How is vitiligo treated?

What medical treatments are available to treat vitiligo?

The vitiligo, a noncontagious skin disorder resulting from the loss of melanocytes—the cells responsible for skin pigmentation—leading to white patches. Its progression is unpredictable and can affect hair and body hair, with possible causes including genetics, certain environmental factors, or oxidative stress. Although vitiligo is not harmful, its cosmetic impact can have significant psychological consequences. This is why it is important to offer patients an appropriate care strategy.

Oral corticosteroids.
Autoimmunity is considered one of the main pathogenic mechanisms of vitiligo, along with an immune system deficiency. Cytokines released by the innate immune system amplify the immune response and recruit other immune cells, such as CD8+ T lymphocytes, which will attack melanocytes. Corticosteroids can 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 of body weight) administered for two months before being tapered over the following two months. The results showed very good efficacy. Oral corticosteroids are now used as a first-line treatment when vitiligo is in its active phase, to prevent progression and induce repigmentation of the white patches.

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87.7%

Patients experienced a halt in the progression of their vitiligo.

70.4%

Average 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, which are responsible for inflammation. At the same time, they promote the production of anti-inflammatory cytokines, thereby helping to modulate the immune response. Moreover, calcineurin inhibitors promote melanocyte migration and proliferation by increasing levels of matrix metalloproteinases and by inducing in melanoblasts the expression of the endothelin B receptor, 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 evaluate the efficacy of calcineurin inhibitors in treating vitiligo. The results show that monotherapy with these inhibitors produced at least slight improvement in 55.0% of patients (21 studies, 560 patients), 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).
Calcipotriene ointment.
Topical calcipotriene has been found to be relatively effective, either as monotherapy or as part of combination therapies—such as PUVA (psoralen plus UVA) treatment—or in conjunction with 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, involved in melanocyte destruction.
A study conducted on 18 children with vitiligo highlighted the efficacy of calcipotriol treatment. The therapy was applied twice daily as a cream (50 µg/g) in nine patients and as an ointment in the others. Its effectiveness was assessed clinically after two weeks, then monthly over a four- to six-month period. Several patients responded positively, as described below. Although the number of participants was relatively small, this study suggests that calcipotriol‐based treatment may be effective against vitiligo.

21.4%

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

28.6%

Of the 77.8% of patients who experienced an improvement, the degree of improvement ranged from 50% to 80%.

21.4%

Among the 77.8% of patients who experienced improvement, 30% to 50% exhibited an improvement magnitude between 30% and 50%.

However, another study involving 24 patients with vitiligo localized or generalized assessed the efficacy of a daily topical calcipotriol treatment over three to six months. The results showed that 87.5% of patients exhibited no repigmentation, while only 12.5% experienced partial repigmentation, with just 8.05% achieving a maximum repigmentation of 20 to 30% of the lesions.

The limited sample size, modest results, and conflicting studies prevent establishing a definitive efficacy of calcipotriene monotherapy in the treatment of vitiligo. Nevertheless, its benefit appears more pronounced when used in combination with other therapies, underscoring the need for further studies to explore this point in greater depth.

Ruxolitinib.
Ruxolitinib is an inhibitor of Janus kinase (JAK) enzymes. These enzymes are involved in inflammatory signaling pathways that contribute to 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 signaling pathway, which stimulates cytotoxic T lymphocytes (CD8+). 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 3 clinical trials evaluated the efficacy of a 1.5% ruxolitinib cream in 674 patients with non-segmental vitiligo. After 24 weeks, about 30% of patients achieved facial repigmentation exceeding 75%, compared to 11% in the placebo group. However, most patients reported pruritus at the application site.
Ruxolitinib cream has demonstrated efficacy, but longer-term studies are necessary to confirm its safety.

Phototherapy to treat vitiligo?

Phototherapy is one of the reference treatments for vitiligo, as the results obtained are highly 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 (PUVA) method.
PUVA therapy is a photochemotherapy combining a photosensitizing drug, psoralen, with UVA phototherapy (320–400 nm). Patients are exposed to these rays, which penetrate deeply into the skin where they are activated by psoralen previously administered orally or topically. The psoralen molecules are then activated to form bonds with the DNA of immune cells, such as T lymphocytes, which are responsible for the inflammatory response, preventing them from functioning properly.
UVB radiation.
Narrowband UVB therapy is based on the use of ultraviolet rays with an emission peak 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 not yet been 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, which is involved in melanin synthesis. At the same time, UVB enhance melanocyte proliferation and activate melanogenesis, thus contributing to skin repigmentation.
The excimer laser.
The excimer laser is an effective option for vitiligo treatment, producing better results when combined with calcineurin inhibitors. It emits high-intensity UVB light at a specific wavelength of 311 nm, enabling it to act directly on the mechanisms involved in depigmentation.
The primary action of the excimer laser relies on inhibiting inflammation and inducing apoptosis of T lymphocytes, thereby reducing the immune response directed against melanocytes. At the same time, the excimer laser promotes repigmentation by stimulating the differentiation of melanocyte stem cells located in hair follicles or the deeper layers of the epidermis. These cells then develop into fully functional melanocytes capable of producing melanin. Moreover, it stimulates melanocyte proliferation and migration, thus aiding the restoration of skin pigmentation.
A controlled study evaluated a 308 nm excimer laser in 25 patients with vitiligo (85 lesions). Patients received three sessions per week for six to ten weeks. At the end of this period, 67% showed follicular repigmentation in at least one lesion. The face, trunk, arms, and legs were the regions with the best response (25% of lesions achieved more than 75% repigmentation), whereas areas such as the hands, elbows, and feet repigmented by only 2%.

What surgical treatments are available for the management of vitiligo?

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

This procedure is typically performed under local anesthesia, since the treated areas are limited. However, general anesthesia may be considered in rare cases, for example when the surfaces to treat are extensive or in children. The principle is based on the transplantation of skin fragments harvested from a healthy, pigmented donor site on the patient’s own body, thereby avoiding any rejection and the need for immunosuppressive therapy. These grafts contain functional melanocytes that will recolonize the depigmented zone. After fixation and healing, repigmentation generally becomes apparent within a few weeks to a few months.