The relationship between the parathyroid glands and pregnancy is a clinical model of adaptive endocrinology in which the maternal body must ensure a continuous flow of calcium to the fetoplacental unit without destabilizing the homeostasis of ionized calcium, phosphate and vitamin D metabolism. Contrary to what might be assumed, pregnancy is not simply a state of increased calcium demand: it is a condition in which set points, compartments and mediators change, with a growing role for placental and mammary signals, particularly parathyroid hormone-related protein (PTHrP), which modify the interpretation of laboratory values and susceptibility to pre-existing disorders.
From a clinical perspective, parathyroid abnormalities during pregnancy are crucial because calcium instability may result in maternal complications, including nephrolithiasis, pancreatitis, gestational hypertension and preeclampsia, arrhythmias, renal impairment, hypercalcemic crisis or severe neuromuscular symptoms, as well as fetal and neonatal complications, including growth restriction, preterm delivery, intrauterine death, neonatal hypocalcemia with tetany or seizures, fetal goiter in selected scenarios and transient or persistent mineral metabolism disorders. Part of the risk derives not only from overt forms of disease, but also from the combination of reduced regulatory reserve, increased fetal requirements and difficulties in interpreting tests performed using reference ranges that are not specific to pregnancy.
Pregnancy requires the progressive formation of the fetal skeleton and, particularly during the second half of gestation, imposes placental calcium transfer that increases with gestational age. The maternal body responds predominantly through an absorptive rather than a demineralizing strategy: intestinal calcium absorption becomes more efficient because of an increase in calcitriol, or 1,25-dihydroxyvitamin D, which may reach concentrations markedly higher than those observed outside pregnancy. This rise in calcitriol is made possible by increased hydroxylation activity and by integrated endocrine and placental signals, with a major contribution from pregnancy-specific mediators that remodel calcium balance.
Within this physiological setting, maternal parathyroid hormone (PTH) does not follow a single standard trajectory throughout pregnancy. During the early stages, it may decrease or remain within the low-normal range, consistently with a more absorptive environment and increased calcitriol. Later in pregnancy, particularly when calcium or vitamin D intake is inadequate or when a pre-existing vulnerability is present, PTH may rise as an adaptive response to preserve serum calcium stability. This variability explains why interpretation of PTH during pregnancy requires clinical context: vitamin D status, ionized calcium, albumin, renal function, phosphate and changes over time are more informative than an isolated result.
A distinctive feature of pregnancy is the increasing importance of PTHrP. The placenta and, later, breast tissue may produce PTHrP, which contributes to calcium transfer to the fetus and may modulate maternal mineral metabolism. Pregnancy therefore introduces a parathyroid-like mediator that can mask or amplify clinical phenotypes: in some rare conditions, excessive PTHrP production may sustain hypercalcemia with suppressed PTH, whereas more commonly PTHrP participates physiologically in maintaining calcium flow to the fetal compartment, particularly when maternal intake is suboptimal.
At the same time, the laboratory determinants of measured serum calcium change. Pregnancy-related hemodilution and reduced plasma albumin may lower total calcium even when ionized calcium remains normal. This is an essential practical point: relying on total calcium without correcting for albumin, or without measuring the ionized fraction when clinically indicated, may lead to an erroneous diagnosis of hypocalcemia or to underestimation of hypercalcemia. Serum phosphate may also vary, and its interpretation should be integrated with PTH, vitamin D and renal function because the maternal axis must maintain a balance between mineral availability, renal excretion and fetal requirements.
Renal physiological changes during pregnancy, including increased glomerular filtration, modify calcium and phosphate handling and may alter the likelihood of nephrolithiasis in the presence of hypercalciuria. In a woman with hyperparathyroidism or inadequately calibrated supplementation, the combination of increased filtration, changes in urinary pH and a high calcium load may promote stone formation and renal complications. These consequences are not exclusively maternal because pain, infection and deterioration of renal function may indirectly affect placental perfusion and fetal growth.
Pregnancy also creates a temporal sequence that influences risk. The fetus becomes progressively dependent on a constant calcium supply and, after birth, the newborn abruptly transitions from continuous placental provision to autonomous homeostasis. If the mother has been hypercalcemic during pregnancy, the fetal parathyroid axis may have been suppressed and, after delivery, the newborn may develop neonatal hypocalcemia because of delayed parathyroid responsiveness. Conversely, in settings of uncontrolled maternal hypocalcemia, fetal compensation may become insufficient to ensure appropriate mineralization and postnatal adaptation, resulting in clinical vulnerability during the first weeks of life.
