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PubMed1996

Delayed endocrine pancreas graft function after simultaneous pancreas-kidney transplantation. Incidence, risk factors, and impact on long-term outcome.

BACKGROUND: The incidence of delayed endocrine pancreas graft function and its impact on long-term outcome after simultaneous pancreas-kidney transplantation are unknown. METHODS: We studied 54 technically successful adult type I insulin-dependent diabetic recipients of cadaver, whole organ, bladder-drained simultaneous pancreas-kidney transplants (mean age, 37.6 years; 65% male, 35% female; 9% pancreas retransplants; 63% on chronic pretransplant dialysis; mean duration of diabetes, 25.1 years). Insulin was administered during the first 2 weeks after transplantation, as needed, to keep blood glucose < 150 mg/dl. Delayed endocrine pancreas graft function was defined as total, cumulative insulin requirement of > 30 U between day 5 and day 10, and/or > 15 U between day 11 and 15. Quadruple immunosuppression was used for all recipients. RESULTS: The incidence of delayed endocrine pancreas graft function was 69%. By univariate analysis, delayed endocrine graft function was associated with pretransplant recipient weight > 80 kg (P = 0.04), donor age > 45 years (P = 0.02), and cardiocerebrovascular (P = 0.06) and nontraumatic causes of donor death (P = 0.02). The incidence of acute pancreas rejection episodes was similar for recipients without and with delayed endocrine pancreas graft function. Pancreas graft survival at 1 and 3 years was 94% and 82% without versus 76% and 59% with delayed endocrine graft function (P = 0.03). CONCLUSIONS: Increased pancreas graft failure after delayed endocrine function was a consequence of insufficient functional reserve (e.g., older donors) rather than increased immunogenicity. Pretransplant reduction of recipient weight and careful donor selection are therefore crucial in order to decrease the incidence of delayed endocrine pancreas graft function and its negative impact on long-term outcome.

Adult↗
PubMed1999

[Organ donation by living donors in isolated pancreas and simultaneous pancreas-kidney transplantation].

We studied retrospectively 106 pancreas transplants from living donors. Of these, 83 were solitary pancreas transplants, done between June 1979 and December 1997 (51 pancreas transplants alone for non-uremic recipients as well as 32 pancreas-after-kidney transplants for previously uremic recipients with a functioning kidney graft), and 23 were simultaneous pancreas-kidney transplants (SPK), done between March 1994 and December 1997. In all, 105 (99%) donors were genetically related to the recipients. Perioperative donor mortality was 0%. Donor complications included 9 splenectomies as well as 4 operatively drained and 7 percutaneously managed peripancreatic fluid collections. We noted hyperglycemia in 3 (3%) donors (all among the initial cases in this series). The 1-year survival rate was 50% for solitary pancreas recipients and 78% (pancreas) and 100% (kidney) for SPK recipients. Of the 5 pancreas graft losses which occurred after SPK, 3 were due to thrombosis, 1 to pancreatitis and infection, and 1 to chronic rejection. Currently, all kidney grafts and 18 pancreas grafts are functioning in these 23 dual organ recipients (with 0% recipient mortality). Living donor pancreas and SPK grafting is associated with low donor morbidity and good graft outcome. With stringent donor criteria and appropriate counseling of the prospective donor/recipient pairs, living donor pancreas transplants may become a more widely applied therapeutic alternative for selected non-uremic and uremic patients with Type I diabetes.

Diabetes Mellitus, Type 2↗
PubMed1992

Intermediate filaments as differentiation markers of normal pancreas and pancreas cancer.

Expression of intermediate filaments (IF) is regulated during development and differentiation. The authors have studied the expression of vimentin and cytokeratins (CK) 4, 7, 8, 13, 18, 19 in normal pancreas, chronic pancreatitis, and pancreas cancer using monoclonal antibodies. Immunohistochemical assays were performed on fresh frozen tissue sections and on cultured pancreas cancer cells using the streptavidin-peroxidase method. In normal pancreas, acinar cells expressed CK 8 and 18, whereas ductal cells expressed CK 7, 8, 18, and 19. CK 4 was expressed by 5-10% of pancreas duct cells in all specimens of normal pancreas. CK 13 was not detected in any epithelial cells of normal pancreas or pancreatitis. CK 7, 8, 18, and 19 were homogeneously expressed in all pancreas cancers, whereas CK 4 was expressed only in 5-50% of cells in 10/16 tumors. Foci of squamous metaplasia expressed CK 13 but showed partial loss of expression of CK 7, 8, 18, and 19. Thirteen pancreas cancer cell lines examined showed homogeneous expression of CK 7, 8, 18, and 19; 2/11 lines expressed CK 4 weakly, and 6/11 expressed vimentin. CK 13 was not detected in any of the lines. These results indicate that pancreas cancer cells consistently express cytokeratin polypeptides characteristic of ductal epithelial cells and that this phenotype is retained in pancreas cancer cell lines. In addition, squamous metaplasia is associated with a coordinate change in the expression of CK polypeptides.

