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)

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.
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PMID:Narcolepsy. Diagnosis and treatment. 105 17

Respiration during sleep was studied in six obese women who had impaired prolactin response to insulin induced hypoglycaemia (non-responders), six obese women with a normal prolactin response to hypoglycaemia (responders), and six lean women. Sleep apnoea did not occur in any subject. All the obese women showed a decrease in haemoglobin oxygen saturation when asleep, which occurred predominantly during periods of rapid eye movement sleep. That the fall in oxygen saturation was significantly greater (p less than 0.05) in the obese non-responders suggests that central as well as mechanical factors may be important for the genesis of nocturnal hypoxia and is evidence for a disturbance of central nervous function in some obese women.
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PMID:Nocturnal hypoxia and prolactin secretion in obese women. 641 59

Central autonomic dysfunctions can be due to primary (degenerative) or secondary disorders. Autonomic failure (AF) may be a major manifestation of multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD). In both MSA and IPD, AF is almost invariably associated with neuronal loss in the intermediolateral cell columns. Dysautonomia in MSA is early, severe, and progressive, including marked orthostatic hypotension and urinary incontinence and is complicated by respiratory disturbances, such as laryngeal stridor and sleep apnea. MSA/AF can be differentiated from primary (or pure) autonomic failure (PAF) without central nervous system involvement. PAF is mainly a disorder of the postganglionic neurons. In contrast to PAF, MSA/AF has preserved basal sympathetic activity, decreased cerebrospinal fluid (CSF) neurotransmitter markers, impaired vasopressin response to hypotension, and impaired adrenocorticotrophic hormone/beta endorphin response to hypoglycemia. AF in IPD is generally less severe than in MSA. Poor response to L-Dopa, abnormal urethral sphincter electromyography, and CSF markers may distinguish MSA from IPD. Secondary autonomic disorders may result from traumatic, vascular, inflammatory, demyelinating, or neoplastic lesions involving corticolimbic, hypothalamic, brainstem, or spinal autonomic network. These disorders can cause AF or autonomic hyperactivity, such as arrhythmia, hypertension, and hyperthermia. However, many disorders may only produce subclinical abnormalities.
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PMID:Central autonomic disorders. 845 95

The mechanisms and pathophysiology of sleep disturbances in patients with endocrine diseases are reviewed. Abnormalities in sleep regulations were demonstrated in patients with thyrotoxicosis and hypothyroidism in a use of electroencephalogram during sleep. Mental disorders are one of the causes of sleep disturbance, for example insomnia due to depression in Cushing's syndrome. Metabolic abnormalities such as hyponatremia and hypoglycemia due to adrenal insufficiency could also contribute to sleep disturbance. Obstructive, central and mixed types of sleep apnea syndrome are known to occur in hypothyroidism, acromegaly and diabetic neuropathy with autonomic dysfunction. Thus, multiple factors are involved in sleep disturbance in patients with endocrine disorders.
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PMID:[Sleep disorders in several pathologic states--endocrine diseases]. 950 51

Respiratory disorders during sleep are a serious medical, economic and social problem. In the submitted review the authors discuss the possible relationship between sleep disorders and diabetes. In the introduction they make the reader familiar with basic information on sleep apnoea, incl. the definition, classification and basic pathomechanisms leading to this disorder. In the subsequent part the authors discuss possible relations between the two diseases, the possible participation of diabetic autonomous neuropathy in the pathogenesis of sleep apnoea, the possible influence of hypoglycaemia on sleep quality and the possible influence of sleep apnoea on the development or deterioration of insulin resistance. The objective of the paper is to provide the professional public, but in particular diabetologists, with an overall review of the problem based on most recent data from the literature and to draw attention to the fact that respiratory sleep disorders in diabetics are relatively frequent and that to this problem attention must be paid in practice and in medical research.
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PMID:[Respiratory disorders during sleep in patients with diabetes mellitus]. 1178 10

Most studies, which are retrospective, show contradictory results regarding the incidence of road traffic accident among diabetic patients. The most frequent cause of accident is hypoglycemia. One should also consider impaired vision (retinopathy, maculopathy), neuropathy (feet insensitivity) and sleep apnoea in overweight patients. Hypoglycemia not only leads to impaired judgement during driving, but also to a reduction in performances, frequent hypoglycemias impair symptom recognition and increase the risk of loss of consciousness. Patients should benefit from teaching about hypoglycemia, i.e. how to recognize and correct it in order to avoid accidents. Generally they should not drive if their glycemia is under 5 mmol/l without correcting it with an adequate amount of carbohydrates.
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PMID:[Diabetes mellitus and driving]. 1763 64

