Laboratory tests

NAME
GGT (Gamma
glutamyltransferase)

MCV (mean
corpuscular volume)

10/7/2013

ROLE
The purpose of this
blood serum chemistry
test is to provide
information about
hepatobiliary diseases,
to assess liver
function, and to
detect alcohol
ingestion. Another
purpose is to
distinguish between
skeletal disease and
hepatic disease when
serum alkaline
phosphatase is
elevated.
MCV = Hct/Hgb

NORMAL

Normal results in
A normal GGT level suggests such elevation stems
females under age 45, from skeletal disease. Serum GGT values vary with
range from 5 to 27 U/L; the assay method used (colorimetric or kinetic). The
in females over age 45 sharpest increases in GGT levels indicate obstructive
and in males, levels
jaundice and hepatic metastasis. Elevations may
range from 6 to 37
indicate any acute hepatic disease, acute
U/L.
pancreatitis, renal disease, alcohol ingestion,
postoperative status, and prostatic metastasis. This
test is nonspecific, providing little data about the
type of hepatic disease. GGT is particularly sensitive
to the effects of alcohol in the liver, and levels may
be elevated after moderate alcohol intake and in
chronic alcoholism, even without clinical evidence of
hepatic injury.
Normal values: MCV:
80 to 95 femtoliter
MCH: 27 to 31
picograms/cell MCHC:
32 to 36
grams/deciliter

4.1 to 8.8 mg/dl

Uric Acid

DIFF

These RBC indices are useful in the differential

diagnosis of types of anemia. Anemias are classified
on the basis of cell size (MCV) and cell color
(MCHC). MCV less than lower limit of normal:
microcytic MCV within normal range: normocytic
MCV greater than upper limit of normal: macrocytic
MCHC less than lower limit of normal: hypochromic
MCHC with normal range: normochromic MCHC
greater than upper limit of normal: hyperchromic
Anemias have been classified as follows:
normocytic/normochromic (NC/NC) anemia: acute
blood loss aplastic anemia (for example, due to
chloramphenicol toxicity) prosthetic heart valves
sepsis tumor microcytic/hypochromic anemia: iron
deficiency lead poisoning thalassemia
microcytic/normochromic anemia: erythropoietin
deficiency secondary to renal failure
macrocytic/normochromic anemia: chemotherapy
folate deficiency vitamin B12 deficiency
Greater-than-normal levels of uric acid
(hyperuricemia) may indicate:

acidosis
alcoholism
diabetes
mellitus
renal failure

gout
leukemia
hypoparathyroidism nephrolithiasis
polycythemia
lead poisoning
vera
toxemia of
purine-rich
pregnancy
diet

severe
exercise
Lower-than-normal levels of uric acid may indicate:

Fanconi's syndrome Wilson's disease SIADH

low purine diet

Cholesterol

Triglycerides
Alanine Aminotransferase
(ALT, SGPT, GPT)

Albumin

Additional conditions under which the test may be

performed: chronic gouty arthritis injury of the
kidney and ureter
140 to 310 mg/dl
atherosclerosis biliary cirrhosis familial
optimal values: 140hyperlipidemias high-cholesterol diet hypothyroidism
220 mg/dl Note: mg/dl myocardial infarction nephrotic syndrome
= milligrams per
uncontrolled diabetes
deciliter
Normal values: 10 to
cirrhosis familial hyperlipoproteinemia (rare)
190 mg/dl Note: mg/dl hypothyroidism low protein in diet and high
= milligrams per
carbohydrates poorly controlled diabetes nephrotic
deciliter
syndrome pancreatitis
Intracellular enzyme
Normal Range: Laboratory- Increased in: Acute viral hepatitis (ALT>AST), biliary tract
involved in amino acid and specific U/L
obstruction (cholangitis, choledocholithiasis), alcoholic
carbohydrate metabolism.
hepatitis and cirrhosis (AST>ALT), liver abscess, metastatic
Present in large
or primary liver cancer; right heart failure, ischemia or
concentrations in liver,
hypoxia, injury to liver ("shock liver"), extensive trauma.
kidney; smaller amounts
Drugs causing cholestasis and other hepatotoxic drugs.
in skeletal muscle and
heart. Released with
Additional: ALT screening of donor blood used in blood banks
tissue damage.
to exclude non-A, non-B hepatitis.
Major component of
Normal Range: 3.4-4.7
increased in: Dehydration, shock, hemoconcentration.

