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PubMed1990

Antihistamine therapy in allergic rhinitis.

Allergic rhinitis is a common disorder that is associated with a high incidence of morbidity and considerable costs. The symptoms of allergic rhinitis are primarily dependent upon the tissue effects of histamine. Antihistamines are the mainstay of therapy for allergic rhinitis. Recently, a second generation of antihistamines has become available. These agents lack the adverse effect of sedation, which is commonly associated with older antihistamines. Current practice of antihistamine therapy in allergic rhinitis often involves random selection among the various agents. Based upon the available clinical trials, chlorpheniramine appears to be the most reasonable initial antihistaminic agent. A nonsedating antihistamine should be used initially if a patient is involved in activities where drowsiness is dangerous. In this comprehensive review of allergic rhinitis and its treatment, the current as well as future options in antihistamine pharmacotherapy are emphasized.

Histamine H1 Antagonists↗
PubMed1990

[Current pathophysiologic aspects of allergic rhinitis. I].

Allergic rhinitis is a classic example of a type I immunological reaction. After allergic provocation tests a biphasic reaction is seen in the respiratory tract that is more pronounced in the lower than in the upper respiratory tract due to the physiological changes during the nasal cycle. The early phase of the immediate reaction starts some minutes after allergen provocation. After 5-10 h the nasal symptoms (discharge, blockage, sneezing and itching of the nose) reappear, a phenomenon which is called the "late-phase response" (LPR). The LPR is of great clinical importance in the pathophysiology of perennial allergic rhinitis and phenomena such as nasal priming and nasal hyper-reactivity. The most important effector cell of the early phase of the immediate reaction is the mast cell, whereas basophils, eosinophils and neutrophil granulocytes seem to be more important for the LPR. There is also evidence for morphological and functional heterogeneity of mast cells in man. The role of the chemotactically immigrated eosinophils in allergic reactions has not been clear until now: the eosinophil-derived mediators may enhance or inhibit the allergic reaction. Also the eosinophils show different morphological and functional states (so-called hypo- and hyperdense eosinophils). The symptoms of allergic rhinitis (sneezing, discharge, blockage, itching of the nose) are caused by different mediators, of which the most important is histamine. Other mediators or modulators of the allergic reactions are leucotrienes, prostaglandins, PAF, serotonin, and the kallikrein-kinine and complement systems. In recent years many regulatory peptides have been detected in the human nasal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1992

Allergic rhinitis.

Allergic rhinitis is a common disease with characteristic symptoms affecting the eyes, ears, and face as well as the nose. A detailed history is the foundation of a correct diagnosis. Laboratory tests may be needed to supplement this in atypical presentations. A combination of pharmacotherapy, immunotherapy, and environmental control may be required to control and prevent symptoms.

Adrenal Cortex Hormones↗
PubMed1989

Management of allergic rhinitis.

Allergic rhinitis is a common complaint and remains an important cause of morbidity. Effective management includes full evaluation of the patient, identification of offending antigens and, if possible, an explanation of antigen avoidance measures. Drug treatment, including topical and oral agents, is effective for most patients, providing it is used correctly.

Humans↗
PubMed1977

Effect of deep inspiration on airway conductance in subjects with allergic rhinitis and allergic asthma.

We measured specific airway conductance (Gaw/Vtg) in a body plethysmograph before and after a deep inspiratory maneuver in 8 subjects with allergic rhinitis and 8 subjects with allergic asthma. In hay fever subjects deep inspiration had no effect on Gaw/Vtg if it was performed in the control state; however, when methacholine-induced bronchoconstriction was present, deep inspiration transiently increased Gaw/Vtg. In asthmatic subjects deep inspiration was followed by a transeint fall in baseline Gaw/Vtg in the control state; however, when bronchoconstriction was present, deep inspiration was followed by small and variable changes in Gaw/Vtg in 7 subjects and marked improvement in Gaw/Vtg in 1 subject. In asthmatic subjects the bronchoconstrictor response to deep inspiration performed in the control state is thought to be due to reflex changes in bronchomotor tone mediated by cholinergic (vagal) nerve pathways. Like asthmatic subjects, hay fever subjects, hay fever subjects also possess cholinergic-mediated airway hyperreactivity compared with normals. Our results indicate that, in spite of their increased airway reactivity, hay fever subjects respond more like normal subjects than like asthmatic subjects after a deep inspiratory maneuver.

