Weitzenblum E, Kessler R, Canuet M, Chaouat A
Service de Pneumologie, Pôle de Pathologie thoracique, Hôpital de Hautepierre, CHU de Strasbourg, France.
Rev Mal Respir. 2008 Apr;25(4):391-403. doi: 10.1016/s0761-8425(08)71582-1.
The obesity-hypoventilation syndrome (OHS), or alveolar hypoventilation in the obese, has been described initially as the "Pickwickian syndrome". It is defined as chronic alveolar hypoventilation (PaO2<70 mmHg, PaCO2 > or =45 mmHg) in obese patients (body mass index>30 kg/m2) who have no other respiratory disease explaining the hypoxemia-hypercapnia.
The large majority of obese subjects are not hypercapnic, even in case of severe obesity (>40 kg/m2). There are three principal causes, which can be associated, explaining alveolar hypoventilation in obese subjects: high cost of respiration and weakness of the respiratory muscles (probably the major cause), dysfunction of the respiratory centers with diminished chemosensitivity, long-term effects of the repeated episodes of obstructive sleep apneas observed in some patients. The role of leptin (hormone produced by adipocytes) in the pathogenesis of this syndrome, has been recently advocated. OHS is generally observed in subjects over 50 years. Its prevalence has markedly increased in recent years, probably due to the present "epidemic" of obesity. The diagnosis is often made after an episode of severe respiratory failure. Comorbidities, favored by obesity, are very frequent: systemic hypertension, left heart diseases, diabetes.
OHS must be distinguished from obstructive sleep apnea syndrome (OSAS) even if the two conditions are often associated. OSAS may be absent in certain patients with OHS (20% of the patients in our experience). On the other hand obesity may be absent in certain patients with OSAS.
Losing weight is the "ideal" treatment of OHS but in fact it cannot be obtained in most patients. Nocturnal ventilation (continuous positive airway pressure and mainly bilevel non invasive ventilation) is presently the best treatment of OHS and excellent short and long-term results on symptoms and arterial blood gases have been recently reported.
肥胖低通气综合征(OHS),即肥胖者的肺泡低通气,最初被描述为“匹克威克综合征”。它被定义为肥胖患者(体重指数>30kg/m²)出现慢性肺泡低通气(动脉血氧分压<70mmHg,动脉血二氧化碳分压≥45mmHg),且无其他可解释低氧血症-高碳酸血症的呼吸系统疾病。
绝大多数肥胖者并非高碳酸血症患者,即使是重度肥胖(>40kg/m²)的情况也是如此。有三个主要原因可解释肥胖者的肺泡低通气,它们可能相互关联:呼吸成本高和呼吸肌无力(可能是主要原因)、呼吸中枢功能障碍伴化学敏感性降低、部分患者中观察到的阻塞性睡眠呼吸暂停反复发作的长期影响。最近有人主张瘦素(脂肪细胞产生的激素)在该综合征发病机制中的作用。OHS通常在50岁以上的人群中出现。近年来其患病率显著增加,可能归因于当前的肥胖“流行”。诊断通常在严重呼吸衰竭发作后做出。肥胖易引发的合并症非常常见:系统性高血压、左心疾病、糖尿病。
OHS必须与阻塞性睡眠呼吸暂停综合征(OSAS)相区分,即使这两种情况常同时存在。某些OHS患者可能不存在OSAS(根据我们的经验,此类患者占20%)。另一方面,某些OSAS患者可能不存在肥胖。
减肥是OHS的“理想”治疗方法,但实际上大多数患者无法实现。夜间通气(持续气道正压通气,主要是双水平无创通气)目前是OHS的最佳治疗方法,最近有报道称其在症状和动脉血气方面取得了出色的短期和长期效果。