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PubMed1996

Mechanism of impaired glucose-potentiated insulin secretion in diabetic 90% pancreatectomy rats. Study using glucagonlike peptide-1 (7-37).

Chronic hyperglycemia causes a near-total disappearance of glucose-induced insulin secretion. To determine if glucose potentiation of nonglucose secretagogues is impaired, insulin responses to 10(-9) M glucagonlike peptide-1 (GLP-1) (7-37) were measured at 2.8, 8.3, and 16.7 mM glucose with the in vitro perfused pancreas in rats 4-6 wk after 90% pancreatectomy (Px) and sham-operated controls. In the controls, insulin output to GLP-1 was > 100-fold greater at 16.7 mM glucose versus 2.8 mM glucose. In contrast, the increase was less than threefold in Px, reaching an insulin response at 16.7 mM glucose that was 10 +/- 2% of the controls, well below the predicted 35-40% fractional beta-cell mass in these rats. Px and control rats then underwent a 40-h fast followed by pancreas perfusion using a protocol of 20 min at 16.7 mM glucose followed by 15 min at 16.7 mM glucose/10(-9) M GLP-1. In control rats, fasting suppressed insulin release to high glucose (by 90%) and to GLP-1 (by 60%) without changing the pancreatic insulin content. In contrast, in Px the insulin response to GLP-1 tripled in association with a threefold increase of the insulin content, both now being twice normal when stratified for the fractional beta-cell mass. The mechanism of the increased pancreas insulin content was investigated by assessing islet glucose metabolism and proinsulin biosynthesis. In controls with fasting, both fell 30-50%. In Px, the degree of suppression with fasting was similar, but the attained levels both exceeded those of the controls because of higher baseline (nonfasted) values. In summary, chronic hyperglycemia is associated with a fasting-induced paradoxical increase in glucose-potentiated insulin secretion. In Px rats, the mechanism is an increase in the beta-cell insulin stores, which suggests a causative role for a lowered beta-cell insulin content in the impaired glucose-potentiation of insulin secretion.

Animals↗

PubMed1989

Compensatory adaption to partial pancreatectomy in the rat.

The aim of the present study was to determine if compensatory adaptions in pancreatic B-cell mass and/or function occur when B-cell mass is reduced without altering glucose tolerance. Islet mass and insulin secretory responses (both in vivo and in vitro) were assessed 19 days after a 40% pancreatectomy (Px) in 5-week-old rats. Plasma glucose and insulin values were unchanged by the 40% Px, both in the fed state and after ip glucose. Also, glucose potentiation of arginine-induced insulin secretion was fully intact when assessed with the in vitro perfused pancreas. Islet mass, assessed using point-counting morphometrics, was 84% of the sham value, not the expected 60%. In contrast, there was no compensatory change in acinar tissue, as judged by pancreatic weight. To determine if the insulin secretory reserve capacity was reduced after the 40% Px, dexamethasone was given on days 14-18. On day 18, the Px rats were midly hyperglycemic, but by the next day, glucose tolerance post-ip glucose was normal, and the insulin responses to the ip glucose in vivo and arginine in vitro were identical in the dexamethasone-treated Px and sham rats. These data show no discernible change in quantitative or qualitative B-cell secretory responses after 40% Px. A key mechanism contributing to this maintenance of normal function was regrowth of much of the excised islet tissue.

Adaptation, Physiological↗

PubMed1990

Glucose turnover and recycling in diabetes secondary to total pancreatectomy: effect of glucagon infusion.

