L. Perfetti
University of Pisa
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Publication
Featured researches published by L. Perfetti.
Allergy | 2009
Gianna Moscato; Gianni Pala; L. Perfetti; M. Frascaroli; P. Pignatti
To cite this article: Moscato G, Pala G, Perfetti L, Frascaroli M, Pignatti P. Clinical and inflammatory features of occupational asthma caused by persulphate salts in comparison with asthma associated with occupational rhinitis. Allergy 2010; 65: 784–790.
Allergy | 2000
Gianna Moscato; L. Perfetti; Eugenia Galdi; V. Pozzi; C. Minoia
Background:u2002HDM distribution varies between geographic areas and may be affected by housing characteristics. We quantified Der p 1 and Der f 1 and assessed the relationships between their levels and housing characteristics in homes of nonallergic subjects.
Allergy | 2002
P. Pignatti; L. Perfetti; Eugenia Galdi; V. Pozzi; A. Bossi; C. Biale; Gianna Moscato
Background:u2002CD69 is a molecule expressed on human eosinophils after cytokine‐activation. Different studies have described the eosinophil activation, evaluated by CD69 expression, at the site of an allergic inflammation. In this study we evaluated the expression of CD69 on peripheral blood eosinophils after a specific inhalation challenge (SIC), in order to better define the state of activation of peripheral blood eosinophils after exposure to sensitizers.
Allergy | 2009
Gianni Pala; P. Pignatti; L. Perfetti; R. Cosentino; Gianna Moscato
role in the development of CSS; (ii) the reduction of corticosteroids, allowed by omalizumab treatment, can unmask CSS, which, beforehand,manifests itself only by asthma, as a forme-fruste of CSS (4). Although the existing evidence seems to indicate that omalizumab can be continued as soon as acute CSS is resolved in order to achieve an optimal control of the asthmatic component (5, 6), we preferred to stop treatment, so as not to expose the patient to a potential risk of further evolution of CSS. In any case, our case suggests to taper corticosteroid with caution and to strictly monitoring patients under omalizumab treatment for signs of CSS, as apparently anti-IgE therapy does not control CSS activity.
Allergy | 2009
Gianni Pala; P. Pignatti; L. Perfetti; M. Caminati; E. Gentile; Gianna Moscato
from 120 before treatment to MFI 22 following omalizumab (data not shown) indicating a decreased IgE load on the basophils. We hypothesize that the favourable clinical response to omalizumab reflects decreased activation of mast cells (similar to the effect in basophils) because of decreased IgE binding to systemic mast cells, which has occurred in this nonatopic individual with an abnormal mast cell population. A BMA performed 7 months after treatment commenced showed persistence of abnormal CD25 and CD2 positive mast cells, consistent with SM, despite the patient’s dramatic clinical improvement. Anaphylaxis associated with SM may have catastrophic consequences. We alert our colleagues to the efficacy of omalizumab for treatment of such patients whether atopic or nonatopic. Jo A Douglass, Robyn O’Hehir and Astrid Voskamp received omalizumab for an investigator initiated study not involving systemic mastocytosis. Jo A Douglass and Robyn O’Hehir participated in contracted research for Novartis. Jo A Douglass received travel sponsorship from Schering-Plough.
Chest | 1999
Gianna Moscato; Antonio Dellabianca; L. Perfetti; Barbara Bramé; Eugenia Galdi; Rosanna Niniano; Pierluigi Paggiaro
American Journal of Respiratory and Critical Care Medicine | 1998
Christophe Leroyer; L. Perfetti; Carole Trudeau; Jocelyne L'Archevêque; Moira Chan-Yeung; J.-L. Malo
Chest | 1998
L. Perfetti; André Cartier; Heberto Ghezzo; Denyse Gautrin; J.-L. Malo
Chest | 1998
L. Perfetti; André Cartier; Heberto Ghezzo; Denyse Gautrin; Jean-Luc Malo
Thorax | 1998
Christophe Leroyer; L. Perfetti; André Cartier; J.-L. Malo