Parekh B
Institute of Metabolic Science, University of Cambridge, Cambridge CB2 0QQ, UK.
Curr Diabetes Rev. 2009 Nov;5(4):210-5. doi: 10.2174/157339909789804387.
The mechanism of dead-in-bed syndrome (DBS), a rare but devastating condition that mainly affects young type 1 diabetes patients, remains mysterious. A new theory is proposed to explain this syndrome. This theory suggests that repeated episodes of hypoglycaemia-induced adaptation in orexin-A neurons cause (i) defective awakening and (ii) hypotonia of upper airway muscles during sleep. Consequently, due to the combined effect of these factors, long-term exposure of intermittent hypoxia occurs, leading to a combination of factors - such as depression of ventilation, increase in sympathetic tone, fluctuations in intrathoracic pressure and cardiac arrhythmias - these in conjunction with an underlying cardiovascular pathology (genetically inherited or acquired) cause cardio-respiratory failure and thus sudden death during sleep. This mechanism can be generalized to explain other cases of sudden unexplained nocturnal deaths including sudden infant deaths (SIDs).
睡死综合征(DBS)是一种罕见但极具破坏性的疾病,主要影响年轻的1型糖尿病患者,其发病机制仍然成谜。本文提出了一种新理论来解释这一综合征。该理论认为,低血糖反复诱发食欲素-A神经元适应性改变,会导致(i)觉醒功能缺陷,以及(ii)睡眠期间上呼吸道肌肉张力减退。因此,由于这些因素的综合作用,会出现间歇性缺氧的长期暴露,进而导致多种因素共同作用——如通气抑制、交感神经张力增加、胸内压波动和心律失常——这些因素与潜在的心血管病变(遗传或后天获得)共同作用,导致心肺功能衰竭,从而在睡眠中突然死亡。这一机制可推广用于解释其他不明原因的夜间猝死病例,包括婴儿猝死综合征(SIDS)。