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.

Activation of transient receptor potential vanilloid 1 (TRPV1), a calcium permeable channel expressed in primary sensory neurons, induces the release of glutamate from their central and peripheral afferents during normal acute and pathological pain. However, little information is available regarding the glutamate release mechanism associated with TRPV1 activation in primary sensory neurons. To address this issue, we investigated the expression of vesicular glutamate transporter (VGLUT) in TRPV1-immunopositive (+) neurons in the rat trigeminal ganglion (TG) under normal and complete Freund’s adjuvant (CFA)-induced inflammatory pain conditions using behavioral testing as well as double immunofluorescence staining with antisera against TRPV1 and VGLUT1 or VGLUT2. TRPV1 was primarily expressed in small and medium-sized TG neurons. TRPV1+ neurons constituted approximately 27% of all TG neurons. Among all TRPV1+ neurons, the proportion of TRPV1+ neurons coexpressing VGLUT1 (VGLUT1+/ TRPV1+ neurons) and VGLUT2 (VGLUT2+/TRPV1+ neurons) was 0.4% ± 0.2% and 22.4% ± 2.8%, respectively. The proportion of TRPV1+ and VGLUT2+ neurons was higher in the CFA group than in the control group (TRPV1+ neurons: 31.5% ± 2.5% vs. 26.5% ± 1.2%, VGLUT2+ neurons: 31.8% ± 1.1% vs. 24.6% ± 1.5%, p < 0.05), whereas the proportion of VGLUT1+, VGLUT1+/TRPV1+, and VGLUT2+/TRPV1+ neurons did not differ significantly between the CFA and control groups. These findings together suggest that VGLUT2, a major isoform of VGLUTs, is involved in TRPV1 activation-associated glutamate release during normal acute and inflammatory pain.

Activation of transient receptor potential vanilloid 1 (TRPV1), a calcium permeable channel expressed in primary sensory neurons, induces the release of glutamate from their central and peripheral afferents during normal acute and pathological pain. However, little information is available regarding the glutamate release mechanism associated with TRPV1 activation in primary sensory neurons. To address this issue, we investigated the expression of vesicular glutamate transporter (VGLUT) in TRPV1-immunopositive (+) neurons in the rat trigeminal ganglion (TG) under normal and complete Freund’s adjuvant (CFA)-induced inflammatory pain conditions using behavioral testing as well as double immunofluorescence staining with antisera against TRPV1 and VGLUT1 or VGLUT2. TRPV1 was primarily expressed in small and medium-sized TG neurons. TRPV1+ neurons constituted approximately 27% of all TG neurons. Among all TRPV1+ neurons, the proportion of TRPV1+ neurons coexpressing VGLUT1 (VGLUT1+/ TRPV1+ neurons) and VGLUT2 (VGLUT2+/TRPV1+ neurons) was 0.4% ± 0.2% and 22.4% ± 2.8%, respectively. The proportion of TRPV1+ and VGLUT2+ neurons was higher in the CFA group than in the control group (TRPV1+ neurons: 31.5% ± 2.5% vs. 26.5% ± 1.2%, VGLUT2+ neurons: 31.8% ± 1.1% vs. 24.6% ± 1.5%, p < 0.05), whereas the proportion of VGLUT1+, VGLUT1+/TRPV1+, and VGLUT2+/TRPV1+ neurons did not differ significantly between the CFA and control groups. These findings together suggest that VGLUT2, a major isoform of VGLUTs, is involved in TRPV1 activation-associated glutamate release during normal acute and inflammatory pain.

BACKGROUND: The aim of this study was to determine whether there is a positive correlation between gamma-glutamyltransferase (GGT) levels and the prevalence of metabolic syndrome and whether GGT can be used as an easily checkable metabolic index using data from the large-scale Korean Genome and Epidemiology Study (KoGES).METHODS: We obtained data of 211,725 participants of the KoGES. The collected data included age, sex, height, weight, waist circumference, and various biochemical characteristics, including serum GGT levels. The data of study participants who ingested more than 40 g/day of alcohol and who were diagnosed with metabolic syndrome at baseline was excluded. We analyzed the prevalence of metabolic syndrome according to GGT quartiles in both genders.RESULTS: The GGT level was significantly higher in subjects with metabolic syndrome compared to normal subjects (37.92±48.20 mg/dL vs. 25.62±33.56 mg/dL). The prevalence of metabolic syndrome showed a stepwise increase with GGT quartiles in both male and female subjects. Compared to the lowest GGT quartile, the odds ratio was 1.534 (95% confidence interval [CI], 1.432 to 1.643), 1.939 (95% CI, 1.811 to 2.076), and 2.754 (95% CI, 2.572 to 2.948) in men and 1.155 (95% CI, 1.094 to 1.218), 1.528 (95% CI, 1.451 to 1.609), and 2.022 (95% CI, 1.921 to 2.218) in women with increasing GGT quartile. The cutoff value of GGT predicting risk of metabolic syndrome was 27 IU/L in men and 17 IU/L in women.CONCLUSION: We suggested that GGT could be an easily checkable marker for the prediction of metabolic syndrome.
Epidemiology ; Female ; gamma-Glutamyltransferase ; Genome ; Humans ; Male ; Odds Ratio ; Prevalence ; Waist Circumference

