A review of hypotheses for the pathophysiology of vitiligo and comorbidities, as well as effective treatment techniques
A review of hypotheses for the pathophysiology of vitiligo and comorbidities, as well as effective treatment techniques
Mohadeseh Jafarnia Kalansara,1,*Sara Seyed Shazileh,2Seyed Mohammad Moshtaghioun,3
1. Department of Biology, Faculty of science, University of Mohaghegh Ardabili, Ardabil, Iran 2. Department of Biology, Faculty of science, Yazd University, Yazd, Iran 3. Department of Biology, Faculty of science, Yazd University, Yazd, Iran
Introduction: Vitiligo is a complicated illness produced by hereditary components, metabolic variables associated with cellular oxidative stress, melanocyte adherence to the epithelium, and immunology (innate and adaptive) that results in melanocyte invasion. Although the condition does not cause immediate physical damage, it can have a significant impact on a patient's psychological well-being resulting in psychosocial distress and social stigmatization.
Several theories have been proposed to explain the pathogenesis of this pigment. However, the exact pathogenesis is still unclear. The most widely accepted theory is that vitiligo is an autoimmune disorder that affects genetically predisposed individuals.
Autoimmune disorders associated with vitiligo include hypothyroidism, thyroiditis, adrenal insufficiency, and pernicious anemia in 20-30% of patients with vitiligo. the average age of onset of vitiligo varies between genders and geographic regions. This disease usually starts at the peak age of 10 to 30 years. It affects around 0.5-2% of the global population, with up to 1.1-2% of Asians affected. It is well-established that vitiligo is not a pure melanocyte defect. This is due to the dynamic interplay between genetic and environmental factors that cause the autoimmune destruction of melanocytes. Melanocytes are localized not only in the epidermis and the region of the hair follicle protrusion, but also in the structures of the inner ear and eyeball, and therefore vitiligo may be accompanied by hearing and vision disorders. A better understanding of individual etiological factors in the Differentiating between vitiligo subtypes is critical for prognosis and deciding on appropriate treatment options. New and evolving treatment approaches Understanding the intracellular molecular and signaling mechanisms, as well as the cytokine profile, in the pathogenesis of vitiligo has paved the way for the development of various innovative vitiligo therapies.
Methods: Three databases were reviewed for relevant research up to 2022: Google Scholar, PubMed, and Medline. Keywords searched: "Associated disorders", "Kinds of vitiligo", "Treatment", "Oxidative stress", "Cell therapy", "Micropigmentation", "Vitamin D analogs ", " TWEAK" Papers on ideas and disorders associated with vitiligo were evaluated first, followed by articles on new research for the creation of effective therapies.
Results: There are no particular topical or systemic medications for vitiligo at the moment.
Studies suggest that miRNAs may play a role in the etiology of vitiligo and may be used as biomarkers. It is important to learn more about miRNAs and their role in order to better understand the molecular process of vitiligo development.
TWEAK is a multifunctional cytokine that belongs to the family of tumor necrosis factor receptor ligands. According to the current findings, TWEAK may play a role in the pathogenesis of vitiligo, differentiate between segmental and nonsegmental vitiligo, be a potential predictor of focal vitiligo fate, and be a promising therapeutic target in vitiligo.
Vitiligo can be caused by the presence of a specific type of cell called TRM cells, which have been shown to play a key role in the development and flare-up of human vitiligo. This suggests targeting these cells might be an effective long-term therapy strategy for the condition.
KRTAP10-11, IP6K2, and C9 were proposed as potential biomarkers for the pathogenesis and prognosis of vitiligo patients' responses to epidermal cell transplantation.
According to existing studies, combining topical calcipotriol or tacalcitol with NB-UVB may improve the therapeutic effects of vitiligo, with tacalcitol having a greater benefit than calcipotriol.
Micropigmentation may be a final resort for vitiligo patients who have not responded to regular medical and surgical therapies.
Conclusion: Despite advancements, the cause of vitiligo remains unknown. The fundamental problem in developing pathophysiology models is integrating various notions, such as oxidative stress and autoimmune response patterns. We now understand that differentiating between types of vitiligo is crucial for evaluating prognosis and selecting viable treatment options. The coexistence of vitiligo with autoimmune diseases is significant and points to an autoimmune etiopathogenesis of the condition. Phototherapy and other non-surgical treatments, such as phototherapy and topical agents, as well as numerous surgical techniques, are available as treatment alternatives for the condition. There is currently no therapy for vitiligo. Several remedies, however, have been developed as a result of advances in understanding vitiligo, with over 80% of individuals having some degree of re-pigmentation.