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Residual radiographic fracture displacement in healed tibial plateau fractures: comparison after treatment with suprapatellar nailing versus lateral plating
No full textOBJECTIVES: Compare maintenance of articular reduction and alignment in bicondylar tibial plateau fractures (OTA/AO 41-C2/C3) treated with suprapatellar intramedullary nailing (IMN) versus dual-plate open reduction and internal fixation (ORIF).
DESIGN: Retrospective Cohort Study.
SETTING: Single Level I academic trauma center.
PATIENTS/PARTICIPANTS: Fifty-eight adults treated between July 2012 and July 2022 (28 IMN, 30 ORIF); groups were matched for age, body mass index, and fracture pattern.
INTERVENTION: Semiextended suprapatellar IMN with ≥1 independent lag screw compared with dual-plate ORIF performed through standard open approaches.
MAIN OUTCOME MEASUREMENTS: Joint-line depression, condylar widening, medial proximal tibial angle (MPTA), and posterior proximal tibial angle (PPTA) at union (12 months).
RESULTS: Initial displacement was greater in the ORIF cohort (joint-line 8.2 mm vs. 5.6 mm, P = 0.014; widening 7.2 mm vs. 5.8 mm, P = 0.150). At 12 months, healed widening (0.6 mm IMN vs. 1.0 mm ORIF, P = 0.856), healed depression (2.0 mm vs. 1.1 mm, P = 0.991), MPTA (89.9° vs. 89.6°, P = 0.699), and PPTA (11.3° vs. 9.8°, P = 0.078) did not differ. No secondary loss of reduction requiring revision occurred.
CONCLUSION: Suprapatellar IMN maintained healed joint line displacement, condylar widening, MPTA, and PPTA in OTA/AO C1, C2, and certain C3 fractures. The MPTA and PPTA were surgically restored and maintained. This technique may be useful in certain circumstances where ORIF of the tibial plateau fractures places the soft tissue envelope at risk or where an intramedullary implant is otherwise preferred.
LEVEL OF EVIDENCE: Level III
Associations between epilepsy-related polygenic risk and brain morphology in childhood
No full textExtensive neuroimaging research in temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) has identified brain atrophy as a disease phenotype. While it is also related to a complex genetic architecture, the transition from genetic risk factors to brain vulnerabilities remains unclear. Using a population-based approach, we examined the associations between epilepsy-related polygenic risk for HS (PRS-HS) and brain structure in healthy developing children, assessed their relation to brain network architecture, and evaluated its correspondence with case-control findings in TLE-HS diagnosed patients relative to healthy individuals We used genome-wide genotyping and structural T1-weighted magnetic resonance imaging (MRI) of 3,826 neurotypical children from the Adolescent Brain Cognitive Development (ABCD) study. Surface-based linear models related PRS-HS to cortical thickness measures, and subsequently contextualized findings with structural and functional network architecture based on epicentre mapping approaches. Imaging-genetic associations were then correlated to atrophy and disease epicentres in 785 patients with TLE-HS relative to 1,512 healthy controls aggregated across multiple sites. Higher PRS-HS was associated with decreases in cortical thickness across temporo-parietal as well as fronto-central regions of neurotypical children. These imaging-genetic effects were anchored to the connectivity profiles of distinct functional and structural epicentres. Compared with disease-related alterations from a separate epilepsy cohort, regional and network correlates of PRS-HS strongly mirrored cortical atrophy and disease epicentres observed in patients with TLE-HS, and highly replicable across different studies. Findings were consistent when using statistical models controlling for spatial autocorrelations and robust to variations in analytic methods. Capitalizing on recent imaging-genetic initiatives, our study provides novel insights into the genetic underpinnings of structural alterations in TLE-HS, revealing common morphological and network pathways between genetic vulnerability and disease mechanisms. These signatures offer a foundation for early risk stratification and personalized interventions targeting genetic profiles in epilepsy
Self-Perceived Hearing Outcomes With Radiation and Cisplatin or Radiation and Cetuximab for Patients With Human Papilloma Virus (HPV)-Positive Oropharyngeal Cancer-Results From NRG Oncology RTOG 1016
No full textPURPOSE: RTOG 1016 was a noninferiority phase 3 trial comparing the efficacy of radiation with either cisplatin (RT + Cis) or cetuximab (RT + Cetux) for patients with Humman Papillomavirus (HPV)+ oropharyngeal cancer (OPC). Perceived hearing handicap was included as a patient-reported outcome (PRO) secondary endpoint. The primary hypothesis was that perceived hearing handicap would be greater for patients receiving RT + Cis compared with RT + Cetux.
