, and critical illness. Diagnosis remains challenging due to heterogeneous manifestations and symptom overlap with other disorders. Current diagnostic strategies integrate standardized screening tools, clinical assessment, and biomarker research. Management primarily targets underlying causes, supportive care optimization, and cautious pharmacological use. Delirium represents a multifaceted neuropsychiatric syndrome closely linked to neurological diseases and adverse patient outcomes. Persistent challenges in its prevention, diagnosis, and management highlight the need for a deeper understanding of its mechanistic pathways and risk factors to inform targeted therapeutic interventions and improve clinical outcomes.
Abstract Background Renal diseases are a major contributor to global morbidity and mortality. However, data describing their clinical spectrum and outcomes in Egypt remain limited. This study aimed to evaluate the burden, management, and outcomes of renal diseases among acutely admitted patients in a tertiary care setting. Methods A prospective observational clinical audit was conducted over six months (February–July 2024) in the internal medicine department at Cairo University Hospitals. All adult patients admitted through the emergency department were included. Patients were categorized into renal and non-renal groups. Data collected included demographics, comorbidities, laboratory and imaging findings, interventions, hospital stay, and outcomes. Statistical analysis included chi-square, t-tests, and multivariable logistic regression to identify predictors of mortality. Results A total of 202 patients were included (median age 54 years), with 52% classified as renal cases. Hypertension (55.9%), diabetes (37.1%), and pre-existing chronic kidney disease (22.8%) were highly prevalent. Among renal patients, acute kidney injury (AKI) was the leading cause of admission (37.1%). Hemodialysis was required in 40.9% of cases. Renal patients had longer hospital stays (mean 9.9 days) and significantly higher costs (median 895–5980 L.E.). Outcomes were less favorable: 37.1% improved, 27.6% progressed to CKD, 26.7% to end-stage renal disease (ESRD), and 8.6% required ICU admission. Mortality was 13.3%. Non-renal patients had better outcomes, with 91.8% improvement and lower resource utilization. Overall mortality was 11.4%. Advanced age and low serum bicarbonate were independent predictors of mortality. Conclusion Renal diseases constitute a substantial clinical and economic burden in hospitalized patients. Early detection, risk stratification, and optimized management strategies are essential to improve outcomes and reduce healthcare costs.
Abstract Background The severity of portal hypertension (PH) is central to risk stratification in chronic liver disease, yet transjugular HVPG testing is resource-intensive. EUS-guided portal pressure gradient (EUS-PPG) has emerged as an endoscopic alternative, but comparative agreement evidence has not been synthesized for severity classification. Methods We performed a systematic review and meta-analysis registered in PROSPERO [CRD420261325781]. MEDLINE (PubMed), Embase, Web of Science, Scopus, and Cochrane CENTRAL were searched from inception with citation searching. We identified 274 records, removed 104 duplicates, screened 170 titles/abstracts, assessed 20 full texts, and included 4 prospective, non-randomized paired comparative studies. Random-effects models were used. The primary outcome was quantitative agreement, assessed using correlation coefficients, intraclass correlation, and Bland–Altman metrics. Secondary outcomes included technical success and procedure-related adverse events. Risk of bias was assessed using ROBINS-I, and certainty of evidence was rated using GRADE. Results Four prospective, non-randomized comparative studies (73 enrolled participants; 69 paired measurements available for analysis) met the inclusion criteria. EUS-PPG showed a high pooled correlation with HVPG ( r = 0.82, 95% CI: 0.72–0.89; p < 0.00001; I² = 0%), with intraclass correlation coefficients ranging from 0.86 to 0.97 and minimal bias on Bland–Altman analysis. The classification accuracy for clinically significant portal hypertension (CSPH) was 100% in two studies. Technical success rates were equivalent (RR 1.00, 95% CI 0.93–1.07), and no significant safety differences were observed (RR 1.23, 95% CI 0.34–4.45). Subgroup analysis by etiology (cirrhosis vs. mixed/non-cirrhotic) showed no difference in agreement. The certainty of evidence was rated very low due to the study design and imprecision. Conclusions EUS-PPG strongly correlates with transjugular HVPG/TJ-PPG and appears to be as feasible and safe as the latter, according to limited comparative data. Until larger outcome-driven studies validate the threshold-based classification, EUS-PPG should be viewed as a complementary hemodynamic tool to inform selected clinical decisions rather than a universal replacement. Trial registration [ID: CRD420261325781].
