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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid deficiency states are now a well recognized cause of the sleep apnea syndrome. The spectrum of disease ranges from mild, asymptomatic hypothyroidism to severe myxedema, and the disorder is associated with both obstructive and central types of sleep apnea. A variety of factors may be involved, including upper airway obstruction with or without obesity, and alterations in ventilatory drive. The definitive therapy is thyroid hormone replacement, which has been shown to diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency. The incidence of thyroid deficiency states in patients with sleep apnea syndrome is not known, but it seems reasonable to evaluate thyroid function in all patients. Thyroid replacement therapy seems logical for the treatment of sleep apnea in patients with previously unrecognized subclinical hypothyroidism. Much remains to be learned about the diagnosis and treatment of sleep apnea syndromes associated with thyroid hormone deficiency, and further studies are needed.
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PMID:Sleep apnea and hypothyroidism. 305 27

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

To determine the incidence and frequency of sleep apnea in persons with hypothyroidism, 11 consecutive patients with newly diagnosed disease were studied before and during thyroid hormone replacement therapy. Nine patients had episodes of apnea, with the number of episodes per hour of sleep ranging from 17 to 176 (mean, 71.8). Six of the nine patients were obese and had 99.5 episodes per hour compared with 16.3 episodes per hour in the 3 nonobese patients (p less than 0.02). After 3 to 12 months of thyroxine replacement therapy, mean apnea frequency decreased from 71.8 +/- 18.0 (SE) to 12.7 +/- 6.1 episodes per hour, without reduction in body weight. There were fewer changes in sleep stage per hour during treatment (22.1 +/- 4.9) than pretreatment (57.6 +/- 14.5). Carbon dioxide response tests done under non-loaded and flow-resistive loaded conditions before and during thyroxine replacement therapy showed increases in the loaded respiratory effort and ventilation during thyroxine treatment. Sleep apnea episodes are common in persons with untreated hypothyroidism, even with normal lung function. Thyroxine replacement therapy decreases apnea frequency, even without change in body weight.
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PMID:Obstructive sleep apnea in hypothyroidism. 647 35

Sleep-disturbed breathing, which includes apneas, hypopneas, and oxygen desaturations, occurs in asymptomatic individuals and increases with age. Obstructive apnea is the most frequent type of respiratory disturbance documented by polysomonography, the gold standard test for assessing sleep-disturbed breathing. Many of the prevalence studies done to date have had one or more methodological weaknesses, including selection biases, varying definitions of obstructive sleep apnea, failure to distinguish types of apneas, failure to control for confounding variables, and small sample size. Although there is consensus on the definitions of sleep-disturbed breathing, the appropriate number of apneas and hypopneas for diagnosing clinically significant obstructive sleep apnea is uncertain. While the cutoff of five or more apneas and hypopneas per hour is historically considered abnormal, the origins of this number are vague, and the longevity of those who have this value on polysomnography is not necessarily reduced. This is particularly true among those without symptoms of obstructive sleep apnea syndrome, which include excessive daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Investigators should be careful to distinguish symptomatic study subjects from asymptomatic subjects, and to exclude central apneas in calculating their estimates. In addition, various studies have used different definitions of sleep apnea syndrome, making comparisons of point estimates difficult. It would be more appropriate for researchers to estimate morbidity and mortality indices with confidence intervals, using several different cutoff points. Subject selection in all studies should follow a two-stage sampling procedure. All subjects with symptoms compatible with obstructive sleep apnea syndrome and a subsample of asymptomatic individuals should be studied with all-night polysomnography. If portable monitoring is used, the validity and reproducibility of this diagnostic method should be assessed. Subjects with significant comorbidity should be excluded from prevalence studies. Factors that clearly increase the risk of sleep-disturbed breathing and obstructive sleep apnea and its related symptoms include age, structural abnormalities of the upper airway, sedatives and alcohol, and probably family history. Although endocrine changes such as growth hormone, thyroid hormone, and progesterone deficiency also have been suggested as risk factors for exacerbating obstructive sleep apnea syndrome, there is minimal epidemiologic evidence to support this. Case-control studies are recommended to assess the relation of endocrine factors to obstructive sleep apnea syndrome in a rigorous fashion. A limited number of mortality studies have suggested decreased survival in persons with the obstructive sleep apnea syndrome, possibly primarily due to vascular-related disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of obstructive sleep apnea. 771 77

