Prostaglandins, leukotrienes and perennial rhinitis

Abstract

Prostaglandins and leukotrienes are implicated in conditions of both the upper and lower airways. In the former they are deranged in nasal polyposis, intrinsic rhinitis and allergic rhinitis while in the latter they are involved in the pathogenesis of asthma. The aim of the present study was to measure mucosal eicosanoid levels in the three types of rhinitis and compare with controls. In addition, the effect of topical steroids on eicosanoid levels in rhinitis was examined. The levels of prostaglandins E(2) (PGE(2)) and D(2) (PGD(2)) and of leukotrienes E(4) (LTE(4)) and B(4) (LTB(4)) were measured in nasal biopsies from the inferior turbinates of patients suffering from perennial rhinitis and a control group. Rhinitis patients were classified into three categories: perennial allergic rhinitis (PAR), non-allergic rhinitis with eosinophilia (NARES) and noneosinophilic non-allergic rhinitis (NENAR) on the basis of symptoms, secretion eosinophilia, nasal resistance and allergy testing. Patients with rhinitis were randomized into two groups. One received fluticasone propionate nasal spray (FPANS) and the other a placebo (PNS) over a period of six weeks prior to the biopsies. One hundred and one patients with PAR, NARES or NENAR were recruited sequentially and the control group consisted of 21 patients with no evidence of rhinitis but with nasal obstruction due to septal deviation. Untreated rhinitics had significantly lower levels of PGE(2), PGD(2) and LTE(4) than non-rhinitic controls. Six-weeks' treatment with FPANS significantly increased the levels of those eicosanoids in patients with PAR and NARES but they were still significantly below normal. Levels of LTB(4) in all three rhinitis groups were not significantly different from controls and treatment with topical steroids had no effect. Their findings are contrary to current thinking that increased levels of eicosanoids, in particular cysteinyl-leukotrienes, play an important role in the pathogenesis of chronic, non-infective upper airway inflammation.

Pathophysiology of nasal obstruction and meta‐analysis of early and late effects of levocetirizine

“…PGD2 provokes a dose‐dependent increase in congestion in patients with and without AR [25, 42]. However, PGF2α increases the nasal patency [25] and PGE2 is a constrictor of nasal vasculature, leading to decongestion [59]. Thus, prostanoids exhibit a complex interplay of effects, and nasal vasoconstriction is most probably the overriding effect in vivo .…”

“…Thus, prostanoids exhibit a complex interplay of effects, and nasal vasoconstriction is most probably the overriding effect in vivo . They may play a role in maintaining normal nasal patency [59].…”

New Evidence of H₁-Receptor Independent COX-2 Inhibition by Fexofenadine HCl in vitro

“…prostaglandins and leukotrienes), which mediate several important physiological and pathological functions, and are also involved in the pathogenesis of many inflammatory airway diseases, including asthma, allergic rhinitis, chronic hyperplastic rhinosinusitis and nasal polyposis [20] . Evidence has shown that COX inhibition is due to inhibition of an antiallergic prostaglandin, most likely PGE 2 , which has been shown to downregulate inflammation by inhibiting the expression of both inflammatory mediators and their receptors [16] .…”

Mechanisms and mediators of nasal symptoms in non‐allergic rhinitis

“…Other research has contradicted this with findings of significantly lower levels of PGE 2 , PGD 2 and LTE 4 in untreated rhinitics compared with controls [110], although there were no changes detected in levels of LTB 4 . Furthermore, this study reported that steroid treatment in these subjects apparently raised the levels of these eicosanoids apart from LTB 4 which was unaffected by the therapy [110]. These findings appear to refute the current thinking that increased levels of eicosanoids are implicated in the pathogenesis of IR.…”

“…One study has reported increased levels of LTC 4 and PGD 2 in nasal lavage in symptomatic IR patients, compared with control subjects [109]. Other research has contradicted this with findings of significantly lower levels of PGE 2 , PGD 2 and LTE 4 in untreated rhinitics compared with controls [110], although there were no changes detected in levels of LTB 4 . Furthermore, this study reported that steroid treatment in these subjects apparently raised the levels of these eicosanoids apart from LTB 4 which was unaffected by the therapy [110].…”