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Calcium, Total
C1 Esterase Inhibitor
C Reactive Protein
C Reactive Protein High Sensitivity Plasma calcium exists in the blood in three forms; 50% is ionized, 40-45% is protein bound,
CA 125 and 5-10% is complexed to anions such as bicarbonate, citrate, sulfate, phosphate, and
CA 153 lactate. Plasma ionized calcium is the biologically active moiety. Total calcium levels are
CA 19.9 maintained between 8.8 and 10.2 mg/dL. Parathyroid hormone and vitamin D regulate normal
CA 27.29 plasma calcium levels by their actions on kidney, intestine, and bone ion transport.
Caffeine
Calcitonin
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Carbon Dioxide
Carbon Monoxide
Carcinoembryonic Antigen
Carcinoid Syndrome The main causes of hypercalcemia are primary hyperparathyroidism, malignant disease, and
Cardiac Marker Panel chronic renal failure. The differential diagnosis of hypercalcemia depends on the clinical setting.
Cardiovascular Risk Panel Overall, primary hyperparathyroidism and malignancy account for 80 - 90% of hypercalcemia
Carotene cases. However, primary hyperparathyroidism is the cause of ~60% of ambulatory cases and
CCP Antibody of ~25% of inpatient cases, whereas malignancy causes ~35% of ambulatory cases and 65%
CD4 Enumeration of inpatient cases.
Celiac Disease Panel
Centromere Antibody Malignancies can raise serum calcium levels by either direct bone destruction or secretion of
Cephalothin Antibody calcemic factors. Patients with squamous cell carcinoma of the lung, metastatic breast cancer,
Cerebrospinal Fluid multiple myeloma, and renal cell carcinoma are most prone to hypercalcemia. These tumors
Ceruloplasmin may produce PTH related protein (PTH-rp) which binds to PTH receptors, but is not detected by
Chemistry Panels standard intact PTH immunoassays. Specific assays for PTH-rp are available.
Chlamydia Detection
Chloride The prevalence of hyperparathyroidism in the general population is 1 to 2 cases per 1000
Cholesterol people, but is more frequent in the elderly and in women. The most common pathological
Cholinesterase lesion is a single parathyroid adenoma (85% of cases) or chief cell hyperplasia (10%).
Clindamycin Resistance Parathyroid carcinoma occurs in 1 to 3% of cases. Hyperparathyroidism also occurs in multiple
Clostridium Difficile endocrine neoplasia type 1 and 2A. Patients identified by laboratory screening are commonly
Coagulation Factor Assays asymptomatic. Presentation with kidney stones is unusual today, but 5% of patients with
Coagulation Factor Inhibitor kidney stone disease have primary hyperparathyroidism. Finding an elevated PTH level in a
Coagulation Screen patient with hypercalcemia makes the diagnosis.
Cold Agglutinin Titer
Colloid Osmotic Pressure The signs and symptoms of hypercalcemia are summarized in the following table.
Complement Profile
Complete Blood Count
Mental Neurological & Skeletal GI & Urological
Congenital Adrenal Hyperplasia
Cord Blood Gases
Cord Blood Studies Fatigue Reduced muscle tone Nausea
Corticotropin Releasing Hormone
Stimulation Test Obtundation Muscle weakness Vomiting
Cortisol
Cortisol in Critical Illness
Cortisol Salivary Apathy Myalgia Polyuria
Cortisol Urine Free
Cortrosyn Stimulation Test Lethargy Pain Polydipsia
Cotinine
Creatine Kinase
Confusion Deep tendon reflexes Dehydration
Creatine Kinase MB
Creatinine
Creatinine Clearance Disorientation Anorexia
Creatinine Kinase Isoenzymes
Crossmatch Coma Constipation
CRP
Cryoglobulin
Cryptococcal Antigen
Cryptosporidium Antigen Evaluation of hypercalcemia usually begins with measurement of total calcium. If total calcium
Crystal Identification is markedly elevated, an ionized calcium level is usually not needed. Slightly to moderately
Cushing Syndrome elevated total calcium should be confirmed by measurement of ionized calcium. The patient's
Cyclosporine history may indicate the cause, such as; immobilization for more than a week, drug therapy,
Cystic Fibrosis hyperthyroidism, adrenal insufficiency, or familial hypocalciuric hypercalcemia. If time permits,
Cytogenetic Studies
2. total calcium levels should be repeated two more times to rule out a transient cause of
Cytomegalovirus Antibody hypercalcemia before undertaking a complete work-up. If hypercalcemia is still evident, serum
Cytomegalovirus Culture albumin and total protein should be determined. Calcium levels should be corrected for
Cytomegalovirus PCR Qualitative elevated albumin levels (see below). If total protein is high, but albumin is normal or low, a
Cytomegalovirus PCR Quantitative monoclonal gammopathy should be ruled out by serum protein electrophoresis. Serum
chloride, phosphorus and intact PTH are also useful in diagnosing the most frequent causes of
hypercalcemia; malignancy and hyperparathyroidism. Serum chloride is mildly elevated in
primary hyperparathyroidism.
