It is hypothesized that the COVID-19 pandemic had a major impact on the epidemiology of malignant melanoma owing to diminished screening, diagnostic, and treatment capacities, resulting in a more advanced stage at initial presentation. The goal of this study is to undertake a systematic analysis of all epidemiological and clinical data on the trends and patient outcomes with malignant melanoma during the ongoing pandemic. Records were identified from PubMed, Cochrane, and Web of Science, selecting a total of 39 articles, narrative reviews, and editorial letters, following the PRISMA guidelines. The vast majority of the studies were published in Europe (28/39), and North America (7/39). A total of 99,860 patients were analyzed during 2020 and 2021 of the COVID-19 pandemic, and it was observed that malignant melanoma TNM staging increased significantly compared to the pre-pandemic period. Before the pandemic, 25.88% of patients had TNM stage II or above, compared to 36.25% during 2020–2021. During the COVID-19 pandemic, the malignant melanoma Breslow depth index grew from 1.59 mm before 2020 to 1.86 mm in 2020 and 2021. Patients decreased by 19.58% in 2020 and 2021 compared to pre-pandemic numbers. The patient–loss ratio indicated lower screening activity and patient addressability to dermatology and plastic surgery departments with skin cancer concerns during the COVID-19 pandemic. This systematic study shows that the identification and management of malignant melanoma during the COVID-19 pandemic faced major challenges which should alert medical systems to the high number of patients with advanced disease stages who may need emergency treatment and become incurable.

A high percentage of oncological patients die yearly because of colorectal cancer (CRC). Worldwide, CRC represents the fourth leading cause of death among oncological patients. Numerous studies have been conducted in order to identify new biomarkers for the early diagnosis of patients with CRC. From this point of view, an ideal biomarker is represented by the expression of microRNAs. In this paper, we wish to summarize the expressions of microRNAs in CRC and to present the pathophysiological and genetic interactions that microRNAs have with protein systems in these patients. For this paper, we looked into the studies available in scientific databases such as PubMed. For the search the following keywords have been used: "miRNAs expression", "colorectal cancer", "genetic polymorphisms in CRC", and "genetic biomarkers in CRC". Modifying the expression of microRNAs can be used successfully both in diagnosing patients with CRC and in following their response to chemotherapy. Numerous studies have shown high specificity for certain microRNA species in the case of CRC. An extraordinary advantage of these biomarkers is represented by their non-invasive sampling from urine and blood. Moreover, a series of connections of microRNAs in some mechanisms involved in the appearance and development of CRC have been shown. Therefore, microRNAs can be named as the biomarker of the future, as well as the epigenetic targeted treatment for patients with CRC. The expression of microRNAs can be successfully used in the evaluation and non-invasive monitoring of patients with CRC. However, further studies are needed regarding the expression of microRNAs and the connections these species have in the pathological mechanisms specific for CRC.

The high mortality risk in severe SARS-CoV-2 infections is tightly correlated to the extreme elevation of inflammatory markers. This acute accumulation of inflammatory proteins can be cleared using plasma exchange (TPE), commonly known as plasmapheresis, although the available data on performing TPE in COVID-19 patients is limited regarding the optimal treatment protocol. The purpose for this study was to examine the efficacy and outcomes of TPE based on different treatment methods. A thorough database search was performed to identify patients from the Intensive Care Unit (ICU) of the Clinical Hospital of Infectious Diseases and Pneumology between March 2020 and March 2022 with severe COVID-19 that underwent at least one session of TPE. A total of 65 patients satisfied the inclusion criteria and were eligible for TPE as a last resort therapy. Of these, 41 patients received 1 TPE session, 13 received 2 TPE sessions, and the remaining 11 received more than 2 TPE sessions. It was observed that IL-6, CRP, and ESR decreased significantly after all sessions were performed in all three groups, with the highest decrease of IL-6 in those who received >2 TPE sessions (from 305.5 pg/mL to 156.0 pg/mL). Interestingly, there was a significant increase in leucocyte levels after TPE, but there was no significant difference in MAP changes, SOFA score, APACHE 2 score, or the PaO2/FiO2 ratio. The ROX index was significantly higher among the patients who underwent more than two TPE sessions, with an average of 11.4, compared to 6.5 in group 1 and 7.4 in group 2, which increased significantly after TPE. Nevertheless, the mortality rate was very high (72.3%), and the Kaplan–Meier analysis identified no significant difference in survival according to the number of TPE sessions. TPE can be used as last resort salvage therapy that can be regarded as an alternative treatment method when the standard management of these patients fails. It significantly decreases the inflammatory status measured via IL-6, CRP, and WBC, as well as demonstrating an improvement of the clinical status measured via PaO2/FiO2, and duration of hospitalization. However, the survival rate does not seem to change with the number of TPE sessions. Based on the survival analysis, one session of TPE as last resort treatment in patients with severe COVID-19 proved to have the same effect as repeated TPE sessions of 2 or more.

