424 General Military Hospital

Reverse total shoulder arthroplasty (rTSA), once reserved for elderly low-demand patients, is increasingly used in younger adults despite concerns regarding complication rates and longevity. This systematic review and meta-analysis evaluate contemporary evidence on primary rTSA in patients aged ≤65 years. Following Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines, PubMed, Scopus, and CENTRAL databases were searched to October 2025. Studies reporting outcomes of primary rTSA in patients ≤65 years with ≥2 years of follow-up were included. Data on indications, functional outcomes, range of motion (ROM), patient-reported outcome measures (PROMs), complications, revisions, and implant survival were recorded and synthesized. Subgroup analyses based on patients' age and comparisons with older rTSA cohorts were also performed. Thirteen studies met our inclusion criteria. Cuff tear arthropathy (27.29%), massive cuff tears (23.39%), and glenohumeral osteoarthritis (22.34%) accounted for most indications. rTSA resulted in significant improvements in ROM and all major PROMs. The overall complication rate was 14.23%, and the revision rate was 2.92%, with instability and infection responsible for 64.2% of revisions. Mid- to long-term implant survival exceeded 85%. When compared with older patients, younger adults demonstrated equivalent ROM outcomes. Concerning PROMs younger patients demonstrated inferior American Shoulder and Elbow Surgeons (mean difference [MD] = -6.43, P = .01), visual analog scale (MD = 0.93, P < .01), Constant score (MD = -4.98, P < .01), University of California Los Angeles (MD = -2.07, P < .01), and Shoulder Pain and Disability Index (MD = 13.56, P < .01), whereas Simple Shoulder Test (MD = -0.7, P = .19) did not differ between the 2 groups. Moreover, younger patients presented a higher revision risk (risk ratio [RR] = 2.21, P < .01). Primary rTSA provides substantial and predictable improvements in pain and shoulder function among young adults, with acceptable early- to mid-term durability. Nevertheless, younger age remains associated with higher revision risk and modestly lower subjective outcomes, likely reflecting greater functional demands and post-operative expectations. These findings highlight the importance of nuanced surgical decision-making and patient counseling as rTSA use continues to expand in this demographic.

Background and Objectives: De Quervain tenosynovitis (DQT) is a stenosing overuse condition of the synovial sheath of the first extensor compartment of the wrist. Open surgical release of the first dorsal compartment remains a standard intervention for DQT when conservative treatments fail. This systematic review evaluated the comparative efficacy of transverse versus longitudinal skin incisions for open release of the first dorsal compartment in DQT. Materials and Methods: Four studies with 259 patients were included in the review. Data from 17 patients were unavailable due to loss to follow-up; therefore, 243 wrists (242 patients) were included in the quantitative analysis. The transverse incision group consisted of 114 cases, and the longitudinal incision group of 129 cases. The primary outcome of the review was the incision-related incidence of injuries to adjacent anatomical structures, including injuries to the superficial branch of the radial nerve (SBRN), tendon injuries, and vein injuries. Secondary outcomes included hypertrophic scar formation, wound infection, and postoperative changes in pain severity measured using a visual analog scale (VAS). Results: Although there was a lower rate of SBRN injury in the longitudinal group (5.4% vs. 7% in the transverse group), the difference did not meet statistical significance (OR = 2.17; 95% CI, 0.39-11.99; p = 0.37; I2 = 30%). Similarly, there was no significant difference in the risk of vein injury (RD = 0.06; 95% CI, -0.03 to 0.14; p = 0.21; I2 = 61%), hypertrophic scar formation (OR = 1.39; 95% CI, 0.32 to 6.04; p = 0.66; I2 = 35%), and wound infection (RD = 0.00; 95% CI, -0.03 to 0.03; p = 0.93; I2 = 0%). Although both approaches resulted in significant pain improvement, no statistically significant difference in postoperative pain was observed between incision types, as assessed by the VAS for pain (mean difference = 0.30; 95% CI, -0.70 to 1.30; p = 0.56; I2 = 43%). Conclusions: No significant differences were identified between incision techniques for DQT in terms of complication rates and postoperative pain outcomes. However, the available evidence is limited, and future high-quality trials are necessary to determine any clinically meaningful difference. Therefore, incision selection should be individualized based on surgeon preference, patient-specific anatomy, and procedural complexity. Despite the technique used, meticulous surgical technique is essential to prevent postoperative complications.

