M. Fernández-Nieto
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Featured researches published by M. Fernández-Nieto.
Allergy | 2003
C. Escudero; Santiago Quirce; M. Fernández-Nieto; J. Miguel; Javier Cuesta; J. Sastre
Background: Bakery workers may develop IgE‐mediated allergy to liquid and aerosolized hens egg proteins that are commonly used in the baking and confectionery industries.
Clinical & Experimental Allergy | 2009
A. Palacin; Javier Varela; Santiago Quirce; V. del Pozo; L. Tordesillas; Pilar Barranco; M. Fernández-Nieto; J. Sastre; A. Diaz‐Perales; G. Salcedo
Background Bakers asthma is an important occupational allergic disease. Wheat lipid transfer protein (LTP) Tri a 14 is a major allergen associated with wheat allergy. No panel of wheat recombinant allergens for component‐resolved diagnosis of bakers asthma is currently available.
Allergy | 2006
Santiago Quirce; M. Fernández-Nieto; Carmelo Escudero; Javier Cuesta; M. de las Heras; J. Sastre
Background: Quantitative relationships between immunological reactivity, non‐specific bronchial responsiveness and bronchial responsiveness to allergens have scarcely been investigated in occupational asthma.
Allergy | 2007
B. Sastre; M. Fernández-Nieto; R. Mollá; E. López; Carlos Lahoz; J. Sastre; V. del Pozo; Santiago Quirce
Background: Eosinophilic bronchitis is a common cause of chronic cough, which like asthma is characterized by sputum eosinophilia, but unlike asthma there is no variable airflow obstruction or airway hyperresponsiveness. We tested the hypothesis that the different airway function in patients with eosinophilic bronchitis and asthma could be caused by an imbalance in the production of bronchoconstrictor (LTC4) and bronchoprotective (prostaglandin E2; PGE2) lipid mediators.
Allergy | 2007
Santiago Quirce; M. Fernández-Nieto; V. del Pozo; B. Sastre; J. Sastre
Eugenol (C10H12O2) and its isomer isoeugenol are well-known skin sensitizers giving rise to allergic contact dermatitis (1) and acute urticaria (2). These fragrance chemicals, however, have not been previously described as a causative agent of occupational asthma (OA). We report the case of a 30-year-old hairdresser, a nonsmoker. In the last year he had developed eczema on his hands and he had suffered from nasal stuffiness and rhinorrhea. Over the last 6 months at work he had also developed episodes of chest tightness, dry cough and shortness of breath upon exposure to perfumes and lacquer. His asthma symptoms worsened progressively and he was treated in the emergency room because of severe asthma attacks on three occasions. He showed a marked improvement away from work. When he was examined in our outpatient clinic he had been on a sick leave for 6 months. At that time spiromety was normal. Blood tests and leukocyte differential count (102 eosinophils/mm) were within normal limits. Total serum IgE was 168 kU/l. Patch testing with European standard series showed positive results to cobalt chloride, potassium dichromate, fragrance mix and isoeugenol (+). Skin prick testing was performed with common aeroallergens, latex and eugenol 2% w/v and all yielded negative results. Specific inhalation challenge (SIC) with eugenol was performed by a 2 min nebulization of the corresponding eugenol dilution in a 7 m challenge chamber (3, 4). Sputum was induced by hypertonic saline inhalation and processed as previously described (4). Sputum samples were analyzed using FC scan cytometry (FACSCalibur flow cytometer; Becton Dickinson, San José, CA, USA). At baseline (visit 1), PC20 methacholine was negative (PC20 > 16 mg/ml). On visit 2 (sham exposure) no significant changes in forced expiratory volume in 1 s (FEV1) were observed over the following 24 h. On visit 3, SIC with eugenol at a dilution of 1/10 000 for 2 min elicited no reaction. On visit 4, the eugenol challenge at 1/1000 elicited rhinitis symptoms and an isolated late asthmatic response. An increase in sputum eosinophils and lymphocytes were observed 24 h after eugenol SIC (Table 1), and methacholine inhalation test became positive (PC20 2 mg/ml). A hairdresser