Disease relevance of ALRH

• Atopic or immunoglobulin E (IgE)-mediated diseases include the common disorders of asthma, atopic dermatitis and allergic rhinitis [1].
• This relation with the serum IgE level was not explained by a concomitant diagnosis of allergic rhinitis or eczema [2].
• Autoantibodies to beta 2-adrenergic receptors have been identified in the serum of one patient with allergic rhinitis ("hay fever") and two patients with asthma [3].
• Exposure to latex in the air elicited allergic rhinitis, conjunctivitis, and asthma [4].
• By Northern blot analysis using a porcine TGF beta 1 cDNA probe, we detected TGF beta 1-specific mRNA in nasal polyp tissues, as well as in the tissue from a patient with allergic rhinitis, but not in the normal nasal mucosa [5].

Psychiatry related information on ALRH

• Sleep disorders, sleep quality, and AR were assessed using validated tools (Sleep Disorders Questionnaire, Epworth Sleepiness Scale, and Score for Allergic Rhinitis) [6].
• Patients with both asthma and allergic rhinitis (n = 76) experienced more physical limitations than patients with allergic rhinitis alone, but no difference was found between these two groups for concepts related to social/mental health [7].
• Our patient suffered from severe viral infections, allergic rhinitis and conjunctivitis, delayed puberty, visual loss, modest achievement in high school, and reactive depression [8].
• Objectives To investigate the association between the magnitude of the skin prick test (SPT) response and the reported symptom severity in patients with allergic rhinitis and the possible modifying role of psychological factors [9].
• OBJECTIVE: We analysed the psychometric properties of a disease-specific instrument, the Rhinoconjunctivitis Quality-of-Life Questionnaire (RQLQ) and the general health instrument, the Medical Outcome Short-Form 36 (SF-36) as they are employed in combination in patients with persistent AR in clinical practice [10].

High impact information on ALRH

• Along with asthma and allergic rhinitis, atopic dermatitis is an important manifestation of atopy that is characterized by the formation of allergy antibodies (IgE) to environmental allergens [11].
• Although allergen immunotherapy is effective for allergic rhinitis, its role in treating asthma is unclear [12].
• These results provide direct evidence of an important role for the 5-lipoxygenase products of arachidonic acid in allergic rhinitis and support the notion that further experiments in this area may lead to new therapeutic approaches to allergic disorders [13].
• Eight subjects with allergic rhinitis underwent nasal challenge on two occasions after an oral dose of 800 mg of A-64077 or an identical-appearing placebo [13].
• Because alpha-adrenergic stimulation causes bronchoconstriction, the alpha-adrenergic responsiveness of 21 subjects with allergic asthma was compared with that of 16 subjects with allergic rhinitis and 38 normal control subjects [14].

Chemical compound and disease context of ALRH

• It has been shown to be safe and efficacious in treating pediatric allergic asthma and treating allergic rhinitis and is being investigated for treating peanut allergy, atopic dermatitis, latex allergy, and others [15].
• We investigated the longevity of allergen-specific Th cells derived from patients suffering from either allergic rhinitis or atopic dermatitis [16].
• This report presents such a patient who was using dexamethasone nasal drops for allergic rhinitis and in whom Cushing's syndrome developed [17].
• Although there are mediators of allergic symptoms in addition to histamine, therapy for allergic rhinitis and urticaria has focused upon the use of antihistamines [18].
• The symptoms and signs of allergic rhinitis were suppressed throughout the study by cetirizine, 5 mg and 10 mg.(ABSTRACT TRUNCATED AT 250 WORDS)[19]

Biological context of ALRH

• From 100 Danish sib-pair families selected for allergy, families containing sib-pairs matching a phenotype definition of both clinical allergic rhinitis and confirmed specific allergy were chosen [20].
• The study revealed one major candidate region on chromosome 4q24-q27 (LOD=2.83) and eight minor candidate regions 2q12-q33, 3q13, 4p15-q12, 5q13-q15, 6p24-p23, 12p13, 22q13, and Xp21 (LOD=1.04-1.63) likely to contain susceptibility genes for allergic rhinitis [20].
• This relation remained significant even after the exclusion of children with diagnosed asthma (P less than 0.0001) and of all children with a history of wheezing, allergic rhinitis, or eczema (P less than 0.0001) [2].
• Therefore, the patients with allergic asthma had significantly enhanced alpha-adrenergic responses when compared both to normal subjects and patients with allergic rhinitis; the possibility that increased alpha-adrenergic activity contributes to the asthmatic diathesis warrants further exploration [14].
• Recurrent staphylococcal abscesses associated with defective neutrophil chemotaxis and allergic rhinitis [21].

