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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiologic evidences suggest that obstructive sleep apnea syndrome(OSAS) itself induces risk factors for cardiovascular diseases(= insulin resistance) independent of obesity. Our data suggest that moderate to severe OSA(AHI = > 20) is a contributing factor to the development of hyperinsulinemia, abnormal glucose metabolism and non-insulin-dependent diabetes mellitus(NIDDM) independent of aging, obesity and hereditary predisposition for DM in patients with OSAS. On the other hand, disagreement exists as to the incidence of OSAS in DM patients. Some authors reported that the incidence of OSAS was high among patients with DM, while others did not find such relationship. In these studies, the number of cases studied was small and, in addition, the selection of patients may have been biased. Future clinical research is needed to answer this issue.
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PMID:[Diabetes mellitus and sleep apnea syndrome]. 1094 40

The prevalence and severity of obesity are increasing in children and adolescents. This raises concerns about the accompanying cardiovascular complications. Such complications include hypertension, dyslipidemia, type II diabetes which may accelerate vascular disease, left ventricular hypertrophy and pulmonary hypertension due to obstructive sleep apnea. The evaluation of an obese child or adolescent should include careful consideration of these possible cardiovascular complications. If they are present, treatment should be directed at both obesity and the risk factor abnormality. This treatment may be important for prevention of future cardiovascular morbidity and mortality. In addition, research is necessary to better understand the mechanisms by which obesity increases the risk of cardiovascular disease.
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PMID:Obesity in the pediatric patient: cardiovascular complications. 1122 43

Severe obstructive sleep apnea (OSAS) is most often accompanied by metabolic syndrome, obesity, diabetes and coronary disease. In its most severe form, it is a life-threatening condition, requiring active and immediate help. Nasal continuous positive airway pressure (CPAP) is the most efficient nonsurgical treatment for patients with OSAS. However, for anatomical, disease-related and subjective reasons, many patients cannot accept this treatment. A permanent tracheostomy may be one alternative in such patients who, in addition, often suffer from extreme obesity and severe heart disease. In this paper, we describe the long-term follow-up results of 7 patients suffering from OSAS and treated with permanent tracheostomy. All the patients (5 men, 2 women) were diagnosed using the static charge sensitive bed method and night-time oximetry for sleep analysis. The mean body mass index (BMI) of the patients ranged from 34 to 60 and the age from 41 to 64 years. All the patients had severe OSAS and long periods of low oxygen saturation (SaO2) levels. Six patients had a CPAP trial before tracheostomy. Only 2 patients tolerated the trial but, despite the continuous use of CPAP, they were nonresponders. Permanent tracheostomy was done according to normal routine in each patient. After primary healing of 2 days, they used silver cannulae, which also allowed them to speak. The patients were evaluated every year after the tracheostomy. After some practical difficulties including proper maintenance of the cannula, all the patients quickly learned the correct management. In postoperative sleep studies, nadir SaO2 levels had improved significantly, obstructive apneas had disappeared and the subjective quality of life had improved. No marked changes in BMI were found.
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PMID:Long-term results of tracheostomy for severe obstructive sleep apnea syndrome. 1135 89

We wished to determine if obstructive sleep apnea (OSA) is associated with increased left ventricular mass (LVM) and impaired left ventricular diastolic function (LVDF) independently of coexisting obesity, hypertension (HTN), and diabetes mellitus (DM). Patients without primary cardiac disease, referred for evaluation of OSA (n = 533), had overnight polysomnography and Doppler echocardiography while awake. Patients were divided, according to the apnea-hypopnea index (AHI), into an OSA group (AHI > or = 5/h, n = 353) and a non-OSA group (AHI < 5/h, n = 180). In men, LVM was greater in the OSA group (98.9 +/- 25.6 versus 92.3 +/- 22.5 g/m, p = 0.023) despite exclusion of those with HTN and DM. A similar trend was noted in women. Regression analysis revealed that LVM was correlated with body mass index (BMI) (beta = 0.480, p < 0.0005), age (beta = 0.16, p = 0.001), and the presence of HTN (beta = 0.137, p = 0.003) in men and with BMI (beta = 0.501, p < 0.0005) in women, but not with AHI or oxygen saturation during sleep. The ratio of peak early filling velocity to peak late filling velocity (E/A), an index of LVDF, was similar in both groups (1.28 +/- 0.32 versus 1.34 +/- 0.31, p = 0.058); it was correlated with age (beta = -0.474, p < 0.0005), but not with AHI or oxygen saturation during sleep. We conclude that OSA is not associated with increased LVM or impaired LVDF independently of obesity, HTN, or advancing age.
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PMID:Impact of obstructive sleep apnea on left ventricular mass and diastolic function. 1140 86

At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish "redox homeostasis." Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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PMID:Free radicals in the physiological control of cell function. 1177 9

The primary aim of this exploratory study was to examine the association between obstructive sleep apnea (OSA) symptoms, nocturia and diabetes in African-American community-dwelling older adults. A pencil and paper survey was used to collect symptoms of OSA, nocturia, excessive daytime sleepiness (EDS), lower urinary tract symptoms (LUT), and self-rated health. The convenience sample of community dwelling African-Americans (n = 87) included a majority of women (61%) and obese persons (60% with BMI > 30). The mean age was 64 years (range 50-91), and 40% were self reported Type 2 diabetics. Diabetics had significantly more OSA symptoms, more nocturia, and decreased self-rated health. Results of a stepwise logistic regression showed that persons with diabetes and those who reported EDS experienced significant three to four-fold risks for OSA. Similarly, diabetics, women, persons with LUT symptoms and those reporting EDS, had significant three to six-fold risks for nocturia > or = 2/night.
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PMID:Sleep apnea symptoms, nocturia, and diabetes in African-American community dwelling older adults. 1185 86