diagnosed with OA caused by persulfates (control subject) underwent the same challenge protocol with eugenol and no relevant changes in FEV1 or PC20 methacholine were observed. Proliferation tests of peripheral blood mononuclear cells from the patient and the control subject were performed by MTS assays (Promega Corp., Madison, WI, USA) with different eugenol dilutions in RPMI-1640 completed with 10% FBS. A striking different in the eugenolinduced proliferation was observed in the patient (15 times higher) as compared to the control subject with the eugenol 1/1000 dilution, whereas no significant difference was observed in the eugenolinduced proliferation between the patient and the control subject at the 1/100 and 1/10 000 dilutions. Baur et al. (5) reported a 44-year-old woman, employed for 26 years in a drugstore, who developed asthma symptoms while presenting customers with various perfume brands. Workplace-related specific challenges with nine different brands of perfumes as well as SIC with one individual perfume in this patient resulted in increased nasal airflow resistance and in significant bronchial obstruction (5). Although the major agents involved in OA and rhinitis in A L L E R G Y 2 0 0 8 : 6 3 : 1 3 7 – 1 4 1 • a 2 0 0 8 T H E A U T H O R S • J O U R N A L C O M P I L AT I O N a 2 0 0 8 B L A C K W E L L M U N K S G A A R D • C O N T R I B U T I O N S T O T H I S S E C T I O N W I L L N O T U N D E R G O P E E R R E V I E W, B U T W I L L B E R E V I E W E D B Y T H E A S S O C I AT E E D I T O R S •
Allergy | 2008
Santiago Quirce; M. Fernández-Nieto; C. Pastor; B. Sastre; J. Sastre
ahead will be to investigate IgE-tp levels in other conditions, such as helminth infection, where total IgE levels are far higher than that for allergy and the Th2 immune response is more prominent (6). We thank Professor Ian Hall for providing access to the Nottingham Family samples. We would also like to thank Professor Sherie Morrison (University of California, Los Angeles) and Dr Ke Zhang (University of California, Los Angeles) for their kind gifts of the recombinant human IgE-Tp and antiIgE-Tp specific monoclonal Ab 367, respectively.
Allergy | 2007
A. Vereda; Santiago Quirce; M. Fernández-Nieto; Borja Bartolomé; J. Sastre
Sampson HA. Fish hypersensitivity. I. In vitro and oral challenge results in fishallergic patients. J Allergy Clin Immunol 1992;89:730–737. 4. Bourne HC, Restani P, Moutzouris M, Katelaris CH. An unusual pattern of meat allergy. Allergy 2005;60:706–707. 5. Restani P, Fiocchi A, Beretta B, Velona T, Giovannini M, Galli CL. Meat allergy: III–Proteins involved and cross-reactivity between different animal species. J Am Coll Nutr 1997;16:383–389. 6. Mamikoglu B. Beef, pork, and milk allergy (cross reactivity with each other and pet allergies). Otolaryngol Head Neck Surg 2005;133:534–537.
Allergy | 2006
E. Compes; Borja Bartolomé; M. Fernández-Nieto; J. Sastre; Javier Cuesta
References 1. Saarinen KM, Pelkonen AS, Mäkelä MJ, Savilahti E. Clinical course and prognosis of cow’s milk allergy are dependent on milk-specific IgE status. J Allergy Clin Immunol 2005;116:869–875. 2. Wilson DR, Lima MT, Durham SR. Sublingual immunotherapy for allergic rhinitis: systematic review and metaanalysis. Allergy 2005;60:4–12. 3. Meglio P, Bartone E, Plantamura M, Arabito E, Giampietro PG. A protocol for oral desensitization in children with IgEmediated cow’s milk allergy. Allergy 2004;59:980–987. 4. Patriarca G, Nucera E, Roncallo C, Pollastrini E, Bartolozzi F, De Pasquale T et al. Oral desensitizing treatment in food allergy: clinical and immunological results. Aliment Pharmacol Ther 2003;17: 459–465. 5. Enrique E, Pineda F, Malek T, Bartra J, Basagana M, Tella R et al. Sublingual immunotherapy for hazelnut food allergy: a randomized, double-blind, placebocontrolled study with a standardized hazelnut extract. J Allergy Clin Immunol 2005;116:1073–1079. 6. Mempel M, Rakoski J, Ring J, Ollert M. Severe anaphylaxis to kiwi fruit: immunologic changes related to successful sublingual allergen immunotherapy. J Allergy Clin Immunol 2003;111:1406–1409.