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Laboratory tests

Albumin

Alkaline Phosphatase

10/7/2013

Major component of
plasma proteins,
influenced by nutritional
state, hepatic function,
renal function, various
diseases.

Alkaline phosphatases
are found in liver, bone,
intestine, placenta.

Normal Range: 3.4-4.7

g/dL

increased in: Dehydration, shock, hemoconcentration.

Decreased in: Decreased hepatic synthesis (chronic liver
disease, malnutrition, malabsorption, malignancy, congenital
analbuminemia [rare]). Increased losses (nephrotic
syndrome, burns, trauma, hemorrhage with fluid
replacement, fistulae, enteropathy, acute or chronic
glomerulonephritis). Hemodilution (pregnancy, CHF). Drugs
(eg, estrogens).

Normal Range: Method

and age dependent

Additional: Serum albumin gives an indication of severity in

chronic liver disease. Useful in nutritional assessment if no
impairment in production or increased loss.
increased in: Obstructive hepatobiliary disease, hepatotoxic
drugs, bone disease (physiologic bone growth, Paget's
disease, osteomalacia, osteogenic sarcoma, bone
metastases), hyperparathyroidism, rickets. Benign familial
hyperphosphatasemia, pregnancy (3rd trimester), GI disease
(perforated ulcer or infarct).
Decreased in: Hypophosphatasia.

ANA (Antinuclear
Antibodies)

ANCA (antineutrophil
cytoplasmic antibodies),
P-ANCA (perinuclear)
C-ANCA (cytoplasmic)

Anti-Cardiolipin
(Anti-Phospholipid)

Anti-DNA

Heterogeneous antibodies Normal Range: < 1:20

to nuclear antigens (DNA
and RNA, histone and
nonhistone proteins).
Antinuclear antibody is
measured in patient's
serum by layering serum
over human epithelial cells
and detecting the
antibody with fluoresceinconjugated polyvalent
anti-human
immunoglobulin.

Tests are on the blood

serum. C-ANCA is most
seen in Wegener's
granulomatosus. C-ANCA
suggests a systemic
vasculitis disease, and is
rarely seen in patients
with lupus. P-ANCA is
most seen in necrotizing,
crescentic
glomerulonephritis and
polyarteritis nodosa. PANCA is found in some
lupus patients.
Anticardiolipin antibodies
are a subset of a group of
antibodies which react
with negatively charged
phospholipids. Antibodies
to cardiolipin have been
associated with an
incresased incidence of
vascular thrombosis,
thrombocytopenia and
recurrent fetal loss in
patients with SLE.
IgG or IgM antibodies
directed against host
double-stranded DNA.

Additional: Normal in osteoporosis. Alkaline phosphatase

isoenzyme separation by electrophoresis or differential heat
inactivation is unreliable. Use g-glutamyl transpeptidase
(GGT), which increases in hepatobiliary disease, to infer
origin of increased alkaline phosphatase (ie, liver or bone).
Elevated in: 1/3-3/4 of patients over age 65 (usually in low
titers), systemic lupus erythematosus (98%), drug-induced
lupus (100%), Sj?gren's (80%), rheumatoid arthritis (3050%), scleroderma (60%), mixed connective tissue disease
(100%), Felty's syndrome, mononucleosis, hepatic or biliary
cirrhosis, hepatitis, leukemia, myasthenia gravis,
dermatomyositis, polymyositis, chronic renal failure.
Additional: A negative ANA test does not completely rule out
SLE, but alternative diagnoses should be considered. Pattern
of staining of ANA may give some clues to diagnoses, but
since the pattern also changes with serum dilution, it is not
routinely reported. Only the rim (peripheral) pattern is highly
specific (for SLE). Not useful as a screening test. Should be
used only when there is clinical evidence of a connective
tissue disease

Normal Range: none

present

Normal Range for anti-IgG: increased in: SLE, some connective tissue diseases, and in
Antiphospholipid Syndrome.
0 - 20 GPL
Normal Range for anti-IgM:
Additional: Patients with acute and chronic infections
0 - 10 MPL.
(including syphilis, HIV, Lyme disease) may also have
increased anti-cardiolipin antibodies

Normal Range: < 1:10 titer increased in: Systemic lupus erythematosus (60-70%,
specificity 95%). Anti-ds-DNA antibody is not found in druginduced lupus.
Additional: High titers are seen only in SLE. Titers of anti-dsDNA correlate well with disease activity and with occurrence
of glomerulonephritis.

