These include: (a) first disease causing skin changes that lead to the occurrence of second disease at the same site; (b) coincidence; (c) the first and second disease affected the same site because of a third, still unknown factor; (d) the locus minoris resistentiae is the actual cause for location of both diseases and each event is caused by a different stimulus. Viral, immunological, neurological and vascular aetiologies have been considered in the context of the second disease. Neurological aetiology seems to be most pertinent in our case. Varicella zoster virus can cause destruction of Aδ and C nerve fibres in the mid and lower dermis. 4 Although nerves are not directly involved in the pathogenesis of a new disease arising on apparently healed herpetic lesions, an indirect influence of the nervous system through interaction with the immune system can not be ruled out. The number of nerves containing immunoreactive calcitonin gene-related peptide (CGRP) and substance-P (SP) are increased in the dermis in prurigo nodularis. Zoster-associated cutaneous nerve damage can mediate the aberrant growth of nerves containing CGRP and SP.
References1 Wolf R, Brenner S, Ruocco V, Filioli FG. Isotopic response. Int J Dermatol 1995; 34: 341-348. 2 Ruocco V, Ruocco E, Ghersetich I, Bianchi B, Lotti T. Isotopic response after herpes virus infection: an update. J Am Acad Dermatol 2002; 46: 90-94. 3 Wyburn-Mason R. Malignant change arising in tissues affected by herpes. BMJ 1955; 2: 1106-1109. 4 Ebert MH. Histologic changes in sensory nerves of the skin in herpes zoster.