Epidemiological studies have implicated obstructive sleep apnea (OSA) as an independent comorbid factor in cardiovascular and cerebrovascular diseases. It is postulated that recurrent episodes of occlusion of upper airways during sleep result in pathophysiological changes that may predispose to vascular diseases. Insulin resistance is a known risk factor for atherosclerosis, and we postulate that OSA represents a stress that promotes insulin resistance, hence atherogenesis. This study investigated the relationship between sleep-disordered breathing and insulin resistance, indicated by fasting serum insulin level and insulin resistance index based on the homeostasis model assessment method (HOMA-IR). A total of 270 consecutive subjects (197 male) who were referred for polysomnography and who did not have known diabetes mellitus were included, and 185 were documented to have OSA defined as an apnea-hypopnea index (AHI) > or =5. OSA subjects were more insulin resistant, as indicated by higher levels of fasting serum insulin (p = 0.001) and HOMA-IR (p < 0.001); they were also older and more obese. Stepwise multiple linear regression analysis showed that obesity was the major determinant of insulin resistance but sleep-disordered breathing parameters (AHI and minimum oxygen saturation) were also independent determinants of insulin resistance (fasting insulin: AHI, p = 0.02, minimum O(2), p = 0.041; HOMA-IR: AHI, p = 0.044, minimum O(2), p = 0.022); this association between OSA and insulin resistance was seen in both obese and nonobese subjects. Each additional apnea or hypopnea per sleep hour increased the fasting insulin level and HOMA-IR by about 0.5%. Further analysis of the relationship of insulin resistance and hypertension confirmed that insulin resistance was a significant factor for hypertension in this cohort. Our findings suggest that OSA is independently associated with insulin resistance, and its role in the atherogenic potential of sleep disordered breathing is worthy of further exploration.
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PMID:Obstructive sleep apnea is independently associated with insulin resistance. 1187 3

Between 1991-2000 2052 patients (81% men and 19% women) were referred to our Sleep Laboratory because of OSA suspision. In 1194 (58%) subjects (88% men and 12% women) diagnosis of obstructive sleep apnoea (OSA, AHI > 10) was confirmed. In 430 of them (36%) mild OSA (AHI 11-25), in 243 (20%) moderate OSA (AHI 26-40), and in 521 (44%) severe OSA (AHI > 40) was diagnosed. Epworth sleepiness scale score in those groups was 10.4, 10.5 and 13.0 points respectively. 908 (76%) of patients with OSA were submitted to nCPAP treatment. Effective CPAP pressure ranged from 5 to 20 milibars, mean 8.4 mbars. In 21 patients upper airway resistance syndrome (UARS) was diagnosed. Central sleep apnoea, most frequently of Cheyne-Stokes respiration type was diagnosed in 13 patients. The most common diseases accompanying OSA were: systemic hypertension (46%), coronary heart disease (29%), diabetes (12%), and COPD (9%). Majority of OSA patients (61%) were obese (BMI > 30 kg/m2), 32% were over weight (BMI 25-30 kg/m2). Only 7% had normal body weight (BMI 20-25 kg/m2). Long-term (more than one year) compliance to treatment was found in 70% of patients prescribed CPAP.
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PMID:[Ten years experience of the sleep laboratory at the Institute of Tuberculosis and Lung Disease in Warsaw]. 1192 60

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.
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PMID:[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome]. 1208 46

The incidence of a cardiovascular disease (CVD) was explored in a consecutive sleep clinic cohort of 182 middle-aged men (mean age, 46.8 +/- 9.3; range, 30-69 years in 1991) with or without obstructive sleep apnea (OSA). All subjects were free of hypertension or other CVD, pulmonary disease, diabetes mellitus, psychiatric disorder, alcohol dependency, as well as malignancy at baseline. Data were collected via the Swedish Hospital Discharge Register covering a 7-year period before December 31, 1998, as well as questionnaires. Effectiveness of OSA treatment initiated during the period as well as age, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP) at baseline, and smoking habits were controlled. The incidence of at least one CVD was observed in 22 of 60 (36.7%) cases with OSA (overnight oxygen desaturations of 30 or more) compared with in 8 of 122 (6.6%) subjects without OSA (p < 0.001). In a multiple logistic regression model, significant predictors of CVD incidence were OSA at baseline (odds ratio [OR] 4.9; 95% confidence interval [CI], 1.8-13.6) and age (OR 23.4; 95% CI, 2.7-197.5) after adjustment for BMI, SBP, and DBP at baseline. In the OSA group, CVD incidence was observed in 21 of 37 (56.8%) incompletely treated cases compared with in 1 of 15 (6.7%) efficiently treated subjects (p < 0.001). In a multiple regression analysis, efficient treatment was associated with a significant risk reduction for CVD incidence (OR 0.1; 95% CI, 0.0-0.7) after adjustment for age and SBP at baseline in the OSA subjects. We conclude that the risk of developing CVD is increased in middle-aged OSA subjects independently of age, BMI, SBP, DBP, and smoking. Furthermore, efficient treatment of OSA reduces the excess CVD risk and may be considered also in relatively mild OSA without regard to daytime sleepiness.
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PMID:Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. 1211 27


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