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Serum Calcium Blood Test

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Serum Calcium Blood Test


 


Introduction:


All cells need calcium in order to work. Calcium helps build strong bones and teeth. It is important for heart function, and helps with muscle contraction, nerve signaling, and blood clotting.
This article discusses the test to measure the total amount of calcium in your blood. Calcium can also be measured in the urine.
This test measures how much calcium is in blood. It is used to assess and manage disorders affecting calcium metabolism (the way the body obtains, transports, uses and disposes of calcium).
Adults have a calcium content of over 1 kg, or approximately 2% of body weight. All but 1% is contained in the bones, where it exists as calcium hydroxyapatite. The extra-osseous intracellular space and extracellular space (ECS) contain a portion of the remaining 1%. A dynamic equilibrium is maintained between the ECS and the rapidly exchangeable fraction of bone calcium.
About 45% of serum calcium is bound to proteins, 5% exists as inorganic complexes, and 50% occurs as free or ionized calcium.
Heart and skeletal muscle contractility are affected by calcium ions; in addition, calcium ions are vital to nervous system function and are associated with blood clotting and bone mineralization.
Indications/Applications
With regard to total serum calcium, serum albumin changes can generally be corrected with the addition of 0.8 mg/dL for every gram that the serum albumin level falls below 4.0 g/dL. In patients with suspected hypercalcemia or hypocalcemia, this principle can be expressed as the following equation:
Corrected total serum calcium level = observed total serum calcium - 0.8 (4.0 - measured serum albumin level in g/dL)
The corrected total serum calcium concentration is normally 8.5-10.2 mg/dL, but there is no sure means of predicting the serum calcium level, for either hypocalcemia or hypercalcemia, at which symptoms will occur. The rapidity of change, as well as the absolute serum calcium concentration, impacts symptom development. It has been found, however, that hypocalcemic symptoms rarely occur if the corrected serum calcium concentration is above 8 mg/dL, while hypercalcemic symptoms rarely develop in patients with a corrected serum calcium level of under 11 mg/dL.
Serum calcium is decreased in the following conditions:

Serum Calcium Blood Test

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Serum Calcium Blood Test

 

Introduction:

All cells need calcium in order to work. Calcium helps build strong bones and teeth. It is important for heart function, and helps with muscle contraction, nerve signaling, and blood clotting.
This article discusses the test to measure the total amount of calcium in your blood. Calcium can also be measured in the urine.
This test measures how much calcium is in blood. It is used to assess and manage disorders affecting calcium metabolism (the way the body obtains, transports, uses and disposes of calcium).
Adults have a calcium content of over 1 kg, or approximately 2% of body weight. All but 1% is contained in the bones, where it exists as calcium hydroxyapatite. The extra-osseous intracellular space and extracellular space (ECS) contain a portion of the remaining 1%. A dynamic equilibrium is maintained between the ECS and the rapidly exchangeable fraction of bone calcium.
About 45% of serum calcium is bound to proteins, 5% exists as inorganic complexes, and 50% occurs as free or ionized calcium.
Heart and skeletal muscle contractility are affected by calcium ions; in addition, calcium ions are vital to nervous system function and are associated with blood clotting and bone mineralization.
Indications/Applications
With regard to total serum calcium, serum albumin changes can generally be corrected with the addition of 0.8 mg/dL for every gram that the serum albumin level falls below 4.0 g/dL. In patients with suspected hypercalcemia or hypocalcemia, this principle can be expressed as the following equation:
Corrected total serum calcium level = observed total serum calcium - 0.8 (4.0 - measured serum albumin level in g/dL)
The corrected total serum calcium concentration is normally 8.5-10.2 mg/dL, but there is no sure means of predicting the serum calcium level, for either hypocalcemia or hypercalcemia, at which symptoms will occur. The rapidity of change, as well as the absolute serum calcium concentration, impacts symptom development. It has been found, however, that hypocalcemic symptoms rarely occur if the corrected serum calcium concentration is above 8 mg/dL, while hypercalcemic symptoms rarely develop in patients with a corrected serum calcium level of under 11 mg/dL.
Serum calcium is decreased in the following conditions:

  • Hypoparathyroidism Vitamin D deficiency
  • Renal insufficiency
  • Pseudohypoparathyroidism
  • Magnesium deficiency
  • Hyperphosphatemia
  • Massive transfusion
  • Hypoalbuminemia

Hypocalcemia results when the parathyroid glands are either absent or impaired. Impaired vitamin-D synthesis can also cause the condition. Owing to an associated decrease in vitamin-D synthesis and the presence of hyperphosphatemia and skeletal resistance to parathyroid hormone (PTH), chronic renal failure is a frequent source of hypocalcemia. Latent or manifest tetany and osteomalacia are characteristic signs of hypocalcemia.