The first clinical decision is which parameters should be measured and which calcium fraction should guide management. During pregnancy, total calcium may be reduced because of lower albumin concentrations. Therefore, when the result is clinically relevant, the most reliable assessment is ionized calcium or albumin-corrected total calcium, with full awareness of the limitations of correction formulas. In the presence of neuromuscular symptoms such as paresthesia, muscle cramps or signs of tetany, arrhythmias, severe hyperemesis, nephrolithiasis, pancreatitis or gestational hypertension, measurement of ionized calcium is particularly useful because it reduces the ambiguity caused by pregnancy-related changes in plasma proteins.
A rational assessment always requires an integrated panel including PTH, phosphate, magnesium, creatinine with estimated renal function, 25-hydroxyvitamin D and, when indicated, calcitriol. Magnesium deserves particular attention because hypomagnesemia may impair both the secretion and action of PTH and may therefore aggravate or mimic functional hypoparathyroidism, making correction of serum calcium unstable. Vitamin D assessment is essential because deficiency may intensify a tendency toward hypocalcemia and increase PTH requirements or, in patients with hypoparathyroidism, increase instability during the titration of calcitriol and calcium.
Practical points that reduce interpretation errors during pregnancy
When hypercalcemia is identified, distinguishing primary hyperparathyroidism, secondary hyperparathyroidism, which is usually not hypercalcemic, and familial hypocalciuric hypercalcemia (FHH) becomes essential. During pregnancy, FHH is a potential diagnostic pitfall because it may mimic mild hyperparathyroidism and lead to unnecessary surgery. It is characterized by chronic mild-to-moderate hypercalcemia, normal or mildly elevated PTH and low urinary calcium excretion, although urinary calcium assessment may be affected by physiological changes in glomerular filtration and calcium intake. When the phenotype is compatible, integration of family history, biochemical findings and, in appropriate cases, genetic evaluation can prevent unnecessary parathyroidectomy.
When hypocalcemia is identified, the differential diagnosis must distinguish true hypoparathyroidism, characterized by inappropriately low PTH relative to the degree of hypocalcemia, from hypocalcemia caused by vitamin D deficiency, malabsorption, chelation or hypomagnesemia. Recognition of hypoparathyroidism is particularly important during pregnancy because treatment with calcium and calcitriol must be calibrated according to ionized calcium and the risk of hypercalciuria, with a target that protects both mother and fetus without inducing nephrocalcinosis or nephrolithiasis.
Imaging during pregnancy must be selected carefully. Neck ultrasonography is safe and useful for documenting thyroid nodules or a suspected parathyroid adenoma, whereas preoperative localization of parathyroid disease using nuclear medicine techniques is generally deferred until after delivery to avoid unnecessary fetal exposure. When the maternal condition requires a surgical decision during pregnancy, the diagnostic strategy often relies on robust biochemical assessment combined with ultrasonography, reserving more complex investigations for settings in which fetal safety can be fully guaranteed.
The assessment strategy should ultimately be structured according to both risk level and timing. In the absence of symptoms and risk factors, there is no single model universally applied across all healthcare systems. However, in women with a history of nephrolithiasis, known hypercalcemia, previous hyperparathyroidism, hypoparathyroidism, cervical surgery, autoimmune disease, chronic kidney disease or a previous newborn with hypocalcemia, early evaluation and scheduled follow-up reduce predictable adverse events. During pregnancy, the window for intervention is limited and trends are often more informative than individual results, provided that blood sampling is standardized and interpreted using the same laboratory method.
Preventing disturbances of mineral metabolism during pregnancy does not simply mean prescribing supplements, but ensuring an intake that is appropriate for both physiological requirements and the underlying disorder. Under physiological conditions, the aim is to provide adequate calcium and vitamin D to support increased intestinal absorption and reduce the likelihood that the body will need to rely on potentially unfavorable compensatory mechanisms. When deficiencies are present, correction is clinically relevant because vitamin D insufficiency may amplify the rise in PTH and promote phosphate disturbances, whereas calcium deficiency may increase serum calcium instability, particularly in women with reduced regulatory reserve or pre-existing disorders.
