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BACKGROUND: Allergic rhinitis (AR) has a substantial socioeconomic impact associated with impaired work productivity. OBJECTIVE: To study the impact of AR on work productivity and estimate the corresponding indirect costs for 40 countries. METHODS: We conducted a cross-sectional study using direct patient data from the MASK-air® app on users with self-reported AR. We used the Work Productivity and Activity Impairment Questionnaire: Allergy Specific to measure the impact of AR on work productivity (presenteeism and absenteeism). Weekly indirect costs were estimated per country, for each level of rhinitis control and considering patients with and without asthma. RESULTS: We assessed data from 677 weeks (364 patients), 280 of which were reported by patients with asthma. Regarding presenteeism, the median impact of AR in weeks of poor disease control was 60.7% (P25-P75=24.9-74.2%), while partial and good disease control were respectively associated with an impact of 25.0% (P25-P75=12.1-42.4%) and 4.4% (P25-75=0.8-12.9%). In poorly-controlled weeks, presenteeism was associated with indirect costs ranging from 65.7 US Dollars purchase power parity (US$ PPPs) (P25-P75=29.2-143.2) in Brazil to 693.6 US$ PPP (P25-P75=405.2-1094.9) in Iceland. Median absenteeism per week was of 0% for all levels of rhinitis control. Patients with AR+asthma showed higher overall work impairment than patients with AR alone, particularly in poorly-controlled weeks (median work impairment in AR alone=39.1% [P25-P75=12.5-71.9%]; median work impairment in AR+asthma=68.4% [P25-P75=54.6-80.2%]). CONCLUSION: Poor AR control was associated with decreased work productivity and increased indirect costs, particularly in patients with AR+asthma. The estimates from this study underpin the economic burden of AR.
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Background: The prevalence of cardiovascular events (CVEs) in patients with asthma varies amongst studies, with little evidence as to their prevalence in patients treated with monoclonal antibodies (mAbs). In this retrospective, observational study, we aimed to evaluate the prevalence of CVEs in patients with T2 and non-T2 asthma and to identify risk factors associated with CVEs. Methods: A total of 206 patients with severe asthma were included. Demographic variables, respiratory comorbidities and cardiovascular risk factors were collected, along with respiratory function, laboratory parameters and respiratory pharmacotherapy, including treatment with mAbs. Results: A total of 10.7% of the patients had any CVE from the date of asthma diagnosis, with a higher risk in those patients with chronic obstructive pulmonary disease (odds ratio [OR] = 5.36, 95% CI 1.76-16.31; p = 0.003), arterial hypertension (OR = 2.71, 95% CI 1.13-6.55; p = 0.026) and dyslipidaemia (OR = 9.34, 95% CI 3.57-24.44; p < 0.001). No association between mAb treatment and a CVE or between time of mAb treatment and the event was found. No significant differences were observed between the T2 and non-T2 cohort. After a multivariate analysis, dyslipidaemia was identified as an independent risk factor (OR = 13.33, 95% CI 4.49-39.58; p < 0.001), whereas regular use of inhaled corticosteroids was associated with a reduced risk of a CVE (OR = 0.103, 95% CI 0.021-0.499; p = 0.005). Further research is needed to fully understand the relationship between severe asthma and CVEs. Conclusions: This study suggests that patients with severe asthma experience a higher percentage of CVEs compared with the general population.
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Derived from the myeloid lineage, granulocytes, including basophils, eosinophils, and neutrophils, along with mast cells, play important, often disparate, roles across the allergic disease spectrum. While these cells and their mediators are commonly associated with allergic inflammation, they also exhibit several functions either promoting or restricting tumor growth. In this Position Paper we discuss common granulocyte and mast cell features relating to immunomodulatory functions in allergy and in cancer. We highlight key mechanisms which may inform cancer treatment and propose pertinent areas for future research. We suggest areas where understanding the communication between granulocytes, mast cells, and the tumor microenvironment, will be crucial for identifying immune mechanisms that may be harnessed to counteract tumor development. For example, a comprehensive understanding of allergic and immune factors driving distinct neutrophil states and those mechanisms that link mast cells with immunotherapy resistance, might enable targeted manipulation of specific subpopulations, leading to precision immunotherapy in cancer. We recommend specific areas of investigation in AllergoOncology and knowledge exchange across disease contexts to uncover pertinent reciprocal functions in allergy and cancer and allow therapeutic manipulation of these powerful cell populations. These will help address the unmet needs in stratifying and managing patients with allergic diseases and cancer.
