Uric acid is the end product of purine metabolism and plays a dichotomous role in the human body. On one hand, it exerts antioxidant and neuroprotective effects; on the other hand, chronic hyperuricemia has been strongly associated with diseases beyond gout, affecting the cardiovascular, renal, metabolic, autoimmune, and central nervous systems (CNS). Excess uric acid promotes oxidative stress, endothelial damage, neurodegeneration, inflammasome activation, and impairs energy metabolism. It exacerbates autoimmune diseases, such as Systemic Lupus Erythematosus (SLE) and antiphospholipid syndrome (APS), by increasing inflammatory and oxidative damage, leading to greater end-organ damage. The British Society for Rheumatology, European League Against Rheumatism, American College of Rheumatology, and National Institute for Health and Care Excellence (NICE) have all established a “treat-to-target” approach for hyperuricemia with serum urate levels below 6 mg/dL and below 5 mg/dL in severe cases. Allopurinol and Febuxostat, xanthine oxidase inhibitors, are used as first-line pharmacological therapies for the treatment of hyperuricemia, whereas uricosurics and Interleukin-1 (IL-1) inhibitors are preferred in cases of refractory hyperuricemia. Lifestyle modifications, such as the Dietary Approaches to Stop Hypertension (DASH) diet, weight reduction, and smoking cessation, are also recommended for the long-term management of the disease. Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors, selective urate transport inhibitors, and plant-derived anti-inflammatory compounds have emerged as new treatments with promising responses. This review synthesizes the current literature on the multifaceted role of uric acid and emphasizes its systemic implications in chronic diseases. It also outlines the already established management options and new innovative therapies for managing this disease. Understanding this dichotomous role is essential for adopting a precise management approach that balances the protective and pathological effects of uric acid.
Epigenetic modifications, particularly aberrant DNA methylation, play an important role in the pathogenesis of both solid and hematologic malignancies. Global hypomethylation and promoter hypermethylation can silence numerous tumor suppressor genes identified in acute myeloid leukemia (AML) and myelodysplastic neoplasm (MDS). Among stemness-associated transcription factors, OCT-4 and SOX-2 are key regulators of pluripotency and stem cell maintenance and have been implicated in cancer stem cell biology and tumor progression. Although their abnormal expression and epigenetic regulation have been reported in various malignancies, limited data are available regarding their promoter methylation status specifically in AML and MDS. Therefore, this study aimed to evaluate the methylation patterns of the transcription factors, specifically OCT-4 and SOX-2, in patients with AML and MDS. The study involved 84 newly diagnosed AML and MDS patients and 16 age, and sex-matched healthy controls. DNA was extracted from blood or bone marrow using a QIAGEN RDNA extraction kit. The SOX-2 and OCT-4 genes were studied using PCR-specific primers for methylated and unmethylated targets. SOX-2 gene methylation was observed in a significantly higher proportion of AML (n=48/77) and MDS (n=4/7) as compared to Controls (n=3/16) (p<0.001). OCT-4 methylation was also observed in a significantly higher proportion of AML (n=44/77) as compared to MDS (n=3/7) and Controls (n=1/16) (p<0.001). Only a few cases in the AML group had both SOX-2 and OCT-4 gene methylation (n=25/77), compared with MDS (n=0/7) and Controls (n=0/16) (p<0.007). This study indicates that SOX-2 and OCT-4 gene methylation is significantly more prevalent in AML and MDS patients than healthy controls, suggesting their potential involvement in leukemogenesis. These findings highlight the potential role of methylation of stemness-associated transcription factors as a biomarker for disease characterization and identification of epigenetic therapeutic targets in AML and MDS.
Teledentistry has evolved from asynchronous communication to real-time consultations, with adoption accelerating during and post-COVID. Concurrently, AI has been leveraged to enhance diagnostic accuracy, efficiency, and accessibility using machine learning, GANs, and connected devices. This scoping review, conducted using Arksey and O'Malley framework and Joanna Briggs Institute guidance, explores the ethical, legal, and economic considerations of AI-driven teledentistry. Following a PRISMA-ScR compliant screening process by two independent reviewers, 137 studies published between 2018 and 2025 were included. Unlike previous reviews that have primarily focused on clinical applications or the general use of AI in healthcare, this review addresses the ethical, legal, and economic considerations of AI in teledentistry in a single paper. It underscores the importance of explainable AI, explores cross-border regulatory challenges, and discusses possible cost models for adoption in smaller practices. This review indicates that AI-powered teledentistry could enhance diagnostic accuracy, facilitate early detection, improve monitoring, and increase accessibility. Nonetheless, these advantages come with critical concerns including data privacy, potential biases, patient autonomy, accountability, and cost. Addressing these issues through governance, oversight, transparency, and economic viability is essential. AI-enabled teledentistry has the potential to transform dental care delivery, but its integration must be approached with careful consideration of its associated challenges.
