Pediatric Hypocalcemia 

Updated: Dec 05, 2016
Author: Yogangi Malhotra, MD; Chief Editor: Sasigarn A Bowden, MD 

Overview

Background

Hypocalcemia is a laboratory and clinical abnormality that is observed with relative frequency, especially in neonatal pediatric patients. Laboratory hypocalcemia is often asymptomatic, and its treatment in neonates is controversial. However, children with hypocalcemia in pediatric intensive care units (PICUs) have mortality rates higher than those of children with normal calcium levels. (See Prognosis, Clinical, Workup, and Treatment.)

The definition of hypocalcemia is based on both gestational and postnatal age in neonates and is different for children. Calcium data are presented as both mg/dL and mmol/L (1 mg/dL = 0.25 mmol/L)

In children, hypocalcemia is defined as a total serum calcium concentration less than 2.1 mmol/L (8.5 mg/dL).

In term infants, hypocalcemia is defined as total serum calcium concentration less than 2 mmol/L (8 mg/dL) or ionized fraction of less than 1.1 mmol/L (4.4 mg/dL)

In preterm infants, hypocalcemia is defined as total serum calcium concentration less than 1.75 mmol/L (7 mg/dL) is defined as hypocalcemia in infants weighing less than 1500 g birthweight. Symptomatology often manifests when the ionized calcium level falls below 0.8-0.9 mmol/L.

Calcium metabolism and function

Calcium is the most abundant mineral in the body. Of the body's total calcium, 99% is stored in bone, and serum levels constitute less than 1%.[1] Various factors regulate the homeostasis of calcium and maintain serum calcium within a narrow range. These include parathormone (PTH), vitamin D, hepatic and renal function (for conversion of vitamin D to active metabolites), and serum phosphate and magnesium levels. (See Etiology and Workup)

Serum calcium is present in two forms: the free (ionized) and the bound form. Only about 50% of circulating calcium is present in the physiologically free form. The rest is either bound to proteins (40%) or complexed (10%) with bicarbonate, citrate, and phosphate. The ionized calcium level varies based on the level of serum albumin, blood pH, serum phosphate, magnesium, and bicarbonate levels, the administration of transfused blood containing citrate and free fatty acid content in total parenteral nutrition. The normal range for ionized calcium is 1-1.25 mmol/L (4-5 mg/dL).

The concentration of calcium in the serum is critical to many important biologic functions, including the following:

  • Calcium messenger system by which extracellular messengers regulate cell function

  • Activation of several cellular enzyme cascades

  • Smooth muscle and myocardial contraction

  • Nerve impulse conduction

  • Secretory activity of exocrine glands

Calcium physiology during pregnancy and Lactation

The fetus requires approximately 30gm calcium to mineralize its skeleton and to maintain normal physiologic processes. The newborn requires more than this amount during the first few months of life from breastmilk. The unique adaptations of the mother’s body allow her to meet the baby’s calcium demands without adverse long-term consequences to the maternal skeleton. The bulk of the calcium transmitted to the fetus during the third trimester is derived from the maternal intestinal absorption. Intestinal absorption of calcium doubles in pregnancy. Serum calcitriol level doubles or triples and stays elevated in pregnancy despite falling PTH level. It is instead increased, as 1-hydroxylase is upregulated by PTH-related Protein (PTHrP), prolactin and placental lactogen. The rise in PTHrP allows for the rise in calcium while protecting the maternal skeleton.

There is an average daily loss of 210 mg of calcium during lactation. Unlike during pregnancy, elevated PTHrP and low estradiol result in temporary demineralization of maternal skeleton to meet the calcium needs of the breastfeeding infant. These bone density losses are significantly reversed within twelve months of weaning.[2]

Pathophysiology

Hypocalcemia manifests as central nervous system (CNS) irritability and poor muscular contractility. Low calcium levels decrease the threshold of excitation of neurons, causing them to have repetitive responses to a single stimulus. Because neuronal excitability occurs in sensory and motor nerves, hypocalcemia produces a wide range of peripheral and CNS effects, including paresthesias, tetany (i.e., contraction of hands, arms, feet, larynx, bronchioles), seizures, and even psychiatric changes in children.

Tetany is not caused by increased excitability of the muscles. Muscle excitability is depressed because hypocalcemia impedes acetylcholine release at neuromuscular junctions and, therefore, inhibits muscle contraction. However, the increase in neuronal excitability overrides the inhibition of muscle contraction. Cardiac function may also be impaired because of poor muscle contractility.

