Stone B G, Gavaler J S, Belle S H, Shreiner D P, Peleman R R, Sarva R P, Yingvorapant N, Van Thiel D H
Department of Medicine, Pittsburgh Veterans Administration Medical Center, Pennsylvania.
Gastroenterology. 1988 Jul;95(1):170-6. doi: 10.1016/0016-5085(88)90307-1.
Individuals with diabetes mellitus are reported to have a twofold to threefold increase in the incidence of cholesterol gallstones. A frequently cited but unproven pathophysiologic mechanism for this phenomenon is reduced gallbladder muscle function, which results in stasis and allows for cholesterol gallstone crystal formation and gallstone growth. To date, gallbladder motor function has not been investigated in a well-characterized diabetic population. Therefore, using radionuclide cholescintigraphy, gallbladder filling and subsequent emptying produced in response to an infusion of the octapeptide of cholecystokinin in 30 diabetic patients and 20 control individuals were studied. No difference in any parameter used to assess gallbladder filling was demonstrated in the diabetics when compared with controls. In contrast, gallbladder emptying induced with cholecystokinin-octapeptide (20 ng/kg body wt . h) was reduced in diabetics compared with controls (55% +/- 5% vs. 74% +/- 4%, p less than 0.01). The peak emptying rate in the diabetics was also decreased (5.0% +/- 0.5% per minute) compared with the controls (7.0% +/- 0.6% per minute, p less than 0.02). The observed decreased gallbladder emptying found in diabetics was not related to obesity, type of diabetes, diabetic control, or presence or absence of peripheral neuropathy. The most severe impairment of gallbladder emptying occurred, however, in diabetics with an associated autonomic neuropathy. This subgroup demonstrated a significant reduction in the percentage of gallbladder emptying (40% +/- 8% vs. 62% +/- 5%, p less than 0.04) and the peak ejection rate (3.5% +/- 0.5% per minute vs. 5.6% +/- 0.6%, p less than 0.02) compared with the diabetics without autonomic neuropathy.
据报道,糖尿病患者胆固醇胆结石的发病率增加了两倍到三倍。这种现象一个经常被引用但未经证实的病理生理机制是胆囊肌肉功能减退,这会导致胆汁淤积,并使胆固醇胆结石晶体形成和胆结石生长。迄今为止,尚未在特征明确的糖尿病患者群体中研究胆囊运动功能。因此,使用放射性核素胆闪烁显像技术,对30例糖尿病患者和20例对照个体在输注胆囊收缩素八肽后产生的胆囊充盈及随后的排空情况进行了研究。与对照组相比,糖尿病患者在用于评估胆囊充盈的任何参数上均未显示出差异。相反,与对照组相比,糖尿病患者中由胆囊收缩素八肽(20 ng/kg体重·小时)诱导的胆囊排空减少(55%±5%对74%±4%,p<0.01)。糖尿病患者的最大排空率也较对照组降低(每分钟5.0%±0.5%对每分钟7.0%±0.6%,p<0.02)。在糖尿病患者中观察到的胆囊排空减少与肥胖、糖尿病类型、糖尿病控制情况或有无周围神经病变无关。然而,胆囊排空受损最严重的是伴有自主神经病变的糖尿病患者。与无自主神经病变的糖尿病患者相比,该亚组的胆囊排空百分比(40%±8%对62%±5%,p<0.04)和最大射血率(每分钟3.5%±0.5%对每分钟5.6%±0.6%,p<0.02)显著降低。