Biomarkers↗
PubMed2005

Pancreas divisum: a study of the cadaveric donor pancreas for islet isolation.

OBJECTIVES: Pancreas divisum, the most frequent congenital variant of pancreatic ductal configuration, might impair intraductal delivery of enzyme for islet isolation. We investigated the frequency of pancreas divisum and its effect on the digestion process in islet isolation. METHODS: Two catheters were placed into the main duct in opposite directions following dissection of the duct in the mid-body of cadaveric donor pancreata. When the majority of outflow was observed through the Santorini orifice by injecting solution through the catheter toward head, a diagnosis of pancreas divisum was made. RESULTS: Twenty-eight cases of a total of 127 pancreata evaluated were described as having pancreas divisum. There were no significant differences in donor demographics, donor instability, pancreas weight, or undigested tissue weight between donors with and without pancreas divisum. In the 28 cases of pancreas divisum, there was moreover no observable difference in the quality of distention between the ventral and dorsal pancreas. Islet yield after digestion was comparable between cases with and without pancreas divisum. CONCLUSION: We found that Santorini's duct was the major drainage route of the pancreas in 22% of individuals. Pancreas divisum did not have a negative impact on the digestion process and outcome of islet isolation.

Cadaver↗
PubMed2002

Serous cystadenoma of the pancreas associated with pancreas divisum.

Pancreas divisum is an embryologic anomaly of the pancreas that is characterized by a lack of fusion of the dorsal and ventral pancreatic ducts. It is rarely associated with pancreatic neoplasms. We report herein a rare association of pancreas divisum and serous cystadenoma of the pancreas. A 46-year-old Japanese woman presented with epigastralgia. Ultrasonography, computed tomography (CT) and magnetic resonance cholangiopancreatography revealed a multilocular cystic mass, measuring 7 cm in diameter, with a central stellate scar, in the body and tail of the pancreas. Angiography demonstrated a relatively hypervascular mass, suppressing the splenic vein. No arterial encasement was evident. Endoscopic retrograde pancreatography through the major papilla demonstrated only the duct of Wirsung; cannulation into the minor papilla was unsuccessful. In addition, CT showed a mildly dilated main pancreatic duct draining into the minor papilla. Distal pancreatectomy and splenectomy were performed, with the tentative diagnosis being serous cystic neoplasm of the pancreas, possibly malignant, and pancreas divisum. The cut surface of the resected specimen had a honeycomb-like appearance and the specimen consisted of multiple cysts of various sizes. Histopathological examination showed multiple cysts lined by a single layer of flat or cuboidal epithelial cells with glycogen in the cytoplasm. There was no evidence of malignancy. The histopathological diagnosis was serous cystadenoma of the pancreas. To the best of our knowledge, only three cases of serous cystadenoma of the pancreas associated with pancreas divisum have been reported. We report the fourth case of such an association, and briefly review the literature.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed2004

Intraductal papillary mucinous tumor of the native pancreas in a pancreas-kidney transplant recipient.

Recent data from the International Pancreas Transplant Registry confirm the benefits of pancreas transplantation, even in high-risk diabetic patients previously considered unqualified for such procedures. With patient survival currently extending into decades, de novo malignancies are now more frequently diagnosed in pancreas recipients. This is the first reported case of an intraductal papillary mucinous tumor of the native pancreas in a high-risk pancreas after kidney recipient. The patient underwent a partial pancreaticoduodenectomy and has remained tumor-free for 9 months. This case report demonstrates that (1) pancreas transplantation can be successfully done in patients with significant cardiocerebrovascular disease, (2) de novo pancreas malignancies can occur within the first year after pancreas transplantation, and (3) tumors of the native pancreas warrant the same surgical treatment in pancreas recipients as in the general population, despite the need for posttransplant immunosuppression and the increased operative risk.

