Postnasal drip and chronic cough: An open interventional study.

BACKGROUND: The postnasal drip (PND) syndrome is often linked as a cause of chronic cough although this is disputed. OBJECTIVES: We examined the effect of specific topical treatment of rhinosinusitis on cough in patients presenting with a chronic cough associated with a postnasal drip or 'nasal catarrh'. METHODS: Patients presenting with a chronic cough and who complained of PND were enrolled and symptoms of PND and cough were assessed by questionnaire and by a capsaicin cough response. Rhinosinusitis was assessed by questionnaires, direct examination of the nose and by high-resolution computed tomography. In an open study, they were treated with fluticasone nasules, ipratropium bromide and azelastine nasal sprays for 28 days, after which they were re-assessed. RESULTS: Eighteen out of 21 patients completed the study. All patients reported having the presence of mucus in the throat. Mean cough score improved post-treatment (p<0.05), but there was no significant change in capsaicin cough sensitivity or nasal catarrh questionnaire score. There was improvement in anterior nasal discharge symptom scores (p=0.005) and in endoscopic nasal scores post-treatment (p<0.01), with a tendency to improved PND scores. CONCLUSION: In a pilot open 'real-life' study treatment targeted towards rhinosinusitis accompanying PND syndrome and chronic cough led to an improvement in cough. A randomised controlled study is now needed to confirm or refute these findings.

Relation of CD4+CD25+ regulatory T-cell suppression of allergen-driven T-cell activation to atopic status and expression of allergic disease.

BACKGROUND: Allergic diseases are frequent and rising in prevalence, and result from activation of T-helper (Th) 2 cells by allergens. CD4+CD25+ regulatory T cells suppress T-cell activation in vitro and prevent pathological findings in animal models of disease. We aimed to investigate whether the amount of inhibition of allergic responses by CD4+CD25+ T cells was related to atopy and allergic disease. METHODS: Blood CD4+CD25+ and CD4+CD25- T cells were isolated from three groups of donors: non-atopic individuals; those atopic with no present symptoms; and patients with hayfever studied during and out of the grass-pollen season. We investigated the ability of CD25+ T cells from these donors to suppress allergen-stimulated T-cell proliferation and cytokine production in vitro. FINDINGS: CD4+CD25+ T cells from non-atopic donors suppressed proliferation and interleukin 5 production by their own allergen-stimulated CD4+CD25- T cells. Inhibition of proliferation by CD4+CD25+ T cells from atopic donors was significantly reduced (p=0.0012), and was even more diminished by CD4+CD25+ T cells isolated from patients with hayfever during the pollen season (p=0.0003). In patients with hayfever, out-of-season suppression remained less than that seen by regulatory cells from non-atopic donors. INTERPRETATION: Allergic disease can result from an inappropriate balance between allergen activation of regulatory CD4+CD25+ T cells and effector Th2 cells. This imbalance could result from a deficiency in suppression by regulatory T cells or strong activation signals could overcome such regulation. Treatment to enhance regulatory T-cell responses, in concert with reduction of Th2 cell activation, might be useful in prevention and treatment of allergic disease.