Maternal Hyperparathyroidism Research Articles

Late-onset hypocalcemia seizure: An interesting presentation of sporadic maternal primary hyperparathyroidism with hypovitaminosis D

Abstract The cardinal manifestation of primary hyperparathyroidism is secondary to hypercalcemia and high bone turnover disease due to sustained elevation of parathyroid hormone. A high index of suspicion for maternal primary hyperparathyroidism should be kept in the setting of neonatal hypocalcemia. Delayed presentation of hypocalcemic seizure secondary to maternal primary hyperparathyroidism is infrequent. Herein, we report a case of a 2-month-old infant who presented with late-onset (>72 h) hypocalcemic seizure, biochemically mimicking pseudohypoparathyroidism, which eventually led to the diagnosis of maternal hyperparathyroidism with vitamin D deficiency.

Asymptomatic parathyroid adenoma in mother as a cause of late-onset persistent hypocalcemia in a newborn

Pregnant women with primary hyperparathyroidism may be asymptomatic or have mild symptoms such as fatigue, thirst, constipation, or transient depression. Transfer of calcium from mother to fetus leads to increased fetal calcium concentrations, suppressing fetal parathyroid hormone synthesis, and stimulating calcitonin secretion leading to neonatal hypocalcemia. Here, we present a report of a newborn admitted on day 10 of life with recurrent tonic convulsions. On investigation, it was found that the baby had severe persistent hypocalcemia which when further evaluated was due to asymptomatic maternal hyperparathyroidism due to parathyroid adenoma.

The Case | A pregnant female with refractory hypocalcemia

A 25-year-old gravida 1 parity 0 female patient at 20 weeks of gestation was found to have asymptomatic hypocalcemia during her prenatal evaluation. Despite calcium and calcitriol supplementation for 4 months, her hypocalcemia persisted. The patient had no medical or surgical history, and there had been no exposure to other medications except prenatal vitamins. Family history was positive for maternal hyperparathyroidism with a history of kidney stones. The patient denied any symptoms including paresthesia, seizures, muscle twitching, or spasms.

Refractory Yet Transient Neonatal Hypocalcemia Due to Hitherto Undiagnosed Asymptomatic Maternal Hyperparathyroidism: A Case Report

Hypocalcemia is one of the common causes of neonatal seizures and can result in significant morbidity. Among the multitude of etiologies, hypoparathyroidism as a consequence of maternal hyperparathyroidism is an uncommon one. We describe a neonate who presented with hypocalcemic seizures with relative hypoparathyroidism that unmasked a previously undiagnosed and asymptomatic maternal hyperparathyroidism, and explore the difficulties encountered in the management. Despite initial recalcitrance of hypocalcemia to therapy, parathyroid suppression was transient and recovered completely in few months.

A neonate with late-onset hypocalcemia due to unrecognized maternal hyperparathyroidism and a systematic overview of similar cases.

Objective: Neonatal seizures are alarming manifestations of an underlying significant disorder demanding immediate attention and intervention. Hypocalcemia, although rare, must be considered in the differential diagnosis of neonatal seizures.Method: We present an unusual case of a 10-day-old infant with unexplained symptomatic hypocalcemia, experiencing multiple episodes of focal tonic-clonic seizures, born by an entirely asymptomatic mother. Moreover, we conducted a systematic search in PubMed and Scopus databases to present a clinical overview of all similar cases.Result: Maternal laboratory investigation revealed markedly increased calcium levels with concomitant high parathyroid hormone levels due to a parathyroid adenoma, undiagnosed during antenatal checkup.Conclusion: This is one of the few cases in the literature where neonatal symptomatology led to the diagnosis of undiagnosed maternal hyperparathyroidism. Early detection and appropriate management of neonatal hypocalcemia could eliminate serious maternal and fetal morbidity.

Unusual Presentation of Primary Hyperparathyroidism: A Rare Case Report

ABSTRACT Aim The aim of this case report is to highlight an exceptional presentation of primary hyperparathyroidism. Background Asymptomatic maternal hyperparathyroidism manifesting in the neonate as hypocalcemic convulsions is exceedingly rare. Case report: Primary hyperparathyroidism has got a varied presentations. We present a case report of neonatal hypocalcemic convulsions secondary to asymptomatic maternal hyperparathyroidism. Here, the challenge in diagnosing this condition and management will be discussed in the context of available literature. Conclusion In the event of nonfebrile seizures in the neonate due to hypocalcemia, the mother has to be evaluated for primary hyperparathyroidism. Clinical significance: Physicians’ awareness of this unique manifestation of primary hyperparathyroidism is essential for the appropriate management of both the mother and the neonate. Timely identification and treatment of this condition will prevent complications in both. How to cite this article Teja VS, Ramakrishnan R. Unusual Presentation of Primary Hyperparathyroidism: A Rare Case Report. World J Endoc Surg 2017;9(1):13-15.

