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PubMedDate not supplied

Lymphoepithelial cysts of the pancreas: case report and review of the literature.

The aim of this report was to describe the clinical and pathologic features of lymphoepithelial cysts of the pancreas, establish the differential diagnosis of other pancreatic cysts, and review the literature. A 53-year-old man was incidentally diagnosed with a pancreatic lesion after an abdominal CT scan. This study showed a solid mass in the tail of the pancreas not enhanced by helical CT. Endoscopic ultrasound examination revealed a low-density tissue mass on the surface of the pancreas, less echogenic than the surrounding parenchyma. Distal pancreatectomy and splenectomy were performed with a suspected diagnosis of mucinous cystic tumor. The patient has had an uneventful postoperative period, and the pathologic finding was a lymphoepithelial cyst of the pancreas. Lymphoepithelial cyst of the pancreas is an unusual and benign entity that must be taken into consideration when evaluating a cystic lesion of the pancreas because a different therapeutic approach may be required.

Diagnosis, Differential↗
PubMed2004

Incidence, timing and site of infections among pancreas transplant recipients.

The incidence, timing and site of infections among the different categories of pancreas transplant recipients were investigated. Patients were divided into three groups: pancreas transplant alone (PTA), pancreas after kidney transplant (PAK), or simultaneous pancreas and kidney (SPK) transplants. Length of follow-up, time to death, pancreas graft survival, incidence, timing and site of bacterial infections were noted. Our study showed that at least 75% of pancreas transplant recipients experienced at least one infection (range from 77.8% in the PTA group to 86.7% in the PAK group). The SPK group presented the highest rate of infections with 35.1 infections per 1000/patient-days. Symptomatic urinary tract infections were the most common cause of infection in all patients. The incidence of infections was higher during the first month after transplantation, except for the SPK transplant group, where infections occurred over a longer time period.

Adult↗
PubMed2004

Enteric conversion after bladder drained pancreas transplantation experience of 14 cases.

The method of exocrine diversion in pancreas allograft continues to be controversial due to the advantages versus disadvantages of bladder versus enteric techniques. Bladder drainage (BD) exposes the patient to urological and metabolic problems that may require conversion to enteric drainage (ED). The purpose of this study was to review our initial experience of conversion from BD to ED for patients who underwent pancreas transplantation originally with bladder diversion. Among 114 pancreas transplantation performed with BD, from January 1996 to April 2003, 60 were simultaneous pancreas-kidney transplantation (SPKT), 35 were pancreas transplantation alone (PA), and 19 were pancreas after kidney transplantations (PAK). Twenty-three (20.2%) cases were excluded due to early death of the patient or the graft, yielding an analyses of 91 patients. Enteric conversion (EC) was performed in 14 (15.4%) patients with a mean follow-up of 15.7 months (range, 3-51 months) after transplantation including 8 (8.8%) SPKT, 4 (4.4%) PAK, and 2 (2.2%) PA. No surgical morbidity or mortality was observed related to EC. All patients had complete resolution of the initial problem with preservation of pancreatic function. EC represents an easy, safe procedure with low morbidity and mortality rates, representing the option of choice for patients with persistent urological or metabolic disturbances.

Humans↗
PubMed2004

Outcomes with the selective use of enteric exocrine drainage in pancreas transplantation.

