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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen combined renal and segmental pancreatic transplantations with enteric exocrine diversion were performed between May 1984 and September 1985. The one year actuarial patient survival rate and pancreatic graft survival rate were 86 and 66 per cent, respectively. Thirteen pancreatic grafts are presently functioning (two to seven months) and all of the recipients are insulin-free. Although graft cold ischemia time was kept low (a mean of 4.6 hours), a moderate graft pancreatitis developed with a peak serum amylase level of 16.8 +/- 2.2 microkatal per liter. Analysis of the fluid drained through an abdominal drain tube placed at the graft site revealed an amylase activity of 280 +/- 110 microkatal per liter on the first postoperative day and rapidly decreasing to a mean of 15 +/- 5 microkatal per liter on day 6. A pancreatic duct catheter was used to divert the exocrine juice to the exterior during the first few postoperative weeks thereby promoting healing of the pancreaticoenteric anastomosis. The volume of pancreatic juice from the ductal catheter was quite low in the first postoperative days but then rose to reach a plateau level of 500 to 600 milliliters. The amylase activity and the lipase concentration in the pancreatic juice was very high (9,100 +/- 2,450 microkatal per liter and 11.1 +/- 4.4 grams per liter, respectively) during the first postoperative day but then gradually decreased to reach a steady level after four to seven days. Intravenous administration of secretin induced a sixfold increase in the flow of pancreatic juice. An intravenous infusion of somatostatin significantly reduced the flow of pancreatic juice and the amylase activity and lipase concentration in the juice but did not abolish the secretin induced increase in pancreatic secretion.
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PMID:Studies on the exocrine secretion of segmental pancreatic grafts in humans. 243 63

In this review, we compared the outcome of 25 studies of experimentally induced pancreatitis in animals with 13 studies of human acute pancreatitis in which the same therapeutic agents were used (aprotinin, glucagon, 5-fluorouracil, somatostatin, peritoneal lavage). Whereas 81% of the animal studies had a positive outcome (improvement in survival), only 7.7% of the human studies showed a positive outcome on survival. Most animal studies suffered from a protocol in which treatment was not significantly delayed after induction of acute pancreatitis. Of the 12 human studies that showed no effect of treatment on survival, none had sufficient statistical power (1 - beta error) for the investigators to have confidence in the negative outcomes. This was due to the fact that the studies had too few patients or that the event rates in the untreated populations were too low. Only five of the human studies reported the complication rates of acute pancreatitis in patients who did not die of their disease. Treatment (by any agent) did not improve the complication rate in these studies, but only one of the five reports had sufficient statistical power for the investigators to have confidence in these negative results. Large multicenter studies with sufficient numbers of patients with severe pancreatitis (high mortality and complication rates) are needed to evaluate new therapies in this disease.
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PMID:Treatment of acute pancreatitis. Comparison of animal and human studies. 244 20

Somatostatin is an inhibitory hormone that decreases the secretion and end organ response of cholecystokinin (CCK). Inhibition of hormonal stimulation of pancreatic exocrine secretion by somatostatin may improve the course of acute pancreatitis. Anesthetized dogs underwent cholecystectomy and cannulation of the pancreatic duct, thoracic duct, and portal vein. Twenty experiments were performed in random order with 5 dogs in each group. Hourly measurements of lymph flow and portal and thoracic duct amylase were made. Portal blood insulin, glucagon, and CCK concentrations were determined by radioimmunoassay on samples obtained at the beginning and end of the experiments. Pancreatitis was induced by injecting, under constant pressure, 10 ml bile into the pancreatic duct during 1 min. Somatostatin was administered intravenously (20 micrograms/kg/hr). After 5 h, the dogs were killed, pancreas glands removed and weighed and tissue samples obtained for histologic evaluation. There was a significant increase in lymph amylase output and portal venous amylase and CCK concentrations in the dogs with pancreatitis compared to the control dogs. In dogs with pancreatitis, lymphatic amylase secretion and portal CCK concentrations were significantly decreased by somatostatin. Somatostatin did not significantly alter portal amylase concentrations, pancreas gland weights or histologic inflammation when compared to values from dogs with pancreatitis not treated with somatostatin.
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PMID:Effects of somatostatin on acute canine experimental pancreatitis. 244 77

