Documente Academic
Documente Profesional
Documente Cultură
With sino-bronchial syndrome, the sinus disease may be caused by allergies or an infection - or it can be chronic. The lung disease can be one of several types such as acute infective bronchitis, recurrent bouts of bronchitis, chronic bronchitis, or asthma thats difficult to manage. It's thought that the sinus disease resulting in lower airway symptoms such as asthma is due to a constant drip of inflammatory and infective secretions from the back of the nose to the back of the throat. This throat irritation may cause bronchial constriction by a reflex transmitted by the nervous system. Or, the post-nasal drip of inflammatory secretions from the upper airway may create a secondary inflammatory reaction of the lungs, causing either asthma or bronchitis. 1999
Sep;57(9):2119-22.
[Sinobronchial syndrome].
[Article in Japanese]
Sugiyama Y. Source
Department of Pulmonary Medicine, Jichi Medical School.
Abstract
A condition characterized by chronic paranasal sinusitis and simultaneous chronic pulmonary infection was recognized and reported as long ago as the early 1900's. This condition was termed "sinobronchial syndrome" (SBS) in 1966. Many types of SBS are reported including Kartagener's syndrome/primary ciliary dyskinesia, Young's syndrome, bare-lymphocyte syndrome, cystic fibrosis and various types of immunoglobulin deficiency. SBS is also found in Japan. Among them, the most important is diffuse panbronchiolitis. The pathogenesis of SBS might involve inherited predisposition, probably accompanied by some deficiencies in the host defense of the respiratory system.
Department of Otorhinolaryngology, St. Luke's International Hospital, Tokyo. Nippon Jibiinkoka Gakkai Kaiho 11/2003; 106(10):1030-7. Source: PubMed ABSTRACT Sinobronchial syndrome (SBS) is characterized by chronic sinusitis with chronic infection of the bronchus. Chronic bronchitis, bronchiectasis and diffuse panbronchiolitis are also examples of complicating lower airway disease. In Japan, the surgical treatment of sinusitis is not considered to improve the lower airway diseases. Most published reports describe the Caldwell-Luc method. However ESS (Endoscopic
Sinus Surgery) can heal sinusitis while maintaining the morphology and function of the paranasal sinus. In addition, its surgical results are satisfactory. This report describes the improvement of patients with SBS who underwent ESS. Twelve patients with sinobronchial syndrome who underwent ESS at our department between 1989 and 1993 were enrolled in the study. Subjective improvement in sinusitis and the lower airway diseases were evaluated using a questionnaire. Objective improvements in sinusitis were evaluated using endoscopic findings of the ethmoid sinuses, while objective improvements in the lower airway diseases were evaluated by measuring the vital capacity and FEV 1.0%. These examinations were performed one year after the operation; the results of long-term follow-up examinations performed more than 6 years after the operation were also studied. In all of the patients, subjective nasal symptoms and objective endoscopic findings were satisfactory, with improvement rates of 91.7% and 83.3%, respectively. Regarding the lower airway symptoms, all the patients subjectively rated the symptoms as having improved, and an improvement in the FEV 1.0% was improved in all of the cases. In the present study, the lower airway symptoms improved after ESS. ESS enables the paranasal sinuses to be treated while maintaining the morphology of the paranasal sinus. Consequently, surgical results are better. The improvement of chronic sinusitis reduces the direct inflow of postnasal drippings into the bronchus. Restoring the normal functions of the nasal sinus defends the lower airway by warning, and humidifying the inspiratory air and removing dusts; these functions are though to have a favorable effect on the lower airway. Source Article: Chronic rhinosinusitis and risk of lung
cancer in the Singapore Chinese Health Study. Woon-Puay Koh, JianMin Yuan, Renwei Wang, Adeline Seow, Hin-Peng Lee, Mimi C Yu [show abstract]
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided
by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
Role of COX-2 in cough reflex sensitivity to inhaled capsaicin in patients with sinobronchial syndrome
Yoshihisa Ishiura1*, Masaki Fujimura2, Hiroki Yamamoto1, Noriyuki Ohkura2 and Shigeharu Myou2
* Corresponding author: Yoshihisa Ishiura ishiura-@p2322.nsk.ne.jp Author Affiliations The Department of Internal Medicine, Toyama City Hospital, Toyama, Japan
Respiratory Medicine, Cellular Transplantation Biology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan For all author emails, please log on. Cough 2010, 6:7 doi:10.1186/1745-9974-6-7 The electronic version of this article is the complete one and can be found online at: http://www.coughjournal.com/content/6/1/7 Receive 7 July 2009 d: Accepte 9 August d: 2010 Publishe 9 August d: 2010 2010 Ishiura et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
Sinobronchial syndrome is a cause of chronic productive cough. Inflammatory mediators are involved in the pathophysiology of chronic productive cough. Accumulating evidences indicate that cyclooxygenase (COX)-2, one of the inducible isoforms of COX, is a key element in the pathophysiological process of a number of inflammatory disorders. However, little is known about the role of COX-2 in chronic productive cough in patients with sinobronchial syndrome known as neutrophilic bronchial inflammation.
