PANCREAS ALERTS
Ann Surg 2002; 236(4):422-8. (AN 22252415, PMID 12368670)
Occlusion of the pancreatic duct versus pancreaticojejunostomy: a prospective randomized trial.
Tran K, Van Eijck C, Di Carlo V, Hop WC, Zerbi A, Balzano G, Jeekel H.
Departments of General Surgery, Erasmus Medical Center Rotterdam, Rotterdam, The Netherlands.
Postoperative complications after pancreaticoduodenectomy are largely due to leakage of the pancreaticoenterostomy. Pancreatic duct occlusion without anastomosis of the pancreatic remnant may prevent these complications.
In this study the authors assessed the postoperative morbidity and pancreatic function after pancreaticoduodenectomy with pancreaticojejunostomy and duct occlusion without pancreaticojejunostomy using a prospective randomized study comprising a nonselected series of 169 patients with suspected pancreatic and periampullary cancer.
Patient characteristics were comparable in both groups and there were no differences in median blood loss, duration of operation, and hospital stay.
The results of the study show that duct occlusion without pancreaticojejunostomy does not reduce postoperative complications but significantly increases the risk of endocrine pancreatic insufficiency after duct occlusion.
In 86 patients the pancreatic duct was occluded without anastomosis to pancreatic remnant, and in 83 patients a pancreaticojejunostomy was performed after pancreaticoduodenectomy.
Postoperative complications were the endpoint of the study.
No significant difference was noted in postoperative complications, mortality, and exocrine insufficiency.
The incidence of diabetes mellitus was significantly higher in patients with duct occlusion.
Pancreas 2002;25(3):283-9. (AN 22258068, PMID 12370540)
Clinical study of chronic pancreatitis with focal irregular narrowing of the main pancreatic duct and mass formation: comparison with chronic pancreatitis showing diffuse irregular narrowing of the main pancreatic duct.
Wakabayashi T, Kawaura Y, Satomura Y, Fujii T, Motoo Y, Okai T, Sawabu N.
Department of Gastroenterology and Department of Surgery, Saiseikai Kanazawa Hospital. Kanazawa, Japan.
Main pancreatic duct-narrowed chronic pancreatitis may be an autoimmune abnormality. It also has been called autoimmune pancreatitis and sclerosing pancreatitis.
The authors reviewed seven cases of chronic pancreatitis with focal narrowing of the main pancreatic duct, evidenced by endoscopic retrograde cholangiopancreatography, and swelling of one or two segments of the pancreas, evidenced by ultrasonography/computed tomography, and indicated the clinicopathologic features of focal-type main pancreatic duct-narrowed chronic pancreatitis.
The patient group comprised six men and one woman, and their age range was 28-75 years, with a mean of 63.7 years.
Affected sites were in the head in two patients, the body in one patient, the tail in one patient, and the body and tail in three patients; endoscopic retrograde cholangiopancreatography showed narrowing in six patients and obstruction in one.
The results indicate that chronic pancreatitis with focal narrowing of the main pancreatic duct is part of the same clinical spectrum as chronic pancreatitis with diffuse narrowing of the main pancreatic duct, and whether the distribution is diffuse or focal seems to be related to the stage or the extent of the disease.
It is unclear whether cases with focal pancreatographic changes are part of the same clinical entity as cases with diffuse main pancreatic duct changes.
Stricture of the lower portion of the common bile duct that caused obstructive jaundice was shown by endoscopic retrograde cholangiopancreatography in two cases in which the pancreas head was affected.
In all six patients, a dynamic study by computed tomography or MRI homogeneously showed delayed enhancement of involved segments of the pancreas.
Serum levels of pancreatic enzyme were elevated in five patients, but only one subject had pancreatitis-like epigastric pain.
Serological evidence suggestive of autoimmune abnormality was detected in only three patients with hypergammaglobulinemia (greater than, or equal to 2.0 g/dL) or positive titers of antinuclear antibody (ANA greater than, or equal to 80).
Histological assessment was available for five patients, who characteristically had dense lymphocytic or plasmocytic infiltration with severe fibrosis that caused luminal narrowing.
The clinical, serologic, and histologic findings as described above were comparable to those for 12 chronic pancreatitis patients with diffuse narrowing of the main pancreatic duct, diagnosed during the same period.
Surgical resection was performed in 5 patients, in 2 of whom a similar inflammatory process recurred in the remnant head of the pancreas, whereas pancreatitis no longer developed in the other 3 patients. One patient was initially treated with steroids, with clinical remission, although there was neither hypergammaglobulinemia nor positive ANA.
It is therefore important to recognize the possible existence of this focal variant to avoid unnecessary surgery.
Pancreas 2002; 25(3):277-82. (AN 22258067, PMID 12370539)
The role of nitric oxide in edema formation in L-arginine-induced acute pancreatitis.
