Gruessner R W, Manivel C, Dunn D L, Sutherland D E
Department of Surgery, University of Minnesota, Minneapolis.
Pancreas. 1991 Jul;6(4):479-88. doi: 10.1097/00006676-199107000-00017.
Pancreas transplantation is usually performed in patients with denovo type I diabetes, who have advanced secondary complications. We report a case in which whole pancreaticoduodenal transplantation, with enteric drainage, was performed to correct both endocrine and exocrine deficiencies in a patient with hyperlabile diabetes and steatorrhea, unresponsive to oral enzyme replacement therapy, following staged total pancreatectomy for idiopathic or familial chronic pancreatitis. The transplant was performed one year after completion of native pancreatectomy and immediately established an insulin-independent euglycemic state, with normal oral and intravenous glucose tolerance test results and correction of steatorrhea. Beginning one year posttransplant, the patient had intermittent episodes of steatorrhea, associated with mild elevation of blood sugar levels, which were presumed to be due to rejection and, indeed, responded to antirejection treatment with antilymphocyte globulin and temporary increases in steroids dosages. At 20 months posttransplant, steatorrhea did not respond to antirejection treatment and an acute abdomen developed. Laparotomy revealed a perforated graft duodenum, which was resected; pathology showed transmural necrosis secondary to chronic rejection. The pancreas graft itself was left in situ, disconnected from the intestinal tract. The patient remained normoglycemic after graft duodenectomy but resumed oral enzyme replacement therapy in an attempt to combat recurrence of severe steatorrhea. However, his overall situation remained improved compared to pretransplant, since the exocrine deficiency was tolerable in the absence of a diabetic state. Ten months postgraft duodenectomy (38 months posttransplant), elevations in blood sugar levels were treated with another course of antirejection treatment and levels temporarily declined. At 14 months postgraft duodenectomy (42 months posttransplant), graft endocrine function again declined and exogenous insulin was resumed. Six months later, four years after the original transplant, a new enteric-drained pancreaticoduodenal graft was placed, once again resulting in an insulin-independent, steatorrheafree state. With improvements in immunosuppression, pancreas transplantation could be offered to selected patients with hyperlabile diabetes, following total pancreatectomy for benign disease; if the enteric drainage technique is used, in the absence of rejection, exocrine deficiency could be corrected as well.
胰腺移植通常用于患有新发I型糖尿病且出现晚期继发性并发症的患者。我们报告了一例患者，该患者因特发性或家族性慢性胰腺炎接受分期全胰切除术后，出现血糖波动较大且对口服酶替代疗法无反应的脂肪泻，为纠正其内分泌和外分泌功能缺陷，进行了带肠内引流的全胰十二指肠移植。移植手术在自体胰腺切除完成一年后进行，术后立即建立了不依赖胰岛素的正常血糖状态，口服和静脉葡萄糖耐量试验结果正常，脂肪泻得到纠正。移植术后一年开始，患者间歇性出现脂肪泻，并伴有血糖水平轻度升高，推测这是由排斥反应引起的，实际上，使用抗淋巴细胞球蛋白进行抗排斥治疗以及临时增加类固醇剂量后症状有所缓解。移植术后20个月，脂肪泻对抗排斥治疗无反应，且出现了急腹症。剖腹探查发现移植的十二指肠穿孔，遂将其切除；病理显示为慢性排斥反应继发的透壁坏死。胰腺移植物本身留在原位，与肠道断开连接。移植十二指肠切除术后患者仍保持血糖正常，但为了对抗严重脂肪泻的复发，重新开始口服酶替代疗法。然而，与移植前相比，他的总体状况仍有所改善，因为在没有糖尿病状态的情况下，外分泌功能缺陷是可以耐受的。移植十二指肠切除术后10个月（移植术后38个月），血糖水平升高，再次进行抗排斥治疗后血糖水平暂时下降。移植十二指肠切除术后14个月（移植术后42个月），移植物内分泌功能再次下降，重新开始使用外源性胰岛素。六个月后，即原移植手术四年后，再次植入了一个新的带肠内引流的胰十二指肠移植物，再次实现了不依赖胰岛素且无脂肪泻的状态。随着免疫抑制治疗的改进，对于因良性疾病接受全胰切除术后患有血糖波动较大的糖尿病的特定患者，可以考虑进行胰腺移植；如果采用肠内引流技术，在没有排斥反应的情况下，外分泌功能缺陷也可以得到纠正。
