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- Bergström, Sten-Erik, et al.
(författare)
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Asthma mortality among Swedish children and young adults, a 10-year study
- 2008
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Ingår i: Respiratory Medicine. - : Elsevier BV. - 0954-6111 .- 1532-3064. ; 102:9, s. 1335-1341
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Previous reports indicate that morbidity and mortality from asthma have increased during the past decades. Here, the mortality rate associated with asthma and possible risk factors in children and young adults in Sweden during the period 1994-2003 were evaluated. METHODS: The medical profession was asked to report suspected cases of death from asthma in individuals 1-34 years of age. All death certificates containing relevant ICD codes were reviewed. Medical records and autopsy reports were assessed and telephone interviews with next-of-kin performed. RESULTS: During the 10-year period 37 deaths due to asthma were identified. The median age at the time of death was 27 years and 6 of the deceased were younger than 15. The overall incidence of death from asthma decreased from 1.54 deaths per million in 1994 to 0.53 per million in 2003. Common risk factors were under-treatment (23/37), poor adherence to prescribed treatment (17/37) and adverse psychosocial situation (19/37). An alarming finding was that 11 of the 37 deaths were probably caused by food allergy and for 8 subjects death was associated with exposure to pet dander. The death certificates were found to contain inaccuracies with 30% of those for whom asthma was reported as the underlying cause having died from other causes. CONCLUSION: Asthma mortality in children and young adults in Sweden decreased between 1994 and 2003. Food allergy and inadequate treatment were the major risk factors for such a death. Recognition and special care of patients with asthma who have shown signs of non-compliance, denial or severe food allergy must be encouraged.
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| 2. |
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| 3. |
- Hedlin, Gunilla, et al.
(författare)
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Astma och KOL
- 2005
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Ingår i: Läkemedelsboken. - Stockholm : Apoteket AB. - 918557452X ; , s. 543-565
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Bokkapitel (populärvet., debatt m.m.)
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| 4. |
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| 5. |
- Hedlin, Gunilla, et al.
(författare)
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Immunmodulerande behandling
- 2009
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Ingår i: Allergi och astma. Hedlin G & Larsson K, red. Studentlitteratur. - 9789144029962 ; , s. 287-300
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 6. |
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| 7. |
- Zetterquist, Wilhelm, et al.
(författare)
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Increased exhaled nitrite in children with allergic asthma is not related to nitric oxide formation
- 2008
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Ingår i: The Clinical Respiratory Journal. - 1752-6981 .- 1752-699X. ; 2:3, s. 166-174
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Nitrite sampled from the upper airways could originate from inflammation-induced nitric oxide (NO), as reports of elevated nitrite in exhaled breath condensate (EBC) from asthmatics suggest, but also through bacterial action in the pharyngo-oral tract. Objectives: To correlate EBC nitrite and nitrate to exhaled NO (FENO, fraction Of expired NO) and other markers of disease activity in children with allergic asthma and thereby further investigate their role and origin. Materials and methods: EBC was collected from 27 asthmatic subjects (ages 6-17 years, all immunoglobulin E-positive for aeroallergens) and 21 age-matched non-atopic healthy controls for fluorometric analysis of nitrite and nitrate. These markers were compared with measurements of FENO, blood eosinophil count (EOS), methacholine reactivity (PD20) and baseline spirometry. Results: EBC nitrite, in contrast to nitrate, was significantly increased (P < , 0.01) in the asthmatic children. They also had increased levels of FENO (P < , 0.001) and EOS (P < , 0.001) along with decreased PD20 (P < , 0-001) and FEV1/FVC (p < , 0.01). However, there was no correlation between EBC nitrite and FENO (r = 0.05) or any other marker of disease activity in the asthmatic children, whereas between the other markers correlations could be established. Conclusion: EBC nitrite is elevated in childhood asthma but the lack of correlation to FENO and other markers, together with simultaneously normal levels of nitrate, make its origin as a metabolite of inflammation-induced NO questionable.
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