5 resultados para Rhinitis

em Deakin Research Online - Australia


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Background: Assessment of allergic sensitization is not routinely performed in infants and young children with eczema.

Objective: To determine whether infants who have atopic eczema (with sensitization) are at a greater risk of developing asthma and allergic rhinitis (AR) than those with non-atopic eczema (without concurrent sensitization).

Methods: The presence of eczema was prospectively documented until 2 years of age in a birth cohort of 620 infants with a family history of atopic disease. Sensitization status was determined by skin prick tests (SPTs) at 6, 12, and 24 months using six common allergens. Interviews were conducted at 6 and 7 years to determine the presence of asthma and AR.

Results: Within the first 2 years of life, 28.7% of the 443 children who could be classified had atopic eczema: 20.5% had non-atopic eczema, 19.0% were asymptomatic but sensitized and 31.8% were asymptomatic and not sensitized. When compared with children with non-atopic eczema in the first 2 years of life, children with atopic eczema had a substantially greater risk of asthma [odds ratio (OR)=3.52, 95% confidence interval=1.88–6.59] and AR (OR=2.91, 1.48–5.71). The increased risk of asthma was even greater if the infant had a large SPT (OR=4.61, 2.34–9.09) indicative of food allergy. There was no strong evidence that children with non-atopic eczema had an increased risk of asthma or AR compared with asymptomatic children.

Conclusion
: In children with eczema within the first 2 years of life, SPT can provide valuable information on the risk of childhood asthma and AR.

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Background Exposure to n-3 polyunsaturated fatty acids (PUFA) in early life is hypothesized to offer protection against atopic disease. However, there is controversy in this area, and we have previously observed that high levels of n-3 fatty acid (FA) in colostrum are associated with increased risk of allergic sensitization.
Objective The aim of the study was to assess the relationship between FA profile in breast milk and risk of childhood atopic disease.
Methods A high-risk birth cohort was recruited, and a total of 224 mothers provided a sample of colostrum (n = 194) and/or 3-month expressed breast milk (n = 118). FA concentrations were determined by gas chromatography. Presence of eczema, asthma and rhinitis were prospectively documented up to 7 years of age.
Results High levels of n-3 22:5 FA (docosapentaenoic acid, DPA) in colostrum were associated with increased risk of infantile atopic eczema [odds ratio (OR) = 1.66 per 1 standard deviation increase, 95% confidence interval (CI) = 1.11–2.48], while total n-3 concentration in breast milk was associated with increased risk of non-atopic eczema (OR = 1.60, 95% CI = 1.03–2.50). Higher levels of total n-6 FA in colostrum were associated with increased risk of childhood rhinitis (OR = 1.59, 95% CI = 1.12–2.25). There was no evidence of associations between FA profile and risk of asthma.
Conclusion In this cohort of high-risk children, a number of modest associations were observed between FA concentrations in colostrum and breast milk and allergic disease outcomes. Further research in this area with larger sample sizes is needed.

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Objective To determine if use of paracetamol in early life is an independent risk factor for childhood asthma.
Design Prospective birth cohort study.
Setting Melbourne Atopy Cohort Study.
Participants 620 children with a family history of allergic disease, with paracetamol use prospectively documented
on 18 occasions from birth to 2 years of age, followed until age 7 years.
Main outcome measures The primary outcome was childhood asthma, ascertained by questionnaire at 6 and 7 years. Secondary outcomes were infantile wheeze, allergic rhinitis, eczema, and skin prick test positivity.
Results Paracetamol had been used in 51% (295/575) of children by 12 weeks of age and in 97% (556/575) by 2 years. Between 6 and 7 years, 80% (495/620) were followed up; 30% (148) had current asthma. Increasing frequency of paracetamol use was weakly associated with increased risk of childhood asthma (crude odds ratio 1.18, 95% confidence interval 1.00 to 1.39, per doubling of days of use). However, after adjustment for frequency of respiratory infections, this association essentially disappeared (odds ratio 1.08, 0.91 to 1.29). Paracetamol use for non-respiratory causes was not associated with asthma (crude odds ratio 0.95, 0.81 to 1.12).
Conclusions In children with a family history of allergic diseases, no association was found between early paracetamol use and risk of subsequent allergic disease after adjustment for respiratory infections or when paracetamol use was restricted to non-respiratory tract infections. These findings suggest that early paracetamol use does not increase the risk of asthma.

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Exposure to airborne pollen from certain plants can cause allergic disease, leading to acute respiratory symptoms. Whole pollen grains, 15–90 μ m-sized particles, provoke the upper respiratory symptoms of rhinitis (hay fever), while smaller pollen fragments capable of depositing in the lower respiratory tract have been proposed as the trigger for asthma. In order to understand factors leading to pollen release and fragmentation we have examined the rupture of Chinese elm pollen under controlled laboratory conditions and in the outdoor atmosphere. Within 30 minutes after immersion in water, 70% of fresh Chinese pollen ruptures, rapidly expelling cytoplasm. Chinese elm flowers, placed in a controlled atmosphere chamber, emitted pollen and pollen debris after a sequential treatment of 98% relative humidity followed by drying and a gentle disturbance. Immunologic assays of antigenic proteins specific to elm pollens revealed that fine particulate material (D p < 2 μ m) collected from the chamber contained elm pollen antigens. In a temporal study of the outdoor urban atmosphere during the Chinese elm bloom season of 2004, peak concentrations of pollen and fine pollen fragments occurred at the beginning of the season when nocturnal relative humidity (RH) exceeded 90%. Following later periods of hot dry weather, pollen counts decreased to zero. The Chinese elm pollen fragments also decreased during the hot weather, but later displayed additional peaks following periods of more moderate RH and temperature, indicating that pollen counts underestimate total atmospheric pollen allergen concentrations. Pollen fragments thus increase the biogenic load in the atmosphere in a form that is no longer recognizable as pollen and, therefore, is not amenable to microscopic analysis. This raises the possibility of exposure of sensitive individuals to pollen allergens in the form of fine particles that can penetrate into the lower airways and pose potentially severe health risks.

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Hypersensitivity to the chicken egg is a widespread disorder mainly affecting 1-2% of children worldwide. It is the second most common food allergy in children, next to cow's milk allergy. Egg allergy is mainly caused by hypersensitivity to four allergens found in the egg white; ovomucoid, ovalbumin, ovotransferrin and lysozyme. However, some research suggests the involvement of allergens exclusively found in the egg yolk such as chicken serum albumin and YGP42, which may play a crucial role in the overall reaction. In egg allergic individuals, these allergens cause conditions such as itching, atopic dermatitis, bronchial asthma, vomiting, rhinitis, conjunctivitis, laryngeal oedema and chronic urticaria, and anaphylaxis. Currently there is no permanent cure for egg allergy. Upon positive diagnosis for egg allergy, strict dietary avoidance of eggs and products containing traces of eggs is the most effective way of avoiding future hypersensitivity reactions. However, it is difficult to fully avoid eggs since they are found in a range of processed food products. An understanding of the mechanisms of allergic reactions, egg allergens and their prevalence, egg allergy diagnosis and current treatment strategies are important for future studies. This review addresses these topics and discusses both egg white and egg yolk allergy as a whole.