Allergy | 2010
L. Manso; S. Heili; M. Fernández-Nieto; B. Sastre; J. Sastre
1. Stevens DA, Moss RB, Kurup VP, Knutsen AP, Greenberger P, Judson MA, Participants in the Cystic Fibrosis Foundation Consensus Conference et al. Allergic bronchopulmonary aspergillosis in cystic fibrosis – state of the art: Cystic Fibrosis Foundation Consensus Conference. Clin Infect Dis 2003; 37(Suppl. 3): S225–S264. 2. Wark PA, Gibson PG, Wilson AJ. Azoles for allergic bronchopulmonary aspergillosis associated with asthma. Cochrane Database Syst Rev 2004;3:CD001108. 3. van der Ent CK, Hoekstra H, Rijkers GT. Successful treatment of allergic bronchopulmonary aspergillosis with recombinant antiIgE antibody. Thorax 2007;62:276–277. 4. Kanu A, Patel K. Treatment of allergic bronchopulmonary aspergillosis (ABPA) in CF with anti-IgE antibody (omalizumab). Pediatr Pulmonol 2008;43:1249–1251. 5. Zirbes JM, Milla CE. Steroid-sparing effect of omalizumab for allergic bronchopulmonary aspergillosis and cystic fibrosis. Pediatr Pulmonol 2008;43:607–610. 6. Hilliard T, Edwards S, Buchdahl R et al. Voriconazole therapy in children with cystic fibrosis. J Cyst Fibros. 2005;4:215–220; Epub. 20 Oct 2005.
Allergy | 2005
Santiago Quirce; M. Fernández-Nieto; A. Jiménez; J. Sastre
Cauliflower (Brassica oleracea var. Botrytis) is a popular foodstuff. It belongs to the family Cruciferae that includes other plants such as cabbage, mustard, broccoli, and rape. Allergic reactions to vegetables occur usually after ingestion or skin contact, and less commonly through the inhalative route. Asthma as a result of inhalation of aerosols from vegetables, such as potato (1), carrot (2) and green bean (3) has been reported. We report on a 41-year-old woman, a nonsmoker, with a past history of allergic rhinoconjunctivitis because of pollen. Her job consisted in supervising the restaurant kitchen of a hotel where she had been employed for 10 years. Since 1998, she had suffered recurrent episodes of ocular and nasal itching, sneezing, watery nose, tearing, dry cough, chest tightness, and dyspnea within a few minutes after inhaling cauliflower and cabbage cooking vapors in the hotel kitchen. In 1999, 6 h after eating cabbage she suffered an acute episode of generalized urticaria, facial and oropharyngeal angioedema that was treated in the emergency room. She had not had problems upon eating these vegetables before. She was able to eat spinaches, Swiss chard, mustard, and lettuce as well as other vegetables without any ill effects. The patient had positive skin prick tests to tree (olive, sycamore, and cypress) and grass pollen. Skin testing with the prick-by-prick method elicited positive responses to raw (4 mm) and stewed cauliflower (3 mm), cabbage (4 mm) and radish (4 mm). The results were negative to turnip, Brussels sprouts, mustard, cress, and broccoli. Total immunoglobulin E (IgE) was 65.4 IU/ml. Determinations of specific IgE (Pharmacia CAP system, Uppsala, Sweden) were positive to cabbage (0.77 kU/l), Brussels sprouts (0.74 kU/l), broccoli (0.63 kU/l), cauliflower (0.40 kU/l), and oilseed rape (0.46 kU/l), and was negative to mustard (<0.35 kU/ l). Spirometry was normal. Methacholine inhalation test showed no airway hyperresponsiveness (PC20 > 16 mg/ml). A specific inhalation challenge test was carried out with cauliflower vapors in a 7 m challenge chamber. The patient was exposed to the vapors coming from the boiling of 324 g of cauliflower in a glass containing 200 ml of distilled water. The concentration of aerosolized particles was measured with an aerosol monitor (DustTrack model 8520, TSI, St Paul, MN, USA). The time of exposure to cauliflower vapor was steadily increased (1, 3, 5 and 10 min). Forced expiratory volume during the first second (FEV1) was registered with a spirometer at baseline and thence at every 5 and 10 min after each inhalation period, and then every 10 min during an hour. Subsequently, FEV1 and peak expiratory flow were monitored with a computerized Asthma Monitor (AM1 Jaeger, Hoechberg, Germany) every hour for the following 24 h. After exposure to cauliflower vapors at a concentration of 0.25 mg/m for 10 min, the patient experienced severe rhinoconjunctivitis and an early asthmatic reaction was observed (20% drop in FEV1 20 min after the challenge). A 15% drop in FEV1 was also observed 10 h after the cauliflower challenge (Fig. 1). Twenty-four hours after provocation, the methacholine inhalation test became positive (PC20 1⁄4 1.41 mg/ml). A control patient with asthma caused by toluene AL LERGY 2 0 0 5 : 6 0 : 9 6 9 – 9 7 4 • COPYRIGHT a 2005 BLACKWELL MUNKSGAARD • ALL R IGHTS RESERVED • CONTRIBUT IONS TO THIS SECT ION WILL NOT UNDERGO PEER REVIEW, BUT WILL BE REV IEWED BY THE ASSOCIATE EDITORS •