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PubMed1994

Ontogeny and regional distribution of hormone-producing cells in the embryonic pancreas of Alligator mississippiensis.

The hormones of the endocrine pancreas are believed to play an important role in early development. The development of the pancreas and the appearance of hormone-producing cells during embryogenesis have been extensively studied in mammals and birds. Relatively little work has been done in other vertebrates, and there are no published studies regarding the order Crocodilia. Given the pivotal phylogenetic position of crocodilians, Alligator mississippiensis provides an interesting species in which to study the embryonic development of the endocrine pancreas. The aims of the present study were (1) to investigate the morphological development of the pancreas and (2) to determine the initial appearance and regional distribution of the pancreatic endocrine cells in the embryonic alligator. At each stage of development serial sections of pancreatic tissue were stained with hematoxylin and eosin to aid in morphological description. Using immunocytochemistry sections were stained to detect the presence of insulin, glucagon, somatostatin, and pancreatic polypeptide. The dorsal pancreatic bud was first observed at stage 8, coincident with the appearance of insulin-containing and glucagon-containing cells. Somatostatin-containing cells were first detected at stage 10. At stage 13 the ventral pancreatic bud was first observed. At stage 14 the dorsal and ventral pancreatic buds fused and insulin, glucagon, and somatostatin were found throughout the pancreas. Not until stage 17 was pancreatic polypeptide first detected. Unlike the other hormones, pancreatic polypeptide was rare or absent in the dorsal region of the pancreas. In later stages of development, somatostatin-containing cells were the most abundant and constituted 35-40% of all hormone-containing cells. The sequence of appearance of insulin and glucagon found in the alligator is the same as that found in mammals and birds.

Alligators and Crocodiles↗
PubMed1995

Characterization of cholecystokinin receptors and messenger RNA expression in rat pancreas: evidence for expression of cholecystokinin-A receptors but not cholecystokinin-B (gastrin) receptors.

It has been previously demonstrated that guinea pig pancreas possesses both cholecystokinin-A (CCK-A) receptors and CCK-B (gastrin) receptors. In contrast to guinea pig pancreas, it is not known whether CCK receptors in rat pancreas are CCK-A receptors, CCK-B (gastrin) receptors, or both. Thus, in the present study, we characterized CCK receptors in rat pancreas at the receptor and mRNA level. 125I-Bolton-Hunter-labeled CCK octapeptide (125I-BH-CCK-8), the specific CCK-A and CCK-B (gastrin) receptor antagonists L364,718 and L365,260, and 125I-labeled gastrin-I were utilized to characterize CCK receptors in normal rat pancreas. Additionally, we utilized 32P-labeled cDNA probes of the CCK-A receptor and CCK-B (gastrin) receptor coding regions in order to examine the expression of CCK receptor subtypes in normal rat pancreas at the mRNA level. The dose-inhibition curve of CCK-8 inhibiting binding of 125I-BH-CCK-8 was significantly best fit by a two-site model with a high-affinity site (Kd = 0.68 +/- 0.13 nM) and a low-affinity site (Kd = 656 +/- 289 nM). L364,718 inhibited binding of 125I-BH-CCK-8 with high affinity, whereas no high-affinity inhibition for L365,260 to inhibit binding of 125I-BH-CCK-8 was detected. L364,718 was 627 times as potent as L365,260 in inhibiting binding of 125I-BH-CCK-8. No saturable binding was present for 125I-labeled gastrin-I. Gastrin-17-I did not inhibit binding of 125I-BH-CCK-8.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Ischemia-reperfusion injury on the pancreas in rats: identification of acinar cell apoptosis.

