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)

Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0+/-2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1+/-3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long-term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (NS) whereas it decreased slightly (NS) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0+/-6.5 versus 55.3+/-6.7%, p<0.05) and at 06:00 h (64.1+/-6.5 versus 45.8+/-7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long-term continuous positive airway pressure treatment may reduce platelet aggregability.
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PMID:Platelet function in patients with obstructive sleep apnoea syndrome. 1110 7

The purpose of this study was to determine the frequency of central and obstructive sleep apnea in adult patients who have echocardiographic evidence of left ventricular dysfunction and pulmonary hypertension. Subjects with left ventricular dysfunction, pulmonary hypertension (pulmonary artery systolic pressure >30 mm Hg) and no lung disease were evaluated for risk factors associated with pulmonary hypertension. Of eight eligible adults, six completed the study. Subjects were from suburban and inner city family practices. Spirometric assessment, pulse oximetry on room air, rheumatologic evaluation, polysomnography, and additional history were taken. All six subjects had sleep apnea (apnea-plus-hypopnea index, or AHI, > or = 20): obstructive, central, or mixed. All were obese, and almost all the subjects had a restrictive pattern on spirometry, which is consistent with obesity. All had a pulmonary artery systolic blood pressure of 35 mm Hg or greater. None had daytime hypoxemia or collagen vascular disease, and none had ever used appetite suppressants. This study found a strong association between pulmonary hypertension and obstructive or central sleep apnea in obese patients with congestive heart failure (CHF). We propose that a pulmonary artery systolic pressure of 35 mm Hg or greater in ambulatory patients with CHF may signify an increased risk of sleep apnea.
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PMID:Left ventricular dysfunction, pulmonary hypertension, obesity, and sleep apnea. 1186 42

Scleredema of Buschke or scleredema diabetorum is a skin complication of diabetes with deposits of collagen and aminoglycans in the dermis. This disease characterized by thickening and hardening of the skin, is usually localized in nape, back and shoulder areas. Consequences could be a decrease in motility of the shoulders and an impairment of respiratory function. Other possible complications are sleep apnoea syndrome and monoclonal gammapathy. Type 1 or type 2 diabetes may be associated with scleredema of Buschke in more than 50% of cases. Diabetes-related risk factors are long duration of the disease, presence of microangiopathy, overweight and need of insulin. Various specific treatments proposed in the literature are poorly validated. In most severe cases, radiation therapy may be useful.
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PMID:Scleredema adultorum of Buschke: an under recognized skin complication of diabetes. 1711 Sep 4

The sinus elevation procedure is a predictable technique to allow for placement of dental implants in the posterior maxilla when the height of the alveolar ridge is limited. The sinus elevation can be performed by various techniques. In the crestal approach, bone graft is utilized to hydraulically elevate the sinus membrane through an osteotomy prepared in the alveolar crest. The implant can be placed either immediately or at a later surgery. This is a case report of an oroantral communication that developed as a complication to a sinus elevation surgery performed with the crestal approach. A 54-year-old female patient presented for dental implant treatment. The patient reported sleep apnea and smoking. Full-thickness flap was reflected in the posterior maxilla and using trephines, an osteotomy was prepared, 1 mm short of the sinus. The trephined core of bone was pushed into the sinus using osteotomes. Particulate bone graft was introduced through the osteotomy to elevate the sinus membrane, and a collagen membrane was used over the bone graft. Six days after surgery, the patient returned to the clinic with an oroantral communication. The patient reported that she was using a positive-pressure breathing mask at night because of sleep apnea. A flap was extended to the tuberosity area and was rotated palatally to achieve closure. The use of the pressure breathing mask was discontinued. The oroantral communication was successfully closed. Relatively few complications have been reported using the osteotome sinus elevation technique. The use of a positive pressure mask may have complicated a sinus elevation surgery. Other factors that may have contributed to this complication include smoking and delayed healing of the area.
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PMID:Oroantral communication as an osteotome sinus elevation complication. 2055 78

