Background: Atopic dermatitis (AD) is a common skin disease with a wide range of symptoms. Due to the rapidly changing treatment landscape, regular updates to clinical guidelines are needed. Objective: This study aimed to update the guidelines for the treatment of AD to reflect recent therapeutic advances and evidence-based recommendations. Methods: The Patient characteristics, type of Intervention, Control, and Outcome framework was used to determine 48 questions related to AD management. Evidence was graded, recommendations were determined, and, after 2 voting rounds among the Korean Atopic Dermatitis Association (KADA) council members, consensus was achieved. Results: This guideline provides treatment guidance on advanced systemic treatment modalities for AD. In particular, the guideline offers up-to-date treatment recommendations for biologics and Janus-kinase inhibitors used in the treatment of patients with moderate to severe AD.It also provides guidance on other therapies for AD, along with tailored recommendations for children, adolescents, the elderly, and pregnant or breastfeeding women. Conclusion KADA’s updated AD treatment guidelines incorporate the latest evidence and expert opinion to provide a comprehensive approach to AD treatment. The guidelines will help clinicians optimize patient-specific therapies.

Background: Atopic dermatitis (AD) is a common skin disease with a wide range of symptoms. Due to the rapidly changing treatment landscape, regular updates to clinical guidelines are needed. Objective: This study aimed to update the guidelines for the treatment of AD to reflect recent therapeutic advances and evidence-based practices. Methods: The Patient characteristics, type of Intervention, Control, and Outcome framework was used to determine 48 questions related to AD management. Evidence was graded, recommendations were determined, and, after 2 voting rounds among the Korean Atopic Dermatitis Association (KADA) council members, consensus was achieved. Results: The guidelines provide detailed recommendations on foundational therapies, including the use of moisturizers, cleansing and bathing practices, allergen avoidance, and patient education. Guidance on topical therapies, such as topical corticosteroids and calcineurin inhibitors, is also provided to help manage inflammation and maintain skin barrier function in patients with AD. Additionally, recommendations on conventional systemic therapies, including corticosteroids, cyclosporine, and methotrexate, are provided for managing moderate to severe AD. Conclusion KADA’s updated AD guidelines offer clinicians evidence-based strategies focused on basic therapies, topical therapies, and conventional systemic therapies, equipping them to enhance quality of care and improve patient outcomes in AD management.

Background: In 2006, the Korean Atopic Dermatitis Association (KADA) working group released the diagnostic criteria for Korean atopic dermatitis (AD). Recently, more simplified, and practical AD diagnostic criteria have been proposed. Objective: Based on updated criteria and experience, we studied to develop and share a consensus on diagnostic criteria for AD in Koreans. Materials and Methods: For the diagnostic criteria, a questionnaire was constructed by searching the English-language literature in MEDLINE and the Cochrane Database of Systematic Reviews. A modified Delphi method composed of 3 rounds of email questionnaires was adopted for the consensus process. Fifty-four KADA council members participated in the 3 rounds of votes and expert consensus recommendations were established. Results: Diagnostic criteria for AD include pruritus, eczema with age-specific pattern, and chronic or relapsing history. Diagnostic aids for AD encompass xerosis, immunoglobulin E reactivity, hand–foot eczema, periorbital changes, periauricular changes, perioral changes, nipple eczema, perifollicular accentuation, and personal or family history of atopy. Conclusion This study streamlined and updated the diagnostic criteria for AD in Korea, making them more practicable for use in real-world clinical field.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

Background: Inflammation following stroke is associated with poor outcomes, and the anti-inflammatory effects of neural stem cells (NSCs) have been reported. However, the direct immunomodulatory effects of NSCs in hemorrhagic stroke remain unclear. In the present study, we investigated the anti-inflammatory mechanism of direct co-culture with NSCs on RAW 264.7 cells stimulated by hemolysate. Methods: RAW 264.7 cells were stimulated with the hemolysate for 4 hours to induce hemorrhagic inflammation in vitro. Regarding direct co-culture, RAW 264.7 cells were cultured with HB1.F3 cells for 24 hours in normal medium and stimulated with hemolysate for 4 hours. Inflammatory cell signaling molecules, including cycloxygenase-2 (COX-2), interleukin-1β (IL-1β), and extracellular signal-regulated kinase (ERK), as well as tumor necrosis factor-α (TNF-α), were evaluated. Results: After stimulation with the hemolysate, levels of the inflammatory markers COX-2, IL-1β, and TNF-α were increased in RAW264.7 cells. Inflammatory marker production was reduced in the group subjected to direct co-culture with HB1.F3 in comparison to that in the RAW264.7 group stimulated by the hemolysate. In addition, direct co-culture with HB1.F3 significantly suppressed the phosphorylation of ERK 1/2 in hemolysate-stimulated RAW 264.7 cells. Moreover, treatment of the ERK inhibitor (U0126) suppressed the expression levels of inflammatory markers in hemolysate-stimulated RAW246.7 cells. Conclusion These results demonstrate that direct co-culture with HB1.F3 suppresses inflammation by attenuating the ERK pathway. These findings suggest that direct NSC treatment modulates the inflammatory response in hemorrhagic stroke.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

