18/07/2025
Vitiligo affecting palmar surfaces exhibits a characteristically recalcitrant course due to unique anatomical, physiological, and immunological factors inherent to acral skin.
The glabrous skin of the palm is devoid of hair follicles, which are considered melanocyte reservoirs capable of repopulating depigmented areas during repigmentation therapies.
This structural deficit contributes significantly to the amelanotic persistence observed in palmar vitiligo.
Furthermore, the epidermal microenvironment in acral regions is relatively inhospitable to melanocyte adhesion, migration, and proliferation.
The basement membrane zone (BMZ) in palmar skin demonstrates differential expression of extracellular matrix proteins, including fibronectin, laminin-332, and collagen IV, which modulate melanocyte, keratinocyte interactions.
Aberrant expression or disruption in these proteins compromises the ability of melanocytes to localize and persist in the lesional dermoepidermal junction.
In addition, mechanical stress and friction-induced Koebnerization are particularly pronounced on the palms, potentiating subclinical inflammation and triggering oxidative stress pathways.
This can result in heightened production of reactive oxygen species (ROS), perpetuating melanocyte apoptosis via activation of caspase-3, p38 MAPK, and JNK pathways.
Moreover, the local immune milieu in vitiliginous palmar skin is often dominated by CD8+ cytotoxic T lymphocytes, secreting interferon-gamma (IFN-γ), which further upregulates CXCL9/10 chemokines through JAK-STAT signaling, creating a hostile cytokine-rich environment that deters melanocyte survival.
From a therapeutic perspective, the absence of follicular melanocytic stem cells, combined with the low vascularity and slow cellular turnover rate in palmar skin, limits the efficacy of both topical immunomodulators and phototherapies such as narrowband UVB (NB-UVB) or excimer laser.