Somatostatin has been reported to promote closure of pancreatic fistulae, but use of the analog SMS 201-995 (Sandoz, Inc.) has not previously been published. We used this analog to treat two patients with end pancreatic fistulae refractory to conventional therapy. One patient had disruption of a pancreaticojejunostomy after pancreaticoduodenectomy and the other had acute necrotizing gallstone pancreatitis and disruption of the pancreatic duct in the tail. SMS 201-995 (100-150 micrograms/d) abruptly decreased fistula output by 50% in both patients but further increases in dosage had no further effect on output. Neither fistula healed after 3-4 wk of therapy. Treatment with somatostatin or its analogs alone will not lead to closure of a pancreatic fistula complicated by factors such as distal obstruction, infection, or foreign body. Somatostatin may promote closure of lateral fistulae and may simplify the management of patients with high output fistulae.
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PMID:Failure of somatostatin or an analog to promote closure of end pancreatic fistulae. 246 17

A prospective study was carried out to evaluate the efficacy of somatostatin in the treatment of acute pancreatitis. Seventy one patients were randomised to control (h = 36), or to the somatostatin group (h = 35) who received somatostatin 100 micrograms/h after a 250 microgram bolus for the first two days. The following were compared in the two groups on admission and two days later: laboratory tests of prognostic significance, severity of pancreatitis, and also morbidity and mortality. Of the nine laboratory tests compared, the white blood cell count, lactate dehydrogenase, and urea concentrations were significantly lower in the somatostatin group two days after admission. Severity of pancreatitis after hospitalisation increased in fewer patients given somatostatin (NS). There was a trend toward fewer complications, especially local, in the somatostatin group. Mortality in both groups was low. Somatostatin appeared to reduce the local complications of acute pancreatitis. A larger trial is necessary to show its beneficial effect conclusively.
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PMID:Somatostatin in the treatment of acute pancreatitis: a prospective randomised controlled trial. 256 34

The aim of the study was to evaluate and control the therapeutic validity of Somatostatin administration and the clinical benefits of parenteral nutrition during acute pancreatitis. We selected 31 patients with 1st and 2nd degree pancreatitis according to Ranson's classification. Diagnosis was based on clinical and humoral data and confirmed by echography and CT examinations. The most common etiological cause was biliary++ lithiasis (74.2%). All the patients in the study were split into two groups and received conventional treatment. The therapeutic schedule administered to group 1 included somatostatin (250 micrograms/h for 72-96 h), while group 2 received total parenteral nutrition with 2,000-2,500 Kal/day trough a central vein. The data obtained from our study demonstrated that both somatostatin and parenteral nutrition are valid tools during the acute phase of the disease. It must be pointed out that the former significantly influences the clinical course and allows a precise control of the painful symptomatology, the objective picture and the curve of the main hematochemical parameters. Parenteral nutrition betters the anabolic response of the organism during the acute phase and carries out an indirect antienzymatic response, so favouring a quicker recovery than observed in the group treated with somatostatin.
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PMID:[Role of somatostatin and parenteral nutrition in the treatment of acute pancreatitis. Personal experience]. 256 58

A series of 172 cases of acute pancreatitis encountered between 1-1-79 and 30-4-88, including 57 treated with somatostatin is presented. A comparison between the latter and the other cases treated with a variety of drugs (aprotinin, cimetidine, ranitidine) led to the following conclusions: 1) somatostatin significantly improves the clinical course of acute oedematous pancreatitis with circumscribed necrosis; 2) it makes no difference to the development of cases with diffuse necrosis and haemorrhage.
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PMID:[Current approach to the treatment of acute pancreatitis with reference to the use of somatostatin]. 257 Mar 82

We describe an infant with pancreas divisum diagnosed by endoscopic retrograde cholangiopancreatography. This infant had chronic and unremitting pancreatitis that only became amenable to surgery following the use of somatostatin analog after the usual and customary treatment for pancreatitis was ineffective.
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PMID:Chronic pancreatitis and pancreas divisum in an infant: diagnosed by endoscopic retrograde cholangiopancreatography and treated with somatostatin analog. 257 Aug 27

