Congestion In Allergic Rhinitis Research Articles

Relationship between Nasal Congestion and Quality of Life of Allergic Rhinitis Patients

Nasal congestion is the most common complaint complained of by allergic rhinitis sufferers. Symptoms of nasal congestion in allergic rhinitis can affect a person's quality of life, resulting in decreased work productivity, academic and social success. Based on previous research, the prevalence of allergic rhinitis is 10 to 30% of the world population, where nasal congestion is the most frequently reported symptom with a prevalence of 60%. The aim of this study was to determine the relationship between nasal congestion and the quality of life of allergic rhinitis sufferers among FK Unissula students. This research is an analytical research with a cross sectional design with sample criteria of Unissula Medical Faculty students Class of 2022 and 2021 who suffer from allergic rhinitis and meet the inclusion and exclusion criteria. The inclusion criteria in this research were students of FK Unissula Class of 2022 and 2021 and were willing to be research subjects. The exclusion criteria in this study were students with anatomical nasal abnormalities and those experiencing chronic rhinosinusitis with or without nasal polyps, deviated septum, adenoid hypertrophy, and neoplasms. There were 50 respondents from FK Unissula students who suffered from allergic rhinitis. It was found that 31 (62%) students had a blocked nose and 19 (38%) students did not experience a blocked nose. The research results showed that the majority of students experienced mild nasal congestion and the quality of life for the majority of students was good. The results of the analysis of the relationship between nasal congestion and the quality of life of allergic rhinitis sufferers using the Spearman test obtained p 0.048 with a correlation coefficient of 0.281. The results of the analysis above showed that there was a significant relationship between nasal congestion and the quality of life of allergic rhinitis sufferers.

15-hydroxy eicosadienoic acid is an exacerbating factor for nasal congestion in mice.

Allergic rhinitis (AR) is one of the most common allergic inflammatory diseases worldwide. In AR, increased blood flow and vascular permeability in nasal mucosa cause rhinorrhea and nasal congestion. We investigated the role of an 11Z,14Z-eicosadienoic acid-derived metabolite, 15-hydroxy-11Z,13Z-eicosadienoic acid (15-HEDE), in functional changes in vasculature and nasal congestion in AR. Repeated intranasal administration of Ovalbumin (OVA) caused AR symptoms, such as sneezing and nasal congestion, in mice. OVA administration increased the level of 15-HEDE in nasal lavage fluid, which reached approximately 0.6ng/ml after ten OVA treatments. Upon measuring vascular contraction, treatment with 0.1-3μM 15-HEDE did not cause contraction in mouse aortae, while it dilated aortae that were pre-contracted by thromboxane receptor stimulation. Pretreatment with the voltage-gated K+ (KV ) channel inhibitor 4-aminopyridine significantly inhibited the 15-HEDE-induced vascular relaxation. Intravital imaging showed that administration of 1μg 15-HEDE dilated blood vessels, and Mile's assay demonstrated that this administration also caused dye leakage, indicating vascular hyperpermeability in mouse ears. Computed tomography scanning and morphological study revealed that administration of 3μg 15-HEDE narrowed nasal passages and thickened nasal mucosa in mice. Finally, we confirmed that treating mice with 3μg 15-HEDE caused rhinitis symptoms, such as abdominal breathing, and reduced respiratory frequency, suggesting nasal congestion. 15-HEDE caused vasodilation by activating KV channels and increased vascular permeability, which may lead to nasal congestion. Furthermore, 15-HEDE might be a new lipid mediator that exacerbates nasal congestion in AR.

A novel concept of immunological and allergy interactions in autism spectrum disorders: Molecular, anti-inflammatory effect of osthole

