Search

Viral community-acquired pneumonia (CAP) is a potentially serious illness, particularly in adult patients with underlying chronic conditions. In addition to the most recent SARS-CoV-2, influenza, and respiratory syncytial virus (RSV) are considered the most relevant causes of viral CAP.To describe the clinical features of hospitalised adults admitted for influenza-A/B and RSV pneumonia and analyse, according to aetiology, factors associated with non-invasive ventilation (NIV) failure and in-hospital death (IHD).This was a retrospective and multi-centre study of all adults who were admitted for laboratory-confirmed influenza-A/B or RSV pneumonia, during two consecutive winter seasons (October-April 2017-2018 and 2018-2019) in three tertiary hospitals in Portugal, Italy and Cyprus.A total of 356 adults were included in the study. Influenza-A, influenza-B and RSV were deemed to cause pneumonia in 197 (55.3%), 85 (23.9%) and 74 (20.8%) patients, respectively. Patients with both obstructive sleep apnoea or obesity hypoventilation syndrome and influenza-A virus pneumonia showed a higher risk for NIV failure (odds ratio (OR) 4.66; 95% confidence interval (CI) 1.42-15.30). Patients submitted to NIV showed a higher risk for IHD, regardless of comorbidities (influenza-A OR 3.00; 95% CI 1.35-6.65, influenza-B OR 4.52; 95% CI 1.13-18.01, RSV OR 5.61; 95% CI 1.26-24.93).The increased knowledge of influenza-A/B and RSV pneumonia burden may contribute to a better management of patients with viral CAP.

Background and objective Average volume-assured pressure support-automated expiratory positive airway pressure (AVAPS-AE) combines an automated positive expiratory pressure to maintain upper airway patency to an automated pressure support with a targeted tidal volume. The aim of this study was to compare the effects of 2-month AVAPS-AE ventilation versus pressure support (ST) ventilation on objective sleep quality in stable patients with OHS. Secondary outcomes included arterial blood gases, health-related quality of life, daytime sleepiness, subjective sleep quality and compliance to NIV. Methods This is a prospective multicentric randomized controlled trial. Consecutive OHS patients included had daytime Pa CO2 > 6 kPa, BMI ≥ 30 kg/m2 , clinical stability for more than 2 weeks and were naive from home NIV. PSG were analysed centrally by two independent experts. Primary endpoint was sleep quality improvement at 2 months. Results Among 69 trial patients, 60 patients had successful NIV setup. Baseline and follow-up PSG were available for 26 patients randomized in the ST group and 30 in the AVAPS-AE group. At baseline, Pa CO2 was 6.94 ± 0.71 kPa in the ST group and 6.61 ± 0.71 in the AVAPS-AE group (P = 0.032). No significant between-group difference was observed for objective sleep quality indices. Improvement in Pa CO2 was similar between groups with a mean reduction of -0.87 kPa (95% CI: -1.12 to -0.46) in the ST group versus -0.87 kPa (95% CI: -1.14 to -0.50) in the AVAPS-AE group (P = 0.984). Mean NIV use was 6.2 h per night in both groups (P = 0.93). NIV setup duration was shorter in the AVAPS-AE group (P = 0.012). Conclusion AVAPS-AE and ST ventilation for 2 months had similar impact on sleep quality and gas exchange.

Introduction Sleep-disordered breathing causes a burden to the sufferer, the health care system and the society. Most studies have focused on obstructive sleep apnea (OSA); however, the prevalence of comorbidities in patients affected by overlap syndrome (OS) and obesity hypoventilation syndrome (OHS) has not been carefully evaluated. Study objectives The principal aim of this study was to identify the presence of comorbidities in patients suffering from OSA, OS, OHS and the differences in three groups of patients. Another purpose was to verify if sleepiness is associated with a greater prevalence of comorbidities. Methods A retrospective analysis in 989 adults referred for sleep diagnostic testing to our sleep center was performed. Patients were classified in OSA (721), OS (123) and OHS (145). Results The prevalence of comorbidities was higher in patients affected by OS and was the highest in the OHS group, while the prevalence of arterial hypertension is the highest in patients affected by OS. The probability of having more than two comorbidities follows the same trend. Excessive daytime sleepiness was associated with an increased rate of arterial hypertension, diabetes mellitus and the presence of multimorbidity in each group of patients. Conclusions The presence and the association of comorbidities seem to be higher in patients suffering from OSA, OS and OHS. Subjects suffering of OHS present a high prevalence of main diseases despite their younger age compared with others patients with SDB. Sleepiness may have a role, at least in a subset of these patients, into the development of comorbidities.

