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)

Forty-five patients with homozygous sickle cell disease who had tonsillectomy for recurrent tonsillitis, when compared with 45 matched controls with haemoglobin genotype AA, showed significant differences in the clinical manifestations and complications of recurrent tonsillitis between the two groups. Although throat swabs in the sickle cell group were mostly negative because they were on prophylactic penicillin, all tonsils harboured Streptococcus pneumoniae when cultured. This study suggests the tonsils to be the more specific source of pneumococcal infection that causes systemic complications which increase morbidity and mortality in sickle cell disease. Although the sickle cell patients may be less clinically symptomatic with tonsillitis, the incidence of serious complications caused by pneumococcal infections, now shown to arise from the tonsils, is significant. Adenotonsillar hypertrophy is linked with an increased risk of a sleep apnoea which causes serious neurological complications such as cerebral infarction and stroke. Tonsillectomy has greatly reduced the incidence of complications from pneumococcal infections in the sickle cell group and should therefore be recommended for sickle cell patients taking prophylactic penicillin and still developing pneumococcal infections.
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PMID:The significance of recurrent tonsillitis in sickle cell disease. 792 45

The goal of the present investigation is to show the clinical significance of arousal response at termination of apnea/hypopnea in patients with sleep apnea syndrome (SAS) after cerebral infarction. We polygraphically assessed "cardiac arousal," which is defined as an abrupt increase in heart rate at a termination of sleep apnea/hypopnea, and electroencephalographic (EEG) arousal. There were six elderly subjects, bedridden after cerebral infarction, with SAS aged 71-87 years (mean 72.3 years) and 11 age-matched patients with SAS aged 61-78 years (mean 62.3 years) as controls. The following sleep parameters were measured: number of apneas per hour (apnea index [AI]), number of hypopneas per hour (hypopnea index [HI]), summation of the two (apnea/hypopnea index [AHI]), and duration in which nocturnal oxygen saturation was decreased below 90% (duration of SaO2 < 90%). We calculated the ratio of apnea/hypopnea per hour with cardiac arousal to total apnea/hypopneas (XI) (% cardiac arousal [XI/AHI x 100]) and the ratio of that with EEG arousal (YI) (% EEG arousal [YI/AHI x 100]). Between the two groups, we found no significant difference in body mass index, the ratio of central apnea to total apnea/hypopnea, AHI, duration of apnea/hypopnea, lowest SaO2, and duration of SaO2 < 90%. Compared with controls, % cardiac and % EEG arousals were significantly lower in patients with cerebral infarction. In contrast, the ratio of HI to AHI was significantly higher in patients with cerebral infarction than in control subjects. Our findings indicate that cardiac and EEG arousals at termination of apnea/hypopnea are significantly suppressed in elderly patients with SAS after cerebral infarction, which may provide useful information on the pathophysiology of SAS in patients with cerebrovascular disease.
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PMID:Suppressed cardiac and electroencephalographic arousal on apnea/hypopnea termination in elderly patients with cerebral infarction. 901 61

Obstructive Sleep Apnea(OSA) is associated with an increased prevalence of cardiovascular complication such as systemic hypertension, ischemic heart disease and stroke, which may lead to unexpected or early death. Sleep in patients with OSA demonstrates a pattern of recurrent arousals, hemodynamic changes, and sympathetic neural activity that have been associated with adverse carviovascular events following awakening in the morning. Neurologic problems in patients with OSA include cognitive impairment, poor memory, and high risk for cerebral infarction. These central nervous system symptoms might be due to hypoxemia and sleep fragmentations. The vascular endothelial damage, platelet aggregation, and hemodynamic changes during sleep apnea are influenced by changes in oxygen and carbon dioxide tension inducing alterations of vascular tone. The cerebral hemodynamics in relation to apneas may not only influence daytime cerebral symptoms but may also have implications for the generation of cerebrovascular disease in OSA. These changes resulted from OSA might play an important role in pathophysiological aspects of the central nervous system. And these changes will be improved after CPAP application.
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PMID:[Abnormality of blood congulation]. 1094 24

