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hsCRP + CRP – All in one

What is CRP and hsCRP?

C-reactive protein (CRP) is protein found in the blood, the levels of which rise in response to

inflammation (i.e. C-reactive protein is an acute-phase protein). Its physiological role is to

bind to phosphocholine expressed on the surface of dead or dying cells (and some types of

bacteria) in order to activate the complement system via the C1Q complex.

CRP is synthesized by the liver in response to factors released by macrophages and fat cells

(adipocytes).

The acute phase response develops in a wide range of acute and chronic inflammatory

conditions like bacterial, viral, or fungal infections; rheumatic and other inflammatory

diseases; malignancy; and tissue injury or necrosis. These conditions cause release of

interleukin-6 and other cytokines that trigger the synthesis of CRP and fibrinogen by the

liver. During the acute phase response, levels of CRP rapidly increase within 2 hours of acute

insult, reaching a peak at 48 hours. With resolution of the acute phase response, CRP declines

with a relatively short half-life of 18 hours. Measuring CRP level is a screen for infectious

and inflammatory diseases. Rapid, marked increases in CRP occur with inflammation,

infection, trauma and tissue necrosis, malignancies, and autoimmune disorders. Because there

are a large number of disparate conditions that can increase CRP production, an elevated

CRP level does not diagnose a specific disease. An elevated CRP level can provide support

for the presence of an inflammatory disease, such as rheumatoid arthritis, polymyalgia

rheumatica or giant-cell arteritis.

The physiological role of CRP is to bind to phosphocholine expressed on the surface of dead

or dying cells (and some types of bacteria) in order to activate the complement system. CRP

binds to phosphocholine on microbes and damaged cells and enhances phagocytosis by

macrophages. Thus, CRP participates in the clearance of necrotic and apoptotic cells.

CRP rises up to 50,000-fold in acute inflammation, such as infection. It rises above normal

limits within 6 hours, and peaks at 48 hours. Its half-life is constant, and therefore its level is

mainly determined by the rate of production (and hence the severity of the precipitating

cause).

Clinical significance

C-reactive protein (CRP) is 1 of the most sensitive acute-phase reactants. Plasma CRP levels

can increase dramatically (100-fold or more) after severe trauma, bacterial infection,

inflammation, surgery, or neoplastic proliferation. Measurement of CRP has been used

historically to assess activity of inflammatory disease, to detect infections after surgery, to

detect transplant rejection, and to monitor these inflammatory processes. While assays for

CRP have been available for many years, the traditional assays lack the sensitivity to measure

basal levels of CRP.

In the mid-1990s, more sensitive methods for measurement of CRP were introduced. These

methods, referred to as high sensitivity CRP (hs-CRP), can accurately measure basal levels of

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CRP throughout the currently accepted cardiovascular risk assessment range (0.20-10.0

mg/L).

These hs-CRP assays were used to assess outcomes in patients with unstable angina and

showed that hs-CRP values in the upper tertile (>3.0 mg/L) were associated with increased

risk of developing myocardial infarction. Data from prospective studies monitoring hs-CRP

in apparently healthy populations also has been published. All prospective studies reported to

date have been positive, with adjusted relative risks of developing cardiovascular disease or

ischemic events ranging from 2.3 to 4.8 in the highest quartile or quintile of data versus the

lowest quartile or quintile. It also has been shown that hs-CRP is additive with total

cholesterol, LDL and HDL, as well as the Framingham 10-year risk score, with respect to risk

prediction.

When is the hsCRP – All in one test done?

High-sensitivity CRP usually is ordered as one of several tests in a cardiovascular risk

profile, often along with tests for cholesterol and triglycerides, when a person's risk of heart

disease is being evaluated. Some experts say that the best way to predict risk is to combine a

good marker for inflammation, like hs-CRP, along with the lipid profile. When hs-CRP is

evaluated, it may be repeated to confirm that a person has persistent low levels of

inflammation.

CRP is useful for: -

1. Monitoring response to antibiotic therapy in patients with known bacterial infections.

2. Warning of intrauterine infections in obstetric patients with premature rupture of

membranes.

