Background: Elevated active glucocorticoids (GCs) are implicated in skin barrier dysfunction, notably in aging and diabetes. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts inactive GCs to active forms, potentially exacerbating this dysfunction. Objective: We aimed to investigate the impact of a novel 11β-HSD1 inhibitor on skin inflammation using both in vitro and in vivo models. Methods: To elucidate the efficacy of a new 11β-HSD1 inhibitor in mitigating skin inflammation induced by various triggers, including dexamethasone treatment, ultraviolet B irradiation, and high glucose levels, in cultured human keratinocytes and the db/db mice as a type 2 diabetes murine model. In cultured keratinocytes, we assessed the effects of the 11β-HSD1 inhibitor on cortisol levels, 11β-HSD1 expression, and cytokine production under conditions simulating inflammation. In db/db mice, we evaluated the inhibitor’s impact on skin barrier function, hemoglobin A1c (HbA1c) levels, corticosterone levels, 11β-HSD1 expression, and cytokine profiles following a 2-week treatment regimen. Results: Our results demonstrated that both the novel 11β-HSD1 inhibitor and a known inhibitor reduced cortisol levels, 11β-HSD1 expression, and inflammatory cytokine production in cultured keratinocytes. In db/db mice, treatment with either inhibitor improved skin barrier function, lowered serum HbA1c levels, and decreased corticosterone, 11β-HSD1, and inflammatory cytokine expression. Conclusion A new 11β-HSD1 inhibitor, “11b-0048,” showed a significant inhibitory effect on the expression of 11β-HSD1 in keratinocytes activated by various conditions and diabetic skin.

Pharmacogenomic variations may significantly influence responses to commonly prescribed stroke medications. Despite accumulating evidence, genetic testing has not yet been widely integrated into stroke care. This review summarizes current evidence and provides practical guidance for clinical implementation. Pharmacogenomic studies and clinical guidelines related to antiplatelet agents, anticoagulants, and statins were reviewed, with particular emphasis on East Asian populations. Substantial evidence supports genotype-guided use of clopidogrel (CYP2C19), warfarin (CYP2C9, VKORC1, CYP4F2), and statins (SLCO1B1, ABCG2). For aspirin, PTGS1/2 and PEAR1 variants have been investigated; however, current data remain insufficient for clinical application. Regarding direct oral anticoagulants (DOACs), candidate genes such as ABCB1 and CES1 demonstrate pharmacokinetic associations, though robust clinical outcome data are lacking. Distinct allele frequencies in East Asians—such as higher prevalence of CYP2C19 and ABCG2 variants—underscore the need for population-specific strategies. Beyond single-gene approaches, polygenic risk scores, pharmacogenomic panels, and integration with multi-omics data and artificial intelligence represent promising directions for personalized therapy. Pharmacogenomic testing can enhance stroke pharmacotherapy, particularly in populations with high frequencies of actionable variants. Broader implementation requires rapid testing platforms, clinician education, tailored clinical guidelines, and real-world validation of aspirin, DOACs, and multi-gene approaches. Future research should expand population-specific studies and integrate pharmacogenomics within the broader framework of precision medicine to ensure equitable clinical benefit.

Background and Objectives: Clinical characteristics and outcomes in acute heart failure (AHF) vary by phenotype. We assessed phenotype-specific features, treatment patterns, and outcomes in a nationwide Korean cohort. Methods: The Korean Heart Failure III registry prospectively enrolled 7,351 AHF admissions at 47 hospitals. Among 6,777 patients with available left ventricular ejection fraction (EF), phenotypes were defined as heart failure with reduced EF (HFrEF, ≤40%), mildly reduced EF (HFmrEF,41–49%), or preserved EF (HFpEF, ≥50%). The primary endpoint was a 12-month composite of all-cause death or heart transplantation, evaluated from index admission and, among hospital survivors, from discharge. We used inverse probability weighting (multinomial generalized boosted models with stabilized, trimmed weights) and weighted Cox proportional-hazards models to estimate hazard ratios (HRs). Results: Phenotype distribution was 58.9% HFrEF, 13.6% HFmrEF, and 27.5% HFpEF. Crude 12-month composite rates from index admission were 13.4% (HFrEF), 12.7% (HFmrEF), and 16.8% (HFpEF). After weighting, from index admission, HFmrEF (HR, 0.892; 95% confidence interval [CI], 0.731–1.088) and HFpEF (HR, 1.101; 95% CI, 0.939–1.291) did not differ from HFrEF; from discharge, HFpEF had modestly higher risk (HR, 1.207; 95% CI, 1.008–1.445) whereas HFmrEF did not (HR, 1.039; 95% CI, 0.844–1.279). Hyponatremia and chronic kidney disease were consistent adverse markers, while angiotensin-converting enzyme inhibitor/ angiotensin II receptor blocker use at discharge was protective. Conclusions Across the EF spectrum, phenotypes showed distinct profiles and risk. Postdischarge risk was modestly higher in HFpEF, supporting phenotype-tailored care and systematic discharge optimization in Korean patients with AHF.

