Table 1.

Mechanism of itraconazole in treatment of dermatologic diseases

Action	Supposed mechanisms	Utilization in nonfungal skin disorders
Anti-malignancy	Anti-Hedgehog signaling pathway; target site on Smoothened	Advanced basal cell carcinoma
Anti-angiogenesis	Inhibition of endothelial cell migration, proliferation, and tube formation via blocking of VEGFR2 trafficking and signaling	Infantile hemangioma Keloid and hypertrophic scar
Anti-inflammation and immunomodulation	Suppression of T-lymphocyte proliferation Phenylpiperazine ring of ITZ related to the immunosuppressive effect	Mycosis fungoides Lichen planus HIV-associated eosinophilic folliculitis Sarcoidosis
	Inhibition of neutrophil chemotaxis and movement Inhibition of interleukin-8 production Inhibition of the formation of pro-inflammatory metabolites (i.e., 5-lipoxygenase)	Palmoplantar pustulosis
Induction of nail growth	Acceleration of nail matrix turnover rate	Yellow nail syndrome
Reduction of hypersensitivity reaction	Modulation of Malassezia species (as an allergen)-induced hypersensitivity reaction	Head and neck dermatitis or refractory atopic dermatitis Reducing irritation of calcipotriol on scalp psoriasis

HIV human immunodeficiency virus, ITZ itraconazole, VEGFR2 vascular endothelial growth factor receptor 2