期刊论文详细信息
Respiratory Research
The prevalence of increased serum IgE and Aspergillus sensitization in patients with COPD and their association with symptoms and lung function
Yongchang Sun1  Xiaofang Liu1  Jianmin Jin1 
[1] Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China
关键词: Aspergillus;    Chronic obstructive pulmonary disease;    Allergy;    Immunoglobulin E;   
Others  :  1137248
DOI  :  10.1186/s12931-014-0130-1
 received in 2014-07-18, accepted in 2014-10-14,  发布年份 2014
PDF
【 摘 要 】

Background

Allergy and Aspergillus hypersensitivity (AH) were shown to be associated with severe symptoms or worse lung function in COPD patients. The prevalence of elevated total IgE (T-IgE) and its association with clinical symptoms and lung function in COPD have not been studied. The prevalence of AH and its correlation with clinical characteristics in a COPD cohort of larger sample size is also lacking.

Methods

273 patients with COPD were evaluated by respiratory symptoms, blood test, chest HRCT, lung function, serum detection of T-IgE and Aspergillus specific IgE. Patients with T-IgE ≥ 1000 KU/L were further investigated for allergic bronchopulmonary aspergillosis (ABPA).

Results

The prevalence of elevated T-IgE and AH in patients with COPD was 47.3% and 15.0%, respectively. Eight patients (2.9%) met the diagnostic criteria for ABPA. Compared with the normal T-IgE group, patients with elevated T-IgE had a longer history of dyspnea (p < 0.01), an earlier onset of dyspnea after chronic cough/expectoration (p < 0.01), and were more likely to wheeze (p < 0.01). They also showed worse lung functions and more severe GOLD staging (p < 0.01). Analysis of the clinical data in male patients with smoking as the risk factor showed the same results. To evaluate the clinical characteristics of COPD with AH, patients with elevated T-IgE were further divided into subgroups with and without AH. When compared with the normal T-IgE group, both the two subgroups showed longer history of dyspnea (p < 0.01), an earlier onset of dyspnea (p < 0.01) and a worse status of lung function (p < 0.05). Correlation analysis demonstrated that T-IgE was correlated positively with the time length of dyspnea (r = 0.401, p < 0.001), and the ratio of duration of dyspnea to that of chronic cough/expectoration (r = 0.59, p < 0.001), but negatively with FEV1/FVC% (r = −0.194, p = 0.001), and FEV1%predicted (r = −0.219, p < 0.001).

Conclusions

There was a high prevalence of elevated serum T-IgE and AH in patients with COPD. Serum T-IgE level was correlated with symptoms such as dyspnea and impairment of lung function. Allergens other than Aspergillus may have similar effects on disease expression or progression of COPD.

【 授权许可】

   
2014 Jin et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150315154716774.pdf 671KB PDF download
Figure 4. 37KB Image download
Figure 3. 34KB Image download
Figure 2. 24KB Image download
Figure 1. 57KB Image download
【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