Anatomical context of ALRH

• Increase of lymphocytes with Fc receptors for IgE in patients with allergic rhinitis during the grass pollen season [22].
• Affinity-purified IgE-binding factors from the plasma of patients with the hyper IgE syndrome (HIE) were assessed for their capacity to enhance IgE synthesis by B cells derived from patients with allergic rhinitis or normal nonatopic donors [23].
• Serial neutrophil function tests revealed normal chemotactic responsiveness when the patients were symptom-free of allergic rhinitis and no longer having abscesses [21].
• Furthermore, in patients with seasonal allergic rhinitis, the concentrations of NGF in nasal secretions correlate with the magnitudes of eosinophilic inflammation in the airway, suggesting a potential clinical implication of eosinophil NGF [24].
• Basophils, recruited from the blood to tissues, have been implicated by their presence in diverse allergic disorders including bronchial asthma, allergic rhinitis, and cutaneous contact hypersensitivity [25].

Associations of ALRH with chemical compounds

• Allergic rhinitis is a common disease of complex inheritance and is characterised by mucosal inflammation caused by allergen exposure [20].
• The pupils of asthmatic subjects dilated by greater than 0.5 mm in response to 1.8 +/- 0.14 per cent phenylephrine, patients with allergic rhinitis required 2.4 +/- 0.16 (P less than 0.01), and normal controls needed 2.7 +/- 0.07 (P less than 0.00001) [14].
• Urinary leukotriene E4 after antigen challenge and in acute asthma and allergic rhinitis [26].
• However, the results also suggest that suppression of the IL-5-eosinophil pathway in this model of allergic rhinitis may not completely suppress clinical symptoms or nasal histamine hyperresponsiveness, because of the existence of other cytokine-progenitor pathways that may induce and maintain the presence of other inflammatory cell populations [27].
• Moreover, BK challenge significantly increased CXCR4 mRNA levels in nasal tissue of mild allergic rhinitis subjects in vivo, but not normal controls [28].

Regulatory relationships of ALRH

• Before treatment, there was no significant difference between the allergic rhinitis patients and controls in the expression of IL-13 mRNA and immunoreactivity [29].
• Heme oxygenase (HO)-1 is upregulated in the nasal mucosa with allergic rhinitis [30].
• These findings may suggest that the greater amounts of NO in the nasal air of patients with allergic rhinitis are mainly induced by iNOS activity [31].
• METHODS: Plasma fractalkine levels were measured by means of ELISA in 19 control subjects and 55 patients with symptomatic allergic rhinitis, asthma, or both, and CX(3)CR(1) function was studied by using triple-color flow cytometry in circulating T-lymphocyte subpopulations [32].
• Eotaxin mRNA and protein expression in chronic sinusitis and allergen-induced nasal responses in seasonal allergic rhinitis [33].

Other interactions of ALRH

• Our findings did not support a previous report of linkage of allergic rhinitis to chromosome 12q14-q24 but they added positive evidence to the asthma and atopy candidate regions 2q33 and 6p23 [20].
• Interleukin-13 (IL-13), a predominantly Th2-derived cytokine, appears to play a central pathological role in asthma, atopic dermatitis, allergic rhinitis, some parasitic infections, and cancer [34].
• Nasal mucosal immunoexpression of the mast cell chemoattractants TGF-beta, eotaxin, and stem cell factor and their receptors in allergic rhinitis [35].
• 12-q23.3 region are contributing to the expression of the clinical phenotype asthma and the strongest evidence for linkage is in a region near the gene encoding IFNG and (2) a susceptibility locus for both asthma and allergic rhinitis maps to this region [36].
• CONCLUSION: Our results suggest that histamine may induce CC chemokine production in the nasal mucosa of patients with allergic rhinitis [37].

Analytical, diagnostic and therapeutic context of ALRH

• Immunotherapy for allergic rhinitis [38].
• We investigated the association of self-reported asthma or allergic rhinitis with serum IgE levels and skin-test reactivity to allergens in 2657 subjects in a general-population study [39].
• Seven recipients either acquired or had an exacerbation of allergic rhinitis, and two recipients without a history of asthma had asthma one year after transplantation [40].
• SUBJECTS: A total of 547910 individuals aged 14 months to 19 years who at the time of measles-mumps-rubella (MMR) vaccination had relevant information collected on the occurrence of measles and allergic rhinitis, eczema, and asthma [41].
• Seven allergic rhinitis patients and five normal volunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage [42].

References