About all

Diabetes and asthma. Asthma and Type 2 Diabetes: Exploring the Complex Relationship and Impact on Health

by alexxlab

How are asthma and type 2 diabetes related. What are the mechanisms linking these two conditions. How does diabetes affect asthma control. What are the implications for patient care and management.

The Global Burden of Asthma and Type 2 Diabetes

Asthma and type 2 diabetes mellitus (T2DM) are two chronic conditions that significantly impact global health. According to the Global Asthma Network, asthma affects an estimated 339 million people worldwide, while the International Diabetes Federation reports that approximately 463 million adults are living with diabetes, with T2DM accounting for about 90% of all cases.

The prevalence of these conditions varies across regions:

  • In Brazil, asthma affects 6.4 million people
  • In the United States, asthma prevalence is around 8% of the population
  • Globally, the prevalence of diabetes is expected to rise to 700 million by 2045

Understanding the relationship between these two conditions is crucial for improving patient care and outcomes. Recent research has uncovered intriguing connections between asthma and T2DM, suggesting a complex interplay of shared risk factors and biological mechanisms.

Epidemiological Evidence: The Asthma-Diabetes Connection

Multiple studies have demonstrated a significant association between asthma and T2DM. For instance:

  • The Singapore Chinese Health Study found that individuals with asthma had a 31% higher risk of developing T2DM compared to those without asthma
  • The Women’s Health Study reported that women with asthma had a 37% increased risk of T2DM
  • A large-scale Korean study revealed that people with diabetes had a 30% higher prevalence of asthma compared to those without diabetes

These findings raise important questions about the nature of the relationship between these two conditions. Are there common underlying factors predisposing individuals to both asthma and T2DM? Or does one condition directly increase the risk of developing the other?

Shared Risk Factors: Obesity and Inflammation

One of the most significant shared risk factors for both asthma and T2DM is obesity. The World Health Organization estimates that over 650 million adults worldwide are obese, a condition that dramatically increases the risk of both respiratory and metabolic disorders.

How does obesity contribute to both asthma and T2DM?

  1. Mechanical effects: Excess weight can compress the lungs, reducing lung volume and altering respiratory mechanics
  2. Inflammatory response: Adipose tissue produces pro-inflammatory cytokines, contributing to systemic inflammation
  3. Insulin resistance: Obesity is a primary driver of insulin resistance, a key feature of T2DM
  4. Altered immune function: Obesity can modulate immune responses, potentially affecting both asthma and T2DM pathogenesis

The link between obesity, asthma, and T2DM highlights the importance of addressing weight management in patients with either or both conditions.

Metabolic Asthma: A New Phenotype?

The concept of “metabolic asthma” has emerged as researchers delve deeper into the connections between metabolic disorders and respiratory health. This phenotype is characterized by:

  • Adult-onset asthma
  • Association with obesity and metabolic syndrome
  • Possible resistance to standard asthma treatments
  • Increased airway inflammation and oxidative stress

Recognizing metabolic asthma as a distinct entity could have important implications for diagnosis and treatment strategies. For instance, addressing underlying metabolic dysfunction might be crucial for achieving optimal asthma control in these patients.

Mechanisms Linking Asthma and Type 2 Diabetes

Several biological mechanisms have been proposed to explain the association between asthma and T2DM:

1. Systemic Inflammation

Both asthma and T2DM are characterized by chronic low-grade inflammation. The pro-inflammatory state in one condition may exacerbate or contribute to the development of the other. Key inflammatory mediators involved in both diseases include:

  • Tumor Necrosis Factor-alpha (TNF-α)
  • Interleukin-6 (IL-6)
  • C-reactive protein (CRP)

2. Oxidative Stress

Increased oxidative stress is a common feature of both asthma and T2DM. Reactive oxygen species (ROS) can damage airway epithelium in asthma and contribute to insulin resistance in T2DM. The interplay between oxidative stress in these conditions may create a vicious cycle, worsening both diseases.

3. Altered Immune Function

T2DM is associated with impaired innate and adaptive immune responses, which may increase susceptibility to respiratory infections and exacerbate asthma symptoms. Conversely, the chronic inflammation in asthma may contribute to insulin resistance and the development of T2DM.

4. Metabolic Dysregulation

Insulin resistance and hyperglycemia in T2DM can affect lung function and airway reactivity. High blood glucose levels may lead to glycation of proteins in the lungs, altering their structure and function.

Impact of Type 2 Diabetes on Asthma Control

The presence of T2DM can significantly affect asthma control and management in several ways:

  1. Increased exacerbations: Patients with both asthma and T2DM may experience more frequent and severe asthma exacerbations
  2. Reduced lung function: T2DM has been associated with decreased lung function, potentially exacerbating asthma symptoms
  3. Medication interactions: Some diabetes medications may interact with asthma treatments, requiring careful management
  4. Comorbid conditions: T2DM increases the risk of other conditions that can worsen asthma, such as obstructive sleep apnea

Understanding these impacts is crucial for developing effective management strategies for patients with both conditions.

Clinical Implications and Management Strategies

The complex relationship between asthma and T2DM has important implications for clinical practice:

  • Screening: Consider screening asthma patients for T2DM and vice versa, especially in the presence of risk factors like obesity
  • Comprehensive approach: Develop treatment plans that address both respiratory and metabolic aspects of health
  • Lifestyle interventions: Emphasize the importance of weight management, physical activity, and dietary modifications
  • Medication management: Carefully consider potential interactions between asthma and diabetes medications
  • Patient education: Educate patients about the links between these conditions and the importance of managing both effectively

By adopting a holistic approach to patient care, healthcare providers can improve outcomes for individuals living with both asthma and T2DM.

Future Directions in Research and Treatment

As our understanding of the asthma-diabetes connection grows, several areas warrant further investigation:

  1. Biomarkers: Identify specific biomarkers that could predict the development of T2DM in asthma patients and vice versa
  2. Targeted therapies: Develop treatments that address the shared inflammatory pathways in both conditions
  3. Personalized medicine: Tailor treatment approaches based on individual patient characteristics and risk factors
  4. Long-term outcomes: Conduct longitudinal studies to better understand the long-term impacts of having both asthma and T2DM
  5. Prevention strategies: Investigate interventions that could simultaneously reduce the risk of both conditions

Advancing research in these areas could lead to significant improvements in the prevention, diagnosis, and treatment of both asthma and T2DM.