This study was designed to evaluate whether chronic deficiency of pancreatic glucagon in patients with diabetes secondary to total pancreatectomy (PX) is responsible for the commonly observed increase in blood concentrations of gluconeogenic precursors (alanine, lactate, and pyruvate). Seven PX patients were studied on two different occasions: 1) after an overnight insulin infusion (0.15 mU/kg.min) and 2) after an overnight insulin/glucagon infusion (2 ng/kg.min). Five type 1 diabetic individuals were also studied after a similar overnight insulin infusion. In the morning of each study day, [6-3H]glucose and [1-14C]glucose were rapidly injected for determination of total glucose turnover rate [( 6-3H]glucose) and glucose recycling (difference between [6-3H]glucose and [1-14C]glucose turnover rate). Basal concentrations of hormones, glucose, and intermediary metabolites were measured. After overnight insulin infusion, plasma glucose concentration (3.8 +/- 0.4 vs. 6.8 +/- 1.4 mmol/L), turnover rate (8.4 +/- 1.0 vs. 13.7 +/- 1.9 mumol/kg.min), and percent glucose recycling (5.6 +/- 3.9% vs. 19.0 +/- 3.8%) were significantly lower in PX patients than in type 1 diabetic individuals (P less than 0.05-0.01). On the contrary, blood alanine (459 +/- 93 vs. 263 +/- 28 mumol/L), lactate (1157 +/- 109 vs. 818 +/- 116 mumol/L), and pyruvate (71 +/- 8 vs. 42 +/- 3 mumol/L) were significantly higher than those values in type 1 diabetic patients (P less than 0.05-0.01). Insulin/glucagon infusion increased plasma glucose concentration (8.7 +/- 1.5 mmol/L), total turnover (18.1 +/- 1.7 mumol/kg.min), and percent recycling (20.4 +/- 6.6%) to values similar to those in type 1 diabetic subjects. The change in glucose metabolism was associated with a significant drop in blood concentrations of alanine (179 +/- 24 mumol/L), lactate (611 +/- 25 mumol/L), and pyruvate (30 +/- 3 mumol/L; all P less than 0.05-0.01 vs. insulin infusion alone). In PX patients, the glucose turnover rate was inversely correlated with blood concentrations of both alanine (r = 0.67) and lactate (r = 0.71; P less than 0.01). In conclusion, chronic deficiency of pancreatic glucagon in PX patients 1) is associated with a decreased rate of glucose turnover, 2) causes a marked impairment in glucose recycling (an index of the activity of hepatic gluconeogenesis), and 3) increases blood concentrations of alanine, lactate, and pyruvate. All abnormalities are reversed by glucagon.

Adult↗

PubMed2000

Persistent hyperinsulinemic hypoglycemia of infancy: long-term outcome following subtotal pancreatectomy.

BACKGROUND: Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is the most common cause of persistent hypoglycemia in infants. The current standard treatment is subtotal pancreatectomy (Px). However, the long-term outcome following surgery needs further attention. METHODS: We analyzed 10 children (7 M, 3 F) with PHHI who underwent partial (65-80%) and subtotal (81-95%) Px. Follow-up ranged from 2 to 9.4 yr (mean = 4.2 yr). We divided them into 2 groups based upon the age at onset of hypoglycemia: early (< 1 mo) and late (> or = 1 mo). RESULTS: The seven patients in the early-onset group underwent 85-95% Px between ages of 18 d and 3 mo. Three of them initially treated by 85-90% Px had persistent hypoglycemia postoperatively. Two out of three required a 2nd operation with 95% Px for controlling hypoglycemia, though both still had persistent hypoglycemia and required medication to control blood glucose. The remaining four had 95% Px and had maintained euglycemia postoperatively. One patient developed diabetes 6 yr after surgery. Six of seven patients had delayed development and subnormal IQ. Three patients of the late-onset group (3 mo, 6 mo and 4 yr) underwent partial Px (80%, 65% and 65%, respectively) and maintained euglycemia postoperatively. Despite 65% Px, one developed diabetes 3 yr after surgery. CONCLUSIONS: These results suggest that children with early-onset hypoglycemia have more severe hyperinsulinism than those with late-onset hypoglycemia. The former require 95% Px for maintaining euglycemia, but long-term complications with diabetes may be common. In contrast, the latter require lower percentage Px which may reduce the incidence of diabetes in the future.

Age Factors↗

PubMed2003

Auto-islet transplantation after pancreatectomy.

Chronic pancreatitis (CP) is an inflammatory disease that causes progressive and irreversible structural changes to the pancreas, resulting in permanent impairment of both endocrine and exocrine functions. In advanced cases of CP, pain can be relieved only with pancreatic resection. However, even partial resection of the pancreas in this setting may cause diabetes. Furthermore, postsurgical diabetes (PSD) always occurs after total or near-total pancreatectomy, which is commonly performed for CP. Auto transplantation of pancreatic islets into the portal vein after pancreatic resection can prevent PSD. The results of this strategy, which are already encouraging, are likely to improve in the near future because of significant progress in the isolation and preservation of pancreatic islets. This review discusses the current status and future prospects for auto-islet transplantation after pancreatic resection for CP.

Diabetes Mellitus↗

PubMed2005

[Laparoscopic distal pancreatectomy for pancreatic cystadenomas].

