How is vitiligo treated?

What medical treatments are available for treating vitiligo?

The vitiligo, a non‐contagious skin disorder resulting from the disappearance of melanocytes responsible for skin pigmentation, leading to white patches. Its progression is unpredictable and can affect hair and body hair, with possible causes such as genetic factors, certain environmental factors or oxidative stress. Although vitiligo is not dangerous, its cosmetic impact can lead to significant psychological repercussions. This is why it is important to offer patients an appropriate management approach.

Oral corticosteroids.
Autoimmunity is regarded as one of the principal pathogenic mechanisms of vitiligo, alongside an impaired immune system. Cytokines released by the innate immune system amplify the immune response and recruit other immune cells, such as CD8+ T lymphocytes, which attack melanocytes. Corticosteroids serve to block the immune response by inhibiting the production of proinflammatory cytokines and can halt the progression of vitiligo, or even lead to skin repigmentation.
A study published in the International Journal of Dermatology evaluated the clinical efficacy of low-dose corticosteroid therapy in 81 patients with vitiligo in active progression. The treatment lasted four months, with a daily oral dose of prednisolone (0.3 mg/kg body weight) administered to patients for two months before being tapered over the following two months. The results demonstrated excellent efficacy. Oral corticosteroids are now used as a first-line treatment when vitiligo is in an active phase, in order to prevent progression and induce repigmentation of the depigmented areas.

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87.7%

Patients experienced a cessation in the progression of their vitiligo.

70.4%

Mean repigmentation of vitiligo lesions.

Calcineurin inhibitors.
Calcineurin inhibitors are used in the treatment of vitiligo because they reduce the production of pro-inflammatory cytokines by inhibiting calcineurin, a protein involved in the activation of T lymphocytes responsible for inflammation. At the same time, they promote the production of anti-inflammatory cytokines, thereby helping to modulate the immune response. Furthermore, calcineurin inhibitors promote melanocyte migration and proliferation by increasing levels of matrix metalloproteinases and inducing expression of the endothelin B receptor in melanoblasts, a protein essential for their proliferation and survival.
A meta-analysis published in the journal JAMA Dermatology examined 46 studies involving 1,499 patients to assess the efficacy of calcineurin inhibitors in the treatment of vitiligo. The results indicate that monotherapy with these inhibitors achieved at least a slight improvement in 55.0% of patients (21 studies, 560 patients), a moderate improvement in 38.5% of patients (23 studies, 619 patients), and marked repigmentation in 18.1% of patients (19 studies, 520 patients) after a median treatment duration of three months (range up to six months).
Calcipotriol ointment.
Topical calcipotriol has been found to be relatively effective, either as monotherapy or as part of combination regimens, such as PUVA (psoralen plus UVA) therapy or alongside topical steroids. Calcipotriol is a synthetic derivative of calcitriol, one of the forms of vitamin D₃. It regulates the proliferation and differentiation of keratinocytes and melanocytes and inhibits the production of pro-inflammatory cytokines, such as interleukin-6, which are involved in the destruction of melanocytes.
A study conducted on 18 children with vitiligo highlighted the efficacy of calcipotriol treatment. The treatment was applied twice daily as a cream (50 μg/g) in nine patients and as an ointment in the others. Its efficacy was assessed clinically after two weeks and then monthly over a period of four to six months. Several patients showed a response, as described below. This study appears to indicate that calcipotriol‐based treatment may be effective against vitiligo, although the number of patients is relatively small.

21.4%

Of the 77.8 % of patients who experienced improvement, complete resolution was observed.

28.6 %

Among the 77.8% of patients who experienced an improvement, the magnitude of that improvement ranged from 50% to 80%.

21.4%

Of the 77.8% of patients who experienced an improvement, the magnitude of improvement ranged from 30% to 50%.

However, another study involving 24 patients with vitiligo localised or generalised, evaluated the efficacy of a daily topical calcipotriol treatment over three to six months. The results showed that 87.5% of the patients exhibited no repigmentation, whereas only 12.5% experienced partial repigmentation, with just 8.05% achieving a maximal repigmentation of 20–30% of the lesions.

The limited sample size, modest results and conflicting studies do not demonstrate a true efficacy of calcipotriol monotherapy in the treatment of vitiligo. However, its benefit appears more pronounced when combined with other therapies, warranting further studies to explore this aspect in depth.