The obesity supine death syndrome refers to a catastrophic cascade of cardiorespiratory complications resulting from the supine positioning of a morbidly obese subject which can ultimately lead to death. It was first described in 1977 in two massively obese patients who were forced to lie down for medical procedures. But surprisingly, despite the current worldwide epidemic of obesity, very few cases have been reported yet. It can be assumed that the syndrome is poorly recognized in clinical practice and may participate in the high rate of unexplained death in morbidly obese patients. Based on the previously published cases and on those we met, this review aims at helping clinicians to early detect at-risk patients, to correctly diagnose this dramatic syndrome and to understand the underlying pathophysiology. More importantly, the main objective is to convince the attending clinicians that they have to do everything in their power to prevent obesity supine death syndrome occurrence by maintaining morbidly obese patients in the sitting or upright position whenever possible. When the syndrome unfortunately occurs, the best therapeutic approach is based on the immediate return to sitting position.

Aims To examine changes and explanatory variables for changes in health-related quality of life in patients treated with long-term mechanical ventilation over a six-year period. Background Long-term mechanical ventilation is a treatment for individuals with chronic hypercapnic respiratory failure, primarily caused by neuromuscular diseases, obesity hypoventilation syndrome, chronic obstructive pulmonary and restrictive thoracic diseases. Studies on long-term outcome on health-related quality of life and factors influencing it are lacking. Design Prospective cohort study. Methods Data were collected from the Norwegian Long-Term-Mechanical-Ventilation Registry and from patient reported questionnaire in 2008 and 2014. Health-related quality of life was measured by the Severe Respiratory Insufficiency questionnaire, containing 49 items and seven subdomains. Linear mixed effects models were used to measure changes and identify factors for changes. Results After six years, 60 patients were still participating, out of 127 at baseline. Health-related quality of life improved significantly in the total score and in four subdomains of the questionnaire. Satisfaction with training in long-term mechanical ventilation was an explanatory variable for improved ‘psychological well-being’ and follow-up for improvement of ‘anxiety’. Side effects of the treatment like facial soreness were associated with the total score. High age and high forced vital capacity were related to lower ‘physical function’ and improved ‘social functioning’, respectively. Conclusion Long-term mechanical ventilation over six years improved health-related quality of life in most patients. Patient training, follow-up and reduction of side effects, largely delivered by trained nurses, contribute to achieve the main goal of the treatment - improved health-related quality of life. This article is protected by copyright. All rights reserved.

Background and objective The prevalence of obesity hypoventilation syndrome (OHS) in the unselected obese is unknown. Our objectives were: (i) to determine the prevalence of OHS in ambulatory obese patients not previously referred to a pulmonologist for suspicion of sleep breathing disorders and (ii) to assess whether venous bicarbonate concentration [HCO3 − v] can be used to detect OHS. Methods In this prospective multicentric study, we measured [HCO3 − v] in consenting obese patients attending pathology analysis laboratories. Patients with [HCO3 − v] ≥ 27 mmol/L were referred to a pulmonologist for comprehensive sleep and respiratory evaluations. Those with [HCO3 − v]

Ekici, Aydanur/0000-0003-1522-6443 WOS:000559013600001 PubMed: 32745286 Introduction Obesity-hypoventilation syndrome occurs with alveolar hypoventilation during sleeping and daytime. Obesity may be a risk factor for venous thromboembolism. However, the venous thromboembolism in the obesity-hypoventilation syndrome is not well characterized. Objective This case series aimed to investigate the presence and clinical features of venous thromboembolism in patients with the obesity-hypoventilation syndrome. Methods Data of eight case reports were collected. Ages ranged from 36 to 73 years. Results All patients had mosaic perfusion and enlarged main pulmonary artery, two had signs of infarction and mostly segmental and subsegmental filling defects. On the basis of this information some conclusions can be drawn carefully. Conclusion Present cases indicate that pulmonary embolism are also very common in patients with obesity-hypoventilation syndrome, anticoagulant therapy is at least as important as the treatment of the current disease. Clinicians will frequently be faced with patients with obesity-hypoventilation syndrome suspected of PE.