Adult↗
PubMed1989

The comparison of allergic responses to Dermatophagoides farinae between bronchial asthma and allergic rhinitis.

The allergic responses of 52 bronchial asthma patients who exhibited a positive bronchoprovocation test with house dust and 50 allergic rhinitis patients who had positive RAST results to Dermatophagoides farinae (D. farinae) were studied, including the measurement of D. farinae-specific IgE using D. farinae-RAST, total IgE and skin reactivity to D. farinae and house dust. A comparison between the allergic rhinitis group in which methacholine PC20 was more than 4.66 mg/mL and the allergic rhinitis group which presented negative results in the methacholine bronchial challenge test, indicated that there were significant differences in skin test reactivity and the ratio of specific IgE to total IgE (P less than .05). The allergic responses we observed were not different between the allergic rhinitis group in which methacholine PC20 was less than 4.66 mg/mL (asthmatic range of methacholine PC20) and the allergic rhinitis group in which methacholine PC20 was more than 4.66 mg/mL. When comparing the bronchial asthma group which showed positive results in D. farinae-RAST and the allergic rhinitis group in which methacholine PC20 was less than 4.66 mg/mL, significant differences were noted in total IgE level (P less than .05). These findings suggest that the development of bronchial asthma in patients with allergic rhinitis might be predicted by measuring the degree of bronchial hyperreactivity and their allergic responses.

Allergens↗
PubMed2026

Phosphoproteomic analysis in a mouse model reveals ERK signaling as a key modulator of inflammatory response in nasal mucosa associated with childhood allergic rhinitis.

Childhood allergic rhinitis (AR) is a multifactorial condition arising from the interplay between genetic predisposition and environmental exposures. Although protein phosphorylation is widely recognized as a key regulator of gene expression across various physiological and pathological states, its global alterations in the nasal mucosa of pediatric patients with AR and their subsequent impact on mucosal function and inflammatory pathways remain incompletely characterized. Our study aimed to elucidate the molecular mechanisms underlying nasal mucosa dysfunction induced by pediatric AR. Our analysis revealed 3,861 proteins encompassing a total of 15,491 phosphorylation sites. Specifically, we detected 441 downregulated phosphorylation sites on 584 proteins and 531 upregulated phosphorylation sites on 722 proteins in the nasal mucosa of the AR group. Our proteomics findings suggest that the dysregulation of immune activation and metabolic regulation may contribute to AR pathophysiology. Through pathway analysis of the identified phosphorylation sites, we found Extracellular Signal-Regulated Kinase (ERK) signaling emerged as an important pathway; notably, upregulation of ERK1/2 phosphorylation was observed as a significant marker associated with AR. Importantly, targeting ERK inhibitors presents a potential therapeutic strategy for modulating key inflammatory response signaling pathways in the context of AR, although this finding is derived from preclinical mouse models and requires rigorous validation in human pediatric nasal mucosal tissues before any clinical translation can be considered. Collectively, these findings highlight that elucidating the molecular mechanisms underlying AR-induced nasal mucosal dysfunction in the mouse model may inform the novel therapeutic targets for pediatric allergy-related diseases. Overall, elucidating these mechanisms has substantial implications for developing targeted interventions aimed at mitigating inflammation associated with allergic rhinitis.

Animals↗
PubMed1989

When hay fever doesn't quit. Diagnosing seasonal and perennial allergic rhinitis.

Seasonal allergic rhinitis is usually easily diagnosed by the seasonal nature of characteristic symptoms combined with evidence of appropriate specific IgE antibodies. Perennial allergic rhinitis, however, may present a diagnostic challenge. The physician may find IgE antibodies to allergens perennially encountered by the patient and should look for other causes of chronic rhinitis. Examination of nasal secretions can be a diagnostic aid, but measurements of eosinophils and total IgE in serum have limited diagnostic value.

Diagnosis, Differential↗
PubMed1989

Allergic rhinitis and aviation.

Allergic rhinitis, or hay fever, is a combination of symptoms that affects approximately 20% of the U.S. population. Symptoms include nasal congestion, sneezing, rhinorrhea, and sleep aberrations. Patients with mild or seasonal cases of allergic rhinitis are perfectly capable of performing adequately in the aviation field. At present, these people are grounded during symptomatic periods. This grounding is due to both Federal Air Regulations and Navy regulations which preclude flying with nasal congestion or with the use of medications. Current therapy of allergic rhinitis is based on the use of three different basic modalities. The first modality is immunotherapy which requires usually weekly injections, and the patient is grounded for 24 h after the injection. The second and most commonly used modality is the use of antihistamine-decongestant preparations. The third group of medications is the topical steroids and cromolyn sodium, which are reviewed in detail because of their improved efficacy and safety. Recommendations are proposed for allowing those persons with allergic rhinitis symptoms that are easily controlled with the topical steroids or cromolyn sodium to continue flying.