Abstract Smoking remains one of the most serious public health concerns, increasing the risk of several diseases, including cardiovascular disease, stroke, chronic respiratory diseases, and cancer. Carbon monoxide (CO), a toxic byproduct of tobacco smoke, induces hypoxia and subsequently stimulates erythropoiesis as a compensatory response. Therefore, this study aimed to assess the hematological parameters of university students who smoke and elucidate the physiological impact of tobacco smoking for awareness efforts. Methods A total of 200 students and staff aged 19–30 years were recruited from the School of Allied Health Science at Badr University in Cairo (BUC) from July to September 2025. The participants were divided into a smoker group ( n = 100) and a nonsmoker control group ( n = 100). Complete blood count (CBC), ferritin level as an acute-phase reactant protein, and erythrocyte sedimentation rate (ESR) were measured, and the results were compared between the groups. Results A highly statistically significant difference was found between smokers and nonsmokers in hemoglobin (Hb) and ferritin levels, mean corpuscular volume (MCV), and red blood cell (RBC), white blood cell (WBC), and platelet (PLT) counts. Smokers exhibited significantly higher Hb and ferritin concentrations, MCV, and RBC and WBC counts (all p < 0.001). Conversely, the median platelet count was significantly lower in smokers than in nonsmokers (221 × 103/µl vs 269 × 103/µl; p < 0.001), while ESR results showed no significant differences between groups. Conclusion Smoking was associated with significant alterations in the hematological profile and iron metabolism among university students. These findings provide potential insights for clinical practitioners to consider smoking status when interpreting routine hematological parameters. Moreover, the inclusion of hematological health education during awareness may support early smoking cessation initiatives targeting young adults.
Heparin, a widely utilized anticoagulant in hemodialysis (HD), is known to sometimes trigger the release of heparin-platelet factor 4 (HPF4) antibodies. These antibodies have been implicated in the development of heparin-induced thrombocytopenia (HIT) and thrombotic complications. To detect the prevalence and diagnostic performance of HPF4 antibodies in chronic kidney disease (CKD) patients undergoing HD and their association with thrombocytopenia and thrombosis, to be used as a marker of hypercoagulability during HD. This cross-sectional study comprised 80 pediatric patients with chronic kidney disease divided into two groups: Group A included patients on maintenance hemodialysis, while Group B included patients on conservative treatment. ELISA was used for determination of HPF4 antibodies. Prevalence of HPF4 antibodies in group A patients was 72.5
Autoimmune polyglandular syndromes (APS) comprise a heterogeneous group of disorders characterized by the coexistence of multiple autoimmune endocrine diseases and, frequently, additional non-endocrine autoimmune manifestations. Adult-onset APS (types 2–4) often evolves over years through sequential glandular involvement, creating a prolonged preclinical phase during which predictive biomarkers may facilitate earlier recognition and individualized surveillance. This narrative review examines the immunogenetic mechanisms underlying adult APS, evaluates the diagnostic and predictive roles of autoantibodies, and discusses emerging risk-stratified screening considerations. The review was informed by a targeted PubMed literature search of English-language publications, with emphasis on recent clinical guidelines, systematic reviews, cohort studies, landmark investigations, and key original studies relevant to adult APS, immunogenetics, autoantibody biomarkers, and screening strategies. Current evidence indicates that organ-specific autoantibodies are among the earliest detectable markers of endocrine autoimmunity and may precede clinical disease by several years. Among the available biomarkers, 21-hydroxylase autoantibodies remain the most informative marker of autoimmune adrenal insufficiency, while glutamic acid decarboxylase (GAD65) and thyroid peroxidase antibodies contribute to identifying individuals at increased risk of autoimmune diabetes and thyroid disease. Multiplex autoantibody platforms further demonstrate the potential to integrate multiple biomarkers within a single assay, supporting comprehensive immunological profiling and future risk-stratified surveillance. However, evidence supporting routine predictive screening in adults remains limited by the absence of validated risk models, standardized surveillance intervals, and prospective outcome studies. Current evidence supports targeted, phenotype-guided surveillance in selected high-risk adults rather than universal screening. Emerging multiplex autoantibody approaches may enhance individualized risk stratification and targeted monitoring but require prospective validation, cost-effectiveness evaluation, and standardized implementation before broad clinical adoption.
