Akademik Veri Yönetim Sistemi
34th EADV Congress, Paris, Fransa, 17 - 20 Eylül 2025, cilt.2, ss.85, (Özet Bildiri)
Introduction & Objectives: Chemical leukoderma is an acquired hypopigmented dermatosis following repeated chemical exposure. It is often misdiagnosed as vitiligo, especially in children. While typically associated with transdermal contact, few cases are linked to systemic drugs, and those involving oral formulations are extremely rare. Transdermal methylphenidate-induced leukoderma has been reported, but oral-related cases remain very limited. Materials & Methods: We present a female adolescent with attention deficit hyperactivity disorder who developed hypopigmented skin lesions following oral methylphenidate use. Results: A 14-year-old female patient presented with newly developed hypopigmented patches on her forearms and hands, which had appeared over the past two weeks while she had been receiving oral methylphenidate for four months. She had no personal or family history of vitiligo, nor any previous drug use, infection, or trauma. A dermatological exam revealed two hypopigmented patches with irregular borders on the left dorsal forearm and one on the right wrist and hand. Wood lamp examination confirmed hypopigmentation. Laboratory tests including vitamin B12, iron, CBC, TSH, T3, T4, and anti-TPO were unremarkable. skin biopsy is not typically helpful in differentiating vitiligo from chemical leukoderma, so it was not performed. methylphenidate-induced leukoderma was diagnosed based on clinical features and exclusion of other causes. According to the Naranjo scale, the case was classified as a “probable” adverse drug reaction. Following psychiatric consultation, methylphenidate was discontinued and replaced with atomoxetine. Dermatological treatment included topical tacrolimus and a topical corticosteroid. Partial repigmentation was observed within two months, with no new lesions developing. Conclusion: Chemical leukoderma presents with acquired hypopigmented macules and patches following repeated exposure to chemicals via skin contact or systemic routes such as oral administration. Methylphenidate, a presynaptic norepinephrine and dopamine reuptake inhibitor, may trigger melanocyte apoptosis by generating reactive oxygen species, as dopamine and its metabolites can induce oxidative stress leading to mitochondrial dysfunction and caspase activation. Although rare, leukoderma can occur with oral methylphenidate use. Rash, pruritus, and urticaria are common cutaneous side effects, yet chemical leukoderma should be considered when hypopigmented lesions are observed. Early drug withdrawal and topical immunomodulators or corticosteroids may yield favorable outcomes. This case contributes to the limited literature on methylphenidate-related cutaneous adverse effects and highlights the need for clinical awareness.