Serum calcium is increased in the following:

  • Hyperparathyroidism
  • Malignancies that secrete PTH–related protein (PTHrP) - Especially squamous cell carcinoma of lung and renal cell carcinoma
  • Vitamin-D excess
  • Milk-alkali syndrome
  • Multiple myeloma
  • Paget disease of bone with immobilization
  • Sarcoidosis
  • Other granulomatous disorders
  • Familial hypocalciuria
  • Vitamin A intoxication
  • Thyrotoxicosis
  • Addison disease

Some drugs that increase serum calcium are as follows:

  • Antacids (some)
  • Calcium salts
  • Chronic diuretic use (eg, thiazides)
  • Lithium

Hypercalcemia results from increased mobilization of calcium from the skeletal system or increased intestinal absorption. The condition is usually caused by primary hyperparathyroidism (pHPT) or bone metastasis of carcinoma of the breast, prostate, thyroid gland, or lung.
In 10% of patients with malignancies, coexistent hyperparathyroidism is the source of hypercalcemia; this indicates that evaluation of serum PTH levels should be performed at initial presentation in all hypercalcemic patients. Surgical removal of 1 or more parathyroid glands is a consideration in patients with pHPT and bone disease, renal stones or nephrocalcinosis, or other signs or symptoms. Severe hypercalcemia may cause cardiac arrhythmia.[1, 2]
Considerations
Because total calcium levels can reflect protein levels, evaluation of serum albumin can be used to interpret calcium concentration. An upward calcium correction of 0.8 mg/dL should be employed for every 1 mg/dL decrease in albumin.
Since gadolinium can interfere with most metals tests, 48 hours must pass between administration of gadolinium-containing contrast media and specimen collection.
Calcium is the chemical element with symbol Ca and atomic number 20. Calcium is a soft gray alkaline earth metal, and is the fifth-most-abundant element by mass in the Earth's crust. Calcium is also the fifth-most-abundant dissolved ion in seawater by both molarity and mass, after sodium, chloride, magnesium, and sulfate.
Calcium is essential for living organisms, in particular in cell physiology, where movement of the calcium ion Ca2+ into and out of the cytoplasm functions as a signal for many cellular processes. As a major material used in mineralization of bone, teeth and shells, calcium is the most abundant metal by mass in many animals.
This test measures the amount of calcium in your blood. Calcium is the most abundant mineral in the body. Your body needs calcium for normal functioning of your nerves and muscles, including the most important muscle of all, your heart. Calcium is also important for healthy bones and teeth. The amount of calcium in your blood is carefully controlled by your body's hormonal (glandular) system.
Serum calcium is a blood test to measure the amount of calcium in the blood. Serum calcium is usually measured to screen for or monitor bone diseases or calcium-regulation disorders (diseases of the parathyroid gland or kidneys).

Calcium is the most abundant mineral element in the body. About 98% of the 1200 g of calcium in the adult is in the form of hydroxyapatite in the skeleton. Hydroxyapatite is a lattice-like crystal composed of calcium, phosphorus, and hydroxide. The remaining calcium is in the extracellular fluid (50%) and in various tissues, especially skeletal muscle. Calcium is maintained within a fairly narrow range from 8.5 to 10.5 mg/dl (4.3 to 5.3 mEq/L or 2.2 to 2.7 mmol/L). Normal values and reference ranges may vary among laboratories as much as 0.5 mg/dl.
The measurement of serum calcium is fraught with possible errors. Several means of contamination might lead to false elevations of serum calcium concentration. Falsely low levels are less common, so if several measurements are obtained, the lowest is usually the most accurate. The precision of the SMAC analysis, an automated colorimetric technique, is usually equal or superior to that of manual analysis. Nevertheless, falsely high or low values may be obtained in patients with liver or renal failure or in patients with lipemic or hemolyzed specimens. Venous occlusion of the arm during venipuncture may increase the total concentration of serum calcium by up to 0.3 mmol/L. This results from an increase in plasma protein concentration caused by hemodynamic changes. Another source of error is posture. If the patient stands up from a supine position, there may be an increase of 0.05 to 0.20 mmol/L in serum calcium. Still another possible source of error is hemolysis. Some methods of measuring calcium are affected by high levels of hemoglobin, and red cells may take up calcium after prolonged contact. If an error is suspected and the measurement is to be redone, the blood should be drawn following an overnight fast because the daily intake of calcium may contribute to the serum calcium concentration as much as 0.15 mmol/L.
Still other variations in the level of serum calcium need to be mentioned. Exercise just before venipuncture tends to increase serum calcium, so the patient should be rested for at least 15 minutes prior to sampling. Men tend to have a higher serum calcium by 0.02 to 0.04 mmol/L during summer versus winter. Postmenopausal women, however, have higher levels of calcium in winter as compared to summer. Men 15 to 45 years of age tend to have serum calcium levels 0.02 to 0.05 mmol/L higher than similarly aged women. While these values generally fall for both sexes during this 30-year period, this trend reverses for women after the age of 45 until they reach 75 when serum calcium levels again tend to fall.
Although all calcium in the body is technically ionized, the term usually only applies to the free ionic fraction that is physiologically active in blood.The portion of total calcium that forms ion couplets with anions such as bicarbonate and/or citrate is known as complexed calcium. Together, the ionized and complexed calcium constitute the diffusible fraction of calcium. This portion may also be called the ultrafilterable calcium, since it passes through biologic membranes. This is unlike protein-bound calcium, which is not diffusible. About 90% of the protein-bound calcium is linked to albumin with the remaining 10% bound to a variety of globulins. There are 12 binding sites on each albumin molecule and only about 10 to 15% are utilized under normal conditions. Therefore, when an excess of calcium in the blood occurs, each of the three calcium fractions (i.e., ionized, complexed, protein-bound) increases in the same ratio, resulting in a constant proportion of ultrafilterable calcium.