Methods
The effect of etodolac, a potent COX-2 inhibitor, on cough response to inhaled capsaicin was examined in 15 patients with sinobronchial syndrome in a randomized, placebo-controlled cross-over study. Capsaicin cough threshold, defined as the lowest concentration of capsaicin eliciting five or more coughs, was measured as an index of airway cough reflex sensitivity.
Results
The cough threshold was significantly (p < 0.03) increased after two-week
treatment with etodolac (200 mg twice a day orally) compared with placebo [37.5 (GSEM 1.3) vs. 27.2 (GSEM 1.3) M].
Conclusions
These findings indicate that COX-2 may be a possible modulator augmenting airway cough reflex sensitivity in patients with sinobronchial syndrome.
Background
Chronic productive cough is one of the most common symptoms in patients with sinobronchial syndrome, a common chronic bronchial disorder, which is defined as a coexisting chronic sinusitis and nonspecific chronic neutrophilic inflammation of the lower airways presenting with expectoration (e.g. chronic bronchitis, diffuse bronchiectasis and diffuse panbronchiolitis [1]). Although clinical efficacy for low-dose and long-term erythromycin therapy (EM therapy) has been established in patients with sinobronchial syndrome [2,3], our previous study has shown that 3-6 months are required to improve the cough, sputum and other symptoms [3]. So, it is important to clarify the mechanisms of chronic productive cough to improve social activity in patients suffering sinobronchial syndrome. Previous studies [2-5] implied the involvement of inflammatory mediators in sinobronchial syndrome, however, exact mechanisms underlying cough in this disorder has been remained obscure [3]. Cyclooxygenase (COX) is an essential enzyme in the pathway of prostaglandin formation from arachidonic acid. The previous studies [6,7] have revealed the existence of two isoforms of COX, namely COX-1 and COX-2, with similar molecular weights. COX-1 is a constituent of healthy cells and is expressed under normal conditions. On the other hand, COX-2 is highly inducible by a number of stimuli including cytokines and is associated with inflammation. It has been suggested that the induction and regulation of COX-2 may be key elements in the pathophysiological process of a number of inflammation [8]. These findings imply the role of COX-2 in controlling cough reflex sensitivity in sinobronchial syndrome, because cough is one of the major symptoms in this disorder. Our previous study showed that non-specific COX inhibitor, indomethacin, could modulate airway cough reflex sensitivity to inhaled capsaicin [9]. Therefore, we conducted this study in patients with sinobronchial syndrome, using etodolac, proven as a potent COX-2 inhibitor [10,11].
Methods
Subjects
Fifteen patients with stable sinobronchial syndrome (5 males and 10 females) with a mean age of 71.6 1.3 ( SEM) (range 55-79) yrs participated in this study. All patients were lifetime nonsmokers or exsmokers without exceeding 10 pack-years to exclude patient with COPD or smoking-induced bronchitis and with no history of viral infection for at least 4 weeks prior to the study. Informed consent was obtained from all subjects. This study was approved by the Ethics Committee of our hospital.