3. Differentiation between active disease and infections in systemic lupus and colitis

ulcerosa.

4. Measure of disease activity and drug response in rheumatoid arthritis.

5. Early detection of complications in postoperative patients.

6. Differentiation between infection and graft-versus-host-disease in bone marrow

transplant patients.

What does the test result mean?

Relatively high levels of hs-CRP in otherwise healthy individuals have been found to be

predictive of an increased risk of a future heart attack, stroke, sudden cardiac death, and/or

peripheral arterial disease, even when cholesterol levels are within an acceptable range.

People with higher hs-CRP values have the highest risk of cardiovascular disease, and those

with lower values have less of a risk. Specifically, individuals who have hs-CRP results at the

high end of the normal range have 1.5 to 4 times the risk of having a heart attack as those

with hs-CRP values at the low end of the normal range.

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The American Heart Association and U.S. Centers for Disease Control and Prevention have

defined risk groups as follows:

Low risk: less than 1.0 mg/L

Average risk: 1.0 to 3.0 mg/L

High risk: above 3.0 mg/L

These values are only a part of the total evaluation process for cardiovascular diseases.

Additional risk factors to be considered are elevated levels of cholesterol, LDL-C,

triglycerides, and glucose. In addition, smoking, high blood pressure (hypertension), and

diabetes also increase the risk level.

For further information, kindly refer to the pack insert.

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Procalcitonin (PCT)

What is Procalcitonin?

Procalcitonin (PCT) is a peptide precursor of the hormone calcitonin, the latter being

involved with calcium homeostasis. It is composed of 116 amino acids and is produced by

parafollicular cells (C cells) of the thyroid and by the neuroendocrine cells of the lung and the

intestine.

The level of procalcitonin in the blood stream of healthy individuals is below the limit of

detection (10 pg/mL) of clinical assays. The level of procalcitonin raises in a response to a

proinflammatory stimulus, especially of bacterial origin. In this case, it is produced mainly by

the cells of the lung and the intestine. It does not raise significantly with viral or non-

infectious inflammations. With the derangements that a severe infection with an associated

systemic response brings, the blood levels of procalcitonin may rise to 100 ng/ml. In serum,

procalcitonin has a half-life of 25 to 30 hours. Remarkably the high procalcitonin levels

produced during infections are not followed by a parallel increase in calcitonin or serum

calcium levels.

Clinical significance

Diagnosis and prognosis of sepsis

Measurement of procalcitonin can be used as a marker of severe sepsis caused by bacteria

and generally grades well with the degree of sepsis, although levels of procalcitonin in the

blood are very low. PCT has the greatest sensitivity (85%) and specificity (91%) for

differentiating patients with systemic inflammatory response syndrome (SIRS) from those

with sepsis, when compared with IL-2, IL-6, IL-8, CRP and TNF-alpha. Evidence is

emerging that procalcitonin levels can reduce unnecessary antibiotic prescribing to people

with lower respiratory tract infections. Currently, procalcitonin assays are widely used in the

clinical environment.

Diagnosis of bacteremia

A meta-analysis reported a sensitivity of 76% and specificity of 70%.

Procalcitonin level can help guide antibiotic therapy. Procalcitonin levels may be useful to

distinguish bacterial infections from nonbacterial infections.

When is the Procalcitonin test done?

The procalcitonin test has been approved by the U.S. FDA (Food and Drug Administration)

for use in conjunction with other laboratory findings and clinical assessments to assist in the

risk assessment of critically ill people for progression to severe sepsis and septic shock. For

diagnostic purposes, it is best used during the first day of presentation. It may be used later on

to monitor the response to treatment.

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Procalcitonin may sometimes be ordered, along with other tests such as a CRP (C-reactive

protein), blood culture, CBC (Complete Blood Count), or CSF (cerebrospinal fluid) analysis

to help detect or rule out sepsis, bacterial meningitis, or bacterial pneumonia in those who are

seriously ill and in children with a fever of unknown origin.

Occasionally, a procalcitonin test may be ordered at intervals to monitor the effectiveness of

antimicrobial treatment.

