Postviral bronchial hyperreactivity syndrome: Recognizing asthma's great mimic

Ostransky, David; Blais, Francis X.

doi:10.1515/jom-1991-900512

Cited by 7 publications

(3 citation statements)

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“…The documented airflow limitation in our 29/30 LC patients, may explain why systemic [ 19 , 20 ], as well as inhaled corticosteroids [ 21 , 22 ], are observed to be effective in LC patients. Recently, findings of continuous elevated inflammation markers in LC patients may explain why the airflow limitation does not seem to be self-limiting within the expected 5–11 weeks [ 10 ], supporting the potential of a persisting condition.…”

Section: Discussionmentioning

confidence: 99%

“…This airflow limitation is a common complication of respiratory tract infections, induced by postviral inflammation with subsequent airway narrowing [ 9 ], commonly referred to as postviral bronchial hyperreactivity [ 9 ]. This condition is self-limited resolving within a 5–11 weeks duration time [ 10 ], in contrast to asthma, which is a chronic condition (>3 months) also associated with airflow limitation as a consequence of inflammation. Typical respiratory symptoms include wheezing, cough, chest tightness/dyspnoea and excessive mucus, which vary by time depending on the varying inflammation [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Assessment of lung function variability documents airflow limitation in many patients with long covid

Reier-Nilsen,

Grønneberg,

Røine

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Assessment of lung function variability documents airflow limitation in many patients with long covid

Reier-Nilsen,

Grønneberg,

Røine

et al. 2024

Heliyon

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“…A recent acute viral infection may also act to sensitise airway responses, with some reports indicating development of a postviral AHR syndrome. In general, this condition resolves spontaneously within 12 weeks 128…”

Section: Lower Airway Dysfunctionmentioning

confidence: 99%

International Olympic Committee (IOC) consensus statement on acute respiratory illness in athletes part 2: non-infective acute respiratory illness

Schwellnus

Adami²,

Bougault

et al. 2022

Br J Sports Med

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Acute respiratory illness (ARill) is common and threatens the health of athletes. ARill in athletes forms a significant component of the work of Sport and Exercise Medicine (SEM) clinicians. The aim of this consensus is to provide the SEM clinician with an overview and practical clinical approach to non-infective ARill in athletes. The International Olympic Committee (IOC) Medical and Scientific Committee appointed an international consensus group to review ARill in athletes. Key areas of ARill in athletes were originally identified and six subgroups of the IOC Consensus group established to review the following aspects: (1) epidemiology/risk factors for ARill, (2) infective ARill, (3) non-infective ARill, (4) acute asthma/exercise-induced bronchoconstriction and related conditions, (5) effects of ARill on exercise/sports performance, medical complications/return-to-sport (RTS) and (6) acute nasal/laryngeal obstruction presenting as ARill. Following several reviews conducted by subgroups, the sections of the consensus documents were allocated to ‘core’ members for drafting and internal review. An advanced draft of the consensus document was discussed during a meeting of the main consensus core group, and final edits were completed prior to submission of the manuscript. This document (part 2) of this consensus focuses on respiratory conditions causing non-infective ARill in athletes. These include non-inflammatory obstructive nasal, laryngeal, tracheal or bronchial conditions or non-infective inflammatory conditions of the respiratory epithelium that affect the upper and/or lower airways, frequently as a continuum. The following aspects of more common as well as lesser-known non-infective ARill in athletes are reviewed: epidemiology, risk factors, pathology/pathophysiology, clinical presentation and diagnosis, management, prevention, medical considerations and risks of illness during exercise, effects of illness on exercise/sports performance and RTS guidelines.

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Asthma as a disruption in iron homeostasis

Ghio

2016

Biometals

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Over several decades, asthma has evolved from being recognized as a single disease to include a diverse group of phenotypes with dissimilar natural histories, pathophysiologies, responses to treatment, and distinctive molecular pathways. With the application of Occam's razor to asthma, it is proposed that there is one cause underlying the numerous phenotypes of this disease and that the responsible molecular pathway is a deficiency of iron in the lung tissues. This deficiency can be either absolute (e.g. asthma in the neonate and during both pregnancy and menstruation) or functional (e.g. asthma associated with infections, smoking, and obesity). Comparable associations between asthma co-morbidity (e.g. eczema, urticaria, restless leg syndrome, and pulmonary hypertension) with iron deficiency support such a shared mechanistic pathway. Therapies directed at asthma demonstrate a capacity to impact iron homeostasis, further strengthening the relationship. Finally, pathophysiologic events producing asthma, including inflammation, increases in Th2 cells, and muscle contraction, can correlate with iron availability. Recognition of a potential association between asthma and an absolute and/or functional iron deficiency suggests specific therapeutic interventions including inhaled iron.

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Postviral bronchial hyperreactivity syndrome: Recognizing asthma's great mimic

Cited by 7 publications

References 0 publications

Assessment of lung function variability documents airflow limitation in many patients with long covid

Assessment of lung function variability documents airflow limitation in many patients with long covid

International Olympic Committee (IOC) consensus statement on acute respiratory illness in athletes part 2: non-infective acute respiratory illness

Asthma as a disruption in iron homeostasis

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