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To inform the clinical practice guidelines' recommendations developed by the European Academy of Allergy and Clinical Immunology systematic reviews (SR) assessed using GRADE on the impact of environmental tobacco smoke (ETS) and active smoking on the risk of new-onset asthma/recurrent wheezing (RW)/low lung function (LF), and on asthma-related outcomes. Only longitudinal studies were included, almost all on combustion cigarettes, only one assessing e-cigarettes and LF. According to the first SR (67 studies), prenatal ETS increases the risk of RW (moderate certainty evidence) and may increase the risk of new-onset asthma and of low LF (low certainty evidence). Postnatal ETS increases the risk of new-onset asthma and of RW (moderate certainty evidence) and may impact LF (low certainty evidence). Combined in utero and postnatal ETS may increase the risk of new-onset asthma (low certainty evidence) and increases the risk of RW (moderate certainty evidence). According to the second SR (24 studies), ETS increases the risk of severe asthma exacerbations and impairs asthma control and LF (moderate certainty evidence). According to the third SR (25 studies), active smoking increases the risk of severe asthma exacerbations and of suboptimal asthma control (moderate certainty evidence) and may impact asthma-related quality-of-life and LF (low certainty evidence).
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Organic dusts are complex bioaerosol mixtures comprised of dust and par ticulate matter of organic origin. These include components from bacteria, fungi, pollen, and viruses to fragments of animals and plants commonplace to several environmental/occupational settings encompassing agriculture/farming, grain processing, waste/recycling, textile, cotton, woodworking, bird breeding, and more. Organic dust exposures are linked to development of chronic bronchitis, chronic obstructive pulmonary disease, asthma, asthma-like syndrome, byssinosis, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis. Risk factors of disease development include cumulative dust exposure, smoking, atopy, timing/duration, and nutritional factors. The immunopathogenesis predominantly involves Toll-like receptor signaling cascade, T-helper 1/T-helper 17 lymphocyte responses, neutrophil influx, and potentiation of manifestations associated with allergy. The true prevalence of airway disease directly attributed to organic dust, especially in a workplace setting, remains challenging. Diagnostic confirmation can be difficult and complicated by hesitancy from workers to seek medical care, driven by fears of potential labor-related consequence. Clinical respiratory and systemic presentations coupled with allergy testing, lung function patterns of obstructive versus restrictive disease, and radiological characteristics are typically utilized to delineate these various organic dust-associated respiratory diseases. Prevention, risk reduction, and management primarily focus on reducing exposure to the offending dust, managing symptoms, and preventing disease progression.
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Polvo , Exposición Profesional , Humanos , Exposición Profesional/efectos adversos , Enfermedades Respiratorias/epidemiología , Animales , Factores de Riesgo , Alérgenos/inmunologíaRESUMEN
Systematic review using GRADE of the impact of exposure to volatile organic compounds (VOCs), cleaning agents, mould/damp, pesticides on the risk of (i) new-onset asthma (incidence) and (ii) adverse asthma-related outcomes (impact). MEDLINE, EMBASE and Web of Science were searched for indoor pollutant exposure studies reporting on new-onset asthma and critical and important asthma-related outcomes. Ninety four studies were included: 11 for VOCs (7 for incidenceand 4 for impact), 25 for cleaning agents (7 for incidenceand 8 for impact), 48 for damp/mould (26 for incidence and 22 for impact) and 10 for pesticides (8 for incidence and 2 for impact). Exposure to damp/mould increases the risk of new-onset wheeze (moderate certainty evidence). Exposure to cleaning agents may be associated with a higher risk of new-onset asthma and with asthma severity (low level of certainty). Exposure to pesticides and VOCs may increase the risk of new-onset asthma (very low certainty evidence). The impact on asthma-related outcomes of all major indoor pollutants is uncertain. As the level of certainty is low or very low for most of the available evidence on the impact of indoor pollutants on asthma-related outcomes more rigorous research in the field is warranted.
