Alcoholic drinks and asthma

Vally, Hassan; Thompson, Philip J.

doi:10.1046/j.1365-2222.2002.01303.x

Cited by 24 publications

(23 citation statements)

References 51 publications

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“…28,29 For the 2 weeks prior to each EVH test, participants were free from any chest or upper respiratory tract infection. 19 On EVH test days participants abstained from caffeine and alcohol as they can influence asthma exacerbations, 30,31 and arrived at the laboratory at least 2 h post-prandial. For each participant, EVH tests were performed at the same time of day.…”

Section: Pulmonary Function and Evh Testmentioning

confidence: 99%

Reproducibility of the bronchoconstrictive response to eucapnic voluntary hyperpnoea

Williams

Johnson

Hunter

et al. 2015

Respiratory Medicine

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Section: Pulmonary Function and Evh Testmentioning

confidence: 99%

Reproducibility of the bronchoconstrictive response to eucapnic voluntary hyperpnoea

Williams

Johnson

Hunter

et al. 2015

Respiratory Medicine

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“…A possible explanation is that changes in lung function may not provide a reliable indication of reactivity to wine in many asthmatics. Some individuals may react to wine only when their asthma has been aggravated by exposure to other irritants or triggers in the environment, or conversely, wine drinking may increase the reactivity of sensitive individuals to other irritants or triggers [8]. In either case, wine challenge under controlled conditions may not elicit a measurable change in lung function.…”

Section: Introductionmentioning

confidence: 99%

Increases in Urinary 9α,11β-Prostaglandin F<sub>2</sub> Indicate Mast Cell Activation in Wine-Induced Asthma

Misso

Aggarwal

Thompson

et al. 2009

Int Arch Allergy Immunol

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Background: Wine-induced asthmatic symptoms may be caused by sulphite additives. Prostaglandin (PG)D₂ and cysteinyl leukotrienes (cysLT) are important mediators of asthmatic responses. To determine whether the sulphite additives in wine alter the production of PGD₂ and cysLT, asthmatic patients with compelling histories of wine sensitivity were challenged with high- and low-sulphite wines; the urinary metabolites of PGD₂ and cysLT were measured before and after challenge. Methods: Eight self-reporting wine-sensitive asthmatic patients completed double-blind challenges with high- and low-sulphite wines on separate days. Urine samples were collected before and after consumption of 150 ml of wine. Urinary concentrations of 9α,11β-PGF₂ and leukotriene (LT)E₄ were measured by enzyme immunoassay. Results: Urinary 9α,11β-PGF₂ concentrations increased in all subjects following challenge with high-sulphite wine, and the median concentration increased 1.6-fold (p < 0.01). Urinary 9α,11β-PGF₂ also increased 1.5-fold after low-sulphite wine challenge, although this did not reach statistical significance (p = 0.08). The median difference in 9α,11β-PGF₂ concentration after high-sulphite wine challenge was not significantly different compared with that after low-sulphite wine challenge. Median urinary LTE₄ concentrations did not change significantly after either wine challenge. Conclusions: Increased urinary 9α,11β-PGF₂ concentrations following wine challenge suggest mast cell activation as a possible mechanism for wine-induced asthma, although this did not appear to be related to the sulphite additives in wine. Urinary 9α,11β-PGF₂ may warrant further assessment as a potential biomarker of reactivity to wine in asthmatic subjects.

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“…Irrespective of these findings, the majority of studies point to the fact that alcoholic beverages on average exacerbate asthma (Cuddy and Li, 2001). Furthermore, alcoholic beverages are known to trigger a wide range of allergic responses (rhinitis, headache, cough, and asthma) (Vally and Thompson, 2002). The sensitivity of EtOH to trigger those adverse effects (particularly among the Asian population) is partly due to a reduced capacity to metabolize AcH (Vally and Thompson, 2003).…”

mentioning

confidence: 99%

“…The sensitivity of EtOH to trigger those adverse effects (particularly among the Asian population) is partly due to a reduced capacity to metabolize AcH (Vally and Thompson, 2003). In addition, other molecules contained in certain alcoholic beverages, such as sulfite additives and histamine (a by-product of the fermentation process of red wine) are thought to be contributing factors in wine-based alcohol-induced asthma (Vally and Thompson, 2002). Nevertheless, the present observation that EtOH per se is able to induce inflammatory responses in a rodent airway model relevant for human asthma suggests that this novel mechanism may also contribute to alcohol-induced asthma.…”

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confidence: 99%

Ethanol Causes Inflammation in the Airways by a Neurogenic and TRPV1-Dependent Mechanism

Trevisani

Gazzieri²,

Benvenuti³

et al. 2004

The Journal of Pharmacology and Experimental Therapeutics

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Ethanol (EtOH) stimulates peptidergic primary sensory neurons via the activation of the transient receptor potential vanilloid-1 (TRPV1). EtOH is also known to trigger attacks of asthma in susceptible individuals. Our aim was to investigate whether EtOH produces airway inflammation via a TRPV1-dependent mechanism and to verify whether this effect is produced via a mechanism distinct from that of acetaldehyde (AcH). EtOH caused a Ca 2ϩ -dependent release of neuropeptides from guinea pigs airways, an effect that was inhibited by both capsaicin pretreatment and the TRPV1 antagonist capsazepine (CPZ). Furthermore, EtOH contracted isolated guinea pig bronchi, showing efficacy similar to that of carbachol: this effect of EtOH was sensitive to capsaicin pretreatment, tachykinin receptor blockade, and TRPV1 antagonism. The EtOH metabolite AcH also contracted isolated guinea pig bronchi, but this action was not affected by capsaicin pretreatment, tachykinin receptor, or TRPV1 antagonism. EtOH by intravenous or intragastric route of administration caused bronchoconstriction and increased plasma extravasation in the guinea pig airways, effects that were abolished selectively by CPZ. In conclusion, we have demonstrated that EtOH stimulates peptidergic primary sensory neurons in the guinea pig airways by TRPV1 activation. This excitatory effect of EtOH, distinct from that of AcH, results in neurogenic inflammatory responses that may contribute to the mechanism of EtOH-induced asthma.

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Alcoholic drinks and asthma

Cited by 24 publications

References 51 publications

Reproducibility of the bronchoconstrictive response to eucapnic voluntary hyperpnoea

Reproducibility of the bronchoconstrictive response to eucapnic voluntary hyperpnoea

Increases in Urinary 9α,11β-Prostaglandin F<sub>2</sub> Indicate Mast Cell Activation in Wine-Induced Asthma

Ethanol Causes Inflammation in the Airways by a Neurogenic and TRPV1-Dependent Mechanism

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