Academic literature on the topic 'Pentagastrine'

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Journal articles on the topic "Pentagastrine"

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Guedj, A. M., I. Julier, N. Jourdan, A. Maubon, P. Fabbro-Peray, and M. Rodier. "P099 - Test à la pentagastrine : marqueur du CMT ou du papillaire…" Annales d'Endocrinologie 65, no. 4 (2004): 329–30. http://dx.doi.org/10.1016/s0003-4266(04)95810-6.

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Pina, G., S. Dubois, A. Murat, et al. "Le dosage ultrasensible de calcitonine basale peut-il remplacer le test à la pentagastrine ?" Annales d'Endocrinologie 73, no. 4 (2012): 271. http://dx.doi.org/10.1016/j.ando.2012.07.113.

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Wion-Barbot, N., J. P. Saint-Andre, A. Minebois, V. Rohmer, J. Ronceray, and J. Cl Bigorgne. "Dépistage des microcarcinomes médullaires de la thyroïde par le dosage immunoradiométrique de la calcitonine, après injection de Pentagastrine." La Revue de Médecine Interne 13, no. 7 (1992): S365. http://dx.doi.org/10.1016/s0248-8663(05)80952-x.

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Rohmer, V., G. Vidal-Trecan, A. Bourdelot, et al. "Prognostic Factors of Disease-Free Survival after Thyroidectomy in 170 Young Patients with a RET Germline Mutation: A Multicenter Study of the Groupe Français d'Etude des Tumeurs Endocrines." Journal of Clinical Endocrinology & Metabolism 96, no. 3 (2011): E509—E518. http://dx.doi.org/10.1210/jc.2010-1234.

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Background: In hereditary medullary thyroid carcinoma (HMTC), prophylactic surgery is the only curative option, which should be properly defined both in time and extent. Objectives: To identify and characterize prognostic factors associated with disease-free survival (DFS) in children from HMTC families. Design: We conducted a retrospective analysis of a multi-center cohort of 170 patients below age 21 at surgery. Demographic, clinical, genetic, biological data [basal and pentagastrine-stimulated calcitonin (CT and CT/Pg, respectively)], and tumor node metastasis (TNM) status were collected. DFS was assessed based on basal CT levels. Kaplan–Meier curves, Cox regression, and logistic regression models were used to determine factors associated with DFS and TNM staging. Results: No patients with a preoperative basal CT <31 ng/ml had persistent or recurrent disease. Medullary thyroid carcinoma defined by a diameter ≥10 mm [hazard ratio (HR): 6.0; 95% confidence interval (95% CI): 1.8–19.8] and N1 status (HR: 20.8; 95% CI: 3.9–109.8) were independently associated with DFS. Class D genotype [odds ratio (OR): 48.5, 95% CI: 10.6–225.1], preoperative basal CT >30 ng/liter (OR: 43.4, 95% CI: 5.2–359.8), and age >10 (OR: 5.5, 95% CI: 1.4–21.8) were associated with medullary thyroid carcinoma ≥10 mm. No patient with a preoperative basal CT <31 ng/ml had a N1 status. Class D genotype (OR: 48.6, 95% CI: 8.6–274.1), and age >10 (OR: 4.6, 95% CI: 1.1–19.0) were associated with N1 status. Conclusion: In HMTC patients, DFS is best predicted by TNM staging and preoperative basal CT level below 30 pg/ml. Basal CT, class D genotype, and age constitute key determinants to decide preoperatively timely surgery.
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Stevens, M. H., R. C. Thirlby, C. T. Richardson, M. A. Fredrickson, R. H. Unger, and M. Feldman. "Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 4 (1986): G453—G459. http://dx.doi.org/10.1152/ajpgi.1986.251.4.g453.

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We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.
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Redfern, J. S., R. Thirlby, M. Feldman, and C. T. Richardson. "Effect of pentagastrin on gastric mucosal histamine in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 3 (1985): G369—G375. http://dx.doi.org/10.1152/ajpgi.1985.248.3.g369.