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Contaminación del Aire Interior , Asma , Compuestos Orgánicos Volátiles , Humanos , Asma/etiología , Asma/epidemiología , Contaminación del Aire Interior/efectos adversos , Compuestos Orgánicos Volátiles/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Hipersensibilidad/etiología , Hipersensibilidad/epidemiología , Incidencia , Plaguicidas/efectos adversosRESUMEN
Epidemiological studies have explored the relationship between allergic diseases and cancer risk or prognosis in AllergoOncology. Some studies suggest an inverse association, but uncertainties remain, including in IgE-mediated diseases and glioma. Allergic disease stems from a Th2-biased immune response to allergens in predisposed atopic individuals. Allergic disorders vary in phenotype, genotype and endotype, affecting their pathophysiology. Beyond clinical manifestation and commonly used clinical markers, there is ongoing research to identify novel biomarkers for allergy diagnosis, monitoring, severity assessment and treatment. Gliomas, the most common and diverse brain tumours, have in parallel undergone changes in classification over time, with specific molecular biomarkers defining glioma subtypes. Gliomas exhibit a complex tumour-immune interphase and distinct immune microenvironment features. Immunotherapy and targeted therapy hold promise for primary brain tumour treatment, but require more specific and effective approaches. Animal studies indicate allergic airway inflammation may delay glioma progression. This collaborative European Academy of Allergy and Clinical Immunology (EAACI) and European Association of Neuro-Oncology (EANO) Position Paper summarizes recent advances and emerging biomarkers for refined allergy and adult-type diffuse glioma classification to inform future epidemiological and clinical studies. Future research is needed to enhance our understanding of immune-glioma interactions to ultimately improve patient prognosis and survival.
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Biomarcadores , Glioma , Hipersensibilidad , Humanos , Glioma/inmunología , Glioma/etiología , Glioma/diagnóstico , Hipersensibilidad/diagnóstico , Hipersensibilidad/inmunología , Hipersensibilidad/etiología , Neoplasias Encefálicas/inmunología , Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/etiología , Susceptibilidad a Enfermedades , AnimalesRESUMEN
BACKGROUND: Drug hypersensitivity reactions (DHRs) to platinum-based drugs are heterogenous and restrict their access, and drug desensitization (DD) has provided a ground-breaking procedure for their re-introduction, although the response is heterogeneous. We aimed to identify the phenotypes, endotypes, and biomarkers of reactions to carboplatin and oxaliplatin and their response to DD. METHODS: Seventy-nine patients presenting with DHRs to oxaliplatin (N = 46) and carboplatin (N = 33) were evaluated at the Allergy Departments of two tertiary care hospitals in Spain. Patient symptoms, skin testing, biomarkers, and outcomes of 267 DDs were retrospectively analyzed. RESULTS: Oxaliplatin-reactive patients presented with type I (74%), cytokine release reaction (CRR) (11%), and mixed (Mx) (15%) phenotypes. In contrast, carboplatin reactive patients presented with predominantly type I (85%) and Mx (15%) but no CRRs. Out of 267 DDs, breakthrough reactions (BTRs) to oxaliplatin occurred twice as frequently as carboplatin (32% vs. 15%; p < .05). Phenotype switching from type I to another phenotype was observed in 46% of oxaliplatin DDs compared to 21% of carboplatin DDs. Tryptase was elevated in type I and Mx reactions, and IL-6 in CRR and Mx, indicating different mechanisms and endotypes. CONCLUSION: Carboplatin and oxaliplatin induced three different types of reactions with defined phenotypes and endotypes amendable to DD. Although most of the initial reactions for both were type I, oxaliplatin presented with unique CRR reactions. During DD, carboplatin reactive patients presented mostly type I BTR, while oxaliplatin-reactive patients frequently switched from type I to CRR, providing a critical difference and the need for personalized DD protocols.
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Antineoplásicos , Hipersensibilidad a las Drogas , Hipersensibilidad , Humanos , Oxaliplatino/efectos adversos , Carboplatino/efectos adversos , Estudios Retrospectivos , Antineoplásicos/efectos adversos , Hipersensibilidad a las Drogas/diagnóstico , Hipersensibilidad a las Drogas/etiología , Hipersensibilidad a las Drogas/terapia , Desensibilización Inmunológica/métodos , Citocinas , Fenotipo , BiomarcadoresAsunto(s)
Hipersensibilidad , Tutoría , Humanos , Mentores , Aniversarios y Eventos Especiales , Hipersensibilidad/terapiaRESUMEN
Drug hypersensitivity reactions are a serious concern in clinical practice because they can be severe and result in lifelong sequelae. An accurate diagnosis and identification of the culprit drug is essential to prevent future reactions as well as for the identification of safe treatment alternatives. Nonetheless, the diagnosis can be challenging. In vivo and in vitro tests can be helpful, although none are conclusive; therefore, the tests are not usually performed in isolation but as part of a diagnostic algorithm. In addition, some in vitro tests are only available in research laboratories, and standardization has not been fully accomplished. Collaborating research is needed to improve drug hypersensitivity reaction diagnosis. In this review, we update the current available in vivo and in vitro tools with their pros and cons and propose an algorithm to integrate them into clinical practice.
