ABSTRACT
La alergia al látex es una respuesta alterada de nuestro organismo al contactar con las proteínas que se encuentran en el látex de caucho natural. Los síntomas de la hipersensibilidad alérgica al látex son bastante parecidos a los de la alergia a los alimentos, siendo menos frecuentes los síntomas digestivos y más típicos los cutáneos tras el uso de guantes de látex, y los nasales y/o el asma tras la inhalación del polvo de los guantes de látex o de los globos. En caso de pacientes muy sensibles puede provocar reacciones alérgicas graves si entra en contacto con mucosas o cavidades internas. Se da la paradoja de que el medio hospitalario, es el lugar de más riesgo dada la cantidad existente de látex, tanto directo como indirecto. Las personas alérgicas al látex presentan a menudo reacciones alérgicas cruzadas, a veces graves, tras ingerir determinadas frutas y vegetales. Las reacciones cruzadas se deben a los alérgenos comunes presentes en el látex y en los diferentes alimentos. Es importante utilizar el análisis molecular de alérgenos para detectar falsos diagnósticos a látex por problemas de reactividad cruzada con proteínas de frutas. Indicamos cómo estas nuevas pruebas han sustituido a análisis menos precisos y eficientes, logrando un considerable ahorro de recursos
Latex allergy is an altered response of the body on contact with proteins found in natural rubber latex. The symptoms of allergic hypersensitivity to latex are quite similar to those of food allergy, with the gastrointestinal symptoms being less frequent and the cutaneous ones being more typical after the use of latex and nasal gloves and / or the asthma after the inhalation of the dust from latex gloves or balloons. In the case of very sensitive patients it can cause severe allergic reactions if it comes in contact with mucous membranes or internal cavities. There is a paradox that the hospital environment is the most risky place, given the existing amount of latex in direct and indirect use. People who are allergic to latex often have cross-allergic reactions, sometimes severe, after eating certain fruits and vegetables. The cross-reactions are due to the common allergens present in latex and in different foods. It is important to use molecular allergen analysis to detect false latex diagnoses due to problems of cross-reactivity with fruit proteins. It is indicated how these new tests have replaced less accurate and efficient analyses, achieving a considerable saving of resources
Subject(s)
Humans , Latex Hypersensitivity/diagnosis , Molecular Diagnostic Techniques/methods , Genetic Testing/methods , Cross Reactions/immunology , Food Hypersensitivity/diagnosis , Allergens/immunology , Hypersensitivity, Immediate/immunologyABSTRACT
BACKGROUND: Quantification of the risk of an allergic drug reaction through the medical history is essential in clinical decision making. However, in normal clinical practice, this evaluation is generally entirely subjective. OBJECTIVE: The objective of this study was to construct a mathematical model to predict the risk of allergic drug reactions using the data collected in the medical history. METHODS: A total of 696 active principles, corresponding to 466 patients aged more than 14 years attending the Allergy Service of the University Hospital of Salamanca, were included. Simple binary logistic regression was used to determine associations between variables from the medical history and the final diagnosis, to construct a predictive model. RESULTS: Variables useful in predicting a final diagnosis of allergic drug reaction were age, sex, drug class, number of active principles, time to the reaction, number of doses, clinical presentation suggestive of allergic disease, and time to medical consultation. True adverse drug reactions were estimated to occur in 20% of active principles. However, possible allergic reactions could only be ruled out in 52.2%. CONCLUSIONS: The use of mathematical models could greatly improve the discriminatory capacity of the medical history. Both the overdiagnosis and underdiagnosis of allergic drug reactions should be considered a public health problem.
Subject(s)
Drug Hypersensitivity/diagnosis , Models, Theoretical , Adult , Allergens/immunology , Analgesics/immunology , Drug Hypersensitivity/epidemiology , Female , Humans , Male , Medical History Taking , Middle Aged , Penicillins/immunology , Prognosis , Risk , Spain/epidemiologyABSTRACT
No disponible
Subject(s)
Humans , Enzyme Activation/immunology , Clinical Laboratory Services/organization & administration , Clinical Laboratory Services/standards , Clinical Laboratory Services , Clinical Laboratory Techniques/methods , Clinical Laboratory Techniques/standards , Clinical Laboratory Techniques , Hypersensitivity/diagnosis , Clinical Laboratory Techniques/instrumentation , Clinical Laboratory Techniques/trends , Food Hypersensitivity/diagnosis , Food Hypersensitivity/immunologyABSTRACT
No disponible
Subject(s)
Humans , Female , Middle Aged , Food Hypersensitivity/immunology , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Anaphylaxis/immunology , Fruit/adverse effects , Risk FactorsABSTRACT
OBJECTIVE: To estimate the attributable and targeted avoidable deaths (ADs; TADs) of outdoor air pollution by ambient particulate matter (PM10), PM2.5 and O3 according to specific WHO methodology. DESIGN: Health impact assessment. SETTING: City of Valladolid, Spain (around 300â 000 residents). DATA SOURCES: Demographics; mortality; pollutant concentrations collected 1999-2008. MAIN OUTCOME MEASURES: Attributable fractions; ADs and TADs per year for 1999-2008. RESULTS: Higher TADs estimates (shown here) were obtained when assuming as 'target' concentrations WHO Air Quality Guidelines instead of Directive 2008/50/EC. ADs are considered relative to pollutant background levels. All-cause mortality associated to PM10 (all ages): 52 ADs (95% CI 39 to 64); 31 TADs (95% CI 24 to 39).All-cause mortality associated to PM10 (<5â years): 0 ADs (95% CI 0 to 1); 0 TADs (95% CI 0 to 1). All-cause mortality associated to PM2.5 (>30â years): 326 ADs (95% CI 217 to 422); 231 TADs (95% CI 153 to 301). Cardiopulmonary and lung cancer mortality associated to PM2.5 (>30â years): Cardiopulmonary: 186 ADs (95% CI 74 to 280); 94 TADs (95% CI 36 to 148). Lung cancer : 51 ADs (95% CI 21 to 73); 27 TADs (95% CI 10 to 41).All-cause, respiratory and cardiovascular mortality associated to O3 (all ages): All-cause: 52ADs (95% CI 25 to 77) ; 31 TADs (95% CI 15 to 45). Respiratory: 5ADs (95% CI -2 to 13) ; 3 TADs (95% CI -1 to 8). Cardiovascular: 30 ADs (95% CI 8 to 51) ; 17 TADs (95% CI 5 to 30). Negative estimates which should be read as zero were obtained when pollutant concentrations were below counterfactuals or assumed risk coefficients were below one. CONCLUSIONS: Our estimates suggest a not negligible negative impact on mortality of outdoor air pollution. The implementation of WHO methodology provides critical information to distinguish an improvement range in air pollution control.
