RESUMEN
Background: Hymenoptera venom allergy is an immunoglobulin (Ig) E mediated hypersensitivity reaction to Hymenoptera venoms. Obvious identification of the culprit insect that causes the clinical symptoms and, hence, the accurate selection of venom for curative treatment, is of great importance for the effectiveness and safety of venom immunotherapy. Objective: In this study, the contribution of component-resolved diagnostics (CRD) is evaluated in the diagnosis of Hymenoptera venom allergy. Method: Ninety-three patients from four different centers in Turkey were included in the study. Conventional tests, including prick and intradermal skin tests, with commercial venom extracts and serum specific IgE (sIgE) levels for whole venoms were performed. An sIgE analysis for venom allergen components, including rApi m 1, rApi m 2, rApi m 10, rVes v 1, rVes v 5, were evaluated by immunoblotting. Results: In conventional test results, 17 of 35 patients with bee venom allergy were positive to honey bee venom, whereas 18 patients were positive to bee and wasp venoms. In 28 of 35 patients with bee venom allergy, the diagnosis was confirmed with CRD. CRD revealed a sensitivity of 80% in patients with bee venom allergy. According to conventional tests, 7 of 24 patients with vespid venom allergy demonstrated sensitivity only to Vespula species, whereas 17 patients revealed double positivity. The total diagnostic sensitivity of Ves v 1 and Ves v 5 was calculated as 87.5%. Ten of 23 patients with a history of hypersensitivity to both venoms showed double sensitivity with CRD; one patient had cross-reactivity, one patient was found to be sensitive only to bee venom, and, eight patients were sensitive only to Vespula species. Eleven patients had an uncertain history in terms of the culprit insect type and six of them had double sensitivity in CRD. Conclusion: CRD seemed to be more helpful in diagnosing vespid venom allergy than bee venom allergy. It can also discriminate clinically significant sensitizations from irrelevant ones.
Asunto(s)
Venenos de Abeja , Himenópteros , Hipersensibilidad , Mordeduras y Picaduras de Insectos , Alérgenos , Animales , Venenos de Artrópodos , Humanos , Himenópteros/inmunología , Hipersensibilidad/diagnóstico , Inmunoglobulina E , Mordeduras y Picaduras de Insectos/diagnóstico , Venenos de AvispasRESUMEN
Alarmins are endogenous, constitutively expressed, chemotactic, and immune activating proteins/peptides that are released as a result of degranulation, cell injury or death, or in response to immune induction. Alarmins are involved in a variety of processes including antimicrobial gene expression regulation, cellular homeostasis, wound healing, inflammation, allergy, autoimmunity and oncogenesis. IL-25, IL-33, thymic stromal lymphopoietin (TSLP) are airway epithelial-derived alarmins and the characteristics of alarmins are that they are rapidly released after nonprogrammed cell death, they activate the immune cells. It is thought that the inhibition of the effects of alarmin on the immune system may be useful in the treatment of asthma. The effects of anti-IL-25 (Brodalumab) and anti-TSLP (Tezepelumab) treatments on asthmatic patients were investigated for that purpose. Brodalumab provided limited benefit only in the asthmatic group with high reversibility. Tezepelumab was found to be the first biological drug to have significant positive effect on two important indicators of asthmatic inflammation such as blood eosinophils and nitric oxide fraction in exhaled air. The effect of anti-IL-33 on airway inflammation was shown in animal experiments and anti-IL-33 was found to be protective by reducing eosinophilia, inflammatory cytokines, airway hypersensitivity. In this review, we aimed to summarize the role of alarmines in the pathogenesis of asthma and the results of studies with anti-alarmin biologics.
Asunto(s)
Alarminas/uso terapéutico , Asma/tratamiento farmacológico , Productos Biológicos/uso terapéutico , Femenino , Humanos , MasculinoRESUMEN
Noninvasive ventilation is the first line treatment of choice in acute respiratory failure in many diseases including post-extubation respiratory failure. Herein we report a case unresponsive to noninvasive ventilation due to tracheal stenosis. A 49- year -old female was admitted to intensive care unit after successful resuscitation of cardiac arrest. During the follow-up, she was extubated on 16th day and then transferred to the coronary ward. Four days later, she started to have progressive dyspnea and difficulty in breathing. Arterial blood gas evaluation showed respiratory acidosis with moderate hypercapnia. Noninvasive ventilation was initiated with the diagnosis of cardiogenic pulmonary edema however she did not respond to noninvasive ventilation therapy. Pulmonary consultation revealed that she had a new onset stridor. She had an urgent fiberoptic bronchoscopy which revealed severe tracheal stenosis. Tracheal stenosis should be considered in patients who do not respond to noninvasive ventilation after extubation like in our case.
Asunto(s)
Ventilación no Invasiva , Estenosis Traqueal/diagnóstico , Estenosis Traqueal/terapia , Análisis de los Gases de la Sangre , Broncoscopía , Diagnóstico Diferencial , Disnea/etiología , Femenino , Humanos , Hipercapnia/etiología , Persona de Mediana Edad , Insuficiencia Respiratoria/diagnóstico , Estenosis Traqueal/complicacionesRESUMEN
BACKGROUND: Data are limited regarding the effectiveness of omalizumab in patients with eosinophilic granulomatosis with polyangiitis (EGPA). Our aim was to evaluate the clinical and functional effectiveness of omalizumab in patients with EGPA in long-term follow-up. METHODS: This study was a retrospective chart review of patients with EGPA who were treated with omalizumab injections between May 2012 and April 2018. Once treatment with omalizumab was started, data were collected at various time points: baseline, the 16th week, 1st year, and annually until the last evaluation. RESULTS: Eighteen patients (16F/2M) with a mean age of 48.61 ± 11.94 years were included. Data were available for all patients for the first year, 12 patients for the second year, 10 patients for the third year, 8 patients for the fourth year and 5 patients for the fifth year. All patients were on mean dosage of 15.77 ± 7.6 mg/day oral corticosteroid (OCS) as daily bases for mean 8.61 ± 4 years besides high-dose inhaler corticosteroid/long-acting beta agonist. Antineutrophil cytoplasmic antibodies (ANCA) were positive in 2 patients, and 8 patients were diagnosed as having vasculitis by skin biopsy, one patient had polyneuropathy, and one patient had cardiac involvement.By considering the individual responses of patients and the level of improvement at the last evalulation, 10 (55.6%) patients responded completely, 1 responded partially, and 7 (38.9%) had no improvement. Omalizumab worked as a steroid-sparing agent in all patients and the daily OCS dose was reduced with a mean dosage of 6.28 mg/day at the end of the first year. The mean OCS reduction time for the whole group was 4 months. A reduction in asthma exacerbations/hospitalizations, improvement in forced expiratory volume in 1 second, and no decrease in the eosinophil count during treatment with omalizumab were also observed. CONCLUSIONS: Omalizumab improved asthma control in some patients with EGPA with uncontrolled asthma by reducing asthma exacerbations and oral steroid requirement. However, more data are needed before recommending widespread use of omalizumab in patients with EGPA.