el Newihi H, Dooley C P, Saad C, Staples J, Zeidler A, Valenzuela J E
Department of Medicine, USC School of Medicine, Los Angeles 90033.
Dig Dis Sci. 1988 Jun;33(6):705-10. doi: 10.1007/BF01540434.
Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.
在一些患有周围神经病变和腹泻的糖尿病患者中观察到外分泌性胰腺功能不全。这种功能不全可能由多种机制引起:(1)胰腺萎缩,(2)胆碱能肠胰反射中断,或(3)血清中胰高血糖素和胰多肽等肽类水平升高,已知这些肽类会抑制胰腺外分泌。为了阐明这种外分泌性胰腺损害所涉及的机制,我们研究了10名患有腹泻和周围神经病变的糖尿病患者。将他们的结果与8名正常志愿者的结果进行比较。每位受试者都接受了标准化的胰腺功能研究,该研究评估了非刺激分泌、空肠内输注氨基酸混合物后的反应以及静脉注射促胰液素和胆囊收缩素(CCK)后的分泌量。在单独的研究中,评估了6名患者和6名正常对照中,背景输注氨甲酰甲胆碱和促胰液素对胰腺对CCK反应的影响。与正常人相比,所有糖尿病患者对所有刺激的酶分泌和碳酸氢盐分泌均显著减少。给予氨甲酰甲胆碱并不能纠正这种减少。糖尿病患者血浆中的胰高血糖素和胰多肽水平并不显著高于对照组。我们得出结论,患有腹泻和周围神经病变的糖尿病患者存在外分泌性胰腺分泌功能受损,并对其可能的机制进行了讨论。