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)

A case of a 63-year-old patient with motor neurone disease (amyotrophic lateral sclerosis) with central sleep apnoea syndrome is being reported. His sleep architecture was fragmented with a high apnea-hypopnea index of 65 per hour and maximum oxygen-desaturation of 78 percent. Total correction of sleep pattern with nasal non-invasive ventilation (BiPAP-ST) was demonstrated.
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PMID:A case of motor neurone disease with sleep apnoea syndrome. 1053 43

Twelve patients (aged 48 +/- 12 y) with ventricular asystole of >3 s due to complete atrioventricular (AV) block (n = 8), sinoatrial (SA) block or sinus node arrest (n = 3) or both (n = 1) associated with obstructive sleep apnoea underwent invasive electrophysiological evaluation of sinus node function and AV conduction properties before and after administration of atropine (0.02 mg kg-1). Ventricular asystole lasted for 5.9 +/- 2.8 s (range 3.1-13 s). Sinus node function was assessed by measurement of sinus node recovery time, sinoatrial conduction time, and the response of sinus rate to atropine. Parameters of AV-conduction assessment included AH- and HV-intervals, AV- and VA-Wenckebach periods, and effective refractory period of the AV node before and after atropine. Sinus node function was normal in 11 of the 12 study patients and moderately abnormal in 1 patient. AV-nodal function was normal in 8 patients and moderately abnormal in 4 patients. A slightly prolonged HV-interval (59-63 ms) was present in 6 patients. Intra- or infra His block was not observed in any patient. In conclusion, normal or only moderately abnormal electrophysiological findings in patients with sleep apnoea-associated ventricular asystole suggest that a neurally mediated cardioinhibitory reflex may cause ventricular asystole in these patients. This sleep apnoea-triggered 'vasovagal' reflex may unmask pre-existing mild to moderate structural abnormalities of the AV conduction system.
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PMID:Invasive electrophysiological evaluation of patients with sleep apnoea-associated ventricular asystole-methods and preliminary results. 1060 94

The case is presented of a 48-year old, slightly overweight, brachymorphic male affected by undiagnosed myxedema, admitted for nocturnal dyspnea present for several years but worsened in the last few weeks. At the age of 19, a paranoid schizophrenia diagnosis was indicated leading to repeated admissions to psychiatric hospitals and continued pharmacological therapy. His sensorium was lucid albeit with a slight psycho-motor slowing down; pharyngeal edema and macroglossia were also apparent, blood O2 saturation was 97%. After the first emergency exams, a hypothyroid condition associated with multinodular goiter and tracheal dislocation was found. Administration of triiodothyronine p.o. and hydrocortisone i.v. was thus initiated. In the doubt of sleep apnea syndrome (SAS) occurrence, pulse oximetry was performed, but after 7 hours, the patient suddenly deceased. Data showed waves of deep O2 desaturation secondary to periods of prolonged apnea. A literature review shows that such a case has never been reported. A posteriori analysis of the patient's clinical management indicates that the obstructive form of SAS, associated with myxedema is a condition which needs to be promptly diagnosed; due to the possible seriousness of its functional evolution, the need for intensive or sub-intensive therapy, with continuous nasal airway positive pressure or with oro-tracheal intubation and assisted ventilation, should be carefully taken into consideration; continuous cardiac monitoring should also be carried out, given the risk for acute coronary complications and ventricular arrhythmias in the early phases of substitutive therapy with thyroid hormone.
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PMID:[Sudden death by sleep apnea syndrome associated with myxedema. A case report and a review of the literature]. 1073 43

Sleep Apnea Syndrome is an understimated disease. We describe its diagnostic criterion and principal epidemiologic data. After a brief rememory about sleep and respiration, its physiopathologic consequences (especially respiratory, cardiovascular and cerebral) were detailed. The diagnostic of its different clinical presentations is suspected clinically but confirmed by polysomnography. His treatment, usually based on the CPAP, permits to prevent its complications.
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PMID:[Sleep apnea syndrome]. 1115 71

We report a case of a 3-year-old child with Prader-Willi syndrome who had severe sleep disordered breathing with daytime hypersomnolence. His daytime blood gases showed type II respiratory failure. He was effectively treated with continuous positive airway pressure (CPAP) and has used this form of therapy for 2 years now with improvement in daytime somnolence, improved mental acuity and normalisation of daytime blood gases.
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PMID:Prader-Willi syndrome with sleep disordered breathing: effect of two years nocturnal CPAP. 1137 May 8