BACKGROUND: Bladder drainage of the exocrine secretions of pancreas transplants has been the standard of practice as it affords the ability to monitor for rejection and is thought to be associated with decreased morbidity. Recently, there has been renewed interest in avoiding the urinary tract complications and metabolic derangements that accompany bladder drainage by draining pancreatic exocrine secretions into the jejunum (enteric drainage). We sought to determine whether enteric drainage of pancreas transplants is safe and offers advantages without compromise in graft function or longevity. METHODS: We retrospectively reviewed all pancreas transplants performed at the University of Washington between 2000 and 2003. Selection of the exocrine drainage method was based on the length of cold ischemia time and whether the pancreas was transplanted alone or in combination with a kidney. Pearson's chi-square and Fisher's Exact tests were used for statistical comparisons in complications or rejections between the groups. RESULTS: Thirty-four pancreas transplants were performed with exocrine drainage into the bladder used in 17 and enteric drainage in 17. The complication rate was 53% in the bladder-drained group and 41% (P=.49) in the enteric-drained group. The incidence of pancreas rejection was 24% in the bladder-drained versus 29% in the enteric-drained patients (P=.50). One graft failed, which was in the bladder cohort. CONCLUSIONS: We found comparable rejection and complication rates between groups. We conclude that enteric drainage is safe when used selectively, and entails no increased risks compared with bladder drainage.

Adult↗
PubMed2005

Successful simultaneous kidney-pancreas transplantation from extreme donors.

UNLABELLED: The purpose of this study was to retrospectively review our experience with "extreme" pancreas donors compared to conventional (CONV) donors. METHODS: "Extreme" (EX) pancreas donors were defined as deceased donors (DDs) age >50 years, <8 years, donation after cardiac death (DCD), and targeted for organ discard. RESULTS: From January 2002 through January 2005, we performed 40 simultaneous kidney-pancreas transplants (SKPT) with Thymoglobulin induction, including 9 (22.5%) from EX and 31 from CONV DDs. Mean DD age was higher in EX DD (41.2 years EX vs 26.0 CONV, P < .05), but mean recipient age and cold ischemia times did not differ between groups. With a mean follow-up of 16.8 months in the EX DD group, patient and kidney graft survival rates are both 100%, and the pancreas graft survival rate is 89%. With a mean follow-up of 21.7 months in the CONV DD group, patient and kidney graft survival rates are both 93.5% and the pancreas graft survival rate is 77.4%. All patients with surviving grafts exhibited good initial (1 case of delayed kidney graft function in a CONV DD) and stable long-term kidney and pancreas graft function. Mean length of initial hospital stay and the incidences of acute rejection, readmissions, operative complications, and infections were similar between groups. CONCLUSIONS: The results of this study suggest that the limits of donor acceptability continue to evolve as excellent outcomes can be achieved in SKPTs from selected EX DDs.

Adolescent↗
PubMed2005

Simultaneous liver and pancreas transplantation in patients with cystic fibrosis.

BACKGROUND: Improved survival in patients with cystic fibrosis (CF) has led to an increased incidence of extrapulmonary complications of this disease. Of these, cirrhosis and pancreatic insufficiency, including CF-related diabetes (CFRD) and exocrine insufficiency, are significant causes of morbidity and mortality. Liver transplantation is the treatment of choice for cirrhosis in this setting, but the addition of an isolated simultaneous pancreas transplant in patients with CFRD has not been reported. METHODS: Two female patients with CF underwent simultaneous pancreas and liver transplantation. Both had pancreatic insufficiency, CFRD, cirrhosis, and preserved renal function. In each case, the liver and pancreas were procured from a single cadaveric donor. The liver transplant was performed first. A lower midline extension was added for improved exposure of the iliac vessels. The donor pancreas transplant was performed with systemic venous drainage and enteric exocrine drainage. Immunosuppression included rabbit anti-thymocyte globulin, tacrolimus, mycophenolate mofetil, and early steroid withdrawal. RESULTS: Both patients recovered well with normal liver function, resolution of portal hypertension, and normal blood glucoses independent of insulin. As a result of the enteric exocrine drainage of the pancreas, they are now independent of supplemental pancreatic enzymes. CONCLUSIONS: Simultaneous liver and pancreas transplantation in CF patients provides the advantages of normalization of glucose and improved nutrition for patients requiring liver transplantation and should be considered in CF patients with CFRD who require liver transplants.

Adolescent↗
PubMed2005

Incidence of pancreas graft thrombosis in portoiliac and portocaval venous anastomosis.