BACKGROUND: Cystic neoplasms are an uncommon group among pancreatic tumors. These lesions are seen more frequently in recent surgical practice, probably because of advances in diagnostic and surgical techniques. Total tumor resection provides the best chance of cure and may remove the risk of malignant transformation of the cystadenomas, particularly of the mucinous type. Minimally invasive techniques have been revolutionary and provide clinical evidence of decreased morbidity and comparable efficacy to traditional, open surgery. However, laparoscopic pancreatic resection is not an established treatment for tumors of the pancreas. AIM: The authors present their initial experience with laparoscopic distal pancreatectomy for pancreatic cystadenomas. MATERIAL AND METHODS: Three female patients (mean age, 55 years) underwent laparoscopic pancreatic resection between September 2001 and December 2003. RESULTS: Laparoscopic pancreatic resection was successfully performed in all patients. Operative time varied between 4 and 6 hours. Intraoperative bleeding was minimal. Due to a thick pancreas, the application of vascular endoscopic stapler was difficult in one patient. Two patients presented postoperative pancreatic leakage with spontaneous resolution. CONCLUSIONS: Resection of the pancreas can be safely performed via the laparoscopic approach with all the potential benefits to the patients of minimally invasive surgery.

Aged↗

PubMed1985

Effect of islet transplantation on diabetes mellitus after subtotal pancreatectomy in rat: a quantitative analysis of islet tissue.

A reproducible model of diabetic state was produced by resecting more than 90% of the pancreatic tissue in Wistar strain male rats. Five rats with diabetic state after the resection received islet transplantation into the liver through the portal vein. All these five rats showed normoglycemia one week after the injection and it lasted about six months. A morphometric analysis using 1190 serial sections of the control rat pancreas showed that the islet distribution accorded satisfactorily with Weibull and gamma distribution, when an islet was regarded as a sphere in the three dimensional space. The estimated value of radius and number of the islets was 0.0155 mm and 131.2/mm3, respectively, whereas volume fractions of the islet tissue in the splenic and gastric segments, and parabiliary and duodenal segments were estimated at 1.45 and 0.98%, respectively. The mean half of the largest diameter of the isolated islets under dissecting microscope reached to 0.080 mm and 500 isolated islets account for about 14% of volume fraction in a whole pancreas. As the remnant pancreas possibly had approximately five percent of islet volume, the transplanted animal contained about 19% of islet volume as compared to the control animal. It could be concluded that transplantation of 500 islets controlled diabetes in the rat with subtotal pancreatectomy. But the transplanted rats eventually became diabetic about six months after the transplantation possibly because of insufficient volume of implanted islets.

Animals↗

PubMed1976

Effects of sub-total gastro-intestinal pancreatectomy of the rat foetus.

Sub-total pancreatectomy in utero was performed in 18-day-old rat foetuses. Pancreatectomized, sham-operated and control foetuses were collected 3 days later and body weight, glucose and insulin levels in blood, and glycogen content and glucose-6-phosphatase (G-6-Pase) activity of the liver were determined. Pancreatectomized foetuses showed only very small pancreatic remnants (less than or equal to 1 mg) and accordingly their insulin levels were much lower (four to five times) than those of sham-operated or control foetuses; their blood glucose levels were slightly increased and liver glycogen content and G-6-Pase activity were slightly reduced; their body weights were also reduced. These results are discussed in relation to other relevant data in the literature. They afford direct experimental evidence of the endogenous origin of insulin in the foetal blood. It is suggested that during the last days of intra-uterine life insulin merely completes the action of the glucocorticoids on glycogen storage in rat foetal liver and probably contributes to foetal body growth. Its relative ineffectiveness on the foetal blood glucose level is not explained. As pancreatectomized foetuses develop sub-normal liver G-6-Pase activity, glucagon is probably not responsible for the increase in this activity occurring during normal development before birth.

Animals↗

PubMed2002

Dual role of the tyrosine kinase GTK and the adaptor protein SHB in beta-cell growth: enhanced beta-cell replication after 60% pancreatectomy and increased sensitivity to streptozotocin.

