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  • 1
    Electronic Resource
    Electronic Resource
    Der Einfluß des Calciums auf den Serumgastrinspiegel und die Magensekretion beim Menschen (1974)
    Springer
    Journal of molecular medicine 52 (1974), S. 433-436 
    Details
    ISSN: 1432-1440
    Keywords: Gastrin ; gastric secretion ; calcium ; normal subjects ; duodenal ulcer ; Zollinger-Ellison syndrome ; Gastrin ; Magensekretion ; Calcium ; Normalpersonen ; Ulcus duodeni ; Zollinger-Ellison-Syndrom
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der Einfluß einer induzierten Hypercalcämie auf die Serumgastrinspiegel und die Magensekretion wurde bei Normalpersonen, Patienten mit Ulcus duodeni und Patienten mit Zollinger-Ellison-Syndrom untersucht. Bei allen Patientengruppen kommt es während der Calciumgluconatinfusion zu einem signifikanten Anstieg der Serumgastrinspiegel. Patienten mit Ulcus duodeni schütten jedoch 2–3mal soviel Gastrin während einer Hypercalcämie aus wie Normal-personen, während die Gastrinausschüttung bei Patienten mit Zollinger-Ellison-Syndrom ein Vielfaches der von Ulcus duodeni-Patienten beträgt. Die integrierte Säureausschüttung während Hypercalcämie ist bei Ulcus duodeni-Patienten ca. 5fach höher als bei Kontrollpersonen. Diese Untersuchungen zeigen, daß die Calcium-induzierte Magensekretion, zumindestens teilweise, durch eine Gastrinfreisetzung hervorgerufen wird.
    Notes: Summary We studied the effect of hypercalcemia on the serum gastrin concentration and gastric secretion in normal man, duodenal ulcer patients and patients with the Zollinger-Ellison syndrome. All subjects showed a significant increase of serum gastrin concentrations during calcium infusion. Patients with duodenal ulcer showed a 2- to 3-fold higher gastrin output during hypercalcemia than normal subjects, but the gastrin output in patients with Zollinger-Ellison syndrome was much higher compared to patients with duodenal ulcer. The integrated gastric secretory response to hypercalcemia is 5-fold higher in duodenal ulcer patients compared to normal subjects. These studies show that, at least in part, the calcium-induced gastric secretion is caused by gastrin release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01468584
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients (1996)
    Springer
    Diabetologia 39 (1996), S. 462-468 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pancreas transplantation ; insulin secretion ; pancreatic hormones ; oral glucose tolerance ; glucagon stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400678
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients (1996)
    Springer
    Diabetologia 39 (1996), S. 462-468 
    Details
    ISSN: 1432-0428
    Keywords: Pancreas transplantation ; insulin secretion ; pancreatic hormones ; oral glucose tolerance ; glucagon stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i.v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p〈0.0001; C-peptide p=0.037). Age (p=0.65), body mass index (p=0.94), immunosuppressive therapy (cyclosporin A p=0.84; predniso(lo)ne p=0.91; azathioprine p=0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (−46%; p=0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p=0.003) and the number of HLA-DR mismatches (p=0.026), but not with HLA-AB-mismatches (p=0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400678
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    242. Zollinger-Ellison-Syndrom (1975)
    Springer
    Langenbeck's archives of surgery 339 (1975), S. 755-755 
    Details
    ISSN: 1435-2451
    Keywords: Zollinger-Ellison syndrome, Diagnostic procedure ; Morphology ; Total gastrectomy ; Zollinger-Ellison-Syndrom ; Diagnostik ; Morphologische Befunde Totale Gastrektomie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die klinische Symptomatik, das diagnostische Vorgehen and die Therapie des Zollinger-Ellison-Syndom (Z.E.S.) sind Gegenstand zahlreicher Diskussionen gewesen. Anhand der eigenen Erfahrung bei 13 Fallen werden das Beschwerdebild und die notwendigen diagnostischen MaBnahmen (Serumgastrinbestimmung, Provokationsteste) dargestellt. Die morphologische Vielfalt der gastrinproduzierenden Tumoren wird durch immunhistologische and elektronenmikroskopische Befunde demonstriert. Als Therapie der Wahl hat die totale Gastrektomie zu gelten, da in einem hohen Prozentsatz die Gastrinome bereits metastasiert haben.
    Notes: Summary The clinical symptomatology, diagnostic procedure and treatment of the Zollinger-Ellison syndrome (Z.E.S.) is discussed extensively. The authors' own experience in 13 cases is described to illustrate the symptoms and the necessary diagnostic steps (serum gastrin determination, provocation tests). The morphologic variety of the gastrin-producing tumors is shown by immunohistologic and electron-microscopic findings. Total gastrectomy is the therapy of choice, since most gastrinomas are metastasizing by the time they are recognized.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01257721
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    Paper (German National Licenses)
    Fulltext
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