BACKGROUND: Pancreas graft thromboses represent more than 70% of all technical failures; multiple risk factors have been implicated. We analyzed the thrombosis rates using portoiliac versus portocaval vein anastomoses. PATIENTS AND METHODS: The series includes 53 patients who underwent pancreas transplantation: 49 simultaneous pancreas-kidney and 4 pancreas after kidney. There were 27 men and 26 women, of mean age of 37.2 +/- 7.0 years. We compared two groups of recipients that were classified according to venous anastomosis: (A) portoiliac (n = 30), and (B) portocaval (n = 23). RESULTS: The recipients did not show significant differences in age, gender, or duration of diabetes mellitus, but body mass index was significantly higher among the portocaval group. A bladder-drained pancreas technique was more frequently performed in the portoiliac group (93% of patients) versus an enteric-drained pancreas in the portocaval group (81%; P < .001). Heparinization was performed in 12 recipients: 11 (36.6%) in the portoiliac group and 1 (4.3%) in the portocaval group (P < .01). Vascular graft thrombosis (venous in six and arterial in one) developed in seven patients (13.2%) all in the portoiliac group (23%) (P < .02). Two-year patient survival was 93% in the portoiliac group and 94% in portocaval group (P = NS). Two-year graft survival was 66.6% in the portoiliac group and 85.9% in portocaval group (P = .07). CONCLUSION: There was no graft thrombosis among patients with a portocaval vein anastomosis.

Adult↗
PubMedDate not supplied

Simultaneous pancreas-kidney transplantation: five-year results from a single center.

We report the 5-year results of our simultaneous pancreas-kidney transplantation (SPKT) program, started on May 2, 2000. Forty-two SPKT were performed on 42 type I diabetic patients with chronic renal failure. The procedure was performed with enteric diversion and vascular anastomosis to the iliac vessels. Immunosuppressive protocol included antithymocyte globulin, tacrolimus, mycophenolate mofetil, and steroids. The 24 women and 18 men had a mean age of 33.5 +/- 6.3 years and mean 22.8 +/- 14.2 years time of diabetes evolution. Forty patients had been on dialysis for 34.3 +/- 24.1 months, and two were preemptive transplantations. Acute rejection episodes were treated in eight patients (19.1%): in three cases they affected both organs; in two only the kidney was affected; and the other three were pancreas graft rejections. The incidence of postoperative complications requiring re-operation was 42.9%, mostly pancreas graft related. Two patients died, one due to cardiovascular disease; the other was transplant related. Three kidney grafts were lost, and the causes were immunologic, thrombosis, and patient death. Pancreas graft loss occurred in seven patients: thrombosis (n = 3); infection (n = 3); immunologic (n = 1). The patients with surviving grafts were doing well, with normal kidney and pancreas function: serum creatinine = 0.89 +/- 0.15 mg/dL; fasting blood glucose = 79 +/- 16 mg/dL; HbA1c = 4.7 +/- 1.1%. The 1-year patient, kidney, and pancreas survival rates were 97.3%, 94.6%, and 83.8% and 5-year values, 91.7%, 89.2%, and 78.7%, respectively. In conclusion, these results are similar to the most recent UNOS/IPTR reports, leading us to consider our experience with SPKT very positive.

Adult↗
PubMed2006

Differential analysis of donor characteristics for pancreas and islet transplantation.

Suitable selection of donors is key to the success of human islet isolation and transplantation. Although several important donor-related factors have been identified previously, they needed to be confirmed in our setting. The aims of this study were: (1) to compare the characteristics of islet donors with those of pancreas donors (national transplant registry). (2) to compare the characteristics of islet donors resulting in a successful isolation in our facility with the characteristics of pancreas donors, and (3) to compare the characteristics of islet donors at this facility, whether or not isolation was successful, with donors elsewhere whose islets were transplanted and included in the Collaborative Islet Transplant Registry. The 35 islet isolations completed at our facility were analyzed for various characteristics. Significant differences were seen in donor age body mass index (BMI), and body weight between our islet donors and our pancreas donors (P < .001). These differences were maintained in the subgroup analysis corresponding to donors of successful isolations compared to pancreas donors (P < .01). Most successful isolations in our islet isolation facility were associated with donors of BMI >25. The percentage of successful isolation (>300,000 IEq) was higher among donors with a body weight >90 kg. We concluded that there was little overlap between the donor profiles for pancreas transplantation and for islet transplantation. More specific selection criteria relative to both BMI and body weight for islet donors may result in greater success of pancreas islet isolation and transplantation.