This review considers the 250+ papers concerning the association of the angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism (rs1799752) and various disease conditions published in 2009. The deletion allele occurs in approximately 55% of the population and is associated with increased activity of the ACE enzyme. It might be predicted that the D allele, therefore, might be associated with pathologies involving increased activity of the renin-angiotensin system. The D allele was seen to be associated with an increased risk of hypertension, pre-eclampsia, heart failure, cerebral infarct, diabetic nephropathy, encephalopathy, asthma, severe hypoglycaemia in diabetes, gastric cancer (in Caucasians) and poor prognosis following kidney transplant. On the positive side, the D allele appears to offer protection against schizophrenia and chronic periodontitis and confers greater up-per-body strength in old age. The I allele, meanwhile, offers improved endurance/athletic performance and aerobic capacity as determined by lung function tests, although it does increase the risk of oral squamous cell carcinoma and obstructive sleep apnoea in hypertensives.
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PMID:Implications of the angiotensin converting enzyme gene insertion/deletion polymorphism in health and disease: a snapshot review. 2153 87

Diabetes affects over 25 million people in the United States, most of whom are over the age of 16 and many of whom are licensed to drive a motor vehicle. Safe operation of a motor vehicle requires complex interactions of cognitive and motor functions and medical conditions that affect these functions often will increase the risk of motor vehicle accidents (MVA). In the case of diabetes, hypoglycemia is the most common factor that has been shown to increase MVA rates. When people with diabetes are compared with nondiabetic controls, systematic analyses show that the relative risk of MVA is increased by between 12% and 19% (Relative Risk Ratio 1.12-1.19). In comparison, the RRR for attention deficit hyperactivity disorder is 4.4 and for sleep apnea is 2.4. Epidemiologic research suggests that patients at risk for hypoglycemia-related MVAs may have some characteristics in common, including a history of severe hypoglycemia or of hypoglycemia-related driving mishaps. Experimental studies also have shown that people with a history of hypoglycemia-related driving mishaps have abnormal counter-regulatory responses to hypoglycemia and greater cognitive impairments during moderate hypoglycemia.
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PMID:Diabetes and driving safety: science, ethics, legality and practice. 2353 55

Evidence for treatment of hypertension in older people is limited to placebo-controlled studies that reduced blood pressure in persons over 60 years who had systolic blood pressure >160 mmHg. Generally, physicians measure blood pressure poorly, failing to look for white coat or masked hypertension, orthostasis, postprandial hypotension, or pseudohypertension. There is evidence that if 24-hour ambulatory blood pressures were obtained, the treatment goal should be substantially lower. Sleep apnea, pain, nocturnal hypoglycemia, drugs, excess aldosterone production, and pheochromocytoma should all be considered as causes of hypertension in older persons. Evidence supports a low-dose diuretic or an angiotensin converting enzyme inhibitor as appropriate first-line therapies in older persons.
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PMID:Treatment of hypertension in older persons: what is the evidence? 2466 34

The carotid body (CB) is a key chemoreceptor organ in which glomus cells sense changes in blood O2, CO2, and pH levels. CB glomus cells have also been found to detect hypoglycemia in both non-primate mammals and humans. O2 and low-glucose responses share a common final pathway involving membrane depolarization, extracellular calcium influx, increase in cytosolic calcium concentration, and neurotransmitter secretion, which stimulates afferent sensory fibers to evoke sympathoadrenal activation. On the other hand, hypoxia and low glucose induce separate signal transduction pathways. Unlike O2 sensing, the response of the CB to low glucose is not altered by rotenone, with the low glucose-activated background cationic current unaffected by hypoxia. Responses of the CB to hypoglycemia and hypoxia can be potentiated by each other. The counter-regulatory response to hypoglycemia by the CB is essential for the brain, an organ that is particularly sensitive to low glucose. CB glucose sensing could be altered in diabetic patients, particularly those under insulin treatment, as well as in other medical conditions such as sleep apnea or obstructive pulmonary diseases, where chronic hypoxemia presents with plastic modifications in CB structure and function. The current review will focus on the following main aspects: (1) the CB as a low glucose sensor in both in vitro and in vivo models; (2) molecular and ionic mechanisms of low glucose sensing by glomus cells, (3) the interplay between low glucose and O2 sensing in CB, and (4) the role of CB low glucose sensing in the pathophysiology of cardiorespiratory and metabolic diseases, and how this may serve as a potential therapeutic target.
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PMID:Glucose sensing by carotid body glomus cells: potential implications in disease. 2536 Jan 17


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