The Role of Comorbidities in Asthma and Diabetes Management

Comorbidities play a crucial role in the management of both asthma and T2DM. Common comorbidities that can affect both conditions include:

  • Obesity
  • Obstructive sleep apnea
  • Cardiovascular disease
  • Depression and anxiety
  • Gastroesophageal reflux disease (GERD)

How do these comorbidities impact asthma and diabetes management?

  1. They can complicate diagnosis and treatment
  2. They may require additional medications, increasing the risk of drug interactions
  3. They can worsen symptoms and outcomes for both conditions
  4. They often share risk factors, creating a complex web of interrelated health issues

Addressing these comorbidities is essential for achieving optimal control of both asthma and T2DM. Healthcare providers should adopt a comprehensive approach that considers the full spectrum of a patient’s health concerns.

Obstructive Sleep Apnea: A Key Player

Obstructive sleep apnea (OSA) deserves special attention in the context of asthma and T2DM. This sleep disorder is highly prevalent in individuals with both conditions and can significantly impact their management:

  • OSA can worsen asthma symptoms and increase the risk of nighttime exacerbations
  • It is associated with insulin resistance and poor glycemic control in T2DM
  • Treatment of OSA, often with continuous positive airway pressure (CPAP), can improve outcomes for both asthma and T2DM

Screening for and treating OSA should be an integral part of the management plan for patients with asthma, T2DM, or both conditions.

The Importance of a Multidisciplinary Approach

Given the complex interplay between asthma, T2DM, and their associated comorbidities, a multidisciplinary approach to patient care is essential. This may involve collaboration between:

  • Pulmonologists
  • Endocrinologists
  • Primary care physicians
  • Nutritionists
  • Exercise physiologists
  • Mental health professionals

By working together, these specialists can develop comprehensive treatment plans that address all aspects of a patient’s health, leading to improved outcomes and quality of life.

Pharmacological Considerations in Managing Asthma and Type 2 Diabetes

The coexistence of asthma and T2DM presents unique challenges in pharmacological management. Healthcare providers must carefully consider potential drug interactions and side effects when treating patients with both conditions.

Asthma Medications and Glycemic Control

Some asthma medications can affect blood glucose levels:

  • Systemic corticosteroids: Can cause significant hyperglycemia, particularly problematic for patients with T2DM
  • Beta-2 agonists: May increase blood glucose levels, although the effect is generally less pronounced with inhaled formulations
  • Leukotriene modifiers: Generally do not significantly affect glycemic control

Strategies for managing these effects include:

  1. Using the lowest effective dose of systemic corticosteroids
  2. Preferring inhaled medications over systemic ones when possible
  3. Monitoring blood glucose levels more closely during asthma exacerbations
  4. Adjusting diabetes medications as needed during corticosteroid treatment

Diabetes Medications and Respiratory Function

Certain diabetes medications may have implications for asthma management:

  • Metformin: Generally well-tolerated, may have anti-inflammatory effects that could benefit asthma control
  • Thiazolidinediones: Can cause fluid retention, potentially exacerbating asthma symptoms in some patients
  • GLP-1 receptor agonists: Some evidence suggests potential benefits for lung function, but more research is needed
  • SGLT2 inhibitors: Limited data on effects in asthma, but may have potential anti-inflammatory benefits

When prescribing diabetes medications for patients with asthma, healthcare providers should consider the potential impacts on respiratory function and choose agents that are least likely to exacerbate asthma symptoms.

Emerging Therapies: Targeting Shared Pathways

Research into the shared inflammatory pathways between asthma and T2DM has led to interest in therapies that could potentially address both conditions:

  • Anti-IL-1β therapies: May improve both glycemic control and airway inflammation
  • PPAR-γ agonists: Could have benefits for both metabolic and respiratory function
  • Anti-TNF-α agents: While not currently recommended for asthma, ongoing research explores potential benefits in specific phenotypes

These emerging therapies highlight the potential for developing treatments that simultaneously target multiple aspects of metabolic and respiratory health.

Patient Education and Self-Management Strategies

Effective self-management is crucial for patients living with both asthma and T2DM. Healthcare providers play a vital role in educating patients about their conditions and empowering them to take an active role in their care.

Key Components of Patient Education

  1. Understanding the relationship between asthma and T2DM
  2. Recognizing symptoms and potential triggers for both conditions
  3. Proper use of medications, including inhalers and blood glucose monitoring devices
  4. Importance of adherence to treatment plans
  5. Lifestyle modifications to improve overall health
  6. When and how to seek medical attention

Self-Management Tools and Techniques

Empowering patients with self-management skills can lead to improved outcomes. Some effective strategies include:

  • Asthma action plans: Written guidelines for daily management and handling exacerbations
  • Blood glucose logs: Tracking blood sugar levels to identify patterns and adjust treatment
  • Peak flow monitoring: Regular measurements to detect changes in lung function
  • Symptom diaries: Recording symptoms for both conditions to identify triggers and patterns
  • Mobile health apps: Utilizing technology to track medication use, symptoms, and health metrics

By providing patients with these tools and the knowledge to use them effectively, healthcare providers can help individuals better manage their asthma and T2DM, leading to improved quality of life and reduced healthcare utilization.

The Importance of Regular Follow-Up

Regular follow-up appointments are essential for patients with both asthma and T2DM. These visits allow healthcare providers to:

  1. Assess disease control and adjust treatment plans as needed
  2. Review medication use and address any concerns or side effects
  3. Reinforce self-management skills and provide additional education
  4. Screen for complications and comorbidities
  5. Offer support and encouragement for ongoing self-care efforts

By maintaining open communication and providing consistent support, healthcare providers can help patients navigate the challenges of managing multiple chronic conditions and achieve better health outcomes.