By investigating the characteristics and prognosis of breast cancer (BC) patients who have undergone hormone replacement therapy (HRT), this study addresses a gap in the existing literature. A total of 17,355 postmenopausal patients with BC were analyzed using data from the Korea Breast Cancer Society database (2000–2014). Among them, 3,585 (20.7%) had a history of HRT before BC diagnosis (HRT group), while 13,770 (79.3%) never received HRT (non-HRT group). The HRT group exhibited an earlier pathologic stage, lower histologic and nuclear grades, and a higher rate of breast conservation surgery compared to the non-HRT group. Furthermore, this group had a higher rate of screening participation and a greater proportion of patients with a normal or overweight body mass index (BMI). The prognosis of the HRT group was better than that of the non-HRT group, with a 5-year overall survival rate of 93.9% versus 91.7% (p < 0.001). The hazard ratio for the HRT group was 0.7 (95% confidence interval, 0.608–0.805; p < 0.001). Increased screening participation, longer HRT duration, and a normal or overweight BMI were associated with a better prognosis in the HRT group. Patients with BC who underwent HRT showed better clinicopathological characteristics and prognosis than those who did not receive HRT. The results highlighted significant differences in patients who underwent screening and those with a normal or overweight BMI. Furthermore, a longer HRT duration was associated with a better prognosis.

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

By investigating the characteristics and prognosis of breast cancer (BC) patients who have undergone hormone replacement therapy (HRT), this study addresses a gap in the existing literature. A total of 17,355 postmenopausal patients with BC were analyzed using data from the Korea Breast Cancer Society database (2000–2014). Among them, 3,585 (20.7%) had a history of HRT before BC diagnosis (HRT group), while 13,770 (79.3%) never received HRT (non-HRT group). The HRT group exhibited an earlier pathologic stage, lower histologic and nuclear grades, and a higher rate of breast conservation surgery compared to the non-HRT group. Furthermore, this group had a higher rate of screening participation and a greater proportion of patients with a normal or overweight body mass index (BMI). The prognosis of the HRT group was better than that of the non-HRT group, with a 5-year overall survival rate of 93.9% versus 91.7% (p < 0.001). The hazard ratio for the HRT group was 0.7 (95% confidence interval, 0.608–0.805; p < 0.001). Increased screening participation, longer HRT duration, and a normal or overweight BMI were associated with a better prognosis in the HRT group. Patients with BC who underwent HRT showed better clinicopathological characteristics and prognosis than those who did not receive HRT. The results highlighted significant differences in patients who underwent screening and those with a normal or overweight BMI. Furthermore, a longer HRT duration was associated with a better prognosis.

Background: Inflammation following stroke is associated with poor outcomes, and the anti-inflammatory effects of neural stem cells (NSCs) have been reported. However, the direct immunomodulatory effects of NSCs in hemorrhagic stroke remain unclear. In the present study, we investigated the anti-inflammatory mechanism of direct co-culture with NSCs on RAW 264.7 cells stimulated by hemolysate. Methods: RAW 264.7 cells were stimulated with the hemolysate for 4 hours to induce hemorrhagic inflammation in vitro. Regarding direct co-culture, RAW 264.7 cells were cultured with HB1.F3 cells for 24 hours in normal medium and stimulated with hemolysate for 4 hours. Inflammatory cell signaling molecules, including cycloxygenase-2 (COX-2), interleukin-1β (IL-1β), and extracellular signal-regulated kinase (ERK), as well as tumor necrosis factor-α (TNF-α), were evaluated. Results: After stimulation with the hemolysate, levels of the inflammatory markers COX-2, IL-1β, and TNF-α were increased in RAW264.7 cells. Inflammatory marker production was reduced in the group subjected to direct co-culture with HB1.F3 in comparison to that in the RAW264.7 group stimulated by the hemolysate. In addition, direct co-culture with HB1.F3 significantly suppressed the phosphorylation of ERK 1/2 in hemolysate-stimulated RAW 264.7 cells. Moreover, treatment of the ERK inhibitor (U0126) suppressed the expression levels of inflammatory markers in hemolysate-stimulated RAW246.7 cells. Conclusion These results demonstrate that direct co-culture with HB1.F3 suppresses inflammation by attenuating the ERK pathway. These findings suggest that direct NSC treatment modulates the inflammatory response in hemorrhagic stroke.