 

Values of Serum Calcium Fractions

Fraction

Milligrams per deciliter (mg/dl)

Percent (%)

Ionized (free ions)

4.40

44

Total diffusible

5.60

56

 Protein-bound

4.60

46

 Complexed

1.00

10

  Total

10.00

100

The ability of protein to bind calcium acts as a buffer that alters the effect of an acute load of calcium on the concentration of ionized calcium by about 50%. Still another consequence of the large number of unfilled binding sites for calcium is that competition by magnesium does not have a significant effect on ionized calcium concentration. The most vital parameter affecting protein binding of calcium is the pH. An alkalemic pH leads to an increase in binding and hence a decrease in the fraction of ionized calcium. The reason for this is twofold: (1) competition between H+ and Ca++ for binding sites; and (2) alteration in configuration of the albumin molecule.
The plasma level of complexed calcium is usually estimated by the difference between ionized and ultrafilterable calcium. As alluded to above, complexed calcium consists of ionic couplets with anions such as HCO3 and HPO4 and with organic ions such as lactate and citrate. The most abundant form seems to be CaHCO+3. As a consequence there is still another mechanism whereby pH alters the ionized calcium concentration. A rise in pH leads to an increase of HCO3, which then forms more complexed CaHCO+3, and therefore a fall in ionized calcium.
A departure of 1.0 g/dl from the normal albumin concentration will account for an alteration of the protein-bound calcium fraction and, hence, the total calcium level of about 0.8 mg/dl.
The calcium homeostatic system depends on several important factors: parathyroid hormone (PTH), vitamin D, phosphate, and magnesium. PTH serves as a receptor arm to correct alterations in the steady-state level of serum calcium. A small fall in ionized calcium will quickly lead to a rise in PTH secretion. The result of this increase in PTH is a rapid release of calcium from bone. This release requires the active form of vitamin D, 1,25-dihydroxycholecalciferol (1,25-DHCC), but is not dependent on bone turnover or an increase in the number of osteoclasts. This effect of PTH most probably is mediated via the transport of calcium from the bone extracellular fluid (ECF). Only if the requirement for calcium is sufficient arid prolonged does PTH affect osteoclast proliferation and increase bone turnover.
PTH also acts to maintain the steady-state level of serum calcium by its action on the kidney. It increases the tubular reabsorption of calcium and magnesium and decreases the tubular reabsorption of phosphate, sodium, bicarbonate, potassium, and amino acids. PTH activates the adenylate cyclase system by binding with receptor sites in the renal cortex. It thus leads to an increase in cyclic adenoside monophosphate.
Vitamin D increases the concentration of serum calcium by several mechanisms. As mentioned above, it potentiates the effect of PTH on the bone. Vitamin D also increases the intestinal absorption of calcium, as well as bone resorption and the tubular reabsorption of calcium. The effects on intestinal reabsorption of calcium and bone resorption seem to be due primarily to the active metabolite 1,25-DHCC, but other metabolites may contribute to some of the other effects on serum calcium.
The serum phosphorus level also plays a role in the maintenance of a steady-state concentration of serum calcium. While there is no exact solubility product for calcium and phosphorus, a rise in serum phosphate usually leads to a fall in serum calcium. Some of this decrement may be caused by enhanced formation of CaHPO4 complexes in the serum. A fall in the level of serum phosphate will conversely lead to an increase in the serum ionized and bone ECF calcium. Some of the mechanisms that contribute to the drop of calcium include hypercalciuria and hypoparathyroidism induced by phosphate depletion.
Alterations of serum magnesium within the normal range (1.5 to 2.5 mEq/L) do not appear to affect the concentration of serum calcium. But hypermagnesemia tends to suppress PTH secretion and may lead to mild hypocalcemia. Conversely, a moderate decrement in serum magnesium may stimulate PTH secretion. With a fall in serum magnesium below a concentration of 1.0 mEq/L, PTH secretion is suppressed and resistance to the action of PTH on target organs develops.
The importance of normal serum calcium concentration can best be appreciated by a review of the clinical manifestations of hypocalcemia and hypercalcemia. The former most often leads to tetany, convulsive seizures, and cardiovascular, psychiatric, and a variety of ectodermal effects. Hypercalcemia is usually associated with soft tissue calcification, tubulointerstitial nephropathy, anorexia, nausea, electrocardiographic disturbances, and a spectrum of neurologic changes from headache to coma.

