A Cantani1, V Ciaschi. 1. Department of Pediatrics, Allergy and Clinical Immunology Division, University "La Sapienza", Rome, Italy.
Abstract
BACKGROUND: The prevalence of Alternaria Alternata (AA), a mold causing in children severe asthma is scarcely known, also due to the underdiagnosis of AA allergy, frequently due to multiple sensitizations to molds. OBJECTIVE: To analyze this issue we prospectively studied all children attending our Division between January 4, 1990 and December 31, 1997. METHODS: A total of 6840 children with asthma or allergic rhinitis were evaluated. Diagnosis was established by family and personal history, physical examination, skin prick tests (SPTs) and RAST (Radio Allergo-Sorbent Test) for inhalants including AA. We further evaluated: (1) sensitization only to AA allergens without positivity for additional inhalants; (2) prevalence of AA positivity among children with asthma or allergic rhinitis; (3) concordance between SPTs and RAST for allergy to molds, (4) proportion of children treated with specific immunotherapy (SIT). RESULTS: Among the 6840 children 213 were positive to AA (3.3%), only 89/6840 children (1.3%) had AA monosensitization (p = 0.0001), a concordance between SPTs and RAST was present in 21/89 (23.6%) children (p = 0.0009), and only 9 children out of 89 were SIT treated. Concerning the clinical manifestations, 83 had asthma or allergic rhinitis, and 6 had asthma associated with atopic dermatitis. Family history was positive in 82.9% of children. The mean onset of AA sensitivity was at age 4 for males, and at age 5 for females. CONCLUSIONS: In childhood, AA allergy is a genetic affection. The SPT concordance with history and clinical examination appears to be operative. Due to life-threatening reactions in children with AA allergy, we suggest that those with suspected inhalant allergy be tested with AA allergens, and treated with SIT if positive.
BACKGROUND: The prevalence of Alternaria Alternata (AA), a mold causing in children severe asthma is scarcely known, also due to the underdiagnosis of AAallergy, frequently due to multiple sensitizations to molds. OBJECTIVE: To analyze this issue we prospectively studied all children attending our Division between January 4, 1990 and December 31, 1997. METHODS: A total of 6840 children with asthma or allergic rhinitis were evaluated. Diagnosis was established by family and personal history, physical examination, skin prick tests (SPTs) and RAST (Radio Allergo-Sorbent Test) for inhalants including AA. We further evaluated: (1) sensitization only to AA allergens without positivity for additional inhalants; (2) prevalence of AA positivity among children with asthma or allergic rhinitis; (3) concordance between SPTs and RAST for allergy to molds, (4) proportion of children treated with specific immunotherapy (SIT). RESULTS: Among the 6840 children 213 were positive to AA (3.3%), only 89/6840 children (1.3%) had AA monosensitization (p = 0.0001), a concordance between SPTs and RAST was present in 21/89 (23.6%) children (p = 0.0009), and only 9 children out of 89 were SIT treated. Concerning the clinical manifestations, 83 had asthma or allergic rhinitis, and 6 had asthma associated with atopic dermatitis. Family history was positive in 82.9% of children. The mean onset of AA sensitivity was at age 4 for males, and at age 5 for females. CONCLUSIONS: In childhood, AAallergy is a genetic affection. The SPT concordance with history and clinical examination appears to be operative. Due to life-threatening reactions in children with AAallergy, we suggest that those with suspected inhalant allergy be tested with AA allergens, and treated with SIT if positive.
Authors: Alan P Knutsen; Hari M Vijay; Barbara Kariuki; Luis A Santiago; Ralph Graff; Jonathan D Wofford; Maulik R Shah Journal: Clin Mol Allergy Date: 2010-03-18