Vitiligo is an autoimmune disease in which CD8+ T-cells target and destroy melanocytes, leaving areas of skin without pigment production. Nonsegmental vitiligo, the classical form of the disease, results in symmetrical, bilateral white patches. Vitiligo is a chronic, unpredictable disease, characterized by flares, with depigmentation and periods of disease arrest alternating. This process can be stressful and negatively impact one’s quality of life. Various hypotheses have been offered, including cellular stress causing degeneration of melanocytes, chemical toxicity causing melanocyte death, and neural changes that influence melanocytes or their ability to produce melanin. Recently, the interaction between oxidative stress and autoimmune-mediated melanocyte loss has been proposed as the primary pathogenesis of vitiligo. It is now well accepted that interferon-γ and/or C-X-C motif chemokine ligand 10 axis is functionally required for both progression and maintenance of vitiligo, making this pathway a potential therapeutic target. Most therapeutic interventions in the management of vitiligo have been developed based on this immunopathogenesis. This article aims to review the current understanding of the vitiligo pathogenesis.

Vitiligo is an autoimmune disease in which CD8+ T-cells target and destroy melanocytes, leaving areas of skin without pigment production. Nonsegmental vitiligo, the classical form of the disease, results in symmetrical, bilateral white patches. Vitiligo is a chronic, unpredictable disease, characterized by flares, with depigmentation and periods of disease arrest alternating. This process can be stressful and negatively impact one’s quality of life. Various hypotheses have been offered, including cellular stress causing degeneration of melanocytes, chemical toxicity causing melanocyte death, and neural changes that influence melanocytes or their ability to produce melanin. Recently, the interaction between oxidative stress and autoimmune-mediated melanocyte loss has been proposed as the primary pathogenesis of vitiligo. It is now well accepted that interferon-γ and/or C-X-C motif chemokine ligand 10 axis is functionally required for both progression and maintenance of vitiligo, making this pathway a potential therapeutic target. Most therapeutic interventions in the management of vitiligo have been developed based on this immunopathogenesis. This article aims to review the current understanding of the vitiligo pathogenesis.

PURPOSE: This study investigated the effects of multiple drilling on the immature capital femoral epiphysis following ischemic injury in a piglet model. MATERIALS AND METHODS: Ischemic necrosis of capital femoral epiphysis was induced bilaterally in 12 piglets using a cervical ligation method. Three weeks later, medial, central, and lateral 3 drill holes were made on the left femoral head using 0.062" K-wire. At 3, 6, 9, and 12 weeks following the multiple drilling, femoral heads were harvested from each three piglets. On histologic examination, percent of revascularization, percent of osteoblast surface, capital femoral epiphyseal quotient and proximal femoral growth plate height were evaluated. Untreated right femoral heads served as control. RESULTS: While percent of revascularization of left capital femoral epiphysis with multiple drilling was significantly higher than untreated control side (p<0.001), percent of osteoblast surface, capital femoral epiphyseal quotient and proximal femoral growth plate height showed no significant difference. CONCLUSION: This study indicates that multiple drilling could promote revascularization of ischemic capital femoral epiphysis, and multiple drilling does not appear to produce bony physeal bars at short-term, if using small diameter drill. However, multiple drilling alone does not seem to prevent femoral head deformity or to promote new bone formation.
Animals ; Bone Remodeling ; Disease Models, Animal ; Epiphyses/*blood supply/pathology/*surgery ; Female ; Femur Head/*blood supply/pathology/*surgery ; Humans ; Ischemia/pathology/*surgery ; Legg-Calve-Perthes Disease/pathology/surgery ; Swine

No abstract available.

PURPOSE: To evaluate the efficacy of the in situ late osteosynthesis for slightly displaced fractures of the lateral humeral condyle. MATERIALS AND METHODS: From 2000 to 2004, 12 patients (8 boys and 4 girls) were managed with in situ late osteosynthesis for fractures of the lateral humeral condyle. The average age at the time of operation was 6 years 1 month (1 year 7 months~9 years 1 month), and the mean amount of fragment displacement was 3.3 mm (2.0~4.5 mm). The operative procedure included curettage and in situ fixation of the fragment RESULTS: Bony union was achieved in all cases after avg. 48 months (33~73 months) follow-up assessment. According to the score system of Dhillon et al, 7 patients had excellent, 3 had good, 2 had fair results. None of the patients developed avascular necrosis or premature closure of the epiphysis. CONCLUSION: We suggest that in situ fixation is an effective method for the late treatment of slightly displaced fracture of the lateral humeral condyle.
Child ; Curettage ; Displacement (Psychology) ; Follow-Up Studies ; Humans ; Necrosis ; Surgical Procedures, Operative

Several studies have previously reported that exposure to stress provokes behavioral changes, including antinociception, in rodents. In the present study, we studied the effect of acute cold-water (4°C) swimming stress (CWSS) on nociception and the possible changes in several signal molecules in male ICR mice.Here, we show that 3 min of CWSS was sufficient to produce antinociception in tailflick, hot-plate, von-Frey, writhing, and formalin-induced pain models. Significantly, CWSS strongly reduced nociceptive behavior in the first phase, but not in the second phase, of the formalin-induced pain model. We further examined some signal molecules' expressions in the dorsal root ganglia (DRG) and spinal cord to delineate the possible molecular mechanism involved in the antinociceptive effect under CWSS.CWSS reduced p-ERK, p-AMPKα1, p-AMPKα2, p-Tyk2, and p-STAT3 expression both in the spinal cord and DRG. However, the phosphorylation of mTOR was activated after CWSS in the spinal cord and DRG. Moreover, p-JNK and p-CREB activation were significantly increased by CWSS in the spinal cord, whereas CWSS alleviated JNK and CREB phosphorylation levels in DRG. Our results suggest that the antinociception induced by CWSS may be mediated by several molecules, such as ERK, JNK, CREB, AMPKα1, AMPKα2, mTOR, Tyk2, and STAT3 located in the spinal cord and DRG.