Causes of Hypocalcemia

PTH deficiency

 Genetic

 Acquired (e.g., surgical, irradiation, neoplastic invasion)

 Transient (e.g., hypomagnesemia)

Vitamin D deficiency

 Cholecalciferol deficiency (e.g., sunlight deprivation, dietary insufficiency, gut malabsorption)

 25-Hydroxycholecaldferol deficiency (e.g., impaired hepatic hydroxylation, hepatobiliary disease, nephrotic syndrome, anticonvulsant therapy)

 1,25-Dihydroxycholecalciferol deficiency (e.g., renal failure, hyperphosphatemia)

Transient hypocalcemia

 Intravascular redistribution (e.g., massive transfusion with acid blood)

 Sudden increase in net deposition in bone

  Decreased bone resorption (e.g., mithramycin, calcitonin)

  Increased mineralization (e.g., treatment of rickets)

  Increased bone formation (e.g., osteoblastic metastasis)

 Failure to increase bone resorption in response to calcium depletion (e.g., medullary carcinoma of thyroid)

  Increased soft tissue deposition (e.g., rhabdomyolysis, pancreatitis, hyperphosphatemia)

 Increased neural excitability is a fairly common manifestation of hypocalcemia. The patient usually describes tingling of the tips of the fingers and around the mouth. If unabated, these symptoms progress in severity and extend to the limbs and face. The patient may also describe numbness over these areas that may be accompanied by pain and carpal spasm. Most of these patients will have a positive Chvostek's and/or Trousseau's sign.
Hypocalcemia may increase central, as well as peripheral, neural excitability, and two types of convulsive seizures may result. First, the patient may suffer from a seizure disorder similar to a patient without hypocalcemia, such as petit mal, jacksonian, or grand mal. Second, systemic tetany may progress to prolonged tonic spasms, which are also referred to as cerebral tetany.
The most common cardiovascular manifestations of hypocalcemia involve disturbances of the electrical rhythm. A fall in serum calcium will delay ventricular repolarization and thus increase the Q-T interval and ST segment. This may progress and produce 2:1 heart block. Chronic hypocalcemia may also lead to less than adequate cardiac performance associated with a reduction in blood pressure.

Causes of Hypercalcemia

Hyperparathyroidism

Metastatic disease of bone

Humoral hypercalcemia

 Ectopic production of PTH-like substance

 Prostagladin induced

 WDHA

Vitamin A/D excess

Milk-alkali syndrome

Sarcoidosis

Immobilization (in setting of posttrauma or osteoporosis)

Hyperthyroidism

Thiazide diuretics

Childhood hypercalcemia

 Idiopathic infantile hypercalcemia

 Hypothyroidism

 Blue-diaper syndrome

 Hypophosphatasia

Proliferative disorders

 Lymphoma

 Sarcoma

 Leukemia

Miscellaneous

 Acromegaly

 Familial hypocalciuric hypercalcemia

 Pheochromocytoma

 Berylliosis

 Tuberculosis

 Rhabdomyolysis with acute renal failure

A variety of psychiatric manifestations may accompany hypocalcemia. These include psychoneurosis, psychosis, and an organic brain syndrome. Following parathyroid surgery and the development of hypocalcemia and hypomagnesemia, an acute psychosis may develop characterized by hallucinations and paranoia. These are reversible on correction of the electrolyte disturbances.
Several defects of the ectoderm are often seen in patients with chronic hypocalcemia. Cataracts are the most common feature. This results from alteration of the local sodium pump with eventual lens degeneration and the development of dystrophic calcifications. Defects in the development of the enamel of teeth may occur if the hypocalcemia precedes the maturation of the respective tooth. Hair and nails may also be affected by chronic hypocalcemia. Both may become dry and brittle; their growth may even be stunted.
Still more unusual effects of hypocalcemia may rarely occur. These include disturbances of blood coagulation, intestinal malabsorption, defective bone mineralization (when associated with vitamin D deficiency), secondary hyperparathyroidism in the neonate of a hypocalcemic mother, slight papilledema, and calcification of the basal ganglion.
The manifestations, and hence the clinical significance, of hypercalcemia consist of five effects: soft tissue calcification, tubulointerstitial renal disease, anorexia and nausea, Q-T prolongation of the electrocardiogram, and an acute brain syndrome.
Three sites of soft tissue calcification occur with hypercalcemia even in the absence of serum phosphate elevations. These are corneal and/or conjunctival calcification, chondrocalcinosis, and renal calcification. While corneal calcifications are usually asymptomatic, conjunctival calcifications often are quite irritating. Band keratopathy is a distinct entity caused by dystrophic calcification often in the setting of hypercalcemia, but less common than either of the other forms of calcification. Calcium pyrophosphate arthritis (i.e., chondrocalcinosis) has an increased incidence in the hypercalcemia of hyperparathyroidism (HPTH), but not in other forms of hypercalcemia.
The clinical characteristics of hypercalcemic renal disease include a mild to moderate fall in creatinine clearance, mild to moderate elevation of blood pressure, mild proteinuria, and impaired concentrating ability associated with polyuria and nocturia. Pathologic changes usually consist of interstitial fibrosis and medullary calcifications which, if severe, appear as calcinosis by x-ray. A variety of tubular dysfunctions may rarely occur in addition to those mentioned. These include glycosuria, phosphaturia, impaired potassium reabsorption, and enhanced hydrogen ion secretion.
The most common gastrointestinal effects of hypercalcemia include anorexia, nausea, and constipation. The constipation is likely the result of dehydration and decreased appetite, while the nausea seems to be a central effect. The incidence of ulcer disease in HPTH remains controversial, whereas the frequency of acute pancreatitis seems to be increased in patients with HPTH.
Even though steady-state levels of serum calcium are important to myocardial function, cardiovascular abnormalities associated with hypercalcemia are limited to shortening of the Q-T interval, rare episodes of heart block, and a tendency to arrhythmias in the presence of digitalis treatment. Hypertension is a fairly common effect of hypercalcemia and may be caused by increased peripheral resistance and/or positive cardiac inotropism.

