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Latex allergen exposure increases exhaled nitric oxide in symptomatic healthcare workers

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The objective of this study was to investigate the clinical and diagnostic impact of baseline exhaled nitric oxide (eNO) levels and latex allergen-induced eNO changes in different healthcare worker groups.Healthcare workers, 31 latex-sensitised and 14 nonsensitised, underwent occupational-type challenge tests with powdered allergenic latex gloves.Sensitised as well as nonsensitised healthcare workers developed a significant eNO increase 1 h after challenge. Conversely, only latex-sensitised employees showed a significant eNO increase 22 h after challenge, which showed a significant relationship with bronchial obstruction (specific airway resistance changes). However, there was no difference in either baseline eNO level or eNO increase after 22 h between asthmatic (n = 13) and rhinitic only (n = 20) responders. The specificity and sensitivity of a 50% eNO increase after 22 h in responders were 100 and 56%, respectively.These results support the assumption that the whole respiratory tract is involved in a combined allergic rhinitis and asthma syndrome. Smoking healthcare workers showed reduced baseline exhaled nitric oxide levels, but, as shown for the first time, an allergen-induced exhaled nitric oxide increase comparable to that of nonsmokers. Corticosteroid therapy inhibited the allergen-induced exhaled nitric oxide change but not the clinical response in the challenge test. These findings suggest that cigarette smoke and corticosteroids initiate distinct molecular mechanisms influencing nitric oxide concentrations in the airways.
European Respiratory Society (ERS)
Title: Latex allergen exposure increases exhaled nitric oxide in symptomatic healthcare workers
Description:
The objective of this study was to investigate the clinical and diagnostic impact of baseline exhaled nitric oxide (eNO) levels and latex allergen-induced eNO changes in different healthcare worker groups.
Healthcare workers, 31 latex-sensitised and 14 nonsensitised, underwent occupational-type challenge tests with powdered allergenic latex gloves.
Sensitised as well as nonsensitised healthcare workers developed a significant eNO increase 1 h after challenge.
Conversely, only latex-sensitised employees showed a significant eNO increase 22 h after challenge, which showed a significant relationship with bronchial obstruction (specific airway resistance changes).
However, there was no difference in either baseline eNO level or eNO increase after 22 h between asthmatic (n = 13) and rhinitic only (n = 20) responders.
The specificity and sensitivity of a 50% eNO increase after 22 h in responders were 100 and 56%, respectively.
These results support the assumption that the whole respiratory tract is involved in a combined allergic rhinitis and asthma syndrome.
Smoking healthcare workers showed reduced baseline exhaled nitric oxide levels, but, as shown for the first time, an allergen-induced exhaled nitric oxide increase comparable to that of nonsmokers.
Corticosteroid therapy inhibited the allergen-induced exhaled nitric oxide change but not the clinical response in the challenge test.
These findings suggest that cigarette smoke and corticosteroids initiate distinct molecular mechanisms influencing nitric oxide concentrations in the airways.

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