Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred one patients diagnosed as having obstructive sleep apnea (OSA) were interviewed 12-24 months after their evaluation regarding those daytime symptoms associated with sleep apnea: sleepiness, fatigue, impaired memory, and snoring. Continuous positive airway pressure (CPAP) was the treatment most often used by severe sleep apnea patients, and this improved daytime alertness in 84% of the patients. Patients with moderate obstructive sleep apnea often had surgery which led to 85% reporting improved daytime alertness. Patients with mild obstructive sleep apnea usually were treated with weight loss or changing sleep position and also improved 64% and 66%. Patients who declined or failed treatment did not improve. Guidelines for the treatment of sleep apnea are suggested.
Conn Med 1992 Mar
PMID:Treatment outcome of sleep apnea. 158 4

Three of six siblings presented with sleep apnea between 18 and 26 months of age. Twin females and a male had normal growth and development without antecedent neurologic or apparent metabolic disorder. The females presented at 25 and 27 months respectively with irregular respiration and episodes of apnea. Twin A succumbed to an apneic episode while sleeping. Central sleep apnea was diagnosed in twin B at the Stanford Sleep Clinic. She died following an apneic episode three months after evaluation. The male presented at 18 months with fatal sleep apnea. A fourth child was evaluated for sleep apnea at 7 weeks of age with several hospitalizations before her death at 31 months. She and remaining family members were extensively studied for inherited neurologic disorders including subacute necrotizing encephalomyopathy (SANE, Leigh disease). This family with lethal sleep apnea presents an association with SANE with minimal neurologic signs and symptoms and neuropathologic involvement. Lesions were confined to the respiratory centers of the lower brain stem, making sleep apnea explicable. This child and family members tested positive or borderline for inhibitor substance thiamine triphosphate (TTP). All testing for TTP inhibitor substance was performed in Professor Jack R. Cooper's laboratory, Department of Pharmacology, Yale University School of Medicine, New Haven, Conn. These cases present an interesting and instructive lesson emphasizing the need for extensive evaluation of children with unsuspected sleep apnea with early demise.
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PMID:Familial lethal sleep apnea. 371 Apr 78

A less-than-normal decline in nocturnal blood pressure (BP) has been associated with excessive hypertensive complications. This is concerning because secondary hypertension is often associated with this so-called nondipper BP profile. A nondipping pattern is more frequently found in the presence of pheochromocytoma, Cushing's syndrome, and sleep apnea syndrome, but the prevalence is unclear in patients with primary hyperaldosteronism. We therefore studied ambulatory BP profiles in 16 hypertensive patients with primary hyperaldosteronism and an equal number of essential hypertensive subjects. The awake-sleep BP difference of the hyperaldosteronism patients was similar to that of essential hypertensives (15/14 +/- 3/2 versus 14/9 +/- 3/2 mm Hg, P=NS). The prevalence of dippers and nondippers (according to two distinct criteria) in the two groups was similar. Repeat ambulatory BP monitoring in 12 subjects with primary hyperaldosteronism after specific intervention (3 after surgical removal of an adrenal adenoma and 9 after commencement and titration of spironolactone therapy) showed highly significant reductions in office BP (22/10 +/- 6/4 mm Hg, P<.05) and awake and sleep BP. However, the extent of nocturnal BP decline was unchanged between the two studies (17/16 +/- 3/3 versus 16/12 +/- 2/2 mm Hg, P=NS). There was no correlation between the awake-sleep difference and serum or urinary aldosterone levels or the aldosterone-to-renin ratio. In this study, we did not detect any differences in the awake-sleep differences between a group of hypertensives with primary hyperaldosteronism and a control group of essential hypertensives.
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PMID:Circadian blood pressure variation in hypertensive patients with primary hyperaldosteronism. 949 70

Obstructive sleep apnea is a state-dependent syndrome. It is characterized by repeated collapse of the upper airway as the result of the loss of waking neuromuscular drive as the brain changes from wakefulness to sleep. This produces a state-dependent decrease in muscle tone, which, together with other predisposing factors such as obesity and anatomical narrowing of the upper airway, results in the spectrum of sleep disordered breathing. Sleep-disordered breathing describes the continuum from simple snoring (pharyngeal vibration), to flow limitation (hypopnea), to complete cessation of breathing (apnea). Obstructive sleep apnea (OSA) is the common description of what is now appreciated as the sleep apnea/hypopnea syndrome. The cardinal symptoms are snoring, observed apneas, and excessive daytime sleepiness. The immediate physical consequences are hypoxia, repeated sympathetic discharges, increased cardiac load, and repeated brain arousals. The repetitive arousals are required to restore airway patency, resulting in severely fragmented sleep and consequent sleep deprivation. The syndrome, untreated, produces significant cognitive and cardiorespiratory morbidity, and potential mortality. Compared to matched controls, patients with undiagnosed sleep apnea use twice the health resources and spend double the health-care dollars in the 10 years prior to diagnosis. Both trends are reversed by successful treatment. It is by definition a sleep-related illness and can be observed and evaluated only when the patient is asleep. Polysomnography is the laboratory procedure to study sleep and its protean dysfunctions. Multiple physiologic parameters are required to document the various types of sleep disorders as well as to establish the origin of pathologic sleep fragmentation. Complete polysomnography includes (but is not limited to) electroencephalogram (EEG), electrooculogram ((EOG), electromyogram (EMG), electrocardiogram (ECG), respiratory effort, air flow, and oxygen saturation. Treatment options for obstructive sleep apnea include continuous positive airway pressure (CPAP), oral appliances, uvulopalatal and/or maxillomandibular surgery, positional control, and weight loss. The efficacy of each depends on the individual anatomy and the severity of the sleep-disordered breathing. CPAP is accepted as the most reliable treatment regardless of anatomy and severity. It is currently the only treatment modality which can be titrated during sleep and requires simultaneous polysomnography.
Conn Med 2000 Aug
PMID:Obstructive sleep apnea, polysomnography, and split-night studies: consensus statement of the Connecticut Thoracic Society and the Connecticut Neurological Society. 1098 71

