
Abstract:
Vitiligo is an acquired skin dyschromia characterised by the loss of epidermal melanocytes. Vitiligo affects around 1% of the population in the United States and 0.1-2% globally. The precise pathophysiology of vitiligo is still unclear and is probably complex. Upon the conclusion of this update, participants should be capable of discussing the epidemiology of vitiligo and summarising the proposed findings mechanisms underlying the development of this disease. Furthermore, they ought to engage in discourse regarding physical matters, findings, patient approach, and several therapy approaches for this condition.
Keywords: Homoeopathic treatment, Vitiligo, epidermal melanocytes.
Introduction:
Vitiligo, an acquired skin condition, results in symmetrical white patches due to pigment cell loss from the epidermis distributed. Lesioned skin is more sunburn-prone due to melanin deficiency. Vitiligo is a global condition with a prevalence of <2%. In the US, it’s estimated to be 1% occurrence. The disease usually starts in childhood or young adulthood and peaks started 10-30 years ago. All races and sexes are impacted equally, but a female predominance reported. Disparity may be skewed by female patients’ expressed more cosmetic concerns. Vitiligo can affect mental health damaging to the patient. This applies mainly to darker-skinned patients. Vitiliginous skin stands out from regular skin due to its colour skin. Vitiligo can impact quality of life, self-esteem, marriage, and work, especially in darker-skinned people and some cultures. Patients may regard pigment loss as a threat to race identity.
Etiopathogenesis:
Vitiligo is polygenic and multifactorial. Although the exact cause is unknown, various theories have been presented to explain the loss of epidermal melanocytes disorder. Possible pathways include autoimmune, biochemical, oxidant, neurological, and viral. Genetics also play a major effect, according to studies of vulnerability to vitiligo.
Vitiligo genetics:
Vitiligo is a non-Mendelian hereditary condition with incomplete penetrance, numerous susceptibility loci, and genetic heterogeneity. It may entail inheritance, Melanin production, oxidative stress, and regulation genes autoimmunity. Because vitiligo often occurs with autoimmune disorders, HLA connections with vitiligo have been studied. Several haplotypes multiple studies have linked to vitiligo.
Immune system role:
There is a well-established link between vitiligo and autoimmune diseases. Vitiligo is often linked to thyroid illnesses including Hashimoto’s thyroiditis and Graves’ disease, as well as other endocrinopathies like Addison’s disease and diabetes mellitus. Some of the links between alopecia areata, pernicious anaemia, systemic lupus erythematosus, inflammatory bowel disease, rheumatoid arthritis, psoriasis, and autoimmune polyglandular syndrome are questionable. The presence of circulating autoantibodies to melanocytes in vitiligo patients’ blood strongly suggests an autoimmune aetiology. Melanocyte cell surface antigen-specific autoantibodies destroy melanocytes in vivo and in vitro.
Vitiligo oxidant-antioxidant function:
In vitiligo, oxidative stress may potentially contribute to its pathogenesis. Melanocytes are destroyed by harmful free radicals, according to several studies. Increased nitric oxide levels in cultured melanocytes and vitiligo patients’ blood may cause auto-destruction of melanocytes. Vitiligo patients’ red cells had lower glutathione levels than controls, which prevents free radical damage. Vitiligo sufferers may have more oxidative stress.
Theory of neurons:
Segmental vitiligo is typically dermatomal. This result led to a neurological theory that nerve ending chemical mediators may reduce melanin synthesis. In vitiligo skin, neuropeptide Y levels are elevated. In some segmental vitiligo patches, perspiration decreases and axons and Schwann cells display minor degenerative or regenerative alterations.
Viral:
The presence of CMV DNA in skin biopsy specimens from some vitiligo patients increases the possibility of melanocyte destruction caused by the virus. Hepatitis C, HIV, and Epstein-Barr viruses may be involved, according to some scientists.