Sinobronchial syndrome is a common chronic bronchial disorder in Japan, which is not related to smoking. We provide some details, as it is not recognized as a diagnostic category by the ATS. Sinobronchial syndrome is defined as a coexisting chronic sinusitis and nonspecific chronic neutrophilic inflammation of the lower airways presenting with expectoration (e.g. chronic bronchitis, diffuse bronchiectasis and diffuse panbronchiolitis [1]). Suzaki et al. [12] reported that the sinobronchial syndrome was found in 10% of 309 patients with chronic sinusitis and in 55% of 74 patients with chronic lower respiratory tract infectious diseases. They suggested that there is a gene controlling the susceptibility to sinobronchial syndrome, especially diffuse panbronchiolitis, which is significantly associated with human leukocyte antigen (HLA)-BW54; this is found specifically in Japanese and not in Caucasians. The obstructive form of sinobronchial syndrome is known as "diffuse panbronchiolitis" [1]. Recognition of the sinobronchial syndrome is very important in Japan because long-term, low dose erythromycin therapy is specifically effective [2,3], as inhaled steroid therapy for bronchial asthma. In our patients, diagnosis of the sinobronchial syndrome was based on the following criteria: 1) productive cough on most days for at least 3 months for 2 consecutive years, 2) chronic sinusitis diagnosed based on symptoms (postnasal drip, nasal discharge and nasal obstruction), physical examinations and plain roentgenogram as indicated by opacities or airfluid levels of one or more paranasal sinuses, 3) no history suggesting to the attending physician that they had bronchial asthma, 4) no history of wheezing syndrome, and 5) no significant emphysema documented by chest computed tomographic scan. Each studied patient did not have perennial or vasomotor rhinitis. They were taking low-dose erythromycin and mucolytic agents, such as carbocysteine and ambroxol, however, not theophylline, 2-adrenoceptor stimulants, or glucocorticosteroids. This study was carried out when their symptoms were mild and stable.
Study protocol
The concomitant medication was stopped at 9.00 p.m. on the previous day to allow a washout time of 12 h or more before the measurement of cough threshold to inhaled capsaicin at 10.00 a.m. on each test day. Each patient attended 4 times separated by 2 weeks, at the same time each day. Control measurement of capsaicin cough threshold was carried out before the first treatment. After two weeks as wash out period, treatment with etodolac and placebo was performed in a randomized, cross-over fashion, putting a washout period of 2 weeks between the treatments. Etodolac tablet (200 mg) or its placebo was taken orally twice a day for 14 days and at 8.00 a.m. on the test day. FEV1 was measured on a dry wedge spirometer (Chestac 11, Chest Co., Ltd., Tokyo, Japan) before capsaicin challenge to assess the bronchoactive effect of the treatment regimens.
Data analysis
Capsaicin cough threshold values were expressed as geometric mean with geometric standard error of the mean (GSEM). Forced vital capacity (FVC) and FEV1 were shown as arithmetic mean values SEM. The cough threshold, the FVC and the FEV1 values were compared between each pair of the four test periods (run-in, placebo treatment, wash out and etodolac treatment) by the Wilcoxon signed-ranks test. Data are transformed to logarithmic values for cough threshold at this test. A p-value of less than 0.05 was taken as significant.
