Pilar García-Ortega

Usefulness of UniCAP‐Tryptase fluoroimmunoassay in the diagnosis of anaphylaxis

Background: Serum tryptase level measured by RIA is the main in vitro tool to confirm the diagnosis of anaphylaxis.

Failure of montelukast to prevent anaphylaxis to diclofenac

1) Digestive problems or rashes could appear after the ingestion of a certain quantity of histamine-rich peanuts. A high content of histamine has already been noticed for some cooked pork meats, fermented cheese, tinned ®sh, etc. This reaction to biogene amines is well known and can be related to a functional de®ciency of the degrading enzymes (4, 5). 2) The worsening of IgE-related allergy may be caused by this associated factor: the high quantity of histamine in some peanut batches. This could explain the differences in the intensity of the disorders occurring after the ingestion of the same quantity of peanuts.

Selective type-1 hypersensitivity to cefixime.

Accepted for publication 3 May 1999 Copyright # Munksgaard 1999 ISSN 0105-4538 References 1. HaÈcki M, WuÈ thrich B, Hanser M. Wildseide: ein aggressives Inhalationsallergen. Dtsch Med Wochenschr 1982;107:166±169. 2. Johansson SG, WuÈ thrich B, Zortea Ca ̄isch C. Nightly asthma caused by allergens in silk®lled bed quilts: clinical and immunologic studies. J Allergy Clin Immunol 1985;75:452±459. 3. Taub SJ. Allergy due to silk. J Allergy 1930;1:539±541. 4. Figley KD, Parkhurst HJ. Silk sensitivity. J Allergy 1933;5:60±69. 5. Parlato SJ, Swarthout G. A study of the silk allergen. J Allergy 1934;5:505±509. 6. Chaoming W, Shitai Y, Lixin Z, Yan Y. Silkinduced asthma in children: a report of 64 cases. Ann Allergy 1990;64:375±378.

Allergy to Diplotaxis erucoides pollen: occupational sensitization and cross-reactivity with other common pollens

Background: Diplotaxis erucoides is a common weed of the Brassicaceae family widespread in southern and central Europe.

Effects of specific immunotherapy on the development of new sensitisations in monosensitised patients

BACKGROUND Specific immunotherapy (SIT) is the only treatment that interferes with the basic pathophysiological mechanisms of allergic disease and is widely used in the management of clinically significant respiratory IgE-mediated diseases. Nevertheless, until recently, information on the influence of SIT on the development of new allergic sensitisations has been scant. METHODS One hundred consecutive patients (45 males and 55 females, aged 6 to 69 years) with respiratory allergic diseases and attending the allergy unit of a general hospital were selected. All had been diagnosed by clinical history and skin prick tests of allergic rhinitis and/or asthma, were monosensitised (71 to Dermatophagoides spp, 22 to Parietaria judaica pollen and 7 to grass pollen) and had been followed up as outpatients between 1990-98. Sixty-six patients had been treated with conventional SIT for at least 3 years, while thirty-four followed only environmental measures and drug treatment. Family atopy status (first-degree relatives), smoking, family pets (cat and/or dog), rhinitis and/or asthma symptom score and inhalant skin prick tests to the same aeroallergens were compared between baseline and after 3 to 5 years of treatment. RESULTS No statistically-significant differences in the development of new sensitisations were observed between the two groups (36.4 % of SIT-treated patients versus 38.2 % in control group, RR = 0.97, CI 95 %: 0.72-1.3). Smoking, family atopy history and pets did not appear to be risk factors for the development of neosensitisations (p < 0.05). Nevertheless, SIT-treated patients presented a better clinical score than the control group, with improvements of 89.4 % and 61.8 %, respectively (p = 0.007). CONCLUSIONS Three-year SIT did not protect against development of new sensitisations in monosensitised allergic rhinitis or asthma. Smoking, family atopy history and pets were not associated with development of new sensitisations. Clinical score improved significantly in the SIT-treated group compared with drug-treated patients.