【 参考文献 】
  • [1]Han MK, Agusti A, Calverley PM, Celli BR, Criner G, Curtis JL, Fabbri LM, Goldin JG, Jones PW, Macnee W, Make BJ, Rabe KF, Rennard SI, Sciurba FC, Silverman EK, Vestbo J, Washko GR, Wouters EF, Martinez FJ: Chronic obstructive pulmonary disease phenotypes: the future of COPD. Am J Respir Crit Care Med 2010, 182:598-604.
  • [2]Jamieson DB, Matsui EC, Belli A, McCormack MC, Peng E, Pierre-Louis S, Curtin-Brosnan J, Breysse PN, Diette GB, Hansel NN: Effects of allergic phenotype on respiratory symptoms and exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2013, 188:187-192.
  • [3]Agarwal R, Agarwal AN, Gupta D, Jindal SK: Aspergillus hypersensitivity and allergic bronchopulmonary aspergillosis in patients with bronchial asthma: systematic review and meta-analysis. Int J Tuberc Lung Dis 2009, 13:936-944.
  • [4]Agarwal R, Hazarika B, Gupta D, Aggarwal AN, Chakrabarti A, Jindal SK: Aspergillus hypersensitivity in patients with chronic obstructive pulmonary disease: COPD as a risk factor for ABPA? Med Mycol 2010, 48:988-994.
  • [5]Bafadhel M, McKenna S, Agbetile J, Fairs A, Desai D, Mistry V, Morley JP, Pancholi M, Pavord ID, Wardlaw AJ, Pashley CH, Brightling CE: Aspergillus fumigatus during stable state and exacerbations of COPD. Eur Respir J 2014, 43:64-71.
  • [6]Hakonarson H, Carter C, Kim C, Grunstein MM: Altered expression and action of the low- affinity IgE receptor FcepsilonRII (CD23) in asthmatic airway smooth muscle. J Allergy Clin Immunol 1999, 104:575-584.
  • [7]Redhu NS, Saleh A, Lee HC, Halayko AJ, Ziegler SF, Gounni AS: IgE induces transcriptional regulation of thymic stromal lymphopoietin in human airway smooth muscle cells. J Allergy Clin Immunol 2011, 128:892-896.
  • [8]Redhu NS, Shan L, Al-Subait D, Ashdown HL, Movassagh H, Lamkhioued B, Gounni AS: IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways. Allergy Asthma Clin Immunol 2013, 9:41-50. BioMed Central Full Text
  • [9]Roth M, Zhong J, Zumkeller C, S’ng CT, Goulet S, Tamm M: The role of IgE-receptors in IgE-dependent airway smooth muscle cell remodelling. PLoS One 2013, 8:e56015.
  • [10]Celli BR, Barnes PJ: Exacerbations of chronic obstructive pulmonary disease. Eur Respir J 2007, 29:1224-1238.
  • [11]Nishimurak K, Izumi T, Tsukino M, Oga T: Dyspnea is a better predictor of 5-year survival than airway obstruction in patients with COPD. Chest 2002, 121:1434-1440.
  • [12]Agarwal R, Maskey D, Aggarwal AN, Saikia B, Garg M, Gupta D, Chakrabarti A: Diagnostic performance of various tests and criteria employed in allergic bronchopulmonary aspergillosis: a latent class analysis. PLoS One 2013, 8:e61105.
  • [13]Schwartz HJ, Greenberger PA: The prevalence of allergic bronchopulmonary aspergillosis in patients with asthma, determined by serologic and radiologic criteria in patients at risk. J Lab Clin Med 1991, 117:138-142.
  • [14]Mahdavinia M, Grammer LC: Management of allergic bronchopulmonary aspergillosis: a review and update. Ther Adv Respir Dis 2012, 6:173-187.
  • [15]Gottlieb DJ, Sparrow D, O’Connor GT, Weiss ST: Skin test reactivity to common aeroallergens and decline of lung function: the Normative Aging Study. Am J Respir Crit Care Med 1996, 153:561-566.
  • [16]Masuko H, Sakamoto T, Kaneko Y, Iijima H, Naito T, Noguchi E, Hirota T, Tamari M, Hizawa N: Lower FEV1 in non-COPD, nonasthmatic subjects: association with smoking, annual decline in FEV1, total IgE levels, and TSLP genotypes. Int J Chron Obstruct Pulmon Dis 2011, 6:181-189.
  • [17]Frew AJ, Kennedy SM, Chan-Yeung M: Methacholine responsiveness, smoking, and atopy as risk factors for accelerated FEV1 decline in male working populations. Am Rev Respir Dis 1992, 146:878-883.
  • [18]Tashkin DP, Altose MD, Connett JE, Kanner RE, Lee WW, Wise RA: Methacholine predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. The Lung Health Study Research Group. Am J Respir Crit Care Med 1996, 153:1802-1811.
