Neonatal acidity and pyloric stenosis of infancy (PS) - the beginning and the end two stories

Abstract

The author tells two stories. Story one describes the beginnings of his research interest into the cause and effect of neonatal acid secretion. It also explains the new proposal that an insensitivity of the usual negative feed-back in adults between neonatal gastrin and gastric acidity is not functioning at birth and takes some weeks to develop. Because of this, gastrin levels and acidity rise together from birth. This means that when feedback maturity occurs, there will be a temporary peak in both gastrin and gastric acidity before mutual restraint is established. The early gap in acid defense is filled by functional maternal gastrin transfer during labor which produces an external source of acid secretion until the neonatal gastric mucosa has matured. Story two relates the effects of these earlier changes to the baby who has inherited an enhanced parietal cell mass. Such babies develop a critical hyperacidity during developmental peak acidity. Acidity- provoked sphincter contractions; sphincter hypertrophy and gastric outlet obstruction (GOO) may then supervene. All the bewildering clinical features are understandable within the framework of this hypothesis.