Adult↗
PubMed2005

Dorsal pancreas agenesis in retinoic acid-deficient Raldh2 mutant mice.

During embryogenesis, the pancreas arises from dorsal and ventral pancreatic protrusions from the primitive gut endoderm upon induction by different stimuli from neighboring mesodermal tissues. Recent studies have shown that Retinoic Acid (RA) signaling is essential for the development of the pancreas in non-mammalian vertebrates. To investigate whether RA regulates mouse pancreas development, we have studied the phenotype of mice with a targeted deletion in the retinaldehyde dehydrogenase 2 (Raldh2) gene, encoding the enzyme required to synthesize RA in the embryo. We show that Raldh2 is expressed in the dorsal pancreatic mesenchyme at the early stage of pancreas specification. RA-responding cells have been detected in pancreatic endodermal and mesenchymal cells. Raldh2-deficient mice do not develop a dorsal pancreatic bud. Mutant embryos lack Pdx 1 expression, an essential regulator of early pancreas development, in the dorsal but not the ventral endoderm. In contrast to Pdx 1-deficient mice, the early glucagon-expressing cells do not develop in Raldh2 knockout embryos. Shh expression is, as in the wild-type embryo, excluded from the dorsal endodermal region at the site where the dorsal bud is expected to form, indicating that the dorsal bud defect is not related to a mis-expression of Shh. Mesenchymal expression of the LIM homeodomain protein Isl 1, required for the formation of the dorsal mesenchyme, is altered in Raldh2--/-- embryos. The homeobox gene Hlxb9, which is essential for the initiation of the pancreatic program in the dorsal foregut endoderm, is still expressed in Raldh2--/-- dorsal epithelium but the number of HB9-expressing cells is severely reduced. Maternal supplementation of RA rescues early dorsal pancreas development and restores endodermal Pdx 1 and mesenchymal Isl 1 expression as well as endocrine cell differentiation. These findings suggest that RA signaling is important for the proper differentiation of the dorsal mesenchyme and development of the dorsal endoderm. We conclude that RA synthesized in the mesenchyme is specifically required for the normal development of the dorsal pancreatic endoderm at a stage preceding Pdx 1 function.

Aldehyde Oxidoreductases↗
PubMed1998

Activation of the urokinase plasminogen activator/urokinase plasminogen activator receptor system and redistribution of E-cadherin are associated with hepatocyte growth factor-induced motility of pancreas tumor cells overexpressing Met.

Because hepatocyte growth factor (HGF) is a potent mitogen for normal human exocrine pancreas cells (NPCs) in vitro, we have analyzed the expression of HGF and its receptor, Met, in NPC and pancreas cancer cells and studied its effects in vitro. Using immunohistochemistry, Northern blotting, and reverse transcription-polymerase chain reaction, we examined the expression of HGF and Met in normal pancreas and pancreas cancer. Scatter assays, wound-healing assays, and migration through transwell filters were used to study HGF-stimulated motility of IMIM-PC-2 cancer cells. In tumors, HGF is mainly detected in stromal cells, whereas Met is overexpressed in cancer cells with an unpolarized distribution. In vitro, HGF stimulates motogenesis but not proliferation in cancer cells. Cell motility is accompanied by a rapid decrease in the cytoskeleton-bound E-cadherin, an acceleration of cellular adhesion to the substrate, an up-regulation of urokinase plasminogen activator (u-PA) RNA and protein, and a change in the solubility and proteolysis of the u-PA receptor. Cell motility is significantly reduced by inhibitors of u-PA proteolytic activity such as antibodies neutralizing u-PA activity, plasminogen activator inhibitor 1, and amiloride. These results show that a paracrine loop of HGF activation may participate in the development or progression of pancreas cancer. In vitro, the HGF-stimulated motogenesis of pancreas cancer cells involves the activation of the u-PA/u-PA receptor proteolytic system, suggesting its role in the invasive stages of tumor progression.