Antinerythrocyte
antibodies (anti-RBC)
also known as Coombs test

The direct Coombs test Normal Range: none

measures the presence of present
antibodies that are bound
to the surface of
circulating RBCs. Indirect
Coombs measures *free*
anti-RBC antibodies. The
sensitivity of this test is in

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Laboratory tests

Antineurofilament antibodies

Anti-Cardiolipin
(Anti-Phospholipid)

Antinerythrocyte
antibodies (anti-RBC)
also known as Coombs test

Antineurofilament antibodies

Antineuronal antibodies

Anti-ribosomal P

Anti-Ro/SS-A

Aspartate Aminotransferase
(AST, SGOT, GOT)

10/7/2013

sensitivity of this test is in

question--but it remains
the standard for detection
of autoimmune anemia.
Limited studies have been Normal Range: non
done with this test.
present
Antibodies against
neurofilaments in blood
serum. 60% of diffuse NP
lupus patients have shown
this antibody.
MPLAnticardiolipin
Normal Range for anti-IgG:
antibodies are a subset of 0 - 20 GPL
a group of antibodies
Normal Range for anti-IgM:
which react with
0 - 10
negatively charged
phospholipids. Antibodies
to cardiolipin have been
associated with an
incresased incidence of
vascular thrombosis,
thrombocytopenia and
recurrent fetal loss in
patients with SLE.
The direct Coombs test Normal Range: none
measures the presence of present
antibodies that are bound
to the surface of
circulating RBCs. Indirect
Coombs measures *free*
anti-RBC antibodies. The
sensitivity of this test is in
question--but it remains
the standard for detection
of autoimmune anemia.
presentLimited studies
Normal Range: non
have been done with this
test. Antibodies against
neurofilaments in blood
serum. 60% of diffuse NP
lupus patients have shown
this antibody.
Most specifically, this is Normal Range: non
IgG neuron-reactive
present
antibody
radioimmunoassay
performed on the
cerebrospinal fluid. In the
general lupus population,
75% with neuro-psyciatric
(NP) lupus are detected,
as compared to 10%
without NP lupus--*false
positive*. Highest titers
are found in patients with
diffuse NP lupus
(seizures, organic brain
syndrome)--90%. 40% of
focal NP are positive
(stroke, cranial
neuropathy, transverse
myelitis).
Antibodies to ribosomal P Normal Range: Negative
protein from blood serum.
80 - 90% positive in NP
lupus that manifests with
psychosis or depression.
Autoantibody against
Normal Range: Negative
acidic nuclear
ribonucleoproteins that is
found in patients with
some connective tissue
diseases, especially
Sjogren's syndrome.
U/LIntracellular enzyme Normal Range: Laboratoryinvolved in amino acid and specific
carbohydrate metabolism.
Present in large
concentrations in liver,
skeletal muscle, brain,
red cells, and heart.
Released into the
bloodstream when tissue
is damaged.

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increased in: SLE, some connective tissue diseases, and in

Antiphospholipid Syndrome.
Additional: Patients with acute and chronic infections
(including syphilis, HIV, Lyme disease) may also have
increased anti-cardiolipin antibodies.

Positive in: Primary Sjogren's syndrome (70%), SLE (40%),

rheumatoid arthritis (10%).
Additional: Anti-La/SS-B is another antibody against acidic
ribonucleoproteins that is less sensitive for Sjogren's (5060%) and SLE (10-15%). Patients with antibodies to SS-A
may have a negative ANA test.
increased in: Acute viral hepatitis (ALT>AST), biliary tract
obstruction (cholangitis, choledocholithiasis),
mononucleosis, alcoholic hepatitis and cirrhosis (AST>ALT),
liver abscess, metastatic or primary liver cancer, myocardial
infarction, myopathies, muscular dystrophy,
dermatomyositis, rhabdomyolysis, ischemic injury to liver
("shock liver") or hypoxia. Hepatotoxic drugs (eg, isoniazid).
Additional: Test not indicated for diagnosis of myocardial
infarction.
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Laboratory tests

Bilirubin

10/7/2013

Bilirubin, a product of
hemoglobin metabolism,
is conjugated in the liver
to the mono- and
diglucuronides and
excreted in bile. Some
conjugated bilirubin is
bound to serum albumin,
so-called D (delta)
bilirubin. Elevated serum
bilirubin occurs in liver
disease, biliary
obstruction, or
hemolysis.