The management of arterial hypertension has experienced great changes during the past years, based on the knowledge of its pathophysiology, as well as the development of new antihypertensive drugs. Recent studies show the effect of the dysfunction of the endothelium in hypertension, sleep apnea and a higher prevalence of primary hyperaldosteronism. The Sixth report of the Joint Committee makes a new classification of this pathology, including a new concept of the stratification of risk for each stage of the disease, and according to it a new way of treatment. This fact marks a new and a more aggressive behaviour to treat the hypertense patient. With respect to the treatment, the emphasis has been on the non-pharmacological measures, and the development of new antihypertensive drugs of long action and high through/peek rate. Prevention continues to be an important goal and main challenge for the clinician, given the high morbidity and mortality rate caused by hypertension.
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PMID:[New concepts in hypertension]. 1126 97

Resistant hypertension is an increasingly common problem faced by primary care physicians and specialists and will undoubtedly become even more common as the adult population ages and gains weight. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), at least 8% of subjects were resistant to treatment based on the need for three or more antihypertensive agents. Characteristics of patients with resistant hypertension include being older, black, obese, and diabetic, and having chronic kidney disease as well as untreated sleep apnea. Hyperaldosteronism is common in patients with resistant hypertension, with a prevalence of approximately 20%. This, however, is likely an underestimation of the role aldosterone excess plays in causing drug resistance. In subjects with resistant hypertension, suppressed renin levels are common, exceeding 75% in our studies, suggesting aldosterone excess effects beyond cases of true primary hyperaldosteronism. Recent studies indicate that aldosterone antagonists provide significant blood pressure reduction when added to antihypertensive regimens of patients with resistant hypertension. Interestingly, the blood pressure reduction with use of spironolactone is not limited to patients with hyperaldosteronism, consistent with the concept of aldosterone excess as a continuum from low-renin hypertension with normal aldosterone levels to true primary hyperaldosteronism.
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PMID:The role of aldosterone antagonists in the management of resistant hypertension. 1615 75

Resistant hypertension affects approximately 10% of the hypertensive patient population. It should be differentiated from white-coat hypertension and pseudo-resistant hypertension. Non-compliance to anti-hypertensive therapy remains the most common cause of resistant hypertension. Primary hyperaldosteronism is not as uncommon as previously thought, but its prevalence depends on the selected population. Low-renin resistant hypertension responds to aldosterone blockade when other drugs are apparently inadequately effective. Sleep apnea syndrome can also contribute to the development of resistant hypertension by stimulating aldosterone secretion, which leads to vascular damage and may promote scarring through more direct actions. Normal blood levels of potassium in resistant hypertension do not exclude the possible presence of hyperaldosteronism.
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PMID:Resistant hypertension: a methodological approach to diagnosis and treatment. 1767 42

Primary aldosteronism (PA) is associated with vascular end organ damage. The aim of the study was to evaluate differences regarding comorbidities depending on tumor size in patients with aldosterone producing adenoma (APA). The retrospective cross-sectional study was done by collection from 6 German centers (German Conn's registry) between 1990 and 2007. Among the 640 registered patients with PA, 60 operated patients with APA were analyzed. The main outcome of measures was the comorbidities depending on tumor size. Thirty-one patients (17 men, 14 women) had an adenoma size <20 mm, and 29 patients (10 men, 19 women) had an adenoma size>/=20 mm. There was no difference in age, preoperative potassium, aldosterone, or creatinine levels, preoperative systolic and diastolic blood pressure, or duration of hypertension between the two groups. In the group with APA <20 mm, cerebrovascular events occurred with a prevalence of 12.9%, cardiac events 16.1%, peripheral vascular events 25.8%, renal insufficiency 16.1%, and sleep apnea 6.4%, respectively. There was no significant difference in comorbidities compared to the group with APA>/=20 mm. Subgroup analysis (n=22) of follow-up data on post-operative systolic and diastolic blood pressure showed no significant difference between these subgroups with regard to potassium, aldosterone or creatinine levels, blood pressure, duration of hypertension, or comorbidities. Our data indicate a high prevalence of comorbidities in patients with APA. However, adenoma size was not correlated with cardio- and cerebrovascular comorbidities, and does not seem to be a prognostic factor for blood pressure outcome.
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PMID:Tumor size of Conn's adenoma and comorbidities. 1954 84

Secondary hypertension occurs in a significant proportion of adult patients (~10%). In young patients, renal causes (glomerulonephritis) and coarctation of the aorta should be considered. In older patients, primary aldosteronism, obstructive sleep apnoea and renal artery stenosis are more prevalent than previously thought. Primary aldosteronism can be screened by taking morning aldosterone and renin levels, and should be considered in patients with severe, resistant or hypokalaemia-associated hypertension. Symptoms of obstructive sleep apnoea should be sought. Worsening of renal function after starting an angiotensin-converting enzyme inhibitor suggests the possibility of renal artery stenosis. Recognition, diagnosis and treatment of secondary causes of hypertension lead to good clinical outcomes and the possible reversal of end-organ damage, in addition to blood pressure control. As most patients with hypertension are managed at the primary care level, it is important for primary care physicians to recognise these conditions and refer patients appropriately.
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PMID:Secondary hypertension in adults. 2721 Dec 5