Carcinoma, Pancreatic Ductal↗
PubMed1998

Pregnancy after pancreas transplantation in the cyclosporine era: report from the International Pancreas Transplant Registry.

BACKGROUND: As of December 31, 1996, a total of 9012 pancreas transplants have been reported to the International Pancreas Transplant Registry (IPTR). Over 75% of these recipients were < or = 40 years of age at the time of their transplant. With continued improvement in short- and long-term outcome after transplant, an increasing number of female recipients have become pregnant. However, outcome after pregnancy in pancreas transplant recipients has not been studied in detail. METHODS: To evaluate the risks of pregnancy after pancreas transplantation in the cyclosporine era, we surveyed the institutions reporting to the IPTR. RESULTS: Nineteen cases of pregnancy in 17 female recipients of simultaneous pancreas-kidney transplants resulted in 19 live births. Metabolic control during pregnancy was good in all cases. Mean duration of gestation was 35.2-2.2 weeks. Mean birth weight was 2150+/-680 g. Two congenital malformations were reported (one bilateral cataract and one double aortic arch). One child developed type I diabetes at age 3 years. Only one pancreas graft and one kidney graft were lost (in two different recipients). The pancreas graft was lost after delivery (because of acute rejection). The kidney graft was lost 3 months after delivery (impaired function due to previous amphotericin B treatment). One case of a worsened secondary complication (retinopathy) was reported. One recipient died of myocardial infarction 7 years after transplant and 5 years after delivery, in spite of a normal pretransplant coronary angiogram and good pancreas function. CONCLUSION: This study shows that simultaneous pancreas-kidney transplantation can restore fertility in uremic type I diabetic female recipients. Thus, both posttransplant contraception and fertility counseling are options for female recipients. However, our analysis demonstrates that, when discussing the possibility of pregnancy with female pancreas recipients, these potential risks must be considered: (1) graft loss, (2) progressive maternal morbidity and mortality even with good glycemic control, and (3) diabetes transmission to offspring.

Adult↗
PubMed2001

The transplanted fetal endocrine pancreas undergoes an inherent sequential differentiation similar to that in the native pancreas. An ultrastructural study in the pig-to-mouse model.

This study examines, at the ultrastructural level, whether the fetal porcine endocrine pancreas (insulin, glucagon, somatostatin, and pancreatic polypeptide [PP]- and islet amyloid polypeptide [IAPP]-containing cells) develops normally after transplantation under the kidney capsule in athymic mice. We have thus used an in vivo pig-to-mouse model for the differentiation of the endocrine pancreas removed from its normal milieu. Islet-like cell clusters (ICCs) were prepared from the fetal porcine pancreas as previously described and transplanted under the renal capsule of athymic mice. At various times after transplantation, the endocrine pancreas was removed and the level of differentiation was compared with the native pancreas of the same biological age. At the ultrastructural level, several sequential steps could be identified based on the morphology and hormone content of the secretory granules of the endocrine cell examined. Applying this approach, we could demonstrate that the ontogeny of the transplanted fetal pig pancreas follows the same sequential differentiation as the native pancreas. The process seems to be under stringent control, apparently directly related to the biological age of the tissue, and independent not only of the new environment under the kidney capsule but also of the adult and xenogeneic milieu provided after transplantation to the athymic nude mouse. Therefore, all four major hormone-producing cells seem to develop normally after transplantation when compared with the development in the native pancreas. IAPP was produced by the pluripotent fetal endocrine cells as well as the adult alpha-, beta-, and delta-cell granules in the native pancreas; however, in the transplanted pancreas, IAPP expression was demonstrated only in beta-cells, delta-cells, and PP cells. No IAPP was found in granules of the alpha-cell lineage. The results suggest a sequential differentiation of all four major types of islet cells from a common pluripotent progenitor cell, which seems to be located in the pancreatic ducts. Therefore, the results presented strongly suggest that the ontogeny of the four major endocrine islet cells is determined by genetic information carried by the progenitor cells and not by the systemic or local environment.

Amyloid↗
PubMed2004

Discrepancy between pancreatographic and histopathological findings in the ventral pancreas of pancreas divisum.

