Citations

Abstract Background Streptococcus agalactiae (group B Streptococcus [GBS]) may cause pneumonia or may colonize the respiratory tract, making its clinical significance uncertain when detected in respiratory specimens. This study aimed to assess whether clinicians interpreted GBS detected by the BIOFIRE Pneumonia Panel (BF-PP) as a pathogen implicated in pneumonia. Methods This retrospective cohort study included adult patients hospitalized with suspected pneumonia at Mayo Clinic, Rochester, between September 2020 and February 2025. Cases were independently classified into pathogen and nonpathogen groups by 2 infectious diseases (ID) specialists, with a third reviewer resolving disagreements. Clinical characteristics and outcomes of both groups were recorded. A subgroup analysis of patients who had an ID consultation was performed. Results A total of 109 cases were included. GBS was considered a pneumonia pathogen in 47.7% of cases and a nonpathogen in 52.3%. ID consultation was performed in 33.0% of cases, with GBS considered a pathogen in 30.6% of those. Common comorbid conditions included pulmonary, gastrointestinal, neurologic, and cardiovascular disease and obesity. Rates of endotracheal intubation were similar in the pathogen and nonpathogen groups (51.9% vs 50.9%, respectively), with the in-hospital mortality rate being numerically but not significantly higher in the former versus the latter (21.2% vs 14.0%; P = .33); findings were similar in the ID-assessed subgroup. In 76.1% of GBS detections, other microorganisms—most commonly Staphylococcus aureus—were codetected. Only 10.2% of BF-PP GBS-positive specimens were culture positive for GBS. Conclusions While GBS is not an uncommon pneumonia pathogen, the clinical significance of its detection by BF-PP is uncertain in many cases.

Proper organization of the enteric nervous system (ENS) is critical for normal gastrointestinal (GI) physiology. Inflammatory bowel disease (IBD) disrupts key GI functions, including bowel motility. However, in many IBD patients, motility disorders persist even during remission, suggesting an irreversible ENS defect secondary to IBD. Here, we show that postinflammatory GI motility dysfunction arises from structural remodeling of the ENS, driven by a combination of neuronal loss and neurogenesis. During mucosal inflammation, enteric neurons upregulate CCL2 expression, facilitating the recruitment of monocytes into the myenteric plexus within the intestinal muscle. Monocyte-derived macrophages infiltrate the myenteric ganglia, contributing to excessive ENS remodeling and postinflammatory motility dysfunction. This neuroimmune axis is counterbalanced by a hypoxia-induced stress response in enteric neurons mediated by HIF1α. Enhancing the neuron-intrinsic hypoxia pathway limits ENS remodeling and preserves motility. In summary, this study presents a mechanistic model of postinflammatory GI motility dysfunction and proposes a therapeutic strategy to maintain ENS integrity and function during inflammation.

Background: Splanchnic venous thrombosis (SVT) is a potentially severe and frequently underdiagnosed complication following splenectomy in patients with hematologic diseases. Despite its clinical importance, no standardized, evidence-based guidelines currently exist to inform perioperative prevention, diagnosis, or treatment in this population. Materials and Methods: A systematic review and meta-analysis were conducted following PRISMA guidelines to estimate the incidence and risk factors for SVT after splenectomy in patients with hematologic diseases. Twenty-eight observational studies comprising 5025 patients were included. Risk factor data were analyzed using random-effects models. In parallel, an international Delphi consensus process was performed involving 35 experts (hematologists and surgeons) from 14 countries. Experts were assigned to five domain-specific groups and developed clinical statements on prophylaxis, diagnosis, and management of SVT. Consensus was defined as ≥80% agreement, and recommendations were graded using the GRADE framework. Results: The pooled incidence of SVT after splenectomy was 11.4%, with higher rates in studies using routine imaging (20.7%) and those conducted at single centers (15.1%). Splenic size and weight were significant risk factors, while age, BMI, and platelet count were not. Disease-specific risk was highest in patients with myeloproliferative neoplasms, lymphoma, and thalassemia. The Delphi process generated 25 consensus statements, 14 of which were classified as strong recommendations. Key guidance included perioperative vaccination, individualized thromboprophylaxis with BMI-adjusted low molecular weight heparin, selective Doppler-based screening in high-risk patients, and stepwise anticoagulation regimens based on thrombus burden and clinical evolution. Conclusion: This study presents the first international consensus-based guidelines for managing SVT after splenectomy in patients with hematologic disease. Developed through systematic evidence synthesis and expert consensus, these recommendations provide a practical framework rather than definitive standards of care and support individualized prevention, detection, and treatment strategies in this high-risk population.