CD36 functions as both a lipid transporter and scavenger receptor, integrating metabolic and inflammatory signaling pathways. It plays a critical role in maintaining cellular homeostasis and influencing disease progression. This review summarizes the structure, ligands, functions, regulation, and clinical implications of CD36 in renal and bladder cancer. Increased CD36 expression promotes enhanced fatty acid uptake, which supports tumor cell proliferation, migration and survival, by mediating metabolic reprogramming and interacting with the tumor microenvironment. In renal cancer, most frequently clear cell renal carcinoma (ccRCC), which has a typical metabolic phenotype, CD36 is involved in lipid accumulation and oxidative stress pathways. Pathogenic mechanisms include hypoxia-inducible factor (HIF)-driven pathways and carnitine palmitoyl transferase 1A (CPT1A) via the PPARα/CD36 axis, which phosphorylate Akt. By using fatty acid oxidation, CD36 lead to the production of reactive oxygen species and to transcription of genes mediating a pro-tumor function, inducing tumor-associated macrophages (TAM). In bladder cancer, CD36 is implicated in tumoral cells proliferation, survival, and adaptation to metabolic stress, epithelial-mesenchymal transition (EMT) and influences the tumor microenvironment, through interactions with tumor-associated macrophages and inflammatory signaling pathways. Although multiple studies propose CD36 as a prognostic biomarker, inconsistencies across cohorts limit its clinical translation. Notably, advances have revealed the regulatory networks governing distinct physiological properties of CD36, thereby identifying targeting CD36 as a potential strategy for cancer treatment. Inhibition of CD36-mediated lipid metabolism and signaling pathways may reduce tumor growth and metastatic potential. However, further research is necessary to clarify its context-dependent functions and to develop effective CD36-targeted therapies. To our knowledge, this is the first review to systematically examine the role of CD36 across both renal and bladder cancer. It could be the first step toward identifying new mechanisms mediated by CD36 in these malignancies.
Ischemic heart disease (IHD) remains the leading cause of cardiovascular mortality worldwide. Although age standardized death rates have declined over the past two decades, the absolute number of deaths continues to rise due to population growth and demographic aging. This Perspective examines the resulting paradox of progress, in which improving mortality rates coexist with an expanding global burden. Emerging evidence from recent global analyses highlights widening disparities across regions, sexes, and age groups. Global Burden of Disease (GBD) studies suggest an increasing burden of early onset IHD among adults aged 15 to 49 years, associated with rising incidence and prevalence, with notable regional variability and links to metabolic and dietary risks. While high income settings continue to achieve sustained mortality reductions, low- and middle-income regions face persistent gaps in prevention and care. These disparities reflect differences in health system capacity, including limited screening, delayed access to acute cardiac care, and suboptimal use of secondary prevention. Scalable strategies such as task-sharing and simplified treatment approaches offer practical solutions but remain underused. A strategic shift toward implementation, life-course prevention, and equity-focused policy reform is essential. Importantly, this perspective bridges the gap between epidemiological trends and health policy, linking epidemiologic trends to scalable implementation strategies for clinicians and policymakers to address the global burden of IHD.
Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of metformin therapy that most commonly occurs in the setting of acute kidney injury (AKI) and impaired drug clearance. Given the widespread use of metformin for type 2 diabetes mellitus, recognition of precipitating factors for MALA remains critically important. We report a case of severe euglycemic diabetic ketoacidosis (DKA) with refractory lactic acidosis in a patient with previously unrecognized obstructive uropathy due to recurrent nephrolithiasis causing bilateral hydronephrosis and severe AKI while on metformin therapy. The patient developed profound metabolic derangements that were unresponsive to conventional medical therapy, with resolution only after emergent hemodialysis. This case highlights the importance of early recognition of AKI from obstructive uropathy as a reversible precipitant of metformin accumulation and emphasizes the role of prompt renal replacement therapy in patients with severe MALA and refractory metabolic acidosis.