PURPOSE: Isolated gonadotropin-releasing hormone (GnRH) deficiency (IGD) is classified as Kallmann syndrome (KS) with anosmia and normosmic idiopathic hypogonadotropic hypogonadism (nIHH). This study was undertaken to investigate the clinical, endocrinological, and molecular characteristics in Korean patients with KS and nIHH. METHODS: Twenty-six patients from 25 unrelated families were included. Their clinical, endocrinological, and radiological findings were analyzed retrospectively. Mutation analysis of the GNRH1, GNRHR, KISS1, KISS1R, PROK2, PROKR2, TAC3, TACR3, FGF8, FGFR1, and KAL1 genes was performed in all patients. CHD7 and SOX10 were analyzed in patients with CHARGE (Coloboma, Heart defects, choanae Atresia, Growth retardation, Genitourinary abnormality, Ear abnormality) features or deafness. RESULTS: Of the 26 patients, 16 had KS and 10 had nIHH. At diagnosis, mean chronologic age was 18.1 years in males and 18.0 years in females; height SDS were -0.67+/-1.35 in males, -1.12+/-1.86 in females; testis volume was 2.0+/-1.3 mL; and Tanner stage was 1.5. There were associated anomalies in some of the KS patients: hearing loss (n=6) and congenital heart disease (n=4). Absence or hypoplasia of the olfactory bulb/sulci was found in 84.62% of patients with KS. Molecular defects in KAL1, SOX10, and CHD7 were identified in 5 patients from 4 families (16.0%, 4/25 pedigrees). After sex hormone replacement therapy, there were improvement in sexual characteristics and the sexual function. CONCLUSION: This study described the clinical, endocrinological, and molecular genetic features in IGD patients in Korea. Although the mutation screening was performed in 10 genes that cause IGD, molecular defects were identified in relatively small proportions of the cohort.
Cohort Studies ; Deafness ; Diagnosis ; Ear ; Female ; Gonadotropin-Releasing Hormone ; Hearing Loss ; Heart ; Heart Defects, Congenital ; Hormone Replacement Therapy ; Humans ; Hypogonadism* ; Immunoglobulin D ; Kallmann Syndrome* ; Korea ; Male ; Mass Screening ; Molecular Biology ; Nasopharynx ; Olfaction Disorders ; Retrospective Studies ; Testis ; Urogenital Abnormalities

Mucous gland adenoma of the bronchus is a rare benign tumor arising from the bronchial mucous gland. It accounts for less than 0.5 % of all lung tumors. In adults, tracheal tumors are most often malignant. Among benign tumors arising in the trachea, mucous gland adenoma of the trachea is extremely rare. First case was reported by Ferguson and Cleeland in 1988, as "Mucous gland adenoma of the trachea". Microscopic study shows it to arise from normal submucosal mucous glands forming glandular or tubular structures composed of mucous secreting cells. Common symptoms were cough, hemoptysis, recurrent and protracted pneumonia, shortness of breath, and wheeze. Duration of symptoms before diagnosis varied from a few weeks to 10 years with prolonged symptoms being usual. Management of these tumors should be complete excision, including pulmonary resection because two instances of recurrence after local excision have been reported.
Adenoma* ; Adult ; Bronchi ; Cough ; Diagnosis ; Dyspnea ; Hemoptysis ; Humans ; Lung ; Pneumonia ; Recurrence ; Trachea*

No abstract available.
Amniocentesis* ; Cytogenetics*

Hydrops fetalis is diagnosed when abnormal fluid collections are manifest in two or more fetal compartments, including abdominal ascites, pleural effusions, pericardial effusions, skin edema, polyhydroamniosis and placental edema. Although fetal hydrops was hystorically most commonly associated with Rh blood group isoimmunization, the availability of Rh immunoglobulin has increased the proportion of fetuses affected due to nonimmune etiologies. We have experienced a case of nonimmune hydrops fetalis at 32 weeks of gestation in a 27-year-old woman and reported that with brief review of related literatures.
Adult ; Ascites ; Edema ; Female ; Fetus ; Humans ; Hydrops Fetalis* ; Immunoglobulins ; Pericardial Effusion ; Pleural Effusion ; Pregnancy ; Skin