Background and Objectives: Genitourinary syndrome of menopause (GSM) is a prevalent and distressing condition in postmenopausal women, often leading to sexual dysfunction characterized by vaginal dryness, pain, and reduced libido. While local estrogen therapy remains the standard treatment, due to safety concerns and contraindications, there is growing interest in the exploration of alternative interventions. This study aimed to compare the effectiveness and safety of intravaginal platelet-rich plasma (PRP) therapy versus local hormonal treatment in improving sexual function and vaginal health in postmenopausal women. Materials and Methods: A prospective, controlled clinical trial was conducted between January 2023 and December 2024 across three private gynecology clinics in Timișoara, Romania. Ninety postmenopausal women aged between 50 and 65 years with FSFI scores ≤ 23 were randomized into two groups: one receiving three monthly sessions of autologous PRP and the other undergoing 12 weeks of vaginal estriol therapy. Outcomes were assessed using validated tools—the Female Sexual Function Index (FSFI), the Vaginal Health Index (VHI), the Patient Global Impression of Improvement (PGI-I), and patient satisfaction scores—at baseline, week 6, and week 12. Results: Both of the treatment groups demonstrated significant improvements in FSFI and VHI scores at 12 weeks, with the PRP group showing a slightly higher, though not statistically significant, mean increase in the total FSFI (+10.1 vs. +9.3 points). Clinical gains were also observed in lubrication, elasticity, and dyspareunia. Patient satisfaction was high in both groups (93.3% PRP vs. 88.9% hormonal), and there were no reports of serious adverse events during the study period. The PRP group exhibited fewer side effects, without systemic symptoms, supporting its favorable safety profile. Conclusions: PRP therapy is a well-tolerated, hormone-free treatment that offers clinically meaningful improvements in sexual function and vaginal health, comparable to estrogen therapy. It may be particularly beneficial for women with contraindications to hormones or in advanced postmenopause. Further long-term studies are needed to confirm these findings and optimize treatment protocols.