Association between Asthma and Type 2 Diabetes Mellitus: Mechanisms and Impact on Asthma Control—A Literature Review

1. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention. Fontana-on-Geneva Lake, WI, USA: Global Initiative for Asthma; 2018. https://ginasthma.org/wp-content/uploads/2019/01/2018-GINA.pdf. [Google Scholar]

2. Shu C. J., Benoist C., Mathis D. The immune system’s involvement in obesity-driven type 2 diabetes. Seminars in Immunology. 2012;24(6):436–442. doi: 10.1016/j.smim.2012.12.001. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

3. Perez M. K., Piedimonte G. Metabolic asthma: is there a link between obesity, diabetes and asthma? Immunology and Allergy Clinics of North America. 2014;34(4):777–784. doi: 10.1016/j.iac.2014.07.002. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

4. Salles C., Terse-Ramos R., Souza-Machado A., Cruz A. A. Obstructive sleep apnea and asthma. Jornal Brasileiro de Pneumologia. 2013;39(5):604–612. doi: 10.1590/s1806-37132013000500011. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

5. Zammit C., Liddicoat H., Moonsie I., Makker H. Obesity and respiratory diseases. International Journal of General Medicine. 2010;3:335–343. doi: 10.2147/IJGM.S11926. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

6. Su X., Ren Y., Li M., Zhao X., Kong L., Kang J. Prevalence of comorbidities in asthma and nonasthma patients. Medicine. 2016;95(22):p. e3459. doi: 10.1097/md.0000000000003459. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

7. Adeyeye O. O., Ogbera A. O., Ogunleye O. O., et al. Understanding asthma and the metabolic syndrome—a Nigerian report. International Archives of Medicine. 2012;5(1):p. 20. doi: 10.1186/1755-7682-5-20. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

8. Global Asthma Network. The Global Asthma Report 2018. Auckland, New Zealand: Global Asthma Network; 2018. http://www.globalasthmanetwork.org/publications/Global_Asthma_Report_2014.pdf. [Google Scholar]

9. International Diabetes Federation. IDF Diabetes Atlas. 9a. Brussels, Belgium: International Diabetes Federation; 2020. https://www.diabetesatlas.org/upload/resources/2019/IDF_Atlas_9th_Edition_2019.pdf. [Google Scholar]

10. World Health Organization. WHO. Obesity and Overweight. Fact Sheets N° 311. Geneva, Switzerland: World Health Organization; 2016. http://http://www.who.int/mediacentre/factsheets/fs311/en/l. [Google Scholar]

11. http://www.brasil.gov.br/saude/2015/01/asma-atinge-6-4-milhoes-de-brasileiros. Brasil. Ministério da Saúde. Portal da Saúde. Brasília: Ministério de Saúde. Asma atinge 6,4 milhões de brasileiros, 2019,

12. Brasil. Ministério da Saúde. Vigitel Brasil 2018—Vigilância de fatores de risco e proteção para doenças crônicas por inquérito telefônico: estimativas sobre frequência e distribuição sociodemográfica de fatores de risco e proteção para doenças crônicas nas capitais dos 26 estados brasileiros e no Distrito Federal em 2018—Brasília: DF, 2019.

13. Papi A., Brightling C., Pedersen S. E., Reddel H. K. Asthma. The Lancet. 2018;391(10122):783–800. doi: 10.1016/s0140-6736(17)33311-1. [PubMed] [CrossRef] [Google Scholar]

14. Mueller N. T., Koh W.-P., Odegaard A. O., Gross M. D., Yuan J.-M., Pereira M. A. Asthma and the risk of type 2 diabetes in the Singapore Chinese Health Study. Diabetes Research and Clinical Practice. 2013;99(2):192–199. doi: 10.1016/j.diabres.2012.11.019. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

15. Song Y., Klevak A., Manson J. E., Buring J. E., Liu S. Asthma, chronic obstructive pulmonary disease, and type 2 diabetes in the Women’s Health Study. Diabetes Research and Clinical Practice. 2010;90(3):365–371. doi: 10.1016/j.diabres.2010.09.010. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

16. Baek J. Y., Lee S. E., Han K., Koh E. H. Association between diabetes and asthma. Annals of Allergy, Asthma & Immunology. 2018;121(6):699–703. doi: 10.1016/j.anai.2018.08.008. [PubMed] [CrossRef] [Google Scholar]

17. Rana J. S., Mittleman M. A., Sheikh J., et al. Chronic obstructive pulmonary disease, asthma, and risk of type 2 diabetes in women. Diabetes Care. 2004;27(10):2478–2484. doi: 10.2337/diacare.27.10.2478. [PubMed] [CrossRef] [Google Scholar]

18. Gershon A. S., Guan J., Wang C., Victo, Charles J. To T. Describing and quantifying asthma comorbidty: a population study. PLoS One. 2012;7 doi: 10.1371/journal.pone.0034967.e34967 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

19. Yun H. D., Knoebel E., Fenta Y., et al. Asthma and proinflammatory conditions: a population-based retrospective matched cohort study. Mayo Clinic Proceedings. 2012;87(10):953–960. doi: 10.1016/j.mayocp.2012.05.020. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

20. Wytrychowski K., Obojski A., Hans-Wytrychowska A. The influence of insulin therapy on the course of acute exacerbation of bronchial asthma. Advances in Experimental Medicine and Biology. 2016;884:45–51. doi: 10.1007/5584_2015_175. [PubMed] [CrossRef] [Google Scholar]

21. Klein O. L., Aviles-Santa L., Cai J., et al. Hispanics/latinos with type 2 diabetes have functional and symptomatic pulmonary impairment mirroring kidney microangiopathy: findings from the hispanic community health study/study of Latinos (HCHS/SOL) Diabetes Care. 2016;39(11):2051–2057. doi: 10.2337/dc16-1170. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

22. Tesse R., Schieck M., Kabesch M. Asthma and endocrine disorders: shared mechanisms and genetic pleiotropy. Molecular and Cellular Endocrinology. 2011;333(2):103–111. doi: 10.1016/j.mce.2010.11.032. [PubMed] [CrossRef] [Google Scholar]

23. Sweeney J., Patterson C. C., Menzies-Gow A., et al. Comorbidity in severe asthma requiring systemic corticosteroid therapy: cross-sectional data from the optimum patient care research database and the British thoracic difficult asthma registry. Thorax. 2016;71(4):339–346. doi: 10.1136/thoraxjnl-2015-207630. [PubMed] [CrossRef] [Google Scholar]

24. Rafacho A., Ortsäter H., Nadal A., Quesada I. Glucocorticoid treatment and endocrine pancreas function: implications for glucose homeostasis, insulin resistance and diabetes. Journal of Endocrinology. 2014;223(3):R49–R62. doi: 10.1530/joe-14-0373. [PubMed] [CrossRef] [Google Scholar]

