ABSTRACT
Allergic mechanisms account for most cases of chronic rhinitis. This condition is associated with significant impairment of quality of life and high indirect costs. The identification of the allergic triggers of rhinitis has been historically based on the performance of atopy test [skin prick test (SPT) and serum allergen-specific (s)IgE]. Nevertheless, these tests only denote sensitization, and atopy and allergy represent two different phenomena. It is now clear that allergic phenotypes of rhinitis can exist in both atopic (allergic rhinitis, AR) and non-atopic (local allergic rhinitis, LAR) individuals. Moreover, both allergic phenotypes can coexist in the same rhinitis patient (dual allergic rhinitis, DAR). Therefore, a diagnostic approach merely based on atopy tests is associated with a significant rate of misdiagnosis. The confirmation of the allergic etiology of rhinitis requires the performance of in vivo test like the nasal allergen challenge (NAC). NAC is mandatory for the diagnosis of LAR and DAR, and helps decide the best management approach in difficult cases of AR. Nevertheless, NAC is a laborious technique requiring human and technical resources. The basophil activation test (BAT) is a patient-friendly technique that has shown promising results for LAR and DAR diagnosis. In this review, the diagnostic usefulness for chronic rhinitis of SPT, NAC, olfactory tests, serum sIgE, BAT and the quantification of inflammatory mediators in nasal samples will be discussed. The accurate performance of an etiologic diagnosis of rhinitis patients will favor the prescription of specific therapies with disease-modifying potential like allergen immunotherapy.
ABSTRACT
BACKGROUND: The measurement of nasal specific IgE (NsIgE) in local allergic rhinitis (LAR) patients is challenging and shows variability. The objective of this work was to evaluate a minimally-invasive method of direct detection of NsIgE in patients with LAR to Dermatophagoides pteronyssinus (DP) using an automated immunoassay. METHODS: Fifty patients participated (LAR, n = 14; allergic rhinitis (AR), n = 20; healthy controls [HC], n = 16). Detection of NsIgE was performed by direct application of the solid phase of a commercial DP ImmunoCAP® test 24 hours after DP nasal provocation. RESULTS: There was no difference in the median volume of secretion absorbed by the solid phase of the ImmunoCAP test in the 3 studied groups (p = 0.17). According to receiver operating characteristic (ROC) curve analysis, NsIgE ≥0.1450 was the optimal cutoff point, obtaining in LAR patients 42.86% sensitivity with the highest specificity (100%), and 75% sensitivity and 100% specificity for AR. CONCLUSION: This study demonstrates the detection of NsIgE to DP in LAR by using a simple, commercial device with high specificity.
Subject(s)
Dermatophagoides pteronyssinus/immunology , Immunoassay/methods , Immunoglobulin E/immunology , Nasal Mucosa/immunology , Rhinitis, Allergic/diagnosis , Administration, Intranasal , Adult , Allergens/immunology , Animals , Female , Humans , Immunoglobulin E/blood , Male , Middle Aged , Nasal Provocation Tests , Rhinitis, Allergic/immunology , Young AdultABSTRACT
La angiotensina II, el péptido efector del sistema renina-angiotensina, está implicado en la patogénesis de la aterosclerosis a distintos niveles. Existen numerosas evidencias experimentales que demuestran que tanto la inhibición de la síntesis de angiotensina II mediante la administración de inhibidores de la enzima de conversión de la angiotensina II como mediante el empleo de antagonistas de su receptor AT1 inhiben la formación y la progresión de la lesión aterosclerótica. La angiotensina II es capaz de estimular la producción de especies reactivas de oxígeno en el vaso que desempeñan un papel clave en la disfunción endotelial y en la oxidación de las lipoproteínas de baja densidad (LDL). Asimismo, la angiotensina II participa en la inducción de la respuesta inflamatoria en la pared vascular mediante la producción de moléculas de adhesión y citoquinas quimiotácticas y proinflamatorias. Este péptido estimula la proliferación y la migración de células de músculo liso y modula su cambio fenotípico, dando lugar a un aumento en la síntesis de la matriz extracelular. Finalmente, la angiotensina II también participa en las complicaciones de la aterosclerosis al favorecer la ruptura de la placa y la trombogenicidad de la misma. Por tanto, la angiotensina II juega un papel importante tanto en el inicio del proceso al favorecer la disfunción endotelial, en la progresión de la lesión ateromatosa, en la ruptura de la placa y en la aparición de accidentes trombóticos (AU)
Angiotensin II, the effector peptide of the renin-angiotensin system, may be involved in various factors affecting the pathogenesis of atherosclerosis. There is abundant experimental evidence that both pharmacological antagonism of angiotensin II formation by angiotensin converting enzyme inhibition and blockade of angiotensin II by angiotensin type I receptor blockade inhibits the formation and progression of atherosclerotic lesions. Angiotensin II is able to stimulate the production of reactive oxygen species in blood vessels, which play a key role in endothelial dysfunction and oxidation of low-density lipoproteins. In addition, angiotensin II participates in the induction of the inflammatory response in the vascular wall through the production of adhesion molecules and chemotaxic and proinflammatory cytokines. This peptide stimulates the proliferation and migration of smooth muscle cells and modulates phenotypic changes in these cells, thus increasing the synthesis of extracellular matrix. Finally, angiotensin II also contributes to the complications of atherosclerosis by favoring plaque rupture and thrombogenicity. Therefore, angiotensin II plays an important role both in the beginning of the process -promoting endothelial dysfunction- in atherosclerotic lesion progression, in plaque rupture, and in the occurrence of thrombotic accidents (AU)