An acute brain syndrome may be the most common side effect of moderate to severe hypercalcemia. Symptoms such as depression, chronic recurrent headache, and memory impairment are often associated with chronic hypercalcemia of a mild to moderate degree. More pronounced elevations of serum calcium usually lead to a spectrum of symptoms ranging from mental confusion or delirium to stupor and coma. The EEC often shows diffuse slowing consistent with a metabolic encephalopathy.
In the present study, serum calcium was affected by age in both genders, with a gradual decrease with age in men and an increase in calcium at the time of menopause in women. This age-related pattern is similar to that described in other epidemiological studies.
We found a highly significant association between serum calcium and both systolic and diastolic BP in both genders, an association that persisted after adjustment for all the other variables in the linear regression model. When the importance of calcium in all aspects of physiology is considered, together with the huge amount of research done on hypertension, there are remarkably few studies on the relation between total serum calcium levels and BP. However, in the few available studies, the results are similar to those presented in this study.
Calcium exists in 3 major forms in plasma. Approximately 50% is in the free or ionized form, which is the physiologically important fraction, 40% is bound to albumin, and the remaining 10% is in soluble complexes with anions such as bicarbonate, phosphate, and lactate. Thus, total serum calcium will not only reflect calcium physiology but also be a function of the serum albumin level. Numerous algorithms have therefore been derived to correct for this effect, but unfortunately, serum albumin data are not included in our study. This could be of considerable importance because in a report by Hu et al, serum albumin also showed a consistent and strong association with systolic and diastolic BP.
In other epidemiological studies on calcium and BP, some investigators have corrected for serum albumin concentration. Thus, in the study by Kesteloot and Geboers of 9321 men in the Belgian army, serum calcium values were not corrected, whereas in the study from Sweden by Lind et al, which included >18 000 men and women, values were corrected and the association was still present and highly significant. On the other hand, in the British Regional Heart Study of 7735 healthy middle-aged men, Phillips and Shaper found that the small but significant association between serum calcium and BP diminished after they corrected for serum albumin and became nonsignificant after they included serum globulins and hematocrit in the model.
There are several reports that ionized serum calcium actually is lower in hypertensive patients than in normal controls. To reconcile this with our findings, because there is a strong correlation between total and ionized serum calcium, one would have to assume that the binding characteristics for calcium and its carrier proteins are abnormal in hypertension. This has been found in a study of 28 hypertensive subjects compared with normotensive controls,14 but until this finding is confirmed in other studies, it must be considered highly speculative.
To make the matter even more complicated, there seems to be a negative association between the intake of dietary calcium and BP,  and the serum calcium level has been reported to increase with calcium intake. To settle these questions, large studies, which consider all of these variables, are needed.
In regards to serum calcium and lipids, there was a particularly strong association with cholesterol in both genders even after correction for age, BMI, and other possible risk factors. Thus, the standardized regression coefficient β for calcium, with cholesterol as dependent variable, was second only to age and the other lipids in the model. Serum calcium was also found to be an independent, significant predictor of the HDL cholesterol level, but the standardized regression coefficient was only half that seen for total cholesterol. In contrast, the association between serum calcium and triglycerides was weaker and disappeared in women, but not in men, in the linear regression analysis.
To the best of our knowledge, the relation between serum calcium and triglycerides has not been previously reported, whereas similar results regarding cholesterol were found by Lind et al. As with hypertension, our results are confounded by the lack of correction for serum albumin, which has been reported to be positively correlated with serum cholesterol. However, the similarity of the results in our study with the study by Lind et al, in which they corrected for serum albumin, makes it unlikely that serum albumin had a major influence.
Our findings on BP and lipids are in agreement with findings in chronic hypercalcemia. Thus, hypertension and hyperlipidemia are common in patients with hyperparathyroidism, and these patients also have an increased mortality rate from cardiovascular diseases. Moreover, serum calcium levels are higher in non–insulin-dependent diabetes mellitus and are also positively associated with blood glucose in the general population. An association between serum calcium and the metabolic syndrome has therefore been suggested.

