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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the last 25 years, 134 patients with chronic pancreatitis were treated surgically in our clinic. According to intraoperative measurement of the pancreatic intraductal pressure, both perfusion pressure and residual pressure in the patients with dilated pancreatic duct were significantly higher than those in control patients. Operative procedures included side-to-side pancreaticojejunostomy in 47 patients, 40%-80% caudal pancreatectomy in 28, pancreaticoduodenectomy in 16, pancreatic sphincteroplasty in 10, and others. The effect of operation on abdominal pain was noted in 97% of the patients. The study of operative effect on abdominal pain and follow-up results showed the excellent maintenance of operative benefit. Surgical treatment, however, could not help improve impaired function of the pancreas. Ten of 34 late deaths were related to the failure of controlling diabetes. Therefore, long-term follow-up care to the pancreatic dysfunction is considered to be necessary even after complete relief of abdominal pain.
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PMID:The role of surgical treatment for chronic pancreatitis. 242 Feb 94

To study incidence and cause of hyperamylasemia in various diseases, serum amylase was determined in 1371 consecutive patients and subsequent isoamylase analysis was carried out in 91 hyperamylasemic sera. Hyperamylasemia was observed in various diseases: acute pancreatitis (5/5), chronic pancreatitis (0/3), mumps (3/3), cerebrovascular diseases (2/39), respiratory diseases (6/69), heart diseases (5/89), liver diseases (16/101), cholelithiasis (0/13), diabetes mellitus (2/66), peptic ulcer (0/46), other digestive diseases (0/33), malignant tumor (9/249), renal failure (21/25), intraabdominal surgery (9/35), extraabdominal surgery (2/20), trauma (1/23), and miscellaneous (10/552). Salivary type hyperamylasemia due to dominant increase of salivary type isoamylase occurred in over half of the hyperamylasemic patients. Knowledge of hyperamylasemia in various diseases and routine isoamylase analysis of hyperamylasemic sera would enhance diagnostic accuracy and exclude unnecessary treatment of pancreatitis solely because of the presence of hyperamylasemia.
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PMID:Clinical value of routine isoamylase analysis of hyperamylasemia. 242 26

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). 246 85

Chronic pancreatitis is associated with glucose intolerance and resultant pancreatogenic diabetes. Using the canine pancreatic duct-ligated model of pancreatitis, we serially evaluated pancreatic histology and electron microscopy, tolerance to intravenous and oral glucose, and insulin response to glucose loading. Pancreatic duct ligation caused microscopic evidence of acute pancreatitis at 1 week, progressing to acinar loss and fibrosis consistent with chronic pancreatitis at time periods up to 6 months. The islets of Langerhans showed degranulation early and appeared to be structurally preserved late. Calculated K values indicated a progressive significant deterioration in intravenous glucose tolerance, falling significantly from 3.46 +/- 0.23 basally to 1.51 +/- 0.17 at 6 months after duct ligation (p less than 0.0001). Oral glucose tolerance deteriorated significantly, with the integrated glucose response rising from 23.7 +/- 1.2 g/dl.minute basally to 32.3 +/- 2.8 g/dl.minute at 6 months after duct ligation (p less than 0.05). Integrated insulin response to both intravenous and oral glucose deteriorated with pancreatitis. Pancreatitis-induced glucose intolerance is a consistent feature of this duct-ligated model. Glucose intolerance stabilizes between 4 and 6 months after duct ligation and is associated with pancreatic acinar fibrosis and pancreatic endocrine structural preservation. While the mechanism of altered glucose tolerance may involve mechanical, neural, humoral, or vascular events, our data clearly support the conclusion that pancreatic ductal stenosis with resultant pancreatic fibrosis and chronic pancreatitis is associated with abnormal islet responsiveness leading to circulating insulin deficiency and glucose intolerance, despite histologic and ultrastructural evidence of intact islets of Langerhans.
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PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