Etiology

Overall, one of the most common causes of hypocalcemia in children is renal failure, which results in hypocalcemia because of inadequate 1-hydroxylation of 25-hydroxyvitamin D and hyperphosphatemia due to diminished glomerular filtration.

Although hypocalcemia is most commonly observed among neonates, it is frequently symptomatic and reported in older children and adolescents, especially in PICU settings. The causes of hypocalcemia can be classified by the child's age at presentation.

Early onset neonatal hypocalcemia

Early neonatal hypocalcemia, which occurs within 48-72 hours of birth, is most commonly seen in preterm and very low birth weight infants, infants asphyxiated or depressed at birth, infants of diabetic mothers, and the intrauterine growth restricted infants. The mechanisms underlying hypocalcemia caused by these conditions are as follows:

  • Prematurity: Possible mechanisms include inadequate nutritional intake, decreased responsiveness of parathyroid hormone to vitamin D, increased calcitonin level, increased urinary losses, and hypoalbuminemia leading to a decreased total (but normal ionized) calcium level.[3]

  • Birth asphyxia: Delayed introduction of feeds, increased calcitonin production, increased endogenous phosphate load due to tissue catabolism, renal failure, metabolic acidosis, and its treatment with alkali therapy all may contribute to hypocalcemia.[4, 5]

  • Infants of a diabetic mother: The degree of hypocalcemia is associated with the severity of diabetes in the mother. Magnesium depletion in mothers with diabetes mellitus causes a hypomagnesemic state in the fetus, which induces functional hypoparathyroidism and hypocalcemia in the infant. In addition, infants of diabetic mothers have higher serum calcium in utero and this may also suppress the parathyroid gland. A high incidence of birth complications due to macrosomia and difficult delivery and, in some cases, higher incidence of preterm birth in infants of diabetic mothers are contributing factors for hypocalcemia.

  • Intrauterine growth restriction: Infants with intrauterine growth restriction may develop hypocalcemia because of decreased transplacental passage of calcium. In addition, decreased accretion is present if they are delivered preterm or have experienced perinatal asphyxia as a result of placental insufficiency.

Late-onset neonatal hypocalcemia

This occurs 3-7 days after birth, although occasionally it is seen as late as age 6 weeks. The following are some important causes of late neonatal hypocalcemia:

  • Exogenous phosphate load: This is most commonly seen in developing countries. The problem results when the neonate is fed with phosphate-rich formula or cow's milk. Whole cow's milk has 7 times the phosphate load of breast milk (956 vs 140 mg/L in breast milk). This may cause symptomatic hypocalcemia in neonates.[6]

  • Vitamin D deficiency: In a review of the medical records of 78 term neonates with hypocalcemia, moderate-to-severe late-onset neonatal hypocalcemia developed more often in male infants and Hispanic infants. It was often a sign of coexistent vitamin D insufficiency or deficiency and hypomagnesemia. The newborns respond well to one or more of the following: calcium supplements, calcitriol, low phosphorus formula (PM 60/40), and magnesium supplements for a limited period of time.[7]

  • Primary immunodeficiency disorder: DiGeorge Syndrome is the most important immunodeficiency disorder to be aware of that is associated with hypocalcemia. DiGeorge Syndrome is a primary immunodeficiency, often but not always, characterized by cellular (T-cell) deficiency, characteristic facies, congenital heart disease and hypocalcemia. Hypoparathyroidism causes hypocalcemia; 90% of infants with the features of DiGeorge syndrome have a 22q11 chromosomal deletion.

  • Data suggest an association between late-onset neonatal hypocalcemia and gentamicin therapy, especially with the newer dosing schedule of every 24 hours.[8]

Other causes of late-onset neonatal hypocalcemia include the following:

  • Magnesium deficiency (usually transient)

  • Transient hypoparathyroidism of newborn

  • Hypoparathyroidism due to other causes

  • Maternal hyperparathyroidism

  • Blood transfusion or sodium bicarbonate (alkali) infusions

  • Phototherapy for hyperbilirubinemia[9]

Hypocalcemia in infants and children

Hypoparathyroidism, abnormal vitamin D production or action, and hyperphosphatemia are among the causes of hypocalcemia in infants and children.