Results
Cough threshold to inhaled capsaicin before each treatment (run-in and washout period) and after treatment with etodolac and placebo are shown in figure 1. Geometric mean values for the cough threshold were 25.9 (GSEM 1.4) M in run-in period, 25.9 (GSEM 1.4) M in washout period, 27.2 (GSEM 1.3) M after placebo treatment and 37.5 (GSEM 1.3) M after etodolac treatment. The cough threshold after the etodolac treatment was significantly greater than the value after run-in period, wash out period and the placebo treatment (p < 0.03). FVC or FEV1 value Though cough is an important protective mechanism for the cleaning of the excessive mucus production [16], chronic cough can be a difficult clinical problem for physicians interfering with patient's quality of life through loss of sleep, interruption of work and social embarrassment. However, mechanism correlating to the cough reflex sensitivity in sinobronchial syndrome remains unclear. Previous investigators demonstrated the efficacy of EM therapy for chronic bronchitic disorders; sinobronchial syndrome and diffuse panbronchiolitis, which is recognized as a severe obstructive form of sinobronchial syndrome [2,3]. EM therapy has excellent effect through the improvement of pulmonary inflammation by reducing the intrapulmonary chemotactic gradient or the ability of the neutrophils to respond to chemotactic factors, ultimately reducing the migration of neutrophils to inflammatory
sites [2,3,17], but at least eight weeks are required to improve the symptoms including chronic productive cough [2,3]. We also failed to improve cough reflex sensitivity to inhaled capsaicin by four-week treatment of clarithromycin, another form of long term therapy for this disorder [18]. Thus it is important to clarify the potential mechanisms of chronic productive cough in patients suffering from sinobronchial syndrome to improve their symptoms more early. COX is the key enzyme in the pathway of prostaglandin formation consisting of at least two isoforms, namely COX-1 and COX-2 [6,7]. COX1 is constitutively expressed in most tissues, and maintains homeostasis of various physiologic functions. COX-2 is, with some exceptions, not generally found in healthy tissues, but its expression is markedly induced in inflammation. It can be induced by various stimuli, including inflammatory cytokines, resulting in further production of inflammatory substances such as prostanoids [6,7]. Previous study suggested that the induction and regulation of COX-2 may be key elements in the pathophysiological process of a number of inflammations [8]. We showed the modulating role of thromboxane, the family of metabolites resulting from enzymes possessing COX activity [19]. We also showed that non selective COX inhibitor, indomethacin, can modulate airway cough reflex sensitivity to inhaled capsaicin [9]. Recently, we conducted another study in patients with bronchial asthma [20], and showed the role of COX-2 for handling cough reflex sensitivity in asthmatic airway with chronic eosinophilic bronchial inflammation. We, therefore, conducted this study using etodolac with potent affinity for the COX-2 enzyme over the COX-1 enzyme, compared with that of celecoxib [10,11]. Unfortunately, we did not evaluate cough symptom scores and C2, but we clearly showed the beneficial effect of two-week treatment with etodolac for cough reflex sensitivity to inhaled capsaicin. So we can consider that COX-2 plays some roles in controlling cough reflex sensitivity in bronchitic airway with chronic neutrophilic bronchial inflammation, not only in asthmatic airway with chronic eosinophilic bronchial inflammation [20]. The precise mechanisms for modulating role of COX-2 in the pathophysiology of cough reflex remains unknown since we did not measure arachidonic metabolites in this study. Possible mechanism is that decreased sputum production caused by COX-2 inhibition may affect our result as shown in previous study [5]. Recently, Kamei and their colleagues [21] reported the effect of COX-2 inhibition in cough reflex sensitivity in guinea pigs and suggested that the inhibition of substance P release might result in the regulation of endogenous prostaglandins by COX-2 inhibitor on the capsaicin-sensitive sensory C-fibers. Therefore we can consider that COX-2, generated in chronic bronchitic airway known as neutrophilic inflammation [2-5,17], modulates airway cough reflex sensitivity through similar mechanisms. Another crucial problem in clinical practice remains about the cardiovascular risks of rofecoxib, celecoxib and valdecoxib in the placebocontrolled trials [22,23], however succeeding study did not found an elevated cardiovascular risk with etodolac [24]. Therefore we hope that adverse reactions in long-term should be clarified in future studies.
Conclusions
In conclusion, the present study clearly showed that two week treatment with a potent COX-2 inhibitor, etodolac, attenuated cough reflex sensitivity to inhaled capsaicin in patients with sinobronchial syndrome. This is the first report indicating the modulating role of COX-2 in airway cough reflex sensitivity of bronchitic airway known as chronic neutrophilic inflammation. Further studies are required for elucidating the inflammatory process in bronchitic airways succeeding COX-2 induction.