Antibodies↗
PubMed1993

Sequential evaluation of islet cell responses to glucose in the transplanted pancreas in humans.

We evaluated the hormonal and metabolic responses of denervated pancreas allografts in nine volunteers 3 to 12 months after the transplant (initial) and again 1 year later (follow-up). Eight of the patients received simultaneous pancreas-kidney transplants. The glucose clamp technique was used to create a square wave of hyperglycemia 5.5 mmol/L above the basal glucose level for 2 hours. A biphasic insulin response was evident in each subject, both initially and at follow-up. The initial plasma insulin response was fourfold higher in patients with pancreas-kidney transplants than in normal volunteers. However, the plasma insulin response of the patients with pancreas-kidney transplants at the follow-up study was more similar to that of the normal controls. The plasma glucagon levels were elevated in follow-up clamp studies. Hepatic glucose production and glucose disposal were similar in both studies. At the follow-up examination only, GLUT4, the major insulin-sensitive glucose transporter, was measured in muscle homogenates by immunoblotting. GLUT4 levels in the patients with pancreas-kidney transplants were only 55% as abundant as in normal volunteers. This may be due, in part, to immunosuppressive therapy or to persistent, albeit reduced, levels of hyperinsulinemia even 2 years after transplantation. We concluded that, despite systemic drainage of the pancreas and immunosuppressive therapy, pancreatic insulin secretion, peripheral insulin levels, and muscle insulin responsiveness are restored toward normal levels approximately 2 years after the transplant.

Adult↗
PubMed1997

Molecular insights into the development of the pancreas.

There is general agreement that the exocrine pancreas derives from the endoderm of the embryonic foregut. The cellular origin of the endocrine pancreas has been debated for a long time. A hypothesis existed that the endocrine cells of the pancreas originated from the neural crest of the embryo. The recent application of microdissection of the mouse embryo and an exquisitely sensitive polymerase chain reaction assay (PCR) indicates that both the exocrine and endocrine cells of the pancreas develop from the endoderm of the foregut as evidenced by the expression of genes responsible for acinar enzymes and islet hormones in the foregut at the site where the future pancreatic diverticulum would form. Furthermore, the mesenchyme surrounding the primitive endoderm cells from which the pancreas would form exerts significant regulation of differentiation of the pancreas. In culture or in vivo explants, these endoderm cells differentiate only into islet cells in the absence of mesenchyme. On the other hand, when these cells are cultured in vitro with mesenchyme, they differentiate to form not only islets but also ducts and acini.

Animals↗
PubMed1998

Effect of hydrogen peroxide on permeability of the main pancreatic duct and morphology of the pancreas.