CONTEXT: Pancreas divisum is a congenital anomaly in which the ventral and dorsal pancreatic ducts do not communicate. CASE REPORT: Autopsy case of pancreas divisum with a history of heavy consumption of alcohol was presented. Pancreatography via the major duodenal papilla showed a short ventral pancreatic duct of 1 cm in length, and hypoplasia of the ventral pancreas was suspected. As large cysts were confined to the dorsal pancreas, isolated dorsal pancreatitis was also suspected. At autopsy, extensive fibrosis was detected in both the ventral and dorsal pancreas. Immunohistochemical examination revealed that PP-rich islets were scattered in the fibrotic area between the ventral pancreatic parenchyma and the neck of the pancreas, suggesting that this fibrotic area originated from the ventral pancreas. These facts suggest that the short ventral pancreatic duct was not induced by hypoplasia of the ventral pancreas but was shortened secondarily by the alcohol-induced fibrosis. CONCLUSIONS: In pancreas divisum, a short ventral pancreatic duct resulting from secondary factors may be confused with that originating from hypoplasia of the ventral pancreas.

Aged↗
PubMed1988

[Changes in carbohydrate metabolism after major resection of the pancreas, with special reference to the fibrotic pancreas caused by ligation of the pancreatic duct].

Fibrotic pancreas was caused by ligation of the pancreatic ducts in mongrel dogs. Four weeks later, reconstruction of the pancreatic duct and major pancreatic resection were performed. Changes of carbohydrate metabolism and functional and morphological changes of islet cells in the remnant pancreas were investigated. 1) Immediately after resection of more than 84% of the fibrotic pancreas, diabetes developed, and insulin and glucagon secretion decreased, accompanied with marked degeneration of B, A and D cells in the islets. 2) During the early periods after 63 to 84% pancreatectomy, secretion of both insulin and glucagon decreased, and then showed a tendency to recover, but later the secretion gradually decreased again and so-called Sandmeyer's diabetes developed. The size of the islets and the number of B cells decreased, but the rate of A and D cells in the islets increased relatively in the remnant pancreas. 3) After resection of less than 63% of the fibrotic pancreas, secretion of both insulin and glucagon decreased temporarily with subsequent recovery. Diabetes did not develop. There were no marked morphological changes in the islets, nor significant changes in the distribution of B, A and D cells of the islets in the remnant pancreas. Diabetes developed after resection of more than 63% of the fibrotic pancreas 4 weeks after ligation of the pancreatic duct, while it developed after resection of more than 74% of the normal pancreas in dogs. Therefore, with regard to carbohydrate metabolism, resectability of the fibrotic pancreas was about 10% less than that of the normal pancreas in dogs.

Animals↗
PubMed1983

Increases in plasma kallikrein-like and pancreas kallikrein-like substances after administration of pancreas or plasma kallikrein.

Differences between the concentration of a kallikrein-like substance in blood obtained by the peptide-MCA method and that obtained by the TAME (N-tosyl-l-arginine methyl ester) method by administering pancreas kallikrein to rabbits have been recognized already and the existence of a Substance X was evaluated. In the present study, it was revealed that administration of pancreas kallikrein resulted in inactivation of kallikrein in the substrate in gut homogenates and homogenates of various organs except for the pancreas. In the pancreas homogenate, inactivation was not observed. On the other hand, there was a possibility that at least part of Substance X existed due to plasma kallikrein. Thus, the concentration of plasma kallikrein in plasma after administration of pancreas kallikrein was determined. A pattern similar to the concentration curve of Substance X was obtained. Thus, it was clarified that plasma kallikrein-like substance, at least, increased when pancreas kallikrein was administered. On the contrary, when plasma kallikrein was administered to the rabbit duodenum, the concentration of pancreas kallikrein-like substance in plasma increased. It was also clarified that plasma kallikrein-like substance increased in vitro by adding pancreas kallikrein to the blood or plasma, whereas the in vitro addition of plasma kallikrein to the blood induced its decomposition and a slight increase in pancreas kallikrein-like substance, and the addition of plasma kallikrein to the plasma induced an increase in plasma kallikrein and a slight increase in pancreas kallikrein-like substance.

Animals↗
PubMed1997

Tacrolimus in pancreas transplantation: a multicenter analysis. Tacrolimus Pancreas Transplant Study Group.

