Background: Biologics effectively improve psoriatic skin lesions, but their impact on itch relief remains unclear. Objective: To evaluate itch improvement in severe psoriasis patients treated with ustekinumab or guselkumab. Methods: This retrospective study analyzed patients with severe psoriasis who completed initial efficacy evaluations after treatment with either biologic. Itch severity was assessed using numerical rating scale (NRS), visual analog scale, and verbal rating scale. NRS improvement was evaluated after three injections. Results: Among 108 patients (74 on ustekinumab, 34 on guselkumab), 77 (71.3%) had moderate-to-severe itch (NRS ≥4) at baseline. Of these, 63 (81.8%) achieved an NRS improvement of ≥4 points. Ustekinumab showed greater itch relief compared to guselkumab in NRS (p=0.033). On the other hand, guselkumab showed more reduction for psoriatic skin lesions than ustekinumab in the Psoriasis Area and Severity Index (p=0.040). In the moderate-to-severe itch group, patients with large plaques experienced significantly greater improvement in NRS than those with small plaques (p=0.012). Conclusion While guselkumab is generally preferred for psoriatic skin lesions, ustekinumab may provide superior itch relief.

Background: Chromosomal alterations serve as diagnostic and prognostic markers in acute leukemia. Given the evolving landscape of chromosomal abnormalities in acute leukemia, we previously studied these over two periods. In this study, we investigated the frequency of these abnormalities and clinical trends in acute leukemia in Korea across three time periods. Methods: We retrospectively analyzed data from 1,787 patients with acute leukemia (319 children and 1,468 adults) diagnosed between 2006 and 2020. Conventional cytogenetics, FISH, and multiplex quantitative PCR were used for analysis. The patient groups were divided according to the following three study periods: 2006–2009 (I), 2010–2015 (II), and 2016–2020 (III). Results: Chromosomal aberrations were detected in 92% of patients. The PML::RARA translocation was the most frequent. Over the 15-yr period, chromosomal aberrations showed minimal changes, with specific fusion transcripts being common among patients.ALL was more prevalent in children than in adults and correlated significantly with the ETV6::RUNX1 and RUNX1::RUNX1T1 aberrations. The incidence of ALL increased during the three periods, with PML::RARA remaining common. Conclusions The frequency of chromosomal abnormalities in acute leukemia has changed subtly over time. Notably, the age of onset of adult AML has continuously increased. Our results may help in establishing diagnoses and clinical treatment strategies and developing various molecular diagnostic platforms.

Enterococcus faecium, particularly in its multidrug-resistant forms, causes invasive nosocomial infections. Given the limited data comparing the effectiveness of the European Committee on Antimicrobial Susceptibility Testing (EUCAST) and the CLSI clinical breakpoints (CBPs) for quinupristin–dalfopristin (QD) resistance and the need to evaluate their practical application, we retrospectively investigated the susceptibility patterns of 287 E.faecium bloodstream isolates from Korean hospitals to QD using the updated EUCAST and CLSI CBPs and two antimicrobial susceptibility testing methods: disk diffusion (DD) and Sensititre broth microdilution (Sensititre). QD resistance rates were 5.9% (CLSI) and 18.8% (EUCAST) for DD and 22.6% (CLSI) and 28.2% (EUCAST) for Sensititre. The most prevalent QD resistance gene types among QD-resistant isolates were ermB+msrC+ or ermB– msrC+. Categorical agreement between DD and Sensititre ranged from 77.7% to 90.7%, depending on the testing method and CBPs applied. The EUCAST zone diameter CBPs more effectively help identify QD-resistant E. faecium isolates using the DD method than the CLSI zone diameter CBPs. In comparison, the CLSI minimum inhibitory concentration (MIC) CBPs provide more reliable results for resistance classification in the Sensititre method than EUCAST MIC CBPs. These findings would help improve clinical decision-making for treating multidrug-resistant E. faecium infections.