Abbreviations
ATS: American Thoracic Society; COX: cyclooxygenase; EM therapy: lowdose and long-term erythromycin therapy; FEV1: forced expiratory volume in one second; FVC: forced vital capacity; GSEM: geometric standard error of the mean; HLA: human leukocyte antigen; NSAIDS: nonsteroidal anti-inflammatory drugs.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
YI recruited the subjects, performed the data collecting and draft the manuscript. MF conceived the study, contributed to its design, data acquisition, data interpretation, and review and correction of the manuscript. HY performed the statistical analysis and data interpretation. NO participated in data acquisition. SM contributed to data interpretation. All authors have given final approval of the version to be published.
References
Homma H, Yamanaka A, Tanimoto S, Tamura M, Chijimatsu Y, Kira S, Izumi T: Diffuse panbronchiolitis; a disease of the transitional zone of the lung. Chest 1983, 83:63-69. PubMed Abstract | Publisher Full Text Kudoh S, Azuma A, Yamamoto M, Izumi T, Ando M: Improvement of survival in patients with diffuse panbronchiolitis treated with low-dose erythromycin. Am J Respir Crit Care Med 1998, 157:1829-1832. PubMed Abstract | Publisher Full Text Ishiura Y, Fujimura M, Saito M, Shibata K, Nomura M, Nakatsumi Y, Matsuda T: Additive effect of continuous low-dose ofloxacin on erythromycin therapy for sinobronchial syndrome. Respir Med 1995, 89:677-684. PubMed Abstract | Publisher Full Text Kurashima K, Fujimura M, Hoyano Y, Takemura K, Matsuda T: Effect of thromboxane A2 synthetase inhibitor, OKY-046, on sputum in chronic bronchitis and diffuse panbronchiolitis. Eur Respir J 1995, 8:1705-1711. PubMed Abstract | Publisher Full Text Tamaoki J, Chiyotani A, Kobayashi K, Sakai N, Kanemura T, Takizawa T: Effect of indomethacin on bronchorrhea in patients with chronic bronchitis, diffuse panbronchiolitis, or bronchiectasis. Am Rev Respir Dis 1992, 145:548-552. PubMed Abstract
Samuelsson B: An elucidation of the arachidonic acid cascade. Discovery of prostaglandins, thromboxane and leukotrienes. Drugs 1987, 33:2-9. PubMed Abstract | Publisher Full Text Smith WL, Dewitt DL: Prostaglandin endoperoxide H synthases-1 and -2. Adv Immunol 1996, 62:167-215. PubMed Abstract | Publisher Full Text Belvisi MG, Saunders MA, Haddad el-B, Hirst SJ, Yacoub MH, Barnes PJ, Mitchell JA: Induction of cyclo-oxygenase-2 by cytokines in human cultured airway smooth muscle cells: novel inflammatory role of this cell type. Br J Pharmacol 1997, 120:910-916. PubMed Abstract | Publisher Full Text | PubMed Central Full Text Fujimura M, Kamio Y, Kasahara K, Bando T, Hashimoto T, Matsuda T: Prostanoids and cough response to capsaicin in asthma and chronic bronchitis. Eur Respir J 1995, 8:1499-1505. PubMed Abstract | Publisher Full Text Warner TD, Mitchell JA: Cyclooxygenases: new forms, new inhibitors, and lessons from the clinic. FASEB J 2004, 18:790-804. PubMed Abstract | Publisher Full Text Warner TD, Giuliano F, Vojnovic I, Bukasa A, Mitchell JA, Vane JR: Nonsteroid drug selectivities for cyclo-oxygenase-1 rather than cyclo-oxygenase-2 are associated with human gastrointestinal toxicity: a full in vitro analysis. Proc Natl Acad Sci USA 1999, 96:7563-7568. PubMed Abstract | Publisher Full Text | PubMed Central Full Text Suzaki H, Ichimura K, Kudoh S, Sugiyama Y, Symposium MaedaH II: Sinobronchial syndrome and its related