An ischemia-reperfusion injury on the pancreas is involved in the pathophysiology of acute pancreatitis or tissue injuries after pancreas transplantation. On the other hand, recent studies have demonstrated that ischemia-reperfusion induces apoptosis in several organs such as kidney, heart, and brain. In the present study, we sought to characterize a pattern of injury during ischemia-reperfusion on the pancreas and determined whether ischemia-reperfusion on the pancreas causes the apoptotic process. Ischemia-reperfusion was induced by blocking the inferior splenic artery and removing the clamp in pentobarbital-anesthetized rats. Rats were sacrificed at 0-72 hr following a 60-min ischemia. Evans blue extravasation showed 3.5-fold increase at 2 hr after reperfusion, indicating a rapid increase of vascular permeability. Tissue myeloperoxidase activity, an index of neutrophil accumulation, significantly increased in a time-dependent manner until 48 hr after reperfusion. Histological analysis revealed the existences of interstitial cell infiltration and edema. DNA breaks of acinar cells were detected by gel electrophoresis and in situ nick end-labeling, and the numbers strikingly increased at 48 hr after reperfusion. Furthermore, Bax protein, an effector of apoptotic cell death, was expressed in acinar cells. The results indicate that an ischemia-reperfusion injury on the pancreas in rats resembles many features of acute pancreatitis. Apoptosis in acinar cells may be one of the specific features of the ischemia-reperfusion injury on the pancreas.

Amylases↗
PubMed1989

Somatomedin C in the pancreas of young and adult, normal and obese, hyperinsulinemic mice.

Immunocytochemical, immunochemical and RNA-hybridization techniques were used to map the distribution of somatomedin C (Sm-C; insulin-like growth factor I; IGF-I) in the pancreas of young and adult lean and obese mice. The D cells in the islets of Langerhans showed intense cytoplasmic Sm-C immunoreactivity, extending into their processes. Only slight Sm-C immunoreactivity was seen in A and B cells, apparently confined to the plasma membranes. In the exocrine pancreas scattered duct cells were immunopositive. Starvation increased, while feeding decreased the Sm-C immunoreactivity in B cells. RNA-hybridization analyses revealed that roughly the same number of Sm-C mRNA molecules, as calculated per DNA amount in the pancreas, could be demonstrated in young and adult, lean and obese mice. Radioimmunoassay (RIA) determinations of total Sm-C showed that there were about equal concentrations in the pancreas of lean and obese mice. There were marked differences between the liver and the pancreas, in that the RIA Sm-C values for the former were twice those in the latter while, in contrast, the corresponding values for the Sm-C mRNA, i.e. the agent determining the synthesis of Sm-C, were about 100 times higher in the liver as compared to that in the pancreas. We interpret our results as follows: The D cells in the islets form and secrete Sm-C in both young and adult, lean and obese mice, while A and B cells bind, but do not necessarily synthesize this peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Resection of the inferior head of the pancreas: report of a case.

We developed a new technique for partial resection of the head of the pancreas with an end-to-side pancreaticoduodenostomy, while preserving the duodenum, the common bile duct, and the upper part of the head of the pancreas around the duct of Santorini. A resection of the inferior head of the pancreas was performed in a patient with an intraductal mucin-producing tumor of the pancreas. This procedure is considered to be appropriate for treating both benign disease and noninvasive malignant disease involving either the uncinate process or the duct of Wirsung, because it removes both the uncinate process and the pancreatic tissue around the duct of Wirsung. We thus believe that a resection of the inferior head of the pancreas with an end-to-side pancreaticoduodenostomy can help play a significant role in the management of patients with benign diseases and localized malignant tumors of the pancreas.

Adenocarcinoma, Papillary↗
PubMed1996

The impact of midline versus transverse incisions on wound complications and outcome in simultaneous pancreas-kidney transplants: a retrospective analysis.

