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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Sleep and sleep disorders play a prominent role in hormone regulation. Given that sleep disordered breathing (SDB) and diabetes mellitus (DM) are thought to result from obesity, it has been assumed that when the two coexist, the diabetes was caused by the obesity. However, new data has shed light on the effects that SDB, sleep deprivation, and snoring have on glucose regulation. It now appears that in addition to causing daytime drowsiness, cardiovascular disease, mood and memory disturbances, impotence, and car wrecks, obstructive sleep apnea (OSA) also promotes insulin resistance. Though data is still sketchy on the optimum management of coexisting DM and OSA, large-scale studies will most likely prove that homeostatic glucose control in patients with sleep apnea will require aggressive treatment of their SDB.
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PMID:Sleep and the endocrine system: new associations to old diseases. 1239 57

The purpose of this article is to review the current state of knowledge on contributions of nocturnal urine overproduction and overactive bladder to the syndrome of nocturia. We review the recent literature and current state of the art in differential diagnosis, pathophysiology, and classification of nocturia. We found that multiple pathologic factors may result in nocturia, including cardiovascular disease, diabetes mellitus or insipidus, third spacing of fluid, sleep apnea, lower urinary tract obstruction, primary sleep disorders, and behavioral and environmental factors. Thus, nocturia may be attributed to nocturnal polyuria (nocturnal urine overproduction), diminished nocturnal bladder capacity, or both. Distinction between these conditions is made by a simple arithmetic analysis of the 24-hour voiding diary. Understanding the manifold origins of nocturia will lead to rational treatment of specific contributing pathophysiologic factors.
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PMID:Nocturnal polyuria versus overactive bladder in nocturia. 1249 48

This article reviews the state of knowledge and the algorithms for the diagnosis, classification, and treatment of nocturia. The state of the art in diagnosis, classification, and treatment of nocturia is presented. Nocturia has been poorly classified and poorly understood. Multiple factors may result in nocturia, among which are pathologic conditions such as cardiovascular disease, diabetes mellitus, lower urinary tract obstruction, anxiety or primary sleep disorders, and behavioral and environmental factors. Nocturia may be attributed to nocturnal polyuria (nocturnal urine overproduction), diminished nocturnal bladder capacity, or a combination of the two. Distinction between these conditions is made by a simple arithmetic analysis of the 24-hour voiding diary. Nocturia has been poorly studied and, only recently, has been classified according to its etiology and pathogenesis. Based on a review of the current state of knowledge, this article presents a scheme for the classification and treatment of patients suffering from loss of sleep resulting from nocturnal micturition.
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PMID:Nocturia. 1449 58

Stroke is a disease with well-defined modifiable risk factors such as arterial hypertension, smoking, diabetes, hyperlipidemia and atrial fibrillation. The need of new risk factors is based on the fact that only half the cardiovascular disease risk is explained by conventional risk factors. Inflammatory markers, infection, homocysteine and sleep-disordered breathing rank as the four most important new risk factors in cerebral atherosclerosis. C-reactive protein is the inflammatory marker that has been most thoroughly studied. Elevated concentrations of C-reactive protein increase the risk of heart disease and thromboembolic stroke in men and women. The role of Chlamydia pneumoniae is still controversial. Influenza vaccination is a simple and effective preventive measure against stroke. Despite the potential relationship between homocysteine and stroke, we should wait to the results of the ongoing trials to know if the reduction of homocysteine levels with vitamin therapy is of clinical benefit. Sleep-disordered breathing is a potential new risk factor with an effective therapy. Neurologists should not forget to look for sleep disorders in their stroke patients and probably manage them with breathing therapy from the acute phase.
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PMID:Cerebral ischemia: new risk factors. 1469 79