Ruxolitinib.
Ruxolitinib is an inhibitor of Janus Kinase (JAK) enzymes. These enzymes are involved in inflammatory signalling pathways that contribute to the depigmentation in vitiligo. JAK enzymes are proteins that transmit signals from cytokine receptors on the cell surface to the nucleus. In vitiligo, certain pro-inflammatory cytokines, such as interferon-gamma, trigger excessive JAK activation. This leads to overactivation of the JAK-STAT signalling pathway, which stimulates cytotoxic CD8+ T lymphocytes. These cells attack and destroy melanocytes. Ruxolitinib blocks JAK enzyme activity, preventing the transmission of pro-inflammatory signals. This reduces the production of inflammatory cytokines and the activation of cytotoxic T lymphocytes.
Two phase III clinical trials assessed the efficacy of a 1.5% ruxolitinib cream in 674 patients with non-segmental vitiligo. After 24 weeks, around 30% of patients achieved facial repigmentation greater than 75%, compared with 11% in the placebo group. However, most patients experienced itching at the application site.
Ruxolitinib cream has proven effective, but longer‐term studies are necessary to confirm its safety.

Phototherapy as a treatment for vitiligo?

Phototherapy is one of the benchmark treatments for vitiligo, as the results obtained are very satisfactory. It is offered to patients whose forms are extensive and resistant and it is also indicated for patients in whom topical corticosteroid therapy has failed.

The psoralen plus UVA method (PUVA).
PUVA therapy is a photochemotherapy that combines a photosensitising drug, psoralen, with UVA phototherapy (320–400 nm). Patients are exposed to these rays, which penetrate deeply into the skin, and the psoralen is activated after prior oral or topical administration. The psoralen thus activated forms bonds with the DNA of immune cells, such as T lymphocytes responsible for the inflammatory response, preventing them from functioning properly.
UVB radiation.
Narrowband UVB therapy relies on the use of ultraviolet rays with an emission peak at around 311 nm. These shorter wavelengths deliver higher energy while limiting the risk of erythema or burns.
Although its mechanism of action in the treatment of vitiligo has yet to be fully elucidated, several beneficial effects have been observed.
UVB at 311 nm exert a local immunosuppressive effect, thereby reducing the autoimmune attack on melanocytes. They also stimulate the production of melanotropic hormone, involved in the synthesis of melanin. In parallel, UVB promote melanocyte proliferation and activate the melanogenesis, thus contributing to the repigmentation of the skin.
The excimer laser.
The excimer laser is an effective option for the treatment of vitiligo, yielding superior results when combined with calcineurin inhibitors. It emits high-intensity UVB light at a specific wavelength of 311 nm, allowing it to act directly on the mechanisms involved in depigmentation.
The primary action of the excimer laser centres on inhibiting inflammation and inducing apoptosis in T lymphocytes, thereby reducing the immune response directed against melanocytes. In parallel, the excimer laser promotes repigmentation by stimulating the differentiation of melanocyte stem cells found in hair follicles or the deeper layers of the epidermis. These cells transform into functional melanocytes capable of producing melanin. Moreover, it stimulates the proliferation and migration of melanocytes, thus facilitating the restoration of skin pigmentation.
A controlled study evaluated the 308 nm excimer laser in 25 patients with vitiligo (85 lesions). Patients received three treatments per week for six to ten weeks. Following this period, 67% exhibited follicular repigmentation in at least one lesion. The face, trunk, arms and legs showed the best response (25% of lesions achieving over 75% repigmentation), whereas areas such as the hands, elbows and feet repigmented by only 2%.

What surgical interventions are available for the management of vitiligo?

Graft procedures are surgical techniques used in the treatment of vitiligo when the lesions are stable, that is, they have not progressed for at least six to twelve months. They are particularly indicated in cases of segmental vitiligo, that is, affecting a well-defined area of the body, with no risk of progression.

This procedure is generally performed under local anaesthesia, as the treated areas are limited. However, general anaesthesia can be considered in rare cases, such as when the areas to be treated are extensive or in children. The principle is based on the transplantation of skin fragments from a healthy, pigmented donor site of the patient, thereby avoiding any rejection and the need for immunosuppressive therapy. These grafts contain functional melanocytes that will recolonise the depigmented area. Once the grafts are secured and have healed, repigmentation typically becomes apparent within a few weeks to a few months.