Indications of reduced pulmonary function in type 1 (insulin-dependent) diabetes mellitus

Innocenti, F.; Fabbri, Alessandro; Anichini, Roberto; Tuci, S.; Pettinà, G; Vannucci, Francesco; Giorgio, L. A. De; Seghieri, Giuseppe

doi:10.1016/0168-8227(94)90004-3

Cited by 61 publications

(60 citation statements)

References 23 publications

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“…This was especially true of the children with poor glycaemic control. Our study therefore extends the existing knowledge on reduced DL CO in adult patients with type 1 diabetes [12,13,14,15,16], suggesting that this lung function index starts to decline in childhood.…”

Section: Discussionsupporting

confidence: 83%

“…This biochemical mechanism would also plausibly explain why patients with the highest HbA 1 c had the lowest DL CO. Published data on lung mechanics in diabetic subjects are conflicting. Some reports describe decreased volumes and flows in diabetic adults [12,13,14,15], adolescents [9,11] and children [17,18] as compared with control subjects or reference values. Others, conversely, report normal lung volumes and flows in diabetic adults [8,16,32,33], adolescents [9,34] and children [19].…”

Section: Discussionmentioning

confidence: 99%

“…Because pulmonary function and gas exchange depend partly on the integrity of the connective tissue and microcirculation within the lung, changes involving these structural components could lead to mechanical lung dysfunction and impaired blood gas exchange [6,7,8]. Studies conducted in adult patients with type 1 diabetes report diminished elastic lung recoil [9,10], reduced lung volumes [11,12,13,14,15] and altered alveolocapillary diffusion [12,14,16]. Various mechanisms have been proposed to explain reduced diffusing capacity, including alveolocapillary membrane thickening due to non-enzymatic glycosylation of lysine and hydroxyproline [5,6] and decreased capillary bloodflow volume [10].…”

Section: Introductionmentioning

confidence: 99%

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Diffusing capacity for carbon monoxide in children with type 1 diabetes

et al. 2004

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Aims/hypothesis. Few data are available on lung dysfunction in children with diabetes. We studied the association of pulmonary function variables (flows, volumes and alveolar capillary diffusion) with disease-related variables in children with type 1 diabetes mellitus. Methods. We studied 39 children with type 1 diabetes (mean age 10.9±2.6 years, disease duration 3.6±2.4 years, insulin·kg −1 ·day −1 0.77±0.31) and 30 healthy control children (mean age 10.4±3.0 years). Pulmonary function tests included spirometry, N 2 wash-out and the single-breath diffusing capacity for carbon monoxide (DL CO Conclusions/interpretation. In children with type 1 diabetes, the diffusing capacity diminishes early in childhood and is associated with poor metabolic control. Although low DL CO /V A levels in these children probably reflect pulmonary microangiopathy induced by type 1 diabetes, other factors presumably influencing CO diffusion capacity measurements (e.g. a left shift in HbA 1 c resulting in high O 2 binding and low CO binding) could explain the apparent capillary and alveolar basal membrane dysfunction.Keywords Children · Lung function · Pulmonary gas exchange · Type 1 diabetes mellitus

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Diffusing capacity for carbon monoxide in children with type 1 diabetes

et al. 2004

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“…The presence of these alterations could be regarded as the manifestation of diabetic microangiopathy. To confirm these considerations, it has been demonstrated that the reduction of DLCO in diabetic patients correlates with the severity of other vascular complications, such as retinopathy and renal microangiopathy [30,34,35,56]. The increased thickness of the alveolarcapillary barrier and the expansion of the interstitium are associated with a reduction of alveolar space and a narrowing of the pulmonary capillary network [21,36].…”

Section: Pulmonary Diffusing Capacity For Carbon Monoxide (Dlco)mentioning

confidence: 99%

“…It was also shown that the diabetes patients had a reduced pulmonary diffusing capacity for carbon monoxide (DLCO) [32]. This effect was attributed to vascular injury of pulmonary capillaries related to diabetic microangiopathy [30,33,34].…”

Section: Pulmonary Diffusing Capacity For Carbon Monoxide (Dlco)mentioning

confidence: 99%

The Diabetic Lung - A New Target Organ?

Pitocco

Fuso²,

Conte³

et al. 2012

Rev Diabet Stud

140

112

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■ AbstractSeveral abnormalities of the respiratory function have been reported in patients with type 1 and type 2 diabetes. These abnormalities concern lung volume, pulmonary diffusing capacity, control of ventilation, bronchomotor tone, and neuroadrenergic bronchial innervation. Many hypotheses have emerged, and characteristic histological changes have been described in the "diabetic lung", which could explain this abnormal respiratory function. Given the specific abnormalities in diabetic patients, the lung could thus be considered as a target organ in diabetes. Although the practical implications of these functional changes are mild, the presence of an associated acute or chronic pulmonary and/or cardiac disease could determine severe respiratory derangements in diabetic patients. Another clinical consequence of the pulmonary involvement in diabetes is the accelerated decline in respiratory function. The rate of decline in respiratory function in diabetics has been found to be two-to-three times faster than in normal non-smoking subjects, as reported in longitudinal studies. This finding, together with the presence of anatomical and biological changes similar to those described in the aging lung, indicates that the "diabetic lung" could even be considered a model of accelerated aging. This review describes and analyses the current insight into the relationship of diabetes and lung disease, and suggests intensifying research into the lung as a possible target organ in diabetes.

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The relationship between nitric oxide and leptin in the lung of rat with streptozotocin‐induced diabetes

Öztay

Kandil

Gúrel

et al. 2007

Cell Biochemistry & Function

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Lung structural changes and immunoreactivity of endothelial (eNOS)- and inducible nitric oxide synthase (iNOS) were investigated by light microscopy in lungs of treated and untreated diabetic rats. Diabetes was induced by a single intraperitoneal (i.p.) injection of 65 mg kg(-1) streptozotocin (STZ) in Wistar albino male rats. Diabetic rats received daily i.p. doses of dexamethasone (2 mg kg(-1)), leptin (0.5 microg kg(-1)) and intramuscular insulin (20 U kg(-1)) or a combination of these drugs for 1 week starting 4 weeks after the STZ injections. After treatment, the blood levels of glucose, leptin, insulin and nitrate/nitrite (NO(3) (-)/NO(2) (-)) were measured. Dilatation of alveoli and alveolar ducts, partial alveolar wall thickening and increased eNOS- and iNOS characterized the diabetic rat lungs. High blood glucose and nitrate/nitrite levels as well as low insulin and leptin levels were also present. Treatment with insulin, dexamethasone and a combination of these drugs resulted in improvement of the structural and immunohistochemical abnormalities. The most effective treatment was insulin therapy. Leptin administration resulted in increased relative amounts of extracellular material, which led to noticeable respiratory efficiency in the diabetic rat lungs. All treatments except leptin lowered blood glucose levels. The combination of insulin and dexamethasone increased blood leptin and insulin, while the remaining diabetic rats had blood with low leptin and insulin concentrations. These results suggest that therapy with insulin plus dexamethasone but not therapy with leptin is beneficial for diabetics.

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Indications of reduced pulmonary function in type 1 (insulin-dependent) diabetes mellitus

Cited by 61 publications

References 23 publications

Diffusing capacity for carbon monoxide in children with type 1 diabetes

Diffusing capacity for carbon monoxide in children with type 1 diabetes

The Diabetic Lung - A New Target Organ?

The relationship between nitric oxide and leptin in the lung of rat with streptozotocin‐induced diabetes

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