25. Ernst P., Suissa S. Systemic effects of inhaled corticosteroids. Current Opinion in Pulmonary Medicine. 2011;18:85–89. [PubMed] [Google Scholar]

26. Moher D., Liberati A., Tetzlaff J., Altman D. G., The PRISMA Group Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. PLoS Medicine. 2009;6(7) doi: 10.1371/journal.pmed.1000097.e100009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

27. Rodbard H. W., Bays H. E., Gavin J. R., et al. Rate and risk predictors for development of self-reported type-2 diabetes mellitus over a 5-year period: the SHIELD study. International Journal of Clinical Practice. 2012;66(7):684–691. doi: 10.1111/j.1742-1241.2012.02952.x. [PubMed] [CrossRef] [Google Scholar]

28. Thomsen S. F., Duffy D. L., Kyvik K. O., Skytthe A., Backer V. Risk of asthma in adult twins with type 2 diabetes and increased body mass index. Allergy. 2011;66(4):562–568. doi: 10.1111/j.1398-9995.2010.02504.x. [PubMed] [CrossRef] [Google Scholar]

29. Hashemzadeh M., Movahed M. R. The occurrence of asthma in hospitalized patients with type 2 diabetes mellitus. Internal Medicine Journal. 2009;39(10):699–701. doi: 10.1111/j.1445-5994.2009.01976.x. [PubMed] [CrossRef] [Google Scholar]

30. Gulcan E., Bulut I., Toker A., Gulcan A. Evaluation of glucose tolerance status in patients with asthma bronchiale. Journal of Asthma. 2009;46(2):207–209. doi: 10.1080/02770900802627302. [PubMed] [CrossRef] [Google Scholar]

31. Verbovoy A. F., Kosareva O. V., Akhmerova R. I. Leptin, resistin, and hormonal and metabolic parameters in women with type 2 diabetes and in those with its concurrence with asthma. Terapevticheskii Arkhiv. 2014;87:37–41. [PubMed] [Google Scholar]

32. Koskela H. O., Salonen P. H., Niskanen L. Hyperglycaemia during exacerbations of asthma and chronic obstructive pulmonary disease. The Clinical Respiratory Journal. 2013;7(4):382–389. doi: 10.1111/crj.12020. [PubMed] [CrossRef] [Google Scholar]

33. Suissa S., Kezouh A., Ernst P. Inhaled corticosteroids and the risks of diabetes onset and progression. The American Journal of Medicine. 2010;123(11):1001–1006. doi: 10.1016/j.amjmed.2010.06.019. [PubMed] [CrossRef] [Google Scholar]

34. Faul J. L., Wilson S. R., Chu J. W., Canfield J., Kuschner W. G. The effect of an inhaled corticosteroid on glucose control in type 2 diabetes. Clinical Medicine & Research. 2009;7(1-2):14–20. doi: 10.3121/cmr.2009.824. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

35. Kankaanranta H., Kauppi P., Tuomist L. E., Ilmarinen P. Emerging comorbidities in adult asthma: risks, clinical associations, and mechanisms. Mediators of Inflammation. 2016;2016:23. doi: 10.1155/2016/3690628.3690628 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

36. Singh S., Prakash Y. S., Linneberg A., Agrawal A. Insulin and the lung: connecting asthma na metabolic syndrome. Journal of Allergy. 2013;1(20):37.627384 [Google Scholar]

37. Yeryomenko G. V., Bezditko T. V. The treatment of patients with asthma and comorbidity. Medicni Perspektivi (Medical Perspectives) 2018;23(1(part 1)):50–59. doi: 10.26641/2307-0404.2018.1(part1).127209. [CrossRef] [Google Scholar]

38. Li C.-Y., Erickson S. R., Wu C.-H. Metformin use and asthma outcomes among patients with concurrent asthma and diabetes. Respirology. 2016;21(7):1210–1218. doi: 10.1111/resp.12818. [PubMed] [CrossRef] [Google Scholar]

39. Koskela H. O., Salonen P. H., Romppanen J., Niskanen L. A history of diabetes but not hyperglycaemia during exacerbation of obstructive lung disease has impact on long-term mortality: a prospective, observational cohort study. BMJ Open. 2015;29(5)e006794 [PMC free article] [PubMed] [Google Scholar]

40. Wouters E. F. M., Reynaert N. L., Dentener M. A., Vernooy J. H. J. Systemic and local inflammation in asthma and chronic obstructive pulmonary disease: is there a connection? Proceedings of the American Thoracic Society. 2009;6(8):638–647. doi: 10.1513/pats.200907-073dp. [PubMed] [CrossRef] [Google Scholar]

41. Wellen K. E., Hotamisligil G. S., Hotamisligil G. S. Inflammation, stress, and diabetes. Journal of Clinical Investigation. 2005;115(5):1111–1119. doi: 10.1172/jci25102. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

42. Lee C. C., Liu S. Role of inflammatory cytokines in type 2 diabetes. Journal of Periodontology. 2008;79:1527–1534. [PubMed] [Google Scholar]

43. Berg A. H., Scherer P. E. Adipose tissue, inflammation, and cardiovascular disease. Circulation Research. 2005;96(9):939–949. doi: 10.1161/01.res.0000163635.62927.34. [PubMed] [CrossRef] [Google Scholar]

44. Bastard J. P., Maachi M., Lagathu C., et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. European Cytokine Network. 2006;17(1):4–12. [PubMed] [Google Scholar]

45. Chesné J., Braza F., Mahay G., Brouard S., Aronica M., Magnan A. IL-17 in severe asthma. Where do we stand? American Journal of Respiratory and Critical Care Medicine. 2014;190(10):1094–1101. doi: 10.1164/rccm.201405-0859pp. [PubMed] [CrossRef] [Google Scholar]

46. Ramalho R., Guimarães C. Papel do tecido adiposo e dos macrófagos no estado de inflamação crónica associada à obesidade: implicações Clínicas. Acta medica portuguesa. 2008;21:489–496. [PubMed] [Google Scholar]

47. Singh S., Bodas M., Bhatraju N. K., et al. Hyperinsulinemia adversely affects lung structure and function. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2016;310(9):L837–L845. doi: 10. 1152/ajplung.00091.2015. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