The role of gender and menopause in obstructive sleep apnoea is well known; however, no study has reported the impact of gender on the clinical presentation and the nocturnal respiratory events in patients with obesity hypoventilation syndrome. Therefore, this study prospectively evaluated differences in the clinical characteristics of women and men with obesity hypoventilation syndrome in a large cohort of patients with obstructive sleep apnoea. During the study period, a total of 1973 patients were referred to the sleep clinic with clinical suspicion of obstructive sleep apnoea. All patients underwent overnight polysomnography, during which time spirometry, arterial blood samples and thyroid tests were routinely obtained. Among 1973 consecutive patients, 1693 (617 women) were diagnosed with obstructive sleep apnoea, among whom 144 suffered from obesity hypoventilation syndrome (96 women). The prevalence of obesity hypoventilation syndrome among women and men was 15.6% and 4.5%, respectively (P

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess the effects of non‐invasive positive airway pressure therapy, compared to usual care, on clinical outcomes among adults with obesity hypoventilation syndrome.

BACKGROUND Obesity-hypoventilation syndrome (OHS) is defined as daytime hypercapnia and hypoxemia in obese patients with sleep-disordered breathing. We evaluated the electrocardiographic P-wave duration and dispersion (PD) and echocardiographic noninvasive indicators of atrial conduction heterogeneity in OHS patients and the impact of CPAP on atrial conduction and atrial fibrillation incidence. METHODS AND RESULTS We enrolled 50 OHS patients and 50 sex- and age-matched obese subjects as control. Study population underwent cardiologic evaluation and polysomnography before enrollment, at 1- and 6-month follow-ups after CPAP therapy. The OHS group showed a significant increase in inter-atrial (35.2 ± 8 milliseconds vs. 20.1 ± 2.7 milliseconds, P < 0.0001), intra-left (30.5 ± 7.2 milliseconds vs. 16.5 ± 2 milliseconds, P < 0.0001), and intra-right atrial electromechanical delays (AEMD)(24.8 ± 10 milliseconds vs. 15 ± 2.6 milliseconds, P < 0.0001) as well as in Pmax (130 ± 7.4 milliseconds vs. 97 ± 7.2 milliseconds, P = 0.002) and PD (56.5 ± 8.5 milliseconds vs. 31 ± 7.2 milliseconds, P = 0.002) compared to the control group. Significant improvement was noted after 6 months of CPAP therapy in inter-atrial (35.2 ± 8 milliseconds vs. 24.5 ± 6.3 milliseconds, P < 0.0001), intra-left (30.5 ± 7.2 milliseconds vs. 20.6 ± 5 milliseconds, P = 0.003), and intra-right AEMD (24.8 ± 10 milliseconds vs. 17 ± 7.5 milliseconds, P < 0.0001), as well as in Pmax (130 ± 7.4 milliseconds vs. 95 ± 10 milliseconds, P < 0.0001) and in PD (56.5 ± 8.5 milliseconds vs. 32.5 ± 6 milliseconds, P < 0.0001) in the OHS group. External loop recorder monitoring detected paroxysmal AF in 19 OHS patients (38%) with significant reduction in paroxysmal AF episodes (12 ± 6 vs. 47 ± 12, P < 0.0001) after 6-month CPAP therapy. CONCLUSION Our findings showed a significant increase of electrocardiographic and echocardiographic indexes of atrial conduction heterogeneity in OHS patients. The CPAP therapy, having a positive impact on atrial conduction time, seems to reduce AF incidence in OHS patients.