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We studied the effect of pentagastrin on histamine content of gastric mucosa obtained from dogs with gastric fistulas to determine whether pentagastrin mobilizes cellular stores of histamine. Experiments were also performed on canine gastric mucosa in vitro to investigate the effects of pentagastrin on histamine release, per se. During in vivo studies basal histamine content averaged 0.9 nmol/mg wet wt tissue or 18.8 nmol/mg tissue prot. No significant difference in gastric mucosal histamine content occurred during intravenous administration of pentagastrin (6 or 16 micrograms . kg-1 . h-1) or saline (control), even though acid output from the gastric fistula increased significantly above control during pentagastrin infusion. Moreover, pentagastrin (10(-5) and 10(-8)M) did not release more histamine from gastric mucosa in vitro than the buffer (control), whereas Triton X-100 and the phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, alone and in combination with calcium ionophore A23187, released significant amounts of histamine above control values. From these experiments we conclude that pentagastrin did not alter histamine content of canine gastric mucosa in vivo, even though acid secretion was stimulated maximally, nor did pentagastrin release histamine in vitro.
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van Megen, H. J. G. M., H. G. M. Westenberg, and J. A. Den Boer. "Evidence for enhanced sensitivity for pentagastrin in panic disorder patients." Acta Neuropsychiatrica 5, no. 2 (1993): 23–28. http://dx.doi.org/10.1017/s0924270800033950.

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SummaryWe studied the effects of pentagastrin, an analogue of the cholecystokinin tetrapeptide (CCK4), in 15 patients with panic disorder and 15 healthy controls. Three different intravenous dosages of pentagastrin (0.1, 0.3 and 0.6 μ/kg) and placebo (saline) were investigated. Subjects were randomly allocated to two of the four dosage groups and tested on two separate occasions, one week apart, using a double-blind incomplete block design. A total of 59 intravenous injections were carried out. The panic rate with pentagastrin, irrespective of the dosage, was 55% (12/22) for patients and 5% (1/22) for controls. None of the subjects panicked with saline. The frequency of panic attacks between the three pentagastrin doses in patients was not different. One control subject had a panic-like attack at the highest dose of pentagastrin. These findings concur with previous studies on the panicogenic effect of CCK4 and pentagastrin and suggest a greater sensitivity for CCK agonists in patients suffering from panic disorder than in healthy controls.
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Nishida, A., A. Kobayashi-Uchida, S. Akuzawa, et al. "Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 5 (1995): G699—G705. http://dx.doi.org/10.1152/ajpgi.1995.269.5.g699.

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Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for > or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats.
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Campbell-Thompson, M. L., and A. M. Merritt. "Basal and pentagastrin-stimulated gastric secretion in young horses." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 6 (1990): R1259—R1266. http://dx.doi.org/10.1152/ajpregu.1990.259.6.r1259.

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Equine gastric secretion was studied using a gastric cannula model after fasting (basal) and pentagastrin infusion. Gastric secretory rate, pH, osmolality, and electrolyte concentrations and outputs were determined over a 5-h period. Dose-response tests estimated that the maximally effective intravenous dose of pentagastrin was between 3 and 6 micrograms.kg-1.h-1. Basal secretory rate was 278 +/- 29 (SE) ml/15 min, and the pH was 2.00 +/- 0.31. Pentagastrin infusion at 6 micrograms.kg-1.h-1 increased secretory rate to 533 +/- 60 ml/15 min and decreased pH to 1.41 +/- 0.11. Basal gastric acid concentration and output were 38 +/- 5 meq/l and 211 +/- 36 mu eg.kg-1.h-1, respectively. Pentagastrin increased acid concentration to 60 +/- 5 meq/l and acid output to 474 +/- 61 mu eq.kg-1.h-1. Gastric fluid osmolality remained hypotonic during both basal and pentagastrin conditions. Sodium concentration remained high in comparison with hydrogen ion concentration, and sodium output increased during pentagastrin infusion. Equine gastric secretion did not attain maximal acid concentrations nor the marked drop in pH, which has been reported for other monogastric species. These data suggest that in the horse a large nonparietal component exists that modifies parietal secretions and is increased by pentagastrin stimulation.
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Heitkemper, M. M., and J. F. Shaver. "Pentagastrin on neurotransmitter enzyme activities in the rat gastrointestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 4 (1986): G546—G552. http://dx.doi.org/10.1152/ajpgi.1986.250.4.g546.

