Radioimmunoassay of Plasmagastrin in Pernicious Anæmia, Achlorhydria Without Pernicious Anæmia, Hypochlorhydria, and in Controls

Ganguli, P. C.; Cullen, D. R.; Irvine, W. J.

doi:10.1016/s0140-6736(71)91932-5

Cited by 115 publications

(30 citation statements)

References 24 publications

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“…Unlike McGuigan and Trudeau (1970b, c), we have found no rise in fasting plasma gastrin concentration with age (Ganguli, Cullen & Irvine, 1971 Food has previously been shown to be a potent stimulant for gastrin secretion (Hansky & Cain, 1969;McGuigan & Trudeau, 1970a;Ganguli, 1970;Walsh, Yalow & Berson, 1971) but the clearly specific effect of protein and the failure of a predominantly (93 %) carbohydrate meal has not been reported.…”

Section: Discussioncontrasting

confidence: 84%

Radio‐immunoassay of gastrin in human plasma

Ganguli¹,

Hunter²

1972

The Journal of Physiology

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SUMMARY1. A radio-immunoassay for gastrin has been developed using partially purified porcine gastrin to raise antibodies and highly purified natural porcine gastrin I for radio-iodination with 1251. The separation of antibodybound from free hormone was performed by a double-antibody method.2. In this assay highly purified natural porcine gastrin I, synthetic human gastrin I, radio-iodinated porcine gastrin I, gastrin in the plasma of a healthy volunteer, a patient with pernicious anaemia and another patientwith the Zollinger-Ellison syndromewereimmunologicallyidentical.3. The fasting plasma gastrin concentration of fourteen gastric ulcer patients was significantly higher than that of the 113 hospital controls with no history of gastro-intestinal disease, while twenty-seven duodenal ulcer patients had gastrin levels within the normal range.4. Plasma gastrin concentration was significantly elevated in pernicious anaemia (fifty-one patients), achlorhydria (thirty-three patients), hypochlorhydria (eleven patients) and in nine patients with histologically proven Zollinger-Ellison syndrome. 5. In human volunteers a protein meal stimulated endogenous gastrin release while a carbohydrate meal did not. Atropine sulphate I.M., and hydrochloric acid orally, produced a significant fall in the level of circulating gastrin.

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Section: Discussioncontrasting

confidence: 84%

Radio‐immunoassay of gastrin in human plasma

Ganguli¹,

Hunter²

1972

The Journal of Physiology

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“…Extensive hyperplasia of ECL cells has been observed in the oxyntic mucosa of pa tients with gastrin-producing tumours (the Zollinger-Ellison syndrome) [49][50][51][52][53][54], These patients regularly display an increased mass of oxyntic mucosa [53,55], usually associ ated with diffuse ECL cell hyperplasia [50] and sometimes noduli of ECL cells [54], Two such patients had multiple ECL cell tumours [53,56], Achlorhydria with or without atrophic gastritis and pernicious anaemia is another condition with greatly increased serum gas trin levels [57,58], Diffuse or focal hyperpla sia of endocrine -mostly ECL -cells has been reported in many such cases [59][60][61][62][63][64][65][66] and also the occurrence of multiple polypoid gastric carcinoids (some of which have been diagnosed as ECLomas). mostly in patients fig.…”

Section: Eci Cells In Man and T Heir Neoplastic Transformationmentioning

confidence: 99%

Activation and Hyperplasia of Gastrin and Enterochromaffin-Like Cells in the Stomach

et al. 1986

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The stomach is rich in endocrine cells, most of which are still unidentified with respect to the peptide hormones they produce. The endocrine cell populations in the antrum usually differ from those in the oxyntic mucosa. Gastrin cells are found in the antrum and respond readily to stimuli from the gastric lumen, such as changes in the pH and the presence of food. In order to study the functional control of the antral gastrin cell, rats were subjected to different kinds of surgery. The serum gastrin concentrations in the various experimental groups were measured 8–10 weeks after the operations. Elevated antral pH raised the serum gastrin concentration. The combination of elevated antral pH and the passage of food over the pyloric glands produced gastrin cell hyperplasia. The operation that was most effective in inducing gastrin cell hyperplasia was removal of the acid-producing part of the stomach. Interestingly, gastrin cell hyperplasia was seen also after bilateral truncal vagotomy, indicating that an intact vagal innervation is not essential for the development of gastrin cell hyperplasia. Enterochromaffin-like (ECL) cells are endocrine/paracrine cells that are numerous in the acid-producing part of the stomach in many species. In the rat, they occur predominantly in the basal half of the oxyntic mucosa and produce and store histamine. The ECL cells have an unknown function and do not seem to respond to stimuli from the gastric lumen. They are activated by circulating gastrin and by vagal excitation. Gastrin mobilises histamine from these cells and activates the histamine-forming enzyme, histidine decarboxylase. Long-term hypergastrinaemia produces diffuse ECL cell hyperplasia, whereas hypogastrinaemia (following removal of the endogenous stores of gastrin by antrectomy) reduces the ECL cell number. Portacaval shunt brings about a marked increase in the number of ECL cells through an unknown mechanism. Also neuronal stimuli are important for the trophic control of the ECL cells. Studies of unilaterally vagotomised rats showed reduced weight and thickness of the oxyntic mucosa as well as a markedly reduced number of ECL cells on the denervated side.

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“…An elevated serum gastrin is not only found in achlorhydria, but also in hvpochlorhydria [3,5,12], The underlying mechanism. which can be assumed to be the same in both conditions, is supposed to be hyperplasia of the G cells due to the lacking inhibition of gastrin secretion by gastric acid, which is per manently absent [1,9].…”

Section: Discussionmentioning

confidence: 99%