1968
DOI: 10.1097/00000658-196809000-00016
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Identification of the Diarrheogenic Hormone Associated with Non-Beta Islet Cell Tumors of the Pancreas

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Cited by 99 publications
(29 citation statements)
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“…In case 2 reported here, plasma PTH was slightly elevated and the autopsy revealed parathyroid hyperplasia, suggesting that the hypercalcemia could be due to the concomitant parathyroid lesion. However, it is difficult to decide whether or not the parathyroid lesions are the cause of hypercalcemia, because there is a case reported (Zollinger et al, 1968) in which hypercalcemia recurred after removal of hyperplastic parathyroid glands but returned to normal after removal of a pancreatic tumor. Therefore, the determination of plasma PTH levels is expected to be of value in recognizing the parathyroid lesions in patients with the WDHA syndrome, although the elevation of the plasma PTH level does not necessarily mean that hypercalcemia is due to parathyroid lesions.…”
Section: Discussionmentioning
confidence: 99%
“…In case 2 reported here, plasma PTH was slightly elevated and the autopsy revealed parathyroid hyperplasia, suggesting that the hypercalcemia could be due to the concomitant parathyroid lesion. However, it is difficult to decide whether or not the parathyroid lesions are the cause of hypercalcemia, because there is a case reported (Zollinger et al, 1968) in which hypercalcemia recurred after removal of hyperplastic parathyroid glands but returned to normal after removal of a pancreatic tumor. Therefore, the determination of plasma PTH levels is expected to be of value in recognizing the parathyroid lesions in patients with the WDHA syndrome, although the elevation of the plasma PTH level does not necessarily mean that hypercalcemia is due to parathyroid lesions.…”
Section: Discussionmentioning
confidence: 99%
“…Glucagon, in doses higher than this value in man, induced smaller changes in intestinal transport [66], More recently discovered intestinal polypeptides, the gastric inhibitory peptide (GIP) [9] and vaso-active intestinal peptide (VIP) [113] have also been shown to be capable of provoking severe diarrhoea in experimental animals [6], In view of these actions it is hardly surprising that several of these hormones have been suggested as aetiological agents for the diarrhoea of the Verner-Morrison syndrome. The cholera-like diarrhoea of this disorder is almost certainly due to liberation of a humoral agent from pancreatic adenomata and secretin [150] and glucagon [5] have both had their protagonists. However, the diarrhoea now seems more likely to be due to overproduction of GIP [36], To my knowledge, there is no published evidence which implicates cAMP in the mode of action of these substances on intestinal transport but this possibility remains to be excluded.…”
Section: 'Physiological' Stimulators O F Intestinal Secretionmentioning
confidence: 99%
“…Small but mul tiple and diffuse hepatic métastasés were found and biopsied. The gallbladcr was large and atonic; bile composition in a peroperative specimen was: Na*: 151 mmol: K.*: 5 mmol/l: HCO5: 76 mmol/l: protein: 0.8 g/dl (normal range: N+: 187 ± 39 mmol/l; K*: 11.5 ± 4.5 mmol'l: HCO3: 9 ± 8 mmol/l) [36]. Before resec tion the portal VIP plasma level was 480 pg/ml and the systemic VIP plasma level was 500 pg/ml.…”
Section: Case Reportmentioning
confidence: 97%
“…The pathogenesis is related to over production of one or more circulating factors by an endocrine tumor. Many humoral agents have been incriminated including se cretin [36], glucagon and gastrin [4], gastric inhibitory polypeptide (GIP) [11], vasoactive intestinal polypeptide (VIP) [6], prostaglan dins [31], pancreatic polypeptide (PP) [24], alone or in combination.…”
mentioning
confidence: 99%