Role of substance P in the pathogenesis of chronic urticaria

Abstract

Chronic urticaria (CU) is a serious issue in clinical allergology. Exact pathogenesis of diseases is unknown despite a fairly large number of studies. From clinical view, CU manifests as wheals and/or angioedema, lasting for more than 6 weeks. It is classified into spontaneous (without obvious triggers) and induced CU (in cases of evident physical and chemical stimuli). It is quite difficult to reveal its cause. Most often, the patients refer to specific foods as a trigger factor. Stress is the second leading cause of CU after breaking the diet. Mental or emotional stress has been shown to cause degranulation of mast cells (MC) and histamine release. Substance P (SP) is a neurotransmitter, which underlies neuroimmune inflammation, being considered the most informative marker of CU. The purpose of our study was to assess a role of SP in the CU pathogenesis and to determine the relationship of SP with known urticaria triggers and comorbidities. We examined 97 patients with CU and 68 apparently healthy individuals matched by sex and age. The levels of histamine and substance P (SP) were determined in blood serum by enzyme immunoassay. The patients were classified into groups, depending on the history of food and drug intolerance, presence of concomitant autoimmune thyroiditis (AIT), influence of stress as a trigger for CU. When analyzing the average levels of histamine and SP in the group of patients suffering from CU, compared with the control group, no significant correlations were found. We detected an almost 3-fold increase of histamine levels in the patients suffering from AIT (28.25 ng/mL versus 83.61 ng/mL). However, when assessing the level of histamine in patients with CU and with a history of food and drug intolerance, trigger stress and AIT, the average values of the indicator did not show significant differences. Meanwhile, when assessing the SP index in patients with a history of drug, food intolerance, AIT and stress as a trigger for CU, we have found a significant increase in SP in the patients when compared with control group (p 0.05). Our results confirm the neuroimmune inflammation system to be involved in genesis of mast cell activation in CU patients. Further studies are required in order to discern a specific phenotype of stress-induced CU and determine the opportunities for its psychopharmacological correction.