Study of an association between chronic obstructive pulmonary diseases and types 1 and 2 diabetes


Cite item

Full Text

Abstract

Aim. To study an association between multifactorial obstructive pulmonary disease (COPD) and asthma and types 1 and 2 diabetes (T1D and T2D).
Subjects and methods. A multicenter study was conducted in two formed cohorts of patients with bronchopulmonary pathology (n = 616) and diabetes (n = 700). Random sampling, retrospective data collection, by applying a blind approach, as well as questioning and, if need be, diagnosis verification and an additional study were accomplished. Statistical methods were employed to make a cross assessment of the prevalence of the diseases in each cohort as compared to a control group in which population-based values were used.
Results. In the cohort of patients with bronchopulmonary pathology, the prevalence of T2D was considerable in patients with COPD, it was 9.49%, which was greater than the control values (3.0; p < 0.01), more than 2.5 times higher (p < 0.05) than that in asthmatic patients in whom the prevalence was 3.64% and it did not differ from the control group. In COPD concurrent with T2D, the prevalence of diabetes was as high as 16.15% (p < 0.001). At the same time, the prevalence of bronchopulmonary pathology in the T2D cohort being 2.3% for COPD and 1.0% for asthma was lower than the population-based value (p < 0.05), 2.6% and 6.1%, respectively.
It was contrastingly found that T1D was absent in the asthmatic patients and the prevalence of asthma (0.33%) was low in patients with asthma (p < 0.05). In parallel, an association between COPD and T1D could not be traced, by taking into account an age difference and other specific features of a pathological process in these patient groups.
Conclusion. Unlike asthma, COPD, in combination with asthma in particular, is an essential risk factor for T2D. Asthma and T1D mutually exclude each other.