BACKGROUND: The direct effect of free oxygen radicals, if any, on the morphology of the pancreas has never been studied in vivo. This study was designed to evaluate the effects of hydrogen peroxide (H2O2) on permeability of the main pancreatic duct (MPD) and morphology of pancreas in cats when administered intraductally or intraarterially. METHODS: Thirty-six mongrel cats were randomly allocated into three groups, and all groups were divided into two subgroups. In group I and III, MPD was perfused with either standard perfusate (group IA and IIIA) or H2O2 at a concentration of 150 microM (group IB and IIIB) for 3 hours. In group II, the splenic artery was infused either with 0.9% sodium chloride (group IIA) or H2O2 (group IIB) for 3 hours. After 3 hours, in group I and II, MPD was perfused with 99mTc labelled dextran, and the percentage of the dextran permeated from the MPD into the portal vein was calculated for the evaluation of the pancreatic duct permeability. Then, tissue samples were obtained for the examination of early histopathological changes in pancreas. In group III, following ductal perfusion studies, the cats were allowed to recover. After 24 hours animals were killed, and samples were taken for the examination of late histological changes in pancreas. In all groups, an inflammatory score was created for each animal based on the pathological changes in pancreas: edema, leukocyte infiltration, parenchymal necrosis, and hemorrhage. RESULTS: Group I: All cats developed acute edematous pancreatitis with significantly higher inflammatory scores than controls (P < 0.01). Desquamation of the single layer of columnar epithelium that normally lined the duct and leukocyte infiltration around the MPD duct were found. Pancreatic duct permeability was found to be increased significantly (P < 0.01). Group II: There were no statistical differences in inflammatory scores and pancreatic duct permeability between experimental and control groups (P > 0.05). Group III: All animals developed gross acute edematous pancreatitis after 3 hours of intraductal H2O2 perfusion. Histopathological changes at 24 hours were much more pronounced in group IIIB than in group IIIA including focal necrosis and hydropic degeneration of acinar cells. CONCLUSION: This study has shown that intraductal H2O2 perfusion induced acute edematous pancreatitis with marked histopathological changes and increased pancreatic duct permeability in cats. Intraarterial H2O2 infusion, however, has no effect on the permeability of the MPD and morphology of pancreas in our model.

Acute Disease↗
PubMed2000

A transgenic mouse expressing human CYP1A2 in the pancreas.

A transgenic mouse line expressing the human cytochrome P450 CYP1A2 in the pancreas under the control of the mouse elastase promoter was established. The expression of CYP1A2 was specific to the transgenic pancreas and was not found in the control wild-type mouse pancreas. The level of CYP1A2 expressed in pancreatic microsomes from transgenic mice was comparable to that of the endogenously expressed CYP1A2 protein in the liver, as judged by western blotting analyses. Estrone metabolism was used to determine the activity of CYP1A2 expressed in the pancreas of the transgenic mouse. The transgenic pancreas exhibited almost one-third to one-half of the activity of wild-type or CYP1A2 transgenic mouse liver, whereas the wild-type pancreas demonstrated no activity. The addition of NADPH-cytochrome P450 oxidoreductase to the reaction mixture containing pancreatic microsomes from the transgenic mice did not increase the estrone metabolism activity significantly. This transgenic mouse line provides another useful tool to study human CYP1A2 and its relation to chemical toxicity and carcinogenesis.

Animals↗
PubMed2003

The Onecut transcription factor HNF-6 (OC-1) is required for timely specification of the pancreas and acts upstream of Pdx-1 in the specification cascade.

The pancreas derives from cells in the ventral and dorsal foregut endoderm that express the transcription factor Pdx-1. These specified cells give rise to the precursors of the endocrine, ductal, and exocrine pancreatic cells. The identification of transcription factors that regulate the onset of Pdx-1 expression is therefore essential to understand pancreas development. No such factor that acts both in the ventral and in the dorsal endoderm is known. We showed previously that the Onecut transcription factor HNF-6 promotes differentiation of the endocrine cell precursors in which it stimulates expression of the proendocrine gene Ngn-3. By analyzing the phenotype of HNF-6 null mice, we now demonstrate that HNF-6 also controls an earlier step in pancreas development. Indeed, the pancreas of Hnf6(-/-) mice was hypoplastic. This did not result from decreased proliferation or from increased apoptosis, but from retarded pancreatic specification of endodermal cells. The onset of Pdx-1 expression was delayed both in the ventral and in the dorsal endoderm, leading to a reduction in the number of endodermal cells expressing Pdx-1 at the time of pancreatic budding. In normal embryos, HNF-6 was detected in the endoderm prior to the expression of Pdx-1. Moreover, HNF-6 could directly stimulate the Pdx1 promoter. Our data therefore identify HNF-6 as the first factor known to control Pdx-1 expression both in the ventral and in the dorsal endoderm. We conclude that HNF-6 controls the timing of pancreas specification and that HNF-6 acts upstream of Pdx-1 in this developmental process. Together with the known role of HNF-6 in pancreatic endocrine cell differentiation, our data point to HNF-6 as a key regulator of pancreas development.

