Jokic R, Zintel T, Sridhar G, Gallagher C G, Fitzpatrick M F
Division of Respiratory Medicine, Royal University Hospital, Saskatoon, Saskatchewan, Canada S7N 0W8.
Thorax. 2000 Nov;55(11):940-5. doi: 10.1136/thorax.55.11.940.
It is unclear why some morbidly obese individuals have waking alveolar hypoventilation while others with similar obesity do not. Some evidence suggests that patients with the obesity hypoventilation syndrome (OHS) may have a measurable premorbid impairment of ventilatory chemoresponsiveness. Such an impairment of ventilatory chemoresponsiveness in OHS, however, may be an acquired and reversible consequence of severe obstructive sleep apnoea (OSA). We hypothesised that, in patients with OHS who do not have coincident severe OSA, there may be a familial impairment in ventilatory responses to hypoxia and hypercapnia.
Sixteen first degree relatives of seven patients with OHS without severe OSA (mean (SD) age 40 (16) years, body mass index (BMI) 30 (6) kg/m(2)) and 16 subjects matched for age and BMI without OHS or OSA were studied. Selection criteria included normal arterial blood gas tensions and lung function tests and absence of sleep apnoea on overnight polysomnography. Ventilatory responses to isocapnic hypoxia and to hyperoxic hypercapnia were compared between the two groups.
The slope of the ventilatory response to hypercapnia was similar in the relatives (mean 2.33 l/min/mm Hg) and in the control subjects (2.12 l/min/mm Hg), mean difference 0.2 l/min/mm Hg, 95% confidence interval (CI) for the difference -0.5 to 0.9 l/min/mm Hg, p=0.5. The hypoxic ventilatory response was also similar between the two groups (slope factor A: 379.1 l/min * mm Hg for relatives and 373.4 l/min * mm Hg for controls; mean difference 5.7 l/min * mm Hg; 95% CI -282 to 293 l/min * mm Hg, p=0.7; slope of the linear regression line of the fall in oxygen saturation and increase in minute ventilation: 2.01 l/min/% desaturation in relatives, 1.15 l/min/% desaturation in controls; mean difference 0. 5 l/min/% desaturation; 95% CI -1.7 to 0.7 l/min/% desaturation, p=0. 8).
There is no evidence of impaired ventilatory chemoresponsiveness in first degree relatives of patients with OHS compared with age and BMI matched control subjects.
目前尚不清楚为何一些病态肥胖个体存在清醒时肺泡通气不足，而其他肥胖程度相似的个体却没有。一些证据表明，肥胖低通气综合征（OHS）患者可能在病前就存在可测量的通气化学敏感性受损。然而，OHS患者的这种通气化学敏感性受损可能是严重阻塞性睡眠呼吸暂停（OSA）的后天性且可逆的后果。我们推测，在没有合并严重OSA的OHS患者中，可能存在对低氧和高碳酸血症通气反应的家族性受损。
对7例无严重OSA的OHS患者的16名一级亲属（平均（标准差）年龄40（16）岁，体重指数（BMI）30（6）kg/m²）和16名年龄及BMI匹配、无OHS或OSA的受试者进行了研究。入选标准包括动脉血气张力和肺功能测试正常，以及夜间多导睡眠图检查无睡眠呼吸暂停。比较了两组对等碳酸血症低氧和高氧性高碳酸血症的通气反应。
亲属组（平均2.33 l/min/mm Hg）和对照组（2.12 l/min/mm Hg）对高碳酸血症的通气反应斜率相似，平均差异0.2 l/min/mm Hg，差异的95%置信区间（CI）为-0.5至0.9 l/min/mm Hg，p = 0.5。两组之间的低氧通气反应也相似（斜率因子A：亲属组为379.1 l/min * mm Hg，对照组为373.4 l/min * mm Hg；平均差异5.7 l/min * mm Hg；95% CI为-282至293 l/min * mm Hg，p = 0.7；氧饱和度下降和分钟通气量增加的线性回归线斜率：亲属组为2.01 l/min/%去饱和，对照组为1.15 l/min/%去饱和；平均差异0.5 l/min/%去饱和；95% CI为-1.7至0.7 l/min/%去饱和，p = 0.8）。
与年龄及BMI匹配的对照组相比，没有证据表明OHS患者的一级亲属存在通气化学敏感性受损。
