Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4473_Библиотеки_им_академика_М_И_Перельмана

to consider changes in the genetic composition of a population in a short time, one of the most pow­erful hypotheses to elucidate this prevalence increase is the hygiene hypothesis. It suggests that exposure early in childhood to microbes and infections leads to an altered immune system, a reduced risk of IgE sensitization, and a decreased risk of AR throughout life. AR is a debilitating disease on individual and social levels, and it has a major negative impact on morbidity, lost work­ing days, high cost for medical treatment, and reduced school performance. Allergic rhinitis occurs when inhaled allergens interact with IgE antibodies on cells in the airway. AR can some­times be a restricted disease without a systemic response of IgE sensitization, like an increase in serum-specic IgE levels or a positive allergen skin test result. Patients with AR may initially present symptoms like nonallergic rhinitis. These patients may have nasal symptoms for longer than 2 years but negative skin test results and absence of serum-specic IgE response to aller­gic disease’s nasal markers. On the other hand, some of the patients with persistent nonallergic rhinitis may have increased eosinophil number, increased specic and total IgE levels, as well as increased T cell counts in their nasal lavage sam­ple compared with healthy control subjects. These ndings must alert us that people who have persistent nonallergic rhinitis based on the allergy skin test and serum-specic IgE test result might have a localized form of allergic rhinitis [8]. In these cases, examination of the nasal mucosa and nasal challenge tests may help to identify these patients.

logically [10, 11]. Epidemiological studies have shown that up to 80% of patients with asthma demonstrate symptoms of rhinitis, while approximately 20–40% of patients with AR have clinical asthma. Both are airway diseases in which IgE antibody sensitization to aeroal­lergens is a prominent feature. The link between asthma and rhinitis in particular has gained much interest. There is evidence that systemic trafcking of inammatory cells from local inammation in one portion of the respiratory tract can induce inammatory changes in the other; segmental bronchial allergen challenge in patients with AR has been shown to result in both bronchial and nasal inammatory responses [10]. There is growing evidence that rhinitis is a risk factor for the development of asthma, inde­pendent of atopy. Additionally, the airway mucosa of the nose and bronchi has many simi­larities, and the clinical and pathophysiological changes in asthma and AR are often very com­parable. Although there are still some differ­ences that should be highlighted, the strong relationship between rhinitis and asthma has introduced the concept of “the united airway disease.”

between the SNPs and serum IgE levels. Based on these data, it was suggested that dysregulation of FOXJ1 may inuence T cell activity.

Fine mapping in three independent Danish populations was performed by Brasch-Andersen

suggestive linkage to two novel regions at 1q31­q32 and 20p12 [25]. The locus has previously been demonstrated to have a suggestive linkage with asthma [26]. Possible candidate genes are the glutathione S-transferase M1 (GSTM1) [27] and acidic mammalian chitinase (CHIA) genes located at 1p12-p13, earlier shown to be associ­ated with asthma [28]. Chromosome 20p12 is also a novel nding in regard to AR.However, it has previously been found to have a linkage with atopy as well as asthma [26].

Several studies have found an association of laggrin (FLG), a lament-associated protein that binds to keratin bers in epithelial cells with various allergic conditions and diseases includ­ing atopy as well as atopic dermatitis (AD), asthma, and AR [29].

mutant allele of TLR2 or TLR4 polymorphisms was signicantly associated with the moderate to severe groups compared to the mild group in both atopic asthmatics and allergic rhinitis groups (P>0.001 for each). In conclusion, their study demonstrated a lack of association of TLR2 and TLR4 polymorphisms with asthma and allergic rhinitis but suggests a signicant association between these genetic variants and the disease severity.

The current and remarkable rise in allergic diseases and the very early onset of disease indi­cate that in utero events have a more essential effect on immune development and allergic sus­ceptibility than genomic inheritance. Above all, as epigenetic modications are commonly revers­ible, this may provide for the development of novel therapeutic compounds that may be efcacious in arresting or even reversing the allergy epidemic [33].

subgroups depending on the presence or absence of NPs [51]. Some researchers determined a sig­nicant correlation between nasal polyposis and the presence of tissue eosinophilia. However, both the presence and degree of eosinophilia in NPs can be quite variable, and researchers did not observe eosinophilia in a large patient group with idiopathic nasal polyposis [53]. These results support the opinion that certain forms of CS such as allergic fungal sinusitis (AFS) [54] and aspirin­exacerbated respiratory disease (AERD) [55] may be more likely to produce NPs and present rich eosinophilic inltrate into the sinus cavity. Polyposis can present as a complication in any form of CS.So it should not be used as the basis for diagnosis or decisions regarding treatment. Evaluation of the presence or absence of NPs can be especially important in clinical practice for identifying patients who are more or less likely to have eosinophilic disease and thereby also identi­fying patients who are more or less likely to respond to eosinophil-targeted medicines. However, it should be emphasized that, in prac­tice, CS presents as a spectrum of disorders in which the level of eosinophilia and predilection for polyposis exist on a continuum. Although we will stress the different features of the pathology of eosinophilic and noneosinophilic forms of these diseases, in daily life patients can generally present with variable overlapping symptoms.

[74]. Despite the diffuse involvement of the sinuses with inammatory tissue, the patient is asymptomatic and compared with acute sinus­itis or NES, patients seldom suffer from head­aches or “sinus pressure.” However, anosmia is one of the consistent complaints and perhaps causes the greatest morbidity.