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Biomedical subjects

W A De Backer

Publications and source records attributed to W A De Backer.

At least 19 recordsLinked to original sources
PubMed2007

Reference values for sleep-related respiratory variables in asymptomatic European children and adolescents.

AIM: Only a limited number of studies, designed to establish normal values for sleep-related respiratory variables in children, have been reported, and all are non-European. The aim of this study was to expand the knowledge on normative data in children. METHODS: Subjects ranging from 6 to 16 years were recruited and underwent full polysomnography. Only subjects without sleep disordered breathing or other sleep problems as assessed by clinical history were included. RESULTS: Sixty subjects were studied ( = 11.7 +/- 2.6 years; 28 boys; = 118.8 +/- 30.6%). was 0.85 +/- 1.06 (range: 0.0-5.5). was 0.06 +/- 0.16 (range: 0.0-0.9); 11 patients had a total of 31 obstructive apneas. Only five obstructive hypopneas were detected with = 0.08 +/- 0.17 (range: 0.0-0.9). was 1.98 +/- 1.39 (range: 0.1-7.2). was 97.0 +/- 0.6% (range: 96.0-98.0); was 91.8 +/- 2.7% (range: 82.0-96.0); <% of total sleep time with SaO2 >or= 95%> was 98.7 +/- 2.1% (range: 90.8-100.0); was 0.8 +/- 0.9 (range: 0.0-4.9) and was 6.1 +/- 1.8 (range: 2.7-10.9). Snoring was detected in 15 patients (4 overweight subjects), with no difference in patient characteristics and sleep-related respiratory variables between snorers and non-snorers. Subjects in the overweight group (n = 22) had a lower SaO2nadir (90.8 +/- 2.7 vs. 92.4 +/- 2.6; P = 0.01) and a higher ODI (1.3 +/- 1.3 vs. 0.4 +/- 0.4; P = 0.0002) than their normal weight peers. CONCLUSION: Our data are in agreement with other non-European studies, designed to establish normal values in children.

Adolescent↗
PubMed2006

Glucocorticosteroids as antioxidants in treatment of asthma and COPD. New application for an old medication?

Inhaled corticosteroids (ICS) are the standard of care in asthma and are widely used in the treatment of patients with COPD. The influence of steroids on inflammatory processes has long been established since glucocorticoids and their receptor belong to the regulatory network involved in inhibition of several inflammatory pathways. Inflammatory processes are usually accompanied by an increased oxidative burden followed by a depletion of antioxidants. Therefore, the effects of steroids on antioxidant status have been investigated revealing possible positive effects on the reduced antioxidant enzyme activity. Nevertheless, the mechanisms of this modulation have not been fully elucidated yet. It is possible that antioxidant enzyme activity is regulated at the level of transcription. Additionally, because of the fact that antioxidant enzymes are trace element dependent, steroids may affect their activity through influence on trace element accumulation. This review summarizes the effects of steroids on the antioxidant enzymes activity in vitro and in vivo in relation to asthma and COPD.

Administration, Inhalation↗
PubMed2006

Antioxidant and anti-inflammatory efficacy of NAC in the treatment of COPD: discordant in vitro and in vivo dose-effects: a review.

In order to develop efficient therapeutic regimes for chronic obstructive pulmonary disease (COPD), N-acetylcysteine (NAC) has been tested as a medication which can suppress various pathogenic processes in this disease. Besides its well-known and efficient mucolytic action, NAC meets these needs by virtue of its antioxidant and anti-inflammatory modes of action. NAC is a thiol compound which by providing sulfhydryl groups, can act both as a precursor of reduced glutathione and as a direct ROS scavenger, hence regulating the redox status in the cells. In this way it can interfere with several signaling pathways that play a role in regulating apoptosis, angiogenesis, cell growth and arrest and inflammatory response. Overall, the antioxidant effects of NAC are well documented in in vivo and in vitro studies. It successfully inhibits oxidative stress at both high and low concentrations, under acute (in vitro) and chronic administration (in vivo). With regard to its anti-inflammatory action, in contrast, the effects of NAC differ in vivo and in vitro and are highly dose-dependent. In the in vitro settings anti-inflammatory effects are seen at high but not at low concentrations. On the other hand, some long-term effectiveness is reported in several in vivo studies even at low dosages. Increasing the dose seems to improve NAC bioavailability and may also consolidate some of its effects. In this way, the effects that are observed in the clinical and in vivo studies do not always reflect the success of the in vitro experiments. Furthermore, the results obtained with healthy volunteers do not always provide incontrovertible proof of its usefulness in COPD especially when number of exacerbations and changes in lung function are chosen as the primary outcomes. Despite these considerations and in view of the present lack of effective therapies to inhibit disease progression in COPD, NAC and its derivatives, because of their multiple molecular modes of action, remain promising medication once doses and route of administration are optimized.