The procalcitonin test may be ordered along with other tests, when a seriously ill person has

symptoms that suggest that they may have a systemic or severe bacterial infection. When

used, it is typically ordered as an early detection tool, within the first day of hospital

admission.

Complications of sepsis may include:

Chills, fever

Nausea

Rapid breathing, rapid heartbeat

Confusion

Decreased urine output

More severe symptoms include inflammation throughout the body and formation of many

tiny blood clots in the smallest blood vessels. One or more organs may begin to stop working

(multi-organ failure, MOF) and there may be a dangerous drop in blood pressure.

Rarely, it may be ordered at intervals to monitor antimicrobial therapy in persons suspected

of having sepsis.

What does the test result mean?

Low levels of procalcitonin in a seriously ill person represent a low risk of sepsis and

progression to severe sepsis and/or septic shock but do not exclude it. Low concentrations

may indicate a localized infection that has not yet become systemic or a systemic infection

that is less than six hours old. It may also indicate that the person's symptoms are likely due

to another cause, such as transplant rejection, a viral infection, or trauma – post-surgery or

otherwise.

High levels indicate a high probability of sepsis, that is, a higher likelihood of a bacterial

cause for the symptoms. They also suggest a higher risk of progression to severe sepsis and

then to septic shock.

Moderate elevations may be due to a non-infectious condition or due to an early infection

and, along with other findings, should be reviewed carefully. Decreasing procalcitonin levels

in a person being treated for a severe bacterial infection indicate a response to therapy.

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Cortisol

What is Cortisol?

Cortisol, known more formally as hydrocortisone, is a steroid hormone, more specifically a

glucocorticoid, produced by the zona fasciculata of the adrenal gland. It is released in

response to stress and a low level of blood glucocorticoids. Its primary functions are to

increase blood sugar through gluconeogenesis; suppress the immune system; and aid in fat,

protein and carbohydrate metabolism.

Clinical significance

A cortisol test may be ordered to screen for and help diagnose Cushing syndrome, a group of

signs and symptoms associated with excess cortisol. Blood cortisol testing evaluates both

protein-bound and free cortisol while urine testing evaluates only free cortisol, which should

correlate with the levels of free cortisol in the blood. Sometimes salivary cortisol is also

ordered to help detect Cushing syndrome.

Blood cortisol is also used to help diagnose adrenal insufficiency and Addison disease,

conditions in which the adrenal glands do not function properly.

Multiple blood and/or saliva cortisol levels collected at different times, such as at 8 am and 4

pm, can be used to evaluate both cortisol concentrations and diurnal variation. Normally, the

level of cortisol in the blood rises and falls in a "diurnal variation" pattern, peaking early in

the morning then declining throughout the day and reaching its lowest level about midnight.

A 24-hour urine cortisol sample will not show diurnal variation; it will measure the total

amount of unbound cortisol excreted in 24 hours.

If an abnormal level of cortisol is detected, a doctor will do additional testing to help confirm

the findings and to help determine its cause:

Dexamethasone Suppression

If a person has a high cortisol level, a doctor may perform a dexamethasone suppression test

to help determine whether the cause is related to excess ACTH production by the pituitary.

This test involves analyzing a baseline sample for cortisol, then giving the person oral

dexamethasone (a synthetic glucocorticoid) and measuring cortisol levels in subsequent timed

samples. Dexamethasone suppresses ACTH production and should decrease cortisol

production if the source of the excess is pituitary-related. There are a few variations of this

test. An overnight test may be used to help screen for Cushing syndrome. Longer tests help

confirm initial findings. For these, the medication is usually given (either low or high dose)

every 6 hours for either 2 or 4 days prior to blood or urine collection. Separate 24-hour urine

samples are collected prior to and throughout the testing period and then the blood and urine

samples are measured for cortisol and evaluated.

ACTH Stimulation

If the findings of the initial blood and/or urine tests indicate insufficient cortisol production, a

doctor may order an ACTH stimulation test. This test involves measuring the concentration

of cortisol in a person's blood before and after an injection of synthetic ACTH. If the adrenal

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glands are functioning normally, then cortisol levels will rise with the ACTH stimulation. If

they are damaged or not functioning properly, then the response will be limited. A longer

version of this test (1-3 days) may be performed to help distinguish between adrenal and

pituitary insufficiency.

