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Calcium, Total

Plasma calcium exists in the blood in three forms; 50% is ionized, 40-45% is protein bound,and 5-10% is complexed to anions such as bicarbonate, citrate, sulfate, phosphate, andlactate. Plasma ionized calcium is the biologically active moiety. Total calcium levels aremaintained between 8.8 and 10.2 mg/dL. Parathyroid hormone and vitamin D regulate normalplasma calcium levels by their actions on kidney, intestine, and bone ion transport.

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The main causes of hypercalcemia are primary hyperparathyroidism, malignant disease, andchronic renal failure. The differential diagnosis of hypercalcemia depends on the clinical setting.Overall, primary hyperparathyroidism and malignancy account for 80 - 90% of hypercalcemiacases. However, primary hyperparathyroidism is the cause of ~60% of ambulatory cases andof ~25% of inpatient cases, whereas malignancy causes ~35% of ambulatory cases and 65%of inpatient cases.

Malignancies can raise serum calcium levels by either direct bone destruction or secretion ofcalcemic factors. Patients with squamous cell carcinoma of the lung, metastatic breast cancer,multiple myeloma, and renal cell carcinoma are most prone to hypercalcemia. These tumorsmay produce PTH related protein (PTH-rp) which binds to PTH receptors, but is not detected bystandard intact PTH immunoassays. Specific assays for PTH-rp are available.

The prevalence of hyperparathyroidism in the general population is 1 to 2 cases per 1000people, but is more frequent in the elderly and in women. The most common pathologicallesion is a single parathyroid adenoma (85% of cases) or chief cell hyperplasia (10%).Parathyroid carcinoma occurs in 1 to 3% of cases. Hyperparathyroidism also occurs in multipleendocrine neoplasia type 1 and 2A. Patients identified by laboratory screening are commonlyasymptomatic. Presentation with kidney stones is unusual today, but 5% of patients withkidney stone disease have primary hyperparathyroidism. Finding an elevated PTH level in apatient with hypercalcemia makes the diagnosis.

The signs and symptoms of hypercalcemia are summarized in the following table.

Mental Neurological & Skeletal GI & Urological

Fatigue Reduced muscle tone Nausea

Obtundation Muscle weakness Vomiting

Apathy Myalgia Polyuria

Lethargy Pain Polydipsia

Confusion Deep tendon reflexes Dehydration

Disorientation Anorexia

Coma Constipation

Evaluation of hypercalcemia usually begins with measurement of total calcium. If total calciumis markedly elevated, an ionized calcium level is usually not needed. Slightly to moderatelyelevated total calcium should be confirmed by measurement of ionized calcium. The patient'shistory may indicate the cause, such as; immobilization for more than a week, drug therapy,hyperthyroidism, adrenal insufficiency, or familial hypocalciuric hypercalcemia. If time permits,

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total calcium levels should be repeated two more times to rule out a transient cause ofhypercalcemia before undertaking a complete work-up. If hypercalcemia is still evident, serumalbumin and total protein should be determined. Calcium levels should be corrected forelevated albumin levels (see below). If total protein is high, but albumin is normal or low, amonoclonal gammopathy should be ruled out by serum protein electrophoresis. Serumchloride, phosphorus and intact PTH are also useful in diagnosing the most frequent causes ofhypercalcemia; malignancy and hyperparathyroidism. Serum chloride is mildly elevated inprimary hyperparathyroidism.

Test Hyperparathyroidism Malignancy

Total calcium (mg/dL) <12.4 >12.4

Chloride (meq/L) >103 <103

Phosphorus normal to low normal

Chloride : phosphorus ratio 29 or greater <29

Intact PTH elevated suppressed

PTH-rp normal elevated

Calcitriol elevated low

Hypocalcemia most commonly results from PTH deficiency or failure to produce 1,25 dihydroxyvitamin D. The most common causes of hypoparathyroidism are parathyroid or thyroid surgeryand parathyroid infiltration by cancer, sarcoid, amyloid or hemochromatosis. Acute illnessessuch as pancreatitis, hepatic failure, sepsis, and various medications can also causehypocalcemia. The normal response to a fall in the plasma ionized calcium level is increasedPTH secretion and 1,25 dihyroxy vitamin D synthesis, leading to increased calcium absorptionfrom the intestine and increased resorption from bone and kidneys.

Some drugs are associated with hypocalcemia. Gentamicin and cisplatin cause renalmagnesium loss, which leads to hypocalcemia. Heparin therapy releases fatty acids that bindcalcium ions and cause transient hypocalcemia. Anticonvulsants such as dilantin andphenobarbital induce the microsomal oxidase pathway which accelerates inactivation of vitaminD. Loop diuretics such as furosemide enhance renal calcium excretion. Phosphate salts bind upcalcium ions causing hypocalcemia.

The laboratory evaluation of a low total plasma calcium level should include measurement ofionized calcium, magnesium, and phosphorus levels. Low ionized calcium rules out artefactualcauses of hypocalcemia, such as hypoalbuminemia. Abnormally high or low magnesium levelsshould be excluded because they can inhibit PTH secretion. A low serum phosphorus level isconsistent with vitamin D deficiency, while a high level suggests chronic renal failure orpseudohypoparathyroidism. Measurement of intact PTH levels helps to differentiate betweenconditions caused by PTH and vitamin D defects. The demonstration of an inappropriately lowintact PTH level in the presence of hypocalcemia is consistent with the diagnosis ofhypoparathyroidism. Serum 25-hydroxyvitamin D levels can be measured to confirm vitamin Ddeficiency.

Total calcium levels are effected by changes in plasma protein concentrations. Most of theprotein bound fraction of calcium is bound to albumin; each 1 g/dL of albumin binds 0.8 mg/dLof calcium. Three formulas have been used to correct calcium for decreased serum albuminlevels:

%Calcium bound = 8 (albumin) + 2(globulin) + 3

Corrected calcium = measured Calcium /0.6 + [total protein/8.5]

Corrected calcium = Calcium - albumin + 4

Each formula will give a slightly different value for corrected calcium. A better approach is todirectly measure ionized calcium levels.

Two of the four approved gadolinium based magnetic resonance (MR) imaging contrast agents,gadodiamide (Omniscan) and gadoversetamide (OptiMARK), have recently been shown tointerfere with calcium measurements on some chemistry analyzers, resulting in falsely lowvalues. Patients with normal renal function may have spuriously low calcium measurements upto 24 hours after administration of these contrast agents, but patients with renal insufficiencymay be affected for up to 4.5 days. However, the Vitros chemistry analyzers used throughoutthe Saint Luke's Health System are not adversely affected (Am J Clin Pathol 2004;121:282-92).

Reference range is 8.8 - 10.2 mg/dL. Calcium levels less than 6.0 mg/dL or greater than 13.0mg/dL are considered critical values.

Specimen requirement is one SST tube or one green top (heparin) tube of blood. Prolongedvenous stasis should be avoided because it can produce artefactual hypercalcemia.

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