http://bmj.bmjjournals.com/cgi/content/full/321/7255/223

Large quantities of calcium (20-30 g) are actively transported across the
placenta from the mother to the fetus to facilitate normal bone mineralisation.5
Most (80%) is transferred in the third trimester. Parathyroid hormone and
calcitonin do not cross the placenta.5 Fetal 1,25-dihydroxyvitamin D,
synthesised in both fetal kidney and placenta, acts as the major stimulus and
regulator of calcium transfer across the placenta. In the fetus, maternal
primary hyperparathyroidism results in high concentrations of serum calcium that
acts to suppress the parathyroid glands, resulting in a low fetal parathyroid
hormone concentration. Fetal calcitonin concentrations are high to encourage
bone mineralisation. At birth, the neonate is suddenly deprived of this rich
source of calcium. It is incapable of mobilising calcium from bone owing to the
low concentrations of parathyroid hormone and high concentrations of calcitonin.
Acute neonatal hypocalcaemia results in tetany and convulsions, usually at 5 to
14 days of age.6 If the infant is breast fed, tetany can be delayed by one month
or more.7 Routine blood tests show hypocalcaemia (calcium concentration <1.75
mmol/l); hypomagnesaemia is also common.5 A parathyroid hormone assay often
shows a low value but the value may be normal or increased. Treatment by oral or
parenteral calcium and magnesium supplements is usually required only for a
short period. Transient hypoparathyroidism resolves within three to five
months.8

Transient neonatal hypocalcaemia in the first few days of life is relatively
common. However, when hypocalcaemia presents towards the end of the first week
(or later) with symptoms such as tetany or convulsions, appropriate
investigations should be carried out.

Primary hyperparathyroidism in pregnancy can result in major morbidity and
mortality for both the mother and the neonate. The hypercalcaemia can manifest
itself in symptoms such as hyperemesis gravidarum, weakness, renal calculi,
pancreatitis, spontaneous abortion, or fetal death.5 The mother may be at risk
in the immediate postpartum period. A hypercalcaemic crisis can result, as the
maternal efflux of calcium to the fetus is suddenly discontinued.

A detailed history may turn up discrete symptoms in the mother such as weakness,
excessive thirst, constipation, or recent depression. Patients, however, often
report no symptoms.8-11 The condition can be diagnosed by screening the mother's
blood for calcium and then for parathyroid hormone. The mother should be
referred to an endocrinologist and surgeon. Further pregnancies should then pose
no risk to the fetus or mother.

The presentation of asymptomatic primary hyperparathyroidism through convulsions
in the infant, although previously documented anecdotally, is exceedingly
rare.9-12 It is unusual for a district general hospital serving a population of
250 000 people to see two such patients within 12 months. The first case
illustrates how easy it is simply to treat neonatal hypocalcaemia without
investigating the cause. Primary hyperparathyroidism went unnoticed in this
mother until neonatal convulsions occurred in her third child. All mothers with
neonates showing tetany or seizures should have serum calcium concentrations
checked to exclude primary hyperparathyroidism.





Views concerning the incidence of tetany in the newly born vary
greatly. One reason for this is that the complete clinical picture
of tetany as seen in older children is rarely encountered in the
newborn. Another complicating factor is that there is no general
agreement concerning the circumstances in which tetany is liable to
occur in the early days of life.

http://www.mgwater.com/Seelig/Magnesium-Deficiency-in-the-
Pathogenesis-of-Disease/chapter3.shtml


The existence of neonatal tetany is considered a sensitive clue to
maternal hyperparathyroidism. Hartenstein and Gardner (1966)
reviewed the literature and found that there were seven reported
families, including their own reports, in which neonatal tetany was
associated with maternal parathyroid adenoma.

http://www.indianpediatrics.net/mar2005/mar-294-295.htm

Neonatal hypocalcemia resulting from maternal primary
hyperparathyroidism (MPH) is usually detected clinically in the
first 2 weeks of life. Occasionally, diagnosis of primary
hyperparathyroidism in a young asymptomatic mother is made when the
infant presents with hypocalcemia. We present an infant with late
onset hypocalcemia resulting from a combination of transient hypo-
parathyroidism due to asymptomatic MPH and vitamin D deficiency.

The presentation of asymptomatic maternal hyperparathyroidism by
convulsion in an infant is exceedingly rare. Hyper-parathyroidism in
asymptomatic mothers might easily have been missed if the maternal
calcium status had not been investigated(1-4) like in our patient's
mother. Suppression of the fetal parathyroid gland by maternal
hypercalcemia often causes transient neonatal hypocalcemia(5). Low
vitamin D levels of the patient might have exacerbated the
hypocalcemia observed in this infant which may due to several
causes : he has not received vitamin D supplement , he has grown
rapidly and there could have been low placental transfer of 25-OH D3
from the mother who had increased conversion of 25-OH D3 to 1,25-OH
D3 due to her hyperparathyroidism. We emphasize that all mothers
with neonates showing tetany or hypocalcemic convulsions should have
serum calcium concentrations measured to exclude primary hyper-
parathyroidism even if the mother is asymptomatic.

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