This follow-up multicenter analysis is based on 362 pancreas allograft recipients at 14 institutions who were given tacrolimus between 1 May 1994 and 15 November 1995. Three groups were studied: (1) recipients given tacrolimus initially for induction and maintenance therapy (n = 250; 215 without, 35 with, a concurrent bone marrow transplant), (2) recipients who converted to tacrolimus for rescue or rejection therapy (n = 89), and (3) recipients who converted to tacrolimus for other reasons (n = 23). Of 215 recipients without a bone marrow transplant in the induction group, 166 (77%) underwent a simultaneous pancreas-kidney transplant (SPK), 29 (14%) a pancreas transplant alone (PTA), and 20 (9%) a pancreas after previous kidney transplant (PAK). Initial antibody therapy was given to 185 (86%) recipients. All 215 received tacrolimus and prednisone; 202 (94%) also received azathioprine (AZA) and 11 (5%) mycophenolate mofetil (MMF). The most common side effects of tacrolimus were neurotoxicity in 21%, nephrotoxicity in 21%, gastrointestinal (GI) toxicity in 13%, and diabetogenicity in 13% of these recipients. No recipient in this group developed new-onset insulin-dependent diabetes mellitus. Of 89 recipients in the rescue group, 71 (79%) had an SPK, 11 (13%) a PTA, and 7 (8%) a PAK. Before conversion, all had been on cyclosporine (CsA)-based immunosuppression; 74% of them had 2 or more rejection episodes previously. The most common side effects were nephrotoxicity in 27%, neurotoxicity in 26%, GI toxicity in 18%, and diabetogenicity in 8% of these recipients. No recipient in this group developed new-onset insulin-dependent diabetes mellitus. In the induction group patient survival at 1 yr was 98% for SPK, 79% for PTA, and 100% for PAK recipients. According to a matched-pair analysis, pancreas graft survival for SPK recipients at 1 yr was 88% with tacrolimus vs. 73% with CsA (p = 0.002); for PTA recipients, 68% vs. 70% (p > 0.35); and for PAK recipients, 85% vs. 65% (p = 0.13). Graft loss from rejection was not different with tacrolimus vs. CsA in all 3 pancreas recipient categories. At 1 yr, 17% of recipients had converted from tacrolimus to CsA for diabetogenicity, nephrotoxicity, or rejection; 23% had converted from AZA to MMF. The incidence of post-transplant lymphoma was < 2%. In the rescue group, patient survival rates at 1 yr were 96% for SPK, 100% for PTA, and 86% for PAK recipients (p < 0.08). Pancreas graft survival at 1 yr was 89% for SPK, 58% for PTA, and 69% for PAK recipients (p = 0.004). Graft loss from rejection was significantly lower for SPK vs. PTA or PAK recipients. At 1 yr, 20% of recipients had reconverted from tacrolimus to CsA for rejection, neurotoxicity, or nephrotoxicity; 19% had converted from AZA to MMF. There were no post-transplant lymphomas in the rescue group. This follow-up multicenter analysis shows that tacrolimus after pancreas transplantation is associated with high graft survival rates when used for induction and with high graft salvage rates when used for rescue therapy. The rate of graft loss from rejection is low in all 3 pancreas recipient categories. The overall incidence of new-onset insulin-dependent diabetes mellitus is < 1%, as is the incidence of post-transplant lymphoma. Converting from tacrolimus to CsA and, in patients on tacrolimus, from AZA to MMF, is safe; interchangeable use of drugs appears to be of immunologic benefit. To determine the best immunosuppressive regimen after pancreas transplantation, a prospective randomized study comparing tacrolimus and MMF vs. Neoral plus MMF is mandatory.

Adult↗
PubMed1983

The duct-ligated pancreas transplant and its effect on the islet cellular composition of the host pancreas. A morphometric analysis.

Rats rendered diabetic by streptozotocin were subjected to pancreas transplantation. After twenty weeks, the duct-ligated pancreas transplant was studied morphometrically to determine the effect of duct occlusion on the various cell populations of the islets. Concomitantly, the streptozotocin-treated host pancreas was examined for a possible influence of the graft on the diabetic pattern of islet cell population. Twenty weeks after pancreas transplantation, the volume fractions of insulin, glucagon, somatostatin and pancreatic polypeptide cells in the graft islets did not differ from those of the normal control pancreas. In the pancreas of nontransplanted diabetic rats, insulin-positive B cells were reduced from 60-65% to less than 10% of the islet volume, whereas non-B cells were significantly increased in volume density. The changes in fractional volume of the various islet cells correlated fairly well with changes in plasma concentration of the corresponding pancreas hormones. In the recipient's own pancreas, the relative volumes of glucagon and somatostatin cells were unaffected by the pancreas transplant. However, the insulin cell mass was significantly increased, and comprised about 20% of the islet volume, while cells containing pancreatic polypeptide were found only sporadically.