Growth Hormone Releasing Hormone (GHRH) is one of the most important hormones in life. Because of its potential clinical importance, its short half-life, and its expensive chemical synthesis, an analog of hGHRH with a prolonged half-life and better activity has been studied for clinical application, especially for the treatment of muscle wasting, type II diabetes, or sleep disorders. The Pro-Pro-hGHRH(1-44) peptide has better activity. The fusion partner gene with 127 amino acid residues of the C-terminus from l-asparaginase was recombined with asp-pro-pro-hGHRH(1-44) gene synthesized by PCR method to form a fusion protein with the unique acid labile linker Asp-Pro. The recombinant protein was expressed to high levels in Escherichia coli BL21 (DE3). The Pro-Pro-hGHRH(1-44) peptide was purified to homogeneity by means of cell disruption, washing, ethanol precipitation, acid hydrolysis, and SP-Sephadex C-25, and Sephadex G-25 column chromatography. The fold of the purification was about 88 times and the yield was 1.1% of the total protein weight of the inclusion body. The peptide molecular mass of 5235.25 Da was determined by ESI mass spectroscopy. Its purity was determined by SDS-PAGE. In the study of the activity, we measured GH release of rat pituitary by using the antiserum kit against human GH. The peptide doses of 0.01, 0.1, 1.0, 7.72, and 20.9 microg/ml used, respectively, released the GH values of 0.1+/-0.1, 12.5+/-7.3, 16.6+/-5.8, 49.8+/-7.6, and 79.5+/-5.7 ng/ml whereas their blank controls, respectively, were 0.5+/-0.8, 4.1+/-2.6, 3.1+/-3.1, 4.7+/-1.8, and 1.2+/-0.3 ng/ml. The activity results of all dose groups except 0.01 microg/ml Pro-Pro-hGHRH(1-44) group and hGHRH(1-40) group showed that there were significant differences between GH released by the peptide and that by its blank control. With the increase of dosage, the differences were more significant. hGHRH(1-40) showed no measured GH release when the dose was up to 2 microg/ml. The activity results show that the Pro-Pro-hGHRH(1-44) peptide is a potential GH releasing analog.
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PMID:Production and enhanced biological activity of a novel GHRH analog, hGHRH with an N-terminal Pro-Pro extension. 1500 64

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia. Thyroid function, hepatic and renal tests, glycemia, TP, TCA, VS, VDRL-TPHA were normal. Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. A neurologic examination was possible because of cooperation. All the tendon reflexes of inferior members were absent. The plantars were in flexion and there was a left inferior member hypoesthesia. The cerebral scan and EEG were normal. Fundic biopsy, realized by fibroscopy, revealed fundic atrophia and intestinal metaplasia compatible with Biermers' disease. The iron deficiency exploration concluded diet deficiency. Mme V. appeared euphoric, her speech was very rapid with play on words and overactivity. This hypomania state totally disappeared 3 days after. Six Months after her hospitalisation, she presented an hypothyroidism (TSH=3,780; T3=1,35; T4=1,08). A thyroid hormones replacement was started and she continued to receive Monthly B12 replacement. Discussion - This case report illustrates psychiatric manifestations of Biermers' disease. The clinical arguments in favour are: white woman, more than 60 Years old, no history of psychiatric problems, atypical symptoms (confusional state with psychiatric symptoms), fluctuation of symptoms (severe depression with confusional state, delusion of persecution and Capgras' syndrome; delusion with lability of mood and hypomania), dramatic improvement after 9 days of vitamin B12 replacement therapy. The biological arguments are: anemia, vitamin B12 deficiency, normal folate level, atrophia and fundic metaplasia, positive antibodies to parietal cells in the serum, association between Biermers' disease and autoimmune disease (Haschimoto thyroidite). Psychiatric manifestations can occur in the presence of low serum B12 levels but in the absence of the other well recognized neurological and haematological abnormalities of pernicious anemia. Mental or psychological changes may precede haematological signs by Months or Years. They can be the initial symptoms or the only ones. Verbank et al. described the case of a patient with vitamin B12 deficiency in whom hypomania, paranoia and depression had been successively presented during a period of 5 Years before anemia have been developed. The case of Mme V. is similar in the succession of severe depression with delusion of persecution and Capgras' syndrome, delusion with lability of mood and hypomania, during a period of two Months. This report seems to be the first one of a sequence of several psychiatric states with pernicious anemia during a period of two Months with normocytosis anemia. To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms. Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. In first intention, B12 deficiency should be researched by serum B12 determination (normal 200-950 pg/ml). Studies of methylmalonic acid and homocysteine showed that they are very sensitive functional indicators of cobalamin status especially when other evidence of cobalamin (B12) deficiency was equivocal. Measurement of methylmalonic acid (normal 73-271 nmol/l) and homocysteine (normal 5,4-13,9 micromol/l) should not replace the measurement of serum cobalamin.
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PMID:[Psychiatric manifestations of vitamin B12 deficiency: a case report]. 1502 91