Aerospace Medicine↗
PubMed1992

A 10-year prognosis for childhood allergic rhinitis.

The prognosis of allergic rhinitis was studied in 154 children aged 3-17 years at diagnosis by means of a detailed questionnaire administered 8-11 years later. The symptoms had completely disappeared in only 15 (10%) patients. The conjunctival symptoms, however, had disappeared or were controlled successfully by topical drug therapy in almost all, and 77 (50%) were managing without medication for allergic rhinitis. Twenty-five (23%) of the 110 children with seasonal allergic rhinitis had a perennial disease at follow-up, in contrast to seven (16%) of 44 with perennial allergic rhinitis originally who had only seasonal symptoms at follow-up. Asthma or wheezing had developed in 29 cases (19%) and was more common (p less than 0.01) among those with perennial allergic rhinitis (15 of 44) than among those with seasonal allergic rhinitis (14 of 110). No significant association was found between age at onset of symptoms, family history of atopic disease or type of treatment for allergic rhinitis and allergic rhinitis still present at follow-up or development of asthma during the observation period.

Adolescent↗
PubMed1992

Dynamics of mast cells in the nasal mucosa of patients with allergic rhinitis and non-allergic controls: a biopsy study.

Mast cell degranulation is thought to be an important component of the pathogenesis of allergic rhinitis. Quantitative studies on mast cells in nasal mucosa after allergen exposure have given widely divergent results, ranging from an overall decrease via redistribution to an overall increase. We investigated this problem by employing a combination of anti-IgE and toluidine blue staining of biopsy specimens. In allergic patients anti-IgE was found to identify all mast cells and toluidine blue to detect mast cells that were not (totally) degranulated. The study was composed of two parts done in different patient groups. In the first part of the study biopsies were performed in 23 patients with isolated grass-pollen allergy, once during natural provocation in the summer and once in the winter. Biopsies were also performed in 12 controls. Non-allergic controls were found to have the same number of mast cells in the lamina propria as asymptomatic allergic patients. The controls seldom have mast cells in the epithelium. The patients with isolated grass-pollen allergy showed an increase in the numbers of mast cells in the lamina propria during natural provocation and the same seemed to occur in the epithelium as well. During natural provocation almost all of the mast cells in the epithelium and half of those in the lamina propria were degranulated. In the second part of the study 17 patients with isolated grass-pollen allergy and four controls were challenged daily with allergen extract during a 2-week period in the winter. During this period biopsies were performed at eight different occasions, i.e. once before, six occasions during and once after the provocation period. The results of this part of the study showed that during provocation mast cells migrate to the surface of the nasal mucosa, where they become degranulated, and that the pool of mast cells in the lamina propria was apparently replenished by migration of mast cells from the vessels in the lamina propria. The total number of mast cells in the lamina propria remained approximately the same while the mast cells residing in an increasingly thick layer measured from the basal membrane into the lamina propria became degranulated. After 2 weeks, 82% of the mast cells in the lamina propria was degranulated and it was only in the deepest layers that some toluidine blue positive cells were found.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1992

New strategies for the prevention and treatment of allergic rhinitis in children.

Allergic rhinitis (AR) is a very common disease in children, often underdiagnosed and with underestimated complications. Its prevalence has increased during the last years, due to changes in environmental factors. The therapeutic strategy will include prevention by identification and eviction of the main allergens, associated to pharmacological therapy. Among antirhinitic drugs, the new generation of non-sedative specific antihistamines represent the main choice. We report our own experience with astemizole, one of these new antihistamines which confirms that astemizole is an effective and safe drug for the management of AR in children.

Allergens↗
PubMed1990

Effects of one-year hyposensitization in allergic rhinitis. Comparison of two house dust mite extracts.