BackgroundAutism spectrum disorder (ASD) is a neurodevelopmental disorder defined by Diagnosis and Statistic Manual 5 (DSM-5) as persistent social interaction and communication deficient across multiple contexts. Various immunological findings have been reported in children with ASD, and co-existing allergic problems have been recorded in children diagnosed with ASD. Osthole, the effective component of Chinese traditional medicine, is reported to have anti-inflammatory effects. This study assessed the anti-inflammatory effect of osthole on the histamine-induced inflammatory responses in PBMC cells. MethodsPeripheral blood mononuclear cells (PBMC's) from children with: (1) ASD group with co-existing allergies/asthma (n = 29); (2) ASD group without allergy/asthma (n = 29); (3) Allergy group (n = 30) and from typically developing age-matched control subjects (n = 28) were stimulated with either histamine, FXF, osthole or mixture of this substances. mRNA COX-2 gene expression, COX-2 production and inhibitory effect of tested substances on COX-2 were assessed after stimulation. ResultsChildren with ASD may show either an innate proinflammatory response or increased activity of COX-2 which could display more impaired behavioral profile than children with non-inflamed. This study indicated that COX-2 may be involved in pathogenesis of ASD and/or allergy, and osthole could be used to decrease the effects of COX-2 in inflammation and ASD development. High incidence of allergy in ASD patients may indicate immune dysregulation that could be of relevance to the pathophysiology, symptomatology or neuroimmunology of ASD. ConclusionsThis study shows that fexofenadine (FXF – antihistamine drug) and osthole exhibit selective COX-2 enzyme inhibitory activity. The selective COX-2 activity of osthole may explain further the anti-inflammatory properties of osthole in relieving congestion in allergic rhinitis, and as distinctive effects between FXF and osthole were observed, individual antihistamines may have different modes of action via the COX enzyme system.

Evaluation of optical rhinometry for nasal provocation testing in allergic and nonallergic subjects

Objective Optical rhinometry is a new method that quantifies light extinction in optical density to assess nasal blood volume as a measure of nasal patency. The purpose of this study is to evaluate optical rhinometry as an objective evaluation of nasal patency using nasal provocation testing with histamine and oxymetazoline. Study Design Prospective pilot. Setting Academic tertiary rhinologic practice. Subjects and Methods Convenience sample of five adult subjects with allergic rhinitis and five adult normal subjects who underwent challenge with histamine and oxymetazoline. Patients underwent challenge with increasing concentrations of histamine to determine the amount of histamine needed to cause a positive optical rhinometry reading. The same subjects then underwent histamine challenge with this amount followed by oxymetazoline. Nasal patency was assessed subjectively after each challenge with the visual analog scale. Results The median histamine amount needed to cause a positive response was statistically lower in allergic rhinitis as compared with nonallergic subjects at 150 μg and 300 μg, respectively ( P = 0.04). When comparing the optical rhinometry with subjective nasal congestion after histamine and oxymetazoline challenges, there was a statistically significant correlation with r = 0.79 ( P = 0.00003). Conclusion This initial study demonstrates a correlation between subjective symptoms of nasal patency and objective measurements with the optical rhinometer. Less histamine amount necessary to incite nasal congestion in allergic rhinitis suggests that these patients may be primed to the effects of histamine. These preliminary data suggest that optical rhinometry is able to assess changes in nasal patency during challenges with histamine and oxymetazoline.

Mechanism of nasal obstruction in patients with allergic rhinitis

SummaryNasal obstruction is a crucial symptom in allergic rhinitis (AR) patients and may affect the quality of life. It is caused mostly by nasal mucosal obstruction, and to a lesser extent, fluid secretion. Mucosal congestion is primarily a vascular phenomenon comprising vasodilatation of capacitance vessels (cavernous sinus) and oedema formation due to plasma leakage from post‐capillary venules. The nose has a complex microvascular anatomy consisting of capacitance vessels, arteriovenous anastomosis, and subepithelial and periglandular capillaries. Nasal congestion is explained by the effects of local mediators exerting potent vasodilatation or increasing permeability of nasal blood vessels and nerves. Capacitance vessels usually constrict because of constant sympathetic tone. They distend by a variety of stimuli such as loss of continuous sympathetic stimulation on the sinusoids, direct vasodilatation by vasoactive substances, contraction of cushion veins, and compression of venules by distended arteries in the intraosseous bony canals of periosteal space. Although topical application of histamine can cause vasodilatation and oedema, histamine is not likely a major mediator causative of nasal congestion in AR. Nasal vascular dilatation elicited by cysleukotriene 1 (cysLT1) may be induced by nitric oxide produced through cysLT1 receptor activation. Thromboxane A2 may cause capacitance vessel dilatation through a contraction of cushion veins. Potentiation of vasoconstrictor action of steroids has been reported since the 1950s. Glucocorticoids (GCs) have two fundamentally different vascular effects: classic action modifying the transcription of pro‐inflammatory genes and acute non‐genomic action (within minutes) that increases the vasomotor tone. The non‐genomic effect is likely related to binding of GCs to the plasma membrane and inhibition of extraneuronal monoamine transporter on vascular smooth muscle cells, thereby increasing noradrenaline concentrations at α1‐adrenoceptors. Genomic vascular effects include the reduction of vessel density, decrease of hyperperfusion, reduction of inflammatory microvascular hyperpermeability, and decreased influx and activation of inflammatory cells. These effects require hours to manifest themselves physiologically.

