25/01/2021
The skin doesn't have its characteristic color because it has lost its melanin. For some reason, the pigment-forming cells known as melanocytes have been destroyed.Autoimmune diseases, such as autoimmune thyroid disease (Hashimoto's thyroiditis) or type 1 diabetes, can also raise your odds.
-GENETIC
The observation that vitiligo was more prevalent in the immediate relatives of patients with vitiligo provided early evidence of its heritability. While vitiligo affects ~1% of the general population, the risk of a patient’s sibling developing the disease is 6%, and for an identical twin it is 23%. In addition, patients with vitiligo and their relatives have an increased risk of developing other autoimmune diseases, including autoimmune thyroiditis, type 1 diabetes, pernicious anemia, and Addison’s disease, suggesting that vitiligo is also an autoimmune disease . These early observations were later confirmed by genome-wide association (GWA) studies, which identified numerous common genetic variants in vitiligo patients encoding for components of both the innate (NLRP1, IFIH1, CASP7, C1QTNF6, TRIF) and adaptive immune system (FOXP3, BACH2, CD80, CCR6, PTPN22, IL2R, alpha GZMB, HLA class I and II).
-OXIDATIVE STRESS
Accumulating evidence suggests that melanocytes from vitiligo patients have intrinsic defects that reduce their capacity to manage cellular stress. Epidermal cells, including melanocytes, are constantly exposed to environmental stressors such as UV radiation and various chemicals, which can increase production of reactive oxygen species (ROS). While healthy melanocytes are capable of mitigating these stressors, melanocytes from vitiligo patients appear to be more vulnerable. For example, melanocytes from perilesional vitiligo skin demonstrate a dilated endoplasmic reticulum (ER) and abnormalities in their mitochondria and melanosome structure, all of which are characteristic of elevated cellular stress. High concentrations of epidermal H2O2 level and a decreased level of catalase, a critical enzyme that protects cells from oxidative damage, have been observed in skin of patients with vitiligo.
-ENVIRONMENT
The earliest triggering events that lead to vitiligo are not fully understood. Multiple studies suggest that a combination of melanocyte intrinsic defects and exposure to specific environmental factors may play a central role in disease onset. This was evident in a group of factory workers who developed vitiligo following exposure to monobenzone, an organic chemical phenol, in their gloves. Later studies confirmed that a history of exposure to other phenolic and catecholic chemicals found in dyes (especially hair dyes), resins/adhesives, and leather was associated with vitiligo.
Melanogenesis is a multi-step process through which the melanocyte produces melanin. Tyrosinase is a rate-limiting enzyme in this process that controls the production of melanin through oxidation of the amino acid tyrosine, a naturally occurring phenol and further discussed in this issue, Harris JE: Chemical-induced vitiligo. In vitro studies demonstrated that chemical phenols can act as tyrosine analogs within the melanocyte, precipitating high levels of cellular stress. This may include increased production of ROS and triggering of the unfolded protein response (UPR).
-INNATE IMMUNITY
As mentioned earlier, GWA studies in vitiligo patients implicated multiple susceptibility loci related to the genes that control the innate immunity. This likely causes dysregulated innate activation in response to melanocyte stress, demonstrated through recruitment of innate populations like natural killer (NK) cells and production and release of high levels of pro-inflammatory proteins and cytokines including heat-shock proteins (HSP), IL-1β, IL6, and IL-8. Among larger HSP molecules, inducible HSP70 (HSP70i) is unique, as it can be secreted to chaperone peptides specific to the originating host cells. Recently, HSP70i has been shown to be important for vitiligo pathogenesis in a mouse model through induction of inflammatory dendritic cells (DCs), which themselves may be cytotoxic or carry and present melanocyte-specific antigens to T cells in lymphoid tissues. This has been proposed to be a key crosstalk step between innate and adaptive immunity leading to the T cell-mediated autoimmune destruction of melanocytes.
-ADAPTIVE IMMUNITY
Ultimately, cytotoxic CD8+ T cells are responsible for the destruction of melanocytes.Cytokines secreted within the skin act as an early signal to help these autoreactive T cells locate stressed melanocytes.This is probably important because the epidermis is not vascularized, and so active mechanisms are required to help them efficiently locate melanocytes. Chemokines are small, secreted proteins that act as chemoattractants to guide T cell migration. IFN-γ and IFN-γ-induced chemokines (CXCL9 and CXCL10) are highly expressed in the skin and blood of patients with vitiligo, as well as a mouse model.In addition, IFN-γ and CXCL10 are required for both disease progression and maintenance in a mouse model of the disease.Recently, a separate study demonstrated that serum CXCL10 was not only higher in patients with vitiligo compared to healthy controls, but its level was associated with disease activity and significantly decreased after successful treatment, suggesting it may be used as a biomarker to monitor the disease activity and treatment response.
Your doctor can usually make a diagnosis of vitiligo by looking at your skin during a physical exam. You might also have other tests, including blood tests and:
-Skin biopsy, where a sample of your skin is sent to a laboratory for further examination
-A Wood's lamp test, where a doctor looks at your skin under UV light
and Home Remedies
There's no known way to prevent or cure vitiligo. But you can make your affected skin look better. Which treatment may work best for you depends on how old you are, how much skin needs improving, and how much your vitiligo affects you.
Medications for vitiligo
Your doctor may prescribe a corticosteroid cream to put on affected skin to try to give it its color back. It may take months to see changes in your skin. You might also see some streaks or lines on your skin, or your skin may get thinner.
If your vitiligo is progressing quickly, your doctor might suggest a corticosteroid pill or injection.
In rare cases, they may suggest an ointment called a calcineurin inhibitor ointment. It affects your immune system to ease inflammation. You might get it if your vitiligo is in a small area, usually around your face and neck. Doctors don't prescribe these often, as these medicines are linked to skin cancer and lymphoma.
-Alternative medicine for vitiligo
A few studies suggest that ginkgo biloba can give you some of your skin color back.
Some experts also say some supplements can help phototherapy be more effective, including:
Alpha-lipoic acid
Folic acid
Vitamin C
Vitamin B12