Background Obesity is a risk factor for both sleep-related breathing disorders (SRBD), including obesity hypoventilation syndrome (OHS) and cardiovascular diseases (CVD). The development of CVD in patients with SRBD is usually attributed to the fact that most patients are obese in addition to conventional cardiovascular risk factors. Aims This study aims to measure the prevalence of certain CVD in patients with OHS in the Auckland region and highlight the importance of the effects of SRBD on the heart. Methods A dataset of all patients with a formal diagnosis of OHS that were under active follow up was compiled from Auckland District Health Board Sleep Disordered Breathing Service. Clinical notes were retrospectively reviewed for echocardiogram reports, blood pressure measurements and electrocardiograms. Results Forty-seven patients were included in the present study. The median age was 60 years, 24 were female (51%), 20 (42.5%) had diabetes, mean HbA1C was 53.5 mmol/mol, mean systolic blood pressure was 127 mmHg, mean body mass index was 49 kg/m2, mean forced expiratory volume in 1 s was 1.7 L, mean estimated glomerular filtration was 71 mL/min/1.73 m2 and there was anti-hypertensive use in 31 (65.9%) patients. Thirty-three patients had poor quality echocardiography views (70.2%). Left ventricular systolic and diastolic function was impaired in 8 (25%) and 18 (60%) respectively. Right ventricular dysfunction and pulmonary hypertension was present in 19 (63.3%) and 13 (52%) respectively. Sixteen patients (34%) had recurrent atrial or ventricular arrhythmias. Conclusion There appears to be a high prevalence of right ventricular impairment, pulmonary hypertension, left ventricle hypertrophy, diastolic dysfunction and arrhythmias in patients with OHS. These findings would appear to be higher than expected in obese patients without OHS. A larger prospective matched cohort study would be needed to confirm the clinical significance of these findings.

Background and objective Obesity hypoventilation syndrome (OHS) prevalence was previously estimated at 9% in patients with obstructive sleep apnoea (OSA) in Japan. However, the definition of OSA in that study was based on an apnoea-hypopnoea index (AHI) of ≥ 20/h rather than ≥ 5/h. Therefore, the prevalence of OHS in OSA was not measured in the same way as for Western countries. Our study objectives were to investigate the characteristics of Japanese patients with OHS. Methods Nine hundred eighty-one consecutive patients investigated for suspected OSA were enrolled. At least 90% of them were from urban areas, including 162 with obese OSA (body mass index (BMI) ≥ 30 kg/m2 and AHI ≥ 5/h). Results The prevalence of OHS (BMI 36.7 ± 4.9 kg/m2) in OSA and that in obese OSA were 2.3% and 12.3%, respectively. Multiple regression analysis revealed that independent of age and BMI, arterial oxygen pressure (contribution rate (R2) = 7.7%), 4% oxygen desaturation index (R2 = 8.9%), carbon monoxide diffusing capacity/alveolar volume (R2 = 8.3%), haemoglobin concentration (R2 = 4.9%) and waist circumference (R2 = 4.9%) were independently associated with arterial carbon dioxide pressure. After 12.3 ± 4.6 months of CPAP treatment, more than 60% of OHS patients no longer had hypercapnia. Conclusions The prevalence of OHS in OSA in Japan was 2.3%. The mean BMI of patients with OHS in Japan was lower than that in Western countries (36.7 kg/m2 vs 44.0 kg/m2).

Background and objective Reduced atmospheric pressure during air travel can cause significant hypoxaemia in some patients with respiratory disease. Our aims were to investigate the degree of hypoxaemia in patients with obesity hypoventilation syndrome (OHS) during hypoxic challenge test (HCT), and to identify any predictors of a positive HCT. Methods Thirteen patients underwent assessment, including HCT, lung function and incremental shuttle walk test. All had OHS well controlled with long-term nocturnal non-invasive ventilation (NIV). Patients with chronic obstructive pulmonary disease were excluded. A positive HCT was defined according to the British Thoracic Society (BTS) recommendation as arterial oxygen tension (PaO2)

Dyspnoea in obese patients can be multifactorial and complex. Mediastinal and pleural lipomatosis can be associated with obesity and is usually considered asymptomatic and benign. We report an obese 39‐year‐old man who presented with progressive dyspnoea, where in addition to obstructive sleep apnoea and obesity hypoventilation syndrome, was found to have massive mediastinal and pleural lipomatosis causing restrictive lung disease. Pleural lipomatosis are generally slow growing so conservative management is recommended. However, complications such as haemorrhage and compression of adjoining organs can occur in pleural lipomas, so surgical excision can be considered in some instances.