subjects: clinical observation in sinobronchial syndrome from a viewpoint of otorhinolaryngology. J Jap Bronchoesophagol Soc 1987, 38:181-186. Fujimura M, Sakamoto S, Kamio Y, Matsuda T: Effects of methacholine-induced bronchoconstriction and procaterolinduced bronchodilation on cough receptor sensitivity to inhaled capsaicin and tartaric acid. Thorax 1992, 47:441445. PubMed Abstract | Publisher Full Text | PubMed Central Full Text Bresalier R, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, Lines C, Riddell R, Morton D, Lanas A, Konstam MA, Baron JA: Adenomatous Polyp Prevention on Vioxx (APPROVe) Trial Investigators: Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med 2005, 352:1092-1103. PubMed Abstract | Publisher Full Text Psaty BM, Furberg CD: COX-2 inhibitors - Lessons in drug safety. N Engl J Med 2005, 352:1133-1135. PubMed Abstract | Publisher Full Text McEwan JR, Choudry NB, Fuller RW: The effect of sulindac on the abnormal cough reflex associated with dry cough. J Pharmacol Exp Exp Ther 1991, 255:161-164. Kadota I, Sakito O, Kohno S, Sawa H, Murae H, Oda H, Kawakami K, Fukushima K, Hiratani K, Hara K: A mechanism of erythromycin treatment in patients with diffuse panbronchiolitis. Am Rev
Respir Dis 1993, 147:153-159. PubMed Abstract Ogawa H, Fujimura M, Amaike S, Matsumoto Y, Matsuda T: Effect of clarithromycin on cough receptor sensitivity to capsaicin in patients with sinobronchial syndrome. J Jap Bronchology 1996, 18:543-547. Ishiura Y, Fujimura M, Yamamori C, Nobata K, Myou S, Kurashima K, Takegoshi T: Thromboxane antagonism and cough in chronic bronchitis. Ann Med 2003, 35:135-139. PubMed Abstract | Publisher Full Text Ishiura Y, Fujimura M, Yamamoto H, Ishiguro T, Ohkura N, Myou S: COX-2 inhibition attenuates cough reflex sensitivity to inhaled capsaicin in patients with asthma. J Investig Allergol Clin Immunol 2009, 19:370-374. PubMed Abstract Kamei J, Matsunawa Y, Saitoh A: Antitussive effect of NS-398, a selective cyclooxygenase-2 inhibitor, in guinea pigs. Eur J Pharmacol 2004, 497:233-239. PubMed Abstract | Publisher Full Text Bresalier R, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, Lines C, Riddell R, Morton D, Lanas A, Konstam MA, Baron JA: Adenomatous Polyp Prevention on Vioxx (APPROVe) Trial Investigators: Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med 2005, 352:1092-1103. PubMed Abstract | Publisher Full Text Psaty BM, Furberg CD: COX-2 inhibitors - Lessons in drug safety. N Engl J Med 2005, 352:1133-1135. PubMed Abstract | Publisher Full Text Motsko SP, Rascati KL, Busti AJ, Wilson JP, Barner JC, Lawson KA, Worchel J: Temporal relationship between use of NSAIDs, including selective COX-2 inhibitors, and cardiovascular risk. Drug Safety 2006, 29:621-632. PubMed Abstract | Publisher Full Text
Sinobronchial syndrome
Department of Pediatric Otorhinolaryngology, Warsaw Medical School, Poland Head: Prof. Mieczysaw Chmielik M.D.
Summary Sinobronchial syndrome occurs in some cases of paranasal sinus disease. The clinical picture of sinobronchial syndrome is based on the evacuation of exudate from sinuses to nasopharynx, larynx, and to the lower respiratory tract. Causes leading to the development of this condition are discussed. The authors, based on their own experience and data from literature, present the pathogenesis, diagnostic methods, and treatment of sinobronchial syndrome. Key words: sinobronchial syndrome.