Taste buds relay taste sensory information to the primary taste neurons but depend on those same neurons for essential components to maintain function. While denervation-induced taste bud degeneration and subsequent regeneration were discovered decades ago, the mechanisms underlying these phenomena (e.g., heterogenous cellular responses to nerve injury and the signaling pathways involved) remain poorly understood. Here, using mouse genetics, nerve injury models, pharmacologic manipulation, and taste bud organoid models, we identify a specific subpopulation of taste cells, predominantly c-Kit-expressing sweet cells, that exhibit superior resistance to nerve injury. We found the c-Kit inhibitor imatinib selectively reduced the number of residual c-Kit-expressing sweet cells at post-operation week 2, subsequently attenuating the re-emergence of other type II cells by post-operation week 4. In taste bud organoids, c-Kit-expressing cells were resistant to R-spondin withdrawal but susceptible to imatinib, while other taste cell types showed the opposite behavior. We also observed a distinct population of residual taste cells that acquired stem-like properties, generating clonal descendent cells among suprabasal keratinocytes independent of c-Kit signaling. Together, our findings reveal that c-Kit signaling confers resilience on c-Kit-expressing sweet cells and supports the broader reconstruction of taste buds during the later regenerative stage following nerve injury.
Animals ; Taste Buds/metabolism* ; Proto-Oncogene Proteins c-kit/metabolism* ; Mice ; Signal Transduction ; Imatinib Mesylate/pharmacology* ; Mice, Inbred C57BL

Background: The diagnosis of tuberculous pleural effusion (TPE) often relies on pleural fluid adenosine deaminase (ADA) levels. The diagnostic utility of ADA, however, is influenced by the prevalence of tuberculosis (TB) in local populations. Malignant pleural effusion (MPE) cases can exhibit moderately elevated ADA levels comparable to those seen in TPE. As population aging potentially impacts ADA levels, global TB incidence is decreasing whereas the burden of malignancy is on the rise. Consequently, epidemiological shifts and temporal changes in ADA distribution complicate the differential diagnosis between TPE and MPE when ADA levels are within the 40–70 IU/L range. Nonetheless, data specific to this subset are scarce. Methods: This retrospective study included consecutive patients aged > 18 years with confirmed TPE and MPE, spanning from 2012 to 2023. ADA levels in pleural fluid were categorized into three groups: < 40 IU/L, 40–70 IU/L, and > 70 IU/L. The study examined annual trends in the frequency of new cases and ADA level distributions over time and identified discriminating factors between TPE and MPE in cases with ADA levels of 40–70 IU/L. Results: In total, 297 TPE and 369 MPE cases were included in this study. Over the study period, the frequency of TPE progressively declined, while that of MPE increased. In the most recent four-year period, new TPE and MPE cases with ADA levels of 40–70 IU/L occurred at comparable numbers. Multivariable analysis identified pleural fluid carcinoembryonic antigen (CEA) levels and the number of focal pleural nodules as independent predictors for MPE. Specifically, the presence of either CEA levels > 15.7 ng/mL or more than eight pleural nodules yielded the highest diagnostic accuracy with a sensitivity of 88%, specificity of 100%, and an area under the curve of 0.95. Conclusion The differential diagnosis between TPE and MPE with pleural ADA levels of 40–70 IU/L has become increasingly critical due to evolving epidemiological patterns and ADA distribution changes over time. Pleural fluid CEA levels and the characteristics of pleural nodules may offer valuable guidance in distinguishing between TPE and MPE within this diagnostic gray zone.

