(1/848) Pancreatic polypeptide hyperplasia causing watery diarrhea syndrome: a case report.
Neuroendocrine tumours of the pancreas can secrete numerous peptides, leading to various recognizable clinical syndromes. The secretion of pancreatic polypeptide has been used as a marker for neuroendocrine tumours but is considered to be a biologically inert peptide. A 37-year-old woman had watery diarrhea syndrome from pancreatic polypeptide hyperplasia. Only 2 other reported cases in the literature have described pancreatic polypeptide hyperplasia; however, this is the first reported case in which the patient was successfully treated by surgical resection, with a 2-year follow-up. This report and review of the literature illustrate that pancreatic polypeptide hypersecretion may present as a clinical endocrinopathy. (+info)
(2/848) The homeodomain protein IDX-1 increases after an early burst of proliferation during pancreatic regeneration.
Islet duodenal homeobox 1 (IDX-1/PF-1/STF-1/PDX-1), a homeodomain protein that transactivates the insulin promoter, has been shown by targeted gene ablation to be required for pancreatic development. After 90% pancreatectomy (Px), the adult pancreas regenerates in a process recapitulating embryonic development, starting with a burst of proliferation in the epithelium of the common pancreatic duct. In this model, IDX-1 mRNA was detected by semiquantitative reverse transcription-polymerase chain reaction in total RNA from isolated common pancreatic ducts at levels 10% of those of isolated islets. The IDX-1 mRNA levels were not significantly different for common pancreatic ducts of Px, sham Px, and unoperated rats and did not change with time after surgery. By immunoblot analysis, IDX-1 protein was only faintly detected in these ducts 1 and 7 days after Px or sham Px but was easily detected at 2 and 3 days after Px. Similarly, IDX-1 immunostaining was barely detectable in sham or unoperated ducts but was strong in ducts at 2-3 days after Px. The increase of IDX-1 immunostaining followed that of BrdU incorporation (proliferation). These results indicate a posttranscriptional regulation of the IDX-1 expression in ducts. In addition, islets isolated 3-7 d after Px showed higher IDX-1 protein expression than control islets. Thus, in pancreatic regeneration IDX-1 is upregulated in newly divided ductal cells as well as in islets. The timing of enhanced expression of IDX-1 implies that IDX-1 is not important in the initiation of regeneration but may be involved in the differentiation of ductal cells to beta-cells. (+info)
(3/848) Relation between hospital surgical volume and outcome for pancreatic resection for neoplasm in a publicly funded health care system.
BACKGROUND: Recent studies from the United States have shown that institutions with higher numbers of pancreatic resection procedures for neoplasm have lower mortality rates associated with this procedure. However, minimal work has been done to assess whether the results of similar volume-outcome studies within a publicly financed health care system would differ from those obtained in a mixed public-private health care system. METHODS: A population-based retrospective analysis was used to examine pancreatic resection for neoplasm in Ontario for the period 1988/89 to 1994/95. Outcomes examined included in-hospital case fatality rate and mean length of stay in hospital. For each hospital, total procedure volume for the study period was defined as low (fewer than 22), medium (22-42) or high (more than 42). Regression models were used to measure volume-outcome relations. RESULTS: The likelihood of postoperative death was higher in low-volume and medium-volume centres than in high-volume centres (odds ratio 5.1 and 4.5 respectively; p < 0.01 for both). Mean length of stay was greater in low- and medium-volume centres than in high-volume centres (by 7.7 and 9.2 days respectively, p < 0.01 for both). INTERPRETATION: This study adds to growing evidence that, for pancreatic resection for neoplasm, patients may have better outcomes if they are treated in high-volume hospitals rather than low-volume hospitals. (+info)
(4/848) Pancreatectomy for chronic pancreatitis.
Of one hundred and forty-nine patients (101 male and 48 female) 4-67 years of age, 117 were alcoholics and underwent pancreatectomy because of episodic or continuous abdominal pain or complications or chronic pancreatitis. Nineteen patients underwent pancreaticoduodenectomy, seventy-seven 80-95% distal resection, anf fifty-three 40-80% distal pancreatic resection. There were 3 operative death and 30 late deaths 6 months to 11 years post pancreatectomy. Twenty-one patients were lost to followup, 1 to 11 years post pancreatectomy. Ninety-five patients are known to be alive, 4 of whom are institutionalized. Indications for pancreatectomy in addition to abdominal pain include recurrent or multiple pseudocysts, failure to relieve pain after decompression of a pseudocyst, pseudoaneurysm of the visceral arteries associated with a pseudocyst, recurrent attacks of pancreatitis unrelived by non-resective operations, duodenal stenosis and left side portal hypertension. The choice between pancreaticoduodenectomy or distal resection of 40-80% or 80-95% of the pancreas should be based on the principle site of inflammation whether proximal or distal in the gland, the size of the common bile duct, the ability to rule out carcinoma, and the anticipated deficits in exocrine and endocrine function. The risk of diabetes is very significant after 80-95% distal resection and of steatorrhea after pancreaticoduodenectomy. When the disease process can be encompassed by 40-80% distal pancreatectomy this is the procedure of choice. (+info)
(5/848) Patient survival after D1 and D2 resections for gastric cancer: long-term results of the MRC randomized surgical trial. Surgical Co-operative Group.