Intraperitoneal placement of the pancreas allograft, usually through a midline incision, has so far achieved the best results in pancreas transplantation. The usefulness and safety of a transverse incision has not been previously reported. The purpose of this study was to compare midline and transverse incisions, with respect to wound complications and outcome, in simultaneous pancreas-kidney transplant recipients with intraperitoneal placement of the pancreatic graft. The incidence of deep abscess formation, superficial abscess formation, wound leak, and fascial dehiscence, as well as graft survival, were retrospectively compared in 41 bladder-drained simultaneous pancreas-kidney recipients with a midline incision and in 15 with a transverse incision. The overall incidence of wound complications was similar (34% vs 20%, P = NS) in the two groups. Deep abscess formation occurred more frequently in the midline group (27% vs 0%, P = 0.02). Staphylococcus epidermidis and Candida albicans were the most common microbial isolates from deep abscesses. Multivariate logistic regression analysis revealed donor age 40 years or older (P = 0.04), the occurrence of a bladder leak (P = 0.05), and a peak serum amylase in the 1st week of 1000 IU/l or greater (P = 0.02) to be independent risk factors for the development of wound complications. The type of incision, however, was not found to be an independent risk factor. Patient (90% vs 83%, P = NS), pancreas allograft (78% vs 82%, P = NS), and kidney allograft (83% vs 70%, P = NS) survival rates were similar for the midline and transverse groups. We conclude that the transverse incision is a reasonable alternative to the midline incision in simultaneous pancreas-kidney transplantation and it is presently the incision of choice at our institution. It offers excellent exposure and is associated with a similar wound complication rate and outcome when compared to the midline incision.

Abscess↗
PubMed1990

Reduction of insulin resistance by combined kidney-pancreas transplantation in type 1 (insulin-dependent) diabetic patients.

To evaluate the effect of combined kidney and pancreas transplantation on insulin action and glucose metabolism, 15 Type 1 (insulin-dependent) diabetic patients who were undergoing combined kidney-pancreas transplantation were studied before transplantation by means of the euglycaemic hyperinsulinaemic clamp technique combined with 3-3H-glucose infusion and indirect calorimetry. Nine of the original 15 patients were studied again after four months and six after 12 months, successful combined kidney-pancreas transplantation with the same experimental protocol. Nine volunteers formed the group of normal subjects. Combined kidney-pancreas transplantation normalised hepatic glucose production and reduced peripheral insulin resistance in Type 1 diabetic uraemic patients, despite chronic immunosuppressive therapy. To further evaluate the hypothesis that residual insulin resistance was due to chronic steroid therapy. 11 additional subjects with chronic uveitis (six of whom were treated with only prednisone, and five treated only with cyclosporin) underwent the same protocol demonstrating a normal hepatic glucose production. The insulin-stimulated peripheral glucose uptake was reduced in the prednisone-treated group, but normal in cyclosporin-treated subjects. Four additional diabetic patients with a kidney transplant were also studied. They showed a peripheral insulin sensitivity intermediate between diabetic uraemic patients and patients after combined transplant. We conclude that short-term (one year) combined kidney-pancreas transplantation improves glucose metabolism by restoring normal rates of hepatic glucose production and reducing peripheral insulin resistance; chronic steroid therapy is the major determinant of residual reduced insulin action. Both kidney and pancreas substitution play a role in reducing peripheral insulin resistance.

Adult↗
PubMed1980

The location of VIP in the pancreas of man and rat.

VIP has powerful stimulatory effects on both endocrine and exocrine pancreas but its localisation within the gland has not been established. In this study, human pancreas was obtained fresh at surgery (eleven) or within four hours of death (seven). The pancreas was also removed from rats (twenty-two). Immunocytochemical staining showed VIP to be present in fine nerve fibres in all areas of the pancreas. Many fibres were seen in the exocrine pancreas, running between the acini, and around ducts and blood vessels. In addition, dense networks of fibres were observed forming meshes around islets and occasional ganglia were found containing immunoreactive cell bodies. In general, there were fewer VIP fibres in the rat pancreas than in the human, but overall distribution was identical. The mean VIP content of whole human pancreatic tissue was 42 +/- 10 pmol/g wet weight (38 +/- 9 pmol/g in head, 49 +/- 6 pmol/g in body and 42 +/- 11 pmol/g in tail). Whole rat pancreatic tissue contained 28 +/- 7 pmol/g wet weight while preparations of isolated islets were found to contain 374 +/- 30 pmol/g. It is possible that the heavy VIP innervation of the islets described here indicates a role in the regulation of islet hormone release.

