Recently attempts have been made to demonstrate the possible role of hypergastrinemia in the production of congenital
hypertrophic pyloric stenosis in infants. Eleven infants with congenital
hypertrophic pyloric stenosis, ranging in age from three to 11 weeks, were evaluated for fasting and postprandial serum
gastrin levels. Two to ten weeks following successful
pyloromyotomy, a similar evaluation was undertaken to demonstrate the possible role of elevated serum
gastrin levels in the etiology of congenital
hypertrophic pyloric stenosis. The average fasting and postprandial serum
gastrin levels in infants with congenital
hypertrophic pyloric stenosis did not differ significantly from levels noted in control infants. Similarly, no statistically significant difference was noted between the pre- and postoperative levels of serum
gastrin in the affected infants. Several experimental studies have been reported within the past few years describing the production of
hypertrophic pyloric stenosis in the offspring of dogs injected with
pentagastrin during pregnancy. The results of our study minimize the direct importance of serum
gastrin in the production of congenital
hypertrophic pyloric stenosis. The role of the
hormone secretin in the etiology of this condition is hypothesized.