Hypoparathyroidism can result from the following:

  • Aplasia or hypoplasia of parathyroid gland -DiGeorge syndrome also known as velocardiofacial (Shprintzen) syndrome or 22q11 deletion syndrome; fetal exposure to retinoic acid; complex of vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, and radial and renal abnormalities (VATER/VACTERL); and association of coloboma, heart defects, choanal atresia, renal abnormalities, growth retardation, male genital anomalies, and ear abnormalities (CHARGE) (Details of DiGeorge syndrome are discussed in the late-onset hypocalcemia section above.)

  • Parathormone (PTH) receptor defects - Pseudohypoparathyroidism

  • Autoimmune parathyroiditis

  • Infiltrative lesions -Hemosiderosis, Wilson disease, thalassemia

  • Activating mutations of the calcium-sensing receptor leading to inappropriately suppressed PTH secretion (e.g. GNA11 mutation)[10]

  • Idiopathic causes

Abnormal vitamin D production or action can be caused by the following:

  • Vitamin D deficiency: Dietary insufficiency and maternal use of anticonvulsants have been reported.

  • Acquired or inherited disorders of vitamin D metabolism

  • Resistance to actions of vitamin D

  • Liver disease: Liver disease can affect 25-hydroxylation of vitamin D; certain drugs (eg, phenytoin, carbamazepine, phenobarbital, isoniazid, and rifampin) can increase the activity of P-450 enzymes, which can increase the 25-hydroxylation and also the catabolism of vitamin D.

Hyperphosphatemia can result from the following:

  • Excessive phosphate intake from feeding cow milk or infant formula with improper (low) calcium to phosphate ratio

  • Excessive phosphate intake caused by inappropriate use of phosphate-containing enemas

  • Excessive phosphate or inappropriate Ca:P ratio in total parenteral nutrition

  • Increased endogenous phosphate load caused by anoxia, chemotherapy, or rhabdomyolysis

  • Renal failure

Other causes of hypocalcemia in infants and children include the following:

  • Malabsorption syndromes

  • Alkalosis: Respiratory alkalosis is caused by hyperventilation; metabolic alkalosis occurs with the administration of bicarbonate, diuretics, or chelating agents, such as the high doses of citrates taken in during massive blood transfusions.

  • Pancreatitis

  • Pseudohypocalcemia (ie, hypoalbuminemia): Serum calcium concentration decreases by 0.8 mg/dL for every 1 g/dL fall in concentration of plasma albumin.

  • “Hungry bones syndrome:" Rapid skeletal mineral deposition is seen in infants with rickets or hypoparathyroidism after starting vitamin D therapy.

Epidemiology

Occurrence in the United States

The incidence of neonatal hypocalcemia varies in different studies. Data on the incidence and prevalence rates in the neonatal period are limited. Hypocalcemia occurs frequently in very low birth weight infants (< 1500 g). In a small study of 19 infants, the reported incidence of early onset hypocalcemia was 37% by 12 hours, 83% by 24 hours, and 89% by 36 hours in very preterm infants less than 32 weeks’ gestation.[11] Among very preterm infants, the onset of hypocalcemia is earlier than in more mature at-risk neonates.

The risk of developing early onset neonatal hypocalcemia is also greater among infants of diabetic mothers (7% [gestational DM], 32% [pregestational]) and infants experiencing perinatal asphyxia. The overall prevalence of moderate-to-severe, late-onset neonatal hypocalcemia (onset 5-10 d after birth) is low and appears to be more common among Hispanic and male infants; the severity of hypocalcemia is greater among infants who also exhibit hyperphosphatemia, hypomagnesemia, and vitamin D deficiency or insufficiency.[12]

International occurrence

No variation is reported across national boundaries. However, late-onset hypocalcemia is more common in infants in developing countries where babies are fed cow's milk or formulas containing high amounts of phosphate than in countries where infants are fed human milk or formulas containing low amounts of phosphate.

Age-related demographics

Most pediatric patients with hypocalcemia are newborns. In older children, hypocalcemia is usually associated with critical illness, acquired hypoparathyroidism, activating mutations of the calcium-sensing receptor, or defects in vitamin D supply or metabolism.

Prognosis

Most cases of early-onset neonatal hypocalcemia resolve within 48-72 hours without any clinically significant sequelae.