Background/Objectives: Psoriatic disease is a systemic inflammatory condition associated with increased cardiometabolic risk, but the impact of contemporary systemic therapies and narrowband ultraviolet B (NB-UVB) phototherapy on vascular and systemic inflammatory markers remains incompletely characterized. We aimed to systematically synthesize prospective evidence on treatment-associated changes in vascular inflammation and systemic inflammatory biomarkers in adults with moderate-to-severe psoriatic disease. Specifically, we evaluated changes assessed by 18F-FDG PET/CT imaging and circulating biomarkers following biologic therapies or NB-UVB phototherapy. Methods: We systematically searched MEDLINE, Embase, Web of Science, Scopus, and CENTRAL from inception to 31 January 2026 for prospective interventional and observational studies in adults with psoriasis or psoriatic arthritis treated with biologic agents targeting TNF-α, IL-12/23, IL-17, or IL-23, or with NB-UVB phototherapy. Eligible studies were required to report serial assessments of vascular inflammation by 18F-FDG PET/CT (typically aortic target-to-background ratio) and/or systemic inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, TNF-α, GlycA, or hematologic indices such as the neutrophil-to-lymphocyte ratio) over at least 8 weeks of follow-up. We imposed no language restrictions and included only full-text, peer-reviewed prospective studies. Risk of bias was evaluated using RoB 2 for randomized trials and ROBINS-I for nonrandomized studies. Random-effects meta-analyses were prespecified for outcomes reported by at least two clinically comparable studies; however, because of substantial heterogeneity in reporting and methodology, effect estimates were summarized using a structured narrative synthesis. Results: Thirteen prospective studies (n ≈ 900 adults, published 2015–2025) met inclusion criteria, including four studies with serial 18F-FDG PET/CT imaging and one additional PET/CT study providing baseline observational data on vascular inflammation, as well as eight biomarker-focused prospective cohorts. Across randomized mechanistic trials and observational studies, biologic therapies reduced aortic target-to-background ratio by approximately 6–12% over 12–24 weeks (e.g., mean change from 2.42 to 2.18 with TNF-α inhibition and from 2.51 to 2.20 with IL-17 blockade), and no study reported worsening of PET-derived vascular indices under effective systemic treatment. Biologic and other systemic therapies produced concordant reductions in hs-CRP (typically by 30–50%), IL-6, TNF-α, GlycA, and blood-count-derived indices including neutrophil-to-lymphocyte ratio, with biomarker improvements frequently paralleling reductions in cutaneous disease activity and cardiometabolic risk markers. Two NB-UVB cohorts demonstrated significant hs-CRP reductions of roughly 20–30% and modulation of vitamin D-related inflammatory proteins, suggesting systemic anti-inflammatory effects, although these changes appeared less pronounced than with biologic therapy and were not accompanied by vascular imaging. Conclusions: Contemporary systemic psoriasis therapies, particularly biologic agents targeting the IL-23/Th17 axis and TNF-α, are associated with consistent reductions in aortic vascular inflammation and broad improvements in systemic inflammatory biomarkers, whereas NB-UVB phototherapy confers more modest but measurable systemic anti-inflammatory effects, although the current evidence does not allow differentiation between individual biologic classes in terms of magnitude of effect. Although reductions in vascular and systemic inflammatory markers were observed across therapies targeting TNF-α, IL-12/23, IL-17, and IL-23, the small number of mechanistic imaging studies and absence of head-to-head comparisons do not allow robust differentiation between biologic classes or support a uniform class effect. The convergence of imaging and biomarker data reinforces psoriasis as a clinically relevant model of inflammation-driven atherosclerosis and supports the concept that effective control of psoriatic inflammation may contribute to cardiovascular risk modification, highlighting the need for integrated cardiovascular risk assessment in routine care. However, the imaging evidence base remains limited to four small mechanistic PET/CT studies with relatively short follow-up, which constrains the strength and generalizability of conclusions regarding vascular inflammation. Larger, adequately powered, event-driven prospective trials with standardized imaging and biomarker endpoints are needed to determine whether these vascular and systemic anti-inflammatory effects translate into reduced cardiovascular events in psoriatic disease; because of methodological and reporting heterogeneity across the 13 included studies, these conclusions are based on a structured narrative synthesis rather than a formal quantitative meta-analysis. PROSPERO registration number: CRD420261296646.

Background/Objectives: Fetal telomere length (FTL) at birth is considered a key marker of early biological aging and future disease risk. While chronic inflammation is known to accelerate telomere attrition in adults, limited evidence exists on how maternal inflammation during pregnancy impacts FTL. This study aimed to investigate the association between maternal systemic inflammatory status in late pregnancy and FTL at birth. Methods: We conducted a prospective cohort study including 150 clinically healthy pregnant women recruited in the third trimester. Participants were stratified post hoc into an inflammation group (n = 67) and a control group (n = 83) based on circulating inflammatory markers: high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), TNF-α, and IL-10. Umbilical cord blood was collected at birth, and telomere length was quantified using real-time PCR. Correlation and multivariable linear regression analyses were performed to evaluate associations between maternal inflammation and FTL. Results: Mothers in the inflammation group had significantly elevated hsCRP, IL-6, and TNF-α levels, and lower IL-10 concentrations. FTL was significantly shorter in this group compared to the controls. Unlike previous investigations that relied on single pro-inflammatory markers, our study tests a composite immune-balance index (IL-6/IL-10 ratio) together with hsCRP in a prospectively followed cohort of clinically healthy pregnancies. Using its correlation coefficient, the IL-6/IL-10 ratio alone explained approximately 28% of the total variance in fetal telomere length—almost double the variance captured by IL-6 assessed in isolation. IL-6 and hsCRP emerged as independent negative predictors of FTL in multivariable models (β = −0.37 and −0.29, respectively). The IL-6/IL-10 ratio showed the strongest inverse correlation with FTL (r = −0.53, p < 0.001). Conclusions: Subclinical systemic inflammation in late pregnancy is independently associated with shorter fetal telomere length at birth, highlighting maternal immune imbalance (especially IL-6/IL-10 ratio) as a modifiable determinant of early biological aging. These findings underscore the need to consider maternal inflammatory profiling in pregnancy as a potential target for early-life preventive strategies.