Diuretic resistance is a major therapeutic challenge in acute decompensated heart failure (ADHF). Acetazolamide, a carbonic anhydrase inhibitor, has emerged as a potential adjunct to conventional loop diuretics, as demonstrated in the ADVOR trial. We present a 74-year-old woman with acute coronary syndrome complicated by cardiogenic shock and refractory pulmonary edema despite inotropic support and guideline-directed therapy. The patient received intravenous acetazolamide 500 mg daily for three days, resulting in marked diuresis and radiographic resolution of pulmonary edema within 72 hours. The patient improved clinically. This case supports the potential utility of acetazolamide as an adjunctive strategy for overcoming diuretic resistance in ADHF.
Spina bifida is a neural tube defect (NTD) that arises when the neural tube fails to close properly during early development. This review focuses on myelomeningocele (MMC), the most common severe form of spina bifida, which often leads to motor and sensory impairments, including lower limb weakness or paralysis, as well as renal, urological, orthopedic, developmental, and psychosocial challenges. We explore the etiology, pathogenesis, prevention, diagnosis, and management of spina bifida, with a special emphasis on in-utero surgical repair. Over the past several decades, researchers and clinicians have made remarkable strides across all stages of care from prevention to postnatal outcomes. Widespread use of folic acid supplementation has significantly reduced the number of new cases. Advances in prenatal imaging and diagnostics now allow for earlier and more accurate detection, enabling timely intervention. In-utero surgical techniques continue to evolve, with innovative hybrid approaches that combine the strengths of open and minimally invasive methods. The momentum in this field shows no sign of slowing. Promising developments in stem cell therapy, biomaterials, robotic-assisted surgery, 3D printing, and enhanced imaging are redefining treatment goals in spina bifida. With each advance, clinicians gain better tools to improve outcomes for both mother and child, minimizing risks and maximizing long-term health and quality of life for both patients.
Cancer remains a leading cause of global mortality, with annual incidence projected to exceed 35 million cases by 2050. Modern antineoplastic therapies have improved survival outcomes at the risk of increasingly associated cardiovascular complications, collectively termed cancer therapy related cardiac dysfunction (CTRCD). Anthracyclines and HER2-targeted therapies remain the most well-characterized cardiotoxic agents. Anthracyclines cause irreversible, dose-dependent myocardial injury through mechanisms including oxidative stress, iron dysregulation, mitochondrial dysfunction, and topoisomerase IIβ inhibition, leading to progressive ventricular dysfunction and heart failure. HER2-directed therapies, such as trastuzumab, interfere with cardioprotective ErbB signaling, typically producing reversible cardiac impairment. Other oncologic treatments - including tyrosine kinase inhibitors, VEGF antagonists, and immune checkpoint inhibitors - contribute to hypertension, ischemic injury, and immune-mediated myocarditis. Newer modalities, such as proteasome inhibitors, histone deacetylase inhibitors, and CAR T-cell therapy, have expanded the spectrum of treatment-associated cardiotoxicity. Early CTRCD detection through multimodal strategies - including echocardiographic assessment with global longitudinal strain, cardiac magnetic resonance imaging, and serial measurement of troponins and natriuretic peptides - facilitates timely intervention. Risk stratification tools such as the HFA-ICOS score enable personalized monitoring and therapeutic planning. Preventive and management strategies incorporate cardioprotective agents like ACE inhibitors, β-blockers, dexrazoxane, and emerging therapies such as SGLT2 inhibitors. Modern cardio-oncology emphasizes a multidisciplinary, precision-based approach integrating early detection, genetic risk assessment, and targeted prophylaxis to preserve cardiac function while maintaining oncologic efficacy, thereby enhancing both survival and quality of life for cancer patients.
Herpes Zoster commonly involves thoracic and cranial dermatomal distributions. It is caused by reactivation of the latent varicella-zoster virus (VZV) due to immunosuppression or increasing age. However, uncommon regional presentation for shingles such as the palmar creases, may lead to a misdiagnosis. We report an unusual case of C7 dermatome presentation, prematurely mistaken as contact dermatitis or scabies due to lack of a clustered appearance. Prevention with vaccination is key and so is avoiding delays in diagnosis due to late complications that may arise.