Obesity causes many undesirable health disorders such as diabetes mellitus, hyperlipidemia, hypertension and so on. Recently, those life style-affecting diseases is increasing, especially the increment of diabetes mellitus is prominent. In 2000, Japan obesity society issued the new standard of the evaluation of obesity and new diagnostic criteria of obesity as a disease for Japanese. According to this issue, obesity was evaluated by body mass index(BMI). And, 18.5 < BMI < 25 is normal, 25 < BMI < 30 is obese 1, 30 < BMI < 35 is obese 2, 35 < BMI < 40 is obese 3, and 40 < is obese 4. Obesity as a disease is defined by two cases. The first category is composed of two items; one is BMI > 25, and the other is having one disease worsen by obesity, such as diabetes mellitus, hyperlipidemia, hypertension, hyperuricemia, coronary heart disease, cerebral infarction, sleep apnea syndrome, fatty liver, deformative arthritis. The second category is the visceral type of obesity with BMI > 25, which was diagnosed by west size, over 85 cm for men, and over 90 cm for women, and by visceral fat area over 100 cm2 in abdominal CT.
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PMID:[Evaluation of obesity and diagnostic criteria of obesity as a disease for Japanese]. 1126 12

Patients suffering from sleep apnea syndrome are known to be at higher risk of cardiac and cerebral infarction. In this case report, we describe bilateral pallidal lesions, which are normally seen after sudden asphyxia due to cardiac arrest or carbon monoxide intoxication. Some epidemiological and pathophysiological observations are cited.
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PMID:[Bilateral pallidal infarction in sleep apnea syndrome]. 1590 92

Stroke is the third leading cause of death in the United States. Stroke survivors often experience medical complications and long-term disability. Disturbances in respiratory system function and complications affecting the respiratory system are common after stroke. The nature of these disorders depends on the severity and site of neurological injury. Alterations in breathing control, respiratory mechanics, and breathing pattern are common and may lead to gas exchange abnormalities or the need for mechanical ventilation. Stroke can lead to sleep disordered breathing such as central or obstructive sleep apnea. Sleep disordered breathing may also play a role in the pathogenesis of cerebral infarction. Venous thromboembolism, swallowing abnormalities, aspiration, and pneumonia are among the most common respiratory complications of stroke. Neurogenic pulmonary edema occurs less often. Close observation of the stroke patient for these potential disturbances, and implementation of prophylactic measures can prevent significant morbidity and mortality.
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PMID:Respiratory complications of stroke. 1608 17

Sleep-disordered breathing (SDB) is more probably the cause rather than the consequence of stroke because: apneas are essentially obstructive rather than central, the frequency of SDB is not different between transient ischemic attack and cerebral infarction; and previous excessive daytime sleepiness is significantly more frequent among stroke patients with SDB than those without. The presence of SDB in stroke patients could lead to a poor outcome. Pathophysiological relationships between strokes and SDB are multiple. Experimental and clinical studies have shown that both short- and long-term factors may play a role in increasing the susceptibility to stroke in patients with obstructive sleep apnea syndrome. The former include changes in cerebral hemodynamics, hematologic alterations, and cardiocirculatory dysfunctions that typically and repeatedly occur during apnea episodes and also may persist during wakefulness. Regarding long-term factors, some changes in the anatomical characteristics of carotid arteries wall have been recognized in SDB patients. This finding seems to suggest that the link between SDB and cerebrovascular disease might be explained, at least in part, by an increase in the progression of the atherosclerosis process involving cerebral vessels. There are several practical implications from the demonstrated significant role of sleep apnea in increasing the predisposition to developing stroke. Specific investigation is fundamental in the presence of a clinical suspect of SDB, especially in patients with history of transient ischemic attacks and stroke. Specific treatment of SDB may reduce the possibility of further cerebrovascular disturbances.
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PMID:Cerebrovascular diseases and sleep-disordered breathing. 1683 28