ULTRASOUND TREATMENT AS INTERVENTION IN INTRAUTERINE HYPERPARATHYROIDISM

Hypocalcemia during pregnancy reduced the normal foetal growth, skeletal mineralization and serum calcium concentration. Untreated maternal hyperparathyroidism associated hypocalcemia predisposed the foetal to intrauterine hyperparathyroidism resulting in adverse effect to skeletal mineralization. In vivo study has discovered that prenatal ultrasound exposure has the ability to reduce the foetal PTH level. Ten-month-old nulliparous New Zealand White (NZW) does were assigned to three different groups; Control (C), healthy NZW does and free from ultrasound exposure; hypoparathyroidism (HyPT), negative control groups having hypocalcemia condition established through external parathyroidectomy surgery and free from prenatal abdominal ultrasound exposure; treatment (T), experimental groups having hypocalcemia condition and receiving prenatal abdominal ultrasound exposure during pregnancy as intervention to hypoparathyroidism. In the treatment group, rabbits were exposed for 30, 60 and 90 minutes to parathyroid ultrasound on the 1st, 2nd and 3rd gestational stage accordingly. Following birth, foetal serum calcium (SCa), body weight (BW), crown-to-rump length (CRL), total body length (TBL), bi-parietal diameter (BPD) and femur length (FL) of the foetal were measured. Maternal hypocalcemia during pregnancy gave birth to litters with small to gestational age (SGA) and the reduction of BW, CRL, TBL, BPD, FL and SCa were also noted. Meanwhile, the outcome of ultrasound exposure given during the middle of 2nd gestational stage resulted in significant increase in progeny mean average BW, CRL, TBL, BPD FL and SCa compared to the HyPT group. Prenatal abdominal ultrasound helps to control the level of foetal parathyroid hormone and while still in the womb limits the postnatal complication.

Neonatal seizure: a rare presentation of maternal hyperparathyroidism

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Vitamin D supplementation in pregnancy.

Vitamin D supplementation in pregnancy.

Neonatal Seizure as a Manifestation of Unrecognized Maternal Hyperparathyroidism

Maternal hypercalcemia suppresses parathyroid activity in the fetus resulting in impaired parathyroid responsiveness to hypocalcemia after birth. Resultant hypocalcemia may be severe and prolonged and rarely may lead to convulsions. Here, we present a newborn infant admitted to the pediatric emergency department at age two weeks with recurrent tonic convulsions due to asymptomatic maternal hyperparathyroidism and vitamin D deficiency. Physicians should be aware that undiagnosed maternal hyperparathyroidism can cause severe hypocalcemia in the newborn.Conflict of interest:None declared.

Elevated Fibroblast Growth Factor 23 Levels in a Newborn With Secondary Hypoparathyroidism

Fibroblast growth factor 23 (FGF-23) is a recently identified hormone that is of prime importance for phosphate homeostasis in humans. FGF-23 is secreted by osteocytes in response to phosphate-loading. It stimulates renal phosphate excretion and suppresses the formation of 1.25-dihydroxy-vitamin D by inhibiting renal 1α-hydroxylase activity. Knowledge about FGF-23 in early infancy is limited. We report here the case of a newborn with transient secondary hypoparathyroidism caused by maternal primary hyperparathyroidism during pregnancy. FGF-23 levels at birth were extremely high in the child (15.850 kilo-Relative Units per liter, kRU/L) (ie, ∼45 times higher than in the mother) and ∼7 times higher than in healthy newborns. The child's FGF-23 levels declined gradually and reached the normal adult range after ∼7 months. We discuss the potential physiologic significance of FGF-23 in newborns.

Three case reports of maternal primary hyperparathyroidism in each trimester and a review of optimal management in pregnancy

Primary hyperparathyroidism (PHPT) during pregnancy is associated with significant maternal and fetal risks. Prompt diagnosis and effective management during pregnancy can improve both maternal and fetal outcomes. However, there is no consensus with regard to conservative versus surgical management especially in the first and third trimester. We report three cases of PHPT associated with pregnancy that underwent parathyroidectomy each in a different trimester. Cases 1 and 2 were found to have hypercalcaemia and elevated parathyroid hormone levels in the second and first trimesters, respectively. Case 3 was known to have PHPT prenatally but previously declined parathyroidectomy. All three cases underwent parathyroidectomies during pregnancy without significant postoperative complications and all achieved favourable maternal and neonatal outcomes. Maternal hyperparathyroidism represents a preventable cause of maternal morbidity, with fetal morbidity and mortality. The benefits of parathyroidectomy with normalization of serum calcium in the mothers outweigh the risks of hypercalcaemia and suppression of the fetal parathyroid, especially where maternal vitamin D concentration is low.