When is the Cortisol test done?

A cortisol test may be ordered when a person has symptoms that suggest a high level of

cortisol and Cushing syndrome, such as

High blood pressure (hypertension)

High blood sugar (glucose)

Obesity, especially in the trunk

Fragile skin

Purple streaks on the abdomen

Muscle wasting and weakness

Osteoporosis

Women may have irregular menstrual periods and increased facial hair; children may have

delayed development and a short stature. This test may be ordered when someone has

symptoms suggestive of a low level of cortisol, adrenal insufficiency or Addison disease,

such as:

Weight loss

Muscle weakness

Fatigue

Low blood pressure

Abdominal pain

Dark patches of skin—this occurs in Addison disease, but not secondary adrenal

insufficiency

Sometimes decreased production combined with a stressor can cause an adrenal crisis that

can be life-threatening and requires immediate medical attention. Symptoms of a crisis may

include:

Sudden onset of severe pain in the lower back, abdomen, or legs

Vomiting and diarrhea, resulting in dehydration

Low blood pressure (hypotension)

Loss of consciousness

Suppression or stimulation testing is ordered when initial findings are abnormal. Cortisol

testing may be ordered at intervals after a diagnosis of Cushing syndrome or Addison disease

to monitor the effectiveness of treatment.

What does the test result mean?

Normal values indicated in the following tables pertain to humans. (Normals vary among

species.)

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Reference ranges for blood plasma content of free cortisol

Time Lower limit Upper limit Unit

09:00 am 140 700 nmol/L

5 25 μg/dL

Midnight 80 350 nmol/L

2.9 13 μg/dL

Normally, cortisol levels are very low at bedtime and at their highest just after waking,

though this pattern will change if a person works irregular shifts (such as the night shift) and

sleeps at different times of the day.

An increased or normal cortisol concentration in the morning along with a level that does not

drop in the afternoon and evening suggest an overproduction of cortisol and Cushing

syndrome. If this excess cortisol is suppressed during a dexamethasone suppression test, it

suggests that the excess cortisol is due to increased pituitary ACTH production. If it is not

suppressed, then the increased cortisol could be due to an ACTH-producing tumor outside of

the pituitary, due to a problem with the adrenal gland, or due to a medication, such as

corticosteroids that may be prescribed to someone with asthma.

If insufficient cortisol is present and the person tested responds to an ACTH stimulation test,

then the problem is likely due to insufficient ACTH production by the pituitary. If the person

does not respond to the ACTH stimulation test, then it is more likely that the problem is

based in the adrenal glands. If the adrenal glands are underactive, due to pituitary dysfunction

and/or insufficient ACTH production, then the person is said to have secondary adrenal

insufficiency. If decreased cortisol production is due to adrenal damage, then the person is

said to have primary adrenal insufficiency or Addison disease.

Once an abnormality has been identified and associated with the pituitary gland, adrenal

glands, or other cause, then the doctor may use other testing such as CT (computerized

tomography) or MRI (magnetic resonance imaging) scans to locate the source of the excess

(such as a pituitary, adrenal, or other tumor) and to evaluate the extent of any damage to the

glands.

Factors generally reducing cortisol levels

Magnesium supplementation decreases serum cortisol levels after aerobic exercise,

but not after resistance training.

Omega-3 fatty acids have a dose-dependent effect in slightly reducing cortisol release

influenced by mental stress, suppressing the synthesis of interleukin-1 and -6 and

enhancing the synthesis of interleukin-2; the former promotes higher CRH release.

Omega-6 fatty acids, on the other hand, have an inverse effect on interleukin

synthesis.

Music therapy can reduce cortisol levels in certain situations.

Massage therapy can reduce cortisol.

Laughing, and the experience of humour, can lower cortisol levels.

Soy-derived phosphatidylserine interacts with cortisol; the correct dose, however, is

unclear.