Renal Epithelials -
Normal Test Hyperparathyroidism Malignancy
ATCC Primary Cell
Solutionsâ„¢ LGC Total calcium (mg/dL) <12.4 >12.4
Standards partnered with
ATCC Chloride (meq/L) >103 <103
www.lgcstandards-atcc.org
Phosphorus normal to low normal
Cytokine Center
Chloride : phosphorus ratio 29 or greater <29
Recombinant cytokines,
ELISPOT Kits ELISA
Intact PTH elevated suppressed
Kits, related antibodies
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PTH-rp normal elevated
Calcitriol elevated low
Calcium carbonate
Ground calcium
carbonate (GCC) fillers & Hypocalcemia most commonly results from PTH deficiency or failure to produce 1,25 dihydroxy
extenders...CaCO3 vitamin D. The most common causes of hypoparathyroidism are parathyroid or thyroid surgery
www.imerys-perfmins.com/ and parathyroid infiltration by cancer, sarcoid, amyloid or hemochromatosis. Acute illnesses
such as pancreatitis, hepatic failure, sepsis, and various medications can also cause
hypocalcemia. The normal response to a fall in the plasma ionized calcium level is increased
PTH secretion and 1,25 dihyroxy vitamin D synthesis, leading to increased calcium absorption
New Diabetes 2 from the intestine and increased resorption from bone and kidneys.
Treatment
First European stem cell Some drugs are associated with hypocalcemia. Gentamicin and cisplatin cause renal
clinic treats your diabetes magnesium loss, which leads to hypocalcemia. Heparin therapy releases fatty acids that bind
calcium ions and cause transient hypocalcemia. Anticonvulsants such as dilantin and
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phenobarbital induce the microsomal oxidase pathway which accelerates inactivation of vitamin
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D. Loop diuretics such as furosemide enhance renal calcium excretion. Phosphate salts bind up
calcium ions causing hypocalcemia.
Protein Evolution The laboratory evaluation of a low total plasma calcium level should include measurement of
Superior to Directed ionized calcium, magnesium, and phosphorus levels. Low ionized calcium rules out artefactual
causes of hypocalcemia, such as hypoalbuminemia. Abnormally high or low magnesium levels
Evolution Next should be excluded because they can inhibit PTH secretion. A low serum phosphorus level is
Generation Technologies consistent with vitamin D deficiency, while a high level suggests chronic renal failure or
www.bioatla.com pseudohypoparathyroidism. Measurement of intact PTH levels helps to differentiate between
conditions caused by PTH and vitamin D defects. The demonstration of an inappropriately low
intact PTH level in the presence of hypocalcemia is consistent with the diagnosis of
hypoparathyroidism. Serum 25-hydroxyvitamin D levels can be measured to confirm vitamin D
deficiency.
Total calcium levels are effected by changes in plasma protein concentrations. Most of the
protein bound fraction of calcium is bound to albumin; each 1 g/dL of albumin binds 0.8 mg/dL
of calcium. Three formulas have been used to correct calcium for decreased serum albumin
levels:
%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 to
directly 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 to
interfere with calcium measurements on some chemistry analyzers, resulting in falsely low
values. Patients with normal renal function may have spuriously low calcium measurements up
to 24 hours after administration of these contrast agents, but patients with renal insufficiency
may be affected for up to 4.5 days. However, the Vitros chemistry analyzers used throughout
the 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 13.0
mg/dL are considered critical values.