Introduction Obesity hypoventilation syndrome (OHS) can be overlooked unless clinicians have a high index of suspicion. The present case-control study aimed to compare characteristics of patients with OHS and obese obstructive sleep apnea syndrome (OSAS), and to identify determinants of hypercapnia in OSAS patients. Methods Demographic and anthropometric features, pulmonary function tests, blood gas analysis and sleep parameters of 59 OHS patients were compared to 295 body mass index-matched OSAS patients. Results The rate of hypertension (67.8% vs 53.2%, respectively, P = 0.027) was higher in OHS than OSAS group. In OHS patients, FVC (%) (P

Background and objective: Although it has been reported that pulmonary hypertension is more frequent in patients with obesity-hypoventilation syndrome than in patients with ‘pure’ obstructive sleep apnoea syndrome, little is known about the haemodynamic repercussions of this entity. The aim was to describe the haemodynamic status, as assessed by echocardiography and 6-min walk test (6MWT), of patients with a newly diagnosed, most severe form of obesity-hypoventilation syndrome, and to evaluate the impact of non-invasive ventilation in these patients. Methods: A prospective, descriptive, and single-centre follow-up study was conducted. At baseline, patients underwent echocardiography, spirometry, static lung volume measurement, 6MWT, overnight pulse-oximetry and polygraphic recording. Changes in echocardiography and 6MWT were assessed after 6 months of non-invasive ventilation. Right ventricular overload was defined on the basis of right ventricular dilatation, hypokinesis, paradoxical septal motion and/or pulmonary hypertension. Results: Thirty patients (20 women; mean age 69 ± 11) were tested. The percentage of patients with right ventricular overload did not change significantly after non-invasive ventilation (43.3–41.6%; P = 0.24). In patients with right ventricular overload at diagnosis, pulmonary artery systolic pressure decreased significantly at six months (58 ± 11 to 44 ± 12 mm Hg; P = 0.014), and mean distance on 6MWT increased from 350 ± 110 to 426 ± 78 m (P = 0.006), without significant changes in body mass index. Conclusions: Right ventricular overload is a frequent finding in patients with the most severe form of obesity-hypoventilation syndrome. Treatment with non-invasive ventilation is associated with a decrease in pulmonary artery systolic pressure at six months and an increase in the distance covered during the 6MWT.

We have coined the term 'malignant obesity hypoventilation syndrome' (MOHS) to describe a severe multisystem disease due to the systemic effects of obesity. Patients with this syndrome have severe obesity-related hypoventilation together with systemic hypertension, diabetes and the metabolic syndrome, left ventricular hypertrophy with diastolic dysfunction, pulmonary hypertension and hepatic dysfunction. This syndrome is largely unrecognized as physicians do not make the association between the patients' multiple medical problems and obesity. Because of the delayed diagnosis and progressive morbidities of this condition, all patients with a body mass index of more than 40 kg m(-2) should be screened for MOHS. The management of patients with MOHS includes short-term measures to improve the patients' medical condition and long-term measures to achieve enduring weight loss. Bariatric surgery reverses or improves the multiple metabolic and organ dysfunctions associated with MOHS and should be strongly considered in these patients.

Obesity hypoventilation syndrome (OHS) is defined as a combination of obesity (body mass index ≥ 30 kg/m(2)), daytime hypercapnia (partial arterial carbon dioxide concentration ≥45 mm Hg) and sleep-disordered breathing after ruling out other disorders that may cause alveolar hypoventilation. Through the prism of the International Classification of Functioning, OHS is a chronic condition associated with respiratory, metabolic, hormonal and cardiovascular impairments, leading to a decrease in daily life activities, a lack of social participation and high risk of hospitalization and death. Despite its severity, OHS is largely underdiagnosed and the health-related costs are higher than those of apnoeic or obese eucapnic patients. The present review discusses the definition, epidemiology, physiopathology and treatment modalities of OHS. Although nocturnal positive airway pressure therapies represent first-line treatment and are effective in improving patient outcomes, there is a need to offer combined treatment strategies and to assess the effect of multimodal therapeutic strategies on morbidity and mortality.

