Long-term outcomes of total pancreatectomy and islet auto transplantation for hereditary/genetic pancreatitis.
Long-term outcomes of total pancreatectomy and islet auto transplantation for hereditary/genetic pancreatitis.
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DOI：
10.1016/j.jamcollsurg.2013.12.037
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发表时间：
2014-04
影响因子：
5.2
通讯作者：
Pruett, Timothy L.
中科院分区：
文献类型：
--
作者：
Chinnakotla, Srinath;Radosevich, David M.;Dunn, Ty B.;Bellin, Melena D.;Freeman, Martin L.;Schwarzenberg, Sarah J.;Balamurugan, A. N.;Wilhelm, Josh;Bland, Barbara;Vickers, Selwyn M.;Beilman, Gregory J.;Sutherland, David E. R.;Pruett, Timothy L.
慢性胰腺炎是一种由多种病因引起的衰弱性疾病。具有遗传/遗传缺陷（HGP）的亚群不仅有慢性疼痛，而且患胰腺癌的风险也增加。TP-IAT治疗由hgp引起的慢性胰腺炎的长期结果尚不清楚。对1977-2012年单中心484例tp - iat前瞻性维护数据库的回顾。对遗传/遗传缺陷(PRSS1 （n=38）、SPINK1 （n=9）、CFTR （n=14）和家族性（n=19）患者接受TP-IAT治疗的结果（疼痛缓解、麻醉使用、β细胞功能、健康相关生活质量测量）进行评估，并与非遗传/遗传病因患者进行比较。所有80例HGP患者均为麻醉依赖患者，内窥镜治疗或直接胰腺手术失败。TP-IAT治疗后，90%的胰腺炎患者无疼痛且持续疼痛缓解；超过65%具有部分或完全β细胞功能。与非遗传性病因相比，HGP患者更年轻（22岁vs.38岁p=<0.001），胰腺炎疼痛持续时间更长（11.6±1.1年vs. 9.0±0.4年p=0.016），胰脏纤维化评分更高（7±0.2 vs. 4.8±0.1 p=<0.001），胰岛产量倾向较低（3435±361 IEQ vs. 3850±128 IEQ p=0.28）。使用多变量logistic回归，(1)非hgp病因（p值=0.019）；(2)胰脏纤维化严重程度较低（p值<0.001）；(3)胰腺炎病程较短（p值= 0.008）；(4)每公斤体重移植IEQ较高（p值=<0.001）更有可能实现胰岛素独立（p值<0.001）。HRQoL的生理和心理部分评分与基线相比，SF-36有显著改善（p <0.001）。在2,936人年的随访期间，整个队列中没有患者在肝脏或其他地方发展为胰腺起源的癌症。TP-IAT治疗由HGP病因引起的慢性胰腺炎患者可长期缓解疼痛（90%）并保存β细胞功能。HGP引起的慢性疼痛性胰腺炎患者具有胰腺癌的高终生风险，应在胰腺炎炎症导致更高程度的胰腺纤维化和胰岛细胞功能丧失之前尽早考虑TP-IAT。
Chronic-pancreatitis is a debilitating-disease resulting from many etiologies. The-subset with hereditary/genetic defects (HGP) not only has chronic-pain, but also an increased-risk for pancreatic-cancer. The long-term-outcomes of TP-IAT for chronic pancreatitis due-to-HGP are not clear. Review of a prospectively-maintained-database of 484 TP-IAT-from-1977-2012 at a single-center. The-outcomes (pain-relief, narcotic-use, β cell-function, health-related quality of-life-measures of patients-that-received TP-IAT for hereditary/genetic-defects (PRSS1 (n=38), SPINK1 (n=9), CFTR (n=14) and Familial (n=19) were-evaluated-and-compared to those with non-hereditary/genetic-etiology. All 80 patients with HGP were narcotic-dependent and failed-endoscopic-management or direct-pancreatic-surgery. Post TP-IAT, 90% of the patients-were-pancreatitis-pain-free with sustained-pain-relief; over 65% had partial or full β-cell-function.-Compared to non-hereditary etiologies, HGP were-younger (22 yrs vs.38 yrs p=<0.001), had-pancreatitis-pain of longer-duration (11.6±1.1 vs. 9.0±0.4 yrs p=0.016), had a higher-pancreas-fibrosis-score (7±0.2 vs. 4.8±0.1 p=<0.001), and-trended-toward-lower-Islet-yield (3,435 ± 361 IEQ vs. 3850± 128 IEQ p=0.28). Using-multivariate-logistic-regression, (1) non-HGP-etiology (p value=0.019) (2) lower severity-of-pancreas-fibrosis (p value < 0.001), (3) shorter-duration-of-years with pancreatitis (p value = 0.008) and (4) higher-transplant IEQ per KG body-weight (p value =<0.001) were-more likely-to-achieve-insulin-independence (p value < 0.001). There was a significant-improvement in HRQoL from-baseline, by SF-36, in physical-and-mental-component HRQoL scores (p <0.001). None-of-the-patients in the entire-cohort-developed-cancer of pancreatic-origin in the liver or elsewhere during 2,936 person-years of follow-up. TP-IAT in patients with chronic pancreatitis due to HGP etiology provides long-term pain relief (90%) and preservation-of-beta-cell-function. Patients with chronic-painful pancreatitis due to HGP with a high-life-time-risk of pancreatic-cancer should be considered earlier for TP-IAT before pancreatic-inflammation results in higher-degree of pancreatic-fibrosis and islet-cell-function-loss.
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