Abstract

BackgroundOur previous findings showed the importance of analysing the peripheral markers of acute phase response (APR) activation, C-reactive protein (CRP) and IL-6 in the context of urticaria activity and severity. However, these biomarkers do not reliably differentiate between APR to infectious and the disease severity.AimIn order to investigate a possible association between the immune-inflammatory activation markers CRP and procalcitonin (PCT).MethodsSerum PCT and CRP concentrations were measured in patients with CU of varying severity as well as in healthy subjects.ResultsSerum PCT and CRP concentrations were significantly increased in more severe CU patients when compared to healthy controls and mild CU, and within the CU population there was a significant correlation between concentrations of PCT and CRP. Serum PCT concentrations remained within normal ranges in most CU patients and were only slightly elevated in some severe CU cases.ConclusionsPCT serum concentration may be only slightly elevated in some cases of severe CU. Upregulation of PCT synthesis accompanied by parallel changes in CRP concentration reflects a low-grade systemic inflammatory response in CU. PCT should be considered as a better marker than CRP to distinguish between APR to infection and an active non-specific urticarial inflammation.

Highlights

  • Spontaneous chronic urticaria (CU) can be identified as a mast cell- and basophil-dependent inflammatory disorder of the skin accompanied by acute phase response (APR) [1]

  • Background Our previous findings showed the importance of analysing the peripheral markers of acute phase response (APR) activation, C-reactive protein (CRP) and IL-6 in the context of urticaria activity and severity

  • Serum PCT and CRP concentrations were significantly increased in more severe CU patients when compared to healthy controls and mild CU, and within the CU population there was a significant correlation between concentrations of PCT and CRP

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Summary

Introduction

Spontaneous chronic urticaria (CU) can be identified as a mast cell- and basophil-dependent inflammatory disorder of the skin accompanied by acute phase response (APR) [1] This process is manifested by increased concentration of biomarkers—IL-6 and C-reactive protein [2,3,4,5], together with activation of the coagulation/fibrinolysis cascade [4, 6, 7], but not blood platelets [8, 9]. Our previous findings showed the importance of analysing the peripheral markers of acute phase response (APR) activation, C-reactive protein (CRP) and IL-6 in the context of urticaria activity and severity.

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