Heart failure (HF) is a major cause of mortality and morbidity in South Korea, imposing substantial physical, emotional, and financial burdens on patients and society. Despite the high burden of symptom and complex care needs of HF patients, palliative care and hospice services remain underutilized in South Korea due to cultural, institutional, and knowledge-related barriers. This position statement from the Korean Society of Heart Failure emphasizes the need for integrating palliative and hospice care into HF management to improve quality of life and support holistic care for patients and their families. By clarifying the role of palliative care in HF and proposing practical referral criteria, this position statement aims to bridge the gap between HF and palliative care services in South Korea, ultimately improving patient-centered outcomes and aligning treatment with the goals and values of HF patients.

Atopic dermatitis (AD) is the most prevalent inflammatory skin condition, with approximately 80% of cases originating in childhood and some emerging in adulthood. In South Korea, the estimated prevalence of AD ranges between 10% and 20% in children and 1% and 3% in adults. Severe/recalcitrant AD manifests as a chronic, relapsing skin disorder, persisting with uncontrolled symptoms even after topical steroid treatment. Corticosteroids and systemic immunosuppression, conventionally the standard care for difficult-to-treat diseases, cause numerous undesirable side effects. When AD persists despite topical steroid application, systemic therapies like cyclosporine or systemic steroids become the second treatment strategy. The desire for targeted treatments, along with an enhanced understanding of AD’s pathophysiology, has spurred novel therapeutic development. Recent advances introduce novel systemic options, such as biological agents and small-molecule therapy, tailored to treat severe or recalcitrant AD. Notably, dupilumab, a monoclonal antibody inhibiting interleukin 4 and 13, marked a transformative breakthrough upon gaining approval from the U.S. Food and Drug Administration (FDA) in 2017, leading to a paradigm shift in the systemic treatment of AD. Furthermore, both dupilumab and Janus kinase inhibitors, including baricitinib, abrocitinib, and tofacitinib, now approved by the Korean FDA, have established their applicability in clinical practice. These innovative therapeutic agents have demonstrated favorable clinical outcomes, effectively addressing moderate to severe AD with fewer side reactions than those associated with previous systemic immunosuppressants. This review summarizes the latest advancements and evidence regarding systemic treatments for AD, including newly approved drugs in Korea.

Objective: This study was performed to evaluate the efficacy and safety of lurasidone (160 mg/day) compared to quetiapine XR (QXR; 600 mg/day) in the treatment of acutely psychotic patients with schizophrenia. Methods: Patients were randomly assigned to 6 weeks of double-blind treatment with lurasidone 160 mg/day (n=105) or QXR 600 mg/day (n=105). Primary efficacy measure was the change from baseline to week 6 in Positive and Negative Syndrome Scale (PANSS) total score and Clinical Global Impressions severity (CGI-S) score. Adverse events, body measurements, and laboratory parameters were assessed. Results: Lurasidone demonstrated non-inferiority to QXR on the PANSS total score. Adjusted mean±standard error change at week 6 on the PANSS total score was -26.42±2.02 and -27.33±2.01 in the lurasidone and QXR group, respectively. The mean difference score was -0.91 (95% confidence interval -6.35–4.53). The lurasidone group showed a greater reduction in PANSS total and negative subscale on week 1 and a greater reduction in end-point CGI-S score compared to the QXR group. Body weight, body mass index, and waist circumference in the lurasidone group were reduced, with significantly lower mean change compared to QXR. Endpoint changes in glucose, cholesterol, triglycerides, and low-density lipoprotein levels were also significantly lower. The most common adverse drug reactions with lurasidone were akathisia and nausea. Conclusion Lurasidone 160 mg/day was found to be non-inferior to QXR 600 mg/day in the treatment of schizophrenia with comparable efficacy and tolerability. Adverse effects of lurasidone were generally tolerable, and beneficial effects on metabolic parameters can be expected.

Gastric cancer is one of the most common cancers in Korea and the world. Since 2004, this is the 4th gastric cancer guideline published in Korea which is the revised version of previous evidence-based approach in 2018. Current guideline is a collaborative work of the interdisciplinary working group including experts in the field of gastric surgery, gastroenterology, endoscopy, medical oncology, abdominal radiology, pathology, nuclear medicine, radiation oncology and guideline development methodology. Total of 33 key questions were updated or proposed after a collaborative review by the working group and 40 statements were developed according to the systematic review using the MEDLINE, Embase, Cochrane Library and KoreaMed database. The level of evidence and the grading of recommendations were categorized according to the Grading of Recommendations, Assessment, Development and Evaluation proposition. Evidence level, benefit, harm, and clinical applicability was considered as the significant factors for recommendation. The working group reviewed recommendations and discussed for consensus. In the earlier part, general consideration discusses screening, diagnosis and staging of endoscopy, pathology, radiology, and nuclear medicine. Flowchart is depicted with statements which is supported by meta-analysis and references. Since clinical trial and systematic review was not suitable for postoperative oncologic and nutritional follow-up, working group agreed to conduct a nationwide survey investigating the clinical practice of all tertiary or general hospitals in Korea. The purpose of this survey was to provide baseline information on follow up. Herein we present a multidisciplinary-evidence based gastric cancer guideline.