If such an association exists, one would expect serum calcium to be related to cardiovascular mortality and morbidity. Indeed, this has been demonstrated prospectively for myocardial infarction in a study in which serum calcium appeared as an independent risk factor in middle-aged men followed for 18 years. Furthermore, in a study by Leifsson and Ahrén that followed 22 000 men for a mean period of 10 years, the risk of premature death in men <50 years of age increased when serum calcium levels rose, even if the increase was within the normal range. As in hyperparathyroidism, this increase was mainly due to cardiovascular diseases.
With our data, we can thus far only perform a retrospective analysis on serum calcium in relation to cardiovascular diseases. In the questionnaire completed by the patients, questions on myocardial infarction, angina pectoris, and stroke were included. Not surprisingly, serum calcium levels were higher in those with infarction and angina, but significantly so only for men with myocardial infarction when analyzed with logistic regression. In this respect, serum albumin is probably not a confounding factor, because serum albumin is found to be inversely related to cardiovascular diseases. However, a positive association is no proof of causative relation. In the case of calcium and hypertension, one should be especially careful because there is an apparent discrepancy between results obtained with ionized and total serum calcium levels.
In men, BP increased with age whereas calcium decreased with age. Accordingly, BP must be influenced by other factors that in this respect are more important than calcium. It must also be recognized that serum calcium could merely be a marker for other factors of greater importance for hypertension and cardiovascular diseases. Thus, in the study by Resnick et al, subjects with hypertension and high plasma renin activity also had elevated serum ionized calcium levels, and Alderman et al reported that a 2 unit increase in plasma renin activity increased the overall incidence of myocardial infarction by 25%. Furthermore, the calcium-regulating hormones calcitonin, calcitriol, and parathyroid hormone have been related to hypertension, partly in association with plasma renin activity. Finally, there may be interactions between serum calcium, phosphate, and magnesium, as well as between calcium and sodium.
Our results are average values of large groups of individuals, and effects in subgroups may not be seen, as shown in the study by Hunt et al. Thus, in their study on 875 subjects, no correlation between plasma ionized calcium and BP was found. However, after the older subjects were divided into tertiles on the basis of renin activity, there was a significant inverse correlation between ionized calcium and BP in the low renin group and a significant positive relation with systolic BP in the high renin group.
In addition to relations between serum calcium and cardiovascular risk factors, certain other observations should be noted. Despite a highly significant correlation between systolic and diastolic BP (correlation coefficient in men of 0.681), in men there was a negative association between cholesterol and systolic BP and a positive correlation between cholesterol and diastolic BP. For systolic BP, this is contrary to that reported by others. However, as shown in Table 1⇑, there was an increase in systolic BP up to the age of 90 years, whereas diastolic BP and serum cholesterol peaked in those in their 60s and thereafter showed a decline. Because the age of our study population was high, this age-related pattern may explain the discrepancy with previous reports.
Furthermore, there was a significant correlation between pulse rate and BP in both genders. Because a highly significant relation between heart rate and the calcium/phosphate ratio has been described, this could have an effect on the relation between calcium and BP. However, when pulse rate was excluded from the multiple linear regression analysis, this increased the corresponding standardized β coefficient in both genders by only 7%.
In conclusion, total serum calcium is strongly related to BP and serum lipids. This relation might be explained in part by covariation with serum albumin and may also be due to the association between serum calcium and other substances related to hypertension and heart disease. Regardless of this, however, total serum calcium appears to be a marker of cardiovascular disease, at least in men.

 

Why is this test done?

A serum calcium blood test is performed to measure a patient's blood-calcium levels. Calcium is necessary for cell function. It helps keep teeth and bones strong. Calcium is also essential for helping with muscle contraction, blood clotting, heart function, and nerve signaling. This test may also be referred to as Ca++ or Ca+2.
If a doctor suspects parathyroid diseases, bone diseases, or kidney diseases, he or she may have the patient have this test done. This test may also be used to monitor such conditions.
This test is usually done to screen for bone diseases or diseases of the parathyroid gland or kidneys. It can also be done to monitor patients with such conditions.
About half of the calcium in the blood is attached to proteins. A separate test measures calcium that is not attached to proteins in your blood. Such calcium is called free or ionized calcium.
Laboratory tests may be done for many reasons. Tests are performed for routine health screenings or if a disease or toxicity is suspected. Lab tests may be used to determine if a medical condition is improving or worsening. Lab tests may also be used to measure the success or failure of a medication or treatment plan. Lab tests may be ordered for professional or legal reasons. You may need this test if you have:

  • Decreased blood calcium
  • Decreased blood magnesium
  • Elevated blood calcium
  • Heat stroke
  • Kidney failure
  • Measles
  • Meningococcal infectious disease
  • Necrotizing fasciitis
  • Pancreatitis
  • Pheochromocytoma
  • Primary hyperparathyroidism
  • Rhabdomyolysis
  • TSS - Toxic shock syndrome
  • Tumor lysis syndrome

