Metabolic Alkalosis, Prostaglandins, Low Chloride, or Something Else?

Abstract

The recent epidemic of metabolic alkalosis in a large number of infants fed soy protein isolate ^(1–3) which was deficient in chloride has prompted a renewed interest in this pathophysiological state. These infants were characterized by having an elevated blood pH, increased serum bicarbonate concentration, and a slight compensatory increase in pCO₂. Under experimental ^{(4, 5)} and clinical conditions, metabolic alkalosis can result from either the gain of base or the loss of acid from extracellular fluid associated with chloride and potassium deficits. Thus, two phases of this disorder can be considered: 1) the mechanisms which produce the metabolic alkalosis, i.e. increased alkali intake, or acid loss through vomiting, and 2) the processes responsible for subsequent maintenance of the alkalosis, i.e. hypochloremia, sodium avid state, etc. The clinical and laboratory evaluation of the infants fed soy formula failed to show the first phase in the development of metabolic alkalosis. Therefore, the composition of the formula itself was considered, namely, the low chloride, high citrate, phytate phosphorus, soy bean protein as well as the hypothetical consideration of prostaglandin precursors or enhancers.