Treatment of congestion in upper respiratory diseases

Congestion, as a symptom of upper respiratory tract diseases including seasonal and perennial allergic rhinitis, acute and chronic rhinosinusitis, and nasal polyposis, is principally caused by mucosal inflammation. Though effective pharmacotherapy options exist, no agent is universally efficacious; therapeutic decisions must account for individual patient preferences. Oral H(1)-antihistamines, though effective for the common symptoms of allergic rhinitis, have modest decongestant action, as do leukotriene receptor antagonists. Intranasal antihistamines appear to improve congestion better than oral forms. Topical decongestants reduce congestion associated with allergic rhinitis, but local adverse effects make them unsuitable for long-term use. Oral decongestants show some efficacy against congestion in allergic rhinitis and the common cold, and can be combined with oral antihistamines. Intranasal corticosteroids have broad anti-inflammatory activities, are the most potent long-term pharmacologic treatment of congestion associated with allergic rhinitis, and show some congestion relief in rhinosinusitis and nasal polyposis. Immunotherapy and surgery may be used in some cases refractory to pharmacotherapy. Steps in congestion management include (1) diagnosis of the cause(s), (2) patient education and monitoring, (3) avoidance of environmental triggers where possible, (4) pharmacotherapy, and (5) immunotherapy (for patients with allergic rhinitis) or surgery for patients whose condition is otherwise uncontrolled.

Targeting congestion in allergic rhinitis: The importance of intranasal corticosteroids

The cardinal nasal symptoms of allergic rhinitis (AR) are sustained by an underlying inflammatory process. Congestion is one of the most prominent and distressing symptoms for patients and is strongly associated with a broadly deteriorated quality of life and significant losses in productivity. The purpose of this study was to explore the role of intranasal corticosteroids (INSs) in down-regulating the inflammatory response to allergen and their clinical efficacy on AR symptoms, particularly congestion. AR is characterized by an influx of inflammatory cells and mediators into the nasal mucosa after antigen exposure. The response is biphasic, encompassing an early and a late phase. Antigen exposure has a priming effect, decreasing the threshold for subsequent allergic reaction on rechallenge and increasing the responsiveness of the nasal mucosa. INSs are a mainstay of therapy for AR and the most effective intervention for nasal congestion and other nasal symptoms, with established superiority to antihistamines, decongestants, and leukotriene antagonists. In addition to symptom relief, INSs suppress numerous stages of the inflammatory cascade, inhibiting the influx of inflammatory cells and mediators. Topical nasal corticosteroids have a low incidence of local adverse effects, negligible systemic absorption, and excellent safety. Congestion is one of the most bothersome symptoms of AR. INS therapy improves AR symptoms, with particular efficacy in relieving congestion, by attenuating nasal hyperresponsiveness. Pretreatment with INSs has been shown to relieve early and late-phase clinical symptoms of AR. Modification of the disease process results in significant relief of symptoms and leads to fewer disease exacerbations.

The pathophysiology, clinical impact, and management of nasal congestion in allergic rhinitis