Polecane ksiki z ksigarni medycznej BORGIS: Otorynolaryngologia dla Chirurgiczna rehabilitacja gosu
Nasofiberosk
po cakowitej laryngektomii
INTRODUCTION
In Nelsons Texbook of Pediatrics we find the following definition of sinobronchial syndrome; The term sinobronchitis is occasionally used to designate the relationship between sinus and lower respiratory tract symptoms; children with this condition may have reactive airways, cystic fibrosis, immunodeficiency, or dyskinetic cilia as the underlying disease (2). The term sinobronchial syndrome is occasionally used in current literature. Symptoms of sinobronchial syndrome are usually described as the symptoms of chronic sinusitis. But chronic sinusitis and sinobronchial syndrome are not the same disease. Jan Danielewicz was one of the first Polish writers who pointed out that sinobronchial syndrome was a separate form of sinusitis in children. Inflammation processes taking place in sinuses in children can not be included among chronic diseases, in his opinion, in spite of the fact that these processes usually return during a few succeeding years in autumn and winter. Sinus mucous membrane changes developing in children suffering from sinusitis are reversible, and the disease retreats spontaneously during pubescence. These cases, on Jan Danielewiczs theory, are said to be against the chronic character of sinusitis in the pediatric group (4). The typical clinical view of sinobronchial syndrome has promped many authors to propose the hypothesis that abnormal defensive mechanism of respiratory tract mucous membrane, and the incomplete response of the immunological system in children, are underlying pathological mechanisms.
PATHOLOGY
The normal physiological function of the paranasal sinuses depends on 3 main factors: structure and function of mucous membrane, mucus drainage, and ventilation. Mucociliary transport plays the main role in the local defensive mechanism of mucous membrane. The predominant immunoglobulin in mucous is IgA, produced by plasma cells in the submucosa. IgG penetrates from blood vessels by a passive diffusion mechanism (8). The immunological system achieves complete efficiency in children at 10-12 years old. That is why infections of the respiratory tract in children follow a different course than in adults. During the first years of life a relative immunodeficiency is observed in children compared to adults. Levels of IgG reach adult values at approximately 3 years of age and IgA levels at 7 to 8 years. Children also have 6 to 7 viral infections per year. Frequent viral infections may influence the immunological response and lead to an abnormal immunological reaction. Recurrent viral infection could also impair mucociliary transport (5). In some children with sinobronchial syndrome, adenoid hypertrophy or septal deviation are diagnosed (10). These pathological circumstances impair the normal ventilation of the sinuses and lead to prolongation of the inflammation process. The pathological process of sinobronchial syndrome, regardless of the
initiating event or predisposing conditions, leads to a local inflammation process. Inflammatory cells and their mediators become resident in the submucosa. Inflammation alters the ciliated epithelium and composition of mucus. Mucociliary transport dysfunction causes an impairment of sinus drainage, with the resultant pooling of secretions. Secretions filling sinuses may become infected, leading to persistence of inflammation (2). Studies of immunological processes in recurrent sinusitis in children, carried out in recent years, confirm the hypothesis about an abnormal immunological response. In a group of children with sinobronchial syndrome, immunoglobulin A level in serum was found to be reduced to the lower limit of the norm for the patients age (9). Shapiro and others showed abnormal results of immunological studies, in 34 of 61 children with chronic sinusitis. Depressed IgG levels and poor response to pneumococcal and Haemophilus influenzae antigens were found. Twentytwo patients had positive prick tests. These findings, sugges an allergic component in the pathogenesis of sinusitis in this group of children (11). Baroody and coworkers compared the structure of mucosa from the sinuses of children suffering from chronic sinusitis with that obtained from the sphenoid sinuses of healthy adults. There were significantly more eosinophils in the tissues of children with chronic sinusitis. Allergy status did not affect the degree of tissue eosinophilia (1). Driscoll and others, in an investigation carried out in the same way, showed significantly more CD4+ cells in the sinus mucosa of children with chronic sinusitis than in normal sinus mucosa. The number of CD8+ cells was not significantly different in either group. This contrasts with published results on adults with chronic sinusitis, in whom CD8+cells predominate in nasal polyps and submucosa. Authors suggest that this possibly reflects a difference in the immunologic response of children and adults (5). Predicted these studies explain only a few immunological mechanisms taking place in sinusitis in children. Further investigations should be carried out to elucitade the immunological processes.