Acetylcysteine↗
PubMed2006

Differences in responses upon corticosteroid therapy between smoking and non-smoking patients with COPD.

Inhaled corticosteroids have a high level of topical anti-inflammatory activity. However, in patients with COPD these drugs have been reported to exert limited effects. A reduction in histone deacetylase (HDAC) activity is suggested to prevent the anti-inflammatory action of corticosteroids. Cigarette smoke is known to reduce HDAC expression. The aim of this study is to compare the outcome of corticosteroid therapy in both smoking and non-smoking COPD patients. Twenty-three smoking patients and 18 ex-smoking patients with COPD were treated with inhaled corticosteroids for a period of 2 months. Blood and induced sputum samples were collected before and after treatment. Values of FEV(1) %-predicted did not change upon the therapy, but there was a trend to improve in the ex-smokers (63.1 -> 64.8%-pred.), compared with a decrease in the smokers (63.3 -> 61.6%-pred.). The levels of the pro-inflammatory cytokine IL-8 increased in the group of smokers from 379 +/-78 to 526 +/-118 ng/ml. Although not significant, a slight decrease from 382 +/-70 to 342 +/-62 ng/ml was observed in the group of ex-smokers. The neutrophil related elastase activity showed similar effects after steroid treatment, it went up from 36.4 +/-12.0 to 113.5 +/-9.7 nmol/l in smokers, and decreased from 346.2 +/-72.1 to 131.1 +/-6.5 nmol/l in ex-smokers with COPD. These results support the evidence that inhaled corticosteroids have no anti-inflammatory effects in COPD patients, but only when these patients are still smoking. Smoking cessation seems the best therapy for COPD patients.

Adrenal Cortex Hormones↗
PubMed2006

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.

Acetylcysteine↗
PubMed2005

First night effect for polysomnographic data in children and adolescents with suspected sleep disordered breathing.

AIMS: To assess the presence of a first night effect (FNE) in children and adolescents and to examine if a single night polysomnography (PSG) is sufficient for diagnosing obstructive sleep apnoea syndrome (OSAS). METHODS: Prospective case study of 70 patients (group 1: 2-6 years, n = 22; group 2: 7-12 years, n = 32; group 3: 13-17 years, n = 16) referred for OSAS. Diagnostic criteria for OSAS: one or more of the following: (1) obstructive apnoea index (OAI) > or =1; (2) obstructive apnoea hypopnoea index (oAHI) > or =2; (3) SaO2 < or =89% in association with obstruction. RESULTS: In all age groups, but mainly in the oldest children, REMS increased during the second night, mainly at the expense of stage 2 sleep. The first night PSG correctly identified OSAS in 86%, 91%, and 100% of the children for groups 1, 2, and 3 respectively. This represents 9% false negatives for OSAS when only the first night PSG was used. All cases missed had mild OSAS, except for one with oAHI >5 on night 2. There were also seven patients with OSAS on night 1 but with a normal PSG on night 2: all had oAHI <5. CONCLUSION: There is a FNE in children and adolescents. A single night PSG is sufficient for diagnosing OSAS, but in cases with a suggestive history and examination and with a negative first night, a second night study might be advisable.

Adolescent↗
PubMed2005

Inhibition of in vitro neutrophil migration through a bilayer of endothelial and epithelial cells using beta2-agonists: concomitant effects on IL-8 and elastase secretion and impact of glucocorticosteroids.