Abstract Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are increasingly used for weight management and cardiometabolic health. Common peroneal neuropathy (CPN) associated with rapid weight loss is attributed to adipose tissue reduction and subsequent nerve compression at the fibular head. Cases of “Slimmer’s Palsy” have been described in conditions involving rapid weight loss, including anorexia, malignancy, and post-biliary surgery, yet it remains underrecognized as a potential complication of GLP-1RA therapy. This case report describes two nondiabetic patients who developed acute foot drop after losing 14% and 18% of their total body weight over 3–6 months of semaglutide and tirzepatide use, respectively. As use of GLP-1RAs continues to rise, peripheral nerve surgeons should be aware of Slimmer's Palsy as a predictable and treatable complication of rapid weight loss and be prepared to intervene before permanent denervation occurs.

Introduction Hypergranulation tissue (excess granulation tissue) is a common complication following penile inversion vaginoplasty (PIV). It often requires repeated treatment with silver nitrate using a speculum to access the neovagina. This study evaluates whether adding betamethasone suppositories to silver nitrate treatment improves the resolution of hypergranulation tissue after PIV. Methods A retrospective chart review was conducted on patients who received supplemental betamethasone suppositories in addition to silver nitrate treatment (betamethasone group) between 01/2023 and 12/2024 and matched to a cohort of patients treated with silver nitrate alone (silver nitrate group). Outcomes, number of treatments, and severity of hypergranulation tissue were compared using t tests for continuous variables and Fisher's exact tests for categorical variables. Results There were 16 patients in each group, with similar average follow-up times: 8.5 ± 5.5 months (silver nitrate group) and 7.8 ± 4.7 months (betamethasone group) ( P = 0.70). At the most recent follow-up, moderate and severe hypergranulation resolved more often in the betamethasone group (86%, 50%) than in the silver nitrate group (60%, 25%). Patients in the betamethasone group with moderate or severe hypergranulation tissue required fewer median treatments for resolution (2 vs 3.5 and 4 vs 5, respectively). After excluding cases that required cauterization under anesthesia, patients in the betamethasone group were significantly more likely to have resolution of their hypergranulation tissue compared to patients in the silver nitrate group ( P = 0.035). Conclusions Betamethasone is an effective addition to silver nitrate for the treatment of hypergranulation tissue, with our results indicating it can improve resolution and lessen treatment burden in patients' post-PIV.

Abstract Vaccine‐induced immune thrombotic thrombocytopenia (VITT) is a new disorder that emerged in the wake of coronavirus disease 2019 (COVID‐19) vaccination. It is a rare but life‐threatening condition that requires an aggressive course of treatment to improve patient outcomes. Currently, the diagnosis of VITT relies on a comprehensive panel of criteria, including a history of recent vaccination, platelet count, positive enzyme linked immunosorbent assays (ELISA) result for a closely related thrombotic disorder, heparin‐induced thrombocytopenia (HIT), and platelet factor 4 (PF4)‐dependent functional assays. The study describes a technically simple antigenic assay designed to detect autoimmune antibodies associated with VITT. It is first shown that cross‐linked platelet factor 4 (c‐PF4) represents an antigenic target specific for VITT/VITT‐like Abs. This antigenic target is then incorporated into a microfluidic electrochemical biosensor and specific and sensitive detection of VITT/VITT‐like antibodies is demonstrated in a fully automated manner while using microliter volumes of patient sera. Fifty‐five serum samples are tested using the microfluidic electrochemical biosensor and demonstrated high accuracy for the detection of VITT sera and VITT‐like monoclonal gammopathy of thrombotic ignificance (MGTS) antibodies compared to healthy controls and HIT patients. It is envisioned that the microfluidic electrochemical biosensor will be used in combination with other clinical criteria to enable timely, sensitive, and specific diagnosis of VITT.

