Prurito e stress: connessione cervello-pelle, misalliance neuroendocrino-immunitaria

Diverse comuni malattie della pelle sono riconosciute essere aggravate da stress psicologico, in particolare dermatosi legate a meccanismi immunitari. Il  prurito (prurito) è  sintomo  comunemente associato alla maggior parte di queste malattie infiammatorie della pelle.

Una ampia serie di mediatori, rilasciati in risposta allo stress nella pelle o in altri sistemi, incrementano la innervazione sensoriale, potenziano  la produzione di altri agenti pruritogeni, sostengono la  infiammazione (neurogena)  e abbassano la soglia del prurito.

Viene sostenuto che le molecole chiave della risposta allo stress, con un forte potenziale pruritogeno, come NGF, CRH (corticotropin-releasing hormone), sostanza P, e i mastociti,  possono essere considerati come ‘ interruttori centrali cellulari della infiammazione pruritogena ‘.

Conoscenze ulteriori saranno utili per più efficaci strategie terapeutiche nella gestione del prurito nelle malattie infiammatorie della pelle influenzabili dallo stress.


Neuroimmunomodulation. 2006;13(5-6):347-56.

From the brain-skin connection: the neuroendocrine-immune misalliance of stress and itch.

Arck P, Paus R.

Perceived stress has long been allied with disturbances of the dynamic equilibrium established between the nervous, endocrine and immune systems, thus triggering or aggravating disease manifestation.

Several common skin diseases are now acknowledged to be worsened by psychological stress, particularly immunodermatoses such as atopic dermatitis, psoriasis, seborrheic eczema, prurigo nodularis, lichen planus, chronic urticaria, alopecia areata and pruritus sine materia.

Itch (pruritus) is perhaps the most common symptom associated with a majority of these inflammatory skin diseases, and acute as well as chronic stress perceptions are recognized to trigger or enhance pruritus.

A wealth of mediators released systemically or locally in the skin in response to stress increase sensory innervation, upregulate the production of other pruritogenic agents, perpetuate (neurogenic) inflammation and lower the itch threshold.

In the present review, we explore recent frontiers in both stress and pruritus research and portray the perpetuation of chronic skin inflammation and itch as a neuroendocrine-immune ‘misalliance’.

We argue that key candidate molecules of the stress response with strong pruritogenic potential, such as nerve growth factor, corticotropin-releasing hormone and substance P, and mast cells, which may be considered as ‘central cellular switchboards of pruritogenic inflammation’, need to be further explored systematically in order to develop more effective therapeutic combination strategies for itch management in chronic, stress-vulnerable inflammatory skin diseases.

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