Treatment-free remission (TFR) is an emerging goal for patients with chronic myeloid leukemia (CML) treated with tyrosine kinase inhibitors (TKI). However, long-term TFR durability in real-world settings remains understudied. The J-SKI study, a large observational study, was conducted to evaluate long-term TFR outcomes in Japanese patients with CML. This interim analysis included 795 eligible patients from the prospective (n = 283) and retrospective (n = 512) cohorts. With a median follow-up of 32 months (range 0.8–168) after TKI discontinuation, the 5-year TFR rate was 65.2
We prospectively evaluated whether cytotoxic T-lymphocyte (CTL) activation and T-cell receptor (TCR) Vβ clonality predict treatment-free remission (TFR) after tyrosine kinase inhibitor (TKI) cessation in chronic-phase chronic myeloid leukemia (CML). Forty-five patients with sustained deep molecular response (DMR) were enrolled (On-TKI, n = 38; Off-TKI, n = 7) and underwent one-year immuno-monitoring from consent. The primary endpoint was 12-month TFR, defined as retention of MR4. Overall, 32/45 patients (71%) maintained TFR at 12 months. Longer TKI exposure and stable DMR were associated with TFR; notably, patients fulfilling "≥7 years of TKI plus ≥1 year of DMR" and exhibiting CTL activation features-CD8 > CD4, memory > effector, and/or highly activated CTL clones on TCR Vβ repertoire-showed the highest likelihood of durable TFR. By contrast, NK cells, effector Tregs, and G-/M-MDSCs did not discriminate TFR status in this cohort. Although antigen specificity against CML stem cells was not directly tested, the memory-dominant CTL phenotype is consistent with immune control after antigen reduction. These findings suggest that a simple, clinically accessible strategy based on flow cytometric CTL profiling and TCR Vβ clonality may help inform TKI discontinuation decisions in CML. External validation is warranted to confirm transportability and refine clinical thresholds.
BACKGROUND:Accurate intraoperative assessment of fracture reduction is essential in trochanteric fracture surgery to prevent mechanical failure. Although restoration of anteromedial cortical support, particularly in the sagittal plane, has been recognized as a critical factor, standard lateral views may fail to detect malreduction because the shadow of the greater trochanter overlaps and obscures the anteromedial cortical line. This study aimed to evaluate the clinical utility of a novel intraoperative anteromedial cortex (AMC) view for assessing fracture reduction. METHODS:This prospective multicenter observational study included 135 trochanteric fractures (AO/OTA 31A1.2, 31A1.3, and 31A2) surgically treated between June 2022 and December 2023. In addition to standard AP and lateral fluoroscopic views, an AMC view was obtained intraoperatively. Reduction on the lateral and AMC views was categorized as anterior malreduction, anatomic reduction, or posterior malreduction. The primary outcome was the concordance rate between the lateral and AMC views. RESULTS:Discordances between lateral and AMC views were observed in 26 of 135 cases (19.3%). Notably, among fractures classified as anatomic reduction on the lateral view, 12 cases (19.4%) were reclassified as anterior malreduction on the AMC view, representing "hidden" anterior malreduction. In 7 of these 12 cases (5.2% of the total cohort), the AMC view findings directly led to a change in the surgical strategy, requiring direct reduction through a small incision. CONCLUSIONS:Approximately one-fifth of trochanteric fractures showed inconsistent reduction patterns between the standard lateral the AMC views. The AMC view provides a more precise intraoperative assessment of the anteromedial cortex and is particularly effective in identifying hidden anterior malreduction that may be overlooked on standard fluoroscopy.
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne viral infection that can rapidly progress to multiple organ failure with a high mortality rate. Pulmonary involvement has been reported, but the radiologic-pathologic correlation remains poorly understood. We report an autopsy-proven fatal case of SFTS in a 79-year-old man with pre-existing collagen vascular disease-associated interstitial lung disease. Serial chest computed tomography (CT) initially demonstrated subtle peripheral ground-glass opacities that progressively expanded over time. On the final CT examination obtained shortly before death, extensive bilateral consolidation with high attenuation on mediastinal window images was observed, suggestive of pulmonary hemorrhage. The patient developed severe thrombocytopenia, disseminated intravascular coagulation, and respiratory failure and died despite intensive treatment. Autopsy revealed diffuse pulmonary hemorrhage, alveolar septal thickening, focal diffuse alveolar damage with hyaline membrane formation, and prominent hemophagocytosis. Immunohistochemical staining demonstrated numerous SFTS virus-infected cells within the lung tissue. This case highlights the CT findings of pulmonary involvement in fatal SFTS and demonstrates a direct radiologic-pathologic correlation. Our findings suggest that cytokine storm and hemophagocytic syndrome play critical roles in the development of pulmonary hemorrhage and lung injury in SFTS.
