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Dm Ii & Sleep Apena

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maxwell18

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Guest jstacy

I saw only one BVA case where Sleep Apnea was claimed secondary to AO exposure. The case was remamded from 1997 and there was no follow up case published. It is possible to claim sleep apnea secondary to DM. The Kicker is Hypertension and getting a Doctor to relate the issues.

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From the University of Maryland Medical Center website:

" Sleep apnea, a disorder in which breathing halts briefly but repeatedly during sleep, is now highly associated with hypertension. A weak but still higher than normal association with high blood pressure has even been observed in those who snore or have mild sleep apnea. The relationship between sleep apnea and hypertension has been thought to be largely due to obesity, but major studies are finding a higher rate of hypertension in people with sleep apnea regardless of their weight. Treating sleep apnea with a device known as nasal continuous positive airway pressure may have modest benefits blood pressure as well."

Hope this helps!

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From the University of Maryland Medical Center website:

" Sleep apnea, a disorder in which breathing halts briefly but repeatedly during sleep, is now highly associated with hypertension. A weak but still higher than normal association with high blood pressure has even been observed in those who snore or have mild sleep apnea. The relationship between sleep apnea and hypertension has been thought to be largely due to obesity, but major studies are finding a higher rate of hypertension in people with sleep apnea regardless of their weight. Treating sleep apnea with a device known as nasal continuous positive airway pressure may have modest benefits blood pressure as well."

Hope this helps!

Do you have the web link to the above quot? I could use the entire document.

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Do you have the web link to the above quot? I could use the entire document.

Sorry, I couldn't find the article source. There's a lot on the internet about sleep apnea and hypertension. Here's an article from the New England Journal of Medicine:

Volume 342:1378-1384 May 11, 2000 Number 19

Prospective Study of the Association between Sleep-Disordered Breathing and Hypertension

Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D.

ABSTRACT

Background Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications).

Methods We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea–hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea–hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes.

Results Relative to the reference category of an apnea–hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea–hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea–hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea–hypopnea index of 15.0 or more events per hour.

Conclusions We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population.

Source Information

From the Departments of Preventive Medicine (P.E.P., T.Y., M.P.), Medicine (J.S.), and Biostatistics and Medical Informatics (M.P.), University of Wisconsin School of Medicine, Madison.

Address reprint requests to Dr. Peppard at the Department of Preventive Medicine, University of Wisconsin, 502 N. Walnut St., Madison, WI 53705, or at ppeppard@facstaff.wisc.edu.

As I said, there's a lot more on this on the internet. But, this is a powerful start!

Ralph

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Do you have the web link to the above quot? I could use the entire document.

Sorry, I couldn't find the article source. There's a lot on the internet about sleep apnea and hypertension. Here's an article from the New England Journal of Medicine:

Volume 342:1378-1384 May 11, 2000 Number 19

Prospective Study of the Association between Sleep-Disordered Breathing and Hypertension

Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D.

ABSTRACT

Background Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications).

Methods We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea–hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea–hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes.

Results Relative to the reference category of an apnea–hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea–hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea–hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea–hypopnea index of 15.0 or more events per hour.

Conclusions We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population.

Source Information

From the Departments of Preventive Medicine (P.E.P., T.Y., M.P.), Medicine (J.S.), and Biostatistics and Medical Informatics (M.P.), University of Wisconsin School of Medicine, Madison.

Address reprint requests to Dr. Peppard at the Department of Preventive Medicine, University of Wisconsin, 502 N. Walnut St., Madison, WI 53705, or at ppeppard@facstaff.wisc.edu.

As I said, there's a lot more on this on the internet. But, this is a powerful start!

Ralph

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Does anyone know if sleep apena is or can be connected to DM II, which was connected by AO rating?

Thanks

Don't know if this connects in the right direction or not, but check this out:

COPYRIGHT © 2006 by the American College of Chest Physicians.

Sleep Apnea: Treatment Options and Comorbid Outcomes

Tuesday, October 24, 2006

12:30 PM - 2:00 PM

THE ASSOCIATION BETWEEN OBSTRUCTIVE SLEEP APNEA SYNDROME AND THE COMPLICATIONS OF DIABETES MELLITUS

Semaan G. Kosseifi, MD*, Alan Peiris, MD, PhD, Beth Bailey, MD, PhD, Robert Price, PhD, Thomas M. Roy, MD, FCCP and Ryland P. Byrd, MD, FCCP

James H. Quillen College of Medicine, Johnson City, TN

PURPOSE: Obstructive sleep apnea syndrome (OSAS) and diabetes mellitus (DM) are commonly encountered diseases, each associated with a substantial risk of morbidity and mortality. Recent evidence suggests that the presence of OSAS may increase the risk of developing insulin resistance and type 2 DM. The purpose of this study was to test our hypothesis, that OSAS and DM complications are related.

METHODS: The electronic charts of all DM patients referred for sleep studies over a one year period were reviewed. Data collected included patient's age and gender, body mass index, glycosylated hemoglobin A1c (HgA1c), evidence of microalbuminuria, presence of microvascular complications (retinopathy and/or neuropathy), presence of macrovascular complications (coronary artery disease, carotid disease, stroke or transient ischemic attack) and multiple OSAS variables produced by sleep study. Analysis involved examining bivariate associations between OSAS variables and metabolic syndrome parameters.

RESULTS: From a total number of 447 patients who over one year period, 127 patients with DM were identified. AHI (Apnea Hypopnea Index) was directly related to diabetic microvascular complications (p <0.05) and macrovascular complications (p <0.1). The number of hypopneas was also direclty related to microalbuminuria (p <0.1). The number of apneas was significantly related to macrovascular (p <0.1) and microvascular complications (p <0.05). Oxygen saturation was significantly inversely related to microalbumin (p< 0.01), macrovascular complications (p <0.1) and microvascular complications (p <0.05). The average HgA1c in our study group was significantly below the national HgA1c average. HgA1c was not associated with any of the sleep parameters.

CONCLUSION: Despite well controlled DM, as reflected in HgA1c, OSAS was directly related to microalbuminuria, microvascular and macrovascular complications. Although OSAS and type II DM are independent diseases, our study support the hypothesis that OSAS may contribute to DM complications.

CLINICAL IMPLICATIONS: Screening diabetic patients for OSAS should be thought about early on in the work up and management of such population since this might be a potentially treatable cardiovascular risk factor.

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