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Hipersensibilidad a las Drogas , Hipersensibilidad , Humanos , Algoritmos , Causalidad , Progresión de la Enfermedad , Hipersensibilidad a las Drogas/diagnóstico , Hipersensibilidad a las Drogas/etiología , Hipersensibilidad/diagnóstico , Hipersensibilidad/etiologíaRESUMEN
Since the discovery of immunoglobulin E (IgE) as a mediator of allergic diseases in 1967, our knowledge about the immunological mechanisms of IgE-mediated allergies has remarkably increased. In addition to understanding the immune response and clinical symptoms, allergy diagnosis and management depend strongly on the precise identification of the elicitors of the IgE-mediated allergic reaction. In the past four decades, innovations in bioscience and technology have facilitated the identification and production of well-defined, highly pure molecules for component-resolved diagnosis (CRD), allowing a personalized diagnosis and management of the allergic disease for individual patients. The first edition of the "EAACI Molecular Allergology User's Guide" (MAUG) in 2016 rapidly became a key reference for clinicians, scientists, and interested readers with a background in allergology, immunology, biology, and medicine. Nevertheless, the field of molecular allergology is moving fast, and after 6 years, a new EAACI Taskforce was established to provide an updated document. The Molecular Allergology User's Guide 2.0 summarizes state-of-the-art information on allergen molecules, their clinical relevance, and their application in diagnostic algorithms for clinical practice. It is designed for both, clinicians and scientists, guiding health care professionals through the overwhelming list of different allergen molecules available for testing. Further, it provides diagnostic algorithms on the clinical relevance of allergenic molecules and gives an overview of their biology, the basic mechanisms of test formats, and the application of tests to measure allergen exposure.
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Hipersensibilidad , Humanos , Hipersensibilidad/diagnóstico , Hipersensibilidad/terapia , Alérgenos , Inmunoglobulina ERESUMEN
Multistep mast cell desensitization blocks the release of mediators following IgE crosslinking with increasing doses of Ag. Although its in vivo application has led to the safe reintroduction of drugs and foods in IgE-sensitized patients at risk for anaphylaxis, the mechanisms of the inhibitory process have remained elusive. We sought to investigate the kinetics, membrane, and cytoskeletal changes and to identify molecular targets. IgE-sensitized wild-type murine (WT) and FcεRIα humanized (h) bone marrow mast cells were activated and desensitized with DNP, nitrophenyl, dust mites, and peanut Ags. The movements of membrane receptors, FcεRI/IgE/Ag, actin, and tubulin and the phosphorylation of Syk, Lyn, P38-MAPK, and SHIP-1 were assessed. Silencing SHIP-1 protein was used to dissect the SHIP-1 role. Multistep IgE desensitization of WT and transgenic human bone marrow mast cells blocked the release of ß-hexosaminidase in an Ag-specific fashion and prevented actin and tubulin movements. Desensitization was regulated by the initial Ag dose, number of doses, and time between doses. FcεRI, IgE, Ags, and surface receptors were not internalized during desensitization. Phosphorylation of Syk, Lyn, p38 MAPK, and SHIP-1 increased in a dose-response manner during activation; in contrast, only SHIP-1 phosphorylation increased in early desensitization. SHIP-1 phosphatase function had no impact on desensitization, but silencing SHIP-1 increased ß-hexoxaminidase release, preventing desensitization. Multistep IgE mast cell desensitization is a dose- and time-regulated process that blocks ß-hexosaminidase, impacting membrane and cytoskeletal movements. Signal transduction is uncoupled, favoring early phosphorylation of SHIP-1. Silencing SHIP-1 impairs desensitization without implicating its phosphatase function.