Liver cirrhosis is increasingly recognized as a multisystemic disorder, profoundly impacting cardiac and renal function, giving rise to tightly coupled cirrhotic cardiomyopathy (CCM) and hepatorenal syndrome (HRS), and creating a vicious cycle of the hepato-cardio-renal axis. In this narrative review, we propose viewing CCM and HRS as triad dysfunction, driven by shared hemodynamic and molecular mechanisms linking portal hypertension, splanchnic vasodilation, hyperdynamic circulation, and systemic inflammation. We further synthesize the progression of intrahepatic resistance and splanchnic vasodilation to the hyperdynamic circuit, leading to triggers for CCM and HRS. Diagnostic biomarkers such as natriuretic peptides, troponins, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), along with emerging imaging techniques like artificial intelligence-cirrhosis-electrocardiogram (ACE), echocardiography, and point-of-care ultrasound (poCUS) are reviewed. We also discuss therapeutic horizons, while vasoconstrictors with albumin and diuretics remain crucial pharmacological care. Beyond drugs, transjugular intrahepatic portosystemic shunt (TIPS), liver transplantation, and lifestyle and nutritional modifications play a vital role. Persistent challenges arise due to constant reliance on the organ-centric approach, lack of true predictors of response, and risk of unmasking latent cardiac and renal vulnerability. Finally, future direction demands a paradigm shift to an integrated axis-aware, genetic, molecular, and cellular approach and the use of artificial intelligence to enable individualized risk stratification and improve long-term outcomes in cirrhotic patients with cardiorenal involvement.
IgG4-related disease is a systemic fibroinflammatory disorder characterized by its tumefactive lesions, elevated serum IgG4 levels, and unique histological findings such as lymphoplasmacytic infiltrates in a storiform pattern. It affects a wide variety of organ systems however, endocrinological manifestations remain uncommon and underdiagnosed due to nonspecific presentations. The thyroid and pituitary glands are the most commonly affected endocrinological organs, with the thyroid presenting as Riedel's thyroiditis or IgG4-related thyroiditis, and the pituitary involvement as hypophysitis. Symptoms could arise either due to direct organ infiltration or a decrease in hormone production and release. Diagnosing IgG4-related disease depends on serological, radiological, and histopathological findings. While immunosuppressive and biological agents are used for more severe or refractory cases, corticosteroids are the mainstay of treatment considering the autoimmune etiology of this disease. Early recognition of endocrinological involvement in IgG4-related disease is imperative for treating and preventing eventual irreversible glandular damage, highlighting the need for increased clinical awareness and multidisciplinary approaches amongst physicians. This review focuses on the endocrinological manifestations, clinical implications, and management strategies of IgG4-related disease.
The paradigm of dental medicine is shifting from a reactive surgical model to precision pediatric caries diagnostics, emphasizing early detection of pathogenic oral microbiota. Rapid point-of-care assays capable of identifying high-density Streptococcus mutans are critical to enable targeted intervention. This pilot study evaluated the diagnostic validity of a high- threshold monoclonal antibody-based lateral flow assay (Saliva-Check Mutans, SCM) relative to selective culture for identifying clinically meaningful S. mutans loads in children. Stimulated saliva samples were collected from 50 schoolchildren aged 9-13 years in Oaxaca, Mexico. Samples were analyzed using SCM and selective culture on Mitis Salivarius Agar (MSA), with presumptive S. mutans colonies confirmed biochemically. Selective culture identified 46% of participants as positive, whereas SCM detected 18% as positive. Relative to culture, SCM demonstrated 39.1% sensitivity (95% CI: 21.5%-60.1%), 100% specificity (95% CI: 87.5%-100%), and 100% positive predictive value (95% CI: 66.4%-100%), with no false positives observed. The results highlight the assay's rule-in capability for high-density pathogenic loads (>10^5 CFU/mL). The diagnostic discordance reflects divergent analytical thresholds, termed the "Threshold Gap". While SCM exhibits limited sensitivity for low-level colonization, its absolute specificity supports its use as a precision high-threshold triage tool, identifying pediatric patients with clinically significant S. mutans burdens who may benefit from intensified preventive strategies. Integration with culture or molecular approaches can enhance risk stratification and precision dentistry workflows.