BACKGROUND: Beta2-agonists and glucocorticosteroids are two common treatments for COPD and they are often used in combination. Glucocorticosteroids mediate the anti-inflammatory response through the glucocorticosteroid receptors (GRs). Beta2-agonists are potent bronchodilators but they can have some anti-inflammatory properties by elevating the level of intracellular cAMP. In this study we aimed to investigate the anti-inflammatory effect of combination therapy in vitro. METHODS: Neutrophils or the bilayer of endothelial and epithelial cells were preincubated with salbutamol, budesonide or budesonide followed by salbutamol. FMLP-induced IL-8, elastase release and neutrophil migration through the bilayer was measured. RESULTS: Salbutamol at concentrations of 10(-4), 10(-5) and 10(-9) M inhibited IL-8, elastase release and migration of neutrophils in an inverse bell-shaped concentration-response manner. When given after budesonide (10(-9) and 10(-8)M), the inhibitory effect on migration was additive. This additive effect was not observed for elastase and IL-8 release. CONCLUSIONS: Salbutamol inhibits neutrophil migration and IL-8 and elastase release in a concentration-dependent manner. Preincubation with low concentration of budesonide enhanced the inhibition of migration achieved by low concentrations of salbutamol.

Adrenergic beta-Agonists↗
PubMed2005

The interrelationship between markers of inflammation and oxidative stress in chronic obstructive pulmonary disease: modulation by inhaled steroids and antioxidant.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is accompanied by both airway and systemic inflammation and by oxidative stress. This study aimed to characterise the relationship between oxidative stress and inflammatory components in induced sputum and blood. MATERIAL & METHODS: We studied blood and sputum samples from stable COPD patients (mean FEV1 60.5+/-7.5% predicted) at baseline (no treatment) and after 10 weeks treatment with either inhaled steroid, fluticasone propionate (FP) (1000 microg/d) or 10 weeks treatment with N-acetylcysteine (600mg/d) (NAC). We assessed the inflammatory markers (IL-8, ECP, sICAM-1, NE) in sputum and serum and we compared them with blood markers of oxidative stress (SOD, GPx, TEAC, albumin, vitamin E and A). RESULTS: At baseline blood sICAM-1 correlated with IL-8 levels (P<0.01, r = 0.62) and negatively with GPx (P<0.01, r = -0.63) and with TEAC (P<0.05, r = -0.53). TEAC correlated positively with GPx (P<0.01, r = 0.70). Correlation between sICAM and IL-8 disappeared after NAC treatment. The correlation between sICAM and GPx disappeared after FP treatment. The correlation between TEAC and GPx was maintained after both NAC and FP. CONCLUSIONS: The relationship between markers of inflammation, adhesion and antioxidant capacity is significantly modulated by treatment with N-acetylcysteine or inhaled corticosteroids.

Administration, Inhalation↗
PubMed2004

Use of ICAM-1 antibodies and antisense oligonucleotides to inhibit transmigration of neutrophils.

OBJECTIVE: The increase in adhesion molecule expression during the initial phase of inflammation leads to transmigration of neutrophils. Inhibition of this transmigration could decrease inflammatory response and tissue damage. MATERIALS AND METHODS: Uptake of fluorescein-labelled oligonucleotides, expression of ICAM-1 and neutrophil migration were studied using the bilayer of epithelial (H292) and endothelial (ECV-304) cell lines and neutrophils from peripheral blood of healthy volunteers. RESULTS: The inhibition of ICAM-1 expression was time dependent for both cell lines, with inhibition of more than 50% after 48 h. Antisense oligos inhibited transmigration already after 4 h of incubation (6.6 +/- 2.5% versus 18.6 +/- 2.5% inhibition, p < 0.01). Antisense was more effective in preventing fMLP-induced neutrophil migration than ICAM-1 antibodies (88 +/- 3.8% versus 67 +/- 7% inhibition, p = 0.02). CONCLUSIONS: Antisense oligos cause a decrease in ICAM-1 expression and inhibit transmigration of neutrophils. However the effectiveness of antisense is higher than monoclonal antibodies, neither of them is able to block the migration completely. This suggests the existence of ICAM-1 independent mechanisms that are responsible for migration.