Recent longitudinal studies have improved the knowledge of the natural history of chronic pancreatitis. This disease is mainly induced by alcohol abuse. Mean age at onset of the disease is 40 years. First symptoms are generally pain, often related to acute pancreatitis. Over the first five years of course, complications as pseudocysts or common bile duct stenoses can occur, often necessitating surgical treatment. In the late course, the disease becomes less symptomatic but the risk of diabetes mellitus increases. Occurrence of pancreatic calcifications is observed with time in the majority of patients. Chronic pancreatitis is associated with overmortality but the causes of death are mainly extrapancreatic (alcoholic liver disease and cancers). Abnormalities of pancreatic secretion induced by alcohol abuse play an important role in the pathophysiology of the disease: it is possible that the decrease of concentration of the "pancreatic stone protein" promotes formation of calcifications. Direct toxicity of alcohol is another possible factor.
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PMID:[The natural history and physiopathology of chronic pancreatitis]. 248 15

Significant obstructive jaundice in chronic pancreatitis is generally considered to be rare. Eleven of 57 consecutive patients with proven chronic pancreatitis have developed significant obstructive jaundice of more than transient duration. Eight presented as jaundice complicating known pancreatitis and three as jaundice of unknown cause. Life table analysis showed a steady rise in the risk of developing jaundice up to the end of 10 years from the onset of chronic pancreatitis. Jaundice was found to occur in the presence of more "destructive" disease, and jaundiced patients had a higher incidence of pancreatic calcification, diabetes and malabsorption at the time of presentation with jaundice. Obstructive jaundice caused by chronic pancreatitis was found to carry a good prognosis for jaundice, for pain and for life. Only one of the 11 patients died in hospital. It is important to distinguish chronic pancreatitis from cancer in these patients. Pre-operative and intra-operative cytology have been helpful. Stent insertion is not an appropriate method of treatment for these patients because of the benign nature of the disease and the possibility of exacerbating the pancreatitis. It is important to be aware of another form of "malignant masquerade" causing obstructive jaundice.
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PMID:Obstructive jaundice in chronic pancreatitis. 248 66

This study was performed to ascertain the role of serum markers and simple clinical data in detecting pancreatic cancer and in distinguishing this malignancy from chronic pancreatitis and other gastrointestinal diseases. Serum CA 19-9, tissue polypeptide antigen and carcinoembryonic antigen were measured in 38 control subjects, 37 patients with pancreatic cancer, 39 with chronic pancreatitis and 44 with extra-pancreatic diseases mainly of gastrointestinal origin. Clinical data recorded included age, sex, presence of pancreatic calcifications, weight loss, pain, jaundice, alcohol abuse, diabetes mellitus. Serum markers gave a correct allocation of the subjects in 48.1% of the cases with pancreatic cancer patients correctly predicted in 62.2%. Clinical data correctly diagnosed 74.2% of subjects. Chronic pancreatitis was identified in 84.6% of the cases and pancreatic cancer in 64.9%. The first clinical variables selected were pain and age. The addition of serum markers to clinical data did not enhance accuracy of the results. We conclude that the diagnosis of chronic pancreatic diseases should first be suspected on the basis of accurately recorded simple clinical data; serum markers seem to be only occasionally useful. Since indicative clinical data and serum markers become positive in the advanced phases of pancreatic cancer, early diagnosis of this malignancy still remains an objective to reach.
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PMID:[Role of serum markers and or various clinical parameters in the diagnosis of pancreatic carcinoma]. 248 91

S-100 protein-containing cells were demonstrated by immunogold silver staining in human islets of Langerhans from patients with chronic pancreatitis (CP) with (n = 6) (Group I) or without (n = 6) (Group II) diabetes mellitus, (DM) and from nondiabetic, non-pancreatic controls (n = 6) (Group III). In all three groups S-100 protein containing cells were observed in all islets of Langerhans throughout the pancreas. Quantitative analysis of cell composition of islets did not reveal significant differences in S-100 protein cell content between the three groups. When double immunohistochemical staining was used to demonstrate different endocrine cell types (insulin, glucagon and pancreatic polypeptide) and S-100 protein immunoreactive cells, the latter proved to be a distinct cell type. Somatostatin-producing cells and S-100 protein-containing cells were usually also present as two distinct cell populations, but positive staining for both S-100 protein and somatostatin was occasionally observed within the same cells.
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PMID:S-100 protein immunoreactivity in human islets of Langerhans. 251 43