Immune checkpoint inhibitors (ICIs) have revolutionized cancer management, leading to unprecedented improvements in clinical outcomes. Several adverse events from ICIs have been documented, but the risk and clinical relevance of bone adverse events (BAEs) remain uncertain. Sporadic reports describe inflammatory cytokine upregulation, osteoporosis onset during ICI treatment, and increased risk of fragility fractures. In this review, original articles written in English and published up to June 2025, were identified in PubMed, Scopus, and WOS databases by using pre-selected keywords. Based on pre-defined inclusion/exclusion criteria, 23 articles were included in the final analysis. As BAEs, we considered the following conditions: fractures, osteoporosis, osteopenia, bone pain, altered bone metabolism markers. Overall, we found 1610 cancer patients developing at least one BAE, whose percentage was highly variable among studies (range 0.3-88.9%), reflecting the differences in study design, patient enrollment, and BAE recording. Median age was > 55 years, and BAEs were reported in patients with various primary solid tumors, most commonly lung cancer patients (10/23 studies), mainly treated with programmed cell death protein-1 (PD-1)/PD-1 ligand (PD-L1) inhibitors. However, several limitations of the studies emerged from the analysis and are highlighted in the manuscript. In conclusion, BAEs may occur more frequently among patients treated with ICIs but are likely to be underreported in most studies. Further investigation is needed to estimate and mitigate the risk of such events, since diagnostic techniques and anti-osteoporotic drugs are widely available in the clinical practice. A research agenda focusing on higher-quality reporting of BAEs from ICIs is warranted.

This study evaluates changes in cellular immunity components, from chronic kidney disease stage V (CKD-V) to long-term transplantation (lKTx). We applied flow cytometry to determine total, CD4+, CD8+, CD28− T-lymphocytes, Natural killer cells (NK) and regulatory T-lymphocytes (Tregs), in peripheral blood of 56 patients with CKD-V, 207 patients on hemodialysis (HD), 149 recently transplanted (rKTx), 26 lKTx patients and 49 healthy volunteers as a control group (CG). Lymphocyte proportion decreased in CKD vs. CG [20.2 (14.4–25.8) vs. 29.7 (24.4–38.1)%, p < 0.001] without further deterioration in HD [19.9 (15.3–23.7)%, p = 0.83 vs. CKD-V] and increased in rKTx [24.7 (20–32.6)%, p < 0.001 vs. HD], and lKTx [25.5 (21.9–35)%, p = 0.16 vs. CG]. Similar kinetics were observed in CD4+ subpopulations, however CD8+ T-cells gradually increased from CG to lKTx. NK remained stable in CKD-V and HD, reduced in rKTx, and marginally increased in lKTx. Tregs gradually declined until HD and suboptimally improved with transplantation. CD28− subpopulations largely increased in lKTx, compared with HD [CD4+CD28−: 12.6 (4.7–27.6) vs. 6 (2.1–13.2)%, p = 0.006, CD8+CD28−: 68.4 (54.4–90.3) vs. 45.5 (28.4–58.9)%, p < 0.001], independently of age for CD8+CD28− (p = 0.33). Cellular immunity subpopulations show significant changes in the spectrum of CKD, with transplantation restoring total lymphocytes and CD4+ T-cells, but not Tregs and NK. LKTx was associated with a large increase in CD28− subpopulations.

BACKGROUNDMassive rotator cuff tears (RCTs) result in impaired shoulder function and quality of life. These tears lead to structural changes in the rotator cuff muscles, which compromise recovery after repair and increase re-tear rates.AIMTo investigate the potential inhibitory effects of alpha-tocopherol (vitamin E) and OTR-4131 on muscle atrophy, fatty infiltration, and fibrosis in rotator cuff muscles following a massive RCT using a Wistar rat model, and establish a standardized methodology for evaluating potential therapeutic agents.METHODSThis protocol outlines a controlled animal study using 40 male Wistar rats, randomized into five groups. The experimental groups will receive either systemic administration of alpha-tocopherol or local administration of OTR-4131 via intramuscular injection into the supraspinatus and infraspinatus muscles. Two sham groups will receive systemic and local saline injections respectively, while a control group will undergo no intervention. The interventions will be administered after surgical transection of the supraspinatus and infraspinatus tendons. Outcomes will be assessed via wet muscle weight measurements, muscle fiber diameter, fatty infiltration percentage, and fibrosis evaluation using histological methods.RESULTSThe study anticipates that alpha-tocopherol and OTR-4131 will reduce muscle atrophy, fatty infiltration, and fibrosis compared to control and sham groups, supporting their potential protective role in rotator cuff muscle degeneration.CONCLUSIONThe results are expected to improve the understanding on the role of alpha-tocopherol and OTR-4131 in rotator cuff muscle protection after massive RCT and may serve as a foundation for further preclinical and clinical research aimed at improving rotator cuff repair outcomes.

