Noda A, Hayakawa T, Aoki I, Horiguchi Y, Toda Y
Am J Dig Dis. 1975 Nov;20(11):1019-26. doi: 10.1007/BF01071189.
Abnormal pancreatic excretion of 5,5-dimethyl-2,4-oxazolidinedione (DMO) was demonstrated in 44 patients with chronic pancreatitis (14 with calcification and 30 without calcification). Pancreatic excretion of DMO in patients with chronic pancreatitis, as well as in normal subjects, depended on plasma DMO concentration and secretory volume. In the postsecretin 60-min period, almost all patients showed a decrease in total DMO output of duodenal aspirate over the observed range of plasma DMO concentration. More than half the patients without calcification gave a discordant pattern between the DMO output and volume, ie, decreased DMO output with normal volume secretion, while most of patients with calcification had low DMO output with decreased volume flow. The data of the pancreozymin-secretin test suggested that chornic pancreatic inflammation was moderate or minimal in patients without calcification and far advanced in those with calcification. From these results the hypothesis was advanced that DMO diffusion into the pancreatic ducts might be primarily impaired in the relatively early stage of chronic pancreatitis, and as the inflammation progressed to the final stage, DMO outflow from the ducts to the duodenum would be disturbed with evolving diffusion impairment of the compound. Total DMO output, when expressed as the output at a level of 10 mg/100 ml of plasma DMO (standard DMO output), was significantly reduced in chronic pancreatitis during a 60-min period after secretin stimulation. DMO in duodenal content, when expressed in terms of maximal concentration ratio of duodenal juice/plasma for the compound (maximal J/P ratio), was significantly low in chronic pancreatitis during the last 40-min period after secretin stimulation. These two parameters can therefore be used as indices of pancreatic excretion of DMO. The present technique may well become an effective diagnostic tool for early detection of chronic pancreatitis.
在44例慢性胰腺炎患者（14例有钙化，30例无钙化）中，证实了5,5 - 二甲基 - 2,4 - 恶唑烷二酮（DMO）的胰腺排泄异常。慢性胰腺炎患者以及正常受试者的胰腺DMO排泄取决于血浆DMO浓度和分泌量。在注射促胰液素后的60分钟内，几乎所有患者在观察到的血浆DMO浓度范围内，十二指肠抽吸物中总DMO输出量均下降。超过一半无钙化的患者在DMO输出量和分泌量之间呈现不一致的模式，即分泌量正常但DMO输出量减少，而大多数有钙化的患者DMO输出量低且分泌量减少。促胰液素 - 胰酶泌素试验的数据表明，无钙化患者的慢性胰腺炎症为中度或轻度，而有钙化患者的炎症则已发展到晚期。基于这些结果，提出了一个假设：在慢性胰腺炎相对早期阶段，DMO向胰管内的扩散可能首先受到损害，随着炎症发展到终末期，该化合物扩散障碍不断演变，DMO从胰管向十二指肠的流出会受到干扰。当以血浆DMO浓度为10mg/100ml水平时的输出量（标准DMO输出量）来表示总DMO输出量时，促胰液素刺激后60分钟内，慢性胰腺炎患者的该值显著降低。当以十二指肠内容物中该化合物的十二指肠液/血浆最大浓度比（最大J/P比）来表示十二指肠中的DMO时，促胰液素刺激后最后40分钟内，慢性胰腺炎患者的该值显著降低。因此，这两个参数可作为胰腺DMO排泄的指标。本技术很可能成为早期检测慢性胰腺炎的有效诊断工具。