Obesity, particularly severe central obesity, affects respiratory physiology both at rest and during exercise. Reductions in expiratory reserve volume, functional residual capacity, respiratory system compliance and impaired respiratory system mechanics produce a restrictive ventilatory defect. Low functional residual capacity and reductions in expiratory reserve volume increase the risk of expiratory flow limitation and airway closure during quiet breathing. Consequently, obesity may cause expiratory flow limitation and the development of intrinsic positive end expiratory pressure, especially in the supine position. This increases the work of breathing by imposing a threshold load on the respiratory muscles leading to dyspnoea. Marked reductions in expiratory reserve volume may lead to ventilation distribution abnormalities, with closure of airways in the dependent zones of the lungs, inducing ventilation perfusion mismatch and gas exchange abnormalities. Obesity may also impair upper airway mechanical function and neuromuscular strength, and increase oxygen consumption, which in turn, increase the work of breathing and impair ventilatory drive. The combination of ventilatory impairment, excess CO2 production and reduced ventilatory drive predisposes obese individuals to obesity hypoventilation syndrome.

The childhood obesity epidemic involves unusual and underrecognized complications associated with this clinical and public health problem. Obesity hypoventilation syndrome (OHS) is defined as the triad of obesity, daytime hypoventilation, and sleep-disordered breathing in the absence of an alternative neuromuscular, mechanical or metabolic explanation for hypoventilation. We herewith report a 12-year-old boy who was diagnosed with OHS. The patient improved with phlebotomy and bi-level positive airway pressure. To the best of our knowledge, this is the first reported case of secondary polycythemia due to OHS requiring therapeutic phlebotomy.

Background and objective The use of continuous positive airway pressure (CPAP) treatment in patients with obesity hypoventilation syndrome (OHS) and obstructive sleep apnoea (OSA) was evaluated, and factors that might predict CPAP treatment failure were determined. Methods A sleep study was performed in 29 newly diagnosed, clinically stable OHS patients. CPAP treatment was commenced if the apnoea–hypopnoea index was >15. Lung function, night-time oximetry, blood adipokine and C-reactive protein levels were assessed prospectively on enrollment and after 3 months. Treatment failure at 3 months was defined as daytime arterial partial pressure of carbon dioxide (PaCO2) >45 mm Hg and/or oxygen saturation (SpO2) 30% of the night-time oximetry study. Results All patients had severe OSA (median apnoea–hypopnoea index = 74.7 (62–100) with a nocturnal mean SpO2 of 81.4 ± 7), and all patients were treated with CPAP. The percentage of time spent below 90% saturation improved from 8.4% (0.0–39.0%) to 0.3% (0.4–4.0%). Awake PaCO2 decreased from 50 (47–53) mm Hg to 43 (40–45) mm Hg. Seven patients failed CPAP treatment after 3 months. PaCO2 at 1 month and mean night-time SpO2 during the first night of optimal CPAP were associated with treatment failure at 3 months (odds ratio 1.4 (1.03–1.98); P = 0.034 and 0.6 (0.34–0.93); P = 0.027). Conclusions CPAP treatment improves night-time oxygenation and daytime hypoventilation in selected clinically stable OHS patients who also have OSA. Patients with worse night-time saturation while on CPAP and higher daytime PaCO2 at 1 month were more likely to fail CPAP treatment.

