Stefano Caccavale1, Tobia Caccavale2, Maddalena La Montagna3. 1. Department of Dermatology, Second University of Naples, Naples, Italy. E-mail: stefano85med@libero.it. 2. Department of Mental and Physical Health and Preventive Medicine, Second University of Naples, Naples, Italy. 3. Department of Psychiatry, University of Foggia, Foggia, Italy.
Sir,We read with great interest the report recently published in the Indian Journal of Dermatology by Dhawan et al.,[1] which describes a case of trigeminal trophic syndrome (TTS) in a child developing as a result of herpes zoster infection.[1]The authors do not fully clarify the pathomechanism involved in the appearance of TTS in the dermatomes previously affected by zoster. Herpes zoster is known to be accompanied by neurological symptoms due to the neurotropism of this virus. These symptoms are provoked by nerve lesions following this herpetic infection. The injury to the sensory fibers may cause permanent damage that results in partial denervation of the affected dermatome.[2] Zoster-affected dermatomes become susceptible to the subsequent development of heterogeneous skin disorders, thus featuring the well-defined “Wolf's post-herpetic isotopic response.” Probably, the documented reduction of peptidergic fibers in zoster-affected dermatomes could provoke an alteration in neuropeptide release leading to an imbalance of local immune control.[2] It should be considered that some neuropeptides are immune stimulators while others are immune suppressors. As a result, the post-herpetic isotopic response can be either reduced or exaggerated depending on the type of neuropeptide each time involved in the nerve damage. Furthermore, depending on incidental circumstances, some neuropeptides can either enhance or inhibit particular immune/inflammatory cell functions.[2] The report of Dhawan et al.[1] is no more than a further mere example of “immunocompromised cutaneous district” (ICD).[3] Whatever the cause,[456789] the concept of ICD refers to a skin site of loco-regional immune dysregulation due to an obstacle to the normal trafficking of immunocompetent cells through lymphatic channels, and/or an interference with the signals that the neuropeptides and neurotransmitters, related to peripheral nerves, send to cell membrane receptors of immunocompetent cells. Depending on which of the neurotransmitters and immune cells are involved, this destabilization could be either defective, thus predisposing to infections and tumors, or excessive, thus favoring the occurrence of some immune disorders or dysimmune reactions at the sites “marked” by prior clinical events or injury.[4]TTS may result from a physical mechanism of self-mutilation, secondary to trigeminal anesthesia and paresthesia. In the past, a “trophic” theory was proposed to explain the ulcer formation. According to this theory, there would be a defective production of certain trophic factors, resulting in an anomalous maintenance of facial skin homeostasis. Lack of neurotrophic factors, such as substance P and alpha-MSH, may be involved. A more complex dysregulation of neuropeptides might have a role in this rare disease, thus featuring the conditions of a typical ICD.[2] The neural compartment of skin immunity plays a key role in immune homeostasis, and this assertion is confirmed by the fact that any neurological injury can give rise to immune destabilization of the innervated area, which becomes a site prone to the occurrence of “opportunistic” skin disorders.We thank the authors for giving us the opportunity to discuss such a complex and interesting topic.