Assessment of dietary intake should consider the entire clinical context, including dairy products, fortified foods, calcium-rich mineral water, dietary habits, nausea and food aversions during the first trimester. In some women, reduced calcium intake is iatrogenic and results from unnecessary advice or fear of kidney stones. In reality, the risk of nephrolithiasis during pregnancy depends mainly on the balance between intake, urinary excretion, hydration and the underlying disorder. Drastically reducing calcium intake may worsen instability and increase reliance on non-physiological supplementation.
Vitamin D management should be based on measurement of 25-hydroxyvitamin D and realistic correction targets. Excess vitamin D is not harmless and may promote hypercalcemia in predisposed women, whereas deficiency may make hypoparathyroidism more difficult to control and may increase PTH to an undesirable degree. Pregnancy increases the physiological importance of calcitriol, but this does not replace the need for adequate substrate availability, particularly in women with limited sunlight exposure or other risk factors for deficiency.
A practical issue concerns interactions between supplementation and other treatments. Calcium salts have variable bioavailability and may be divided into several daily doses to improve absorption and reduce peaks in urinary calcium excretion. In women taking iron, temporal separation may reduce gastrointestinal adverse effects and improve adherence, although the interaction is more relevant to levothyroxine than to calcium itself. During pregnancy, adherence is often impaired by nausea, constipation and complex obstetric treatment regimens. The most effective preventive strategy is therefore simple and consistent counseling that avoids unnecessarily complex schedules and supports continuity.
The safety of supplementation changes substantially in the presence of hyperparathyroidism or hypercalcemia. In a woman with PTH-dependent hypercalcemia, indiscriminately increasing calcium or vitamin D may worsen hypercalcemia and increase renal and pancreatic complications. In these settings, prevention does not mean increasing intake, but controlling the cause of hypercalcemia, maintaining adequate hydration, avoiding excessive loads and performing close monitoring. Exposure to iodine loads or certain medications is not the central issue in this context, but any intervention that alters renal function or electrolyte balance may affect calcium stability.
Prevention also includes preconception planning when a parathyroid disorder is already known. In a woman with primary hyperparathyroidism, definitive treatment before pregnancy reduces the risk of complications and simplifies management. In a woman with hypoparathyroidism, stabilizing the serum calcium target and establishing a monitoring plan before conception reduce fluctuations and urgent hospital visits during gestation. Pregnancy is not the ideal time to devise a therapeutic strategy: it is the time to apply an already planned strategy, with adjustments guided by biochemical and clinical findings.
Hypoparathyroidism during pregnancy is a condition with a high risk of instability because fine regulation of ionized calcium is lost precisely when the maternal system must sustain a continuous calcium flow to the fetus. The most common cause in women of reproductive age is postsurgical hypoparathyroidism, although autoimmune, genetic and functional forms may emerge or be recognized during pregnancy. The typical biochemical phenotype is hypocalcemia with relative hyperphosphatemia and inappropriately low PTH, often accompanied by neuromuscular instability and, in the most severe cases, a risk of tetanic crises or arrhythmias.
Treatment during pregnancy aims to maintain a serum calcium level that protects the mother and reduces neonatal risk without exposing the patient to chronic hypercalciuria. In practical terms, standard treatment is based on oral calcium and calcitriol, with native vitamin D when deficiency is documented and correction of magnesium when reduced. Pregnancy may alter treatment requirements. In some women, the physiological rise in calcitriol and the presence of PTHrP may reduce the need for exogenous calcitriol. In others, particularly those with nausea, malabsorption or vitamin D deficiency, instability increases and more frequent adjustments are required. This variability makes close monitoring essential, especially after changes in treatment.
A critical clinical issue is the choice of target. Raising serum calcium toward the upper range may reduce maternal symptoms but increase urinary calcium excretion and the risk of nephrolithiasis or nephrocalcinosis, whereas maintaining excessively low values increases the risk of tetany and may theoretically affect fetal mineral balance, particularly when hypocalcemia is severe or prolonged. International recommendations therefore generally favor a serum calcium target within the low-normal or lower-middle range, taking symptoms, urinary calcium and renal function into account and prioritizing stability rather than maximization of the value.