Transgenic CBA mice expressing either the tyrosine kinase GTK (gut tyrosine kinase) or the adaptor protein SHB (Src homology 2 protein of beta-cells) under the control of the rat insulin promoter exhibited an increased beta-cell mass, but also elevated cytokine-induced islet cell death compared with control mice. To further investigate the importance of GTK and SHB for beta-cell death and proliferation, these mice were subjected to a 60% partial pancreatectomy (Px) or a sham-operation and beta-cell replication was determined by autoradiographic detection of [(3)H]thymidine incorporation into islet cells positively stained for insulin. The Px-operated control mice exhibited a moderate and insignificant increase in beta-cell replication 4 days after Px compared with the sham-operated mice (0.27+/-0.08% vs 0.08+/-0.02%). In contrast, the Px-induced beta-cell proliferation was significantly increased in both the GTK- and SHB-transgenic mice compared with the corresponding sham-treated animals (0.64+/-0.12% vs 0.11+/-0.04% and 0.44+/-0.11% vs 0.09+/-0.04% respectively). This effect was dependent on intracellular signal transduction pathways activated or enhanced by GTK and SHB overexpression, since the proliferation of acinar cells, located in the vicinity of the islets, was equal in the transgenic and control mice. GTK- and SHB-transgenic mice, treated with a sub-diabetogenic dose of the beta-cell toxin streptozotocin (STZ) on day 0 and subjected to a glucose tolerance test on day 3, exhibited an impaired glucose tolerance in comparison with the STZ-treated control mice. Pretreatment with STZ blunted the regenerative response to Px in the transgenic mice. Furthermore, the SHB-transgenic islets were significantly more damaged with respect to beta-cell loss, compared with the islets of the control mice. Previous and present data suggest a dual role of GTK and SHB for beta-cell growth: whereas these proteins increase the beta-cell mass and induce beta-cell proliferation after 60% Px, SHB and GTK also enhance beta-cell death under certain stressful conditions.

Animals↗

PubMed2006

Regulation of pancreatic beta-cell regeneration in the normoglycemic 60% partial-pancreatectomy mouse.

beta-Cell mass is determined by a dynamic balance of proliferation, neogenesis, and apoptosis. The precise mechanisms underlying compensatory beta-cell mass (BCM) homeostasis are not fully understood. To evaluate the processes that maintain normoglycemia and regulate BCM during pancreatic regeneration, C57BL/6 mice were analyzed for 15 days following 60% partial pancreatectomy (Px). BCM increased in Px mice from 2 days onwards and was approximately 68% of the shams by 15 days, partly due to enhanced beta-cell proliferation. A transient approximately 2.8-fold increase in the prevalence of beta-cell clusters/small islets at 2 days post-Px contributed substantially to BCM augmentation, followed by an increase in the number of larger islets at 15 days. To evaluate the signaling mechanisms that may regulate this compensatory growth, we examined key intermediates of the insulin signaling pathway. We found insulin receptor substrate (IRS)2 and enhanced-activated Akt immunoreactivity in islets and ducts that correlated with increased pancreatic duodenal homeobox (PDX)1 expression. In contrast, forkhead box O1 expression was decreased in islets but increased in ducts, suggesting distinct PDX1 regulatory mechanisms in these tissues. Px animals acutely administered insulin exhibited further enhancement in insulin signaling activity. These data suggest that the IRS2-Akt pathway mediates compensatory beta-cell growth by activating beta-cell proliferation with an increase in the number of beta-cell clusters/small islets.

Actins↗

PubMed1988

Discordance of exocrine and endocrine growth after 90% pancreatectomy in rats.

As we have previously shown, by 8 wk after 90% pancreatectomy (PX) in the rat, there is considerable regeneration of both exocrine and endocrine pancreas. In this study we examine the growth of both the exocrine and endocrine tissue 3, 7, 14, and 21 days after PX by following the pancreatic content of insulin, glucagon, and amylase as well as the mitotic indices for exocrine and islet beta-cells. By 7 days the pancreatic remnant weighed more than the anatomically equivalent tissue in the sham, the remnant equivalent. The growth of the exocrine tissue and the endocrine beta-cells was discordant during these initial weeks after PX, as shown by the mitotic index. The mitotic index, measured as accumulated mitotic figures after a 4-h colchicine treatment, for both the exocrine and beta-cells in the sham animals was low and unchanging at the different time points (approximately 0.5%). At 3 and 7 days after PX, both the exocrine and beta-cells had mitotic indices three- to fourfold that of the sham animals. At 14 days after PX, the exocrine cells had a slightly, albeit significantly, elevated mitotic index, whereas that of the beta-cells was still double that of the shams. By 21 days there was no difference in mitotic index for exocrine tissue, but the beta-cells on the PX animals had a mitotic index still double that of the shams. Another index of growth, the cell birthrate, was estimated at 7 days from the slope of regression lines of the mitotic frequency accumulated 1, 2, 3, and 4 h after colchicine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Reduced insulin, GLUT2, and IDX-1 in beta-cells after partial pancreatectomy.

