Vitiligo

Pathophysiology & Progression

The precise etiology of vitiligo remains incompletely understood. Current scientific consensus leans toward a complex autoimmune mechanism in which autoreactive cytotoxic T-cells selectively target and destroy epidermal melanocytes. Another leading theory emphasizes high levels of intracellular oxidative stress, which trigger cellular damage and melanocyte apoptosis. Vitiligo is most likely caused by a combination of both mechanisms: patients exhibit autoantibodies against melanocytes alongside elevated concentrations of hydrogen peroxide (H₂O₂), a recognized marker for oxidative stress. Which of these mechanisms acts as the primary initiator remains an area of ongoing research.While it was long assumed that lesional skin completely lacked functional melanocytes, recent studies have demonstrated that dormant melanocytes often persist within affected areas, albeit with a total loss of physiological function.Vitiligo can manifest at any age and follows a highly variable, individual course. While the disease progresses rapidly in some patients, it may remain stable or even show spontaneous repigmentation in others. Early dermatological evaluation is therefore essential to assess disease activity and initiate tailored therapeutic strategies. 

Diagnostics

Diagnosing vitiligo is typically straightforward and based on a thorough medical history and detailed clinical examination. In patients with lighter skin phototypes, examination under a Wood's lamp (UVA 351 nm) significantly enhances visualization of depigmented areas.

Prof. Karin Schallreuter and an international team of researchers demonstrated that vitiligo skin produces specific oxidation products (oxidized pteridines) that emit a characteristic fluorescence under Wood's light. This physiological phenomenon is absent in other hypopigmentary or depigmentary skin disorders, and fluorescence intensity can vary depending on active disease status. Additionally, we evaluate individual risk factors during the initial consultation, such as a family history of autoimmune diseases or co-occurring thyroid disorders.

Treatment & Therapy Options

A range of modern therapeutic modalities is available today, tailored to disease activity, progression rate, and total affected body surface area (BSA). Dr. med. Katharina Rübsam actively continues the clinical work and scientific legacy of Prof. Dr. Karin Uta Schallreuter and the Institute for Pigmentary Disorders. Following an initial consultation and clinical diagnostic evaluation, an individualized treatment plan is established. Prof. Schallreuter continues to support the practice in an advisory capacity with her extensive expertise.

Overview of Modern Treatment Modalities

1. Topical Corticosteroids (TCS): First-line anti-inflammatory therapy for localized disease.

2. Protopic® (Tacrolimus 0.03%–0.1%)  Topical Calcineurin Inhibitors | Not an FDA/EMA-approved therapy (off-label use): Calcineurin inhibitors reduce T-cell-mediated inflammation. Does not cause skin atrophy; local skin irritation may occur as a side effect.

3. Opzelura® (Ruxolitinib 1.5%) Topical Janus Kinase Inhibitor (JAK) | 

   • Modulates key cytokine signaling pathways (specifically the IFN-γ axis).

   • First officially approved topical therapy for non-segmental vitiligo in patients aged 12 and older.

   • Indications: Vitiligo with facial involvement, with a total treatment area not exceeding 10% of body surface area.

4. RINVOQ® (Upadacitinib) | Janus kinase (JAK) inhibitor – the first targeted systemic therapy for the treatment of non-segmental vitiligo in adults and adolescents aged 12 and older. Requires regular laboratory monitoring prior to and during treatment, which is administered as a daily oral tablet.

5. PCKUS (Pseudocatalase + Narrowband UVB) | 

   • Reduces epidermal hydrogen peroxide (H₂O₂) levels, mitigating oxidative stress and promoting repigmentation.

   • Shows excellent clinical results on the face and trunk, with more limited response on acral surfaces (hands and feet).

   • Mechanism of Action: Elevated epidermal (H₂O₂) levels are reduced using a topically applied pseudocatalase complex activated by short exposures to narrowband UVB (311 nm) radiation.

   • Key Studies:

     1. Schallreuter et al., 2002: Combination of Dead Sea climatotherapy + PCKUS led to significantly faster repigmentation compared to climatotherapy alone or placebo.

     2. Schallreuter et al., 2008 (Pediatric cohort, n = 71): Achieved ≥ 75% repigmentation in 66% of pediatric patients after 12 months of treatment.

Lifestyle Guidelines & Factors to Avoid

• Skincare Containing Coenzyme Q10 (Ubiquinone): Current clinical studies suggest that topical application of products containing Q10 can exacerbate active vitiligo.

• Psychological Stress: Emotional and psychological stress can significantly trigger and accelerate disease activity.

• Mechanical Trauma & Friction: Avoid skin injuries or prolonged, localized pressure. Many patients exhibit the Koebner phenomenon, where new depigmented macules develop at sites of mechanical friction or trauma.

• Smoking: Nicotine abuse has been shown to worsen vitiligo progression, particularly around the perioral area.