Background: Nasal congestion is a cardinal symptom of allergic rhinitis (AR). It is difficult to treat and is associated with decreased quality of life. Objective: This article reviews the clinical features of nasal congestion, its complex pathophysiology in the context of AR, its clinical impact, and the strengths and weaknesses of available treatments. Methods: Primary studies and reviews in the peerreviewed, English-language literature were identified through searches of MEDLINE (1966–2008) and the Cochrane Library (1996–2008) using the terms nasal congestion, allergic rhinitis, pathophysiology, quality of life, and burden. Additional references were obtained by searching the reference lists of the identified articles. Abstracts from the 2006 and 2007 meetings of the American Academy of Allergy, Asthma, and Immunology were also searched. Pertinent articles were included in the review if they were recently published and patient-focused, and if their authors were recognized leaders in the field. Results: A survey of 2355 patients with AR or their guardians found that almost half of respondents rated nasal congestion the most bothersome symptom; in a survey of 2500 adults with AR, 78% rated nasal congestion either extremely or moderately bothersome. Histamine and leukotrienes are major mediators of the allergic inflammation associated with nasal congestion, as indicated by reductions in nasal cross-sectional area in response to histamine challenge ( P < 0.001) and increases in nasal airway resistance in response to leukotriene challenge ( P < 0.05).Therapy for nasal congestion in AR is often hampered by limitations associated with the individual agents; for example, decongestants are effective in the control of nasal congestion, but their use is restricted by their adverse-event profiles. A metaanalysis of 16 controlled studies involving 2267 patients with AR found that intranasal corticosteroids provided significantly greater relief of nasal congestion than oral antihistamines (95% CI for combined standardized mean difference, −0.73 to −0.53). The results of several clinical trials have suggested that leukotriene-receptor antagonists may be associated with reduced nasal congestion; however, no agents in this class are currently approved for the treatment of nasal congestion in AR. Conclusion: There is a need for therapies that are well tolerated and effective in relieving nasal congestion in AR.

Mometasone furoate monohydrate nasal spray for the treatment of nasal congestion in allergic rhinitis

Allergic rhinitis (AR) affects an estimated 20–40 million Americans annually. It is a multifaceted condition comprising a range of symptoms, including nasal congestion, arguably the most bothersome symptom. Of the various types of medications available for the treatment of AR, intranasal corticosteroids are considered the most effective. Mometasone furoate nasal spray is an intranasal corticosteroid with anti-inflammatory properties. It is indicated for the treatment of the nasal symptoms of seasonal AR and perennial AR in adults and children, for the prophylaxis of nasal symptoms of seasonal AR and for the treatment of nasal polyps. Numerous clinical trials have demonstrated that mometasone furoate nasal spray effectively relieves nasal congestion in adults and children with AR, while providing excellent safety and tolerability.

The effect of MK-0524, a prostaglandin D2 receptor antagonist, on prostaglandin D2-induced nasal airway obstruction in healthy volunteers

Nasal congestion in allergic rhinitis results from tissue edema and vasodilatation in the nasal mucosa. Of the mediators released by mast cells in response to allergens, prostaglandin (PG) D(2) is regarded as the most potent inducer of nasal congestion. Intranasal administration of PGD(2) reproduces the nasal blockade experienced by patients with seasonal allergic rhinitis (SAR) via its action on the PGD(2) (DP) receptor to induce nasal vasodilatation. Intranasal challenge with PGD(2) can be a useful tool for evaluating DP-receptor antagonists. The main purpose of this study was to examine the ability of MK-0524, a DP receptor antagonist in development for the treatment of SAR, to block PGD(2) induced nasal congestion in healthy volunteers. To this end, a double-blind, placebo-controlled, randomized, 3-period study was performed in 15 healthy subjects. During each period, subjects received MK-0524 25 mg, MK-0524 100 mg or placebo qd for 3 days. Twenty-four hours following the last dose, nasal provocations with PGD(2) were performed to determine the PD(75), which is the intranasal dose of PGD(2) that provokes a 75% increase in baseline total nasal airway resistance as performed by active anterior rhinomanometry. Following treatment with MK-0524, the PD(75) (mean+/-SD) was significantly shifted from 15.8 +/- 18.3 mug/nostril during the placebo period to more than 512 mug/nostril both following the 25- and 100-mg (maximum challenge dose tested) dose regimen. Whether this >45 fold increase in PD(75) will induce a clinically meaningful effect of MK-0524 will require clinical study in participants with SAR.

New Evidence of H1-Receptor Independent COX-2 Inhibition by Fexofenadine HCl in vitro