Severe late-onset neonatal hypocalcemia due to unrecognized maternal hyperparathyroidism

Severe late-onset neonatal hypocalcemia due to unrecognized maternal hyperparathyroidism

Transient neonatal hypoparathyroidism in two siblings unmasking maternal normocalcemic hyperparathyroidism

Hypoparathyroidism is one of the recognized causes of late-onset neonatal hypocalcemia. Maternal hypercalcemic hyperparathyroidism has been shown to suppress fetal parathyroid glands, causing transient neonatal hypoparathyroidism. We report two siblings (6 years apart) with transient hypoparathyroidism presented with hypocalcemic seizures during the first 2 weeks of life. Subsequent investigation revealed an unrecognized normocalcemic hyperparathyroidism with nephrocalcinosis in the mother. Maternal hyperparathyroidism was caused by two parathyroid adenomas. In conclusion, our report highlights the importance of careful evaluation of neonatal hypoparathyroidism in uncovering an unrecognized, asymptomatic hyperparathyroidism in the mother.

Hypocalcemic tetany in the newborn as a manifestation of unrecognized maternal primary hyperparathyroidism

Primary hyperparathyroidism (PHP) during pregnancy is a very rare event that increases maternal and perinatal morbidity and mortality. We present a case in which hypocalcemic tetany of the neonatal infant - caused by transient hypoparathyroidism in the child - finally revealed asymptomatic maternal PHP. An apparently healthy 30-year-old woman had an uneventful pregnancy and delivery. On the 15th postpartal day, the newborn developed hypocalcemic tetany. After receiving supplementation of calcium and vitamin D, the child developed without further pathological findings. Laboratory and radiological studies in the mother led to a diagnosis of maternal PHP. An adenoma of the right lower parathyroid gland was subsequently removed. The search for the cause of hypocalcemia in a newborn should not focus on the patient alone. Examining the apparently healthy mother and approaching the case in a multidisciplinary fashion may benefit both the child and the mother.

Maternal primary hyperparathyroidism: Discordant outcomes in a twin pregnancy

The case reports a neonate (twin 2 of a twin girl pregnancy) presenting with seizures due to hypocalcaemia. The presumptive cause of the hypocalcaemia was maternal hyperparathyroidism with concurrent vitamin D deficiency. The first twin remained free of hypocalcaemia and was vitamin D replete, despite similar exposure in the pregnancy and similar postnatal care.

Neonatal Tetany Leading to the Diagnosis of Maternal Hyperparathyroidism

Neonatal Tetany Leading to the Diagnosis of Maternal Hyperparathyroidism

Maternal and Neonatal Hyperparathyroidism as a Consequence of Maternal Renal Tubular Acidosis

Neonatal hyperparathyroidism secondary to maternal hypocalcemia in pregnancy is a rare disorder.1 The effects of secondary hyperparathyroidism in patients with renal failure, including renal osteodystrophy, are well described.2 Neonatal hyperparathyroidism in the presence of maternal renal disease and secondary hyperparathyroidism has not previously been reported. We here present a unique situation in which a neonate developed congenital hyperparathyroidism secondary to maternal hypocalcemia as a consequence of renal tubular acidosis. This report emphasizes the significance of maternal serum calcium concentrations in pregnancy in determining the parathyroid state of the fetus and neonate. METHODS For this report, the following biochemical methods were employed and normal ranges, as measured in our laboratory, are indicated in the tables.

Bioactive parathyroid hormone in pregnant rats and fetuses

Parathyroid function at the end of gestation (day 21) was investigated by measuring plasma calcium (PCa), immunoreactive parathyroid hormone (iPTH), bioactive parathyroid hormone (bioPTH; cytochemical bioassay), and bone histology in intact and thyroparathyroidectomized (TPTX; day 12, ether anesthesia) rats and their fetuses. In pregnant intact rats, PCa was significantly lower, and iPTH, bioPTH, and osteoclast number were higher than in nonpregnant rats. In fetuses, PCa was higher than maternal PCa and correlated with fetal bioPTH. TPTX suppressed maternal bioPTH and decreased iPTH and osteoclast number, whereas fetal iPTH and bioPTH were decreased with no change in osteoclast number. Fetal PCa was near normal and was correlated with maternal PCa but not with fetal bioPTH. The fetomaternal calcium gradient was maintained and even increased. This study shows that there is maternal physiological hyperparathyroidism and functional fetal parathyroid glands at the end of gestation in the rat. Parathyroid hormone does not seem to be responsible for maintaining the high fetomaternal calcium gradient in TPTX animals.

Endocrine Regulation of Calcium Homeostasis During Pregnancy

The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.