Four of the 708 snorers (0.56%), referred to our sleep breathing disorders clinic for the past 2 years were diagnosed as having narcolepsy-cataplexy. Detecting HLA DRB1*1501/DQB1*0602 positive was informative for differentiating genuine narcolepsy from non-sleep apnea syndrome (non-SAS) hypersomnia in our clinic. A non-SAS obese boy, diagnosed as having essential hypersomnia syndrome, was found to be HLA DRB1*1502/DQB1*0601 positive. His hypocretin concentration was 206 pg/mL in the cerebrospinal fluid.
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PMID:Narcolepsy and other non-SAS hypersomnia in sleep breathing disorders clinic. 1142 42

We describe a case of diabetes mellitus complicated by neurosensory hearing loss, cardiomyopathy, and sleep apnea syndrome. A 48-year-old man who was admitted for treatment of a lacerated tendon of the right shoulder was also found to require preoperative control of diabetes, a condition that had been diagnosed 4 years earlier. The family pedigree suggested maternal inheritance of diabetes. The patient also had neurosensory hearing loss and the central type of sleep apnea syndrome. His myocardium was hypertrophic and the ultrastructural analysis showed morphologically abnormal mitochondria. On the basis of the apparent characteristic manifestations, we speculated that he had a mitochondrial disease. To elucidate the responsible mutation of mitochondrial DNA, we sequenced the patient's entire mitochondrial DNA derived from blood leukocytes and found 40 sequence variants. Three of those, 5466 A/G, 7912 G/A, and 10601 T/C, have not yet been reported. Nine of the 40 variants were accompanied by an amino acid replacement, including 5466 A/G. Although we could not determine the most significant mutation, the variants of mitochondrial DNA may have been associated with this patient's unusually variable clinical manifestations.
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PMID:A case of diabetes, deafness, cardiomyopathy, and central sleep apnea: novel mitochondrial DNA polymorphisms. 1200 77

Two cases of sleep apnea syndrome caused by primary hypothyroidism are reported. The first patient was a 66-year-old man who complained of sleep apnea; his apnea-hypopnea index (AHI) was 50.8, as assessed by all-night monitoring. Hypothyroidism was subsequently suspected when he showed delayed recovery from general anesthesia following surgery involving uvulopalatopharyngoplasty. Hypothyroidism was diagnosed on the basis of blood tests His snoring and apnea improved after 2 months of levothyroxine sodium administration and the AHI fell from 50.8 to 13.0. The second patient was a 73-year-old man with an AHI of 41.3, as assessed by all-night monitoring. Hypothyroidism was diagnosed on the basis of blood tests and was suspected because of his slow speech. He was similarly treated with levothyroxine sodium. The AHI did not decrease after 4 months of treatment. His desaturation rate (rate of O2 saturation < 90%) improved however, from 56.6% to 31.9%, and the symptoms of hypothyroidism also improved markedly. In both patients, elevated creatine phosphokinase, a dull facial expression, peripheral edema and slow speech were recognized, and these symptoms were suggestive of hypothyroidism. The type of sleep apnea was mainly obstructive in both patients.
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PMID:Two cases of sleep apnea syndrome caused by primary hypothyroidism. 1273 45

As President of the United States from 1909 to 1913, William Howard Taft's minimum body mass index was 42 kg/m(2). This article presents evidence that he suffered from obstructive sleep apnea, manifested by excessive daytime somnolence, snoring, systemic hypertension and, perhaps, cognitive and psychosocial impairment. As president, Taft's hypersomnolence was severe and obvious, but never prompted official discussion of his fitness to govern. Within 12 months of leaving office, Taft permanently lost over 60 pounds. His somnolence resolved. As Chief Justice of the United States from 1921 to 1930, he was not somnolent. President Taft's case illuminates historical puzzles of his performance as President, raises public awareness of sleep apnea, and informs discussions of presidential disability and the 25th Amendment to the Constitution of the United States.
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PMID:Taft and Pickwick: sleep apnea in the White House. 1507 79

A 74-year-old man with ischemic cardiomyopathy was repeatedly admitted for congestive heart failure. His left ventricular ejection fraction was 21% and diastolic left ventricular dimension was 73.5mm by echocardiography. He was treated with biventricular pacing and heart failure improved from New York Heart Association class III to II. Before the treatment, brain natriuretic peptide was 600.5 pg/ml. Apnea hypopnea index was 23.8 and all events were central type. After biventricular pacing, apnea hypopnea index was improved to 21.9 after 11 days, 14.0 after 33 days, and 4.8 after 48 days. His left ventricular ejection fraction was 36%, diastolic left ventricular dimension was 71.4mm, and brain natriuretic peptide was 383.8 pg/ml. In this patient, central sleep disordered breathing was improved by biventricular pacing therapy after only 48 days.
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PMID:[Improvement of central sleep disordered breathing with severe congestive heart failure by biventricular pacing therapy: a case report]. 1647 70


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