Purpose: To evaluate the sentinel lymph node (SLN) protocol for staging endometrial carcinomas, assessing its impact on surgical management, and determining indications for adjuvant therapies. The study also examines factors that may influence SNL mapping, particularly focusing on the failure of the technique due to obesity. Methods: A retrospective analysis was conducted on the medical records of patients with a histological diagnosis of endometrial carcinoma, who underwent surgical staging with SLN biopsy. The lymph node status was compared between non-obese (group 1) and obese (group 2) patients. Results: 71 women were included in the study, of which 33 were non-obese (46.5%) and 38 were obese (53.5%). The failure detection rate was higher in obese patients (14, 36.8%) compared to non-obese patients (5, 15.2%) (p = 0.039). The risk of mapping failure increased by 1.6 times for every 5-unit increase in body mass index (BMI) (OR 1.672, 95% CI 1.024–2.730, p = 0.040). BMI was confirmed as an independent risk factor for mapping failure in both univariate (OR 3.267, 95% CI 1.027–10.395, p = 0.045) and multivariate analyses (OR 5.779, 95% CI 1.320–25.297, p = 0.020). Conclusion: SLN detection in obese patients requires great care, as obesity may alter the sensitivity of the technique.
Systemic sclerosis (SSc) is a complex autoimmune disease characterized by vasculopathy and tissue fibrosis affecting the skin and internal organs. Genetic and environmental factors influence susceptibility, severity, and onset. Current treatments are limited and not always effective, leading researchers to investigate new approaches, such as the use of adipose-derived mesenchymal stem cells (ADSCs) through fat grafting. This review seeks to understand how ADSCs may impact the development and progression of SSc, with a particular focus on how these cells could alter immune responses and reduce fibrosis. ADSCs have been found to affect various immune cells, including T cells, B cells, macrophages, and dendritic cells, by releasing cytokines, chemokines, and growth factors. These interactions generally suppress inflammation and promote a regulatory immune environment. Additionally, ADSCs can influence the extracellular matrix, helping to prevent fibrosis through signaling molecules like exosomes. ADSCs show promise as a treatment for SSc due to their ability to modulate the immune system and reduce fibrosis. Early clinical studies are encouraging, but more research is needed to fully understand how they work and to develop effective treatment protocols.
Background: Platelets have conventionally been viewed as cellular fragments crucial for hemostasis; nonetheless, their extensive secretome of cytokines and growth factors has been increasingly acknowledged as a significant regulator of inflammation and tissue healing at the ocular surface. Aims: The objective of this narrative review is to synthesize existing knowledge of platelet biology with new findings about the therapeutic use of platelet-derived products in dry eye disease (DED). Methods: A qualitative review of the PubMed, Scopus, and Web of Science databases up to June 2025 identified preclinical, translational, and clinical studies assessing platelet-rich plasma (PRP), plasma rich in growth factors (PRGF), platelet lysate, and autologous serum tears for dry eye disease (DED) and associated ocular surface disorders. Results: Platelet-derived formulations have exhibited reliable immunomodulatory and regenerative effects by diminishing inflammatory signaling, lowering cytokine expression, and facilitating epithelial and neurotrophic restoration. Clinical investigations have indicated enhancements in tear film stability, corneal staining, and patient-reported symptoms, especially in cases of moderate-to-severe or refractory illness. Nonetheless, methodological diversity, inconsistent preparation techniques, and restricted sample sizes have impeded comparability among experiments. Conclusions: Platelet-derived treatments constitute a biologically viable and clinically promising strategy for the management of dry eye disease (DED). Future research must emphasize the standardization of preparation protocols, the identification of predictive biomarkers such as transforming growth factor-β1 (TGF-β1), nerve growth factor (NGF), and matrix metalloproteinase-9 (MMP-9), as well as the design of multicenter randomized controlled trials to guarantee reproducible, GMP-compliant clinical applications.
Urothelial carcinoma predominantly affects older patients, who often exhibit frailty, comorbidities, renal impairment, and reduced physiological reserve. We evaluated overall survival (OS) and progression-free survival (PFS) with first-line immune-based strategies in patients aged ≥65 years with advanced or metastatic urothelial carcinoma. The aim was to characterize treatment effects within this age-defined subgroup, not to determine whether age modifies treatment efficacy compared with younger patients. Methods: We conducted a systematic review and meta-analysis of phase 3 randomized trials published from January 2015 to May 2026 reporting age-specific survival outcomes. Combination regimens were compared with platinum-based chemotherapy using random-effects models. Results: Combination strategies improved OS versus chemotherapy (HR 0.79, 95% CI 0.64–0.96), although heterogeneity was substantial (I2 = 69.7%) and the prediction interval crossed the null (0.48–1.27). Class-specific HRs were 0.56 (95% CI 0.26–1.20) for ADC plus ICI, 0.85 (0.77–0.95) for ICI plus chemotherapy, and 0.91 (0.34–2.42) for dual-checkpoint inhibition. PFS favoured experimental treatment but remained imprecise (HR 0.54, 95% CI 0.27–1.08; I2 = 89.5%). Excluding ADC plus ICI trials attenuated the OS effect (HR 0.88, 95% CI 0.80–0.96), indicating that the pooled estimate was influenced by these trials. ICI monotherapy did not improve OS. Conclusions: First-line immune-based combinations improved survival in selected patients aged ≥65 years, but benefit varied across treatment classes and should not be considered uniform across regimens. These findings do not establish whether age modifies treatment efficacy. Age-specific safety data were insufficient to define the benefit–risk profile of individual strategies.