Black tea may hasten recovery from a high-cortisol condition.

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Regular dancing has been shown to lead to significant decreases in salivary cortisol

concentrations.

Factors generally increasing cortisol levels

Caffeine may increase cortisol levels.

Sleep deprivation

Intense (high VO2 max) or prolonged physical exercise stimulates cortisol release to

increase gluconeogenesis and maintain blood glucose. Proper nutrition and high-level

conditioning can help stabilize cortisol release.

The Val/Val variation of the BDNF gene in men, and the Val/Met variation in

women, are associated with increased salivary cortisol in a stressful situation.

Hypoestrogenism and melatonin supplementation increase cortisol levels in

postmenopausal women.

Burnout is associated with higher cortisol levels.

Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged

periods.

Subcutaneous adipose tissue regenerates cortisol from cortisone.

Anorexia nervosa may be associated with increased cortisol levels.

The serotonin receptor gene 5HTR2C is associated with increased cortisol production

in men.

Commuting increases cortisol levels relative to the length of the trip, its predictability

and the amount of effort involved.

Stimuli associated with sexual intercourse can increase cortisol levels in gilts (a young

female pig that has not produced her first litter).

Severe calorie restriction causes elevated baseline levels of cortisol.

Disorders of cortisol production

Hypercortisolism: Excessive levels of cortisol in the blood. (See Cushing's

syndrome.)

Hypocortisolism (adrenal insufficiency): Insufficient levels of cortisol in the blood.

The relationship between cortisol and ACTH, and some consequent conditions, are as

follows:

The disorders of cortisol secretion

Plasma ACTH

↓ ↑

Plasma

Cortisol

↑ Primary hypercortisolism

(Cushing's syndrome)

Secondary hypercortisolism (pituitary or

ectopic tumor, Cushing's disease, pseudo-

Cushing's syndrome)

↓

Secondary hypocortisolism

(pituitary tumor, Sheehan's

syndrome)

Primary hypocortisolism (Addison's

disease, Nelson's syndrome)

A 2010 study has found that serum cortisol predicts increased cardiovascular mortality in

patients with acute coronary syndrome.

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Ferritin

What is Ferritin?

Ferritin is a ubiquitous intracellular protein that stores iron and releases it in a controlled

fashion. The amount of ferritin stored reflects the amount of iron stored. The protein is

produced by almost all living organisms, including algae, bacteria, higher plants, and

animals. In humans, it acts as a buffer against iron deficiency and iron overload.

Ferritin is a globular protein complex consisting of 24 protein subunits and is the primary

intracellular iron-storage protein in both prokaryotes and eukaryotes, keeping iron in a

soluble and non-toxic form. Ferritin that is not combined with iron is called apoferritin.

Clinical significance

Serum ferritin levels are measured in medical laboratories as part of the iron studies workup

for anemia and for restless legs syndrome. The ferritin levels measured usually have a direct

correlation with the total amount of iron stored in the body. However, ferritin levels may be

artificially high in cases of anemia of chronic disease where ferritin is elevated in its capacity

as an acute phase protein and not as a marker for iron overload.

Normal Ranges

A normal ferritin blood level, referred to as the reference interval is determined by many

testing laboratories. The ranges for ferritin can vary between laboratories but are usually

between 30–300 ng/mL (=μg/L) for males, and 15–200 ng/mL (=μg/L) for females.

Low

If the ferritin level is low, there is a risk for lack of iron, which could lead to anemia.

In the setting of anemia, low serum ferritin is the most specific lab test for iron deficiency

anemia.[19]

However it is less sensitive, since its levels are increased in the blood by infection

or any type of chronic inflammation,[20]

and these conditions may convert what would

otherwise be a low level of ferritin from lack of iron, into a value in the normal range. For

this reason, low ferritin levels carry more information than those in the normal range.

Low ferritin may also indicate hypothyroidism, vitamin C deficiency or celiac disease

In adolescents and teenagers, ferritin levels that are low but yet above those causing anemia

and sickness (12 to 50 ng/mL) may cause symptoms of restless legs syndrome.

