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Gastrin processing and secretion in patients with end-stage renal failure
G D Ciccotosto1, J K Dawborn, K J Hardy
1University of Melbourne, Department of Surgery, Victoria, Australia.
The Journal of Clinical Endocrinology and Metabolism
|September 1, 1996
Summary
Hypergastrinemia in end-stage renal failure (ESRF) is underestimated due to unmeasured gastrin forms. Helicobacter pylori (HP) infection and reduced somatostatin levels contribute to elevated gastrin in ESRF patients.
Area of Science:
- Endocrinology
- Nephrology
- Gastroenterology
Background:
- Elevated gastrin levels are observed in end-stage renal failure (ESRF) patients.
- The specific forms of gastrin elevated and secretory profiles post-stimulation in ESRF remain unclear.
- Helicobacter pylori (HP) infection influences gastrin secretion and needs consideration.
Purpose of the Study:
- To quantify all processed and partially processed forms of circulating gastrin in ESRF patients before and after meal stimulation.
- To investigate the impact of HP infection on gastrin levels and secretory profiles in ESRF.
- To assess the role of somatostatin in regulating gastrin secretion in ESRF.
Main Methods:
- Measurement of fasting and post-meal plasma gastrin-amide, gastrin-Gly, and total gastrin in ESRF patients and controls.
- Determination of HP status in all study participants.
- Measurement of fasting plasma somatostatin levels.
Main Results:
- Fasting gastrin-amide, gastrin-Gly, and total gastrin were significantly higher in ESRF patients, especially those with HP infection.
- The proportion of nonamidated gastrin products was significantly higher in ESRF patients.
- Meal-stimulated gastrin response was potentiated in ESRF/HP+ patients, and somatostatin levels were lower in ESRF patients.
Conclusions:
- Hypergastrinemia in ESRF is underestimated when only amidated forms are measured.
- HP infection partially explains the potentiated gastrin meal response in ESRF.
- Reduced somatostatin and decreased gastrin metabolism contribute to increased circulating gastrin in ESRF, potentially explaining gastrointestinal hypertrophy.