Reduction of GLUT2 is associated with loss of glucose-induced insulin secretion in genetic and chemical diabetes and in transplanted islets exposed to chronic hyperglycemia. To examine the mechanisms for this loss of GLUT2 in normal islets exposed to hyperglycemia, we performed studies on Sprague Dawley rats 4 weeks after a 90% partial pancreatectomy (Px), a well-characterized model of hyperglycemia. GLUT2 immunofluorescence in the beta-cell of Px rats was greatly reduced. Western blot analysis of homogenates of isolated Px islets also showed a reduction in GLUT2 protein; densitometry measurements were 36 +/- 3% of values from islets of sham-operated controls. Insulin protein levels were decreased to a similar extent. Islet GLUT2 and insulin mRNA were measured with quantitative reverse transcriptase-polymerase chain reaction. The level of GLUT2 mRNA from Px islets was 24 +/- 4% of that of islets from sham-operated controls; similar results were obtained for insulin. Because both these beta-cell-specific messages were reduced, we analyzed the Px islets for the pancreas-duodenum-specific transcription factor IDX-1(IPF-1, STF-1, PDX-1) protein. It was markedly reduced (approximately 80%) in islets from the Px rats. These data suggest that 1) the loss of GLUT2 protein associated with hyperglycemia is at least partially explained by reduced levels of the GLUT2 gene transcripts; 2) the reduction of beta-cell insulin content during chronic hyperglycemia may not be completely due to degranulation (reduced levels of gene transcripts may play a role); and 3) the reduction in the transcription factor IDX-1 raises the possibility that dysregulation of transcription factors may contribute to the abnormal beta-cell function found in states of chronic hyperglycemia.

Animals↗

PubMed2002

Vascularized islet cell transplantation in miniature Swine: islet-kidney allografts correct the diabetic hyperglycemia induced by total pancreatectomy.

We have previously reported the preparation of vascularized islet-kidneys (IKs) by transplantation of islets under the autologous kidney capsule. Here, we compare the efficacy of transplanting vascularized versus nonvascularized islets into diabetic allogeneic swine recipients. In the vascularized islet transplantation (5,000 islet equivalents [IE]/kg), recipients received minor-mismatched (n = 4) or fully-mismatched (n = 2) IKs after pancreatectomy, with a 12-day course of cyclosporine A (CyA) or FK506, respectively. For the nonvascularized islet transplantation (7,000 IE/kg), three recipients received minor-mismatched islets alone and two recipients received minor-mismatched donor islets placed in a donor kidney on the day of transplantation. All recipients of nonvascularized islets were treated with a 12-day course of CyA. With vascularized islet transplantation, pancreatectomized recipients were markedly hyperglycemic pretransplant (fasting blood glucose >300 mg/dl). After composite IK transplantation, all recipients developed and maintained normoglycemia (<120 mg/dl) and stable renal function indefinitely (>3 months), and insulin therapy was not required. Major histocompatibility complex-mismatched recipients demonstrated in vitro donor-specific unresponsiveness. In contrast, recipients of nonvascularized islets remained hyperglycemic. In conclusion, IK allografts cured surgically induced diabetes across allogeneic barriers, whereas nonvascularized islet transplants did not. These data indicate that prevascularization of islet allografts is crucial for their subsequent engraftment and that composite IKs may provide a strategy for successful islet transplantation.

Animals↗

PubMed2003

Role of endogenous glucagon-like peptide-1 in islet regeneration after partial pancreatectomy.

A reduction in beta-cell mass is an important causative factor in type 1 and type 2 diabetes. Glucagon-like peptide-1 (GLP-1) and the long-acting agonist exendin 4 (Ex-4) expand beta-cell mass by stimulating neogenesis and proliferation. In the partial pancreatectomy (Ppx) model, exogenous Ex-4 promotes islet regeneration, leading to sustained improvement in glucose tolerance. In this study, we investigate the potential role of endogenous GLP-1 in islet growth. We examined beta-cell mass regeneration after 70% Ppx in mice receiving the GLP-1 antagonist Ex9-39 and in GLP-1R(-/-) mice. In Ex9-39-treated sham-operated mice, persistent fasting hyperglycemia was observed, but beta-cell mass was not diminished. In pancreatectomized mice, persistent glucose intolerance was noted, but this was not further exacerbated by Ex9-39. Accordingly, beta-cell mass recovery of Ppx mice was not impaired by Ex9-39. In contrast, GLP-1R(-/-) CD1 mice showed worse glucose intolerance after Ppx compared with wild-type CD1 Ppx mice, and this correlated with a significant defect in beta-cell mass regeneration. The recovery of beta-cell mass differed markedly in the BALB/c and CD1 control mice, indicating a significant role of genetic background in the regulation of beta-cell mass. These studies point to a role for endogenous GLP-1 in beta-cell regeneration after Ppx in mice.