Animals↗
PubMed1989

Pancreas-specific protein. New serum marker for graft rejection in pancreas-transplant recipients.

A radioimmunoassay for a novel human pancreatic protein (pancreas-specific protein, PASP) has been developed. We studied the possibility that serum PASP levels reflect pancreas-graft rejections in human pancreas-transplant recipients. Ten patients subjected to combined pancreas-kidney transplantation and 4 patients subjected to pancreas transplantation alone were studied. Twelve kidney recipients served as control subjects. On several occasions, PASP levels were elevated at kidney rejections in patients with combined pancreas-kidney grafts and then decreased after antirejection therapy, although no other indications for concomitant pancreas-graft rejection were at hand. In the recipients of pancreas grafts alone, PASP levels increased before or at the same time as graft rejections were indicated by current methods. In two cases of chronic graft rejection, PASP rose to high levels long before hyperglycemia occurred. In the control group of kidney-graft recipients, PASP levels were stable and were not affected by high serum creatinine levels, kidney-rejection episodes, or antirejection therapy. This study indicates that PASP may be a good serum marker for pancreas-graft rejection.

Adult↗
PubMed2004

Intraductal papillary-mucinous adenoma developed in the ventral pancreas in a patient with pancreas divisum.

A 34-year-old man was admitted to our hospital with the chief complaints of back pain and epigastralgia. The physical examinations on admission disclosed no abdominal tumor. The serum concentration of total bilirubin was 1.4 mg/dl. The serum elastase-1 level was elevated to 526 ng/dl. Computed tomography showed a cystic lesion, 1 cm in diameter, in the head of the pancreas, without dilatation of the main pancreatic duct. Endoscopic retrograde cholangiopancreatography via the papilla of Vater and the accessory papilla revealed an enlarged ventral pancreatic duct and pancreas divisum. The preoperative diagnosis was mucin-producing pancreatic tumor in the ventral pancreas of a patient with pancreas divisum. A pylorus-preserving pancreatoduodenectomy was performed. The gross findings of the cut surface of the resected specimen disclosed mural nodules in the dilated duct of the ventral pancreas. A histological examination of the mural nodules in the ventral pancreas revealed mucin and intraductal papillary adenoma. Benign tumors associated with pancreas divisum are rare; to the best of our knowledge, only three cases have been reported. Although in these three patients the tumor developed in the dorsal pancreas, the tumor developed in the ventral pancreas in our patient.

Adenoma↗
PubMed2004

Pancreas head carcinoma with total fat replacement of the dorsal exocrine pancreas.

We report a case of pancreas head carcinoma associated with fat replacement of the body and tail. A 68-year-old man presented with obstructive jaundice and was admitted to our hospital. Ultrasonography and computed tomography showed pancreas head tumor with a neighboring cystic lesion and fatty replacement of parenchyma of the pancreas body and tail. By endoscopic retrograde pancreatography, abruption of the main pancreatic duct and the presence of an accessory duct were detected. After percutaneous transhepatic biliary drainage, pancreatoduodenectomy was successfully performed. At laparotomy, the pancreas head was easily dissected from the replaced fatty tissue of the body and tail without continuity of the ductal system or parenchyma. Microscopic examination revealed the existence of an infiltrating ductal adenocarcinoma and a neighboring. cyst in the pancreas head. The dorsal exocrine pancreas was completely replaced by the fat tissues, in which viable Langerhans' islets were scattered. The patient's postoperative course was uneventful, and exogenous insulin administration was unnecessary for the maintenance of normal blood sugar level. Acquired fat replacement of the body and tail of the pancreas is an uncommon disorder, mimicking congenital agenesis of the dorsal pancreas. Though the mechanism is controversial, obstruction of the main pancreatic duct by a cystic lesion or carcinoma in the pancreas head is a possible cause of fatty degeneration of the pancreatic parenchyma.

Adipose Tissue↗