Plasma von Willebrand factor (VWF), produced in and released from vascular endothelial cells by various stimuli including hypoxia, induces platelet aggregation under high shear stress and plays dual pivotal roles in haemostasis and thrombosis within arterioles, which are regulated by the size of vWF multimers (VWFMs). Patients with obstructive sleep apnoea (OSA) have increased risk of thrombotic cardiovascular events, but the pathogenesis is unclear. We examined the relationship between VWF and OSA by measuring VWF antigen (VWF:Ag), VWFMs, VWF collagen binding activity (VWF:CB) and a disintegrin-like, metalloproteinase, and thrombospiondin type 1 motifs 13. A total of 58 OSA patients were enrolled. Blood samples were collected before sleep, after sleep, and after one night of nasal continuous positive airway pressure therapy. Based on VWFM analysis, OSA patients were classified into three groups; consistently normal VWFMs (group 1, n=29), increased high molecular weight (HMW)-VWFMs at 06:00 h (group 2, n=18), and decreased or absent HMW-VWFMs at 06:00 h (group 3, n=11). Patients in group 3 had significantly worse apnoea/hypopnoea index; VWF:CB followed a similar pattern. We observed a significant decrease in platelet count between 21:00 h and 06:00 h in OSA patients, potentially associated with reduced larger VWFMs together with decreased VWF:Ag levels. Severe OSA may contribute to an arterial pro-thrombotic state.
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PMID:Reduced larger von Willebrand factor multimers at dawn in OSA plasmas reflect severity of apnoeic episodes. 2236 56

Obstructive sleep apnea aggravates asthma, but its mechanisms are unknown. Chronic intermittent hypoxia is one hallmark feature of sleep apnea. In this study, we tested the effects of chronic intermittent hypoxia on allergen-induced inflammation in rats. Four groups (n = 9-11/group) of ovalbumin (OVA)-sensitized Brown-Norway rats underwent intermittent hypoxia (10% oxygen, 30 cycles/h, 10 h/d) or normoxia for 30 days concurrent with weekly OVA or vehicle challenges. Lung physiology, differential leukocyte counts from bronchoalveolar lavage, and histology (Picro Sirius Red staining for collagen content) were compared between groups 2 days after the last challenge. Gene expression in bronchoalveolar lavage cells was quantified by quantitative PCR. Compared with normoxia, chronic intermittent hypoxia reduced the FEV0.1/FVC ratio (P = 0.005), peak expiratory flow (P = 0.002), and mean midexpiratory flow (P = 0.004), predominantly in medium and large airways; decreased the baseline eosinophil number (P = 0.01) and amplified the effect of OVA on monocyte number (P = 0.02 for the interaction); in proximal airways, increased (P = 0.008), whereas in distal airways it decreased (P = 0.004), collagen density; induced qualitative emphysematous changes in lung periphery; and increased expression of the M2 macrophage marker YM-1 and augmented OVA-induced expression of plasminogen activator inhibitor-1. Chronic intermittent hypoxia alters immune response to allergen toward a more TH-1-predominant cellular phenotype with collagen deposition and matrix degradation, leading to airflow limitation. These findings highlight the potential of sleep apnea to aggravate airway dysfunction in patients with preexistent asthma.
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PMID:Effects of chronic intermittent hypoxia on allergen-induced airway inflammation in rats. 2500 9

Lung and kidney functions are intimately related in both health and disease. The regulation of acid-base equilibrium, modification of partial pressure of carbon dioxide and bicarbonate concentration, and the control of blood pressure and fluid homeostasis all closely depend on renal and pulmonary activities. These interactions begin in fetal age and are often responsible for the genesis and progression of diseases. In gestational age, urine is a fundamental component of the amniotic fluid, acting on pulmonary maturation and growth. Moreover, in the first trimester of pregnancy, kidney is the main source of proline, contributing to collagen synthesis and lung parenchyma maturation. Pathologically speaking, the kidneys could become damaged by mediators of inflammation or immuno-mediated factors related to a primary lung pathology or, on the contrary, it could be the renal disease that determines a consecutive pulmonary damage. Furthermore, non immunological mechanisms are frequently involved in renal and pulmonary diseases, as observed in chronic pathologies such as sleep apnea syndrome, pulmonary hypertension, progressive renal disease and hemodialysis. Kidney damage has also been related to mechanical ventilation. The aim of this review is to describe pulmonary-renal interactions and their related pathologies, underscoring the need for a close collaboration between intensivists, pneumologists and nephrologists.
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PMID:Kidney-lung connections in acute and chronic diseases: current perspectives. 2694 Mar 39