Predicting exocrine insufficiency following pancreatic resection.
Predicting exocrine insufficiency following pancreatic resection.
复制标题
预测胰腺切除术后的外分泌功能不全。
DOI：
10.1016/j.jss.2010.06.033
复制
发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Hines,OJoe
中科院分区：
文献类型：
--
作者：
King,JonathanC;Hines,OJoe
我们饶有兴趣地阅读了中村博士等人的文章"胰腺实质厚度减少表明胰腺切除术后胰腺外分泌功能不全"。[1]他们的工作提出了一个潜在的有效工具，胰腺外科医生可以治疗他们的病人手术后，以减轻胰腺外分泌功能不全（EPI）的影响。重要的是，他们研究的指标，术前和术后计算机断层扫描（CT）扫描的胰腺实质厚度，是现成的，很容易转化为当前的临床实践，使他们的结果立即适用。特别值得注意的是，他们发现术前胰管与实质比与术后EPI相关，14.5 mm的临界值为67.6%的敏感性和72.2%的特异性。[1]虽然直觉上认为EPI（临床定义为脂肪性胰腺炎的发作）与切除范围直接相关，但预防术后EPI所需的残留胰腺体积尚不清楚，且可能高度可变;潜在疾病过程的程度和术前胰腺功能可能发挥作用，如慢性胰腺炎中所见的实质纤维化。一般来说，在EPI的临床症状出现之前，必须损失90 - 95%的胰酶排泄。[2]此外，同时切除十二指肠或胃会影响前肠的神经激素轴，改变胃泌素、胆囊收缩素和胰多肽，从而对胰腺产生营养和促分泌作用。这些肠激素的丢失影响胰腺残端的萎缩率及其消化功能。[3]第一章
We read with interest the article,“Reduced Pancreatic Parenchymal Thickness Indicates Exocrine Pancreatic Insufficiency After Pancreatoduodenectomy” by Dr. Nakamura et al.[1] Their work presents a potentially potent tool by which the pancreatic surgeon may treat their patients following surgery to alleviate the effects of exocrine pancreatic insufficiency (EPI). Importantly the metric they investigated, pancreatic parenchymal thickness on pre-and postoperative computed tomography (CT) scans, is readily available and easily translatable to current clinical practice making their results immediately applicable. Of particular interest was their finding that the preoperative pancreatic duct to parenchyma ratio was correlated to postoperative EPI with a cutoff of 14.5 mm being 67.6% sensitive and 72.2% specific.[1]While it is intuitive that EPI, clinically defined as the onset of steatorrhea, is directly related to the extent of resection, the volume of residual pancreas needed to prevent postoperative EPI is unknown and probably highly variable; the extent of the underlying disease process and preoperative pancreatic function may play a role as exemplified by parenchymal fibrosis seen in chronic pancreatitis. Generally, 90–95% of pancreatic enzyme excretion must be lost before clinical signs of EPI develop.[2] Additionally, the concurrent resection of the duodenum or stomach affects the neurohormonal axis of the foregut with alterations in gastrin, cholecystokinin, and pancreatic polypeptide which exert trophic and secretogogue effects on the pancreas. Loss of these enteric hormones affects the rate of atrophy of the pancreatic remnant as well as its digestive function.[3]