Intended for healthcare professionals

Clinical Review

ABC of allergies: Summer hay fever

BMJ 1998; 316 doi: (Published 14 March 1998) Cite this as: BMJ 1998;316:843
  1. Stephen Durham

    Summer hay fever causes considerable morbidity and affects quality of life at a time usually considered as the best of the year. Its prevalence has increased over the past 20 years despite falling pollen counts.

    Antihistamines and nasal corticosteroid sprays are first line treatment

    Environmental triggers

    The main cause of hay fever in Britain is grass pollen, particularly perennial rye (Lolium perenne) and timothy grass (Phleum pratense). Symptoms peak during June and July. Symptoms in spring are commonly due to tree pollens, whereas symptoms in late summer and autumn may be due to weed pollens and mould spores. Rape seed may also provoke symptoms of rhinitis, although usually through irritant rather than allergic mechanisms. It has been suggested that emissions of nitrogen dioxide and ozone from vehicle exhausts have been increasing the sensitivity to airborne allergens.

    Perennial rye grass (Lolium perenne)—common in Britain

    Pollen calendar for Britain

    Mechanisms of rhinitis

    The symptoms of rhinitis are caused by an interaction between grass pollen and IgE on the surface of sensitised mucosal mast cells (type 1 hypersensitivity). The cells release mediators such as histamine and leukotrienes, which produce itch, sneeze, watery anterior nasal discharge, nasal congestion, and symptoms affecting the eyes.

    Hypothesis on mechanisms of summer hay fever (rationale basis for treatment). IL=interleukin, VCAM=vascular cell adhesion molecules, GM-CSF=granulocyte macrophage colony stimulating factor

    Allergens are also recognised and processed by mucosal dendritic cells (Langerhans' cells) or macrophages, which then stimulate T lymphocytes to release interleukins, which promote tissue eosinophilia and IgE production. These compounds act to produce ongoing rhinitis, symptoms …

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