Obstructive sleep apnoea syndrome in patients living with diabetes: Which patients should be screened?

AIM: Because type 2 diabetes (T2D) is related to obesity, it is often associated with obstructive sleep apnoea syndrome (OSAS), although OSAS is also frequently diagnosed in patients with type 1 diabetes (T1D) and may promote gestational diabetes. Thus, this systematic review of the scientific evidence aimed to evaluate the epidemiological association between OSAS and all forms of diabetes, the current understanding of the pathophysiological mechanisms behind these associations, the expected benefits and limitations of OSAS treatment in patients with diabetes and, finally, to propose which patients require screening for OSAS. METHODS: A panel comprising French expert endocrinologists and pneumologists was convened. Two of these experts made a search of the relevant literature for each subpart of the present report; all panel experts then critically reviewed the entire report separately as well as collectively. RESULTS: There is little evidence to support the notion that OSAS treatment improves glycated haemoglobin, although it may improve nighttime blood glucose control and insulin sensitivity. However, there is robust evidence that OSAS treatment lowers 24-h blood pressure. CONCLUSION: The high prevalence of OSAS in patients with T1D and T2D justifies screening for the syndrome, which should be based on clinical symptoms, as the benefits of OSAS treatment are mainly improvement of symptoms related to sleep apnoea. There are also several clinical situations wherein screening for OSAS seems justified in patients with diabetes even when they have no symptoms, particularly to optimalize control of blood pressure in cases of resistant hypertension and microvascular complications.

[Update on the respiratory management of patients with chronic neuromuscular disease]. / Mise au point dans la prise en charge respiratoire des maladies neuromusculaires chroniques.

BACKGROUND: Neuromuscular diseases include a wide range of conditions that may involve potentially life-threatening respiratory complications (infection, respiratory failure). SURVEILLANCE AND PULMONARY FUNCTION TESTS: For patients with neuromuscular diseases, clinical assessment of respiratory function and regular pulmonary function tests are needed to screen for nocturnal respiratory disorders, weakness of the diaphragm and potential restrictive disorders and/or chronic hypercapnic respiratory insufficiency, possibly with couch deficiency. MANAGEMENT OF NOCTURNAL RESPIRATORY DISORDERS AND CHRONIC RESPIRATORY FAILURE: Nocturnal respiratory assistance is an important phase of care for nocturnal respiratory disorders and chronic respiratory failure. This may involve continuous positive airway pressure, adaptative servo-ventilation or non-invasive ventilation with a facial or nasal mask. As needed, diurnal assistance may be proposed by mouthpiece ventilation. Should non-invasive ventilation prove insufficient, or if significant swallowing disorders or recurrent bronchial obstruction develop, or in case of prolonged intubation, tracheotomy may be required. LOWER AIRWAY OBSTRUCTION: In case of lower airway infection with ineffective cough, physical therapy, associated with air stacking, intermittent positive pressure breathing or mechanical in-exsufflation may be proposed. PATIENT-CENTERED MANAGEMENT: Care for swallowing disorders, nutritional counseling (cachexia, obesity), vaccinations and therapeutic education are integral elements of patient-centered management aiming to prevent the negative impact of infection and to manage respiratory failure of chronic neuromuscular disease.

[Sleep apneas, metabolic syndrome and cardiovascular risk: Data from the Pays de la Loire sleep cohort]. / Apnées du sommeil, syndrome métabolique et risque cardiovasculaire : données de la cohorte sommeil des Pays de la Loire.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a prevalent disease characterized by recurrent episodes of partial or complete obstruction of upper airway during sleep. Untreated moderate to severe OSAHS is recognized as a cardiovascular (CV) risk factor. Data from the Pays de la Loire sleep cohort and other clinic- or population-based cohorts demonstrate a strong association between OSAHS and the different components of the metabolic syndrome including systemic hypertension, diabetes and impaired lipid metabolism. Beside sleep-disordered breathing severity, these factors contribute to increase the risk of CV events in OSAHS patients. Continuous positive airway pressure (CPAP) therapy of OSAHS is associated with a modest but clinically significant blood pressure reduction. Conversely, there is no clear evidence in support of a metabolic impact of CPAP in OSAHS patients. Considering the multifactorial pathophysiology of CV risk in OSAHS patients and the beneficial impact of various lifestyle and pharmacologic interventions on blood pressure and metabolic dysfunction, combined modality therapy is a promising strategy to improve CV outcomes in individuals with OSAHS.

[Vascular dysfunction in obstructive sleep apnoea: Implication of microparticules]. / Atteinte vasculaire associée au syndrome d'apnées hypopnées obstructives du sommeil : rôle des microparticules.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular diseases, including myocardial infarction and stroke and promotes cardiovascular risk factors including diabetes and hypertension. OSA has also been proposed to have a direct proatherogenic effects. Recent studies have investigated the role of microparticles (MPs) in the atherogenic process. MPs are small plasma membrane vesicles that can be released by a variety of vascular or blood cells and that contain membrane and cytosolic elements. Case-control studies have suggested that OSA is associated with an increase in circulating platelet-, endothelial- and leukocyte-derived MPs. MPs from OSA patients injected to mice have also been shown to induce vascular inflammation and endothelial dysfunction. In this article, we provide an overview of the main characteristics of MPs expressed in OSA and their potential role in the atherogenic process.

Adaptive servo-ventilation: How does it fit into the treatment of central sleep apnoea syndrome? Expert opinions.

The preliminary results of the SERVE-HF study have led to the release of safety information with subsequent contraindication to the use of adaptive servo-ventilation (ASV) for the treatment of central sleep apnoeas in patients with chronic symptomatic systolic heart failure with left ventricular ejection fraction (LVEF) ≤ 45%. The aim of this article is to review these results, and to provide more detailed arguments based on data from the literature advocating the continued use of ASV in different indications, including heart failure with preserved LVEF, complex sleep apnoea syndrome, opioid-induced central sleep apnea syndrome, idiopathic central SAS, and central SAS due to a stroke. Based on these findings, we propose to set up registers dedicated to patients in whom ASV has been stopped and in the context of the next setting up of ASV in these specific indications to ensure patient safety and allow reasoned decisions on the use of ASV.

[Drug-induced pneumonitis in a patient treated with venlafaxine and propanolol]. / Pneumopathie médicamenteuse sous traitement par venlafaxine et propranolol.

INTRODUCTION: Venlafaxine and propranolol have rarely been identified as causes of pulmonary pathology. We describe a case of drug-induced pneumonitis occurring in a patient treated with these two medications. CASE REPORT: A 55 years old woman with liver cirrhosis treated with venlafaxine for 1 year and propranolol for 1 month was admitted to the intensive care unit because of acute respiratory failure. A Mycoplasma pneumoniae pneumonitis was diagnosed. After initial improvement under antibiotics, a new deterioration of respiratory status was observed 4 days after the reintroduction of venlafaxine and propranolol. Spontaneous recovery occurred after these treatments were withheld. Co administration of venlafaxine and propranolol, 2 drugs with affinity for the same cytochrome P450 isoenzyme (CYP2D6), may have contributed to drug accumulation and pulmonary toxicity. The liver cirrhosis of our patient may also have contributed to decreased cytochrome P450 enzymatic activity. CONCLUSIONS: Venlafaxine and propranolol share the same metabolic pathway and their co-administration may be complicated by drug induced pneumonitis.