DIFFERENTIATION
Sinobronchial syndrome should be differentiated from bronchitis and
pneumonitis. In bronchitis and pneumonitis a cough is steady symptom, and there are typical auscultatory signs. Other causes of cough are: - cough variant asthma (S. Corrao), - cough due to foreign body in airways, - drug-induced cough, - psychogenic cough, - other disorders, which stimulate a cough receptor of afferen neurones in the cough reflex arc.
DIAGNOSIS
Diagnosis of sinobronchial syndrome is based on typical clinical symptoms (4). Sometimes we need to take X-rays of the sinuses and chest to confirm the diagnosis. In patients with frequent recurrences of sinusitis and bronchitis or pneumonitis it is necessary to exclude diseases which may appear as sinobronchial syndrome: mucoviscidosis, immotile cilia syndrome and congenital or acquired immunodeficiency. For this purpose we need to carry out diagnostic examinations such as: - bacteriological examination of excudate from sinuses or bronchi, - X-ray examination, CT scans, - immunological tests, - examination of structure and function of cilia, - tests to exclude mucoviscidosis. In cases where immunodeficiency, immotile cilia syndrome and mucoviscidosis have been excluded, we can accept that sinobronchial syndrome is one form of sinusitis in children, connected with abnormal defensive mechanisms in the mucous membrane and in incomplete response of the immunological system as the underlying pathology.
TREATMENT
Treatment of sinobronchial syndrome includes a topical or oral application of an immunomodulating preparation. Mucolytics are also recommended. During acute exacerbation of sinobronchial syndrome symptoms antibiotics should be administrated for 10 to 14 days. In cases of a patient with sinobronchial syndrome, and with concominant adenoid hypertrophy or nasal septal deviation, operative treatment should be taken into concideration.
Polecane ksiki z ksigarni medycznej BORGIS: Otorynolaryngologia dla studentw medycyny i stomatologii
Pimiennictwo
1. Baroody F.M.et al.: Eosinophilia in Chronic Childhood Sinusitis. Arch. Otolarygol. Head. Neck. Surg. 1995, 121:1396-1402. 2. Behrman R.E.: Podrcznik Pediatrii. Nelson, pod red. M. Sieniawskiej, Wyd. Naukowe PWN, Warszawa 1996, str 875. 3. Chazan R.: Zakaenia ukadu oddechowego. a-medica press, Warszawa 1998, 5761. 4. Danielewicz J.: Klinika i patogeneza zespou zatokowo-oskrzelowego u dzieci. Ped. Pol. 1981, 61:11-12, 1311-15. 5. Driscoll P.V. et al.: CD4 Lymphocytes Are
Increased in the Sinus Mucosa of Children With Chronic Sinusitis. Arch. Otolaryngol. Head. Neck. Surg. 1996, 122:1071-76. 6.Gul E. et al.: Kilka uwag na temat zapale zatok przynosowych u dzieci na podstawie analizy materiau Oddziau Laryngologii Wojewdzkiego Szpitala we Wrocawiu z lat 1987-1992. Otolaryng. Pol. 1994, 48, supl., 136139. 7. Kossowska E.: Podsumowanie obrad pierwszego dnia kongresu Otolaryng. Pol. supl., I Europejski Kongres Otolaryngologii Pediatrycznej 5-7.09.1979 Warszawa, 76. 8. Krzeski A., Janczewski G.: Choroby nosa i zatok przynosowych. Sanmedia Warszawa 1997, 4849. 9. akota A. i wsp.: Poziom magnezu w surowicy i jego wpyw na leczenie zespou zatokowooskrzelowego u dzieci. Otolaryng. Pol. 1994, 48, supl. 18, 125-132. 10. Nowak W. et al.: Zesp zatokowooskrzelowy u dzieci leczonych w Szpitalu Miejskim w Bytomiu w latach 1976-1978. Otolaryng. Pol. supl. I Europejski Kongres Otolaryngologii Pediatrycznej 57.09.1979 Warszawa, 5051. 11. Shapiro G.G. et al.: Immunological Defect in Patients With Refractory Sinusitis Pediatrics 1991, 87, 3:311-16.