Background: The diagnosis of tuberculous pleural effusion (TPE) often relies on pleural fluid adenosine deaminase (ADA) levels. The diagnostic utility of ADA, however, is influenced by the prevalence of tuberculosis (TB) in local populations. Malignant pleural effusion (MPE) cases can exhibit moderately elevated ADA levels comparable to those seen in TPE. As population aging potentially impacts ADA levels, global TB incidence is decreasing whereas the burden of malignancy is on the rise. Consequently, epidemiological shifts and temporal changes in ADA distribution complicate the differential diagnosis between TPE and MPE when ADA levels are within the 40–70 IU/L range. Nonetheless, data specific to this subset are scarce. Methods: This retrospective study included consecutive patients aged > 18 years with confirmed TPE and MPE, spanning from 2012 to 2023. ADA levels in pleural fluid were categorized into three groups: < 40 IU/L, 40–70 IU/L, and > 70 IU/L. The study examined annual trends in the frequency of new cases and ADA level distributions over time and identified discriminating factors between TPE and MPE in cases with ADA levels of 40–70 IU/L. Results: In total, 297 TPE and 369 MPE cases were included in this study. Over the study period, the frequency of TPE progressively declined, while that of MPE increased. In the most recent four-year period, new TPE and MPE cases with ADA levels of 40–70 IU/L occurred at comparable numbers. Multivariable analysis identified pleural fluid carcinoembryonic antigen (CEA) levels and the number of focal pleural nodules as independent predictors for MPE. Specifically, the presence of either CEA levels > 15.7 ng/mL or more than eight pleural nodules yielded the highest diagnostic accuracy with a sensitivity of 88%, specificity of 100%, and an area under the curve of 0.95. Conclusion The differential diagnosis between TPE and MPE with pleural ADA levels of 40–70 IU/L has become increasingly critical due to evolving epidemiological patterns and ADA distribution changes over time. Pleural fluid CEA levels and the characteristics of pleural nodules may offer valuable guidance in distinguishing between TPE and MPE within this diagnostic gray zone.

Purpose: Claudin 18.2 (CLDN18.2) has emerged as a promising therapeutic target for CLDN18.2-expressing gastric cancer (GC). We sought to examine the heterogeneity of CLDN18.2 expression between primary GC (PGC) and metastatic GC (MGC) using various scoring methods. Materials and Methods: We retrospectively analyzed data from 102 patients with pathologically confirmed paired primary and metastatic gastric or gastroesophageal junction adenocarcinomas. CLDN18.2 expression was evaluated through immunohistochemistry on formalin-fixed paraffin-embedded tissue samples. We assessed CLDN18.2 positivity using multiple scoring approaches, including the immunoreactivity score, H-score, and the percentage of tumor cells showing moderate-to-strong staining intensity. We analyzed the concordance rates between PGC and MGC and the association of CLDN18.2 positivity with clinicopathological features. Results: CLDN18.2 positivity varied from 25% to 65% depending on the scoring method, with PGC consistently showing higher expression levels than MGC. Intratumoral heterogeneity was noted in 25.5% of PGCs and 19.6% of MGCs. Intertumoral heterogeneity, manifesting as discordance in CLDN18.2 positivity between PGC and MGC, was observed in about 20% of cases, with moderate agreement across scoring methods (κ=0.47 to 0.60).In PGC, higher CLDN18.2 positivity correlated with synchronous metastasis, presence of peritoneal metastasis, poorly differentiated grade, and biopsy specimens. In MGC, positivity was associated with synchronous metastasis, presence of peritoneal metastasis, and metastatic peritoneal tissues. Conclusions CLDN18.2 expression demonstrates significant heterogeneity between PGC and MGC, with a 20% discordance rate. Comprehensive tissue sampling and reassessment of CLDN18.2 status are crucial, especially before initiating CLDN18.2-targeted therapies.

We updated the Korean Society of Gynecologic Oncology (KSGO) practice guideline for the management of ovarian cancer as version 5.1. The ovarian cancer guideline team of the KSGO published announced the fifth version (version 5.0) of its clinical practice guidelines for the management of ovarian cancer in December 2023. In version 5.0, the selection of the key questions and the systematic reviews were based on the data available up to December 2022.Therefore, we updated the guidelines version 5.0 with newly accumulated clinical data and added 5 new key questions reflecting the latest insights in the field of ovarian cancer between 2023 and 2024. For each question, recommendation was provided together with corresponding level of evidence and grade of recommendation, all established through expert consensus.

We describe the updated Korean Society of Gynecologic Oncology (KSGO) practice guideline for the management of cervical cancer, version 5.1. The KSGO announced the fifth version of its clinical practice guidelines for the management of cervical cancer in March 2024. The selection of the key questions and the systematic reviews were based on data available up to December 2022. Between 2023 and 2024, substantial findings from large-scale clinical trials and new advancements in cervical cancer research remarkably emerged. Therefore, based on the existing version 5.0, we updated the guidelines with newly accumulated clinical data and added 4 new key questions reflecting the latest insights in the field of cervical cancer. For each question, recommendation was formulated with corresponding level of evidence and grade of recommendation, all established through expert consensus.