Several studies have previously reported that exposure to stress provokes behavioral changes, including antinociception, in rodents. In the present study, we studied the effect of acute cold-water (4°C) swimming stress (CWSS) on nociception and the possible changes in several signal molecules in male ICR mice.Here, we show that 3 min of CWSS was sufficient to produce antinociception in tailflick, hot-plate, von-Frey, writhing, and formalin-induced pain models. Significantly, CWSS strongly reduced nociceptive behavior in the first phase, but not in the second phase, of the formalin-induced pain model. We further examined some signal molecules' expressions in the dorsal root ganglia (DRG) and spinal cord to delineate the possible molecular mechanism involved in the antinociceptive effect under CWSS.CWSS reduced p-ERK, p-AMPKα1, p-AMPKα2, p-Tyk2, and p-STAT3 expression both in the spinal cord and DRG. However, the phosphorylation of mTOR was activated after CWSS in the spinal cord and DRG. Moreover, p-JNK and p-CREB activation were significantly increased by CWSS in the spinal cord, whereas CWSS alleviated JNK and CREB phosphorylation levels in DRG. Our results suggest that the antinociception induced by CWSS may be mediated by several molecules, such as ERK, JNK, CREB, AMPKα1, AMPKα2, mTOR, Tyk2, and STAT3 located in the spinal cord and DRG.

Sarcoidosis is a multisystem granulomatous disease of unknown etiology. A range of factors including tuberculous infection, beryllium exposure, and cold climate have been implicated in the pathogenesis of the condition. A 45-year-old woman presented with a 4-month history of an asymptomatic eyelid swelling and multiple erythematous papules on the neck. Histological examination of the neck, orbital soft tissue, and lacrimal gland was consistent with sarcoidosis. Ziehl−Neelsen stains and polymerase chain reactions (PCRs) for tuberculosis on the skin biopsy specimens were negative. However, the orbital soft tissue specimen was positive for non-tuberculous mycobacteria (NTM) PCR. The patient was finally diagnosed with sarcoidosis associated with NTM. Treatment with systemic steroid and hydroxychloroquine was started, resulting in an improvement of skin lesions. We herein report a case of sarcoidosis associated with NTM infection with review of the literature, as only little is known regarding the role of mycobacteria in sarcoidosis.

Background: Vulvar pruritus is a common complaint among women presenting to dermatologists. However, few studies have analyzed the dermatologic conditions that cause it. Objective: This retrospective study aims to evaluate the clinical features and causes of pruritic skin lesions of the female external genitalia. Methods: This study included 161 female patients with vulvar pruritus between 2008 and 2018 at CHA Bundang Medical Center. Data were collected by reviewing the electronic medical records retrospectively. The age, diagnosis, and histopathologic findings of the patients were reviewed. Results: The patients’ mean age was 49 years. On physical examination, 71.4% of patients (n=115) had definite skin lesions, and 28.6% (n=46) had ‘vulvar pruritus without skin rash’. The most common diagnostic category, confirmed by skin biopsy, was inflammatory dermatoses (53.4%, n=86), including lichen sclerosus et atrophicus, lichen simplex chronicus, nonatopic eczema, atopic eczema, and psoriasis. Moreover, 7.5% of patients (n=12) were diagnosed with infectious diseases, including candidiasis, herpes simplex virus, syphilis, and scabies; 5.6% (n=9) were diagnosed with neoplastic diseases, including vulvar intraepithelial neoplasia, squamous cell carcinoma, extramammary Paget’s disease, and Bowen’s disease. Conclusion The causes of vulvar itch are vast, and often, multiple causes coexist simultaneously. Therefore, it requires a systemic approach to establish the correct diagnosis. Dermatologists should actively participate in the diagnosis and treatment.

Background: Vulvar pruritus is a common complaint among women presenting to dermatologists. However, few studies have analyzed the dermatologic conditions that cause it. Objective: This retrospective study aims to evaluate the clinical features and causes of pruritic skin lesions of the female external genitalia. Methods: This study included 161 female patients with vulvar pruritus between 2008 and 2018 at CHA Bundang Medical Center. Data were collected by reviewing the electronic medical records retrospectively. The age, diagnosis, and histopathologic findings of the patients were reviewed. Results: The patients’ mean age was 49 years. On physical examination, 71.4% of patients (n=115) had definite skin lesions, and 28.6% (n=46) had ‘vulvar pruritus without skin rash’. The most common diagnostic category, confirmed by skin biopsy, was inflammatory dermatoses (53.4%, n=86), including lichen sclerosus et atrophicus, lichen simplex chronicus, nonatopic eczema, atopic eczema, and psoriasis. Moreover, 7.5% of patients (n=12) were diagnosed with infectious diseases, including candidiasis, herpes simplex virus, syphilis, and scabies; 5.6% (n=9) were diagnosed with neoplastic diseases, including vulvar intraepithelial neoplasia, squamous cell carcinoma, extramammary Paget’s disease, and Bowen’s disease. Conclusion The causes of vulvar itch are vast, and often, multiple causes coexist simultaneously. Therefore, it requires a systemic approach to establish the correct diagnosis. Dermatologists should actively participate in the diagnosis and treatment.