Amino Acid Sequence↗
PubMed1990

Pathologic observations of intrahepatic peribiliary glands in 1000 consecutive autopsy livers. Heterotopic pancreas in the liver.

One thousand consecutively autopsied livers were examined for intrahepatic heterotopic pancreas. Heterotopic pancreas in the liver was found in 41 (4.1%) of the 1000 livers. It occurred with nearly equal frequency in "normal" livers and variously diseased livers. Histologically, heterotopic pancreas was situated exclusively in the large- and medium-sized portal tracts, and its size ranged from 250-900 microns in diameter. It was intermingled with intrahepatic peribiliary glands and appeared to communicate with bile duct lumina. Heterotopic pancreas consisted of three cell types: acinar cells with eosinophilic zymogenlike granules, clear cells resembling centriacinar cells, and ductular elements. Langerhans' islets were not found in any cases. Immunohistochemically, constituent cells of heterotopic pancreas contained pancreatic alpha-amylase and trypsin but lacked argentaffin and argyrophilic cells as well as insulin-, glucagon-, and somatostatin-immunoreactive endocrine cells. Ultrastructurally, acinar cells contained many dense granules regarded as zymogen granules. It is indicated that intrahepatic heterotopic pancreas occurs in large portal tracts. It may modify hepatic bile by secreting pancreatic enzymes into intrahepatic bile duct lumina.

Adolescent↗
PubMed1998

Dynamic imaging of the pancreas using real-time endoscopic ultrasonography with secretin stimulation.

BACKGROUND: Obstructive disorders of the pancreas, including strictures, stones, sphincter of Oddi dysfunction, and pancreas divisum, are diagnostic and therapeutic challenges. Conventional extracorporeal ultrasound with secretin stimulation has been used as a noninvasive study to detect obstruction and predict outcome of therapy. Inconsistent results have been obtained because of the inherent limitations of standard ultrasonography. The aim of this study was to evaluate the behavior of the main pancreatic duct by endoscopic ultrasonography during secretin stimulation and to diagnose obstructive disorders of the pancreas. METHODS: Secretin-stimulated endoscopic ultrasound (SSEUS, 1 IU/kg secretin) was performed in 20 control subjects (no pancreatic or biliary disease), 40 patients with symptomatic chronic pancreatitis, 40 patients with symptomatic pancreas divisum, 20 patients with suspected sphincter of Oddi dysfunction, and 20 patients with suspected occlusion of pancreatic duct stents. Ductal diameter was measured by endoscopic ultrasonography at baseline and at 1-minute intervals, after administration of secretin, for 15 minutes. A result was determined to be abnormal when a 1 mm or greater dilation of the pancreatic duct was observed from baseline after secretin administration. RESULTS: Of the 40 patients with symptomatic chronic pancreatitis, SSEUS correctly predicted obstructive pathology (stones, strictures) in 12 of 13 patients (92%). Of the 40 patients with symptomatic pancreas divisum, 22 underwent stent therapy (16 of 22 with resolution of symptoms). SSEUS accurately predicted response to stent therapy in 13 patients (81%). Seven of twenty patients with suspected sphincter of Oddi dysfunction had abnormal sphincter manometry. SSEUS accurately predicted sphincter dysfunction in only 4 of 7 patients (57%). Finally, 20 patients with suspected occlusion of pancreatic duct stents were studied. Of the 14 stent occlusions confirmed at ERCP, SSEUS correctly predicted premature occlusion in 12 patients (86%). CONCLUSIONS: SSEUS appears to be a useful diagnostic modality in the evaluation of patients with suspected obstructive disorders of the pancreas and it can predict which patients may respond to endoscopic therapy.

Case-Control Studies↗