Human Newborn Hypergastrinemia: An Investigation of Prenatal and Perinatal Factors and Their Effects on Gastrin


Summary: Because gastrin is a potent gastric acid stimulus and gastric acid secretion begins soon after birth, we measured umbilical cord serum gastrins. We also examined multiple factors present during the gestation, labor, delivery, and immediate postpartum period to see what effect, if any, these might have on the serum gastrins.

Two groups were studied: 217 newborn infants and 802 adults without Zollinger-Ellison syndrome. The newborns' median serum gastrin was 100 pg/ml compared to the adult median of 39 pg/ml. The newborn mean was 135 pg/ml and the corresponding adult value was 40 pg/ml (P < 0.001). Twenty-nine newborns had gastrin determinations greater than 200 pg/ml; five were greater than 500 pg/ml. All adult values were less than 200 pg/ml.

Thirty-five neonatal and maternal factors were analyzed to determine their effect on the gastrin levels found. No factor was found to have a significant effect except that Negro infants and maternal sickle cell trait were found to be associated with increased values. Nineteen maternal medications were also evaluated. None, including oxytocin and atropine, were found to have any effect.

Serum gastrin levels continued to be elevated at hour 4 (x = 80 pg/ml) and hour 8 (x = 72 pg/ml) of life. The newborns secreted small amounts of gastric acid in response to this stimulus (range = 0.010 to 0.022 mEq/kg/hr).

Speculation: During the transition to extrauterine life, the fetus is exposed to many varied stimuli. Increased vagal activity and catecholamine secretion are two physiologic reactions which occur in response to these stimuli. Both of these are known to stimulate gastrin release from G cells during extrauterine life and may account for the increased levels found at the time of delivery. The elevated gastrin levels found after birth may also be in response to these factors; however, decreased metabolism may play a role too. It is known that the kidney is the major site for gastrin metabolism in adults. The newborn kidney may not be capable of rapidly metabolizing the large gastrin load presented to it during these first hours of extrauterine life. Continued high secretion of gastrin by the G cell may also play a role in the elevated serum levels found.

The low gastric acid secretion in response to these high gastrin levels may be due to decreased parietal cell responsiveness during this period of life. Decreased parietal cell mass could also be responsible. Finally, if the predominant gastrin molecule was not the G-17 moiety, decreased acid secretion would be expected.

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Correspondence to Arthur R Euler.

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Euler, A., Ament, M. & Walsh, J. Human Newborn Hypergastrinemia: An Investigation of Prenatal and Perinatal Factors and Their Effects on Gastrin. Pediatr Res 12, 652–654 (1978).

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  • Acid secretion
  • gastrin
  • hypergastrinemia
  • newborn

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