Her er lidt jeg fandt på Medline....håber du kan bruge det. beklager at jeg
ikke har tid til at oversætte!
hilsener, jonas.
The pathophysiology of idiopathic rhinitis is unknown but the disease is
classified as being non-allergic on the basis of negative serum IgE
radioallergosorbent assay (RAST) and skin prick tests. In contrast, allergic
rhinitis has a Th2 type inflammatory pathology mediated by IgE and mast
cells. OBJECTIVE: To test the null hypothesis that there would be no
difference in the cellular infiltrate for key Th2-associated inflammatory
cells between allergic and idiopathic rhinitis.
It is important to differentiate seasonal rhinitis from non-allergic
disorders including infectious rhinitis, structural or anatomic problems
such as nasal polyps or septal deviation, rhinitis medicamentosa (due to the
overuse of topical vasoconstrictors), hormonal rhinopathy (e.g., pregnancy,
hypothyroidism), non-allergic vasomotor rhinopathy, non-allergic
inflammatory rhinitis with eosinophils (NARES), or rarely, a neoplasm. A
knowledge of the epidemiologic and clinical presentation of allergic
rhinitis together with these pathophysiologic mechanisms is essential for a
modern-day diagnostic and therapeutic approach to the patient who suffers
from allergic rhinitis.
Little is known about the epidemiology of rhinitis, particularly the
perennial and non-allergic forms. The aim of this study was to compare the
symptoms, atopic state, and medical history of individuals with seasonal and
perennial rhinitis. DESIGN: Of 7702 adults aged 16-65 years registered with
a London general practice, 2969 (30%) were screened by postal questionnaire.
Samples of 113 subjects without rhinitis, 51 with seasonal symptoms alone,
128 with perennial symptoms and seasonal exacerbations were then
interviewed. Atopic and non-atopic subjects were distinguished by skinprick
testing with five common allergens. RESULTS: The estimated minimum
prevalence of rhinitis was 24%: 3% had seasonal symptoms only, of whom 78%
were atopic; 13% had perennial symptoms only, of whom 50% were atopic; and
8% had perennial symptoms with seasonal exacerbations, of whom 68% were
atopic. Seasonal rhinitis was characterised by sneezing, itching, and a high
prevalence of diurnal variation in symptoms. The most common provoking
factors were dust, pollens, and infections. By comparison, perennial
rhinitis was characterised by a higher prevalence of nasal blockage and
catarrh, and a lower prevalence of diurnal variation and provocation by
pollen. There were no significant differences among the groups in the
sociodemographic characteristics examined. Subjects with seasonal rhinitis
were more likely to be atopic and to have eczema and a family history of
hayfever than those without rhinitis. Those with perennial rhinitis were
more likely to have past or current eczema or migraine, be wheezy or
labelled asthmatic, or have a family history of nose trouble other than
hayfever. Subjects with both seasonal and perennial symptoms presented an
intermediate clinical picture. CONCLUSIONS: Seasonal and perennial rhinitis
differ in their atopic state, clinical presentation, and medical history.
The extent to which these differences are genetically or environmentally
determined requires further investigation
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