The effects of somatostatin (SRIF) and its long-acting analogue, SMS 201-995 on the prevention and treatment of acute pancreatitis were studied in rats. Acute pancreatitis was established by ligating the bile duct at the point of entry into the duodenum, thereby allowing reflux of bile into the pancreas. Administration of SRIF (4 micrograms kg-1 body wt IV followed by a 12 h infusion of 4 micrograms kg-1 body wt h-1) or SMS 201-995 (2 micrograms kg-1 body wt SC) at the time of bile duct ligation prevented the increase in the serum concentrations of amylase and lipase observed in control rats 12 h after bile duct ligation. Moreover, SRIF and SMS 201-995 administration prevented development of the histological changes consistent with acute pancreatitis observed in control animals. These results suggest that SRIF or SMS 201-995 may be of value in preventing acute pancreatitis following ERCP or after surgery on the pancreas. In rats with established pancreatitis, SRIF (IV bolus of 4 micrograms kg-1 body wt followed by a 24 h continuous infusion of 4 micrograms kg-1 body wt h-1) or SMS 201-995 (2 micrograms kg-1 body wt SC followed by a similar dose 12 h later): (1) significantly improved survival; (2) produced histological changes in the pancreas consistent with organization and healing; (3) prevented the accumulation of ascitic fluid; (4) reduced the serum levels of amylase and lipase. These results suggest that SRIF and SMS 201-995 may prove valuable in the treatment of established acute pancreatitis in man.
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PMID:Effects of somatostatin and a long-acting somatostatin analogue on the prevention and treatment of experimentally induced acute pancreatitis in the rat. 258 47

Octreotide is an analogue of somatostatin. Like endogenous somatostatin, it exerts a potent inhibitory effect on the release of anterior pituitary growth hormone and thyroid-stimulating hormone, and peptides of the gastroenteropancreatic endocrine system, while overcoming some of the shortcomings of exogenously administered somatostatin, namely a short duration of action, a need for intravenous administration and postinfusion rebound hypersecretion of hormone. Clinical studies have shown that octreotide is effective in the treatment of acromegaly and thyrotrophinomas. In comparative trials octreotide was significantly superior to bromocriptine in patients with acromegaly. Octreotide also appears to provide a significant advantage over existing therapies in the management of the carcinoid syndrome and offers considerable therapeutic potential in reversing carcinoid crises which may be life-threatening. Trials in patients with tumours producing vasoactive intestinal peptide demonstrated that octreotide may be an effective first-line choice for this condition, which has usually metastasised and become refractory to traditional symptomatic therapy. In limited studies in patients with high-output secretory diarrhoea, including cryptosporidium-related diarrhoea associated with AIDS and in patients with small bowel fistulas, octreotide has been shown to be effective in reducing stool/fistula output. However, well-designed clinical trials are still required to confirm its long term usefulness in these disorders. Similarly, although the use of octreotide in other conditions such as neonatal hypoglycaemia caused by nesidioblastosis, reactive pancreatitis, insulin-dependent diabetes mellitus, postprandial hypotension and the dumping syndrome has provided encouraging preliminary results, more studies are needed to clarify the place of octreotide in their treatment. Overall, octreotide appears to be well tolerated with the most frequently reported reactions being pain at the site of injection and gastrointestinal symptoms such as abdominal cramps, nausea, bloating, flatulence, diarrhoea and steatorrhoea. These adverse effects usually abate with time. Additionally, octreotide, like endogenous somatostatin, may also result in cholelithiasis, presumably by altering fat absorption and possibly by decreasing motility of the gallbladder. Thus, octreotide represents a new departure from traditional therapies in the treatment of various pathophysiological states associated with excessive peptide production and secretion. It offers a significant advantage over existing therapies in the medical management of patients with acromegaly, thyrotrophinomas, the carcinoid syndrome, tumours producing vasoactive intestinal peptide and severe secretory diarrhoea in whom conventional management options have either become exhausted or have provided suboptimal symptomatic relief.
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PMID:Octreotide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in conditions associated with excessive peptide secretion. 268 36


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