Animals↗
PubMed1988

Effect of diabetes mellitus on pancreatic exocrine secretion from isolated perfused pancreas in rats.

We studied pancreatic exocrine function in response to cerulein and carbamylcholine in isolated perfused pancreas obtained from control, streptozotocin-induced diabetic, and insulin-treated diabetic rats. The time course of pancreatic juice, protein, amylase, and trypsinogen secretion in response to cerulein or carbamylcholine in diabetic rats was similar to that in control rats. Basal as well as cerulein- or carbamylcholine-stimulated output of amylase from diabetic rat pancreas was significantly reduced, whereas that of trypsinogen was similar to the control. Amylase and trypsinogen outputs in response to 620 pM (1.0 ng/ml) cerulein from insulin-treated diabetic rat pancreas were significantly lower than those from control rat pancreas, although the pancreatic contents of these enzymes were similar to or greater than those in control rats. The dose-response curves of pancreatic juice, protein, amylase, and trypsinogen for cerulein and carbamylcholine were biphasic in both control and diabetic rats. The minimal and the maximal release in response to cerulein occurred with higher concentrations in diabetic rats compared with control rats. In contrast, the maximal responses were obtained with 1 microM carbamylcholine in control rats and with 0.1-1 microM carbamylcholine in diabetic rats. The present study demonstrates that the concentration of cerulein required to elicit maximal response was increased, whereas that to carbamylcholine was reduced in diabetic rat pancreas, and that the protein and enzyme outputs in response to cerulein were significantly reduced in insulin-treated diabetic rat pancreas despite restoration of the pancreatic enzyme contents to control levels.

Animals↗
PubMed1994

The venous drainage of the pancreas.

With the aim of clarifying certain contradictory aspects of the description of the venous drainage of the pancreas, a review of the literature and an anatomic study were carried out. Fifty duodeno-pancreatic blocks were studied by the injection-corrosion technique, of which 45 were available for study of the right pancreas and 37 for that of the left pancreas. The venous drainage of the duodeno-pancreas is effected via two territories: a posterosuperior and an anteroinferior, the former draining toward the portal v. and the second into the superior mesenteric v. The borderline between the two is represented by the inferior posterior pancreatico-duodenal (IPPD) v. Four veins ensure duodeno-pancreatic drainage: the superior anterior, inferior anterior, superior posterior and inferior posterior pancreatico-duodenal vv. (SAPD, IAPD, SPPD and IPPD). The major vein of the ventral aspect is the SAPD; that of the dorsal aspect is the SPPD. Two arches, anterior and posterior, were found in the majority of cases. The left pancreas drains into the splenic v. via several collateral branches. Other veins participate in the venous drainage of the isthmus, body and tail of the pancreas, including the inferior or transverse pancreatic v.

Adult↗
PubMedDate not supplied

Clinical experience in pancreas transplantation in Lyon: long-term survival of duct injected pancreatic grafts.