A DEA approach for evaluating the efficiency

Abstract Background and Aims Systemic lupus erythematosus (SLE), as a multifaceted autoimmune disease, is characterized by significant alterations in adaptive immunity. T follicular helper (TFH) cells are specialized to select high-affinity B cells in germinal centers. As their role in peripheral circulation is still unknown, we aimed to investigate the interaction between peripheral B and TFH cells in patients with SLE Method In this cross-sectional study, flow cytometry was performed estimate B lymphocytes and their subpopulations, IgD+CD27−, IgD+CD27+, IgD−CD27+, IgD−CD27−, in 63 patients with SLE and 48 healthy controls (HC), and results were correlated with peripheral TF cells, and their subtypes, TFH1, TFH2, TFH17, TF regulatory (TFR) and TF cells expressing ICOS (TFICOS). SLE patients were classified as active and non-active disease based on systemic lupus erythematosus disease activity index 2000 (SLEDAI-2K). Results Patients with SLE (Male/Female 5/58, Age = 39 ± 13.5 yrs, 50/63 with lupus nephritis) compared to healthy Controls (HC), had significantly increased levels of neutrophils, 4728 (3200) vs. 3400 (1100)/μL, P &amp;lt; 0.001 and neutrophil/lymphocyte ratio 3.08 (3.7) vs. 1.9 (1.2), P &amp;lt; 0.001, reduced Lymphocytes 1537 (871) vs. 2000 (1000)/μL, P &amp;lt; 0.001, CD19 78.5 (144) vs. 186 (100) P &amp;lt; 0.001 and their subtypes IgD+CD27−, IgD+CD27+, IgD−CD27+, IgD−CD27− [39 (101) vs. 107 (76) P = &amp;lt;0.001, 4.3 (9.1) vs. 17 (27) &amp;lt;0.001, 15.7 (18) vs. 26 (44) &amp;lt;0.001, 10.7 (20) vs. 19 (23) 0.003 respectively). TFH1 and TFICOS proportion predominated in SLE patients (P = 0.005, P = 0.02) as well as the ratio of TFH1/TFH2 (P = 0.008). There were no significant differences in B lymphocytes between patients with active (n = 32) and non-active (n = 31) disease, although a substantial redistribution of B cell subpopulations included increase in IgD−-CD27− cells. In non-active SLE patients (SLEDAI-2K ≤4) strong correlations were evident between TF with CD19, IgD+CD27−, IgD+CD27+, IgD−CD27+ and IgD−CD27− (r = 0.6, P = 0.04; r = 0.6, P = 0.04; r = 0.6, P = 0.02; r = 0.7, P = 0.003, respectively). Moreover, IgD−CD27+ cells also correlated with TFH1, TFH2, TFH17 (r = 0.7, P = 0.01; r = 0.7, P = 0.01; r = 0.6, P = 0.02, respectively). No such correlations were evident in the active SLE group (SLEDAI-2K &amp;gt;4). Conclusion Immune alterations still exist in non-active SLE, including redistribution of B lymphocyte subtypes and their significant cross talk with peripheral TF cells, which may act as a memory reservoir to sustain B lymphocytes activation.

ObjectivePostsurgical chronic hypoparathyroidism (HypoPT) has been linked to an increased cardiovascular risk, but the underlying pathophysiological mechanisms remain incompletely understood. Emerging evidence suggests a potential direct role of parathyroid hormone (PTH) in modulating platelet function and oxidative stress, both contributors to atherothrombosis.Our study aimed to investigate the impact of PTH on platelet function and activation, with a particular focus on NOX2-mediated platelet activation in patients with HypoPT.MethodsWe conducted a cross-sectional study involving 24 patients with HypoPT and 40 age- and sex-matched healthy controls. Clinical, biochemical, and platelet function parameters were assessed. In a subgroup of five HypoPT patients, changes were evaluated after 24 months of PTH (1–34) therapy. Platelet aggregation, oxidative stress biomarkers (sNOX2-dp, H2O2, 8-OHdG), and thrombus formation (T-TAS) were measured. The in vitro effect of PTH (1–34) was tested on isolated platelets.ResultsPatients with HypoPT exhibited enhanced platelet activation, increased oxidative stress, and accelerated thrombus formation compared to controls. Enhanced platelet activation and increased oxidative stress observed in HypoPT were further amplified in HypoPT subjects treated with PTH (1–34). In vitro, PTH (1–34) increased oxidative stress and platelet aggregation only in platelets from HypoPT patients, through a specific signaling pathway involving PTH1R activation, intracellular calcium release, protein kinase C (PKC) activation and NOX2-dependent ROS generation.ConclusionHypoPT is associated with heightened platelet reactivity and thrombotic risk. PTH therapy may exacerbate these alterations through a defined molecular mechanism. These findings highlight the need for careful cardiovascular monitoring in HypoPT patients, particularly those receiving PTH analogues.