Abstract
Hypocalcemia, defined as a serum calcium (Ca) concentration ≤ 7.5 mg/dl, constitutes a frequent development during the neonatal period. Since Ca is transferred across the placenta into the fetus at daily rates of up to 150 mg/kg of fetal weight during the last trimester of pregnancy, it is not surprising that upon delivery, the sudden interruption of such a rich supply of calcium should result in hypocalcemia. The latter has two main peaks of occurrence: during the first 48 hours following delivery (early hypocalcemia), or after the second part of the initial week of life (late hypocalcemia or classical neonatal tetany) (1). Early hypocalcemia is dealt with in detail in another chapter of this volume; however, since several mechanisms seem to be operative in both early and late hypocalcemia, some degree of overlap is unavoidable. This chapter attempts to summarize the available information related to the pathogenetic mechanisms involved in late neonatal hypocalcemia (Table 1).