Surveillance should include not only calcium and phosphate, but also creatinine, magnesium and, when indicated, urinary calcium. Urine collection may be logistically difficult during pregnancy, but the underlying concept remains relevant: a patient with hypoparathyroidism who requires increasing doses of calcium and calcitriol may develop hypercalciuria even when serum calcium is not elevated because the kidney does not receive the PTH-dependent signal that promotes tubular calcium reabsorption. This is one reason why true hormone replacement, when available and appropriate, is conceptually more physiological. During pregnancy, however, management remains centered on safety and on the clinical experience reflected in current guidelines.
Clinical complications of hypoparathyroidism during pregnancy include neuromuscular symptoms, cardiovascular instability and hospital admission for severe hypocalcemia, particularly in the presence of vomiting, diarrhea or reduced adherence. Another relevant phase is the postpartum period: after breastfeeding begins, increased mammary PTHrP may rapidly alter calcium balance and reduce treatment requirements, exposing the patient to hypercalcemia if doses are not reassessed. The monitoring plan must therefore extend into the puerperium and the first weeks of lactation, with scheduled testing and simple instructions for recognizing symptoms of hypercalcemia and hypocalcemia.
In women with hypoparathyroidism, neonatal management is part of high-quality care. Maternal stability reduces the risk of neonatal instability, but the transition to extrauterine life remains a vulnerable phase. The neonatal team should be informed of the maternal condition and treatment so that neonatal calcium can be assessed and any neuromuscular signs or seizures can be managed promptly.
Hypercalcemia during pregnancy is less common than hypocalcemia, but when present it may cause clinically significant maternal and fetal complications. The most common cause of PTH-dependent hypercalcemia during pregnancy is primary hyperparathyroidism, generally due to a parathyroid adenoma and less frequently to multiglandular hyperplasia or parathyroid carcinoma. Hypercalcemia may remain unrecognized because symptoms such as nausea, vomiting, fatigue and constipation may be attributed to pregnancy itself. Consequently, the diagnosis is sometimes made only after nephrolithiasis, pancreatitis, hypertension or renal deterioration develops.
In the mother, hypercalcemia increases the risk of nephrolithiasis, polyuria and dehydration and may precipitate a hypercalcemic crisis in the setting of vomiting, reduced fluid intake or infection. Pancreatitis is a serious complication because it may destabilize the pregnancy and require intensive care. Observational studies and clinical series have also reported an association between hyperparathyroidism during pregnancy and an increased risk of obstetric complications, including gestational hypertension and preeclampsia, as well as preterm delivery and pregnancy loss, with risk generally increasing as serum calcium rises.
In the fetus and newborn, the central pathophysiological mechanism is suppression of the fetal parathyroid axis in response to maternal hypercalcemia. The fetus is exposed to an environment with elevated calcium concentrations and reduces parathyroid secretion. After birth, when placental calcium transfer ceases and serum calcium physiologically falls, the newborn may fail to activate PTH promptly and may develop neonatal hypocalcemia with tetany or seizures. This mechanism explains why a maternal hypercalcemic disorder may result in a neonatal hypocalcemic disorder, an apparently paradoxical but biologically coherent outcome.
The diagnosis of hyperparathyroidism during pregnancy requires rigorous biochemical confirmation: hypercalcemia with non-suppressed PTH and often reduced phosphate, together with assessment of vitamin D and renal function. The differential diagnosis includes FHH, which generally does not benefit from surgery and usually follows a more benign course, and PTH-independent forms in which PTH is suppressed. These include vitamin D-mediated causes, malignancy-related hypercalcemia, immobilization and, more rarely, excessive PTHrP production during pregnancy or lactation. Diagnostic accuracy is essential because the definitive treatment of primary hyperparathyroidism is surgical, whereas other causes require entirely different strategies.
Hypercalcemic crisis during pregnancy is rare but represents both an endocrine and obstetric emergency. The typical clinical picture includes severe dehydration, neurological impairment, worsening renal function and possible hemodynamic instability. The priority is stabilization with hydration and correction of electrolyte disturbances in a monitored setting, together with multidisciplinary assessment involving an endocrinologist, obstetrician, anesthetist and, when necessary, nephrologist. Surgery may become more urgent in this setting, but the decision requires consideration of gestational timing and disease severity, balancing anesthetic risk against the risk of persistent hypercalcemia.