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Actinas , Mastocitos , Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatasas , Animales , Humanos , Ratones , Inmunoglobulina E , Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatasas/genética , Monoéster Fosfórico Hidrolasas , Receptores de IgE , Tubulina (Proteína)RESUMEN
The current monkeypox disease (MPX) outbreak constitutes a new threat and challenge for our society. With more than 55,000 confirmed cases in 103 countries, World Health Organization declared the ongoing MPX outbreak a Public Health Emergency of International Concern (PHEIC) on July 23, 2022. The current MPX outbreak is the largest, most widespread, and most serious since the diagnosis of the first case of MPX in 1970 in the Democratic Republic of the Congo (DRC), a country where MPX is an endemic disease. Throughout history, there have only been sporadic and self-limiting outbreaks of MPX outside Africa, with a total of 58 cases described from 2003 to 2021. This figure contrasts with the current outbreak of 2022, in which more than 55,000 cases have been confirmed in just 4 months. MPX is, in most cases, self-limiting; however, severe clinical manifestations and complications have been reported. Complications are usually related to the extent of virus exposure and patient health status, generally affecting children, pregnant women, and immunocompromised patients. The expansive nature of the current outbreak leaves many questions that the scientific community should investigate and answer in order to understand this phenomenon better and prevent new threats in the future. In this review, 50 questions regarding monkeypox virus (MPXV) and the current MPX outbreak were answered in order to provide the most updated scientific information and to explore the potential causes and consequences of this new health threat.
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Monkeypox virus , Mpox , Niño , Femenino , Humanos , Embarazo , Brotes de Enfermedades , Mpox/diagnóstico , Mpox/epidemiologíaRESUMEN
This review article provides an overview of short-acting beta-agonist (SABA) use and prescribing trends in Europe, summarizing updated data on the results from the industry-funded SABINA program (SABA use IN asthma) and other studies on this matter. SABA use continues to increase worldwide. Overuse has been defined as ≥3 canisters/year. Almost a third of European patients with asthma, at all severity levels, overuse SABA. Guidelines recommend close monitoring of patients who overuse SABA and avoiding over-reliance on SABA monotherapy. SABA overuse is associated with increased risk of asthma exacerbations and mortality, increased use of health services and negative physical and mental health outcomes. Reliance on SABA monotherapy can be unsafe and therefore it is necessary to change asthma treatment approaches and policies. Changes in physician and patient behaviours towards SABA use are required to ensure that patients with asthma are not over-reliant on SABA monotherapy. Notwithstanding, the limitations of the studies on the use of SABA should be considered, taking into account that the prescription/purchase of medication canisters does not always represent the actual use of the medication and that associations between SABA overuse and poor asthma outcomes may not be directly causal. National health systems and asthma guidelines must align asthma management with global recommendations and adjust them to local needs.
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Antiasmáticos , Asma , Humanos , Asma/tratamiento farmacológico , Asma/epidemiología , Asma/inducido químicamente , Europa (Continente)/epidemiología , Administración por Inhalación , Antiasmáticos/efectos adversosRESUMEN
INTRODUCTION: Hypersensitivity reactions (HSRs) have been observed with the use of biologics in children. The management of HSRs in children is mainly based on experiences from the adult population. Recently, data from different centers experienced in managing these reactions, including desensitization in children, have been published, allowing clinicians to have an appropriate global overview and compare results. AREAS COVERED: This review highlights the published data on hypersensitivity reactions to biologics in children and drug desensitization protocols adapted to the pediatric population. EXPERT OPINION: With regard to HSRs to biologics in children, few data are available. Compared with the adult population, there is a lack of knowledge in the endophenotypes, management and the standardization of protocols including premedication regimens in children. An international consensus is needed to provide clinicians with new insight on how to apply personalized management and to perform tailored desensitization protocols in pediatric populations. Various specialists including allergists, pediatricians, oncologists, hematologists, rheumatologists, and pharmacists, should build a multidisciplinary management team to keep pediatric patients on their best treatment options in the safest manner.