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The effects of three doses (5, 100, and 250 micrograms/kg) of pentagastrin on the activities of choline acetyltransferase (ChAT) and acetylcholine esterase (AChE), the neurotransmitter enzymes that synthesize and degrade acetylcholine, and monoamine oxidase (MAO), the degradation enzyme for catecholamines, were investigated. Enzyme activities were assayed in 6 gastrointestinal segments of 21- and 28-day-old and adult rats. All animals were injected intraperitoneally for 7 days with pentagastrin, and the results were compared with age-matched controls receiving saline for 7 days. Plasma and adrenal corticosterone levels were measured. No consistent differences in adrenocortical variables existed between pentagastrin- and saline-treated animals. Similarly, no consistent pentagastrin dose responses of ChAT, AChE, and MAO activities were evident. However, at the highest dose pentagastrin generally produced increases in ChAT activities in 21- and 28-day-old rats, while producing decreases in AChE and MAO activities in 21-day-old rats and increases in 28-day-old animals. There were few significant differences in enzyme activities in adult rats receiving pentagastrin as compared to saline.
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Dissertations / Theses on the topic "Pentagastrine"

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CERF, ISABELLE. "Depistage du cancer medullaire de la thyroide par le dosage irma de la calcitonine sous stimulation par la pentagastrine." Angers, 1991. http://www.theses.fr/1991ANGE1072.

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RIBARD, DIDIER. "Effet inhibiteur de l'octapeptide c-terminal de l'oxyntomoduline sur la secretion acide gastrique stimulee par la pentagastrine chez l'homme." Montpellier 1, 1989. http://www.theses.fr/1989MON11040.

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Ferroudji, Sai͏̈d. "Effet inhibiteur de l'octapeptide C-terminal de l'oxyntomoduline sur la sécrétion acide gastrique stimulée par la pentagastrine chez l'homme : essai d'étude dose-effet." Montpellier 1, 1990. http://www.theses.fr/1990MON11196.

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Strang, Isobel. "In vivo and in vitro studies of the CCK←B receptor in anxiety." Thesis, University of the West of Scotland, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311768.

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Elwerr, Malik [Verfasser], Kerstin [Gutachter] Lorenz, Nada [Gutachter] Rayes, and Katharina [Gutachter] Holzer. "Calcium vs. Pentagastrin Stimulation bei der C-Zell-Erkrankung der Schilddrüse : eine Matched-Pair Analyse / Malik Elwerr ; Gutachter: Kerstin Lorenz, Nada Rayes, Katharina Holzer." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2020. http://d-nb.info/1226762115/34.

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Abuazab, Mohammed Ibrahim Mahmoud [Verfasser], K. [Gutachter] Lorenz, Oliver [Gutachter] Gimm, and Thomas J. [Gutachter] Musholt. "Korrelation des intraoperativen Pentagastrin-Stimulationstestes und der Kompartiment-orientierten Lymphknotendissektion zur Prädiktion des onkologisch adäquaten Resektionsausmaßes beim medullären Schilddrüsenkarzinom / Mohammed Ibrahim Mahmoud Abuazab ; Gutachter: K. Lorenz, Oliver Gimm, Thomas J. Musholt." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2017. http://d-nb.info/1210731606/34.

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Abuazab, Mohammed Ibrahim Mahmoud [Verfasser], K. Gutachter] Lorenz, Oliver [Gutachter] [Gimm, and Thomas J. [Gutachter] Musholt. "Korrelation des intraoperativen Pentagastrin-Stimulationstestes und der Kompartiment-orientierten Lymphknotendissektion zur Prädiktion des onkologisch adäquaten Resektionsausmaßes beim medullären Schilddrüsenkarzinom / Mohammed Ibrahim Mahmoud Abuazab ; Gutachter: K. Lorenz, Oliver Gimm, Thomas J. Musholt." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2017. http://nbn-resolving.de/urn:nbn:de:gbv:3:4-1981185920-255284.

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Hüller, Mareike. "Stellenwert der basalen im Vergleich zur Pentagastrin-stimulierten Kalzitoninbestimmung in der Nachsorge des C-Zellkarzinoms." Doctoral thesis, 2009. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-37292.