During pregnancy, the term parathyroid disease encompasses highly heterogeneous conditions that require different strategies. Sporadic primary hyperparathyroidism due to an adenoma is the most common PTH-dependent cause of hypercalcemia and, when clinically significant, may benefit from parathyroidectomy. The second trimester is often considered the most favorable period when surgery cannot be deferred. Genetic and syndromic phenotypes also exist in which the disease is multiglandular, recurrent or associated with other endocrinopathies, and pregnancy may be the period in which the condition becomes clinically apparent or is reassessed.
Familial hypocalciuric hypercalcemia deserves specific attention. It is typically a benign condition characterized by mild-to-moderate hypercalcemia, non-suppressed PTH and relative hypocalciuria, and it is not corrected by parathyroidectomy. During pregnancy, it may be mistaken for mild hyperparathyroidism and lead to unnecessary surgery. The principal issue therefore becomes accurate communication and neonatal management: in some families, the genetic background may influence the newborn's calcium level and adaptive response, and neonatal surveillance should be planned according to the clinical context.
Genetic syndromes such as multiple endocrine neoplasia type 1 (MEN1) or CDC73-related disorders, which encompass tumor-associated hyperparathyroidism and, in selected cases, an increased risk of parathyroid carcinoma, have more complex implications. In these conditions, hyperparathyroidism may be multiglandular and the family history is often informative. During pregnancy, management must balance the urgency of controlling hypercalcemia against the need to plan a complete diagnostic pathway that includes assessment of other syndromic components without unnecessarily exposing the patient to procedures during gestation.
Parathyroid carcinoma during pregnancy is exceptional, but it should be considered when hypercalcemia is marked and PTH is very high, particularly in the presence of a palpable cervical mass, local signs or severe early complications. In these cases, the diagnostic strategy is guided by biochemical assessment and ultrasonography, and management generally favors surgery by an experienced team because calcium control and the quality of the first operation are major determinants of prognosis. Pregnancy again requires strict clinical discipline: delays caused by underestimation must be avoided, but unnecessary and unsafe diagnostic procedures must also be prevented.
PTH-independent causes of hypercalcemia may also have specific features during pregnancy, including excessive placental or mammary PTHrP production, vitamin D-mediated hypercalcemia and hypercalcemia associated with granulomatous or other rare disorders. These conditions are distinguished by suppressed PTH and require a different diagnostic and therapeutic pathway in which parathyroidectomy has no role and management must focus on identifying the underlying cause and selecting the safest approach for both mother and fetus.
Therapeutic management of parathyroid disorders during pregnancy is based on a fundamental principle: the target is not simply to normalize a laboratory value, but to prevent maternal complications and protect the newborn by maintaining stability and minimizing fluctuations. In hypoparathyroidism, standard treatment with calcium and calcitriol remains the cornerstone, together with close monitoring and a target of stable serum calcium while avoiding chronic hypercalciuria. Treatment must remain flexible because requirements may change during pregnancy and particularly after delivery when breastfeeding begins. Correction of magnesium and native vitamin D deficiency reduces instability and allows more predictable dose titration.
For primary hyperparathyroidism, the definitive treatment is parathyroidectomy. In women with clinically significant hypercalcemia or complications, surgery may be indicated during pregnancy and, when necessary, the second trimester is often considered the most favorable period from an obstetric and anesthetic perspective. The decision should integrate the serum calcium level, symptoms, renal or pancreatic complications, obstetric history and the feasibility of conservative monitoring. In mild disease, a conservative approach based on hydration, avoidance of excessive calcium intake, symptom control and monitoring may be considered, but the strategy should be reassessed promptly if serum calcium rises or complications develop.
Pharmacological treatment of hypercalcemia during pregnancy is complex. Hydration is the safest and most immediate measure, whereas treatments commonly used outside pregnancy require caution. Calcimimetics such as cinacalcet have been used in selected cases, but evidence during pregnancy is limited and decisions should be individualized in expert centers after careful assessment of the risk-benefit ratio. Bisphosphonates are generally not a first-line option during pregnancy because of their prolonged retention in bone and uncertainties regarding fetal safety. Calcitonin may temporarily lower serum calcium and has been considered as bridging treatment in some situations, but its efficacy is limited and management remains focused on stabilization and, when indicated, surgery.
Management of hypercalcemic crisis requires an emergency protocol involving intravenous hydration, electrolyte and cardiac monitoring, assessment of renal function, identification of the underlying cause and rapid determination of definitive management. The immediate goal is to reduce systemic maternal risk and maintain placental perfusion through close collaboration with the obstetric team. Even in advanced pregnancy, impulsive decisions should be avoided. In some cases, management may include stabilization followed by planned surgery or coordination of delivery timing according to maternal safety, always on a multidisciplinary basis.