METS-IR and SIRI associations with RCC remain observational. Diagnostic intensity and repeat-attendance selection may influence estimates. Trajectory findings do not establish reversibility of RCC risk.
Ebola Virus Disease (EVD) remains among the most lethal zoonotic hemorrhagic fevers, with case fatality rates (CFRs) of 25
Vitamin B12 deficiency is traditionally recognized through megaloblastic anemia, yet accumulating evidence shows a broad spectrum of non‑hematological manifestations and clinically relevant associations with elevated serum B12. Understanding these dimensions is essential for timely diagnosis and rational management across diverse populations. To synthesize current evidence on the non‑hematological clinical manifestations, diagnostic challenges, and management implications of Vitamin B12 deficiency and excess, with emphasis on high‑risk groups and emerging therapeutic approaches. A narrative review of human studies was conducted using PubMed, MEDLINE, Embase, Cochrane CENTRAL, Web of Science, Scopus, and Google Scholar from 1950 to 2024, supplemented by guideline documents and reference snowballing. Eligible publications examined non‑hematological outcomes or diagnostic and therapeutic aspects of vitamin B12 status; data were synthesized qualitatively with critical appraisal of study quality. Vitamin B12 deficiency is linked to neurological, cognitive, psychiatric, cardiovascular, reproductive, renal, dermatological, and oncologic manifestations that may occur in the absence of anemia. Functional deficiency often arises despite serum Vitamin B12 concentrations within the conventional reference range, making methylmalonic acid, homocysteine, and holotranscobalamin valuable adjunctive biomarkers, although interpretation is influenced by renal function and assay availability. High‑dose oral supplementation is generally non‑inferior to intramuscular therapy for correcting biochemical deficiency, while severe neuropsychiatric presentations and malabsorptive states frequently warrant parenteral regimens. Persistent hypervitaminemia B12 more commonly reflects underlying systemic disease—such as malignancy, liver or kidney dysfunction—than true toxicity, underscoring the need for etiological investigation rather than dose reduction alone. Elderly individuals, vegetarians/vegans, pregnant women, and post‑bariatric surgery patients constitute key risk groups requiring proactive screening and long‑term follow‑up. Vitamin B12 imbalance extends far beyond hematological abnormalities and should be considered in a wide range of neuropsychiatric, cardiometabolic, reproductive, and systemic presentations. Integrating functional biomarkers into diagnostic algorithms, individualizing replacement strategies, and prioritizing high‑risk populations may improve outcomes and align clinical practice with emerging evidence. Future research should focus on standardized diagnostic thresholds, long‑term neurocognitive and cardiovascular endpoints, and pharmacogenomic and novel delivery strategies to support precision supplementation.
Acute kidney injury (AKI) refers to a condition in which the kidneys abruptly lose their ability to effectively filter waste products from the bloodstream. This work aimed to assess the dynamic changes in platelet count of intensive care unit (ICU) admission and determine their correlation with ICU mortality. This prospective cohort study involved 150 adult patients aged 18 years or older who were admitted to ICU with a confirmed diagnosis of sepsis and had available serial platelet measurements from Day 0 to Day 2. All patients underwent a comprehensive baseline assessment, baseline laboratory investigations. Platelet decline showed a strong and consistent association with AKI development. Lower platelet counts from Day 1 to Day 2 significantly increased the odds of AKI, with the most predictive parameter being Platelet Day 2 (OR = 0.984, 95
Abstract Background Current evidence regarding the efficacy of desmopressin in combination therapy for nocturnal polyuria (NP) in elderly patients remains limited. This meta-analysis aimed to evaluate the efficacy and safety of desmopressin combined with different medications for treating NP in the elderly population. Methods A systematic search was conducted across CNKI, PubMed, the Cochrane Library, Scopus, Web of Science, Wanfang Data, and VIP databases for randomized controlled trials (RCTs) published up to February 2025 that evaluated desmopressin-based combination therapy in participants with a mean age ≥ 55 years and a primary diagnosis of nocturnal polyuria. This study adhered rigorously to the PRISMA guidelines. The quality of the studies included in the review was assessed. Data on therapeutic effectiveness and the incidence of adverse events were extracted and analyzed. Results Two studies involving a total of 133 elderly patients (72 in the combination therapy group and 61 in the monotherapy group) were included. The results indicated that desmopressin tablets combined with other drugs significantly reduced nocturnal voiding frequency ( P = 0.002) and nocturnal urine volume ( P < 0.0001) compared to monotherapy with an α-blocker or tolterodine. No significant increase in adverse events was observed in the combination therapy group. Conclusion This meta-analysis provides the first comprehensive evaluation of desmopressin combination therapy for nocturnal polyuria, confirming its potential efficacy, particularly in the 60–70 age group. However, given the limited data, these findings are preliminary and require validation in larger, well-designed multicenter RCTs with standardized outcome definitions.
