Gene/Protein Disease Symptom Drug Enzyme Compound
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6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Very frequently in acute and chronic pancreatitis, the surgical treatment is indispensable. The disease itself is accompanied by metabolic disturbances, protein deficiency, hepatic lesion, by diabetes and malabsorption syndrome. Following the laboratory parameters we were able to perform partial or total hyperalimentation, correction of acid-base dis-equilibrium and to obtain the positive nitrogen balance, and in this way keep the patients in optimal conditions pre- and postoperatively.
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PMID:[Metabolic disorders and current treatment of the surgical patient with pancreatitis]. 85 52

Marked weight loss is the major nutritional defect in chronic pancreatitis. Inadequate food intake owing to recurrent or near continuous pain usually accounts for the initial 10 to 20 per cent of loss of body weight, which decreases again with the onset of diabetes and is often precipitous with the development of steatorrhea. Treatment of pain, control of diabetes, and intensive pancreatic replacement therapy for steatorrhea usually causes weight gain, but seldom to ideal weight. It appears that the patient's body weight gets set at a new "weight-stat." Although isolated abnormalities of small bowel function tests can be elicited and deficiencies of fat-soluble vitamins, calcium, zinc, selenium, and so forth may be demonstrated, these rarely lead to clinical syndromes, as with demonstrable low B12 uptake in some 10 to 15 per cent of patients. In the late stage of the disease and particularly in NATP, extreme protein-calorie malnutrition may occur, which may not be correctable even by hyperalimentation. Although the mortality of the disease was reportedly higher in areas of socioeconomic deprivation, it appears from recent studies in Switzerland and other developed countries that mortality during a 12-year period may be in the region of 50 per cent worldwide.
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PMID:Nutritional deficiencies in chronic pancreatitis. 268 Sep 66

Islet transplantation is successful in animals and holds considerable promise as endocrine replacement therapy for patients with diabetes mellitus, but clinical application to diabetic patients has been difficult. We have shown the technical feasibility of human islet transplantation by autotransplantation of dispersed pancreatic islet tissue into the portal vein in three patients with chronic pancreatitis and incapacitating, intractable pain who underwent near-total (greater than 97%) pancreatectomy. In all three patients, the excised pancreas was dispersed by collagenase digestion, but no effort was made to purify the islets. Islet yield, as judged by tissue insulin content, ranged from 24 to 55%. The first patient, who never received insulin after the pancreatectomy and islet autotransplantation, had a normal oral glucose tolerance test by 3 wk and has remained normoglycemic for over 2 yr. In the second patient, viable islets were histologically identified in the liver parenchyma. The third patient was treated with hyperalimentation for 3 wk after the pancreatectomy and islet autotransplantation and, during this period, required insulin. After cessation of hyperalimentation and initiation of oral geedings, the patient was withdrawn from insulin. Although abnormalities of carbohydrate metabolism were present, the patient did not require insulin for more than 1 yr. Seven diabetic renal allograft recipients have received allografts of dispersed pancreatic islet tissue prepared in the same way. No patients were cured of diabetes, although transient evidence of islet function--increase in serum or urinary C-peptide levels or decrease in exogenous insulin requirements--occurred in some. Although rejection was probably responsible for most of the failures, transplantation of allogeneic human islet tissue as a free graft is metabolically inefficient. With the current state of immunosuppressive therapy, the primary role of islet transplantation may be in a situation where rejection cannot occur: as an autograft to obviate the occurrence of diabetes after extensive pancreatectomy for benign disease.
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PMID:Transplantation of dispersed pancreatic islet tissue in humans: autografts and allografts. 676 13

A case of chronic pancreatitis localized in the head of the pancreas with pancreas divisum was treated by laparoscopic pylorus-preserving pancreatoduodenectomy. The laparoscopic technique of resection and reconstruction with a gastrojejunostomy, hepaticojejunostomy, and pancreaticojejunostomy is described. The postoperative period was complicated by a jejunal ulcer and delayed gastric emptying necessitating a prolonged hospitalization and intravenous hyperalimentation. No fistulas occurred, a follow-up CT scan revealed no pancreatic abnormalities, and the patient was discharged in good condition on the 30th postoperative day. Although technically feasible, the laparoscopic Whipple procedure may not improve the postoperative outcome or shorten the postoperative recovery period.
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PMID:Laparoscopic pylorus-preserving pancreatoduodenectomy. 791 34