ABSTRACT Background Isolated chromosome 5/5q losses (–5/5q) without TP53 mutations are associated with favorable outcomes in myeloid neoplasms (MN) with <5% blasts. However, the clinical implication of concurrent −5/5q and TP53 aberrations in MN with ≥5% blasts is poorly understood. Methods Patients with TP53 ‐mutated MN carrying ≥5% blasts assessing the prognostic impact of ‐5/5q on 24‐month overall survival (OS24) were examined. Results Of 587 patients, 515 (88%) exhibited −5/5q overwhelmingly in the context of a complex karyotype (98.3% vs. 61.1% complex karyotype without −5/5q; p < .0001) and multihit TP53 allelic state (88.3% vs. 56.9%; p < .0001). Proportions of patients with blasts ≥20% were comparable between groups with and without −5/5q; p = 0.26. Notably, patients with −5/5q exhibited significantly fewer coalterations; p < .0001. Looking at outcomes, presence of −5/5q was associated with shorter median 24‐month overall survival (7.8 months vs. 11.2 months; p Log‐rank = .012), an effect restricted to subgroups with blasts <20% ( p = .039; N = 163), absent −7/7q ( p = .007; N = 225), or WHO5‐defined single hit allelic state ( p = 0.030; N = 91). Importantly, −5/5q retained independent adverse prognostic significance regardless of TP53 allelic state in a multivariable model. Furthermore, among the subset of 75 (13%) patients undergoing allogeneic stem cell transplantation, −5/5q predicted significantly shorter median 5‐year posttransplant survival (16.2 months vs. median not reached; p Log‐rank = .009). Conclusions These findings emphasize the independent prognostic relevance of chromosome 5/5q losses underscoring the clinical relevance of cytogenetic testing for −5/5q even in this high‐risk cohort.

Abstract Background Eligibility criteria for clinical trials are crucial for maintaining safety and study integrity. However, overly restrictive criteria can result in unrepresentative trial populations, leading to gaps in understanding real‐world treatment efficacy. Addressing potentially modifiable exclusions (PMEs) could enhance trial accessibility and participation without compromising safety. Methods The authors retrospectively analyzed screen‐failed patients with biliary tract cancer or pancreatic cancer between August 2019 and November 2024 at The University of Texas MD Anderson Cancer Center. Screen‐failed patients were those who provided informed consent but did not participate for any reason. Clinical data were obtained from screening logs and electronic health records. PMEs were identified and validated by two independent medical oncologists. Results Of 585 screen‐failed patients from 18 trials, 509 were analyzed (367 with pancreatic cancer and 142 with biliary tract cancer) after excluding 76 because of incomplete data. Leading causes of screen failure were declined participation (19%), comorbidities (12%), suboptimal organ function (11%), absence of a biomarker (10%), and insufficient biospecimens (7%). Reasons for declining included preference for standard care (23%), travel (22%), and competing trials (5%). The authors identified 69 patients (13.6%) who had PMEs (primarily borderline laboratory abnormalities), including liver function (23%), kidney function (20%), platelet count (12%), hemoglobin (7%), and white blood cell count (6%) abnormalities. Other PMEs included previous or concurrent malignancies (9%) and viral hepatitis (4%). PMEs were evenly distributed across trials. Conclusions Rigid eligibility criteria exclude stable patients who might benefit from investigational treatments. Easing criteria related to incidental or asymptomatic laboratory abnormalities could broaden trial accessibility and improve enrollment in populations that are more representative of real‐world use.