Catecholamines and Vitiligo
- 1 March 1992
- journal article
- research article
- Published by Wiley in Pigment Cell Research
- Vol. 5 (2) , 65-69
- https://doi.org/10.1111/j.1600-0749.1992.tb00003.x
Abstract
The levels of some catecholamine metabolites, namely homovanillic acid (HVA), vanil‐mandelic acid (VMA), 3‐methoxytyramine (MT), normetanephrine (NMN), metanephrine (MN), 3,4‐dihydroxy mandelic acid (DOMAC), and 3,4‐dihydroxy phenylacetic acid (DOPAC), have been evaluated in the 24 hr urines of 150 patients affected with different types of vitiligo and in 50 healthy age‐matched individuals. The patients were divided into three groups according to the different phases of the disease. The first group included subjects affected either with the early active phase or with progressive increase in both number and/or the size of previous lesions. The second group included patients in whom no new lesions had appeared for between 4‐8 months. In the third group the white areas had been stable for 1‐5 years. The first and second groups showed values of HVA and VMA from 4 to 10 times and from ½ to 3 times higher respectively than those of controls, while no significant differences were found between the third group and controls. Our results clearly show that a significant increase of urinary levels of HVA and VMA, deriving respectively from dopamine and from norepinephrine and epinephrine characterizes the onset and the progressive active phases of vitiligo, irrespective of the type of distribution. The increased release of catecholamines from the autonomic nerve endings in the microenvironment of melanocytes in the affected skin areas might be involved in the etiopathogenesis of vitiligo through two main mechanisms: (1) a direct cytotoxic action of catecholamines and/or their o‐diphenol catabolites; (2) an indirect action. Skin and mucosa arterioles possess α receptors, activation of which by catecholamine discharge may cause a severe vasoconstriction, leading to epidermal and dermal hypoxia with hyperproduction of toxic oxyradicals generated by different pathways. In both cases a genetic predisposition due to insufficient radical scavengers in the affected areas should be taken into account.Keywords
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