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  • Andrén Sandberg, Ake, et al. (författare)
  • Early prediction of severity in acute pancreatitis. Is this possible?
  • 2002
  • Ingår i: Journal of the Pancreas. - 1590-8577. ; 3:5, s. 25-116
  • Tidskriftsartikel (refereegranskat)abstract
    • One out of ten cases of acute pancreatitis develops into severe acute pancreatitis which is a life threatening disorder with a high mortality rate. The other nine cases are self limiting and need very little therapy. The specificity of good clinical judgement on admission, concerning the prognosis of the attack, is high (high specificity) but misses a lot of severe cases (low sensitivity). The prediction of severity in acute pancreatitis was first suggested by John HC Ranson in 1974. Much effort has been put into finding a simple scoring system or a good biochemical marker for selecting the severe cases of acute pancreatitis immediately on admission. Today C-reactive protein is the method of choice although this marker is not valid until 48-72 hours after the onset of pain. Inflammatory mediators upstream from CRP like interleukin-6 and other cytokines are likely to react faster and preliminary results for some of these mediators look promising. Another successful approach has been to study markers for the activation of trypsinogen such as TAP and CAPAP. This is based on studies showing that active trypsin is the initial motor of the inflammatory process in acute pancreatitis. In the near future a combined clinical and laboratory approach for early severity prediction will be the most reliable. Clinical judgement predicts 1/3 of the severe cases on admission and early markers for either inflammation or trypsinogen activation should accurately identify 50-60% of the mild cases among the rest, thus missing only 2-4% of the remaining severe cases. One problem is that there is no simple and fast method to analyze any of these parameters.
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  • Höglund, Erika, et al. (författare)
  • Growth Hormone Increases Beta-Cell Proliferation in Transplanted Human and Fetal Rat Islets
  • 2009
  • Ingår i: Journal of the Pancreas. - 1590-8577. ; 10:3, s. 242-248
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective The aim of the study was to increase the number of human islet beta-cells after transplantation with injections of human growth hormone (hGH). Interventions Human islets and fetal rat islets were transplanted under the left kidney capsule and under the right kidney capsule, respectively in nude normoglycemic mice which were then given a daily injection of 200 µg hGH for 1-4 weeks. Main outcome measure Beta-cell proliferation was determined using thymidine incorporation and the beta-cell area was assessed using light microscopy. Results Mice given hGH increased their body weight one week after transplantation and had a more efficient removal of glucose after 3 and 4 weeks. Treatment with hGH resulted in increased beta-cell proliferation in human and fetal rat beta-cells, and the beta-cell area tended to increase. However, serum insulin concentrations and pancreas insulin content remained unchanged. Conclusions hGH increased the proliferation of transplanted human beta-cells as well as improving the glucose tolerance of the transplanted mice.
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  • Vujasinovic, Miroslav, et al. (författare)
  • Is Pancreatic Exocrine Insufficiency a cause of Malabsorption in Patients after Bariatric Surgery?
  • 2016
  • Ingår i: Journal of the Pancreas. - : E S Burioni Ricerche Bibliografiche. - 1590-8577. ; 17:4, s. 402-405
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction It is known that afferent and efferent loop syndromes can develop following gastric surgery procedures, which can result in accelerated intestinal transit time as well as colonization by pathogenic bacteria in the upper gastrointestinal tract with inadequate stimulation and poorly synchronized pancreatic enzyme secretion. This condition is known as pancreaticocibal asynchrony and can cause pancreatic exocrine insufficiency. The aim of our study was to determine whether pancreatic exocrine insufficiency is impaired in patients after bariatric surgery. We are presenting the results of a pilot study. Patients and methods Patients were selected from the bariatric surgery outpatient clinic of the Slovenj Gradec General Hospital (Slovenian centre of excellence for bariatric surgery). All patients were Caucasians over 18 years of age. The eligibility criteria for surgery were determined according to European guidelines body mass index ≥40 kg/ m2 or ≥35 kg/m2 in patients with obesity-related comorbidities). All procedures were performed by laparoscopic surgery (as Roux-en-Y or mini-omega loop gastric bypass). All patients received standard supplementation after surgery. Faecal elastase-1 (FE1) measurements were performed using the enzyme-linked immunosorbent assay method. Results Twenty-two consecutive patients were included in the study: 21 (95.5%) female and 1 (4.5%) male; the mean age was 42.0±9.2 years, with a range of 24 to 57 years. Patients were included in the study one year after bariatric surgery. Weight outcomes Body mass index pre-surgery: 42.5±4.0 (range 34.9-49.1). Body mass index present: 27.4±3.2 (range 23.1-34.6). Pre-surgery weight: 119.5±15.0 kg (range 97-149). Lowest post-surgery weight (present weight): 76.7±9.6 kg (range 63-100). Total weight loss: 42.8±7.3 kg. Pancreatic exocrine insufficiency was present in two patients (9.1%): mild to moderate pancreatic exocrine insufficiency (FE1 191 μg/g) in a 39-year-old male and severe pancreatic exocrine insufficiency (FE1 15 μg/g) in a 52-year-old female. Serum nutritional markers were low in both patients (vitamin D, iron, selenium). Conclusions Our results show that pancreatic exocrine insufficiency is possible in patients one year post-surgery and could be an additional cause of malabsorption in this group of patients.
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