Prostaglandins, leukotrienes and perennial rhinitis.
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.
Shahab
Riad
R
Head and Neck Oncology Group, Faculty of Medicine, University of Liverpool, UK.
Phillips
David E
DE
Jones
Andrew S
AS
D000403:Airway Resistance; D000730:Androstadienes / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D002908:Chronic Disease; D015232:Dinoprostone / Q000032:analysis; D004311:Double-Blind Method; D004804:Eosinophils / Q000473:pathology; D000068298:Fluticasone; D006801:Humans; D007958:Leukocyte Count; D007975:Leukotriene B4 / Q000032:analysis; D017999:Leukotriene E4 / Q000032:analysis; D015289:Leukotrienes / Q000032:analysis*; D009297:Nasal Mucosa / Q000737:chemistry / Q000473:pathology; D009298:Nasal Polyps / Q000378:metabolism; D015230:Prostaglandin D2 / Q000032:analysis; D011453:Prostaglandins / Q000032:analysis*; D012220:Rhinitis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D012221:Rhinitis, Allergic, Perennial / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D015289:Leukotrienes; D011453:Prostaglandins; D007975:Leukotriene B4; D017999:Leukotriene E4; D000068298:Fluticasone; D015232:Dinoprostone; D015230:Prostaglandin D2