Vitiligo – A Window in the Darkness

Dr. Wiete Westerhof, Netherlands institute for Pigmentary Disorders, IWO Building, Academic Medical Center, Meibergdreef 35, NL-1105AZ Amsterdam (The Netherlands) In this issue (p. 223), a new treatment protocol for vitiligo applied to 33 patients in a pilot study under the direction of K.U. Schallreuter at the Department of Dermatology, University of Hamburg, is reported. The research and development of this new approach in repigmentation is the result of continuous basic research on vitiligo by the same group. Earlier work by the Hamburg group in collaboration with M. Pittelkow (Mayo Clinic, Rochester, Minn., USA) showed that vitiliginous keratinocytes established under in vitro conditions had a defect in calcium transport in association with the expression of ß2-adrenoceptors [1, 2]. The high density of these receptors on keratinocytes led to the discovery that these cells have the full capacity for cate-cholamine synthesis themselves [3]. Therefore, the release of the hormones from the compartment epidermis seems not to depend on presynaptic nerve endings. In addition, Schallreuter’s group found that catechola-mine biosynthesis is defective in vitiligo yielding increased norepinephrine levels in both epidermis and plasma of these patients [4]. These results supported earlier findings by Dunerva [5] and, more recently, by Morrone et al. [6], who found elevated levels of catecholamines and metabolites in the urine and plasma of patients with active vitiligo. Our own group in Amsterdam discovered increased catechol-ö-methyltransferase (COMT) activities in the lesional skin of vitiligo patients [7]. COMT is an enzyme that methylates catecholamines, thereby inactivating these potentially cytotoxic compounds. The rise in COMT is probably a response to the elevated level of catechols in vitiliginous skin. Recently, more detailed examination on regulation of catecholamines led to the fundamental discovery that the