the incidence in pregnant reproductive age women is reported to be 8 patients per 100 000 per year .
the most common cause of primary hyperparathyroidism in pregnancy , as in the general population , is a single adenoma . in 1938 , friedrichsen described symptomatic hypocalcemia in an infant unmasking the mother 's hyperparathyroidism .
since this initial anecdotal publication , there have been fewer than 20 published cases of similar presentations of neonatal hypocalcemia leading to a diagnosis of maternal hyperparathyroidism .
neonatal hypocalcemia , while fortunately rare , can be physiologic in origin and generally resolves shortly after birth .
late - onset or symptomatic hypocalcemia , however , can cause seizures in infants and warrants investigation of both the child and the mother . during the third trimester of pregnancy , calcium
parathyroid hormone ( pth ) and calcitonin , on the other hand , do not cross the placental barrier and serum calcium of a neonate is often higher than that of the mother at birth .
after birth , serum calcium regulation of the child is no longer dependent on the mother . within the first 48 h ,
this is a normal transition phase due to the new dependence on their own immature pth secretion , limited dietary calcium intake , immature renal reabsorption , minimal skeletal calcium stores and vitamin d status .
other causes of hypocalcemia are abnormalities of vitamin d metabolism , hyperphosphatemia , hypomagnesemia and hypercalcitonemia , which typically occur within 1224 h of life .
hypocalcemia can result in convulsions , arrythmias , tetany and/or paresthesias in the hands , feet and perioral regions .
additionally , hypocalcemia may result in petechiae , hyperactive reflexes , prolonged qt waves and laryngospasms .
while most patients with hyperparathyroidism are diagnosed outside of pregnancy , neonatal manifestations of hypocalcemia can be a rare initial presentation of maternal hyperparathyroidism . here , we present a case of a female with multiglandular hyperparathyroidism diagnosed only after her newborn child presented with seizures due to severe hypocalcemia .
a 7-day - old male infant born to a healthy 33-year - old female at 37 weeks of gestation presented to the local emergency department ( ed ) with sudden - onset tonic  clonic seizures .
he was healthy at birth , with no prenatal complications , and was stable at discharge following birth .
laboratory testing revealed extreme hypocalcemia ( ionized calcium of 3.2 mg / dl ) and undetectable pth ( < 10 pg / ml ) .
concomitant evaluation of the mother revealed both elevated ionized calcium ( 5.9 mg / dl ) and pth ( 116 pg / ml ) . upon further review ,
the mother reported a history dating back several years with vague symptoms of constipation , labile mood and fatigue during and prior to her pregnancy .
she denied any history of bone pain , kidney stones or abdominal pain , and denied any family history of calcium disorders . with a diagnosis of primary hyperparathyroidism ,
in - office ultrasound revealed an essentially normal thyroid with only a small subcentimeter nodule in the right inferior pole .
evaluation of the surrounding tissue for parathyroid abnormalities revealed a large 2- to 3-cm , hypodense area inferior to the right inferior thyroid pole .
this area lacked blood flow but was not classic for parathyroid adenoma due to the almost anechoic appearance .
evaluation of the left side of the neck revealed similar hypodense changes in the lower neck but nothing as significant as seen on the right .
a parathyroid nuclear scan was performed showing two sites of sestamibi hyperconcentration , slow washout and discordance in the left neck .
the patient was diagnosed with primary hyperparathyroidism likely due to multiglandular disease and was prepared for parathyroidectomy .
after an extensive exploration , three significantly enlarged cystic glands were identified and removed ( fig .  1 ) .
intraoperative pth levels dropped appropriately after parathyroidectomy , thyroid lobectomy and cervical thymectomy from a baseline of 104 pg / ml to a final value of 41.1 pg / ml .
pathology noted three hypercellular , cystic parathyroid glands with mucoid degeneration weighing 6.200 , 1.846 and 0.110 g as well as a separate 3 mm focus of hypercellular parathyroid tissue in the pretracheal tissue .
given the cystic appearance , age of the patient and presence of multiglandular disease , evaluation for familial cystic parathyroid adenomatosis ( hyperparathyroidism - jaw bone - tumor syndrome ) and men 1 were undertaken , both of which were normal .
he returned to the ed with seizures at 1 month of age . after increasing calcium supplementation appropriately ,
he has since been maturing well with no further seizure activity and normal calcium levels .
this represents a unique case of undiagnosed maternal primary hyperparathyroidism manifesting with intrauterine parathyroid suppression and hypocalcemic seizures in the newborn .
after ruling out multiple syndromes contributing to our patient 's hyperparathyroidism , it was concluded that our patient suffered from isolated multiglandular primary hyperparathyroidism .
fortunately , the infant in our case was able to recover parathyroid function over the course of 9 months of calcium supplementation .
not all cases of intrauterine parathyroid suppression are able to recover and wean from supplemental calcium .
undiagnosed maternal hyperparathyroidism can lead to disastrous complications for infants and therefore must be considered in both hypercalcemic pregnant patients and hypocalcemic neonates .
after 2448 h , a child presenting with symptomatic hypocalcemia can represent a potentially fatal condition indicating severely suppressed parathyroid function and an underlying maternal hyperparathyroidism .
this potentially fatal presentation of the disease highlights the importance of diagnosis and treatment of hypercalcemia in the pregnant patient .
we recommend considering surgery at the time of diagnosis , even during pregnancy , to minimize dangers to both mother and infant .
 a 7-day - old male infant born to a healthy 33-year - old female at 37 weeks of gestation was brought to the local emergency department ( ed ) with sudden - onset tonic  clonic seizures . 
 laboratory testing revealed extreme hypocalcemia ( ionized calcium of 3.2 mg / dl ) and undetectable parathyroid hormone ( pth < 10 pg / ml ) . 
 concomitant evaluation of the mother revealed both elevated ionized calcium ( 5.9 mg / dl ) and pth ( 116 pg / ml ) . 
 the mother underwent preoperative ultrasound localization and sestamibi scan , followed promptly by parathyroidectomy . given the cystic appearance and presence of multiglandular disease , evaluation for familial cystic parathyroid adenomatosis ( hyperparathyroidism - jaw bone - tumor syndrome ) and men 1 were undertaken . 
 the infant was stabilized and discharged home . 
 he returned to the ed with seizures at 1 month of age . after increasing calcium supplementation appropriately , 
 he was monitored with weekly office visits . 
 this represents a unique case of undiagnosed maternal primary hyperparathyroidism manifesting with intrauterine parathyroid suppression and hypocalcemic seizures in the newborn . 
INTRODUCTION
CASE REPORT
DISCUSSION
CONFLICT OF INTEREST STATEMENT