Chronic pancreatitis of biliary origin, frequently located in the cephalic portion of the organ, etiopathogenically dependent on biliary lithiasis, the anatomoclinical evolution of which is complicated by their presence, have a better prognosis, and are usually reversible following therapy of the biliary affections. Persistent chronic pancreatitis proper, usually of the recurrent type, associated with calcification and the development of pancreatic stones, and with pseudocysts, although rare in our country, raise diagnostic difficulties from the standpoint of surgery, and have a reserved prognosis. The authors have evaluated a total of 321 cases hospitalized between 1960 and 1987 with chronic pancreatitis of biliary origin (252 cases--78.5%), and chronic pancreatitis proper, not associated to biliary affections (69 cases--21.5%). Male patients totalled 33.6% of all cases. The authors stress the high frequency of chronic pancreatitis associated to biliary lithiasis (181 cases), in contrast with pancreatitis associated to nonlithiasic cholecystopathies (38 cases), or to postoperative cholecystic disturbances (33 cases). Chronic pancreatitis non-associated to biliary affections totalled 69 cases, of which 24 were of the persistent type, 13 were of the recurrent type, one had calcifications, two had pancreatic stones, four followed acute pancreatitis, six were complicated by pancreatic abscesses, and 9 were complicated by pseudocysts. The duration of biliary and pancreatic disturbances was between 3 and 5 years in 43.9% of the cases, and between 6 and 10 years in 21.3%. Chronic pancreatitis achieves a complex clinical syndrome, the dominant feature being the painful biliopancreatic syndrome associated to obstructive jaundice (42.4%), angiocholitis (47.6%), weight loss (46%), hepatic and renal failure (10.9%), diabetes (8.4%), and a tumoral mass (15.7%). Indirect surgical interventions aimed at suppressing the biliary factor were carried out in 291 patients, with very good results in 56% of the cases, good results in 32%, mediocre in 7%. In 2.4% of the cases surgery failed to improve the condition of the patients. Direct interventions on the pancreas, which consisted either in pancreatic decompression or in exeresis of the gland have been performed in 30 patients. Drainage of pancreatic abscesses was done in 6 patients (2 deaths), cystic-digestive anastomoses were performed in 8 patients, Wirsung-jejunostomy in 3 patients (1 death), cystostomy in one patient, distal pancreatectomy in one patient (deceased), viscerolysis and novocaine infiltration in 11 patients. In the 321 cases of chronic pancreatitis operated by direct and indirect procedures very good
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PMID:[Chronic pancreatitis: anatomico-clinical and surgical therapy characteristics. Our experience with 321 cases]. 252 82

Insulin-like growth factor II is secreted primarily by the liver and is reported to be transcribed in many primary hepatocellular carcinoma (PHC) cell lines. We have studied diagnostic significance of serum IGF-II in chronic liver diseases using specific enzyme immunoassay. Serum IGF-II levels (mean +/- SE) were decreased in chronic hepatitis (538 +/- 51 ng/ml; N = 29), liver cirrhosis (427 +/- 45; 50) and PHC (260 +/- 41; 17) compared to controls (830 +/- 49; 57). Serum IGF-II was not different from controls in any of nonhepatic diseases such as diabetes (1032 +/- 97; 19) pancreatic cancer (1413 +/- 282; 8), chronic pancreatitis (999 +/- 126; 17), peptic ulcer (1186 +/- 43; 11), irritable bowel syndrome (1002 +/- 109; 12), gastrointestinal tract cancer (1250 +/- 216; 21) and chronic renal failure (733 +/- 135; 14). In liver diseases serum IGF-II showed a significant correlation with liver function test (negative with retention of indocyanine green and total bile acids; positive with albumin, thrombo-test, and cholinesterase). These results suggest that serum IGF-II reflects a reduced production of IGF-II in the liver and that it can be an index for the residual capacity of liver function.
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PMID:Serum insulin-like growth factor II in chronic liver disease. 253 15


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