Abstract
Importance:Exact etiopathogenesis of chronic spontaneous urticaria (CSU) remains elusive. Infections, pseudoallergens, autoimmunity, and contact sensitization are various postulated factors. Few studies are available measuring cytokine levels in CSU.Objectives:The aim was to study various etiological factors of CSU and levels of IL-6 and IFN-ϒ in cases and controls, and correlation between various etiologies with the levels of the abovementioned interleukins in the cases.Design:Case-control study performed over 2 years with no follow-up of the participants.Setting:It was a referral-center-based study.Participants:Sixty patients of CSU and equal age and sex-matched healthy controls were recruited on the basis of convenience sampling.Exposures:Biochemical and hematological investigations with hepatitis serology, thyroid function tests, anti-thyroid antibodies, and levels IL-6 and IFN-ϒ were performed in all cases and controls. All cases were subjected to ASST. Cases with all above negative tests were patch-tested with Indian standard series. Urticaria activity score (UAS7) was calculated for all the cases and repeated in patients with positive etiological factor after 3 weeks (improvement after allergen or drug avoidance, treatment of infection).Outcomes:To study the various etiological factors (food, infection, autoimmunity, autoreactivity, and contact sensitization) and the levels of IL-6 and IFN- γ in patients of chronic spontaneous urticaria.Results:Etiology was ascertained in 75% of patients (autoimmunity: 50%, contact sensitization: 21.67%, food and drug allergy: 1.67% each). Mean values of the interleukins and anti-thyroid antibodies were significantly higher in cases versus controls. Levels of IFN-ϒ were significantly elevated in patients with higher UAS7 scores.Conclusion:Antithyroid antibodies, ASST, and patch testing are important tools and should be considered in patients of CSU after a thorough history and history-based workup. Elevated levels of IL-6 and IFN- ϒ in cases suggest that both Th1 and Th2 type of immune responses are implicated in pathogenesis of CSU.
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