METHODS AND MATERIALS: Perceived hearing handicap was measured at baseline, end of treatment, and 3, 6, and 12 months posttreatment using the Hearing Handicap Inventory for Adults Screening Version (HHIA-S), a 10-item self-assessment questionnaire designed to measure patients\u27 reactions to their hearing loss. Mixed ordinal logistic models were used to determine the treatment effect on HHIA-S scores and handicap categories (2-sided α = 0.05).
RESULTS: The PRO substudy included 375 eligible patients. No significant differences in patient/tumor characteristics were found between patients who participated in the HHIA-S study versus those excluded. For total HHIA-S scores and social and emotional subscales, RT + Cetux had significantly lower (ie, better) scores from end of treatment. Change score from baseline to end of treatment for RT + Cis (4.32; 95% confidence interval [CI], 2.57-6.07]) was greater than RT + Cetux (0.08; 95% CI, -1.15 to 1.31). For hearing handicap category, RT + Cis had a significantly higher percentage of mild/moderate and severe cases at the end of treatment (32%) compared with RT + Cetux (20%) (P \u3c .0001). Adjusted conditional odds of higher self-perceived hearing handicap category for RT + Cis compared with RT + Cetux was 3.73 (95% CI, 2.10-6.62).
CONCLUSION: Patients have significantly worse self-perceived hearing handicap after receiving RT + Cis treatment than with RT + Cetux. This was consistent across time through 1 year posttreatment. These findings inform hearing-related outcomes for patients with HPV-associated OPC and indicate the need for ototoxicity monitoring with RT + Cis treatment
Socioeconomic Disparities in Prostate Cancer Presentation: The Impact of ADI on Prostate Cancer Stage at Diagnosis
No full textOBJECTIVES: To investigate the impact of socioeconomic deprivation, as measured by Area Deprivation Index (ADI), on PCa stage at diagnosis in a North-American statewide cohort.
METHODS: The Michigan Department of Health and Human Services (MDHHS) was queried to identify men aged ≥ 30 with a confirmed diagnosis of PCa at prostate biopsy between 2004 and 2022. An ADI score was assigned to each patient based on their residential census block group. Individuals were further categorized into quartiles, where the fourth 1 (ADI 75-100) represented those living in the most deprived areas. Logistic regression analysis tested the impact of ADI on diagnosis with NCCN high-risk PCa (T3-T4 or PSA \u3e20 ng/ml or ISUP GG ≥ 4) or metastatic PCa (N1 or M1) at presentation.
RESULTS: We included 78018 patients, 17% of whom were Non-Hispanic Black (NHB). Median (IQR) age was 66 (59-72) years. Patients in the most disadvantage quartile (Q4) were more likely to be NHB (40.1% vs. 5.4%), had higher proportion with PSA\u3e20 ng/ml (10.6 % vs. 5.1%), GG ≥ 4 (55.4% vs. 53.1%), clinical T ≥ 3 (4% vs. 3%) and metastasis (3.3% vs. 1.8%) at diagnostic presentation, compared to those in the least disadvantaged quartile (Q1) (all P \u3c .0001). At MVA, for each 10-unit increase in ADI percentile, the relative odds of being diagnosed with NCCN high-risk and metastatic PCa increases by 2% (95% CI, 1.01-1.02) and 4% (95% CI, 1.02-1.05), respectively. Moreover, when compared to NHW men, NHB men had a 1.16 (95% CI, 1.12-1.22) and a 1.52-fold (95% CI, 1.38-1.68) higher relative odds of being diagnosed with NCCN high-risk PCa and metastatic PCa, respectively (P \u3c .001).