Controversy still exists on the optimal surgical resection for potentially curable gastric cancer. Much better long-term survival has been reported in retrospective/non-randomized studies with D2 resections that involve a radical extended regional lymphadenectomy than with the standard D1 resections. In this paper we report the long-term survival of patients entered into a randomized study, with follow-up to death or 3 years in 96% of patients and a median follow-up of 6.5 years. In this prospective trial D1 resection (removal of regional perigastric nodes) was compared with D2 resection (extended lymphadenectomy to include level 1 and 2 regional nodes). Central randomization followed a staging laparotomy. Out of 737 patients with histologically proven gastric adenocarcinoma registered, 337 patients were ineligible by staging laparotomy because of advanced disease and 400 were randomized. The 5-year survival rates were 35% for D1 resection and 33% for D2 resection (difference -2%, 95% CI = -12%-8%). There was no difference in the overall 5-year survival between the two arms (HR = 1.10, 95% CI 0.87-1.39, where HR > 1 implies a survival benefit to D1 surgery). Survival based on death from gastric cancer as the event was similar in the D1 and D2 groups (HR = 1.05, 95% CI 0.79-1.39) as was recurrence-free survival (HR = 1.03, 95% CI 0.82-1.29). In a multivariate analysis, clinical stages II and III, old age, male sex and removal of spleen and pancreas were independently associated with poor survival. These findings indicate that the classical Japanese D2 resection offers no survival advantage over D1 surgery. However, the possibility that D2 resection without pancreatico-splenectomy may be better than standard D1 resection cannot be dismissed by the results of this trial. (+info)
(6/848) Pancreatic exocrine and endocrine function after pancreatectomy for persistent hyperinsulinaemic hypoglycaemia of infancy.
AIM: To evaluate long term detailed pancreatic endocrine and exocrine function in children with persistent hyperinsulinaemic hypoglycaemia of infancy (PHHI) after 85-95% pancreatectomy. METHODS: Six children with PHHI between 0.9 and 12.7 years after pancreatic resection underwent clinical and investigative follow up at 1.0 to 14.9 years of age. One child with PHHI who had not had pancreatectomy was also assessed. Standard endocrine assessment, pancreatic magnetic resonance imaging (MRI), and detailed direct and indirect tests of exocrine pancreatic function were performed. RESULTS: Pancreozymin-secretin stimulation test results were normal in only one child, borderline in two, and deficient in four, one of whom requires daily pancreatic enzyme supplements. Pancreolauryl tests performed in three children were borderline in two and abnormal in the other. Only one child had low faecal chymotrypsin values. One child developed insulin dependent diabetes at 9 years and two children at 1.0 and 13.3 years require diazoxide to maintain normoglycaemia. MRI showed no major regrowth of the pancreatic remnant after resection (n = 5). CONCLUSIONS: Clinical evidence of endocrine or exocrine dysfunction has developed in only two patients to date, but detailed pancreatic function testing suggests subclinical deficiency in all but one of our patients with PHHI. Although 95% pancreatectomy results in postoperative control of blood glucose, subclinical pancreatic insufficiency is present on long term follow up and development of diabetes mellitus and exocrine failure remain ongoing risks. (+info)
(7/848) Long-term follow up of persistent hyperinsulinaemic hypoglycaemia of infancy.
Twenty six children with hypoglycaemia were diagnosed and followed between 1975 and 1995. Diagnosis was confirmed by a high insulin:glucose ratio, and low free fatty acid and 3-hydroxybutyrate on fasting. All patients were treated with diazoxide at a maximum dose of 20 mg/kg/day. Requirement of a higher dose was considered as a failure of medical treatment and an indication for surgery. Sixteen children Responded to diazoxide; 10 failed to respond and underwent pancreatic resection. Six of the latter group started with symptoms in the neonatal period. Eleven of the 26 children have neurological sequelae. Head growth and neurological outcome correlated well. Additionally, non-specific electroencephalogram abnormalities (slow waves) appear to be indicative of subclinical hypoglycaemia during follow up. (+info)
(8/848) Regulation of protein synthesis after acute resistance exercise in diabetic rats.
These studies determined whether insulin-like growth factor-I (IGF-I) involvement in exercise-stimulated anabolic processes becomes more evident during hypoinsulinemia. Male Sprague-Dawley rats (n = 6-12/group) were made diabetic (blood glucose congruent with 300 mg/dl) by partial pancreatectomy (PPX) or remained nondiabetic (glucose congruent with 144 mg/dl). Rats performed acute resistance exercise by repetitive standing on the hindlimbs with weighted backpacks (ex), or they remained sedentary (sed). Resistance exercise caused increases in rates of protein synthesis (nmol Phe incorporated. g muscle-1. h-1, measured for gastrocnemius muscle in vivo 16 h after exercise) for both nondiabetic [sed = 154 +/- 6 (SE) vs. ex = 189 +/- 7] and diabetic rats (PPXsed = 152 +/- 11 vs. PPXex = 202 +/- 14, P < 0.05). Arterial plasma insulin concentrations in diabetic rats, congruent with180 pM, were less than one-half those found in nondiabetic rats, congruent with444 pM, (P < 0.05). The activity of eukaryotic initiation factor 2B (eIF2B; pmol GDP exchanged/min) was higher (P < 0.05) in ex rats (sed = 0.028 +/- 0.006 vs. ex = 0.053 +/- 0.015; PPXsed = 0.033 +/- 0.013 vs. PPXex = 0.047 +/- 0.009) regardless of diabetic status. Plasma IGF-I concentrations were higher in ex compared with sed diabetic rats (P < 0.05). In contrast, plasma IGF-I was not different in nondiabetic ex or sed rats. Muscle IGF-I (ng/g wet wt) was similar in ex and sed nondiabetic rats, but in diabetic rats was 2- to 3-fold higher in ex (P < 0.05) than in sed rats. In conclusion, moderate hypoinsulinemia that is sufficient to alter glucose homeostasis does not inhibit an increase in rates of protein synthesis after acute moderate-intensity resistance exercise. This preserved response may be due to a compensatory increase in muscle IGF-I content and a maintained ability to activate eIF2B. (+info)