Ninety-seven pancreatic grafts in 92 insulin-dependent diabetic patients were performed during the last 11 years. Eighty-three of these grafts were carried out after neoprene duct injection, the other patients underwent pancreato-duodenal transplantation. In 80 cases, a double pancreas and kidney graft was performed. Five different immunosuppressive protocols were subsequently applied. Actuarial survival of patients and pancreata was 75.1% and 47%, after one year and 54.6% and 22.1%, respectively, 4 years after transplantation. Slightly better results were observed in double pancreas and kidney transplantation. The survival of both patients and pancreas improved when the most recent immunosuppressive protocols including cyclosporin A and only small doses of steroids were applied. The main causes of loss of the pancreatic graft were rejection, vascular thrombosis and death of the patient with functioning organ. Metabolic studies showed good insulin secretion with normal or impaired glucose tolerance as well as good short and half-term glycemic control. Whole pancreas grafts with enteric diversion yielded prompter and higher insulin secretion but the incidence of surgical complications was increased. In comparison to the data recorded at 6 months after pancreas transplantation, 5 patients of our series with still functioning organ showed an equally satisfactory and unchanged glycemic control after more than 4 years from surgery. In these patients, the previously high insulinemic values decreased to normal levels. However, 3 of these patients showed a decrease in post-prandial peaks as confirmed also by OGTT. However, mean blood glucose level was not altered. In our series the suppression of exocrine pancreatic secretion by neoprene duct injection did not appear to represent a relevant cause of decrease in endocrine function. The results obtained do not yet allow us to draw definite conclusions as to the efficacy of pancreas transplantation in the treatment of degenerative complications in diabetic patients.

Adult↗
PubMed1977

Experimental study of transductal dissemination of cancer of the pancreas.

Experimental studies on the mechanims of transductal dissemination of the pancreas carcinoma was made in rabbit by injection of VX2 carcinoma suspension into the pancreatic duct. Ductal occlusion was conductive to nidation and growth in the pancreas of intraductal floating cancer cells, but tumor growth also occured in 40% of animals in which the duct was not occluded. The mechanisms of nidation in the pancreas of intraductal floating cancer cells were direct embedding into the ductal wall, and leakage of cancer cells from the duct in the process of pancreatic fibrosis due to ductal obstruction. Expansive tumor growth in the pancreas was more vigorous the smaller the degree of fibrosis of the pancreas, and was most active where associated acute pancreatitis was seen or where the pancreas was X-irradiated one week before injection of carcinoma suspension.

Animals↗
PubMed1997

On the etymology of "pancreas".

It is said that the pancreas was described first by Herophilus of Chalcedon in about 300 BC, and the organ was named by Rufus of Ephesus in about 100 AD. However, it is an established fact that the word pancreas had been used by Aristotle (384-322 BC) before Herophilus. In Aristotle's Historia Animalium, there is a line saying "another to the so-called pancreas." It is considered that the words "so-called pancreas" imply that the word pancreas had been popular at the time of Aristotle, but it had not been authorized yet as an anatomical term. However, the word pancreas presumably has been accepted as an anatomical term since Herophilus.

History, Ancient↗
PubMed2003

Netrin-1 expression in fetal and regenerating rat pancreas and its effect on the migration of human pancreatic duct and porcine islet precursor cells.

AIMS/HYPOTHESIS: We investigated the expression and function of netrin-1, a diffusible laminin-like protein known to regulate neuronal-cell migration in the pancreas. We questioned whether this factor regulates migration of pancreatic epithelial cells and whether this could be involved in islet neogenesis. METHODS: We studied fetal and adult rat pancreas wherein duct ligation induced islet neogenesis. Netrin-1 expression was analysed by RT-PCR, western blot and immunohistochemistry. In vitro cell migration was measured with a human pancreatic duct cell line (CAPAN-2) and with fetal porcine islet cells. We also studied the expression of two netrin-receptors, neogenin and deleted in colorectal cancer. RESULTS: We found a transient expression of netrin-1 mRNA and protein in fetal pancreas from E15 to E18, and in adult pancreas after duct ligation. In normal adult pancreas there was very little netrin-1 expression. Netrin-1 expression was observed both in endocrine and exocrine cells. At the immunohistochemical level, it was expressed by islet cells during tissue regeneration. We could show that netrin-1 increases the migration of fetal islet cells and of a ductal cell line, mainly via a chemokinetic effect. From the two well-established netrin receptors, DCC and neogenin, we only found neogenin to be expressed in the pancreas. Neogenin expression coincided with the period of netrin-1 up-regulation. CONCLUSION/INTERPRETATION: Netrin-1 is involved in pancreatic morphogenesis and tissue remodelling and plays a role in the regulation of duct-cell and fetal-islet cell migration. This can be of importance in islet regeneration, where migration of islet precursors takes place.

