[On the use of "cholecystokinin" in radiological examinations of the biliary tract].
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Recurrent bleeding from an obscure gastrointestinal source is a common but often frustrating clinical challenge. Frequently these bleeds can be attributed to vascular anomalies in the upper or lower gastrointestinal tract. Traditional management has included surgical resection and endoscopic fulguration. However, these methods are often ineffective when vascular lesions are diffuse, difficult to identify, or endoscopically inaccessible. Hormone therapy with a combination of oestrogen and progesterone represents a promising alternative. Since initial reports of success in patients with epistaxis from hereditary haemorrhagic telangiectasia, growing evidence supports its role in reducing bleeding from gastrointestinal vascular anomalies. Existing literature is critically reviewed and management strategies incorporating hormone therapy are suggested.
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Insulin-like growth factor-I (IGF-I) has been demonstrated to exert a nitrogen sparing effect, both experimentally and in patients after abdominal surgery. IGF-I is a major mediator for the anabolic effects of growth hormone (GH). Whether elevated circulating IGF-I levels are the sole mediator of the anabolic effects following GH has not been clarified. IGF-I influences glucose metabolism, both through its own specific receptor and by activating the insulin receptor, and has also been proposed to influence pancreatic islet secretion directly. In the present study, the postoperative effects of IGF-I on plasma levels of other gastrointestinal and pancreatic islet hormones and growth factors were measured in patients after abdominal surgery. Fifteen patients who were candidates for large bowel resection were randomly divided into two groups: IGF-I-treated (n=8) and placebo-treated (n=7). The IGF-I group received daily two s.c. injections of human recombinant IGF-I (80 microg/kg body weight) for five days, beginning on the morning of the first postoperative day. The other group received placebo injections. Fasting plasma levels of gastrointestinal growth factors (epidermal growth factor, transforming growth factor-alpha, IGF-II), gastrointestinal hormones (gastrin, enteroglucagon, peptide YY), and islet hormones (insulin, islet amyloid polypeptide (IAPP) and pancreatic glucagon) were determined by RIA preoperatively and after five days of treatment. No significant effects of IGF-I on other growth factors or gastrointestinal hormones were seen. A marked increase in plasma insulin postoperatively compared with the preoperative levels (42+/-3 vs 61+/-5 pM, P<0.05) was seen in the placebo group, whereas the postoperative levels in the IGF-I-treated patients remained unchanged (44+/-3 vs 45+/-4 pM). A similar pattern was observed for IAPP and cortisol concentrations. No differences in glucagon concentrations were seen. In conclusion, these results suggest that IGF-I does not influence production of other gastrointestinal hormones thought to be involved in alimentary growth or pancreatic glucagon. In contrast, IGF-I caused a marked reduction of insulin and IAPP secretion. The inhibition of beta-cell secretion could be direct or, alternatively, could involve an improvement in postoperative insulin resistance, perhaps by reducing serum cortisol.
OBJECTIVE: The authors studied the effect of exogenous glutamine (GLN), with and without growth hormone (GH), pretreatment, on gastrointestinal, hepatic, femoral, and renal GLN fluxes. SUMMARY BACKGROUND DATA: Growth hormone treatment increases gastrointestinal uptake of GLN despite a reduced skeletal muscle and whole body release. METHODS: Piglets were randomized to a GH + GLN group (n = 8), a GLN group (n = 8), a GH group (n = 8), and a control group (CON; n = 8). Genotropin (Pharmacia, Stockholm, Sweden; 24 international units; correspondingly saline in the GLN and the CON group) was given daily 3 days before and at the onset of trauma (surgery). Organ fluxes and whole body release of GLN were determined 1 and 5 hours after surgery. An infusion of GLN 36 micrograms/kg per minute was started after the first measurement in the GH + GLN and the GLN groups. RESULTS: Both GH treatment and exogenous GLN increased gastrointestinal GLN uptake (p = 0.001 and p = 0.02, respectively). Growth hormone treatment reduced hepatic GLN uptake (p = 0.001). Hepatic GLN uptake was lower in the GH + GLN group versus the GH group (p = 0.02), but not in the GLN group versus the CON group (p = 0.98). Growth hormone treatment reduced femoral and whole-body GLN release (p = 0.0001 and p = 0.02, respectively). Renal GLN uptake was higher in the two GH-treated groups (p = 0.003). CONCLUSION: Both exogenous GLN and GH increased gastrointestinal GLN uptake, and the combination was additive. In contrast to exogenous GLN, GH reduced hepatic uptake and consequently facilitated the increased gastrointestinal GLN uptake that occurred despite reduced femoral and whole-body release.
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A commercial preparation of chorionic gonadotrophin inhibited gastric acid secretion induced by carbachol in rats. When the preparation was incubated for 10 min at 100 degrees C and pH 7, its gonadotrophic activity, as measured by a simple quantal assay based on the male toad spermiation response, was reduced by 92%. The inhibition of gastric acid secretion by the preparation was not significantly reduced by this treatment. It is concluded that the two activities are separable.
In 100 subjects the cholecystokinin test has been used in conjunction with the secretin test of gall bladder function. The response of the normal gall bladder to a standard dose of pancreozymin has been studied and the results in patients following cholecystectomy and in the presence of biliary tract disease have been recorded and contrasted with the results obtained by the secretin test and oral cholecystography. These are sufficiently characteristic to warrant the conclusion that used in this way the cholecystokinin test provides a new and valuable semi-quantitative estimate of gall bladder function.
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