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Der spezifischste und sensitivste biochemische Tumormarker in der Diagnostik und Verlaufskontrolle des MTC ist Kalzitonin. Der hCT-Spiegel sollte nach totaler Thyreoidektomie nicht mehr messbar sein. Ein messbares hCT weist nach Therapie auf ein Rezidiv oder eine Metastasierung hin. Die hCT-Sekretion kann durch Gastrin stimuliert werden, was beim Pentagastrin-Stimulationstest genutzt wird. Im Rahmen dieser Arbeit wurde untersucht, welchen Stellenwert die Bestimmung des basalen Kalzitonin im Vergleich zum Pentagastrin-stimulierten hCT in der Nachsorge des MTC einnimmt. Hierzu wurden 129 Pentagastrintests von MTC-Patienten der Klinik und Poliklinik für Nuklearmedizin der Universität Würzburg retrospektiv ausgewertet. Bei sechs Prozent der Patienten fand sich nach anfänglicher biochemischer Remission ein hCT-Anstieg. Die im Pentagastrintest stimulierten hCT-Werte zeigten den Anstieg früher an als die lediglich basal gemessenen Werte. Das Ergebnis dieser Arbeit lässt den Schluss zu, dass der Pentagastrintest weiterhin ein wichtiger Bestandteil in der Nachsorge von Patienten mit MTC ist, da die stimulierten hCT-Werte im Einzelfall eine noch subklinische residuelle Erkrankung, Metastasierung oder ein Rezidiv frühzeitig detektieren
Calcitonin is the most specific and most sensitive biochemical marker in diagnostic investigation and follow up of patients with medullary thyroid carcinoma. hCT-level should be incapable of measurement after complete thyroidectomie. A measurable hCT after therapy indicates recrudescence or metastases. hCT-secretion can be stimulated by gastrin, which is used in the pentagastrin-stimulationtest. In the context of this study the significance of basal calcitonin compared to pentagastrin-stimulated hCT in the after-care of patients with medullary thyroid carcinoma was analysed. Therefore 129 pentagastrin-tests of MTC-patients from the ´Klinik und Poliklinik für Nuklearmedizin der Universität Würzburg´ were evaluated retrospectively. In a percentage of 6 an increase of hCT could be found after initial biochemical remission. The pentagastrin-stimulated hCT-values indicated the increase earlier than the basal values. To draw a conclusion the pentagastrin-stimulationtest remains an important component in the follow-up of patients with MTC because stimulated hCT-levels can - in individual cases - detect subclinical residual disease, metastases or recrudescence early
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Kuo, Shu-Chuan, and 郭淑娟. "Effect of Lipopolysaccharide on Pentagastrin-induced Gastric Acid Secretion:Involvement of Nitric Oxide and Bradykinin B1 mRNA." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/71725018425701239625.

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碩士
台北醫學院
醫學研究所
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英文摘要 Lipopolysaccharides (LPS), also termed endotoxins, are a family of toxic phosphorylated glycolipids derived from the cell envelope of gram—negative bacteria. In the present study, we attempted to evaluate the effects of LPS on gastric acid secretion:involvement of nitric oxide and bradykinin B1 mRNA. LPS (1 mg/kg) reduced pentagastrin (8 mg/kg/h)-stimulated gastric acid secretion. The inhibitory effect of LPS on pentagastrin stimulated gastric acid secretion was blocked by a potent bradykinin B1 receptor antagonist, [Des-Arg10] HOE 140 (H-158) of 20 mg/kg, or a NO synthase (NOS) inhibitor, NG-nitro arginine methyl ester, L-NAME of 5 mg/kg. LPS significantly decreased spontaneous acid secretion, but L-NAME (5 mg/kg) significantly increased the spontaneous acid secretion. H-158 did not affect the spontaneous acid secretion. H-158 was found to decrease plasma NO in spontaneous acid secretion. LPS was found to increase plasma NO production by two folds while LPS decreased pentagastrin-stimulated acid secretion. Furthermore, Western blot and RT-PCR were performed for iNOS protein and bradykinin B1 gene expression, respectively. LPS-treatment increased iNOS protein and bradykinin B1 mRNA in stomachs in a dose-dependent manner. These results suggest that LPS suppressed pentagastrin stimulated acid secretion via the production of NO. NO might play an important role in the regulation of acid secretion at least by an involvement of bradykinin B1 receptors. Key words:Lipopolysaccharide;pentagastrin;nitric oxide;bradykinin;induced nitric oxide synthase ;B1 bradykinin receptor;western blot ;RT-PCR
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Doyle, Patricia. "Neubestimmung des Referenzbereiches für Serum-Calcitonin basal sowie nach Stimulation mit Pentagastrin bzw. Calcium bei gesunden Probanden." Doctoral thesis, 2010. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-51805.

