All Rights Reserved. Vitiligo Explore the latest in vitiligo, including advances in understanding the genetics and management of the disease. Add to My Interests. All Publications. Check All. Uncheck All. JAMA Dermatology JAMA Ophthalmology 3.
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Create a free personal account to download free article PDFs, sign up for alerts, and more. Purchase access Subscribe to the journal. Early diagnosis and meticulous use of steroids has remained as the mainstay treatment, however, poor prognosis for individuals who presented with complications in the initial consultation has been associated with a poor final visual acuity. The main objective of presenting this classic case of Vogt-Koyanagi-Harada disease is describing its chronic systemic course, and the possible medical and surgical management for the disease and its complications.
Mechanisms of repigmentation induced by photobiomodulation therapy in vitiligo. Photobiomodulation PBM therapy is based on the exposure of biological tissues to low-level laser light coherent light or light-emitting diodes LEDs; noncoherent light , leading to the modulation of cellular functions, such as Photobiomodulation PBM therapy is based on the exposure of biological tissues to low-level laser light coherent light or light-emitting diodes LEDs; noncoherent light , leading to the modulation of cellular functions, such as proliferation and migration, which result in tissue regeneration.
PBM therapy has important clinical applications in regenerative medicine. Vitiligo is an acquired depigmentary disorder resulting from disappearance of functional melanocytes in the involved skin. Vitiligo repigmentation depends on available melanocytes derived from a melanocyte stem cells located in the bulge area of hair follicles and b the epidermis at the lesional borders, which contains a pool of functional melanocytes.
Since follicular melanoblasts MBs are derived from the melanocyte stem cells residing at the bulge area of hair follicle, the process of vitiligo repigmentation presents a research model for studying the regenerative effect of PBM therapy. Previous reports have shown favourable response for treatment of vitiligo with a low-energy helium-neon He-Ne laser.
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This review focuses on the molecular events that took place during the repigmentation process of vitiligo triggered by He-Ne laser Monochromatic radiation in the visible and infrared A IRA range sustains matrix metalloproteinase MMP , improves mitochondrial function, and increases adenosine triphosphate ATP synthesis and O2 consumption, which lead to cellular regenerative pathways.
Cytochrome c oxidase in the mitochondria was reported to be the photoacceptor upon which He-Ne laser exerts its effects.
Mitochondrial retrograde signalling is responsible for the cellular events by red light. The impact on cytochrome c oxidase within the mitochondria, an event that results in activation of CREB cyclic-AMP response element binding protein -related cascade, is responsible for the He-Ne laser promoting functional development at different stages of MBs and boosting functional melanocytes.
He-Ne laser irradiation induced a melanocyte stem cell differentiation; b immature outer root sheath MB migration; c differentiated outer root sheath MB melanogenesis and migration; and d perilesional melanocyte migration and proliferation. These photobiomodulation effects result in perifollocular and marginal repigmentation in vitiligo. Ultraviolet B UVB induces development of early melanocytic progenitors via increased oxidative stress in vitro suggesting the use of antioxidants after regimentation in UVB phototherapy for vitiligo.
Association study between melanocortin-1 receptor gene polymorphisms and occurrence of vitiligo in a Taiwanese population: possible explanation for lack of increased UV-related damage in vitiligo skin. Noninvasive cutaneous blood flow as a response predictor for visible light therapy on segmental vitiligo: a prospective pilot study.
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Currently, it is difficult to predict individual patients' Currently, it is difficult to predict individual patients' response to visible light therapy. Laser Doppler flowmetry was used to evaluate the cutaneous blood flow over SV lesions and contralateral normal skin. The pretreatment blood flow evaluation consisted of two stages: stage 1, following cold stress without prior visible light irradiation, and stage 2, following cold stress with prior visible light irradiation.
Subsequently, the patients received regular visible light treatment for 3months, and a comparison of the pretreatment blood flow patterns between the visible light responding and nonresponding groups was carried out at the end of the study period. The visible light responding group showed a more consistent occurrence of increased blood flow after stage 2 of the pretreatment evaluation while the nonresponding counterpart showed no significant changes.
