Specific Antibody Response Against the 23-Valent Pneumococcal Vaccine in Patients With α1-Antitrypsin Deficiency With and Without Bronchiectasis

Miravitlles, Marc; Gracia, Javier de; Rodrigo, María-José; Cruz, María Jesús; Vendrell, Montserrat; Vidal, Rafael; Morell, Ferrán

doi:10.1378/chest.116.4.946

Cited by 30 publications

(15 citation statements)

References 33 publications

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“…In addition to these more common antibody deficiency disorders, there is an established and growing recognition of an important association between bronchiectasis and defects of specific antibody production 22 71 83 88–90. Additional disease co-factors, such as α 1 -antitrypsin deficiency, may play a role which is contributory to, and cumulative with, infection-associated airway damage in some immunocompromised patients 78 80. The frequency and importance of such interactions remain to be fully elucidated, particularly in progressive disease which responds poorly to treatment.…”

Section: Summary Of Recommendationsmentioning

confidence: 99%

British Thoracic Society guideline for non-CFbronchiectasis

Pasteur

Bilton²,

Hill³

2010

Thorax

848

416

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Section: Summary Of Recommendationsmentioning

confidence: 99%

British Thoracic Society guideline for non-CFbronchiectasis

Pasteur

Bilton²,

Hill³

2010

Thorax

848

416

View full text Add to dashboard Cite

“…By favouring colonisation, chronic mucus hypersecretion may facilitate the growth of bacteria and rapid achievement of a cfu concentration above the threshold [64]; 5) Impairment of host defences. Any impairment in host defences, either locally within the bronchial mucosa or systemically, such as impairment of antibody responses [65], may facilitate bacterial adhesion and faster growth; 6) Nonspecific factors. Elderly patients or patients with significant comorbid conditions may feel worse with lower levels of bronchial inflammation and thus the threshold for these patients may be lower.…”

Section: Frequency and Outcomes Of Exacerbations: Risk Factors For Rementioning

confidence: 99%

Exacerbations of chronic obstructive pulmonary disease: when are bacteria important?

Miravitlles¹

2002

European Respiratory Journal

100

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The progressive course of chronic obstructive pulmonary disease (COPD) is often aggravated by exacerbations, the majority of them produced by bronchial infection. Frequent exacerbations have been demonstrated to have a negative impact on quality of life and pulmonary function in patients with COPD, particularly in active smokers. Furthermore, acute exacerbations are the most frequent cause of medical visits, hospital admissions and death among patients with chronic lung disease.Evidence indicates that the number of patients with pathogenic bacteria in respiratory secretions and the bronchial bacterial load increase during exacerbations. Furthermore, the local inflammatory response of the host parallels the increase in bacterial load. From these observations, it can be speculated that, for symptoms of acute exacerbation to appear, there must be a minimum bacterial load in the airways, i.e. a threshold above which the inflammatory reaction is severe enough to elicit clinical symptoms of exacerbation. This threshold may vary from patient to patient owing to different modifying factors. Some of these factors may be the recognised risk factors for relapse, such as increasing age, impairment of lung function, comorbid conditions or frequent exacerbations in the past.Relapse rates after ambulatory treatment of acute exacerbation of COPD may be as high as 20-25% of cases. Relapses are associated with significant mordibity and increased costs.A number of unanswered questions remain regarding exacerbations of chronic obstructive pulmonary disease. These include the role of viral infection, the importance of residual bacterial colonisation and the impact of new antibiotics on the treatment of exacerbations. Chronic obstructive pulmonary disease (COPD) is one of the most prevalent diseases in developed countries. Furthermore, the number of individuals affected has grown since the 1980s [1]. In Spain, the prevalence of COPD is 9% in adults aged 40-70 yrs, although only 22% of these are diagnosed [2]. Tobacco smoking is the main aetiological factor for COPD. In a population-based study in Spain, 25% of the population aged 40-70 yrs were smokers and another 25% former smokers [3]. Only 15-20% of smokers will develop COPD, and smokers with COPD exhibit higher tobacco consumption and greater dependence on nicotine than smokers who do not have COPD, and more than one-third have never tried to stop smoking [3]. These figures indicate that the problem of COPD in most developed countries will continue to increase in the near future.The chronic and progressive course of COPD is often aggravated by short periods of increasing symptoms, particularly increasing cough, dyspnoea and production of sputum which can become purulent.

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“…We totally agree that a sizeable fraction of patients with bronchiectasis of unknown cause can now be classified as bronchiectasis associated with polysaccharide antibodyresponse deficiency [1,8,10,11]. However, before this diagnosis can be established and substitution therapy with immunoglobulins can be indicated, comprehensive immunological evaluation is mandatory.…”

Section: Antibody Deficiency In Bronchiectasismentioning

confidence: 69%

Antibody deficiency in bronchiectasis

Miravitlles¹

2005

European Respiratory Journal

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Specific Antibody Response Against the 23-Valent Pneumococcal Vaccine in Patients With α1-Antitrypsin Deficiency With and Without Bronchiectasis

Cited by 30 publications

References 33 publications

British Thoracic Society guideline for non-CFbronchiectasis

British Thoracic Society guideline for non-CFbronchiectasis

Exacerbations of chronic obstructive pulmonary disease: when are bacteria important?

Antibody deficiency in bronchiectasis

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