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Ziel: Im Mittelpunkt dieser prospektiven Studie steht die Neubestimmung eines geschlechtspezifischen Referenzbereiches für Calcitonin-Konzentrationen, sowohl basal als auch nach Stimulation mit Pentagastrin bzw. Calcium unter Verwendung eines vollautomatischen Assays (Analyseautomat IMMULITE®2000). Aufgrund des gewählten Studiendesigns ist es möglich, die Wertigkeit des etablierten Pentagastrin-Stimulationstests im Vergleich zu einem alternativen Calcium-Stimulationstest zu beurteilen. Methodik: Insgesamt wurden 50 schilddrüsengesunde, nichtrauchende Versuchspersonen (davon 25 weiblich) im Alter von 20 bis 60 Jahren (Mittelwert: 33 Jahre) in die Studie eingeschlossen. Im Vorfeld wurde bei jedem Probanden mittels sonographischer und labortechnischer Untersuchungen (fT3, FT4, TSH, TPO-Antikörper, TG-Antikörper) das Vorliegen krankhafter Veränderungen der Schilddrüse ausgeschlossen. Um einen intraindividuellen Vergleich der intravenösen Stimulationsverfahren zu ermöglichen, erfolgten die Stimulationsversuche unter gleichen Bedingungen (Nahrungskarenz >4h) in einem zeitlichen Abstand von mehreren Wochen. Die Anzahl der Probanden, die an beiden Versuchen teilnahmen, lag bei 42 (davon 18 Frauen). Die Durchführung des Pentagastrin-Tests erfolgte nach dem in unserer Klinik etablierten Protokoll: 0,5 μg Pentagastrin/ kg Körpergewicht Injektion innerhalb von 10 sec.. Die Dosierung des Stimulans Calcium richtete sich nach Angaben der Literatur. Die Stimulation mit Calcium wurde mit Calciumgluconatlösung durchgeführt (2,5 mg Calcium/kg Körpergewicht, mit einer Injektionsgeschwindigkeit von etwa 10ml/min). Vor der Stimulation wurde jeweils der basale Calcitoninspiegel bestimmt. Weitere Blutabnahmen erfolgten direkt im Anschluss an die Injektion sowie 2, 5 und 15 Minuten nach Injektionsende. Sämtliche Calcitoninkonzentrationen wurden mit Hilfe eines Festphasen, Enzym-markierten, Sandwich, immunometrischen Chemilunineszenz Assay (IMMULITE®2000 Calcitonin) bestimmt. Ergebnisse Bei der Betrachtung der 95. Perzentile des basalen Calcitoninspiegels zeigte sich kein deutlicher geschlechtspezifischer Unterschied (95. Perzentile: Männer: 5,0 pg/ml vs. Frauen: 5,7 pg/ml; Mittelwert: Männer: 2,6±1,3 pg/ml vs. Frauen 1,6±1,3 pg/ml). Bei den Stimulationsverfahren hingegen lagen die Calcitoninkonzentrationen in der Gruppe der Männer im Vergleich zur Gruppe der Frauen jeweils signifikant höher (Pentagastrin-Test: p=0,001; Calcium-Test: p=0,004; Mann-Whitney Test). In beiden Testverfahren wurde der Calcitonin Peak nach 2 bis 5 Minuten erreicht. Bei der Gegenüberstellung des Pentagastrin-Tests und des Calcium-Tests bewirkte letzterer den größeren Calcitoninanstieg (Männer: p<0,001, Frauen: p<0,001). Im Einzelnen lag der Wert der 95. Perzentile – zum Zeitpunkt der 2-Minuten-Messung - für Männer im Pentagastrin-Test bei 37,8 pg/ml (Frauen: 26,2 pg/ml) und im Calcium Test bei 95,4 pg/ml (Frauen: 90,2 pg/ml). Die Daten zeigten keinen Anhalt für einen Einfluss von Alter oder Gewicht. Schlussfolgerung Die mit Hilfe eines verbreiteten Analyseautomaten ermittelten geschlechtsspezifischen Referenzbereiche für Calcitonin liegen unterhalb der bisherigen für andere Messverfahren erarbeiteten Angaben. Bei einem schilddrüsengesunden Kollektiv bewirkte die Stimulation mit Calcium im Vergleich zu Pentagastrin einen stärkeren Calcitoninanstieg
Background: Calcitonin (hCT) - produced by the C-cells of the thyroid gland - plays an essential part in diagnosis and follow-up of medullary thyroid cancer. To increase specificity of this tumor marker, several stimulation tests have been developed e.g. pentagastrin-stimulation test. Since pentagastrin is no longer available in the United States of America, it seems important to evaluate whether calcium stimulation is equivalent to pentagastrin stimulation for this purpose. Our aim was to investigate healthy adults in order to determine the normal range of stimulated serum hCT levels (applying the two-site chemiluminescent immunometric assay IMMULITE®2000 Calcitonin) and to compare intravenous calcitonin stimulation in an intraindividual study set-up using either pentagastrin or calcium as agent. Methods: Having obtained approval from the local Ethics Committee we included 50 healthy, non-smoking volunteers aged 22 - 57 years (25 women) showing no evidence of thyroid abnormality in a preceding screening. 42 subjects – after having given written informed consent – participated in both intravenous stimulation tests, which were performed on separate days using either Pentagastrin (0.5 μg/kg bodyweight over 10 seconds) or calcium gluconate 10% (calcium 2.5 mg/kg bodyweight at a rate of 10ml/min). Tested subjects were committed to fasting before stimulation; drawing of blood samples (at baseline, immediately after application and after 2, 5 and 15 min.). We used a solid phase, enzyme-labeled, two-site chemiluminescent immunometric assay (IMMULITE 2000 Calcitonin) to measure serum hCT. Results: Baseline values did not differ significantly between males and females (mean: 2.6±1.3 vs. 1.6±1.3 pg/ml; 95th percentile 5.0 vs. 5.7 pg/ml). Calcium yielded a greater rise in hCT than did pentagastrin (men: p<0.001; women: p<0.001). Referring to the value of the 95th percentile: after Pentagastrin stimulation maximal hCT-peak of 37.8 pg/ml in men (26.2 pg/ml in women); after calcium stimulation maximal hCT-peak of 95.4 pg/ml in men (90.2pg/ml in women). Conclusions: We established a reference range for basal and stimulated hCT for healthy adults using an automated chemiluminescent assay, which are lower than reported for other methods. Our results emphasize that adequate reference values need to be validated individually for the assay used as well as for the method of stimulation. see also: Journal of Clinical Endocrinology & Metabolism (Aug 2009, 94 (8): 2970-4) Potency and Tolerance of Calcitonin Stimulation with High-Dose Calcium versus Pentagastrin in Normal Adults. Patricia Doyle, Christian Düren, Kai Nerlich, Frederik A. Verburg, Inge Grelle, Hanne Jahn, Martin Fassnacht, Uwe Mäder, Christoph Reiners, and Markus Luster
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Book chapters on the topic "Pentagastrine"

