European review for medical and pharmacological sciences · 2004
Epidemiology of alternaria alternata allergy: a prospective study in 6840 Italian asthmatic children.
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Cantani A, Ciaschi V
Аннотация
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.
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.