The aim of the present study was to evaluate the efficacy and safety of zolpidem in elderly subjects with disorders of sleep and comorbidities. The patients of this study had to present the following requirements: age over 70 years, reported disorders of sleep such as insomnia, and they had to be affected with diabetes and arterial hypertension. Patients presenting diseases that could interfere with sleep, i.e., anxiety, depression, panic attacks,alcohol abuse, some drugs were excluded from the study. All the jobs potentially causing insomnia carried out in the past from the patients were considered, too. A questionnaire of sleep was administered to all the patients (World Psychiatric Association: WPA, 1971).Insomnia, whenever present, was classified according to the criteria of the American Sleep Disorders (ASD) Society and the American Professional Sleep Society (APSS). The following scales were also administered: instrumental activities of daily living scale (IADL),activities of daily living (ADL), geriatric depression scale (GDS), cumulative illness rating scale (CIRS), short portable mental status questionnaire (SPMSQ), mini nutritional assessment (MNA), disease medical index (DMI), sleep questionnaire, social and environmental status. Two groups of patients were evaluated. Group A: 50 patients, 35 women and 15 men, mean age 78.9 years, with a history of insomnia, and Group B 30 patients, 20 women and 10 men, mean age 78.4 years, with onset of insomnia in the last three weeks. The two groups were further divided into three subgroups, diabetic, hypertensive and healthy patients. Zolpidem showed to be effective and well tolerated in both groups of patients.
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PMID:Use of zolpidem in over 75-year-old patients with sleep disorders and comorbidities. 1520 2

The purpose of the study was to find out if snoring, sleep apnea and daytime sleepiness are independent indices of obesity related to type two diabetes (T2D), and whether depression is independently associated with features of sleep apnea. A population-based cohort study was conducted among 593 subjects (245 men and 348 women) born in 1935 and living in Oulu in 1996-1998. Glucose status was determined with a standard 2h oral glucose tolerance test, and sleeping disorders were recorded on the Epworth sleepiness scale (ESS) and in a questionnaire of five questions about sleeping and snoring. Depression was measured by the Zung self-rated depression scale. Insulin sensitivity was measured by quantitative insulin sensitivity check index. Habitual snoring was more common in diabetic subjects than in subjects with impaired glucose regulation (IGR) or normal glucose tolerance (NGT). All sleep disorders associated with neck circumference, waist circumference and body mass index (BMI). There was also a relationship between impaired insulin sensitivity and habitual snoring in bivariate analysis. In multiple logistic regression analysis, depression associated independently with daytime sleepiness (OR 3.00, 95% CI 1.40-6.46). Type 2 diabetes (T2D) (OR 1.93, 95% CI 1.04-3.57) and smoking (OR 1.69, 95% CI 1.00-2.84) associated independently with habitual snoring. BMI (OR 1.20, 95% CI 1.09-1.34) and male gender (OR 2.61, 95% CI 1.05-6.72) associated independently with sleep apnea. In a multiple regression model, BMI, neck circumference and habitual snoring associated independently with T2D. Habitual snoring was associated with T2D and impaired insulin sensitivity. Daytime sleepiness seemed to be linked with depression but not with using sleep medication, IGR and T2D.
Diabetes Res Clin Pract 2005 Jan
PMID:The relationship of glucose tolerance to sleep disorders and daytime sleepiness. 1562 Apr 38

Orexins are a pair of neuropeptides expressed by a population of neurons located in the lateral hypothalamic area (LHA). Prepro-orexin- or orexin receptor type 2-deficient animals exhibit a phenotype remarkably similar to the human sleep disorder, narcolepsy, which is characterized by sleep/wakefulness fragmentation. Human narcolepsy is known to be associated with metabolic abnormalities, including an increased frequency of obesity and non-insulin-dependent diabetes mellitus. Complex disruption of energy homeostasis in orexin neuron-deficient transgenic mice (orexin/ataxin-3 mice) is also manifested as late-onset obesity despite eating less. Here, we report that the development of obesity in orexin neuron-ablated narcoleptic mice is critically dependent on their genetic background and environmental factors, and the phenotype is different from that of prepro-orexin knockout mice even under the same genetic background and environmental factors, suggesting that factors that co-localize in orexin neurons might have important roles in the regulation of energy homeostasis. Our observation also suggests that the obesity observed in orexin neuron-deficient narcolepsy is dependent on the genetic background and environmental factors.
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PMID:Difference in obesity phenotype between orexin-knockout mice and orexin neuron-deficient mice with same genetic background and environmental conditions. 1586 93


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