Antibodies↗
PubMed2002

The inflammatory marker serum eosinophil cationic protein (ECP) compared with PEF as a tool to decide inhaled corticosteroid dose in asthmatic patients.

The objective of this study was to compare the inflammatory marker eosinophil cationic protein (ECP) with peak expiratory flow (PEF) in determining the therapeutic needs of inhaled corticosteroids in asthma patients assessed as asthma symptoms. A randomized, single-blind study over 6 months was performed at six specialist centres in Europe. In total, 164 adult patients with moderate to severe symptomatic asthma and regular use of inhaled corticosteroids were included. After a run-in period of 2 weeks patients were randomly allocated to the ECP or the PEF monitoring group. The dose of inhaled cort costeroids was adjusted every fourth week based on the current serum ECP value or pre-bronchodilator morning PEF values as surrogate markers of therapeutic needs. At the end of the study there were no statistically significant differences in the mean daily symptom score or the percentage of symptom-free days between the two groups. The mean daily dose of inhaled corticosteroids was similar in the two groups at the start of the study but the algorithms used to adjust the dose of inhaled corticosteroids resulted in an increased use of inhaled corticosteroids in both groups. The mean daily dose of inhaled corticosteroids over the whole study period was significantly lower in the ECP group compared withthe PEF group (1246 vs. 1667 microg, P = 0.026). In the ECP group, forced expiratory volume in I sec (FEV)% predicted was lower at the end ofthe study compared with the begining (92% vs. 87%, P = 0 .0009), although there was no significant difference between the two groups. None of the used algorithms for ECP and PEF led to improvement in symptom scores, in spite of increased doses of inhaled corticosteroids. In this respect, both methods were equivalent and insufficient. Recommendations suggesting lung function tests in current guidelines may be difficult to translate into clinical practice, however, a combination of inflammatory markers, lung function and symptoms may still improve asthma control.

Administration, Inhalation↗
PubMed2001

Continuous positive airway pressure and lung inflation in sleep apnea patients.

BACKGROUND: It was shown in normals that an important decrease in upper airway resistance can be obtained with continuous positive airway pressure (CPAP). It was suggested that lung inflation in patients with sleep apnea syndrome (SAS) could also be a mechanism of action of CPAP. OBJECTIVE: In the present study we wanted to evaluate the effects of nocturnal CPAP on the daytime lung function pattern in patients with SAS. METHODS: We measured arterial blood gases and possible changes in static lung volumes in 57 SAS patients (37 with normal lung function, 10 with COPD and 10 with restrictive lung disease) after at least one month of CPAP therapy. RESULTS: A significant increase in PaO(2) (from 79 to 84 mm Hg, p = 0.01) and a decrease in AaDO(2) (from 23 +/- 1 to 16 +/- 1, p < 0.01) was only observed in SAS patients with normal lung function. This improved gas exchange was parallelled by a small but non significant change in the FRC (from 96.5 +/- 3.2 to 105.4 +/- 3.7%pred, p = 0.07) and TLC (from 101.3 +/- 1.7 to 104.1 +/- 1.4%pred, p = 0.15). Similar changes in TLC and FRC were also observed in SAS patients with obstructive and restrictive lung disease. CONCLUSIONS: Chronic nocturnal CPAP therapy can improve daytime gas exchange and may influence lung inflation during the daytime. The small changes seem to be a functional effect but of no clinical relevance.

Female↗
PubMed2000

Induced sputum of patients with chronic obstructive pulmonary disease (COPD) contains adhesion-promoting, therapy-sensitive factors.

