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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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