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.

Background: Oxidative stress is generally accepted as one of the principal pathogenesis of vitiligo, and keratinocyte-melanocyte interactions are also thought to play critical roles. It is well-known that antioxidant response and autophagy protect cells against oxidative damage, but the details and the compensatory relationship between the two mechanisms in the keratinocytes of vitiligo lesions remain unclear. Objective: To evaluate the antioxidant response and autophagy status of patients with vitiligo and to explore the interactions between these two mechanisms. Methods: Ten patients with clinicopathologically proven vitiligo and 10 normal controls were enrolled in our Department of Dermatology, Soonchunhyang University Hospital, Bucheon, Korea. Tissue samples of vitiligo lesions in the patient group and normal skin in the control group were immunohistochemically stained for nuclear factor erythroid 2-related factor 2 (Nrf2), Beclin-1, microtubule-associated protein light chain 3 (LC3)-II, and p62. The immunopositivity of epidermal keratinocytes was evaluated. Results: Keratinocytes in vitiligo lesions had a significantly lower expression of Nrf2 (p=0.002) than that in the cells of normal controls. The levels of autophagy markers did not differ significantly between the two groups, but decreases in the Beclin-1 and LC3-II levels, and an increase in the p62 level in the patient group may indicate a small decrease in autophagy of patients with vitiligo. Conclusion Decreased antioxidant response and reduced autophagy may trigger melanocyte apoptosis in vitiligo lesions.

Multiple miliary osteoma cutis (MMOC) is a rare variant of osteoma, characterized by multiple eruptive hard nodules on the face. A 70-year-old female presented with multiple solid skin-colored papules on both cheeks, unresponsive to conventional medical treatments. She reported receiving an injection of an unknown cosmetic filler substance into her face by an unlicensed medical practitioner 20 years ago. Facial computed tomography showed multiple small calcifications immediately adjacent to foreign material assumed to be the filler substance in the dermis. Histological examination revealed osteoclasts, osteocytes, and eosinophilic bony tissue in the dermis, suggestive of osteoma cutis. Although the pathogenesis remains unclear, inflammation caused by injected foreign material may induce metaplastic transformation of multipotent mesenchymal cells into osteoblasts, resulting in heterotopic ossification. Dermatologists should be aware that MMOC may occur following injection of foreign material by unlicensed practitioners. Performing a detailed history and clinical evaluation may aid in the diagnosis of such recalcitrant skin lesions.

Congenital insensitivity to pain with anhidrosis (CIPA) is an extremely rare disease characterized by insensitivity to pain, anhidrosis, and intellectual disability. CIPA is caused by a genetic mutation in the neurotrophic tyrosine receptor kinase 1 (NTRK1) gene on chromosome 1. The anhidrosis leads to cutaneous changes such as skin dryness, lichenification, and impetiginization. Moreover, patients with CIPA may experience repeated trauma and recalcitrant eczema due to excessive scratching of wounds on their skin, because they do not feel any pain. Severe whole-body eczema in a patient with CIPA may be overlooked, leading these patients to be frequently diagnosed with atopic dermatitis and common eczema.Indeed, in patients with treatment-resistant or atypically distributed eczema and underlying anhidrosis, CIPA should be considered as a potential causative disease. Increased awareness of CIPA among dermatologists is necessary to ensure that patients receive an appropriate diagnosis. Herein, we report a rare case of generalized xerotic eczema in a patient with CIPA.

Benign cephalic histiocytosis (BCH) is an uncommon subtype of non-Langerhans cell histiocytosis. A 5-month-old boy presented with multiple yellowish facial papules and plaques, which later spread to his trunk and both extremities. Laboratory tests, including lipid profile, were normal. Histological examination revealed non-foamy histiocytes, lymphocytes, and some eosinophils in the dermis. Immunohistochemical staining was positive for CD68and factor XIIIa, but negative for CD1a and S-100. Additionally, the patient developed multiple café-au-lait spots with axillary and inguinal freckling. Next-generation sequencing identified a pathogenic variant of the neurofibromatosis type 1 (NF1) gene. Herein, we report a rare case of BCH in a patient with NF1. Although many cases of NF1 accompanied by juvenile xanthogranuloma have been reported, the association between BCH and NF1 has not been elucidated. However, considering that BCH may be a clinicopathological variant of juvenile xanthogranuloma, an association between the two diseases can be considered.

Purpose: Atrial fibrillation (AF) patients with low to intermediate risk, defined as non-gender CHA2DS2-VASc score of 0–1, are still at risk of stroke. This study verified the usefulness of ABCD score [age (≥60 years), B-type natriuretic peptide (BNP) or N-terminal pro-BNP (≥300 pg/mL), creatinine clearance (<50 mL/min/1.73 m2 ), and dimension of the left atrium (≥45 mm)] for stroke risk stratification in non-gender CHA2DS2-VASc score 0–1. Materials and Methods: This multi-center cohort study retrospectively analyzed AF patients with non-gender CHA2DS2-VASc score 0–1. The primary endpoint was the incidence of stroke with or without antithrombotic therapy (ATT). An ABCD score was validated. Results: Overall, 2694 patients [56.3±9.5 years; female, 726 (26.9%)] were followed-up for 4.0±2.8 years. The overall stroke rate was 0.84/100 person-years (P-Y), stratified as follows: 0.46/100 P-Y for an ABCD score of 0; 1.02/100 P-Y for an ABCD score ≥1. The ABCD score was superior to non-gender CHA2DS2-VASc score in the stroke risk stratification (C-index=0.618, p=0.015; net reclassification improvement=0.576, p=0.040; integrated differential improvement=0.033, p=0.066). ATT was prescribed in 2353 patients (86.5%), and the stroke rate was significantly lower in patients receiving non-vitamin K antagonist oral anticoagulant (NOAC) therapy and an ABCD score ≥1 than in those without ATT (0.44/100 P–Y vs. 1.55/100 P-Y; hazard ratio=0.26, 95% confidence interval 0.11–0.63, p=0.003). Conclusion The biomarker-based ABCD score demonstrated improved stroke risk stratification in AF patients with non-gender CHA2DS2-VASc score 0–1. Furthermore, NOAC with an ABCD score ≥1 was associated with significantly lower stroke rate in AF patients with non-gender CHA2DS2-VASc score 0–1.