  • [19]Agarwal R, Chakrabarti A, Shah A, Gupta D, Meis JF, Guleria R, Moss R, Denning DW: Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy 2013, 43:850-873.
  • [20]O’Connor GT, Sparrow D, Weiss ST: The role of allergy and nonspecific airway hyperresponsiveness in the pathogenesis of chronic obstructive pulmonary disease. Am Rev Respir Dis 1989, 140:225-252.
  • [21]Agarwal R, Chakrabarti A: Allergic bronchopulmonary aspergillosis in asthma: epidemiological, clinical and therapeutic issues. Future Microbiol 2013, 8:1463-1474.
  • [22]Chakrabarti A, Sethi S, Raman DS, Behera D: Eight-year study of allergic bronchopulmonary aspergillosis in an Indian teaching hospital. Mycoses 2002, 45:295-299.
  • [23]Newby C, Agbetile J, Hargadon B, Monteiro W, Green R, Pavord I, Brightling C, Siddiqui S: Lung function decline and variable airway inflammatory pattern: Longitudinal analysis of severe asthma.J Allergy Clin Immunol 2014, in press.
  • [24][http://dx.doi.org/10.1155/2013/824781] webcite Zedan M, Attin G, Zedan MM, Osman A, Abo-Elkheir N, Maysara N, Barakat T, Gamil N: Clinical asthma phenotypes and therapeutic responses.ISRN Pediatr 2013, 824781.
  • [25]Bourdin A, Serre I, Flamme H, Vic P, Neveu D, Aubas P, Godard P, Chanez P: Can endobronchial biopsy analysis be recommended to discriminate between asthma and COPD in routine practice? Thorax 2004, 59:488-493.
  • [26]Vroling AB, Duinsbergen D, Fokken WJ, van Drunen CM: Allergen induced gene expression of airway epithelial cells shows a possible role for TNF-alpha. Allergy 2007, 62:1310-1319.
  • [27]Tsai JJ, Liao EC, Hsu JY, Lee WJ, Lai YK: The differences of eosinophil- and neutrophil-related inflammation in elderly allergic and non-allergic chronic obstructive pulmonary disease. J Asthma 2010, 47:1040-1044.
  • [28]Liu XF, Sun YC, Jin JM, Li R, Liu Y: Allergic bronchopulmonary aspergillosis in patients with chronic obstructive pulmonary disease: report of 3 cases. Zhonghua Jie He He Hu Xi Za Zhi 2013, 36:741-745.
  • [29]Mir E, Shah A: Allergic bronchopulmonary aspergillosis in a patient with chronic obstructive pulmonary disease. Prim Care Respir J 2012, 21:111-114.
  • [30]Agarwal R, Srinivas R, Jindal SK: Allergic bronchopulmonary aspergillosis complicating chronic obstructive pulmonary disease. Mycoses 2007, 51:83-85.
  • [31]Simpson JL, Powell H, Baines KJ, Milne D, Coxson HO, Hansbro PM, Gibson PG: The effect of azithromycin in adults with stable neutrophilic COPD: a double blind randomised, placebo controlled trial. PLoS One 2014, 9:e105609.
  • [32]Bade G, Khan MA, Srivastava AK, Khare P, Solaiappan KK, Guleria R, Palaniyar N, Talwar A: Serum cytokine profiling and enrichment analysis reveal the involvement of immunological and inflammatory pathways in stable patients with chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis 2014, 9:759-773.
  • [33]de Deus CR, Chiarion Sassi F, Davison Mangilli L, Jayanthi SK, Cukier A, Zilberstein B, de Andrade CR F: Swallowing transit times and valleculae residue in stable chronic obstructive pulmonary disease. BMC Pulm Med 2014, 14:62. BioMed Central Full Text
  • [34]Seemungal TAR, Donaldson GC, Bhowmik A, Jeffries DJ, Wedzicha JA: Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000, 161:1608-1613.
  • [35]Donaldson GC, Seemungal TA, Bhowmik A, Wedzicha JA: Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax 2002, 57:847-852.
  • [36]Wouters EF: The burden of COPD in the Netherlands: results from the Confronting COPD survey. Respir Med 2003, 97:S51-S59.
  • [37][http://www.goldcopd.org] webcite Global initiative for chronic obstructive pulmonary disease, globle strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, updated 2014. []
  文献评价指标  
  下载次数:90次 浏览次数:126次