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101.
Teodorikez-Wilfox Jimenez-Rodriguez María Pilar Berges-Gimeno Ruth Barranco Joan Bartra María del Carmen Diéguez Inmaculada Doña Montserrat Fernández-Rivas Maria Del Mar Gandolfo-Cano Gabriel Gastaminza-Lasarte Eloína González-Mancebo Belén de la Hoz Caballer Leticia Sánchez-Morillas María José Torres Arantza Vega Rosa Muñoz-Cano 《Allergy》2021,76(7):2249-2253
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Isabel J. Skypala Joan Bartra Didier G. Ebo Margaretha Antje Faber Montserrat Fernández-Rivas Francisca Gomez Olga Luengo Stephen J. Till Riccardo Asero Domingo Barber Lorenzo Cecchi Araceli Diaz Perales Karin Hoffmann-Sommergruber Elide Anna Pastorello Ines Swoboda Anastasios. P. Konstantinopoulos Ronald van Ree Enrico Scala European Academy of Allergy & Clinical Immunology Task Force: Non-specific Lipid Transfer Protein Allergy Across Europe 《Allergy》2021,76(8):2433-2446
Sensitization to one or more non-specific lipid transfer proteins (nsLTPs), initially thought to exist mainly in southern Europe, is becoming accepted as a cause of allergic reactions to plant foods across Europe and beyond. The peach nsLTP allergen Pru p 3 is a dominant sensitizing allergen and peaches a common food trigger, although multiple foods can be involved. A frequent feature of reactions is the requirement for a cofactor (exercise, alcohol, non-steroidal anti-inflammatory drugs, Cannabis sativa) to be present for a food to elicit a reaction. The variability in the food and cofactor triggers makes it essential to include an allergy-focused diet and clinical history in the diagnostic workup. Testing on suspected food triggers should also establish whether sensitization to nsLTP is present, using purified or recombinant nsLTP allergens such as Pru p 3. The avoidance of known trigger foods and advice on cofactors is currently the main management for this condition. Studies on immunotherapy are promising, but it is unknown whether such treatments will be useful in populations where Pru p 3 is not the primary sensitizing allergen. Future research should focus on the mechanisms of cofactors, improving diagnostic accuracy and establishing the efficacy of immunotherapy. 相似文献
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Alzheimer’s disease (AD) is a neurodegenerative process that inexorably leads to progressive deterioration of cognition function and, ultimately, death. Central pathophysiologic features of AD include the accumulation of extracellular plaques comprised of amyloid-β peptide (Aβ) and the presence of intraneuronal neurofibrillary tangles. However, a large body of evidence suggests that oxidative stress and inflammation are major contributors to the pathogenesis and progression of AD. To date, available pharmacologic treatments are only symptomatic. Clinical trials focused on amyloid and non-amyloid-targeted treatments with small molecule pharmacotherapy and immunotherapies have accumulated a long list of failures. Considering that around 90 % of the circulating Aβ is bound to albumin, and that a dynamic equilibrium exists between peripheral and central Aβ, plasma exchange with albumin replacement has emerged as a new approach in a multitargeted AD therapeutic strategy (AMBAR Program). In plasma exchange, a patient’s plasma is removed by plasmapheresis to eliminate toxic endogenous substances, including Aβ and functionally impaired albumin. The fluid replacement used is therapeutic albumin, which acts not only as a plasma volume expander but also has numerous pleiotropic functions (e.g., circulating Aβ- binding capacity, transporter, detoxifier, antioxidant) that are clinically relevant for the treatment of AD. Positive results from the AMBAR Program (phase 1, 2, an 2b/3 trials), i.e., slower decline or stabilization of disease symptoms in the most relevant clinical efficacy and safety endpoints, offer a glimmer of hope to both AD patients and caregivers. 相似文献
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