Background and objectiveThe use of continuous positive airway pressure (CPAP) treatment in patients with obesity hypoventilation syndrome (OHS) and obstructive sleep apnoea (OSA) was evaluated, and factors that might predict CPAP treatment failure were determined. MethodsA sleep study was performed in 29 newly diagnosed, clinically stable OHS patients. CPAP treatment was commenced if the apnoea-hypopnoea index was >15. Lung function, night-time oximetry, blood adipokine and C-reactive protein levels were assessed prospectively on enrollment and after 3 months. Treatment failure at 3 months was defined as daytime arterial partial pressure of carbon dioxide (PaCO2) >45mmHg and/or oxygen saturation (SpO(2)) 30% of the night-time oximetry study. ResultsAll patients had severe OSA (median apnoea-hypopnoea index=74.7 (62-100) with a nocturnal mean SpO(2) of 81.47), and all patients were treated with CPAP. The percentage of time spent below 90% saturation improved from 8.4% (0.0-39.0%) to 0.3% (0.4-4.0%). Awake PaCO2 decreased from 50 (47-53) mmHg to 43 (40-45) mmHg. Seven patients failed CPAP treatment after 3 months. PaCO2 at 1 month and mean night-time SpO(2) during the first night of optimal CPAP were associated with treatment failure at 3 months (odds ratio 1.4 (1.03-1.98); P=0.034 and 0.6 (0.34-0.93); P=0.027). ConclusionsCPAP treatment improves night-time oxygenation and daytime hypoventilation in selected clinically stable OHS patients who also have OSA. Patients with worse night-time saturation while on CPAP and higher daytime PaCO2 at 1 month were more likely to fail CPAP treatment.

Objective: Obese patients demonstrate a variety of biochemical, metabolic, and pulmonary abnormalities. Inflammatory mediators such as tumor necrosis factor-α and interleukin-6 (IL-6) may have a direct effect on glucose and lipid metabolism. Hypoxemia in itself induces release of IL-6. The aim of this study was to examine the relationship between IL-6 levels in healthy volunteers (control group) and three different groups of obese patients: patients without obstructive sleep apnea syndrome (OSAS), patients with OSAS, and patients with obesity hypoventilation syndrome (OHS) (daytime baseline oxygen saturation of 35 kg/m2) and 12 healthy women. Results: The results demonstrate statistically significant differences in serum IL-6 levels between the control group (1.28 ± 0.85 pg/mL) and obese patients without OSAS (7.69 ± 5.06 pg/mL, p < 0.05) and with OSAS (5.58 ± 0.37 pg/mL, p < 0.0005). In the patients with OHS, IL-6 concentrations were highest (43.13 ± 24.27 pg/mL). Discussion: We conclude that serum IL-6 is increased in obese patients. The highest IL-6 levels were found in the patients with OHS.

Fourteen children with the Prader-Willi syndrome have been managed at the Royal Alexandra Hospital for Children between the years 1964-1980--twelve male, two female. Six male children developed features of the obesity hypoventilation syndrome. The age of onset of this complication ranged from 4.0 to 12.6 years. With one exception those children with the obesity hypoventilation syndrome were more obese than those without it. At the time of onset of the syndrome, five of six patients had weights greater than or equal to 6.5 standard deviations above ideal body weight. Those children without the obesity hypoventilation syndrome had a range of standard deviations 1.0 to 4.2 above the ideal body weight. In four of six cases weight reduction and a cardiac failure regimen resulted in reversal of the obesity hypoventilation syndrome. With two of the six children there had been cardiomegaly and increased pulmonary venous vascularity on x-ray at a chronological age of three months. Two of the six children died.

Recently the association of hypersomnia and respiratory insufficiency without lesion in the respiratory organ has attracted attention of many investigators. Obese patients with such a condition have been called the Pickwickian syndrome. In this report, two non-obese patients with a similar condition were presented, one with micrognathia and frequent apneic episodes during sleep, and the other with laryngeal stenosis due to paralysis of the bilateral laryngeal nerves and chronic laryngitis. Tracheostomy had a prompt and long-lasting therapeutic effect to make their sleep stable and also to relieve their excessive daytime sleepiness. These findings suggest that the obstruction or stenosis of the upper airway during sleep disturbed their nocturnal sleep, and that their excessive daytime sleepiness was a phenomenon compensating for their disturbed nocturnal sleep.

Pronounced tonsilar hypertrophy was found in two obese patients suffering from hypersomnolence, periodic attacks of apnea and disturbing snoring at night. Both patients underwent tonsillectomy. Immediately after the operation the hypersomnolence disappeared, the breathing became normal, and the disturbing snoring at night ceased. Follow-up over a period of three years did not reveal any recurrence of these symptoms, even though the patients had not lost any weight during this period.