Takacs T, Czako L, Morschl E, Laszlo F, Tiszlavicz L, Rakonczay Jr Z, Lonovics J.
First Department of Medicine and Department of Pathology, Faculty of Medicine, University of Szeged. Szeged, Hungary.
Nitric oxide (NO) has been implicated in the regulation of the pancreatic circulation, the promotion of the capillary integrity, and the inhibition of leukocyte adhesion.
The authors investigated the rates of changes in the pancreatic constitutive NO synthase (cNOS) and inducible NOS (iNOS) activities and the role of NO in the vascular permeability changes during the development of L-arginine (Arg)-induced acute pancreatitis.
Acute pancreatitis was induced in male Wistar rats by injecting 250 mg/100 g body weight of Arg i.p. twice at an interval of 1 hour, as a 20% solution in 0.15 NaCl (group I).
The serum amylase level was already increased at 6 hours in group I animals, peaked at 12 hours after the Arg injection (11.800±590 versus 6.618±252 U/L in group II), and returned to the control level at 48 hours.
In conclusion endogenous NO is involved in the formation of pancreatic edema in Arg-induced acute pancreatitis by increasing the vascular permeability and protein extravasation. L-NAME treatment decreased the cNOS activity and edema formation but did not prevent the histologic damage in Arg-induced acute pancreatitis.
The control rats received the same quantity of glycine (group II).
In group III, 30 mg/kg N -nitro-L-arginine methyl ester (L-NAME) was injected i.p. 19 hours after the first Arg injection.
The rats were killed at 6, 12, 24, or 48 hours following Arg administration, and the plasma amylase concentration and the pancreatic weight/body weight (pw/bw) ratios were evaluated.
NOS activity was determined via the conversion of L- C-Arg monohydrochloride to C-citrulline.
The vascular permeability was examined by means of the extravasation of Evans blue dye (20 mg/kg bw) into the pancreatic tissue.
The pw/bw ratio peaked at 24 hours in group I (6.63±0.52 versus 4.02±0.22 mg/g in group II) and returned to the control level at 48 hours.
The cNOS activity was depleted at 6 hours in group I (0.02±0.003 versus 0.23±0.02 pmol/min/mg protein in group II); it then gradually increased to a level significantly higher than that in group II and decreased thereafter (0.45±0.03 and 0.13±0.01 pmol/min/mg protein at 24 and 48 hours).
The iNOS activity was significantly increased at 24 and 48 hours versus that in group II (0.15±0.05 and 0.07±0.01 versus 0.04 0.01 pmol/min/mg protein).
The pancreatic concentration of Evans blue dye was significantly higher in group I than in group II (138.59±11.04 versus 43.57±2.67 g/dry weight).
Treatment with L-NAME significantly reduced the amylase activity, pw/bw, Evans blue concentration, and cNOS activity of the pancreas but did not exert any beneficial effect on the histologic score at 24 hours after the onset of pancreatitis, as compared with those values in group I (6.528±673 U/L, 4.56±0.65 mg/g, 86.84±3.9 (g/dry weight, 0.14±0.04 pmol/min/mg protein).
Pancreas 2002; 25(3):270-6. (AN 22258066, PMID 12370538)
Experimental pancreatitis causes acute perturbation of energy metabolism in the intestinal wall.
Ederoth P, Sun Z, Nordstrom CH, Andersson R.
Departments of Anesthesiology, Neurosurgery, and Surgery, Lund University Hospital. Lund, Sweden.
The systemic inflammatory response syndrome (SIRS) may be initiated by a number of underlying conditions such as acute pancreatitis.
The aim of the study was to evaluate whether severe acute pancreatitis in the rat affects energy metabolism in the pancreas and whether the focal inflammation also causes biochemical deterioration in remote organs such as the liver and intestine.
Two groups of eight rats each were studied: the sham (control) group and the pancreatitis group.
In the pancreatitis group, glucose concentration significantly increased in the pancreas and lactate levels significantly increased in the pancreas and intestinal wall.
The authors concluded that the induction of severe acute pancreatitis results in immediate metabolic alterations in the pancreas. In the intestinal wall a severe perturbation of energy metabolism is observed after only 1 hour. This implies a rapid onset of metabolic disturbances, not only in the local, challenged organ, i.e. the pancreas, but also in remote organs.
The association between the local inflammatory reaction, the systemic response, and potential concomitant dysfunction of remote organs is not quite clear.
Under general anesthesia, microdialysis probes were inserted in the pancreas, liver, and small intestine. Acute pancreatitis was induced by intraductal injection of 5% sodium taurodeoxycholate, and the animals were studied for 3 hours thereafter.
The microdialysis fluid was analyzed for glucose, lactate, and pyruvate.
The lactate/pyruvate ratio in the intestine of the pancreatitis group was significantly higher than in the sham group.