Adenocarcinoma↗
PubMed2005

Expression and function of leukaemia inhibitory factor and its receptor in normal and regenerating rat pancreas.

AIMS/HYPOTHESIS: It was recently reported that culturing adult exocrine cells in the presence of epidermal growth factor and leukaemia inhibitory factor (LIF) resulted in their transdifferentiation into endocrine beta cells. The aim of this study was to examine the expression and function of LIF in the pancreas. MATERIALS AND METHODS: We studied the expression of LIF and its receptor components, LIF-receptor-beta and gp130, by immunohistochemistry, western blotting and RT-PCR in normal rat pancreas, pancreas with duct ligation-induced islet neogenesis, and in pancreatic cell cultures. Isolated duct fragments were cultured in the presence of LIF and a janus kinase 2 (JAK2) inhibitor. RESULTS: LIF was detected by immunohistochemistry, western blot and RT-PCR in the ducts of the normal pancreas. Both LIF-receptor-beta and gp130 were detected by RT-PCR in the pancreas. Immunostaining revealed gp130 exclusively in the ducts and centro-acinar cells. After duct ligation-induced tissue injury, upregulation of LIF and its receptor occurred in rat pancreas. Metaplastic exocrine cells also started to express LIF and this was increased after alloxan treatment. Signalling via LIF-receptor-beta/gp130 involves the JAK/signal transducer and activator of transcription (STAT) pathway. LIF induced increased activation of STAT3 in pancreatic cells. In isolated duct fragments, addition of LIF resulted in a significant increase in duct cell proliferation, while a specific inhibitor of the JAK/STAT signalling pathway inhibited proliferation. CONCLUSION/INTERPRETATION: Our observations show that LIF and its receptor are expressed in cells from pancreatic ducts. The cytokine plays a role in pancreatic physiology, controls duct cell proliferation and is involved in repair processes following pancreatic injury.

Animals↗
PubMed2000

Comparison of progression of macrovascular diseases after kidney or pancreas and kidney transplantation in diabetic patients with end-stage renal disease.

AIMS/HYPOTHESIS: The aim of the study was to examine the effect of pancreas-kidney transplantation on the progression of macrovascular diseases in Type I diabetic patients with end-stage renal disease. METHODS: The progression of cerebrovascular disease, coronary heart disease and peripheral vascular disease in uraemic patients with Type I (insulin-dependent) diabetes mellitus and who had had simultaneous pancreas-kidney transplantation was compared with that of recipients of a kidney transplant alone. Between 1986 and 1998 a total of 11 uraemic diabetic patients received a simultaneous pancreas-kidney transplantation and 10 diabetic patients a kidney transplant alone. All transplants functioned for at least 24 months, the mean observation period was 69 +/- 37 compared with 70 +/- 33 months in both patient groups. Macroangiopathic diseases were classified in four stages as described earlier. RESULTS: In the group with simultaneous pancreas-kidney transplantation progression of cerebrovascular and coronary heart disease was observed in four patients (36%) and progression of peripheral vascular disease in five subjects (45%). In the cohort with kidney transplant alone four patients (40%) showed progression of cerebrovascular and coronary heart disease and five progression of peripheral vascular disease (50%); the difference is not significant. Mean values of HbA1c (5.8 +/- 0.2 vs 7.5 +/- 0.6%, p < 0.001) and serum triglycerides (1.2 +/- 0.4 vs 2.0 +/- 1.0 mmol/l, p < 0.05) were significantly lower in the patients with pancreas-kidney transplantation than in the patient group with kidney transplant alone. Serum cholesterol concentrations and blood pressures were similar in both cohorts. CONCLUSION/INTERPRETATION: From our results we concluded that pancreas-kidney transplantation reduces risk factors for the development of macroangiopathy but fails to halt progression of macrovascular diseases similar to Type I diabetic patients with kidney transplant alone.