Doxorubicin (DOX), an anthracycline antibiotic, is pivotal in managing osteosarcoma (OS). Although a cornerstone in the multimodal treatment regimen, its usage is limited by its associated toxicities, such as cardiotoxicity, myelosuppression, and neurotoxicity. This review provides an in-depth discussion of the emerging research aimed at enhancing the overall efficacy and mitigating the undesired side effects of DOX in treating OS. We explore the various drug delivery systems, including polymer-based injectable hydrogels, hydroxyapatite-based systems, and various nanoparticle-based systems such as calcium carbonate nanocrystals and cerium-substituted hydroxyapatite. We also discuss various innovative combination therapies, such as pegylated liposomal DOX with cisplatin and DOX with platinum nanoparticles. Moreover, emerging research into light-sensitive nano-micelles have been highlighted. These methods improve DOX's cytotoxicity and potentially reduce the need for high systemic doses and their associated side effects. The review aims to highlight the promising future in OS treatment by integrating these methodologies to maximize the therapeutic action of DOX and reduce its systemic side effects.
Preeclampsia remains a significant complication of pregnancy which emerges after the 20th week mark and is identified by proteinuria and hypertension. This review explores the multifaceted nature of preeclampsia, beginning with its complex pathology involving endothelial, platelet dysfunction and the imbalance in the factors that regulate angiogenesis. Diagnosis relies on monitoring blood pressure and assessing proteinuria, supported by laboratory tests and imaging studies to detect organ involvement. Biomarkers including Soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF) play a critical role in early detection and risk stratification. The imbalance in the ratio between these two biomarkers serves as a key in diagnosing and predicting preeclampsia. Vascular homeostasis is upset by this imbalance, which results in clinical symptoms such as hypertension and urinary protein excretion. Elevated sFlt-1 and reduced PlGF in high risk pregnancies, including those with chronic hypertension, correlate with greater clinical severity and predict adverse outcomes for maternal and fetal health. Management strategies include the use of antihypertensive medicines, fetal monitoring and delivery of the fetus based on disease severity. Despite ongoing research into predictive biomarkers and preventative measures, preeclampsia remains a challenge and necessitates a multidisciplinary approach for the well-being of both the fetus and the mother. This review serves as a comprehensive resource for clinicians and healthcare workers and by consolidating current knowledge and practical approaches allows them to stay updated on the evolving role of biomarkers in improving diagnostic accuracy.
Atrial fibrillation (AF) is the most common arrhythmia worldwide with treatments such as anticoagulants, rate control, and catheter ablation only aiming to reduce complications. Ischemic preconditioning (IPC), defined as brief cycles of ischemia followed by reperfusion, has emerged as a promising cardioprotective strategy. This review aims to provide a comprehensive review on and discuss recent trials surrounding the use of ischemic preconditioning as a promising therapeutic alternative in the treatment of atrial fibrillation. Clinical trials in both surgical and interventional settings have shown encouraging evidence that these protective mechanisms can lead to meaningful reductions in atrial arrhythmia. Despite these encouraging findings, heterogeneity persists likely due to differences in patient selection, anesthetic regimens, and the timing or protocols of preconditioning. The collective evidence highlights the therapeutic potential surrounding the use of ischemic preconditioning in atrial fibrillation. With recent trials on the rise, IPC's potential impact on rhythm control, pharmacologic responsiveness, cardioversion outcomes, and complication rates is highly promising for the treatment of atrial fibrillation. Further research is required to translate these findings into routine clinical practice, particularly in high-risk populations such as those with concurrent heart failure or structural heart disease.