Late-onset neonatal hypocalcemia secondary to exogenous phosphate load and magnesium deficiency responds well to phosphate restriction and magnesium repletion. A renewed emphasis on exclusive breastfeeding and use of contemporary infant formulas with more appropriate Ca:P ratios for mothers choosing not to breastfeed reduce this risk. Early supplementation with vitamin D in breastfeeding infants is another important prevention strategy.

When caused by hypoparathyroidism, hypocalcemia requires continued therapy with vitamin D metabolites and calcium salts. The period of therapy depends on the nature of the hypoparathyroidism, which can be transient, last several weeks to months, or be permanent.

Higher mortality rates have been reported in children with hypocalcemia than in normocalcemic children in PICU settings.[13]

 

Presentation

History

In patients with hypocalcemia, the history varies depending on age. In newborns, patient history can include the following:

  • Possibly no symptoms exhibited

  • Lethargy

  • Poor feeding

  • Vomiting

  • Abdominal distension

  • Prematurity

  • Difficult birth/low Apgar score

  • Maternal diabetes/hyperparathyroidism

  • Jitteriness

  • Seizure

  • Apnea

History in children can be as follows:

  • Seizures

  • Twitching

  • Cramping

  • Laryngospasm, a rare initial manifestation

Physical Examination

Children’s symptoms include the following:

  • Lethargy

  • Cyanosis

  • Tremulousness

  • Seizures

  • Apnea

  • Tetany and signs of nerve irritability, such as the Chvostek sign, carpopedal spasm, the Trousseau sign, and stridor

  • Abdominal distension

  • Cardiac murmur

  • Features of a "syndrome"

 

DDx

Diagnostic Considerations

Conditions to consider in the differential diagnosis of hypocalcemia include the following:

  • Anoxia

  • Intracranial bleeding

  • Narcotic withdrawal

  • Pseudohypoparathyroidism

  • Rickets, osteomalacia, or rachitis (i.e., vitamin D deficiency)

  • Hyperphosphatemia

  • Hypoalbuminemia

  • Hypomagnesemia

  • Renal failure

  • Metabolic disease affecting vitamin D, seizures

  •  Di George Syndrome (22q deletion)

  •  Congenital hypoparathyroidism

  • Familial hypoparathyroidism

  • Maternal hyperparathyroidism

  • Surgery of thyroid gland

  • Autoimmune hypoparathyroidism

Differential Diagnoses

 

Workup

Laboratory Studies

The following should be assessed in patients with hypocalcemia:

  • Total and ionized serum calcium levels

  • Serum magnesium levels

  • Serum electrolyte and glucose levels

  • Phosphorus levels

  • Parathormone levels

  • Vitamin D metabolite (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) levels

  • Urine calcium, magnesium, phosphorus, and creatinine levels

  • Serum alkaline phosphatase levels

Total and ionized serum calcium levels

Measuring ionized calcium level is essential to differentiate true hypocalcemia from a mere decrease in total calcium concentration. A decrease in total calcium can be associated with low serum albumin concentration and abnormal pH.

Serum magnesium levels

Serum magnesium levels may be low in patients with hypocalcemia, which may not respond to calcium therapy if hypomagnesemia is not corrected. Severe hypomagnesemia (0.46 mmol/L) causes hypocalcemia by impairing the secretion and action of parathormone (PTH).

Serum electrolyte and glucose levels

Seizures and irritability in newborns and children can be associated with hypoglycemia and sodium abnormalities. Low bicarbonate levels and acidosis may be associated with Fanconi syndrome and renal tubular acidosis.

Phosphorus levels

Estimating the phosphate level is essential to establish the etiology of hypocalcemia. Phosphate levels are increased in cases of exogenous and endogenous phosphate loading and renal failure and are usually high in patients with hypoparathyroidism. Phosphate levels are low in cases of vitamin D abnormalities and rickets.

Parathormone levels

Hormone studies are indicated if hypocalcemia persists in the presence of normal magnesium and normal or elevated phosphate levels.

Low PTH levels suggest hypoparathyroidism; serum calcium rises in response to PTH challenge. Oppositely, PTH levels are elevated in patients with vitamin D abnormalities and pseudohypoparathyroidism, and calcium levels do not rise in response to PTH challenge.

The N -terminal fragment of PTH is the only biologically active fragment of PTH. It is difficult to measure because of its short half-life of 2-5 minutes. Circulating PTH levels are determined by assaying for intact PTH peptide.

Vitamin D metabolite (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) levels

These may be assessed, along with hormone concentrations, to eliminate uncommon causes of hypocalcemia (e.g., malabsorption, disorders of vitamin D metabolism).

Urine calcium, magnesium, phosphorus, and creatinine levels

These values should be assessed in patients with suspected renal tubular defects and renal failure. Urine should also be evaluated for pH, glucose, and protein.

In patients with renal defects, calcium excretion is high in presence of hypocalcemia. A urine calcium-to-creatinine ratio of more than 0.3 on a spot sample in presence of hypocalcemia suggests inappropriate excretion.

Serum alkaline phosphatase levels

Values are generally elevated in patients with rickets.

A practical approach to investigation of the etiology of hypocalcemia is a classification system based on the level of circulating PTH level in presence of hypocalcemia. A low/undetectable serum PTH level is seen in cases of hypoparathyroidism or hypomagnesemia. A normal PTH level is inappropriate and is seen in cases of abnormally functioning calcium sensing receptor. An elevated PTH level is a normal physiologic response. However, persistent hypocalcemia despite elevated PTH level indicates a vitamin D disorder or end-organ failure as seen in pseudohypoparathyroidism.[14]

 

Imaging Studies

Chest radiography - Evaluate for thymic shadow, which may be absent in patients with DiGeorge syndrome

Ankle and wrist radiography - Evaluate for evidence of rickets; changes appear at an early stage in the radius and ulna (the distal ends are widened, concave, and frayed)

Other Tests

Additional tests

Additional tests in the diagnosis of hypocalcemia include the following:

  • Malabsorption workup

  • Total lymphocyte and T-cell subset analyses - Findings are decreased in patients with DiGeorge syndrome

  • Electrocardiography - A prolonged QTc (>0.4 s), a prolonged ST segment, and T-wave abnormalities may be observed; measurements of specific intervals are of little value in predicting hypocalcemia (see the image below)

    Electrocardiogram (ECG) findings in severe hypocal Electrocardiogram (ECG) findings in severe hypocalcemia.
  • Karyotyping - To assess for 22q11 and 10p13 deletion

  • Maternal and family screening - This is helpful in familial forms of hypocalcemia, such as those caused by activating mutations of the calcium-sensing receptor

 

Treatment

Approach Considerations

Treatment of asymptomatic patients with hypocalcemia remains controversial, especially with regard to neonates. Some authorities suggest that treating such patients is unnecessary. Most newborns with hypocalcemia remain asymptomatic and can be treated in a regular newborn nursery. If persistent, the newborns can be treated with special formula PM 60/40 that provides 2:1 calcium-to-phosphate ratio. Oral calcium supplements can be added to increase the calcium-to-phosphorus ratio to 4:1 to correct the hypocalcemia until PTH function normalizes.

Most clinicians agree, however, that hypocalcemia should be promptly treated in any symptomatic neonate or older child because of the condition’s serious implications for neuronal and cardiac function. Any child with symptomatic hypocalcemia should be admitted to the hospital unless the diagnosis is hyperventilation.

Oral calcium therapy is used in asymptomatic patients and as follow-up to intravenous (IV) calcium therapy. IV treatment is usually indicated in patients having seizures, those who are critically ill, and those who are planning to have surgery.

However, IV infusion with calcium-containing solutions can cause severe tissue necrosis; this can result in contractures and may require skin grafting. Integrity of the IV site should be ascertained before administering calcium through a peripheral vein.

Necrosis of the liver can occur after calcium infusion through an umbilical vein catheter placed in a branch of the portal vein. The position of all umbilical vein catheters must be confirmed on a radiograph before infusing calcium-containing solutions.

Rapid infusion of calcium-containing solutions through arterial lines can cause arterial spasm and, if administered via an umbilical artery catheter, intestinal necrosis.

Seizures

General medical care in patients with hypocalcemia involves stabilization with management of the patient's airway and breathing if seizures occur. Anticonvulsants are commonly administered before hypocalcemia is confirmed in a new patient. However, seizures usually do not respond to the usual antiepileptic medications until calcium is intravenously administered.

Additional considerations

Magnesium administration is necessary to correct any hypomagnesemia because hypocalcemia does not respond until the low magnesium level is corrected.

Administration of phosphate-lowering agents may be necessary if hypocalcemia is associated with hyperphosphatemia.

In certain conditions, such as pancreatitis and rhabdomyolysis, full correction of hypocalcemia should be avoided. After the primary condition is resolved, these patients may develop hypercalcemia due to the release of complexed calcium.

In patients with concurrent acidemia, hypocalcemia should be corrected first. Acidemia increases the ionized calcium levels by displacing calcium from albumin. If acidemia is corrected first, ionized calcium levels decrease.

Vitamin D analogs may be appropriate in increasing intestinal absorption of calcium.

Replacement therapy with PTH has recently become available. The recombinant human PTH (1-84) allows for better control of serum calcium without the need for high doses of oral calcium and Vit D, and with possible prevention of long term consequences like renal and brain calcifications. [15]

Diet

A diet high in calcium and low in phosphate is required in most instances. Infants drinking regular cow's milk or evaporated milk must be given humanized infant formula instead. Patients with renal failure should be given a low-solute, low-phosphate formula, such as Similac PM 60/40.

Consultations

Consult with the follow specialists as needed:

  • Pediatric endocrinologist

  • Geneticist

 

Medication

Medication Summary

Calcium therapy is the mainstay of treatment for hypocalcemia. Therapy with IV calcium is the most effective and rapid means of elevating serum calcium concentration. After hypocalcemia is controlled, follow-up treatment with oral therapy can be given. However, in patients with asymptomatic hypocalcemia, therapy with oral calcium alone may be sufficient.

Vitamin D, in one of its various forms, is also indicated, depending on the metabolic abnormality present. However, the use of vitamin D formulations in newborns to prevent hypocalcemia has not been effective. The most important aspect of management is resolution of the primary cause (e.g., hyperphosphatemia, hypomagnesemia).

The American Academy of Pediatrics (AAP) published revisions to guidelines for adequate vitamin D intake in infants, children, and adolescents.[16] The revised guidelines now recommend a minimum daily intake of 400 IU of vitamin D beginning in the first few days following birth and continuing through adolescence. Symptomatic hypocalcemia may occur during periods of rapid growth with increased metabolic demands, long before any physical findings or radiologic evidence of vitamin D deficiency occurs.

Although not used routinely due to the suggested risk of osteosarcoma, the administration of recombinant PTH in an infant with hypocalcemia refractory to calcitriol and calcium supplementation was reported to be effective.[17]

Calcium compounds

Class Summary

Calcium is the most abundant mineral in the human body. It is essential for blood coagulation and the development and/or function of bone, teeth, nerves, and muscles. Calcium also functions as an enzymatic cofactor and affects endocrine secretory function. Supplements are used to increase serum calcium concentrations in patients with hypocalcemia. Oral preparations are prescribed to reduce phosphate absorption from the intestine in patients with hyperphosphatemia.

Calcium Gluconate and Calcium Chloride infusions

Calcium gluconate 10% (100 mg/mL) IV solution contains 9.8 mg/mL (0.45 mEq/mL) elemental calcium; calcium chloride 10% (100 mg/mL) contains 27 mg/mL (1.4 mEq/mL) elemental calcium.

Calcium chloride is more irritating to the veins and may affect pH; therefore, it is typically avoided in pediatric patients.

Calcium gluconate can also be given orally. However, it is hypertonic and may potentially increase risk of necrotizing enterocolitis in preterm infants at risk for this condition.

Calcium glubionate (Calcionate)

This is an oral calcium supplement. It is available as a liquid product containing glubionate salt (1800 mg/5 mL) and elemental calcium (115 mg /5 mL).

Calcium carbonate (Oyster Cal, Caltrate, Tums, Oysco 500)

Calcium carbonate is an oral supplement. In many ways, it is the calcium supplement of choice, because it provides 40% elemental calcium. (Therefore, 1 g of calcium carbonate provides 400 mg of elemental calcium.) It is well absorbed orally and is unlikely to cause diarrhea. Calcium carbonate is available in tablet and liquid form.

Vitamin D metabolites

Class Summary

The active forms of vitamin D regulate calcium absorption and its uses in the body. They increase calcium levels by promoting absorption of calcium in the intestines and retention of it in the kidneys.

Calcitriol (Calcijex, Rocaltrol, Vectical)

This is an active metabolic form of vitamin D (i.e., 1,25-dihydroxycholecalciferol). It is especially useful in liver or renal impairment because these cause an inability to hydroxylate vitamin D to its active forms. Generally, the product is rapid-acting, but it may act slowly in neonates (36-48 h). Preterm infants may be resistant to calcitriol's actions. Calcitriol is also used to treat acute hypocalcemia.