Adult↗
PubMed2000

Increased O-GlcNAc transferase in pancreas of rats with streptozotocin-induced diabetes.

AIMS/HYPOTHESIS: Streptozotocin (STZ), a chemically reactive analogue of N-acetylglucosamine, induces necrosis of the beta cells, resulting in diabetes mellitus. Glucose-induced insulin resistance is mediated by increased activity of the hexosamine pathway. We aimed to examine the regulation of O-GlcNAc transferase expression and activity in the normal and streptozotocin diabetic pancreas. METHODS: Rats were made diabetic by an injection of streptozotocin (65 mg/kg). The expression of O-GlcNAc transferase protein was examined by immunoblot analysis. Activity of O-GlcNAc transferase was assayed by the incorporation of [3H]GlcNAc into the synthetic peptide. Localization of O-GlcNAc transferase was done by immunohistochemistry. The change of O-GlcNAc modification of proteins was examined by immunoblot analysis. RESULTS: In the STZ-induced diabetic pancreas, a severe loss of beta cells was observed, whereas alpha cells had increased in number. The diabetic pancreas showed an increase in the expression of O-GlcNAc transferase at the protein level and the O-GlcNAc transferase activity in it was increased significantly (p < 0.05). An increase in the immunostaining intensity in the cytoplasm of islet beta cells was also observed in the diabetic pancreas, whereas exocrine cells and islet cells other than beta cells showed little change in immunostaining intensity. The pancreas of STZ-diabetic rats showed a 3.1-fold increase in total cellular O-GlcNAc-modified proteins. CONCLUSION/INTERPRETATION: These findings indicate that O-GlcNAc transferase plays an important part in the modulation of O-GlcNAc concentrations in the pancreas and suggest that the increase in O-GlcNAc modification of the proteins correlates closely with diabetes.

Animals↗
PubMed2000

Vascular complications following bladder drained, simultaneous pancreas-kidney transplantation: the University of Miami experience.

Vascular complications remain a significant nonimmunologic source of pancreas allograft loss. From February 1993 through January 1998, we performed 98 simultaneous pancreas-kidney transplantations (SPK) using pancreatic exocrine bladder drainage in patients with type 1 insulin-dependent diabetes mellitus and end-stage renal disease. They originally received quadruple immunosuppression, and since May 1997 triple immunosuppression protocol (tacrolimus, mycophenolate mofetil, and steroids). The patients' mean age was 37 years (range 24-53 years), including 50 women and 48 men with a mean follow-up of 42 months. The overall rate of vascular complications was 6% (5 patients). The vascular complications were as follows: late thrombosis of the Y with persistent pancreas allograft function (n = 1), rupture of a pseudoaneurysm of the superior mesenteric artery (PSMA) with an arteriovenous fistula (AVF) (n = 1), thrombosis of the splenic vein (SV) (n = 3), complete thrombosis of the superior mesenteric vein (SMV) and splenic vein (n = 1). The patient with PSMA underwent surgical correction of the AVF and PSMA with preservation of the allograft pancreas function. The other patient with late thrombosis of the Y-graft required no treatment. All 3 patients with SV thrombosis were systemically heparinized followed by oral anticoagulation. The patient with complete thrombosis required surgical thrombectomy of the SMV and SV followed by heparinization and oral anticoagulation. All 6 patients including the 4 with thrombosis had preservation of the pancreas function. Serial pancreas ultrasound showed resolution and improvement with recanalization of the splenic vein and superior mesenteric vein in those patients with thrombosis. We describe our vascular experience with salvage of the pancreatic allograft function. Surgery seems to be the best treatment option in the case of AVF or complete thrombosis of the allograft. Intravenous heparin followed by oral anticoagultion could be a conservative approach for SV thrombosis.

Adult↗