Asthma, mite sensitization, and sleeping in bunks

BACKGROUND Mattresses and bedding are the main reservoirs of house dust mites. OBJECTIVE Subjects sleeping in the bottom bunk may be exposed to house dust particles detached from bedding of the top bunk. Our aim was to ascertain whether this exposure could influence the development of mite sensitization and/or allergic symptoms in these individuals. METHODS Symptoms of allergic respiratory disease were recorded and mite skin tests performed in 94 consecutive bunk-sleeping subjects (47 pairs of siblings) from an outpatient allergy clinic. Levels of Der p I, Der f I, and Der II were determined by enzyme-immunoassay in 16 randomly selected bedding dust samples (8 pairs of bunks). RESULTS Mite sensitization rate and prevalence of allergic respiratory disease were similar for the top-bed and bottom-bed groups, whereas prevalence of asthma was significantly higher in the latter. Mite sensitization was significantly associated with family atopy background, whereas other factors such as house pets, indoor smoke exposure or types of mattress or bunks were not. Der p I levels higher than 2 microg/g dust were found in 12 of the 16 mattresses and the median of the 8-bed-bottom group was over 10 microg/g. CONCLUSIONS Sleeping in bunks constitutes a greater risk of developing asthma for subjects sleeping in the bottom bed. Bunk sleeping should be discouraged in families with an atopic background and sensitized subjects should use the top bed.

Moth plant (Araujia sericifera) allergy

TARC/CCL17 levels in EAE or NEAE patients. Our results showed that plasma levels of TARC/CCL17 in NEAE patients decreased according to the reduction in symptoms and eosinophilia. Therefore, TARC/CCL17 may be useful as a serological marker and may facilitate assessment of the degree of disease activity in NEAE patients. Our results also suggested that Th2 cells contribute to the pathogenesis of NEAE by recruiting eosinophils to the skin. *Institute of Rheumatology Tokyo Women’s Medical University 10-22 Kawada-cho Shinjuku Tokyo 162-0054 Japan Tel: +81-3-5269-1725 Fax: +81-3-5269-1726 E-mail: hokamoto@ior.twmu.ac.jp

Urticaria crónica: cambiando de siglo

1. Al contrario de lo que muchas veces se considera, la urticaria cronica no es una molestia banal, sino un trastorno con repercusion sobre la calidad de vida que afecta al quehacer cotidiano, el cuidado personal y del hogar, la deambulacion, el sueno, la actividad laboral y las relaciones sociales, e incluso puede llegar a ser incapacitante en los casos de urticaria por presion o en los que cursan con angioedema asociado 2 . La urticaria cronica y el angioedema son trastornos frustrantes tanto para el paciente como para el medico, ya que a su prolongada duracion ‐mas de 10 anos en una quinta parte de los casos‐ y a sus variados desencadenantes ‐ejercicio, alimentos, farmacos, estres‐ une la ausencia de etiologia conocida en mas de un 80% de las ocasiones 3,4 . A pesar de que frecuentemente se atribuye a causas alergicas, en la mayor parte de los casos no esta implicado un mecanismo patogenico dependiente de IgE, y de hecho la atopia no se asocia significativamente a urticaria cronica

Antibiotic-induced NSAID intolerance

References 1. ROSENBERG M, PATTERSON R, MINTZER R, COOPER BJ, ROBERTS M, HARRIS KE. Clinical and immunologic criteria for the diagnosis of allergic bronchopulmonary aspergillosis. Ann Intern Med 1977; 86:405±414. 2. VARKEY B. Allergic bronchopulmonary aspergillosis. Clinical perspectives. Immunol Allergy Clin North Am 1998;18:479±501. 3. GLANCY JJ, ELDER JL, MCALEER R. Allergic bronchopulmonary fungal disease without clinical asthma. Thorax 1981;36:345±349. 4. BERKIN KE, VERNON DR, KERR JW. Lung collapse caused by allergic bronchopulmonary aspergillosis in non-asthmatic patients. BMJ (Clin Res Ed) 1982; 285:552±553. 5. AUBRY MC, FRASER R. The role of bronchial biopsy and washing in the diagnosis of allergic bronchopulmonary aspergillosis. Mod Pathol 1998;11:607±611. 6. BOSKEN CH, MYERS JL, BREENBERGER PA, KATZENSTEIN AL. Pathologic features of allergic bronchopulmonary aspergillosis. Am J Surg Pathol 1988;12:216±222. 7. SULAVIK SB. Bronchocentric granulomatosis and allergic bronchopulmonary aspergillosis. Clin Chest Med 1988;9: 609±621. Antibiotic-induced NSAID intolerance