Abstract
Airway inflammation is related to increased nitric oxide production. It can be assessed noninvasively with exhaled nitric oxide measurement. As airway inflammation was supposed to be present in chronic urticaria and angioedema patients we hypothesized increased exhaled nitric oxide in this group. Twenty-six symptomatic chronic urticaria patients with an acute episode of pharynx angioedema (17 women and 9 men, median age 35) were included in the study group. None of the patients reported a history of asthma, allergic rhinitis or cigarette smoking. The control group consisted of 29 non-smoking healthy subjects (19 women and 10 men, median age 22) without any history of atopy. Exhaled nitric oxide measurement was performed in all subjects. Exhaled nitric oxide levels in the angioedema group did not differ statistically significantly from those detected in healthy subjects (15.5 ppb and 17.0 ppb respectively). Our results indicate the lack of airway inflammation in chronic urticaria patients with pharynx angioedema.
Highlights
Nitric oxide (NO) is generated from l-arginine by different isoforms of synthases.Contrary to endothelial and neural isoforms, one form of NO synthase, i.e., inducible and calcium-dependent is not expressed in normal conditions
Since chronic spontaneous urticaria (CSU) and angioedema is characterized as an inflammatory disorder, we aimed to analyze exhaled NO (eNO) levels in the course of acute upper airway angioedema symptoms
We examined thirty four consecutive non-smoking chronic spontaneous urticaria patients referred to our department because of the symptoms of acute pharynx angioedema
Summary
Contrary to endothelial (eNOS or NOS-3) and neural (nNOS or NOS-1) isoforms, one form of NO synthase, i.e., inducible and calcium-dependent (iNOS or NOS-2) is not expressed in normal conditions. Expressed synthases produce NO as a result of receptor stimulation whereas iNOS is expressed in response to diverse stimuli such as inflammatory cytokines having microbidial and pro-inflammatory effects [1,2]. NO may produce beneficial or adverse effects in humans. It expresses proinflammatory activity including increased vascular permeability [4]. On the other hand, when inhibiting mast cell degranulation NO shows an anti-inflammatory activity [5]. The pro- or anti-inflammatory properties of NO may vary according to different conditions [1,4]
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