Background/Aims: Fexofenadine HCl (FEX) has previously been shown to have anti-inflammatory properties in relieving nasal congestion in allergic rhinitis. The objective of this study was to further elucidate the mechanism of action behind the anti-inflammatory properties of FEX in addition to its H₁-receptor antagonism. Methods: The effects of two antihistamines, FEX and loratadine (LOR), were investigated on cyclooxygenase (COX)-1 and -2 enzymesin vitro. FEX (10^–9–10^–3 mol/l) and LOR (10^–9–10^–4 mol/l) were incubated with arachidonic acid in a COX screening assay with either ovine COX-1 or COX-2 or human COX-2. COX-2 enzyme inhibitory activity for the antihistamines was compared with the known selective COX-2 inhibitor DuP-679. Results: High concentrations of FEX (10^–3 mol/l) significantly inhibited arachidonic acid-mediated ovine COX-1 activity, but low concentrations had no effect. Low concentrations of FEX (10^–8 mol/l) inhibited ovine COX-2 activity, and this inhibition decreased with increasing concentrations. The inhibition of COX-2 activity by FEX was similar to that seen with the selective COX-2 inhibitor, DuP-679. Conversely, LOR inhibited COX-1 activity at low concentrations (10^–8 mol/l), but had little inhibitory effect on COX-1 at high concentrations. LOR (10^–5 mol/l) markedly stimulated COX-2 activity. Conclusion: FEX showed selective arachidonic acid-mediated COX-2 inhibitory enzyme activity, which differed markedly from the COX inhibitory enzyme activity of LOR. This selective COX-2 inhibitor activity by FEX may contribute to its anti-inflammatory properties in relieving nasal congestion in allergic rhinitis.

Efficacy and Safety of an Oral Formulation of Cetirizine and Prolonged-Release Pseudoephedrine versus Budesonide Nasal Spray in the Management of Nasal Congestion in Allergic Rhinitis

The aim of this study was to compare the decongestant properties and tolerability of oral cetirizine and pseudoephedrine in a prolonged release form with those of nasal (aqueous spray) budesonide. Thirty-six individuals experiencing allergic rhinitis to house dustmites (HDM) participated in a study according to a randomized, crossover, two-period, two-treatment design with at least a 2-week washout period between treatments. In each period of 4 consecutive days, medications were taken twice daily. On day 1, immediately after the first intake of medication, individuals were exposed to HDM extract in the Vienna Challenge Chamber (VCC) for 5 hours. The primary efficacy parameter was nasal congestion, assessed by active anterior rhinomanometry and rating of nasal cavity photos. Rhinomanometry and nasal cavity photos both indicated that cetirizine/pseudoephedrine efficacy was statistically superior to budesonide in the management of nasal congestion during VCC sessions. The efficacy of cetirizine/pseudoephedrine was similar to that of budesonide from the end of day 1 up to day 4 when individuals were exposed to their natural environment post exposure to the aeroallergens. This study confirms the efficacy of cetirizine/pseudoephedrine and budesonide in the management of nasal congestion associated with allergic rhinitis. Both medications were well-tolerated. Cetirizine/pseudoephedrine was more effective than budesonide during HDM exposure, whereas budesonide became as effective as cetirizine/pseudoephedrine several hours post exposure to the allergens.

Antihistamines alone and in combination with leukotriene antagonists in nasal congestion

Summary Although antihistamines are first-line treatment for allergic rhinitis and are effective at combating the majority of nasal and ocular symptoms associated with this disease, they are traditionally considered to be less effective at dealing with nasal congestion. Combination therapy with antihistamines and antileukotrienes has been shown to be an alternative treatment strategy in dealing with nasal symptoms, including congestion. However, recent studies have suggested that some of the newer antihistamines are effective in reducing nasal congestion in allergic rhinitis when used alone. For example, fexofenadine has been shown to have a beneficial effect on nasal congestion in a number of clinical studies investigating its efficacy and safety, as well as in combination therapy studies. This paper aims to review the available literature looking at combinations of antihistamines and antileukotrienes and single antihistamine therapy for reducing nasal congestion in allergic rhinitis, using subjective symptom scoring and/or objective measurements.

Vascular effects of slow reacting substance (SRS) in the cat nasal mucosa and the appearance of a SRS-like principle in cat nasal secretion on nerve stimulation.

Stimulation of parasympathetic secreto-vasomotor nerve fibres in cat nasal mucosa produced nasal secretions with biological activity similar to cat paw SRS. The biologically active principle was purified by ethanol extraction, Amberlite XAD-2 and anion exchange chromatography. It had elution characteristics common with cat paw SRS but different to those of prostaglandin F2 alpha. The biological activity on the guinea pig ileum was antagonized by FPL 55712. In the cat intraarterial administration of cat paw SRS resulted in a dose-dependent but modest increase in nasal blood flow whereas local blood content was not affected. Provided SRS has similar effects on human nasal blood flow the importance for SRS as a mediator for nasal congestion in allergic rhinitis or parasympathetically induced vasomotor rhinitis seems less likely.