Abstract Objective Drug-induced liver injury (DILI) is a significant global health concern, and herbal medicines are increasingly being used to treat herb-induced liver injury (HILI). Withania somnifera ( Ashwagandha ), which is widely used for its health benefits, has been associated with emerging cases of liver toxicity. This systematic review synthesizes the literature regarding the clinical presentation, diagnostic findings, treatment strategies, and outcomes of Ashwagandha -induced liver injury. Methods A systematic search of PubMed, Medline, Google Scholar, ScienceDirect, and Web of Science was conducted following PRISMA guidelines. Case reports and series documenting Ashwagandha -associated liver injury were included. The extracted data included patient demographics, symptoms, liver function tests, imaging findings, treatment interventions, and outcomes. The Joanna Briggs Institute critical appraisal tool was used to assess the quality of the included reports. Results The analysis was performed on 19 studies involving 26 patients. The mean age was 37.8 ± 15.1 years, with 53.9% of patients being male. The most reported symptoms were jaundice (88.5%) and pruritus (72.9%). Liver injury manifests as hepatocellular, cholestatic, or mixed patterns, with elevated bilirubin, AST, and ALT levels. Most cases demonstrate probable or possible causality on the basis of RUCAM scores (Roussel Uclaf Causality Assessment Method). Discontinuation of Ashwagandha led to recovery in most cases, although severe cases required intensive care or liver transplantation. Conclusion Despite its apparent safety, Ashwagandha can cause liver damage and injury. These findings underscore the importance of vigilant clinical assessment, early recognition, and prompt discontinuation of the supplement in suspected cases.
The gut microbiome has long been recognized as a critical regulator of host metabolism, yet the fungal component the mycobiome remains comparatively understudied. Emerging evidence implicates gut fungi in endocrine and metabolic homeostasis through distinct mechanisms including bile acid modification, immune modulation, and cross-kingdom interactions with bacteria. This narrative review synthesizes current evidence on the role of the gut mycobiome in obesity, insulin resistance (IR), and polyendocrine metabolic ovarian syndrome (PMOS), with emphasis on mechanistic pathways, clinical implications, and therapeutic potential. The healthy gut mycobiome is characterized by dominance of Candida, Saccharomyces, Cladosporium, and Malassezia genera, though considerable variability exists based on geography, diet, age, and sex. Fungal dysbiosis typically manifesting as reduced diversity and overgrowth of pro-inflammatory taxa such as Candida albicans has been consistently documented in obesity, IR, and PMOS. Mechanistically, fungi influence host metabolism through: (1) production of bioactive metabolites (short-chain fatty acids, tryptophan derivatives); (2) modulation of bile acid pools and farnesoid X receptor (FXR) signaling; (3) immune priming via β-glucan-mediated Th17 responses; and (4) regulation of gut barrier integrity through fungal-bacterial crosstalk. In PMOS specifically, mycobiome alterations correlate with hyperandrogenemia, insulin resistance, and chronic inflammation, with emerging evidence implicating the gut-brain-ovary axis. Therapeutic strategies under investigation include probiofungals (Saccharomyces boulardii), dietary modulation, and selective antifungal interventions. The gut mycobiome represents a novel, modifiable determinant of metabolic health with particular relevance to obesity, IR, and PMOS. Future research priorities include longitudinal cohort studies, mechanistic validation in gnotobiotic models, and randomized controlled trials of mycobiome-targeted interventions. Integration of mycobiome assessment into clinical practice may enable personalized approaches to metabolic disease management.