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Lascelles, P. T., and D. Donaldson. "Pentagastrin Stimulation Test." In Diagnostic Function Tests in Chemical Pathology. Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1846-7_59.

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Lascelles, P. T., and D. Donaldson. "Pentagastrin Stimulation Test9." In Diagnostic Function Tests in Chemical Pathology. Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1846-7_60.

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Seibert-Grafe, M. "Pentagastrin stimulierte Magensäuresekretion — eine pharmakodynamische Methode für die klinische Pharmakologie." In Pharmakodynamische Modelle für die Arzneimittelentwicklung. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-50229-3_9.

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Eggstein, S., and A. Imdahl. "Der Einfluß von Pentagastrin und Proglumid auf das Wachstum humaner colorectaler Carcinome." In 105. Kongreß der Deutschen Gesellschaft für Chirurgie München, 6.–9. April 1988. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73472-4_5.

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Walder, Claire E., C. Thiemermann, and J. R. Vane. "Inhibition of EDRF Synthesis Reduces the Pentagastrin-Induced Hyperaemia of the Rat Gastric Mucosa." In Vascular Endothelium. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_62.

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Iwasa, K., A. K. Sandvik, and H. L. Waldum. "Pentagastrin-Stimulated Histamine Release and Acid Secretion from the Totally Isolated Vascularly Perfused Rat Stomach." In New Perspectives in Histamine Research. Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7309-3_34.

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"Pentagastrin." In Meyler's Side Effects of Drugs. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01238-5.

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"Pentagastrin." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/00600-8.

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9

"PENTAGASTRIN." In Litt's Drug Eruption Reference Manual Including Drug Interactions. CRC Press, 2004. http://dx.doi.org/10.3109/9780203492079-137.

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"Pentagastrin-Test." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_312921.

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