Asthma is the most common chronic respiratory disease associated with an increasing prevalence characterized by airway inflammation, mucus production, and airway hyperresponsiveness [ 1 ]. Bronchial
Aspergillosis is one of the frequent causes of exacerbation of asthma depending on the geographical regions. The specific serum IgG level for aspergillus is a major diagnostic criterion in aspergillosis.Ninety-six asthmatic patients, with mean age of 5.4 ± 3.0 years who were referred to the asthma clinic of the Mofid Children’s Hospital, were enrolled in this study. Serum specific IgG for aspergillus was measured and its association with severity of asthma was evaluated.Nineteen asthmatic patients (10 females and 9 males) had aspergillus IgG antibody. Among them, severe persistent asthma and moderate persistent asthma were detected in 5 and 13 cases, respectively, whereas only one patient suffered from mildpersistent asthma. A total of 36.5% of the 96 patients had a history of atopy, while 26% had allergic rhinitis. There was an association between the severity of asthma and the presence of aspergillus IgG antibody. Moreover, the positivity for aspergillus IgG antibody was higher in older patients.Our results indicated an association between aspergillus antibody level and severity of asthma. It could be recommended that the IgG titer for aspergillus is measured in pediatric patients with asthma, whereas co-morbidity of aspergillosis and asthma increases the risk of asthma exacerbation.
In the first part of this series of papers (Székely and Pataki, 102) the pathogenesis of asthma was approached as a pathological antigen-antibody complex induced vago-vagal axon reflex. In the next part (103) the contribution of individual hormonal predisposition, the environmental and the most frequent allergizing factors have been reviewed. In the first section of this last (third) part of the review the genetic factors contributing to the asthma are surveyed. In this field a great progress has been made during the last decade, a lot of genes have been pinpointed which contribute to the heredity of the disease. In the second section of this last paper on the etiology of asthma an attempt is made to summarize the previously reviewed data and some new ones. Actually a new hypothesis is proposed that beyond the multitude of genetic, environmental and hormonal factors the underlying biochemical mechanism is simple: the disequilibrium of two functionally opposing second messenger systems in the airways: the Ca
liberating PLC-PKC cascade and the Ca
level reducing cAMP mediated one with preponderance of the former.
The novel data on the pathogenesis of asthma are summarized in this three-part review. Its immunological background is well established but it is more than an immunological disorder. Multiple lines indicate that both peripheral and central neural mechanisms are also involved in the pathogenesis of asthma. In the present first part of the review asthma is described as vago-vagal axon reflex brought about by multiple positive feed-back mechanisms, receptor upregulation, wind-up, phenotypic switch and formation of a pathological conditioned reflex. In the coming second part the main dispositional (mostly hormonal) and external contributing factors are reviewed, while the third part deals with the role of inheritance, i.e. with gene alleles leading to enhanced production of mediators of asthma.
Asthmatic inflammation during pregnancy poses a risk for maternal and fetal morbidities. Circulating T cell immune phenotype is known to correlate with airway inflammation (detectable by fractional concentration of nitric oxide present in exhaled breath (FENO)) in non-pregnant allergic asthmatics. The aim of this study was to assess the relationship of peripheral T cell phenotype to FENO and clinical variables of asthma during pregnancy.We examined 22 pregnant women with allergic asthma in the 2nd/3rd trimester. The prevalence of Th1, Th2, regulatory T (Treg) and natural killer (NK) cell subsets was identified with flow cytometry using cell-specific markers. FENO, Asthma Control Test (ACT) total score and lung function were evaluated.Peripheral blood Th1, Th2, Treg, and NK cell prevalence were not significantly correlated to airway inflammation assessed by FENO in asthmatic pregnant women (all cells p > 0.05; study power > 75%). However, an inverse correlation was detected between Th2 cell prevalence and ACT total scores (p = 0.03) in asthmatic pregnancy.Blunted relationship between T cell profile and airway inflammation may be the result of pregnancy induced immune tolerance in asthmatic pregnancy. On the other hand, increased Th2 response impairs disease control that supports direct relationship between symptoms and cellular mechanisms of asthma during pregnancy.
In this second part of the review on the pathogenesis of asthma the hormonal factors and adverse external events are shortly reviewed which skew the balance of Th1 vs. Th2 CD4+ lymphocytes towards the latter ones and this way increase the probability of atopic diseases. Among other the role of transplacental priming, insulin, insulin-like and other growth factors, lack of the usual microbial infections in the early childhood (the so-called hygiene hypothesis), gender, diminished testosterone production, gastroesophageal reflux, adverse effects during pregnancy are discussed. A separate chapter deals with the role of central nervous system in the etiology and finally the most common allergizing and airway tissue damaging agents are listed in tabulated form.