References

  1. Concannon P., Erlich H. A., Julier C. et al. Type 1 diabetes: evidence for susceptibility loci from four genome-wide linkage scans in 1,435 multiplex families. Diabetes 2005; 54 (10): 2995-3001.
  2. Rich S. S., Concannon P., Erlich H. et al. The Type 1 Diabetes Genetics Consortium. Ann. N. Y. Acad. Sci. 2006; 1079: 1-8.
  3. Pauwels R. A., Buist A. S., Ma P. et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: National Heart, Lung, and Blood Institute and World Health Organization Global Initiative for Chronic Obstructive Lung Disease (GOLD): executive summary. Respir. Care 2001; 46: 798-825.
  4. Global Initiative for Chronic Obstructive Lung Disease (GOLD) Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Workshop report. The 2006 reportb is available on www.goldcopd.com. (see also UPDATED 2007).
  5. Global Initiative forAsthma (GINA). Global strategy for asthma management and prevenrtion. 2004. www.ginasthma.org; accessed January. 2007.
  6. Дедов И. И. Сахарный диабет в Российской Федерации: проблемы и пути решения. Сахар. диабет 1998; 1: 4-7.
  7. Majori M., Corradi M., Caminati A. et al. Predominant TH1 cytokine pattern in peripheral blood from subjects with chronic obstructive pulmonary disease. J. Allergy Clin. Immunol. 1999; 103 (3, pt1): 458-462.
  8. Chung K. F. Cytokines in chronic obstructive pulmonary disease. Eur. Respir. J. Suppl. 2001; 34: 50S-59S.
  9. Oudijk E., Lammers J., Koenderman L. et al. Systemic inflammation in chronic obstructive pulmonary disease. Eur. Respir. J. 2003; 22: 5S-13S.
  10. Perng D. W., Wu C. C., Su K. C. et al. Inhaled fluticasone and salmeterol suppress eosinophilic airway inflammation in chronic obstructive pulmonary disease: relations with lung function and bronchodilator reversibility. Lung 2006; 184 (4): 217-222.
  11. Groenewegen K. H., Postma D. S., Hop W. C. et al. Increased systemic inflammation is a risk factor for COPD exacerbations. Chest 2008; 133 (2): 350-357.
  12. Renauld J. C. New insights into the role of cytokines in asthma. J. Clin. Pathol. 2001; 54: 577-589.
  13. Pradhan A. D., Manson J. E., Rifai N. et al. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. J. A. M. A. 2001; 286: 327-334.
  14. Hu F. B., Meigs J. B., Li T. Y. et al. Inflammatory markers and risk of developing type 2 diabetes in women. Diabetes 2004; 53: 693-700.
  15. Wouters E. F. M., Karin H. G., Mieke A. D. et al. Systemic inflammation in chronic obstructive pulmonary disease. The role of exacerbations. Proc. Am. Thorac. Soc. 2007; 4: 626-634.
  16. Dahl M., Vestbo J., Lange P. et al. C-reactive protein as a predictor of prognosis in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2007; 175 (3): 250-255.
  17. Wouters E. F. Chronic obstructive pulmonary disease. 5. Systemic effects of COPD. Thorax 2002; 57: 1067-1070.
  18. Congleton J. The pulmonary cachexia syndrome: aspects of energy balance. Proc. Nutr. Soc. 1999; 58: 321-328.
  19. Mador M. J. Muscle mass, not body weight, predicts outcome in patients with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2002; 166: 787-789.
  20. Schols A. M., Buurman W. A., Staal van den Brekel A. J. et al. Evidence for a relation between metabolic derangements and increased levels of inflammatory mediators in a subgroup of patients with chronic obstructive pulmonary disease. Thorax 1996; 51: 819-824.
  21. Pitsiou G., Kyriazis G., Hatzizisi O. et al. Tumor necrosis factor-alpha serum levels, weight loss and tissue oxygenation in chronic obstructive pulmonary disease. Respir. Med. 2002; 96: 594-598.
  22. Takabatake N., Nakamura H., Abe S. The relationship between chronic hypoxemia and activation of the tumor necrosis factor-alpha system in patients with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2000; 161: 1179-1184.
  23. Hotamisligil G. S., Murray D. L., Choy L. N., Spiegelman B. M. Tumor necrosis factor alpha inhibits signaling from the insulin receptor. Proc. Natl. Acad. Sci. USA 1994; 91: 4854-4858.
  24. Hotamisligil G. S. The role of TNFalpha and TNF receptors in obesity and insulin resistance. J. Intern. Med. 1999; 245: 621-625.
  25. Lazarus R., Sparrow D., Weiss S. T. Baseline ventilatory function predicts the development of higher levels of fasting insulin and fasting insulin resistance index: the Normative Aging Study. Eur. Respir. J. 1998; 123: 641-645.
  26. Engstrom G., Janzon L. Risk of developing diabetes is inversely related to lung function: a population-based cohort study. Diabet. Med. 2002; 19: 167-170.
  27. Rahman I., Gilmour P. S., Jimenez L. A., MacNee W. Oxidative stress and TNF-alpha induce histone acetylation and NF-kappaB/AP-1 activation in alveolar epithelial cells: potential mechanism in gene transcription in lung inflammation. Mol. Cell. Biochem. 2002; 234-235: 239-248.
  28. Rahman I. Oxidative stress, chromatin remodeling and gene transcription in inflammation and chronic lung diseases. J. Biochem. Mol. Biol. 2003: 36: 95-109.
  29. Rosen P., Nawroth P. P., King G. et al. The role of oxidative stress in the onset and progression of diabetes and its complications: a summary of a Congress Series sponsored by UNESCO-MCBN, the American Diabetes Association and the German Diabetes Society. Diabet. Metab. Res. Rev. 2001; 7: 189-212.
  30. Daniel M., Cargo M. Association between smoking, insulin resistance and beta-cell function in a Northwestern First Nation. Diabet. Med. 2004; 21 (2): 188-193.
  31. Hota Y., Yatsuya H., Toyoshima H. et al. Low leptin but high insulin resistance of smokers in Japanese men. Diabet. Res. Clin. Pract. 2008; 81 (3): 358-364.
  32. Измеров Н. Ф., Кузмина Л. П., Попкова А. М., Ханыкина О. В. Состояние протеиназно-ингибиторной системы у больных сахарным диабетом 2-го типа в сочетании с хронической обструктивной болезнью легких. Вестн. РАМН 2006; 3: 15-17.
  33. Sethi S., Maloney J., Crove L. et al. Airway inflammation and bronchial bacterial colonization in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2006; 173 (9): 991-998.
  34. Abusriwil H., Stockley R. A. The interaction of host and pathogen factors in chronic obstructive pulmonary disease exacerbations and their role in tissue damage. Proc. Am. Thorac. Soc. 2007; 4 (8): 611-617.
  35. Blackburn D., Hux J., Mamdani M. Quantification of the risk of corticosteroid-induced diabetes mellitus among the elderly. J. Gen. Intern. Med. 2002; 17: 717-720.
  36. Кобылянский В. И., Бабаджанова Г. Ю., Сунцов Ю. Н. и др. Связь хронических воспалительных заболеваний легких и сахарного диабета. В кн.: XII Национальный конгресс по болезням органов дыхания. Казань; 2007. 59.
  37. Бабаджанова Г. Ю. Бронхиальная астма и сахарный диабет: анализ взаимоотношений двух мультифакториальных заболеваний: Дис. ... д-ра мед. наук. М., 2002.
  38. Renauld J. C. New insights into the role of cytokines in asthma. J. Clin. Pathol. 2001; 54 (8): 577-589.
  39. Шмелев Е. И. Бронхиальная астма в сочетании с хронической обструктивной болезнью легких: стратегические проблемы терапии. Consilium medicum, 2006; 8 (3): 846-851.
  40. Чучалин А. Г., ред. Респираторная медицина: Руководство. М.: ГЭОТАР-Медиа; 2007; т. 1.
  41. Cardwell C. R., Shields M. D., Carson D. J., Patterson C. C. A meta-analysis of the association between childhood type 1 diabetes and atopic disease. Diabet. Care 2003; 26 (9): 2568-2574.
  42. Rosenbauer J., Herzig P., Giani G. Atopic eczema in early childhood could be protective against type 1 diabetes. Diabetologia 2003; 46 (6): 784-788.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2010 Consilium Medicum

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
 

Address of the Editorial Office:

  • Novij Zykovskij proezd, 3, 40, Moscow, 125167

Correspondence address:

  • Alabyan Street, 13/1, Moscow, 127055, Russian Federation

Managing Editor:

  • Tel.: +7 (926) 905-41-26
  • E-mail: e.gorbacheva@ter-arkhiv.ru

 

 © 2018-2021 "Consilium Medicum" Publishing house


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies