European Journal of Cardiovascular Medicine

Type 2 diabetes mellitus (T2DM) represents one of the most significant global health challenges of the 21st century, affecting over 463 million adults worldwide as of 2019, with projections indicating this number will rise to 700 million by 2045 (1). This chronic metabolic disorder, characterized by insulin resistance and progressive beta-cell dysfunction, is well-recognized for its devastating complications affecting multiple organ systems, including the cardiovascular, renal, neurological, and ocular systems (2). However, the potential impact of diabetes on pulmonary function has received relatively limited attention in clinical practice and research, despite emerging evidence suggesting that the lungs may represent an underrecognized target organ in diabetic complications (3).

The pathophysiological mechanisms underlying diabetic complications share common pathways involving chronic hyperglycemia, advanced glycation end products (AGEs) formation, oxidative stress, and chronic low-grade inflammation (4). These same mechanisms may potentially affect pulmonary structure and function through several interconnected pathways. The lung's extensive microvascular network, comprising the largest capillary bed in the human body, makes it particularly susceptible to diabetic microangiopathy, similar to that observed in diabetic retinopathy and nephropathy (5). Furthermore, chronic hyperglycemia leads to nonenzymatic glycosylation of structural proteins, including collagen and elastin in lung tissues, potentially altering pulmonary mechanics and reducing lung elasticity (6).

Pulmonary function tests (PFTs), particularly spirometry, provide objective and reproducible measures of respiratory function that can detect subclinical abnormalities before the onset of clinical symptoms (7). Spirometry measures various parameters including forced vital capacity (FVC), forced expiratory volume in one second (FEV1), their ratio (FEV1/FVC), and peak expiratory flow rate (PEFR), which collectively provide insights into both restrictive and obstructive pulmonary pathology (8). The identification of pulmonary dysfunction in diabetic patients could have significant clinical implications, potentially serving as an early marker of systemic microangiopathy and influencing treatment strategies.

Glycemic control, typically assessed through glycated hemoglobin (HbA1c) levels, represents the cornerstone of diabetes management and is strongly associated with the development and progression of diabetic complications (9). HbA1c reflects average blood glucose levels over the preceding 2-3 months and serves as the primary target for therapeutic interventions in diabetes care (10). The relationship between glycemic control and traditional diabetic complications is well-established, with landmark studies demonstrating that intensive glycemic control significantly reduces the risk of microvascular complications (11). However, the specific relationship between glycemic control and pulmonary function in diabetic patients requires further elucidation.

Previous research investigating the association between diabetes and pulmonary function has yielded mixed results, with some studies reporting significant reductions in lung function parameters among diabetic patients, while others have found minimal or no association (12). A systematic review by Klein et al. suggested that diabetic patients may have reduced FVC and FEV1 compared to non-diabetic controls, but the relationship with glycemic control was not consistently demonstrated across studies (13). Similarly, van den Borst et al. conducted a meta-analysis that found modest but significant reductions in pulmonary function parameters in diabetic patients, though the clinical significance of these findings remained unclear (14).

The potential mechanisms linking poor glycemic control to pulmonary dysfunction are multifaceted and complex. Chronic hyperglycemia promotes the formation of AGEs through nonenzymatic glycosylation of proteins, including structural proteins in the lung parenchyma and chest wall (15). These AGEs accumulate in collagen and elastin fibers, leading to increased cross-linking and reduced tissue elasticity, which may manifest as restrictive pulmonary dysfunction. Additionally, diabetic microangiopathy affects pulmonary capillaries, potentially leading to thickening of the alveolar-capillary membrane and impaired gas exchange, similar to the pathological changes observed in diabetic nephropathy and retinopathy.

Understanding the relationship between glycemic control and pulmonary function has important clinical implications for the comprehensive management of diabetic patients. If poor glycemic control is indeed associated with pulmonary dysfunction, this could provide additional motivation for intensive diabetes management and could potentially serve as an early marker for systemic diabetic complications. Furthermore, the identification of pulmonary dysfunction in diabetic patients might prompt earlier interventions to prevent progression to clinically significant respiratory impairment, thereby improving overall patient outcomes and quality of life.

Aims

To evaluate the correlation between pulmonary function tests and glycemic control (HbA1c) in patients with type 2 diabetes mellitus.

Study Design and Setting

This observational cross-sectional study was conducted at the Department of General Medicine, The Oxford Medical College Hospital and Research Centre, Bangalore, Karnataka, India, over a period of 18 months from May 2023 to September 2024. The study protocol was approved by the Institutional Ethics Committee, and all procedures were conducted in accordance with the Declaration of Helsinki.

Study Population and Sampling

The study population comprised patients visiting the outpatient department and admitted to the inpatient department of General Medicine who were diagnosed with Type 2 Diabetes Mellitus. Consecutive sampling was employed, where all eligible patients meeting the inclusion criteria were enrolled until the calculated sample size was achieved.

Sample Size Calculation

Sample size was calculated based on a previous study by Ashok Kumar et al., considering the mean and standard deviation of pulmonary function tests among Type 2 DM patients. Using the formula n = (Z²×sd²)/d², where mean = 2.14, standard deviation = 0.61, and precision (d) = 0.10, the calculated sample size was 143 patients.

Inclusion Criteria

Adults aged 30-60 years diagnosed with Type 2 Diabetes Mellitus according to American Diabetes Association (ADA) criteria were included in the study.

Exclusion Criteria

Patients were excluded if they had: (1) cardiovascular diseases such as heart failure, valvular heart disease, or ischemic heart disease; (2) physical disabilities affecting lung function, including kyphoscoliosis, pectus carinatum, or pectus excavatum; (3) history of smoking; (4) previous history of respiratory diseases or occupational exposure that could compromise lung function; (5) known contraindications to spirometry such as acute myocardial infarction or increased intracranial/intraocular pressure as per American Thoracic Society guidelines.

Data Collection

After obtaining written informed consent, demographic data and detailed medical history were collected using a standardized questionnaire. Particular attention was given to smoking history, duration of diabetes, and current medications. Physical examination was performed, and anthropometric measurements were recorded.

Anthropometric Measurements

Height was measured using a stadiometer to the nearest 0.1 cm, and weight was recorded using a calibrated weighing scale to the nearest 0.1 kg. Body Mass Index (BMI) was calculated as weight in kilograms divided by the square of height in meters (kg/m²).

Laboratory Investigations

Under aseptic precautions, blood samples were collected for fasting blood sugar (FBS), postprandial blood sugar (PPBS), and glycated hemoglobin (HbA1c). All biochemical analyses were performed using photometric technique on EM-360 machine. HbA1c levels were categorized as: good control (<7%), moderate control (7-8%), and poor control (>8%).

Pulmonary Function Testing

Pulmonary function tests were performed using a computerized spirometer (SPIROMETER HELIOS 401) according to American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines. The procedure was explained to each participant, and proper technique was demonstrated. Each participant performed at least three acceptable spirometry maneuvers, with the best of the three selected for analysis. The parameters measured included Forced Vital Capacity (FVC), Forced Expiratory Volume in one second (FEV1), FEV1/FVC ratio, and Peak Expiratory Flow Rate (PEFR). All measurements were expressed both in absolute values and as percentage of predicted values based on age, sex, height, and ethnicity. All spirometry tests were conducted by a trained technician who was blinded to the participants' clinical status.

Pulmonary Function Pattern Classification

Based on spirometry results, patients were classified into three categories: (1) Normal pattern: FEV1 ≥80% predicted, FVC ≥80% predicted, and FEV1/FVC ≥0.70; (2) Restrictive pattern: FVC <80% predicted with FEV1/FVC ≥0.70; (3) Obstructive pattern: FEV1/FVC <0.70.

Statistical Analysis

Data were entered in Microsoft Excel and analyzed using Statistical Package for Social Sciences (SPSS) version 15.0. Descriptive statistics including means, standard deviations, and frequencies were calculated for all variables. Pearson correlation coefficient was used to assess the relationship between HbA1c levels and pulmonary function parameters. Independent t-tests were used for comparing means between groups. A p-value of <0.05 was considered statistically significant. All correlation analyses were performed to evaluate the relationship between glycemic control and various pulmonary function parameters.

Ethical Considerations

The study maintained strict patient confidentiality throughout the research process. All procedures were performed by trained healthcare professionals to minimize patient discomfort. Participants were informed that they could withdraw from the study at any time without affecting their medical care.

Baseline Characteristics

This cross-sectional study included 143 patients with Type 2 Diabetes Mellitus. The gender distribution showed a male predominance with 82 patients (57.3%) being male and 61 patients (42.7%) being female. The age distribution was relatively balanced across the study range, with 54 patients (37.8%) in the 30-40 years age group, 41 patients (28.7%) in the 41-50 years age group, and 48 patients (33.6%) in the 51-60 years age group, indicating a mean age distribution that allowed for comprehensive analysis across different age decades.

The Body Mass Index distribution revealed that the majority of patients were overweight or obese. Specifically, 82 patients (57.3%) were classified as obese (BMI >27.5 kg/m²), 30 patients (21%) were overweight (BMI 23-27.4 kg/m²), 21 patients (14.7%) had normal BMI (18.5-22.9 kg/m²), and 10 patients (7%) were underweight (BMI <18.5 kg/m²). This distribution indicated that 78.3% of the study population had BMI ≥23 kg/m², reflecting the strong association between elevated body weight and Type 2 Diabetes Mellitus.

Regarding the duration of diabetes, the distribution was relatively even across different time periods. Fifty-three patients (37.1%) had diabetes for less than 5 years, 43 patients (30.1%) had diabetes for 5-10 years, and 47 patients (32.9%) had diabetes for more than 10 years. This balanced distribution across duration categories provided an opportunity to assess the impact of disease duration on pulmonary function parameters.

Glycemic Control Status

The assessment of glycemic control revealed concerning findings regarding diabetes management in the study population. Only 32 patients (22.4%) achieved good glycemic control with HbA1c levels below 7%, while 31 patients (21.7%) had moderate control with HbA1c levels between 7-8%. The majority of patients, 80 individuals (55.9%), demonstrated poor glycemic control with HbA1c levels exceeding 8%. This distribution indicated that more than three-quarters of the study population had suboptimal glycemic control, with over half having significantly elevated HbA1c levels.

Pulmonary Function Test Results

The pulmonary function test parameters showed the following mean values: FVC was 3.78±0.64 L with a percentage predicted of 87.1±14.8%, FEV1 was 3.11±0.53 L with a percentage predicted of 86.4±14.7%, the FEV1/FVC ratio was 0.82±0.049 with a percentage predicted of 82.29±4.97%, and PEFR was 7.22±1.29 L with a percentage predicted of 88.6±13.6%. These values indicated mild reductions in lung volumes and flow rates compared to predicted normal values for the study population.

The analysis of pulmonary function test patterns revealed significant abnormalities in the majority of patients. Normal pulmonary function was observed in 52 patients (36.4%), while 81 patients (56.6%) exhibited a restrictive pattern characterized by reduced lung volumes with preserved FEV1/FVC ratio. Only 10 patients (7%) demonstrated an obstructive pattern. The predominance of restrictive dysfunction suggests that diabetes-related changes primarily affect lung compliance and expandability rather than airway obstruction.

Correlation Between HbA1c and Pulmonary Function Tests

The primary objective of this study was to evaluate the correlation between glycemic control and pulmonary function parameters. The analysis revealed statistically significant negative correlations between HbA1c levels and several pulmonary function parameters. HbA1c showed a significant negative correlation with FVC percentage predicted (r=-0.213, p=0.01), indicating that higher HbA1c levels were associated with reduced forced vital capacity. Similarly, HbA1c demonstrated a significant negative correlation with FEV1 percentage predicted (r=-0.202, p=0.02), suggesting that poor glycemic control was associated with decreased forced expiratory volume in one second.

The correlation analysis also revealed a significant negative relationship between HbA1c and PEFR percentage predicted (r=-0.172, p=0.04), indicating that elevated HbA1c levels were associated with reduced peak expiratory flow rates. Interestingly, HbA1c showed a positive correlation with the FEV1/FVC ratio (r=0.178, p=0.03), which is consistent with a restrictive pattern where both FEV1 and FVC are reduced proportionally, but FVC reduction is more pronounced, resulting in a relatively preserved or even elevated FEV1/FVC ratio.

Analysis by HbA1c Categories

To further understand the relationship between glycemic control and pulmonary function, patients were stratified according to their HbA1c levels. Patients with HbA1c levels below 7% (good control) had mean FVC of 3.94±0.65 L and mean FEV1 of 3.19±0.55 L. Those with HbA1c levels between 7-8% (moderate control) had mean FVC of 3.85±0.59 L and mean FEV1 of 3.15±0.51 L. Patients with HbA1c levels above 8% (poor control) demonstrated the lowest values with mean FVC of 3.71±0.63 L and mean FEV1 of 3.07±0.49 L. Although the differences between groups did not reach statistical significance in direct comparison, the declining trend was consistent with the correlation analysis and demonstrated a dose-response relationship between glycemic control and pulmonary function parameters.

The percentage predicted values also followed similar patterns, with patients having better glycemic control generally showing higher percentage predicted values for FVC, FEV1, and PEFR compared to those with poor glycemic control. This finding supports the hypothesis that chronic hyperglycemia has a detrimental effect on pulmonary function in patients with Type 2 Diabetes Mellitus.

Table 1: Baseline Characteristics of Study Population

Table 2: Pulmonary Function Test Parameters

Table 3: Distribution of Pulmonary Function Test Patterns

Table 4: Correlation of HbA1c with Pulmonary Function Tests

*Statistically significant (p<0.05)

Table 5: Pulmonary Function Parameters by HbA1c Categories

The present study demonstrates a significant association between poor glycemic control and reduced pulmonary function in patients with Type 2 Diabetes Mellitus, with the majority of patients exhibiting a restrictive pattern of pulmonary dysfunction. These findings contribute to the growing body of evidence suggesting that the lungs may represent an underrecognized target organ in diabetic complications, with important implications for the comprehensive management of diabetic patients.

The observed negative correlation between HbA1c levels and pulmonary function parameters (FVC % predicted: r=-0.213, p=0.01; FEV1 % predicted: r=-0.202, p=0.02) aligns with several previous studies that have investigated this relationship. Agarwal et al. reported similar findings in their study of 100 diabetic patients, demonstrating significant negative correlations between HbA1c and both FVC (r=-0.37, p<0.01) and FEV1 (r=-0.34, p<0.01), with correlation coefficients stronger than those observed in our study (16). This difference might be attributed to variations in study population characteristics, duration of diabetes, or degree of glycemic control between the two studies.

Aparna et al. conducted a comparative study involving 60 diabetic patients and found that patients with HbA1c levels above 8% had significantly lower FVC (2.89±0.48 L vs 3.21±0.52 L, p<0.01) and FEV1 (2.34±0.41 L vs 2.67±0.45 L, p<0.01) compared to those with better glycemic control (17). These findings are consistent with our observations, where patients with HbA1c >8% demonstrated lower mean FVC (3.71±0.63 L) and FEV1 (3.07±0.49 L) values compared to those with HbA1c <7% (FVC: 3.94±0.65 L; FEV1: 3.19±0.55 L), though the differences in our study did not reach statistical significance in direct group comparisons.

The predominance of restrictive pulmonary dysfunction (56.6%) observed in our study is consistent with the pathophysiological mechanisms underlying diabetic lung disease. Klein et al., in their systematic review of 40 studies involving over 3,000 diabetic patients, found that diabetes was consistently associated with reduced lung volumes, particularly FVC and total lung capacity, supporting a restrictive pattern of impairment (18). The restrictive pattern observed in our study aligns with the concept of "diabetic lung disease," where chronic hyperglycemia leads to structural changes in lung parenchyma through nonenzymatic glycosylation of proteins and microangiopathy.

The positive correlation between HbA1c and FEV1/FVC ratio (r=0.178, p=0.03) observed in our study further supports the restrictive nature of pulmonary dysfunction in diabetes. This finding indicates that while both FEV1 and FVC are reduced in diabetic patients, the reduction in FVC is proportionally greater, resulting in a relatively preserved or even elevated FEV1/FVC ratio. This pattern is characteristic of restrictive lung disease and contrasts with obstructive conditions where the FEV1/FVC ratio is typically reduced.

Shah et al. investigated pulmonary function in 50 diabetic patients and found that 34% had restrictive abnormalities, which is somewhat lower than our finding of 56.6% (19). However, their study included patients with a shorter mean duration of diabetes (6.2±4.3 years) compared to our more diverse population with varying disease durations. This difference suggests that the prevalence of restrictive dysfunction may increase with longer exposure to hyperglycemia, supporting the concept of progressive pulmonary damage in diabetes.

The pathophysiological mechanisms underlying the observed correlations likely involve multiple interconnected pathways. Chronic hyperglycemia promotes the formation of advanced glycation end products (AGEs) through nonenzymatic glycosylation of structural proteins in the lung, including collagen and elastin. These AGEs accumulate in lung tissues, leading to increased cross-linking and reduced elasticity, which manifests as restrictive pulmonary dysfunction. Marvisi et al. demonstrated that diabetic patients had significantly elevated markers of collagen metabolism compared to controls, supporting this mechanism (20).

Additionally, diabetic microangiopathy affects the pulmonary capillary bed, potentially leading to thickening of the alveolar-capillary membrane and impaired gas exchange. Weynand et al. used electron microscopy to demonstrate thickening of alveolar epithelial and pulmonary capillary basal laminae in diabetic patients, with the degree of thickening correlating with the severity of diabetic complications in other organs (21). This finding suggests that pulmonary changes in diabetes may parallel those occurring in other target organs such as the kidneys and retina.

The chronic inflammatory state associated with diabetes may also contribute to pulmonary dysfunction. Elevated levels of inflammatory markers such as C-reactive protein, interleukin-6, and tumor necrosis factor-alpha in diabetic patients can promote pulmonary inflammation and fibrosis, leading to structural changes that impair lung function. This inflammatory pathway may explain why patients with poor glycemic control, who typically have higher levels of systemic inflammation, demonstrate greater reductions in pulmonary function parameters.

Our findings have important clinical implications for the management of diabetic patients. The significant correlation between HbA1c and pulmonary function suggests that achieving and maintaining optimal glycemic control may help preserve lung function in diabetic patients. This provides additional motivation for intensive diabetes management beyond the well-established benefits for preventing traditional diabetic complications such as retinopathy, nephropathy, and neuropathy.

The high prevalence of restrictive pulmonary dysfunction (56.6%) in our diabetic population suggests that pulmonary function assessment should be considered as part of the comprehensive evaluation of diabetic patients, particularly those with poor glycemic control. Early detection of subclinical pulmonary dysfunction could prompt more aggressive diabetes management and potentially prevent progression to clinically significant respiratory impairment.

However, our study has several limitations that should be acknowledged. The cross-sectional design limits our ability to establish causality between poor glycemic control and pulmonary dysfunction. Longitudinal studies would be needed to definitively establish whether improving glycemic control leads to improvements in pulmonary function. Additionally, our study excluded patients with known respiratory diseases and smoking history, which may limit the generalizability of findings to the broader diabetic population.

The single-center design and specific demographic characteristics of our study population may also limit the generalizability of findings to other populations with different ethnic backgrounds, environmental exposures, or healthcare access patterns. Furthermore, we did not assess other potential confounding factors such as physical activity levels, nutritional status, or presence of diabetic complications in other organs, which might influence the relationship between glycemic control and pulmonary function.

Despite these limitations, our study provides valuable evidence supporting the relationship between glycemic control and pulmonary function in diabetic patients. The consistent negative correlations observed between HbA1c and multiple pulmonary function parameters, combined with the high prevalence of restrictive dysfunction, suggest that pulmonary complications should be considered an important aspect of diabetic care.

This study demonstrates a significant negative correlation between glycemic control (HbA1c) and pulmonary function parameters in patients with Type 2 Diabetes Mellitus. Poor glycemic control, as indicated by elevated HbA1c levels, was associated with reduced FVC, FEV1, and PEFR, predominantly manifesting as a restrictive pattern of pulmonary dysfunction. The majority of diabetic patients (56.6%) exhibited restrictive pulmonary dysfunction, with only 36.4% maintaining normal pulmonary function. These findings suggest that the lungs represent an important target organ in diabetic complications, and pulmonary dysfunction may serve as an early marker of systemic diabetic microangiopathy.

The clinical implications of these findings are significant, as they suggest that regular pulmonary function assessment should be considered in the comprehensive care of diabetic patients, particularly those with poor glycemic control. The correlation between HbA1c and pulmonary function parameters provides additional motivation for achieving and maintaining optimal glycemic control, as this may help preserve lung function and prevent progression to clinically significant respiratory impairment.

Early detection of subclinical pulmonary dysfunction through spirometry could prompt more intensive diabetes management strategies and potentially improve long-term outcomes for diabetic patients. Healthcare providers caring for diabetic patients should be aware of the potential for pulmonary complications and consider incorporating pulmonary function assessment into routine diabetic care, especially for patients with persistently elevated HbA1c levels.

Future research should focus on longitudinal studies to establish causality and determine whether improvements in glycemic control lead to corresponding improvements in pulmonary function. Additionally, studies investigating the effectiveness of specific interventions targeting both glycemic control and pulmonary function in diabetic patients would provide valuable insights for optimizing patient care and outcomes.

1. Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res Clin Pract. 2019;157:107843.
2. American Diabetes Association. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2023. Diabetes Care. 2023;46(Suppl 1):S19-S40.
3. Lecube A, Simó R, Pallayova M, Punjabi NM, López-Cano C, Turino C, et al. Pulmonary Function and Sleep Breathing: Two New Targets for Type 2 Diabetes Care. Endocr Rev. 2017;38(6):550-573.
4. Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54(6):1615-25.
5. Pitocco D, Fuso L, Conte EG, Zaccardi F, Condoluci C, Scavone G, et al. The diabetic lung - a new target organ? Rev Diabet Stud. 2012;9(1):23-35.
6. Geerlings SE, Hoepelman AI. Immune dysfunction in patients with diabetes mellitus (DM). FEMS Immunol Med Microbiol. 1999;26(3-4):259-65.
7. Miller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, Coates A, et al. Standardisation of spirometry. Eur Respir J. 2005;26(2):319-338.
8. Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R, et al. Interpretative strategies for lung function tests. Eur Respir J. 2005;26(5):948-68.
9. Nathan DM, Genuth S, Lachin J, Cleary P, Crofford O, Davis M, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329(14):977-86.
10. American Diabetes Association. Glycemic targets: Standards of medical care in diabetes-2023. Diabetes Care. 2023;46(Suppl 1):S97-S110.
11. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352(9131):837-53.
12. Kinney GL, Black-Shinn JL, Wan ES, Make B, Regan E, Lutz S, et al. Pulmonary function reduction in diabetes with and without chronic obstructive pulmonary disease. Diabetes Care. 2014;37(2):389-395.
13. Klein OL, Krishnan JA, Glick S, Smith LJ. Systematic review of the association between lung function and Type 2 diabetes mellitus. Diabet Med. 2010;27(9):977-987.
14. van den Borst B, Gosker HR, Zeegers MP, Schols AM. Pulmonary function in diabetes: a metaanalysis. Chest. 2010;138(2):393-406.
15. Singh VP, Bali A, Singh N, Jaggi AS. Advanced glycation end products and diabetic complications. Korean J Physiol Pharmacol. 2014;18(1):1-14.
16. Agarwal AS, Singh NP, Kumar A, Sinha N. Pulmonary function tests in type 2 diabetes mellitus and their correlation with anthropometric and metabolic parameters. J Clin Diagn Res. 2013;7(8):1588-91.
17. Aparna S, Nanda N, Sreekanth Y, Prasad KVK. Evaluation of pulmonary function tests in type 2 diabetes mellitus: a comparative study. Int J Adv Med. 2018;5(3):626-30.
18. Klein OL, Meltzer D, Carnethon M, Krishnan JA. Type II diabetes mellitus is associated with decreased measures of lung function in a clinical setting. Respir Med. 2011;105(7):1095-1098.
19. Shah SH, Sonawane P, Nahar P, Vaidya S, Salvi S. Pulmonary function tests in type 2 diabetes mellitus and their association with glycemic control and duration of the disease. Lung India. 2013;30(2):108-12.
20. Marvisi M, Bartolini L, Del Borrello P, Brianti M, Marani G, Guariglia A, et al. Pulmonary function in non-insulin-dependent diabetes mellitus. Respiration. 2001;68(3):268-72.
21. Weynand B, Jonckheere A, Frans A, Rahier J. Diabetes mellitus induces a thickening of the pulmonary basal lamina. Respiration. 1999;66(1):14-9.