Evaluation of cutaneous blood flow with and without prior visible light irradiation on cold-stressed SV lesions may serve as a treatment response predictor. Gastroparesis cured by gastrectomy. Successful management of insulin allergy and autoimmune polyendocrine syndrome type 4 with desensitization therapy and glucocorticoid treatment: a case report and review of the literature. Insulin allergy is a rare complication of insulin therapy, especially in type 1 diabetes mellitus T1DM.
Key manifestations are hypersensitivity-related symptoms and poor metabolic control. T1DM, as well as insulin allergy, T1DM, as well as insulin allergy, may develop in the context of autoimmune polyendocrine syndrome APS , further complicating management.
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Case Report. A year-old male patient, diagnosed with T1DM, was treated with various insulin therapy schemes over several months, which resulted in recurrent anaphylactoid reactions and poor glycemic control, after which he was referred to our Endocrinology and Immunology Department. A prick test was carried out for all commercially available insulin presentations and another insulin scheme was designed but proved unsuccessful. A desensitization protocol was started with Glargine alongside administration of Prednisone, which successfully induced tolerance.
Observation of skin lesions typical of vitiligo prompted laboratory workup for other auto Systemic analyses of immunophenotypes of peripheral T cells in non-segmental vitiligo: implication of defective natural killer T cells. Although it is widely believed that non-segmental vitiligo NSV results from the autoimmune destruction of melanocytes, a clear understanding of defects in immune tolerance, which mediate this uncontrolled self-reactivity, is still Although it is widely believed that non-segmental vitiligo NSV results from the autoimmune destruction of melanocytes, a clear understanding of defects in immune tolerance, which mediate this uncontrolled self-reactivity, is still lacking.
However, percentages of peripheral iNKT cells were significantly decreased in NSV patients compared to that in healthy controls. MicroRNA expression profiling identifies potential serum biomarkers for non-segmental vitiligo. Recent GWAS studies have identified vitiligo susceptibility genes that are related to immune Recent GWAS studies have identified vitiligo susceptibility genes that are related to immune regulation and immune targeting of melanocytes Spritz, We Zhou et al. However, the exact molecular mechanisms are still unclear. An update on new and emerging options for the treatment of vitiligo.
Vitiligo is an acquired leukoderma that results from the loss of epidermal melanocytes, and is characterized by macules and patches of depigmented skin. With a relatively high rate of prevalence, vitiligo occurs in localized, generalized, With a relatively high rate of prevalence, vitiligo occurs in localized, generalized, or segmental patterns; it can run a rapidly progressive course or remain stationary. The pathogenesis of vitiligo is not yet fully understood, but the autoimmune hypothesis is the most commonly accepted one, based on which, many treatment modalities have been described.
Although many therapeutic options exist and new modalities are still emerging, treatment challenges persist, as not all patients respond to available therapies. Variables that affect the choice of treatment include the extent, distribution, and progression rate of the lesions.
Vitiligo and social acceptance
Another challenge is the lack of a standardized scoring system, which hampers the production of level 1a evidence studies for the treatment of this condition. A clinical trial and molecular study of photoadaptation in vitiligo. Melanocytorrhagy and apoptosis in vitiligo: Connecting jigsaw pieces.
Vitiligo is an acquired depigmenting disorder characterized by a chronic and progressive loss of melanocytes from the epidermis and follicular reservoir. The mechanism of melanocyte disappearance has never been clearly understood. This review discussed the data supporting the theory of melanocytorrhagy and apoptosis as one of the primary defects underlying melanocyte loss. Theory of melanocytorrhagy proposes that non-segmental vitiligo is a primary melanocytorrhagic disorder with altered melanocyte responses to friction and possibly other types of stress, inducing their detachment and subsequent transepidermal loss.
Melanocytes detachment induces apoptosis whereas adherence to basement membrane suppresses apoptosis.
The study of apoptosis, mechanisms of its induction, and the ways to block apoptosis is one possible way to find both the causes of depigmentation and medications to prevent its progression.