In an open study, 21 patients suffering from chronic non-seasonal rhinitis and allergic to house mites (HDM) have been treated for 1 year with either a new extract (Pharmalagen; n = 10) or an allergoid, pyridine denatured, extract (Alavac; n = 11), both precipitated with AlOH3 (depot). The following investigations were performed before and after therapy: clinical scoring (for 4 weeks), quantified skin prick tests (SPT) and nasal provocation tests (NPT) with HDM, and determination in serum of HDM-specific IgE and IgG. Both groups were compared with six patients who remained untreated and underwent the same investigations. Hyposensitization with either extract induced an improvement in clinical scores (P less than 0.05), a decrease in SPT reactivity (Pharmalgen: P less than 0.001; Alavac: P less than 0.01), a marked increase in the nasal tolerance to HDM (P less than 0.001) and in HDM-specific IgG (P less than 0.001). In the group of untreated patients, all these parameters remained unchanged. Compared with the Alavac extract, the Pharmalgen extract was more active in decreasing SPT reactions (P less than 0.05) and inducing a HDM-specific IgG rise (P less than 0.05). Although both extracts induced some untoward allergic reactions, no adrenaline was used at any time during the study. These data suggest that hyposensitization with depot extracts of HDM can be considered a safe and active adjunct to the treatment of allergic rhinitis.

Adolescent↗
PubMed1987

[Therapy of allergic rhinitis in childhood].

Allergic rhinitis is the most common of all allergic disorders. After summarising the clinical features and diagnostic approach with regard to differential diagnosis, we will discuss the therapeutic modalities. As with all long-term therapy measures, it is essential to persuade both the child and the parents to participate in the treatment and to get their co-operation.

Asthma↗
PubMed1990

[Immediate and late phases of allergic rhinitis].

The allergic reaction of the human nasal mucosa (Type I Coombs and Gell) can be divided in an immediate- and a late-phase reaction. The degranulation of IgE-bearing mast cells is crucial for the initiation of the immediate phase (app. 30 min). Mediators of these cells - especially histamine - cause the typical allergic symptoms. Some of the patients develop a late-phase reaction after a symptom-free interval. Eosinophils migrate into the epithelial lining and release mediators. Furthermore, mast cells increase in number in the epithelium. Other cells like macrophages and T lymphocytes may be involved as well. While the released mediators cause an unspecific mucosal hyperreactivity, the increased number of IgE-bearing mast cells leads to a specific immunological augmentation of the nasal reaction ("priming effect"). The allergic pathomechanism can be reduced by drugs at different points.

Cell Degranulation↗
PubMed1989

Nasal histamine challenges in symptomatic allergic rhinitis.

Twenty subjects (seven with perennial allergic rhinitis, seven with symptomatic seasonal allergic rhinitis, and six normal control subjects) underwent assessment of nasal sensitivity to histamine. Nasal resistance was measured by posterior rhinometry under control conditions and after log incremental doses of histamine solution pipetted into the nose (0.5 to 5000 micrograms). Allergic subjects exhibited a twofold rise of nasal resistance with doses of 0.5, 5, or 50 micrograms of histamine, whereas the nasal resistance in normal subjects remained unchanged until 500 or 5000 micrograms of histamine had been administered. Nasal reactivity to histamine was not correlated with symptoms on the day of testing but was correlated with the number of positive wheals to skin prick testing. It was concluded that nasal resistance is more sensitive to histamine in subjects with allergic rhinitis than in normal control subjects and that this difference may be used as the basis of a diagnostic test.

Administration, Intranasal↗
PubMed1989

[Rush immunotherapy of perennial allergic rhinitis].

In treating perennial allergic rhinitis sensitive to house-dust (HD)-mite (Dermatophagoides farinae), rush immunotherapy with HD antigen and classical immunotherapy were applied to 2 different patient groups, and the results obtained were compared. The results were as follows. 1. There was no significant difference in clinical efficacy between both groups. 2. The titer of the anti-mite IgE antibody was not changed in both groups during the course of treatment. 3. The titer of the anti-mite IgG4 antibody was increased in both groups during the course of treatment. In rush immunotherapy, the increase began within 3 months after the initiation of treatment, whereas about 6 months after the initiation in classical immunotherapy. 4. In rush immunotherapy, a smaller dose amount of antigen could increase the titer of the anti-mite IgG4 antibody. 5. It was not clear whether the increased anti-mite IgG4 antibody titer exerted clinical effects on allergic symptoms. Patients with perennial allergic rhinitis may receive benefit from rush immunotherapy. The antigen-specific IgG4 antibody seems to be an index in evaluating immunotherapy objectively.

Adolescent↗