Pancreatojejunal sutural insufficiency occurring after pancreatoduodenectomy and countermeasures are discussed. In the Department of Surgery at Kurume University School of Medicine, 318 patients underwent pancreatoduodenectomies. The present study includes 15 of these patients, all of whom had pancreatojejunal sutural insufficiency. The frequency of sutural insufficiency was 4.7%. Five patients had bile duct cancer, 5 had cancer of the papilla of Vater, 2 had a carcinoma of the pancreatic head, 1 each had gallbladder cancer, chronic pancreatitis, and papillitis. Six (40%) of the 15 patients died during hospitalization. The presence or absence of sutural insufficiency was confirmed mainly by radiography and determining the properties and amylase levels of the drainage fluid. There was no significant difference due to the method of anastomosis. End-to-side anastomosis had a rate of 5 (5.9%) of 85 patients, while end-to-end had 10 (4.3%) of 233 patients. The sutural insufficiency was manifested as a major leakage in 6 patients and a minor leakage in 9. The degree of lymph node dissection was D0 in 6.1%, D1 in 1.4%, D2 in 4.8% and D3 in 10.8%, with a high incidence of sutural insufficiency in D3 patients. The pancreatic duct diameter was smaller than 4 mm in 10, 5-7 mm in 4 and over 8 mm in 1 patient. The intraoperative pancreatic findings were a soft pancreas in 8, slightly hard in 3, and hard in 4 patients. Fibrosis of the pancreas was normal to slight in 11 and moderate in 4 patients. Drainage by relaparotomy was performed in 4 of the 6 patients with major leakages to control sutural insufficiency, and the other 2 underwent continuous aspiration with an intraperitoneal drain inserted during the operation. The 9 patients with minor leakage underwent conservative treatment including continuous aspiration via an intraperitoneal drain inserted during surgery, fasting, intravenous hyperalimentation, and antibiotic administration. All of the patients with major leakage died from an associated occurrence of hepatic insufficiency, renal insufficiency, intraperitoneal hemorrhage or diffuse peritonitis during hospitalization. However, 8 of the 9 patients with minor leakage had some healing, and the 1 remaining patient developed a pancreatic fistula. The frequency of pancreatojejunal sutural insufficiency was high in patients with minimal pancreatic fibrosis, with soft pancreatic tissue without dilatation of the pancreatic duct, and with relatively good pancreatic function.
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PMID:Pancreatojejunal sutural insufficiency occurring after pancreatoduodenectomy and countermeasures. 866 93

Pancreatic fistulas can be internal or external and the consequence of acute or chronic pancreatitis, malignancy, or trauma (to include pancreatic surgery, pseudocyst drainage, and percutaneous biopsy). Contingent on the presence of concomitant pseudocyst, downstream ductal obstruction, or a disconnected duct syndrome, treatment may include maneuvers to decrease pancreatic secretion (NPO, hyperalimentation, pancreatic enzymes, octreotide), attempts to effect serosal apposition (diuretics, thoracentesis, paracentesis), various types of percutaneous tube manipulation, or surgery. Transpapillary pancreatic duct stents have recently been used for refractory ductal leaks and may work either by direct occlusion of the fistula or by lowering the duodenal-pancreatic pressure gradient.
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PMID:Pancreatic fistulas: etiology, consequences, and treatment. 895 97

Thoracoscopic splanchnicectomy is a minimally invasive procedure used in the treatment of recalcitrant abdominal pain in patients with chronic pancreatitis or pancreatic carcinoma. Chylothorax, an uncommon complication of thoracoscopic splanchnicectomy, may lead to a protracted, costly hospital course of treatment usually consisting of central venous hyperalimentation, restricted oral intake, and tube thoracostomy. In our series of 25 patients who underwent thoracoscopic splanchnicectomy, 2 developed postoperative chylothorax. Both patients failed conservative management and ultimately underwent operative reintervention, at which time, leaking lymphatics were easily identified and closed using minimally invasive techniques. On the basis of this experience, we advocate early thoracoscopic reintervention in patients with chylothorax after thoracoscopic splanchnicectomy.
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PMID:Management of chylothorax after thoracoscopic splanchnicectomy. 1041 45

The development of new drug formulations of pancreatine based on the principle of microdosage with a pH-sensitive coating produced the most demonstrative clinical result--a considerable increase in duration and quality of life of patients with chronic pancreatitis and cystofibrosis, most of which are children. Clinical studies confirmed high efficiency and safety of Panzytrat in open and double blind comparative clinical studies with the participation of 4,557 patients with chronic pancreatitis, mucoviscidosis, and pancreathogenous digestion disorders. In addition to the above-mentioned symptoms, indications for application of Panzytrat also include any clinical symptoms of the pancreas relative excretory insufficiency, in particular, states after oncological diseases and surgical operations (obstruction of ducts, resection, cholecystectomy, etc.) up to a failure to adhere to a diet and overeating.
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PMID:[Use of Panzytrat in the replacement therapy of exocrine pancreatic insufficiency (an analytical review)]. 1250 76

Original WBN/Kob male rats commonly develop chronic pancreatitis by the age of 3 months, while diabetes mellitus occurs at 9 months. In contrast, female rats of this strain do not show pancreatitis or diabetes. The WBN/Kob-fatty rat is a homozygous (fa/fa) congenic strain for the fa allele of the leptin receptor gene (Lepr). In WBN/Kob-fatty rats, both females and males provide a model of non-insulin-dependent diabetes with obesity. The leptin receptor fatty gene (Lepr(fa)) induces obesity and hyperphagia. In the present study, we examined the effect of dietary restriction on pancreatitis and diabetes in female WBN/Kob-fatty rats. Five female fatty rats comprised a restricted feeding group with paired-feeding from 3 to 13 weeks of age, and five female lean rats comprised a control group with paired-feeding. At 13 weeks of age, two of the five female fatty rats of the control group developed diabetes mellitus, while no female fatty rats of the restricted feeding group developed diabetes mellitus. At this stage, pathological changes of the pancreas were observed in female fatty rats. All female fatty rats showed severe interlobular, intra-lobular and intra-islet fibrosis. In female fatty rats of the restricted feeding group, pathological changes of the pancreas were milder those of the free-feeding fatty group. Although dietary restriction could not completely prevent pancreatitis in female fatty rats, the development of diabetes was inhibited by its reduction of the severity of pancreatitis.
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PMID:The influence of dietary restriction on the development of diabetes and pancreatitis in female WBN/Kob-fatty rats. 2103 Jul 90