A falsely low blood ferritin (equivalent to a false positive test) is very uncommon, but can

result from a hook effect of the measuring tools in extreme cases.

Vegetarianism may contribute to low levels of serum ferritin, with one study finding 40% of

vegetarians tested with low serum ferritin levels.

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Elevated

If ferritin is high, there is iron in excess or else there is an acute inflammatory reaction in

which ferritin is mobilized without iron excess. For example, ferritins may be high in

infection without signalling body iron overload.

Ferritin is also used as a marker for iron overload disorders, such as hemochromatosis or

hemosiderosis. Adult-onset Still's disease, some porphyrias, and hemophagocytic

lymphohistiocytosis/macrophage activation syndrome are diseases in which the ferritin level

may be abnormally raised.

As ferritin is also an acute-phase reactant, it is often elevated in the course of disease. A

normal C-reactive protein can be used to exclude elevated ferritin caused by acute phase

reactions.

According to a study of anorexia nervosa patients, ferritin can be elevated during periods of

acute malnourishment, perhaps due to iron going into storage as intravascular volume and

thus the number of red blood cells falls.

When is the Ferritin test done?

The ferritin test is ordered to assess a person's iron stores in the body. The test is sometimes

ordered along with an iron test and a TIBC (Total Iron Binding Capacity) to detect the

presence and evaluate the severity of an iron deficiency or overload.

The ferritin test may be ordered, along with other iron tests, when a routine CBC shows that a

person's hemoglobin and hematocrit are low and their red blood cells are smaller and paler

than normal (microcytic and hypochromic), suggesting iron deficiency anemia even though

other clinical symptoms have not yet developed.

Early iron deficiency usually causes no physical effects at all. If a person is otherwise

healthy, symptoms seldom appear before the hemoglobin in the blood drops below a certain

level (10 g per deciliter). However, as the iron-deficiency progresses, symptoms may begin to

develop and a doctor may order ferritin as wells as other iron-related tests. The most common

symptoms of iron deficiency anemia include:

Chronic fatigue/tiredness

Weakness

Dizziness

Headaches

As iron stores continue to be depleted, there may be shortness of breath, ringing in the ears

(tinnitus), drowsiness, and irritability. If the anemia progresses in severity, chest pain,

headaches, leg pains, shock, and even heart failure may occur. Children may develop learning

(cognitive) disabilities. Besides the general symptoms of anemia, there are certain symptoms

that are characteristic of iron deficiency. These include pica (cravings for specific substances,

such as licorice, chalk, dirt, or clay), a burning sensation in the tongue or a smooth tongue,

sores at the corners of the mouth, and spoon-shaped finger- and toe-nails.

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A ferritin level may also be ordered when iron overload is suspected. Symptoms of iron

overload will vary from person to person and tend to worsen over time. They are due to iron

accumulation in the blood and tissues. Symptoms may include:

Joint pain

Fatigue, weakness

Lack of energy

Abdominal pain

Loss of sex drive

Heart problems

To confirm the presence of iron overload, other iron tests (iron, TIBC) and a genetic test for

hereditary hemochromatosis may be ordered as well.

What does the test result mean?

Ferritin levels are often evaluated in conjunction with other iron tests. A summary of the

changes in iron tests seen in various diseases of iron status is shown in the table below.

Disease Iron TIBC/

Transferrin

UIBC %Transferrin

Saturation

Ferritin

Iron Deficiency Low High High Low Low

Hemochromatosi

s

High Low Low High High

Chronic Illness Low Low Low/Normal Low Normal/Hig

h

Hemolytic

Anemia

High Normal/Low Low/Normal High High

Sideroblastic

Anemia

Normal/Hig

h

Normal/Low Low/Normal High High

Iron Poisoning High Normal Low High Normal

Ferritin levels are low in people who have iron deficiency and are elevated in those with

hemochromatosis and other excess iron storage disorders and in those who have had multiple

blood transfusions.

Ferritin is an acute phase reactant and thus may be increased in people with inflammation,

liver disease, chronic infection, autoimmune disorders, and some types of cancer. Ferritin is

not typically used to detect or monitor these conditions.