48. Thuesen B. H., Husemoen L. L. N., Hersoug L.-G., Pisinger C., Linneberg A. Insulin resistance as a predictor of incident asthma-like symptoms in adults. Clinical & Experimental Allergy. 2009;39(5):700–707. doi: 10.1111/j.1365-2222.2008.03197.x. [PubMed] [CrossRef] [Google Scholar]

49. Agrawal A., Prakash Y. S. Obesity, metabolic syndrome, and airway disease. Immunology and Allergy Clinics of North America. 2014;34(4):785–796. doi: 10.1016/j.iac.2014.07.004. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

50. Lugogo N. L., Bappanad D., Kraft M. Obesity, metabolic dysregulation and oxidative stress in asthma. Biochimica et Biophysica Acta (BBA)—General Subjects. 2011;1810(11):1120–1126. doi: 10.1016/j.bbagen.2011.09.004. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

51. Brumpton B. M., Camargo C. A., Romundstad P. R., Langhammer A., Chen Y. , Mai X.-M. Metabolic syndrome and incidence of asthma in adults: the HUNT study. European Respiratory Journal. 2013;42(6):1495–1502. doi: 10.1183/09031936.00046013. [PubMed] [CrossRef] [Google Scholar]

52. Cottrell L., Neal W. A., Ice C., Perez M. K., Piedimonte G. Metabolic abnormalities in children with asthma. American Journal of Respiratory and Critical Care Medicine. 2011;183(4):441–448. doi: 10.1164/rccm.201004-0603oc. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

53. Klein O. L., Krishnan J. A., Glick S., Smith L. J. Systematic review of the association between lung function and Type 2 diabetes mellitus. Diabetic Medicine. 2010;27(9):977–987. doi: 10.1111/j.1464-5491.2010.03073.x. [PubMed] [CrossRef] [Google Scholar]

54. Aronson D. Hyperglycemia and the pathobiology of diabetic complications. Advances in Cardiology. 2008;45:1–16. doi: 10.1159/000115118. [PubMed] [CrossRef] [Google Scholar]

55. Yu D., Simmons D. Association between lung capacity measurements and abnormal glucose metabolism: findings from the Crossroads study. Diabetic Medicine. 2014;31(5):595–599. doi: 10.1111/dme.12346. [PubMed] [CrossRef] [Google Scholar]

56. O’Byrne P. M., Rennard S., Gerstein H., Radner F., Peterson S., Lindberg B. Risk of new onset diabetes mellitus in patients with asthma or COPD taking inhaled corticosteroids. Respiratory Medicine. 2012;106:1487–1493. [PubMed] [Google Scholar]

57. Katsuyama T., Sada K.-E., Namba S., et al. Risk factors for the development of glucocorticoid-induced diabetes mellitus. Diabetes Research and Clinical Practice. 2015;108(2):273–279. doi: 10.1016/j.diabres.2015.02.010. [PubMed] [CrossRef] [Google Scholar]

58. Van Raalte D. H., Ouwens D. M., Diamant M. Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options? European Journal of Clinical Investigation. 2009;39(2):81–93. doi: 10.1111/j.1365-2362.2008.02067.x. [PubMed] [CrossRef] [Google Scholar]

59. Slatore C. G., Bryson C. L., Au D. H. The association of inhaled corticosteroid use with serum glucose concentration in a large cohort. The American Journal of Medicine. 2009;122(5):472–478. doi: 10.1016/j.amjmed.2008.09.048. [PubMed] [CrossRef] [Google Scholar]

60. Regateiro F., Moura A. L., Faria E. Novos biológicos para o tratamento da asma. Revista Portuguesa de Imunoalergologia. 2017;25:99–113. [Google Scholar]

61. Yalcin A. D., Gorczynski R. M., Cilli A., Strauss L. Omalizumab (anti-IgE) therapy increases blood glucose levels in severe persisten tallergic asthma patients with diabetes mellitus: 18-month follow-up. Clinical Laboratory. 2014;60:1561–1564. doi: 10.7754/clin.lab.2013.130302. [PubMed] [CrossRef] [Google Scholar]

62. Hamada S., Kuroe A., Tsukino M. Does omalizumab impair glucose homeostasis in a patient with severe persistent asthma and type 2 diabetes mellitus? Revista Portuguesa de Pneumologia (English Edition) 2017;23(5):303–304. doi: 10.1016/j.rppnen.2017.05.002. [PubMed] [CrossRef] [Google Scholar]

63. Ferreira L., Moniz A. C., Carneiro A. S., et al. The impact of glycemic variability on length of stay and mortality in diabetic patients admitted with community-acquired pneumonia or chronic obstructive pulmonary disease. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2019;13(1):149–153. doi: 10.1016/j.dsx.2018.08.028. [PubMed] [CrossRef] [Google Scholar]

64. Xia C., Rao X., Zhong J. Role of T Lymphocytes in type 2 diabetes and diabetes-associated inflammation. Journal of Diabetes Research. 2017;2017:6. doi: 10.1155/2017/6494795.6494795 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

65. Black M. H., Anderson A., Bell R. A., et al. Prevalence of asthma and its association with glycemic control among youth with diabetes. Pediatrics. 2011;128(4):e839–e847. doi: 10.1542/peds.2010-3636. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

66. Rogliani P., Calzetta L., Capuani B., et al. Glucagon-like peptide 1 receptor: a novel pharmacological target for treating human bronchial hyperresponsiveness. American Journal of Respiratory Cell and Molecular Biology. 2016;55(6):804–814. doi: 10.1165/rcmb.2015-0311oc. [PubMed] [CrossRef] [Google Scholar]

67. Mitchell P. D., Salter B. M., Oliveria J. P., et al. Glucagon-like peptide-1 receptor expression on human eosinophils and its regulation of eosinophil activation. Clinical & Experimental Allergy. 2017;47(3):331–338. doi: 10.1111/cea.12860. [PubMed] [CrossRef] [Google Scholar]

68. Barros L. L., Souza-Machado A., Corrêa L. B., et al. Obesity and poor asthma control in patients with severe asthma. Journal of Asthma. 2011;48(2):171–176. doi: 10.3109/02770903.2011.554940. [PubMed] [CrossRef] [Google Scholar]

69. Forno E., Zhang P., Nouraie M., Courcoulas A., Mitchell J. E., Wolfe B. The impact of bariatric surgery on asthma control differs among obese individuals with reported prior or current asthma, with or without metabolic syndrome. PLoS One. 2019;14(4) doi: 10.1371/journal.pone.0214730.e0214730 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

Asthma in adults with diabetes: treat their diabetes with metformin, improve their asthma?

  • Journal List
  • HHS Author Manuscripts
  • PMC5021626

As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.

Learn more about our disclaimer.

Respirology. Author manuscript; available in PMC 2017 Oct 1.

Published in final edited form as:

Respirology. 2016 Oct; 21(7): 1144–1145.

Published online 2016 Aug 17. doi: 10.1111/resp.12869

PMCID: PMC5021626

NIHMSID: NIHMS812900

PMID: 27533627

, M.D., M.P.H.

Author information Article notes Copyright and License information Disclaimer

After decades of increasing prevalence in numerous countries, asthma affects over 300 million people worldwide. Similarly, the prevalence of obesity has doubled since the 1980s, and according to the World Health Organization it now affects over 600 million people around the world (with an additional 1.3 billion being overweight)1. Obesity is a major risk factor for diabetes, and it is also associated with higher risk of asthma. Obese people with asthma tend to have more symptoms, more frequent exacerbations, lower quality of life, and decreased response to asthma medications2–4. The pathways linking obesity to asthma have not yet been fully elucidated, but are likely multifactorial and include a mechanical effect on the lungs and the airways, genetic predisposition, epigenetic modification, dietary changes, a pro-inflammatory state, and others.

The metabolic complications of obesity –insulin resistance, the metabolic syndrome, and diabetes– likely play an important role in the pathophysiology of “obese asthma”5,6. The association between obesity and asthma is greater in the presence of insulin resistance7. Independent of obesity, subjects with diabetes may be at higher risk of asthma8. Similarly, insulin resistance and the metabolic syndrome have been associated to lower lung function among obese adolescents, with a more pronounced decreased among obese adolescents with asthma9. In light of these and other similar studies, it is crucial to determine whether preventing or adequately treating and controlling these complications of obesity may reduce asthma morbidity.

In this issue of Respirology, Li et al. use data from the Taiwan National Health Insurance Research Database (NHIRD) to evaluate whether the use of metformin among subjects with asthma and diabetes is associated with the risk of asthma exacerbations, emergency room visits, or hospitalizations10. Using a retrospective cohort approach, the authors analyzed insurance claims and medication data from 1,332 patients with concomitant asthma and diabetes: 444 taking metformin for their diabetes, and 888 age- and sex-matched subjects who were not using metformin. For each subject, they looked at data over a period of three years after the first prescription of metformin. After adjusting for several clinical covariates, they found that metformin use was associated with significantly reduced risk of asthma exacerbations (OR=0.39, 95% confidence interval [CI]=0.19–0.79%) or hospitalizations (OR=0.21, 95% CI=0.07–0.63%).

Metformin is one of the most commonly prescribed oral anti-diabetic drugs; its mechanism of action is not completely understood, but proposed pathways include the activation of AMP-activated protein kinase (AMPK), an enzyme that plays an important role in the regulation of insulin signaling and glucose metabolism11. It also increases insulin sensitivity and may antagonize glucagon, thereby reducing blood glucose levels12. Metformin has been shown to attenuate allergic eosinophilic airway inflammation in obese mice, normalizing levels of eotaxin and tumor necrosis factor alpha (TNF-α) in bronchoalveolar lavage, and restoring levels of AMPK in lung tissue13. It may also inhibit airway smooth muscle cell proliferation through AMPK-dependent pathways14. Interestingly, AMPK induction by metformin ameliorates sodium and water transport in cystic fibrosis airway epithelial cell cultures15. Thus, there is evidence that metformin may have a potential role in the treatment of asthma. The study by Li and colleagues expands our current knowledge in two key aspects: First, it adds another important step to establish causality in the association between insulin resistance (or hyperglycemia) and asthma morbidity in humans. Second, and more importantly, it demonstrates an important clinical benefit among adults with asthma and diabetes taking metformin.

The present study has several strengths, including the use of matched data from a large, population-based cohort; the longitudinal nature of the analysis; the use of both diagnostic code and medication records to ensure accuracy; and the adjustment for multiple covariates and potential confounders such as short- and long-acting beta-agonists (SABA and LABA), inhaled corticosteroids (ICS), and oral steroids. At the same time, the study has limitations that are inherent to claims and coding database analysis. For instance, several covariates were not available in the NHIRD database that could be important confounders, including information on body mass index, tobacco smoking, race and ethnicity, socioeconomic status, allergen or pollution exposures, etc. Importantly, the database provides no information on medication compliance (for either asthma or diabetes), asthma severity, or blood glucose levels. Thus, we cannot ascertain whether the results are directly related to the use of metformin, to better diabetes control with improved glycaemia, or to other potential confounders.

In a world with 1.9 billion overweight/obese people, 400 million people with diabetes, and over 300 million people with asthma, the results reported in this issue of Respirology are novel and important, and certainly merit further investigation. Future studies should build on these findings, and improve on the current limitations by conducting prospective studies in cohorts specifically designed to address the effect of metformin on asthma outcomes. It is premature to recommend clinicians to modify their management of these patients, but if the results were replicated in independent cohorts, they would likely constitute sufficient grounds to consider randomized clinical trials. Future research will also have to address whether the effects of metformin on asthma are limited to patients with diabetes, or whether it may also be beneficial in subjects with obesity, insulin resistance, or the metabolic syndrome.

Funding from the National Heart, Lung, and Blood Institute at the US National Institutes of Health (HL125666) is acknowledged.

1. Obesity and Overweight. WHO; 2016. Accessed July 19, 2016, at http://www.who.int/mediacentre/factsheets/fs311/en/ [Google Scholar]

2. Dixon AE, Holguin F, Sood A, et al. An official American Thoracic Society Workshop report: obesity and asthma. Proc Am Thorac Soc. 2010;7:325–35. [PubMed] [Google Scholar]

3. Tay TR, Radhakrishna N, Hore-Lacy F, et al. Comorbidities in difficult asthma are independent risk factors for frequent exacerbations, poor control and diminished quality of life. Respirology. 2016 [PubMed] [Google Scholar]

4. Sutherland ER, Camargo CA, Jr, Busse WW, et al. Comparative effect of body mass index on response to asthma controller therapy. Allergy Asthma Proc. 2010;31:20–5. [PubMed] [Google Scholar]

5. Baffi CW, Wood L, Winnica D, et al. Metabolic Syndrome and the Lung. Chest. 2016;149:1525–34. [PMC free article] [PubMed] [Google Scholar]

6. Periyalil HA, Gibson PG, Wood LG. Immunometabolism in obese asthmatics: are we there yet? Nutrients. 2013;5:3506–30. [PMC free article] [PubMed] [Google Scholar]

7. Cardet JC, Ash S, Kusa T, Camargo CA, Jr, Israel E. Insulin resistance modifies the association between obesity and current asthma in adults. Eur Respir J. 2016 [PMC free article] [PubMed] [Google Scholar]

8. Thomsen SF, Duffy DL, Kyvik KO, Skytthe A, Backer V. Risk of asthma in adult twins with type 2 diabetes and increased body mass index. Allergy. 2011;66:562–8. [PubMed] [Google Scholar]

9. Forno E, Han YY, Muzumdar RH, Celedon JC. Insulin resistance, metabolic syndrome, and lung function in US adolescents with and without asthma. J Allergy Clin Immunol. 2015;136:304–11 e8. [PMC free article] [PubMed] [Google Scholar]

10. Li C-Y, Erickson SR, Wu CH. Metformin use and asthma outcomes among patients with concurrent asthma and diabetes. Respirology. 2016 doi: 10.1111/resp.12818. [PubMed] [CrossRef] [Google Scholar]

11. Zhou G, Myers R, Li Y, et al. Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest. 2001;108:1167–74. [PMC free article] [PubMed] [Google Scholar]

12. Miller RA, Chu Q, Xie J, Foretz M, Viollet B, Birnbaum MJ. Biguanides suppress hepatic glucagon signalling by decreasing production of cyclic AMP. Nature. 2013;494:256–60. [PMC free article] [PubMed] [Google Scholar]

13. Calixto MC, Lintomen L, Andre DM, et al. Metformin attenuates the exacerbation of the allergic eosinophilic inflammation in high fat-diet-induced obesity in mice. PLoS One. 2013;8:e76786. [PMC free article] [PubMed] [Google Scholar]

14. Ratnovsky A, Mellema M, An SS, Fredberg JJ, Shore SA. Airway smooth muscle proliferation and mechanics: effects of AMP kinase agonists. Mol Cell Biomech. 2007;4:143–57. [PubMed] [Google Scholar]

15. Myerburg MM, King JD, Jr, Oyster NM, et al. AMPK agonists ameliorate sodium and fluid transport and inflammation in cystic fibrosis airway epithelial cells. Am J Respir Cell Mol Biol. 2010;42:676–84. [PMC free article] [PubMed] [Google Scholar]

The combination of bronchial asthma and diabetes: synergism or antagonism? | Ivanov

1. Lowder T.W., Kunz H.E. Regulatory T cells in asthma and airway hyperresponsiveness. J. Allergy Ther. 2011; Suppl. 1:1–8.

2. Karlstad O., Nafstad P., Tverdal A. et al. Comorbidities in an asthma population 8–29 years old: a study from the Norwegian Prescription Database. Pharmacoepidemiol. drug. Saf. 2012; 21:1045–1052.

3. Shi H.N., Walker W.A. T helper cell subclasses and clinical disease states. Curr. Opin. Gastroenterol. 2002; 18:711–716.

4. Mineev V.N. The concept of bronchial asthma as a membrane-receptor pathology. Immunopathology, allergology, infectology. 2005; 3:68–85. / Mineev V.N. An approach to bronchial asthma as to membrane and receptor pathology. Immunopathology, allergology, infektologiya. 2005; 3: 68–85 (in Russian).

5. Vianna E.O., Garcia-Leme J. Allergen-induced airway inflammation in rats. Role of insulin. Am. J. Respir. Crit. care. Med. 1995; 151:809–814.

6. Insuela D.B.R., Silva P.M.R., Martins M.A., Carvalho V.F. The Yin Yang of hormones that control glucose homeostasis in asthma. J. Allergy Ther. 2013; 11:3–8.

7. Kolychev A.P., Mineev V.N., Bulatova N.Yu., Fedoseev G.B. Features of insulin-receptor interactions in bronchial asthma. Pulmonology. 1994; 2:48–51. / Kolychev A.P., Mineev V.N., Bulatova N.Yu., Fedoseev G.B. Insulin-receptor interactions in bronchial asthma. Pul’monologia. 1994; 2: 48–51 (in Russian).

8. Hashemzadeh M., Movahed M.R. The occurrence of asthma in hospitalized patients with type 2 diabetes mellitus. Intern. Med. J. 2009; 39(10): 699–701.

9. Sheiner E., Mazor M., Levy A. et al. Pregnancy outcome of asthmatic patients: a population-based study. J. Matern. Fetal neonate. Med. 2005; 18:237–40.

10. Rapaport M.J., Bistritzer T., Aharoni D. Th2/Th3 cytokine secretion of first degree relatives of T1DM patients. Cytokine. 2005; 30(5): 219–227.

11. Kononenko I.V., Prokofiev S.A., Smirnova O.M. The functional state of β-cells, immunological and clinical and biochemical characteristics in patients with slowly progressive autoimmune diabetes in adults. Problems of endocrinology. 2004; 50(1): 18–22. / Kononenko I.V., Prokof’ev S.A., Smirnova O.M. Functional status of β-cells and immunological, clinical and biochemical features of adult patients with slowly-progressive autoimmune diabetes mellitus. Problemy endocrinology. 2004; 50 (1): 18–22 (in Russian).

12. Saprina T.V., Lazarenko F.E., Prokhorenko T.S. The role of Th2/Th3 imbalance of the immune response in determining the clinical features of autoimmune diabetes mellitus in adults. Diabetes. 2011; 2:12–17. / Saprina T.V., Lazarenko F.E., Prokhorenko T.S. et al. A role of Th2/Th3 immune imbalance for clinical course of diabetes mellitus in adults. Sakharny diabetes. 2011; 2:12–17 (in Russian).

13. Brealey D., Singer M. Hyperglycemia in critical illness: a review. J. Diabetes. sci. Technol. 2009; 3:1250–1260.

14. McMahon G.T., Arky R.A. Inhaled insulin for diabetes mellitus. N. Engl. J. Med. 2007; 356:497–502.

15. Mineev V.N., Bulatova N.Yu. Features of the influence of glucose inhalations on bronchial reactivity in bronchial asthma. Clinical medicine. 2001; 79(8):37–39. / Mineev V.N., Bulatova N.Yu. An influence of inhalational glucose on bronchial reactivity in patients with asthma. Clinical Meditsina. 2001; 79 (8): 37–39 (in Russian).

16. Viardot A., Gray S. T., Mackay F., Chisholm D. Potential antiinflammatory role of insulin via the preferential polarization of effector T cells towards a T helper 2 phenotype. endocrinology. 2007; 148:346–353.

17. Shore S.A., Schwartzman I.N., Mellema M.S. et al. Effect of leptin on allergic airway responses in mice. J. Allergy Clin. Immunol. 2005; 115:103–109.

18. Giannessi D., Maltinti M., Del Ry S. Adiponectin circulating levels: a new emerging biomarker of cardiovascular risk. Pharmacol. Res. 2007; 56:459–467.

19. Shore S.A., Terry R.D., Flynt L. et al. Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice. J. Allergy Clin. Immunol. 2006; 118:389–395.

20. Sherman M.S., Lazar E.J., Eichacker P. A bronchodilator action of glucagon. J. Allergy. Clin. Immunol. 1988; 81:908–911.

21. Imbruce R., Goldfedder A., ​​Maguire W. et al. The effect of glucagon on airway resistance. J.Clin. Pharmacol. 1975; 15:680–684.

22. Olsen P. C., Coelho L.P., Costa J.C. et al. Two for one: cyclic AMP mediates the anti-inflammatory and anti-spasmodic properties of the non-anesthetic lidocaine analog JMF2-1. Eur. J Pharmacol. 2012; 680:102–107.

23. Hu C.P., Zou Y.Q., Feng J.T., Li X.Z. The effect of unilateral adrenalectomy on transformation of adrenal medullary chromaffin cells in vivo: a potential mechanism of asthma pathogenesis. PLOS One. 2012; 7:e44586.

24. Scola A.M., Loxham M., Charlton S.J., Peachell P.T. The long-acting beta-adrenoceptor agonist, indacaterol, inhibits IgE-dependent responses of human lung mast cells. Br. J Pharmacol. 2009; 158:267–276.

25. Goleva E., Dunlap A., Leung D.Y. Differential control of Th2 versus Th3 cell responses by the combination of lowdose steroids with beta2-adrenergic agonists. J. Allergy Clin. Immunol. 2004; 114:183–191.

26. Giordano R., Guaraldi F., Berardelli R. et al. Glucose metabolism in patients with subclinical Cushing’s syndrome. endocrine. 2012; 41:415–423.

27. Torres R.C., Insuela D.B.R., Carvalho V.F. Mecanismos celulares e moleculares da acao antiinflamatoria dos glicocorticoides. Corpus et Scientia. 2012; 8:36–51.

28. Maneechotesuwan K., Yao X., Ito K. et al. Suppression of GATA-3 nuclear import and phosphorylation: a novel mechanism of corticosteroid action in allergic disease. PLOS Med. 2009; 6: e1000076.

29. Ammit A.J., Burgess J.K., Hirst S.J. et al. The effect of asthma therapeutics on signaling and transcriptional regulation of airway smooth muscle function. Pulm. Pharmacol. Ther. 2009; 22:446–454.

30 Barnes P.J. Biochemical basis of asthma therapy. J Biol. Chem. 2011; 286:32899–32905.

31. Rajala M.W., Obici S., Scherer P.E., Rossetti L. Adiposederived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production. J.Clin. Invest. 2003; 111:225–230.

32. Condliffe A.M., Cadwallader K.A., Walker T.R. et al. Phosphoinositide 3-kinase: a critical signaling event in pulmonary cells. Respir. Res. 2000; 1:24–29.

33. Fedoseev G.B., Trofimov V.I., Petrova M.A., red. Many-sided bronchial asthma, diagnosis, treatment and prevention. St. Petersburg: Nordmed-Izdat; 2011. / Fedoseev G.B., Trofimov V.I., Petrova M.A., eds. Multifaceted Bronchial Asthma: Diagnosis, Treatment, Prevention. St. Petersburg: Nordmed-Izdat; 2011 (in Russian).

Bronchial asthma and diabetes mellitus

Bronchial asthma and diabetes mellitus occur against the background of impaired functioning of the immune system. Diabetes mellitus develops as an autoimmune disease with the production of antibodies against the pancreas’ own cells. In bronchial asthma, plant pollen, food, animal hair, bacteria, etc. act as an antigen. The risk of developing asthma in diabetics is higher than in people without autoimmune diseases.

There is also a risk of impaired carbohydrate metabolism for asthmatics using glucocorticosteroids for treatment. With this combination, the development of diabetes as a complication of steroid therapy is less common than osteoporosis or other side effects, but all steroids and a number of other drugs used to treat bronchial asthma worsen the course of existing diabetes, as they increase blood sugar levels.

Patients with asthma who are diagnosed with steroid diabetes usually have severe asthma, which is the reason for the prescription of systemic steroids. Their use in high doses or for a long time leads to obesity. Obesity, in turn, worsens the course of diabetes.

Bronchial asthma in diabetes mellitus occurs more often in the first, insulin-dependent type. There was no association between type 2 diabetes and the incidence of asthma.

For patients with bronchial asthma, a complete cessation of smoking is necessary, since this factor leads to frequent attacks of suffocation and causes circulatory disorders, vasospasm. In diabetes mellitus, in conditions of angiopathy, smoking increases the risk of developing diabetic neuropathy, heart disease, destruction of the glomeruli of the kidneys and kidney failure.

In order to prevent complications of diabetes in the treatment of bronchial asthma, patients are recommended to:

1. Constant monitoring of blood sugar levels and dose adjustment while prescribing glucocorticoids.