Xanthogranulomatous pyelonephritis (XGP) is a rare inflammatory disease caused by chronic urinary tract obstruction or suppuration that occurs in the renal parenchyma. It results in an enlarged, nonfunctioning kidney with diffuse parenchymal damage due to obstructive renal calculi and granulomatous inflammation. Differentiating XGP from renal cell carcinoma, renal tuberculosis, and pyonephrosis can be challenging both clinically and radiologically; therefore, histological investigation after nephrectomy is typically used to confirm the diagnosis. We aimed to study the clinicopathological features of XGP cases confirmed by histopathological examination following surgery. This was a retrospective analysis conducted on 55 nephrectomy specimens diagnosed as XGP over a period of 6.25 years. Clinical details, laboratory and radiological findings were retrieved from the Hospital Information System. The gross and microscopic findings were reviewed. The study included 55 cases, ranging from 6 to 73 years (mean 38 ±18.3 years). The right kidney was involved in 45.5% of patients, and the left was affected in 54.5%. The most common presenting complaint was lumbar/flank pain, followed by recurrent urinary tract infection, fever, hydronephrosis, and an abdominal mass. Surgical interventions included simple nephrectomy (n=48), nephroureterectomy (n=4), radical nephrectomy (n=2), and partial nephrectomy (n=1). Renal/ureteric stones were identified in 49 cases. After histopathological analysis, 40 patients were diagnosed with pure XGPN, 7 with associated chronic pyelonephritis, 3 with hydronephrosis, 2 with pyonephrosis, 1 with nephrocutaneous fistula, 1 with high-grade urothelial carcinoma and 1 with serositis. A positive urine culture was noted in 13 cases. Histologically, all cases revealed sheets of foamy histiocytes, along with a few multinucleated giant cells and chronic inflammation. Cases with associated chronic pyelonephritis were characterised by periglomerular fibrosis, tubular atrophy, thyroidization, and interstitial fibrosis. XGP remains an important mimicker of renal malignancy, both clinically and radiologically. Accurate histopathological diagnosis is crucial to avoid overtreatment and ensure appropriate management. Increased awareness of its clinicopathological spectrum can aid in better diagnostic accuracy and reduce unnecessary radical surgeries.
Lymphatic filariasis, though often asymptomatic, remains a pervasive parasitic disease in endemic regions worldwide. The incidental identification of microfilariae on fine-needle aspiration cytology (FNAC) smears is rare and their coexistence with thyroid neoplasms is exceedingly uncommon. To our knowledge, very few cases of thyroid malignancy with coexistent microfilarial infestation have been documented. We describe a compelling case of a 68-year-old female who presented with a thyroid nodule and underwent FNAC. Cytological analysis revealed features diagnostic of a Hürthle cell neoplasm, accompanied by the unexpected presence of Wuchereria bancrofti microfilariae. Remarkably, the patient exhibited no clinical signs of filarial infection, and peripheral blood examination showed neither microfilaremia nor eosinophilia. This rare cytological finding underscores the diagnostic breadth of FNAC, not only in the evaluating thyroid pathology but also in revealing occult parasitic infestations. It highlights the necessity of meticulous smear evaluation, especially in patients from endemic regions presenting with chronic nodular lesions. The detection of neoplastic and parasitic elements together illustrates the complex interplay between infectious and neoplastic processes and reaffirms FNAC's utility in identifying unexpected pathological associations.
Ganaxolone, a neuroactive steroid that increases GABAergic inhibition, has been tested in many trials for the resolution of different epileptic disorders. Based on these, our study implemented a systematic review to evaluate the general benefit of ganaxolone for seizures. Pubmed, google scholar, European PubMed Central, Cochrane Library, and U.S. National Library of Medicine Clinical Trials were searched for relevant randomized controlled trials (RCTs) up to March 2023 and 12 RCTs were included in this review. We included 1337 patients from 12 RCTs to evaluate the efficacy and safety of ganaxolone. As results showed, across all trials, 26.3% of participants reported >50% reduction from baseline in seizure frequency. The analysis revealed that the nervous system was the most impacted, with dizziness, somnolence, headache, and seizures being the most frequently reported treatment-related adverse events (TRAEs). The results of these trials suggest that ganaxolone may be effective in reducing seizure frequency in patients with various types of epilepsy, including CDKL5 deficiency disorder, Lennox-Gastaut syndrome, and Protocadherin 19. However, further studies are needed to determine its safety and efficacy in a larger patient population.
Low-grade fibromyxoid sarcoma (LGFMS) is a rare fibroblastic neoplasm with an indolent clinical course. It is a distinctive subclass of soft tissue sarcoma with metastasizing potential and sometimes a long interval between tumor presentation and metastasis. This case report describes a 60-year-old female with an unresectable pleural LGFMS initially misdiagnosed as malignant mesothelioma. Pleural LGFMS remains exceedingly rare, with only four prior cases reported. Given its histologically benign appearance, LGFMS poses diagnostic challenges and risks of local recurrence or metastasis. This case underscores the importance of accurate diagnosis using MUC4 and it explores endocrine therapy as a promising palliative option for unresectable LGFMS, contributing valuable insights into management strategies for this rare entity.