CONCLUSIONS: Living in more deprived areas was associated with higher relative odds of newly diagnosed PCa with unfavorable features. Our study underscores the silent barrier that socioeconomic deprivation poses to cancer early diagnosis and echo the call for tailored interventions to bridge this gap
Seconds to Scan: Reducing Stroke Arrival to CT Times
No full texthttps://scholarlycommons.henryford.com/nursresconf2025/1009/thumbnail.jp
Improving RN–NA Collaboration and Communication: A Structured Approach to Enhance Patient Outcomes on Medical-Surgical Units
No full texthttps://scholarlycommons.henryford.com/nursresconf2025/1016/thumbnail.jp
Experience to Evidence: A Nurse-Initiated Framework for Mechanical Circulatory Support Withdrawal
No full texthttps://scholarlycommons.henryford.com/nursresconf2025/1023/thumbnail.jp
Impact of graft-versus-host disease on mortality, length of stay, and hospitalization costs in bone marrow transplant patients: A retrospective analysis using the 2021 NIS database
No full textBackground: Graft-versus-host disease (GVHD) is a significant complication of bone marrow transplantation (BMT), influencing patient outcomes, length of stay (LOS), and hospitalization costs. This study evaluates the prevalence of GVHD in hospitalized BMT patients and its impact on outcomes using the 2021 National Inpatient Sample (NIS) database. Methods: We conducted a retrospective analysis of the NIS 2021 dataset. Patients who underwent BMT and patient\u27s who developed GVHD were identified using the appropriate ICD-10 codes. Survey-weighted descriptive statistics were used to analyze patient demographics, mortality rates, LOS, and total hospitalization charges (TOTCHG). Multivariable logistic and linear regression models evaluated GVHD\u27s impact on outcomes, adjusting for age, sex, race, income quartiles, Charlson comorbidity index (CCI), hospital region, teaching status, and bed size. The top principal diagnoses were ranked by weighted counts. Results: A total of 20,165 weighted BMT hospitalizations were analyzed, of which 10.9% (95% CI: 9.8%-12.1%) were associated with GVHD. GVHD patients had a significantly higher mortality rate compared to non-GVHD patients (6.4% vs. 4.5%, p=0.04), longer LOS (10.7 vs. 7.2 days, p,0.001) and GVHDpatients had significantly higher mean hospitalization charges (≥235,485 vs. ≥113,706). Adjusted regression showedGVHDwas associated with a50%higher odds of mortality (aOR: 1.50,95%CI: 1.03-2.31, p=0.031), 3.3 additional hospitalization days (95% CI: 1.70-4.87, p,0.001), and ≥112,376 higher total charges (95% CI: ≥54,212-≥170,539, p,0.001). Significant adjusted predictors of mortality included age (OR = 1.01, p = 0.009) and Charlson Comorbidity Index (OR = 1.47, p \u3c 0.001). Length of stay was significantly influenced by CCI (0.51 days, p = 0.022), and teaching hospital status (1.76 days, p \u3c 0.001). Hospital charges were significantly higher with CCI (≥13,646.94, p = 0.023), and at teaching hospitals (≥45,054.57, p \u3c 0.001). The most common primary diagnoses among BMT patients with GVHD included septicemia (650 cases), pneumonia (202 cases), acute kidney failure (320 patients) and COVID-19 (130 cases). Conclusions: GVHD significantly exacerbates the clinical and economic burden of BMT, leading to increased mortality, LOS, and healthcare costs. Age, Charlson Comorbidity Index, and teaching hospital status were also significant predictors of mortality, length of stay, and hospital charges. The most common primary diagnoses among GVHD patients included septicemia, pneumonia, acute kidney failure, and COVID-19, underscoring the complexity and resource-intensive care required for this population. These findings emphasize the need to focus on early detection strategies and innovative treatment modalities to mitigate the impact ofGVHDinBMTpatients
AML-1263: Transcriptomic Profiling of Acute Myeloid Leukemia Before and After Induction Therapy: A Public Data-Based Analysis