OBJECTIVE: The aim of this study was to investigate whether sputum of COPD patients before and after treatment with inhaled corticosteroids (IHC) or N-acetylcysteine (NAC) exerts any effect on the adhesion of isolated polymorphonuclear cells (PMNs) to cultured endothelial cells. METHODS: A human endothelial cell line was grown to confluence before use in adhesion experiments. PMNs were obtained from normal, non-smoking volunteers and preincubated (30 min, 37 degrees C) with diluted sputum sol obtained from COPD patients before the cells were put on the endothelial cells. RESULTS: Basal adhesion of unstimulated PMNs after 30 min at 37 degrees C in 5% CO2 was 15.9+/-1.1% (mean +/- SEM, n = 9). A significant enhancement of the adhesion to 33.0+/-1.4% (n = 11, P<0.0001) was observed with sputum obtained from COPD patients before treatment with IHC, and 34.6+/-1.5% (n = 10, P<0.0001) before treatment with NAC. Administration of IHC for 8 weeks resulted in an adhesion of 27.7+/-2.4%, which is an inhibition of 31% (n = 11, P<0.05). However, treatment for 8 weeks with NAC showed no change in the adhesion of stimulated PMNs. Long-term treatment with NAC showed a gradual decrease of adhesion (n = 9, P<0.05), whereas long-term treatment with IHC lead to an increase in adhesion (n = 10, P<0.02). CONCLUSIONS: These results indicate that factors locally produced in the airways of COPD patients may promote adhesion of neutrophils to endothelium. They further suggest that glucocorticoids may only have a short-term transient effect on adhesion, whereas NAC showed effects on the adhesion after administration for longer periods.

Acetylcysteine↗
PubMed2000

Morphometric analysis of the uvula in patients with sleep-related breathing disorders.

The upper-airway mucosa in obstructive sleep apnea (OSA) patients and snorers is often described as edematous and hyperplastic. The morphologic aspects of the pharyngeal mucosa, and in particular the mucosa of the uvula and soft palate, in OSA patients are, however, not well described. The aim of the present retrospective study therefore was to perform histologic examination of the pharyngeal mucosa obtained from patients with various forms of sleep-related breathing disorders, including primary snoring. A midsagittal section of uvulas obtained by uvulopalatopharyngoplasty (UPPP) was investigated in 34 OSA patients and 9 non-apneic snorers. Control tissues were taken by autopsy in 19 patients not known to have OSA or snoring. A morphometric point counting technique was used to determine the tissue composition. The data showed that OSA patients and non-apneic snorers had a significantly greater percentage of intercellular space than controls (65.7% vs 54.0%; P = 0.006). Control uvulas contained more muscle than OSA and snorers (14.0% vs 7.8%; P = 0.006). Moreover, the covering epithelium was significantly thicker in OSA and snorers than in controls (variance ratio = 7.64; P = 0.008). When taking body mass index (BMI) into account, no correlation was found between fat deposition and BMI. Findings showed that an increased clinical severity of OSA did not affect the tissue composition. Indeed, uvula morphology was similar in OSA patients with respect to non-apneic snorers. Since the increased amount of intercellular space is the expression of edema, we hypothesize that these mucosal changes together with hyperplasia of the covering epithelium are secondary effects to snoring. They presumably play a minor role in the etiopathogenesis of OSA, but may increase the severity of OSA by further narrowing the pharyngeal lumen.

Female↗
PubMed2000

Abbreviated method for assessing upper airway function in obstructive sleep apnea.

STUDY OBJECTIVES: Previous studies have shown that the level of flow through the upper airway in patients with obstructive sleep apnea (OSA) is determined by the critical closing pressure (Pcrit) and the upstream resistance (RN). We developed a standardized protocol for delineating quasisteady-state pressure-flow relationships for the upper airway from which these variables could be derived. In addition, we investigated the effect of body position and sleep stage on these variables by determining Pcrit and RN, and their confidence intervals (CIs), for each condition. DESIGN: Pressure-flow relationships were constructed in the supine and lateral recumbent positions (nonrapid eye movement [NREM] sleep, n = 10) and in the supine position (rapid eye movement [REM] sleep, n = 5). SETTING: University Hospital Antwerp, Belgium. PATIENTS: Ten obese patients (body mass index, 32.0+/-5.6 kg/m(2)) with severe OSA (respiratory disturbance index, 63.0+/-14.6 events/h) were studied. INTERVENTIONS: Pressure-flow relationships were constructed from breaths obtained during a series of step decreases in nasal pressure (34.1+/-6.5 runs over 3.6+/-1.2 h) in NREM sleep and during 7.8+/-2.2 runs over 0.8+/-0.6 h in REM sleep. RESULTS: Maximal inspiratory airflow reached a steady state in the third through fifth breaths following a decrease in nasal pressure. Analysis of pressure-flow relationships derived from these breaths showed that Pcrit fell from 1.8 (95% CI, -0.1 to 2.7) cm H(2)O in the supine position to -1.1 cm H(2)O (95% CI, -1.8 to 0.4 cm H(2)O; p = 0.009) in the lateral recumbent position, whereas RN did not change significantly. In contrast, no significant effect of sleep stage was found on either Pcrit or RN. CONCLUSIONS: Our methods for delineating upper airway pressure-flow relationships during sleep allow for multiple determinations of Pcrit within a single night from which small yet significant differences can be discerned between study conditions.