Management must also include an educational component. Women with hypoparathyroidism should recognize symptoms of hypocalcemia and hypercalcemia and know when medical assessment is required. Women with hyperparathyroidism should understand the importance of hydration, avoiding inappropriate supplementation and monitoring renal or gastrointestinal symptoms. During pregnancy, adherence and understanding reduce the fluctuations that otherwise lead to emergency visits and delayed interventions, which carry the greatest risk.
Specific fetal surveillance becomes relevant when the maternal condition may directly alter fetal mineral balance or when treatments cross the placenta and may affect the fetal thyroid or mineral metabolism. In the context of parathyroid disease, the most typical scenario is maternal primary hyperparathyroidism with persistent hypercalcemia. The principal neonatal risk is neonatal hypocalcemia caused by suppression of the fetal parathyroid axis. This risk increases with higher serum calcium levels and longer exposure and may present during the first hours or days of life with irritability, tremors, tetany or seizures.
Surveillance during pregnancy is based on integrating maternal data with obstetric monitoring. Serial assessment of serum calcium and the PTH-dependent biochemical profile guides risk stratification and the need for more intensive follow-up. Fetal ultrasonography assesses growth, amniotic fluid volume and fetal well-being and, in severe or unstable conditions, closer monitoring may be required to identify early signs of placental compromise or growth restriction. There is no single pathognomonic ultrasound marker of fetal calcium disorders, so clinical decisions remain primarily based on the severity and stability of the maternal condition.
In the newborn, the most effective preventive measure is organizational: the neonatal team should be informed before delivery when the mother has hyperparathyroidism, hypercalcemia or hypoparathyroidism requiring active treatment so that neonatal serum calcium measurement and early symptom management can be planned. Neonatal hypocalcemia may require calcium and, in selected cases, calcitriol, together with close monitoring. Prompt management reduces neurological complications and stabilizes postnatal adaptation.
In women with hypoparathyroidism, maternal stability protects the fetus and facilitates more regular neonatal adaptation. However, the postpartum period, particularly during breastfeeding, may rapidly alter maternal calcium balance and treatment requirements. Surveillance should therefore be viewed as a continuum extending through pregnancy, delivery and the puerperium, supported by a written plan shared among endocrinology, obstetric and neonatal teams.
The postpartum period is a phase of rapid transition during which calcium balance may change more quickly than during pregnancy. When breastfeeding begins, mammary PTHrP production increases and may promote mobilization of calcium from the maternal skeleton to support lactation. In a woman with hypoparathyroidism, this may reduce calcium and calcitriol requirements and create a risk of hypercalcemia if doses are not reassessed. In a woman with hyperparathyroidism or pre-existing hypercalcemia, lactation may, in rare situations, further aggravate hypercalcemia and require closer monitoring.
During the puerperium, clinical manifestations may easily be mistaken for nonspecific postpartum symptoms. Fatigue, insomnia, irritability and gastrointestinal disturbances may be attributed to the postpartum period even though they may reflect hypocalcemia or hypercalcemia. In patients with known parathyroid disease, postpartum follow-up is therefore not optional. Scheduled assessment of serum calcium and calcium-phosphate metabolism during the first weeks allows treatment to be adjusted before severe symptoms or renal complications develop.
Postpartum planning also includes the patient's future reproductive care. In women with primary hyperparathyroidism managed conservatively during pregnancy, definitive assessment and, when indicated, surgery should be scheduled after delivery at a time compatible with maternal needs and breastfeeding. In women with hypoparathyroidism, establishing a stable postpartum dose and managing treatment during lactation reduce fluctuations, improve quality of life and prepare the patient for future pregnancies with an already structured plan.
Overall, the maternal and neonatal prognosis is favorable when the disorder is recognized early, laboratory tests are interpreted correctly, with particular attention to ionized calcium and clinical context, and a coordinated plan extends through pregnancy, delivery and the puerperium. The poorest outcomes mainly result from delayed diagnosis, unrecognized clinically significant hypercalcemia or unstable and inadequately monitored hypocalcemia, situations in which the window for intervention narrows and clinical complexity increases rapidly.