Classification of Vitiligo:
The classification of vitiligo includes segmental, acrofacial, generalised, universal, and focal, mixed, and mucosal variants based on involvement pattern.
- Most often, focal vitiligo has a single macule or a few scattered macules in the trigeminal nerve distribution, but the neck and trunk are also affected. This kind is frequent in kids.
- Unilateral dermatomal or quasi-dermatomal macules characterise segmental vitiligo. This type starts early and is not linked to thyroid or autoimmune illnesses like the others. The pathogenesis involves neuronal peptide alteration. More than half of segmental vitiligo patients develop poliosis.
- Acrofacial vitiligo causes distal finger and periorificial depigmentation.
- Vitiligo vulgaris is generalised vitiligo. The most prevalent pattern. Depigmented patches are widespread and symmetrical.
- Universal vitiligo causes depigmented macules and patches across the body and is linked to multiple endocrinopathies syndromes.
Only mucous membranes are affected by mucosal vitiligo.
Clinical Variants:
Trichrome vitiligo includes depigmented and hypo-coloured macules, as well as properly pigmented skin. Hypopigmented areas naturally depigment. Quadrichrome vitiligo has marginal or perifollicular hyperpigmentation. This variety is more common in darker skin, especially in repigmentation areas. Additionally, pentachrome vitiligo exhibits blue–gray hyper-pigmented macules, indicating melanin incontinence. A rare variety of vitiligo is small hypomelanotic macules are present in these patients. Erythema at macule edges characterises inflammatory vitiligo
Laboratory Tests in Patients with Vitiligo:
- Thyroid-stimulating hormone
- Complete blood count
- Total IG E count
- Antinuclear antibody
- Antithyroglobulin antibodies
- Antithyroid peroxidase antibodies
Management:
Vitiligo can cause cosmetic disfigurement, stigma, and significant psychological issues in daily life. It affects 0.5% of the global population and is equally common in men and women. Genetics, immunology, neurology, toxic metabolites, and melanocyte development factors may be involved. Since there is no gene treatment, current techniques aim to arrest progression and achieve repigmentation to mend the morphology and function of depigmented skin. Narrowband ultraviolet (UV) B (311nm) therapy, corticosteroid cream + UVA therapy, and autologous pigment cell transplantation are newer treatments. Depigmentants remove remaining pigment in extensive vitiligo. Sunscreens, disguise, and guidance may help patients manage with the condition.
Homoeopathic Management:
Numerous successful homoeopathic treatments have been used to cure vitiligo. Homoeopathy corrects auto-immune disorders and restores normal immunity. It stimulates melanocytes and increases melanin synthesis, restoring skin colour.
Homoeopathic prescriptions go to the root of the problem by understanding the patient psychologically. Homoeopathy expands with this personalized approach.
- Ars Sulph Flavum is an uncommon but effective remedy for treating vitiligo in dry skin with fissures. This cure causes scaling, itching, and white patches.
- Hydrocotyle Asiatica: Promotes skin pigmentation in discoloured areas. Pricking various skin areas on the body.
- Indications for Ammi visnaga include loss of pigmentation, resulting in white patches on the skin. This substance exhibits phototherapeutic effects similar to psoralens. Some people have repigmentation after using A.visnaga and being exposed to the sun.
- Calc Carb is effective for treating milky white spots on fair, overweight, flabby, and perspiring individuals.
- Kali Carb: Dry skin with light-colored patches around the body. Skin sensation of burning and lancinating.
Numerous therapies and symptoms of vitiligo exist. Treatment should only be administered by an experienced homoeopath after a thorough case investigation. When used properly, homoeopathy treats vitiligo well.
Conclusion:
Vitiligo can be considered a psychologically terrible disorder. This applies especially to patients of colour. Vitiligo has several psychosocial effects. In treating vitiligo, a multidisciplinary approach including early psychology or psychiatry consultation may be helpful. Rotational therapy may be needed to reduce side effects and improve vitiligo repigmentation.
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