Airway Resistance↗
PubMed1999

Two months follow up of auto-CPAP treatment in patients with obstructive sleep apnoea.

BACKGROUND: Continuous positive airway pressure (CPAP) with fixed mask pressure is the current standard treatment for obstructive sleep apnoea (OSA). Auto-CPAP devices apply at any time the minimally required pressure to normalise breathing and may improve patient comfort and compliance. We present an open descriptive study of auto-CPAP treatment at home in patients previously managed with conventional CPAP. METHODS: Fifteen patients with obstructive sleep apnoea (OSA), previously treated for at least one year with standard CPAP, were followed prospectively for a two month period on auto-CPAP. Outcome measures were both subjective evaluation by the patients and objective (polysomnographic) data obtained at one and two months of follow up. RESULTS: The Epworth sleepiness score did not change significantly between baseline and follow up after one and two months and no systematic changes in CPAP related side effects were reported. Compared with the baseline polysomnographic values without treatment, a significant improvement in both respiratory and sleep parameters was observed during auto-CPAP. These results were not significantly different from those obtained with standard CPAP. A significant correlation was found between the effective CPAP pressure (Peff) and the amount of time spent below Peff during auto-CPAP treatment (r = 0.6, p = 0.01). CONCLUSION: Long term auto-CPAP treatment in these patients with severe OSA appears to provide comparable efficacy to that of standard CPAP treatment.

Adult↗
PubMed1998

Methods and clinical significance of studying chemical drives.

Studying chemical control of ventilation implies evaluation of both chemoreceptor functions taken into account however the mechanical factors influencing the effector organs. The role of abnormal chemical drives has been demonstrated in COPD patients. More recently the role of abnormal chemical drives was studied during sleep. Absent or severely depressed drives may facilitate the development of central apneas and hypoventilation. High drives may lead to periodic breathing eventually with central apneas as well. Most intriguing therefore is the role of chemical drives in the pathogenesis of the obstructive and central sleep apnea syndrome. There is accumulating evidence that fluctuations in the drive to breathe may adversely affect the upper airway patency and facilitate upper airway closure and obstructive apneas. Interaction with chemical drives (eg by administration of acetazolamide) has been shown to improve central (and eventually also obstructive) sleep apnea. Studying chemical drives will probably be clinically useful in solving the complex mechanisms controlling ventilation during sleep in patients with and without underlying airway or lung disease.

Acetazolamide↗
PubMed1997

Site of upper airway obstruction in obstructive apnoea and influence of sleep stage.

Various sites along the upper airway (UA) are prone to narrow and collapse in patients affected by obstructive sleep apnoea. Sleep stages may eventually alter these sites. The present study was designed to determine the site(s) of UA obstruction and the influence of sleep stage on the pattern of obstruction. Twenty eight obstructive sleep apnoea patients underwent UA pressure measurements during polysomnography. Solid-state pressure sensors were located at the nasopharynx, oropharynx, tongue base, hypopharynx and oesophagus and the lower limit of UA obstruction was determined relying on the observed pressure pattern. The site of UA obstruction varied among consecutive apnoeas in all but two patients. The lower limit of UA obstruction was predominantly located at the nasoand oropharynx. Rapid eye movement (REM) sleep was associated with a tendency for obstruction to extend towards lower levels of the UA and nasopharyngeal occlusion was significantly less observed during REM compared to oropharyngeal obstruction. Upper airway obstruction involves more than one specific site of the upper airway in the majority of sleep apnoea patients. Obstruction at lower levels of the upper airway is more likely to be observed during rapid eye movement sleep.

Humans↗