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.
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PMID:[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords]. 795 87

Because the incidence of sleep apnea is known to increase in both hypothyroidism and with age, elderly hypothyroid patients may experience more sleep apnea than younger hypothyroidism patients. However, the features of nocturnal disturbed breathing in elderly hypothyroid patients have not been fully elucidated. Concise polysomnographic studies including respiratory movement and oxyhemoglobin saturation (SaO2) were done on 18 elderly subjects with hypothyroidism (73.6 +/- 5.9 years old) before and after thyroid hormone replacement therapy. Fourteen of the patients exhibited a significant incidence of nocturnal apnea. Lower incidence of nocturnal apnea and higher nocturnal nadir SaO2 were observed in the patients 3 to 6 months after thyroxine therapy. Although the levels of thyroid hormones returned to normal in the patients, 9 patients had more than 5 bouts of nocturnal apnea per hour after the hormone replacement therapy. Further, no relationship was found between the level of thyroid hormones and the frequency of nocturnal apnea. These results suggest that levels of thyroid hormones are not indicators of the potential severity of nocturnal apnea in elderly hypothyroid patients, and that sleep studies may be necessary to assess the efficacy of thyroid hormone replacement therapy in the treatment of nocturnal apnea.
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PMID:[Effects of thyroid hormone replacement therapy on nocturnal apnea in elderly patients with hypothyroidism]. 980 9

Primary sleep apnea-hypopnea syndrome (obstructive sleep apnea [OSA]) and hypothyroidism have many signs and symptoms in common. The overlap in clinical presentation, and the sleep-disordered breathing that can accompany hypothyroidism, create a significant risk of misdiagnosis of sleep apnea among patients referred to sleep clinic who have undiagnosed hypothyroidism. We determined the point prevalence of hypothyroidism in our sleep clinic patients with newly diagnosed sleep-disordered breathing. Of 290 sequential patients referred to sleep clinic, 200 (69%) patients judged at high risk for OSA underwent polysomnography (PSG) and biochemical screening for hypothyroidism. Of these, 124 (62%) were judged to have sleep apnea. This included three patients (1.5% of patients undergoing PSG or 2. 4% of those judged to have OSA) who were also discovered to have previously undiagnosed hypothyroidism. These three patients with "secondary" sleep apnea were treated with thyroxine therapy alone, and followed with sequential sleep studies and serum thyroid hormone assays; symptoms, sleep-disordered breathing, nocturnal hypoxia, and thyroid deficiency resolved simultaneously. We conclude that biochemical screening for hypothyroidism is required to prevent inadvertent misdiagnosis of hypothyroid sleep-disordered breathing as primary sleep apnea, and that it is a cost-effective component of the investigation of sleep apnea.
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PMID:Screening for hypothyroidism in sleep apnea. 1043 Jul 54

The current literature recommends that patients who have symptoms of sleep disordered breathing should be evaluated for hypothyroidism. Thyroid hormone replacement therapy has been reported by some authors to be effective in treating obstructive sleep apnea in hypothyroid patients. The present study prospectively evaluated the prevalence of hypothyroidism in 1,000 consecutively presenting patients who came to the office for evaluation of snoring or obstructive sleep apnea syndrome. The authors also examined the efficacy of treatment for hypothyroidism on sleep apnea in patients with both disorders. Of the 1,000 patients, routine thyroid testing was performed on 834; only 10 of these patients (1.2%) were discovered to have previously undiagnosed clinical hypothyroidism. Four of the 10 patients with newly diagnosed clinical hypothyroidism had obstructive sleep apnea syndrome, and they received thyroid hormone replacement therapy. Once these four patients achieved a euthyroid state, repeat polysomnography showed that there was no significant difference between their pre- and posttreatment respiratory disturbance index. Based on the results of our study, we conclude the following: 1) The prevalence of hypothyroidism in patients who are evaluated for sleep disordered breathing is no greater than that of the general population. 2) Thyroid replacement therapy results in little or no improvement in sleep apnea in patients with clinical hypothyroidism. 3) Routine thyroid function screening is not indicated for patients who are being evaluated for sleep disordered breathing.
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PMID:Thyroid testing and thyroid hormone replacement in patients with sleep disordered breathing. 1054 33

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


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