Animals↗

PubMed1998

Nonfunctioning islet cell carcinoma--a twenty-one years survival case after distal pancreatectomy.

A case of nonfunctioning islet cell carcinoma was reported. A 40-year-old woman was admitted with epigastralgia. Abdominal angiography and other diagnostic modalities suggested pancreatic malignancy. After distal pancreatectomy, histopathological study revealed her pancreatic tumor to be a nonfunctioning islet cell carcinoma. Fourteen years later, postoperative computed tomographic examination (CT) detected the recurrence of para-aortic lymph node metastases. Five years later, distal gastrectomy was performed to control bleeding from a gastric ulcer. Twenty-one years after the original operation, she died because of underlying metastatic carcinoma. In this case, slow growth and a low grade malignancy were characteristic. Operative removal of the tumor would be the treatment of choice even if metastatic lesions existed.

Adenoma, Islet Cell↗

PubMed1980

The effect of glucose on plasma immunoreactive secretin in normal man and after gastrectomy or pancreatectomy.

Oral intake of glucose increased the peripheral plasma immunoreactive secretin (IRS) concentration in patients after total pancreatectomy with duodenectomy (p < 0.05) and in patients after total gastrectomy (p < 0.01). In young healthy volunteers and in patients after partial gastrectomy, no effect on IRS was observed. Intravenous glucose reduced the IRS concentration in pancreatectomized patients (p < 0.05), whereas IRS was only reduced in young healthy volunteers when intravenous glucose was followed by oral glucose after an interval of 10 min (p < 0.025). The abnormal IRS release in pancreatectomized patients and in patients after total gastrectomy might be due to rapid intestinal passage and/or increased splanchnic blood flow induced by hypertonic glucose. A third possibility is that a glucose-induced increase in bile flow might release IRS.

Administration, Oral↗

PubMed1982

The effect of early pancreatectomy and peritoneal lavage on the development of experimental haemorrhagic pancreatitis in pigs.

Forty-seven piglets were operated on; haemorrhagic pancreatitis was induced in 42 of them. The effects of pancreatic resection and peritoneal lavage on the development of the disease were compared. Since the pancreatic phospholipase A2 value has been shown to be important in the pathophysiology of the disease, the effect of pancreatic resection on the enzyme serum activities was studied. Early pancreatic resection and early peritoneal lavage were equally effective in reducing the mortality of the animals. When the pancreatic resection was performed later, most of the animals died. The difference in mortality between the groups was statistically significant (p less than 0.01). In the animals with late pancreatectomy the high serum phospholipase A2 activities fell to normal levels within a few hours after the operation. This strongly suggests that the enzyme is of pancreatic origin.

Animals↗

PubMedDate not supplied

Intra-operative color Doppler ultrasonography for assessing splenic blood supply during spleen-preserving distal pancreatectomy: a case report.

A 67 year-old Japanese woman presented with a cystic tumorous lesion, measuring 5 cm in diameter, in the tail of the pancreas. She underwent a spleen-preserving distal pancreatectomy (SPDP), in which the splenic artery and vein were divided because they were involved in scar formation around the lesion. Intra-operative color Doppler ultrasonography (CDUS) confirmed that splenic circulation via collaterals (short gastric and left gastroepiploic vessels) was preserved throughout the salvaged spleen. Histology of the resected specimen showed localized pancreatitis with a pseudocyst without neoplastic tissue. The patient's post-operative course was uneventful with no evidence of splenic failure and she was discharged 20 days after the operation. A literature review suggests that SPDP without preserving the splenic artery and vein may result in failure of the preserved spleen due to inadvertent injury to the remaining collaterals. Based on the experience of our case, we think that intra-operative CDUS is useful for assessing splenic circulation after SPDP with division of the splenic artery and vein.

Aged↗