Antonelli Incalzi Raffaele, Fuso Leonello, Pitocco Dario, Basso Salvatore, Trové Andrea, Longobardi Anna, Calcagni Maria Lucia, Giordano Alessandro, Ghirlanda Giovanni
Department of Geriatrics Campus Biomedico University, Rome, Italy.
Diabetes Metab Res Rev. 2007 May;23(4):311-6. doi: 10.1002/dmrr.688.
Type 1 diabetes mellitus complicated by autonomic neuropathy (AN) is characterized by depressed cholinergic bronchomotor tone and neuroadrenergic denervation of the lung. We explored the effects of AN on the rate of decline of pulmonary sympathetic innervation and respiratory function during a 5-year follow-up.
Twenty diabetic patients, 11 with AN, were enrolled in 1998 and then followed-up until 2003. During follow-up, glycosylated haemoglobin (HbA1c) was measured every 3 months. In 1998 and 2003 the patients underwent respiratory function tests and a ventilatory scintigraphic study of neuroadrenergic bronchial innervation using 123I-MIBG.
During follow-up 4 patients, all with AN, were lost, and 1 developed AN. Forced vital capacity (FVC), and diffusing capacity of the lung for carbon monoxide (DLCO) showed comparable rates of decrease in patients with and without AN. The yearly decline of forced expiratory volume in 1 s (FEV1) was about double the physiologic rate, in both AN and AN-free patients. The MIBG clearance significantly increased both in patients with AN (T1/2: 118.88 +/- 30.14 min at baseline and 92.10 +/- 24.52 min at the end of follow-up) and without AN (135.14 +/- 17.09 min and 92.68 +/- 13.52 min, respectively), indicating a rapidly progressive neuroadrenergic denervation. The rate of the neuroadrenergic denervation was inversely related to the severity of autonomic dysfunction at baseline (Spearman's rho - 0.62, p = 0.017). Neither respiratory function indexes nor MIBG clearance changes correlated with the overall HbA1c values.
Neuroadrenergic denervation of the lung parallels the decline of respiratory function indexes in diabetic patients both with and without AN and seems to be independent from the quality of glycemic control.
1型糖尿病合并自主神经病变(AN)的特征为胆碱能支气管运动张力降低以及肺部神经肾上腺素能去神经支配。我们在5年的随访期间探讨了AN对肺交感神经支配率下降和呼吸功能的影响。
1998年纳入20例糖尿病患者,其中11例患有AN,随后随访至2003年。随访期间,每3个月测量糖化血红蛋白(HbA1c)。1998年和2003年,患者接受呼吸功能测试以及使用123I-MIBG进行的神经肾上腺素能支气管支配的通气闪烁显像研究。
随访期间,4例患者失访,均为患有AN的患者,1例患者出现AN。有AN和无AN的患者的用力肺活量(FVC)和肺一氧化碳弥散量(DLCO)下降率相当。1秒用力呼气量(FEV1)的年下降率在患有AN和未患AN的患者中均约为生理下降率的两倍。MIBG清除率在患有AN的患者(T1/2:基线时为118.88±30.14分钟,随访结束时为92.10±24.52分钟)和未患AN的患者(分别为135.14±17.09分钟和92.68±13.52分钟)中均显著增加,表明神经肾上腺素能去神经支配进展迅速。神经肾上腺素能去神经支配率与基线时自主神经功能障碍的严重程度呈负相关(Spearman秩相关系数为-0.62,p = 0.017)。呼吸功能指标和MIBG清除率变化均与总体HbA1c值无关。
无论糖尿病患者是否患有AN,肺部神经肾上腺素能去神经支配均与呼吸功能指标的下降平行,且似乎与血糖控制质量无关。