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Productos Biológicos , Hipersensibilidad a las Drogas , Hipersensibilidad , Adulto , Humanos , Niño , Hipersensibilidad a las Drogas/diagnóstico , Hipersensibilidad a las Drogas/etiología , Hipersensibilidad a las Drogas/terapia , Productos Biológicos/efectos adversos , Hipersensibilidad/etiología , Desensibilización Inmunológica/efectos adversos , Desensibilización Inmunológica/métodosRESUMEN
The immune system interacts with many nominal 'danger' signals, endogenous danger-associated (DAMP), exogenous pathogen (PAMP) and allergen (AAMP)-associated molecular patterns. The immune context under which these are received can promote or prevent immune activating or inflammatory mechanisms and may orchestrate diverse immune responses in allergy and cancer. Each can act either by favouring a respective pathology or by supporting the immune response to confer protective effects, depending on acuity or chronicity. In this Position Paper under the collective term danger signals or DAMPs, PAMPs and AAMPs, we consider their diverse roles in allergy and cancer and the connection between these in AllergoOncology. We focus on their interactions with different immune cells of the innate and adaptive immune system and how these promote immune responses with juxtaposing clinical outcomes in allergy and cancer. While danger signals present potential targets to overcome inflammatory responses in allergy, these may be reconsidered in relation to a history of allergy, chronic inflammation and autoimmunity linked to the risk of developing cancer, and with regard to clinical responses to anti-cancer immune and targeted therapies. Cross-disciplinary insights in AllergoOncology derived from dissecting clinical phenotypes of common danger signal pathways may improve allergy and cancer clinical outcomes.
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Hipersensibilidad , Neoplasias , Humanos , Hipersensibilidad/diagnóstico , Hipersensibilidad/etiología , Hipersensibilidad/terapia , Inmunidad , Inflamación , Neoplasias/etiología , Neoplasias/terapia , Transducción de SeñalRESUMEN
INTRODUCTION: Nivolumab is a fully human IgG4 monoclonal antibody (moAb) against programmed cell death protein 1, approved for the treatment of over ten types of cancer. The use of this and other moAbs has augmented considerably in recent years and this in turn has caused an increase of hypersensitivity reactions (HSR). CASE REPORT: We present the case of a patient with metastatic renal cell cancer (RCC) who developed a grade 3 cytokine release reaction (CRR) to nivolumab. The maintenance of the symptoms despite of the administration of symptomatic treatment and slowing down the infusion rate of nivolumab during the 1st and 2nd reaction required an allergy evaluation of our patient. MANAGEMENT AND OUTCOME: Skin testing to Nivolumab with negative results and baseline tryptase within the normal range were observed during the allergy workout. A desensitization protocol with specific premedication was applied to reintroduce the moAb, with no further issues. Moreover, a follow up of the patient in the oncology setting was done showing disease stabilization. DISCUSSION: The CRR should be treated by desensitization, in contrast to infusion reactions. The diagnosis of CRR phenotype is based on the clinical presentation and recently, and elevation of IL-6 levels has been shown to be a useful biomarker along with negative skin testing. We can conclude that after a HSR and an appropriate allergy diagnosis of CRR, nivolumab can be safely reintroduced by desensitization without reducing the target dose or the appropriate dilution concentration.
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Hipersensibilidad a las Drogas , Nivolumab , Algoritmos , Anticuerpos Monoclonales/efectos adversos , Citocinas , Hipersensibilidad a las Drogas/diagnóstico , Hipersensibilidad a las Drogas/etiología , Hipersensibilidad a las Drogas/terapia , Humanos , Nivolumab/efectos adversos , Pruebas Cutáneas/efectos adversosRESUMEN
Allergies to grass pollen affects about 20% of the population worldwide. In the last few decades, the South American grass Cortaderia selloana (CS, Pampas grass) has expanded worldwide in a variety of countries including the USA, Australia and Western Europe. In many of these locations, CS has strikingly spread and has now been classified an invasive species. Many pernicious consequences of CS have been reported for local biodiversity, landscape and structures. However, the effect on human health has not been studied. To investigate this issue, we have chosen a European region on the northern cost of Spain where CS spread is overwhelming, Cantabria. We obtained CS pollen extract and analysed the allergenic reaction of 98 patients that were allergic to pollen of local grasses. We determined the skin reaction and the presence of specific IgE antibodies (sIgE) to CS or to a typical autochthonous grass, Phleum pratense. We also compared the seasonal symptoms with reported grass pollen counts in the area. The results strongly suggest that CS can cause respiratory allergies at a similar extent to the local grasses. Given that CS pollinises later than the local grasses, this would extend the period of grass allergies in the region for about three months every year, as stated by most of the patients. This is the first study reported on the effects of the striking expansion of CS on human health. Considering the strong impact that respiratory allergies have on the population, our results suggest that CS can currently constitute a relevant environmental health issue.