All cells require calcium to function. Calcium is especially important in the structure of bones and in neuromuscular (nerves and muscles) activity. A deficiency of calcium in the body fluids causes hyperexcitable nerves and muscles. Excess calcium has the opposite effect.
Calcium and Phosphate are often requested together as part of a “metabolic bone profile”. These tests are usually normal in osteoporosis (“thinning of the bones”) but are helpful to exclude other metabolic bone conditions.
The symptoms of hypercalcaemia (high calcium level in the blood) can be quite non-specific and include the so-called “bones, groans and kidney stones”, namely bony pain (due to a process within the bones causing a high calcium level), and abdominal pain which may be diffuse (“groans”) or localsied to the kidney area as in kidney stones (renal colic, ureteric colic). Hypercalcaemia may also cause thirst, lethargy, and very rarely, an altered conscious state. Patients with some haematological cancers, or cancers which arise in bones or spread to bones, are more prone to this condition.
Low serum calcium (hypocalcaemia) is quite rare and is almost confined to people who have had their parathyroid glands removed or damaged by surgery. It causes painful muscle spasms, known as tetany (not to confused with tetanus, an infectious disease caused by the bacterium Clostridium tetani).
This test is usually done to screen for bone diseases or diseases of the parathyroid gland or kidneys. It can also be done to monitor patients with such conditions.

About half of the calcium in the blood is attached to proteins. A separate test measures calcium that is not attached to proteins in your blood. Such calcium is called free or ionized calcium.
Serum calcium is the name given to the level of calcium found in our blood which is determined by a performing a special blood test. Serum calcium indicates whether we are calcium deficient or have abnormally high level of calcium in our blood stream. These conditions are termed as hypocalcaemia and hypercalcaemia respectively.
Serum calcium definition tells us that both these conditions are dangerous for long-term health. Extremely low levels of calcium in the blood cause fatigue, indigestion, muscle cramps, osteoporosis and many other health complications. Calcium deficiency may indicate that the parathyroid glands are not working properly and very small amount of parathyroid hormone is being produced by them.
Hypocalcaemia also indicates that we are not getting enough calcium from our everyday diet. Either this or too much calcium is lost through urine because of a high protein diet, too much sugar or too much phosphoric acid in our diet. Carbonated soft drinks contain phosphoric acid which interferes with calcium absorption and as a result causes more and more calcium to be lost through urine.
Serum calcium definition should also indicate that abnormally high levels of calcium in the blood are sometimes caused due to hyperactivity of the parathyroid glands. Hypertension, high blood pressure, hypercalcaemia and the complications associated with this condition are the outcomes of abnormally high serum calcium.
Both hypocalcaemia and hypercalcaemia can be treated by using medication or calcium supplements. On average we need about 1000 mg of calcium on a daily basis. If this requirement is not fulfilled we may end up being calcium deficient or other serious complications.
When the blood is unable to receive calcium from food, it starts robbing it from the bones to carry out various activities like proper circulation, proper digestion and absorption of other minerals, blood clotting and other functions. As a result there is a chance of developing degenerative diseases especially osteoporosis when the bones start becoming weaker and weaker.
Women above the age of 40 are advised to increase their daily calcium intake to about 1500 mg. They should also be aware of serum calcium definition and keep a track of their calcium readings taken after every 6 months. Postmenopausal women are most likely victims of bone disease. Although almost every 4 women out of 5 above the age of 40 are calcium deficient, they should also watch out not to consume more than 2500 mg of calcium daily.

How is the test done?

Blood is typically drawn from a vein, usually from the inside of the elbow or the back of the hand. The site is cleaned with germ-killing medicine (antiseptic). The health care provider wraps an elastic band around the upper arm to apply pressure to the area and make the vein swell with blood.
Next, the health care provider gently inserts a needle into the vein. The blood collects into an airtight vial or tube attached to the needle. The elastic band is removed from your arm.
Once the blood has been collected, the needle is removed, and the puncture site is covered to stop any bleeding.
In infants or young children, a sharp tool called a lancet may be used to puncture the skin and make it bleed. The blood collects into a small glass tube called a pipette, or onto a slide or test strip. A bandage may be placed over the area if there is any bleeding.
Collection details are as follows:

  • Preferred container/tube: Serum gel
  • Acceptable container/tube: Red top
  • Submission container/tube: Plastic vial
  • Specimen volume: 0.5 mL, 0.25 mL minimum volume
  • Specimen stability: Frozen or refrigerated

How to prepare for the test
Your health care provider will instruct you, if necessary, to discontinue drugs that may interfere with the test.
Drugs that can increase calcium levels include:

  • Calcium salts (may be found in nutritional supplements or antacids)
  • Lithium
  • Thiazide diuretics
  • Thyroxine
  • Vitamin D
  • Drinking too much milk (two or more quarts a day) or taking too much vitamin D as a dietary supplement can also increase blood calcium levels.

How the test will feel
When the needle is inserted to draw blood, some people feel moderate pain, while others feel only a prick or stinging sensation. Afterward, there may be some throbbing.

 

 

 

 

What does the test result mean?