No full textAcute myeloid leukemia (AML) presents a variable response to induction therapy, necessitating the identification of early transcriptomic biomarkers that reflect treatment effectiveness. Publicly available gene expression data offer a noninvasive approach to study such shifts. Objective: To identify differentially expressed genes (DEGs) in patients with AML before and after induction chemotherapy, and to elucidate biological pathways associated with treatment response. Design: A secondary analysis of publicly available microarray data (GSE10358) using GEO2R. Samples included paired bone marrow aspirates from patients collected pre- and postchemotherapy. DEGs were filtered by adjusted P \u3c 0.05 and |log2FC| \u3e1. Functional enrichment was performed using Enrichr. Setting: Data were collected from an academic oncology research center, archived on the NCBI Gene Expression Omnibus platform. Patients or Other Participants: Ten adult patients with AML with paired samples (n = 20 total). Inclusion was based on dataset availability and treatment label metadata. No additional selection criteria were applied beyond dataset-defined identifiers. Interventions: All patients received standard induction chemotherapy (details not disclosed in dataset). The analysis was observational and did not involve clinical interventions by the investigators. Main Outcome Measures: Differential gene expression levels pre- and posttreatment; significantly enriched pathways relevant to AML biology. Results: A total of 324 DEGs were identified posttreatment, including 145 upregulated and 179 downregulated genes. Post-treatment upregulation was noted for genes such as CDKN1A, GADD45B, and BCL2A1, implicated in DNA damage response and apoptosis. Downregulated genes included MYC, CDC20, and CCNA2, consistent with suppression of proliferation. Enrichment analysis revealed significant activation of p53 signaling and apoptotic pathways, alongside repression of cell cycle and mitotic progression. Conclusions: Transcriptomic changes in AML following chemotherapy demonstrate a shift from proliferative signaling toward cellular stress and apoptotic regulation. Public data mining can reveal candidate biomarkers of early treatment response. Further validation in prospective studies is warranted before clinical implementation
Phase 1b/2 study evaluating telisotuzumab adizutecan (ABBV-400; Temab-A) in combination with budigalimab in patients (pts) with advanced non-squamous (NSQ) non-small cell lung cancer (NSCLC) with no prior treatment for advanced disease and no actionable genomic alterations
No full textBackground: c-Met (MET) protein expression is frequently increased in NSCLC and is associated with poor prognosis. 24% of pts with NSQ EGFR wildtype (WT) NSCLC exhibit increased c-Met protein expression, ie, ≥25% 3+ via IHC. Addition of programmed cell death (ligand) 1 (PD-[L]1) inhibitors to chemotherapy (CT) has improved treatment of NSCLC regardless of PD-(L)1 expression. However, more-effective therapies are needed, particularly for pts with no known actionable genomic alterations. Temab-A is an antibody-drug conjugate comprising the c-Met protein-targeting antibody telisotuzumab and the potent topoisomerase 1 inhibitor adizutecan payload attached via a stable cleavable linker. In an ongoing phase 1 study (NCT05029882), Temab-A monotherapy demonstrated manageable safety and promising efficacy in pts with advanced/metastatic (a/m) NSQ EGFR WT NSCLC in second line and later, with an objective response rate (ORR) of 48% (23/48) across all c-Met expression levels and clinical benefit rate of 85% (41/48) (De Miguel et al. Ann Oncol. 2024;35:S805-S806). Herein, we describe a study evaluating Temab-A in combination with the PD-1 inhibitor budigalimab. Methods: This multicenter, global, open-label, phase 1b/2, randomized (in part 2) study (NCT06772623) will enroll ∼172 pts (≥18 yr) with a/m NSQ NSCLC. Eligible pts have ECOG 0 or 1, measurable disease per RECIST v1.1, and documented EGFRWTand PD-L1 status. Primary objectives are to evaluate safety and tolerability, assess efficacy as measured by ORR by blinded independent central review, and select the recommended phase 3 dose of Temab-A combined with budigalimab. Secondary objectives include assessment of efficacy outcomes (PFS, DOR, OS, and disease control rate), characterization of PK and immunogenicity, and evaluation of PD and potential predictive biomarkers. The study has 2 parts: a safety dose-escalation part 1 and a dose-optimization part 2. Part 1 enrolls ∼12 pts who have received #1 prior systemic therapy for a/m NSCLC, including platinum-based CT, an immune checkpoint inhibitor, or targeted therapy. Pts receive escalating doses of Temab-A IV Q3Wguided by BOIN design in combination with a fixed dose of budigalimab IV Q3W. Dose-limiting toxicities are evaluated during cycle 1. Part 2 enrolls ∼160 pts who have not received prior systemic therapy for a/m NSCLC. Pts are randomized 1:1:1:1 to Temab-A at 1 of 2 doses determined in part 1 + budigalimab, to budigalimab + CT, or to SOC (pembrolizumab + CT) arms. Randomization is stratified by PD-L1 expression and history of brain metastases. Treatment continues until disease progression, intolerable toxicity, or other discontinuation criteria are met. The first dosing of the first patient enrolled is planned in March 2025