Normal values range from 8.5 to 10.2 mg/dL.
Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.
Reference Ranges: Serum Calcium


Age

mg/dL

SI Units (mmol/L)

Cord Blood

8.2-11.2

2.05-2.80

Prem

6.2-11.0

1.55-2.75

0-10d

7.6-10.4

1.90-2.60

10d-24mo

9.0-11.0

2.25-2.74

24mo-12yr

8.8-10.8

2.20-2.70

12yr +

8.5-10.2

2.12-2.55

What abnormal results mean
Higher than normal levels may be due to:

  • Addison's disease
  • Excessive vitamin D level
  • Excessive calcium intake (also called milk-alkali syndrome)
  • HIV/AIDS
  • Hyperparathyroidism
  • Infections that cause granulomas such as tuberculosis and certain fungal and mycobacterial infections
  • Metastatic bone tumor
  • Milk-alkali syndrome
  • Multiple myeloma
  • Overactive thyroid gland (hyperthyroidism) or too much thyroid hormone replacement medication
  • Paget's disease
  • Prolonged immobilization
  • Sarcoidosis
  • Tumors producing a parathyroid hormone-like substance
  • Use of certain medications such as lithium, tamoxifen, and thiazides

Lower than normal levels may be due to:

  • Hypoparathyroidism
  • Kidney failure
  • Liver disease (decreased albumin production)
  • Magnesium deficiency
  • Malabsorption (inadequate absorption of nutrients from the intestinal tract)
  • Osteomalacia
  • Pancreatitis
  • Rickets
  • Vitamin D deficiency

Additional conditions under which the test may be performed:

  • Delirium
  • Dementia
  • Multiple endocrine neoplasia (MEN) II
  • Multiple endocrine neoplasia (MEN) I
  • Renal cell carcinoma
  • Secondary hyperparathyroidism

What the risks are

  • Excessive bleeding
  • Fainting or feeling lightheaded
  • Hematoma (blood accumulating under the skin)
  • Infection (a slight risk any time the skin is broken)
  • Multiple punctures to locate veins

Because Calcium is transported in the blood mostly bound to the protein Albumin, a serum Calcium level needs to be taken in context of the Albumin level, and there are various formulas for calculating this “corrected Calcium”. In uncommon circumstances, an arterial blood sample may have to be taken to check the ionised Calcium level, which is the biochemically active fraction of calcium not bound to Albumin.
The 3 components of total serum calcium are as follows:

  • A protein-bound component - About 45% is protein bound (predominantly bound to albumin); this component is biologically inert
  • A component that is complexed or chelated to citrate - About 5%; this component is also biologically inert
  • An ionized or free component - About 50%; this component is metabolically active

Measurement of the ionized calcium component is generally obtained in special laboratories and through a special procedure. In most laboratories, autoanalyzers are used measure the total serum calcium level accurately and reproducibly, although atomic absorption spectrophotometers probably provide even greater accuracy.
Unless serum proteins contain abnormalities, total serum calcium concentration is normally between 8.5 and 10.2 mg/dL of serum. Because ionized calcium is the only component of the total serum calcium level that is regulated by calciotropic hormones, decisions on the total serum calcium concentration should not be made unless changes in concentrations of plasma proteins, particularly albumin, are considered. Total serum calcium is less difficult to measure than the ionized calcium component is, and ionized calcium measurements are rarely needed if serum protein concentrations can be measured.
Patients with myeloma are a possible exception to this. In these patients, excessive binding of calcium to the myeloma protein occasionally raises the total serum calcium concentration, yet the ionized calcium level may be normal in these individuals. Assessment of ionized calcium would be useful in such patients.

A tourniquet should not be used when blood is drawn for evaluation of serum calcium. It is important to keep in mind the pH-associated changes that can occur in ionized calcium that do not cause changes in the total calcium level. Alkalosis and acidosis cause a decrease and an increase, respectively, in the ionized calcium component. Although serum calcium levels above 11.5 mg/dL commonly cause symptoms, patients may be asymptomatic at this level. Critical levels are reached above 12.0 mg/dL, with levels above 15.0 mg/dL (severe hypercalcemia) being a medical emergency.
Adults have a calcium content of over 1 kg, or approximately 2% of body weight. All but 1% is contained in the bones, where it exists as calcium hydroxyapatite. The extra-osseous intracellular space and extracellular space (ECS) contain a portion of the remaining 1%. A dynamic equilibrium is maintained between the ECS and the rapidly exchangeable fraction of bone calcium.
The reference range for serum calcium is as follows:
Males

  • Younger than 12 months: Not established
  • Age 1-14 years: 9.6-10.6 mg/dL
  • Age 15-16 years: 9.5-10.5 mg/dL
  • Age 17-18 years: 9.5-10.4 mg/dL
  • Age 19-21 years: 9.3-10.3 mg/dL
  • Age 22 years and older: 8.9-10.1 mg/dL

Females

  • Younger than 12 months: Not established
  • Age 1-11 years: 9.6-10.6 mg/dL
  • Age 12-14 years: 9.5-10.4 mg/dL
  • Age 15-18 years: 9.1-10.3 mg/dL
  • Age 19 years and older: 8.9-10.1 mg/dL

 

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