Blood Urea Nitrogen (BUN) Urea, an end product of

protein metabolism, is
excreted by the kidney.
BUN is directly related to
protein intake and
nitrogen metabolism and
inversely related to the
rate of excretion of urea.
Urea concentration in
glomerular filtrate is the
same as in plasma, but
its tubular reabsorption is
inversely related to the
rate of urine formation.
Aspartate Aminotransferase Intracellular enzyme
involved in amino acid and
(AST, SGOT, GOT)
carbohydrate metabolism.
Present in large
concentrations in liver,
skeletal muscle, brain,
red cells, and heart.
Released into the
bloodstream when tissue
is damaged.
Bilirubin, a product of
Bilirubin
hemoglobin metabolism,
is conjugated in the liver
to the mono- and
diglucuronides and
excreted in bile. Some
conjugated bilirubin is
bound to serum albumin,
so-called D (delta)
bilirubin. Elevated serum
bilirubin occurs in liver
disease, biliary
obstruction, or
hemolysis.

Blood Urea Nitrogen (BUN) Urea, an end product of

C3

Normal Range: 0.1-1.2

Direct (conjugated to
glucuronide) bilirubin, 0.10.4 mg/dL (< 7 mol/L);
Indirect (unconjugated)
bilirubin, 0.2-0.7 mg/dL (<
12 mol/L) mg/dL

Normal Range: 8-20

mg/dL

Additional: Assay of total bilirubin includes conjugated

(direct) and unconjugated (indirect) bilirubin plus delta
bilirubin (conjugated bilirubin bound to albumin). It is usually
clinically unnecessary to fractionate total bilirubin. The
fractionation is unreliable by the diazo reaction and may
underestimate unconjugated bilirubin. Only conjugated
bilirubin appears in the urine and it is indicative of liver
disease; hemolysis is associated with increased
unconjugated bilirubin. Persistence of delta bilirubin in serum
in resolving liver disease means that total bilirubin does not
effectively indicate time course of resolution.
increased in: Renal failure (acute or chronic), urinary tract
obstruction, dehydration, shock, burns, CHF, gastrointestinal
bleeding. Drugs with renal toxicity, eg, gentamicin.

Additional: Urease assay

method commonly used. Decreased in: Hepatic failure, nephrotic syndrome, cachexia
BUN/Cr ratio (normally
(low-protein and high-carbohydrate diets).
12:1-20:1) decreased in
acute tubular necrosis,
advanced liver disease, low
protein intake, following
hemodialysis. BUN/Cr ratio
increased in dehydration,
GI bleeding, increased
catabolism.
Normal Range: Laboratory- increased in: Acute viral hepatitis (ALT>AST), biliary tract
specific U/L
obstruction (cholangitis, choledocholithiasis),
mononucleosis, alcoholic hepatitis and cirrhosis (AST>ALT),
liver abscess, metastatic or primary liver cancer, myocardial
infarction, myopathies, muscular dystrophy,
dermatomyositis, rhabdomyolysis, ischemic injury to liver
("shock liver") or hypoxia. Hepatotoxic drugs (eg, isoniazid).
Additional: Test not indicated for diagnosis of myocardial
infarction.
. Normal Range: 0.1-1.2 increased in: Acute or chronic hepatitis, cirrhosis, biliary
Direct (conjugated to
tract obstruction, toxic hepatitis, congenital liver enzyme
glucuronide) bilirubin, 0.1- abnormalities (Dubin-Johnson, Rotor's, Gilbert's, Crigler0.4 mg/dL (< 7 mol/L);
Najjar syndromes), fasting, hemolytic disorders. Hepatotoxic
Indirect (unconjugated)
drugs.
bilirubin, 0.2-0.7 mg/dL (<
12 mol/L) mg/dL
Additional: Assay of total bilirubin includes conjugated
(direct) and unconjugated (indirect) bilirubin plus delta
bilirubin (conjugated bilirubin bound to albumin). It is usually
clinically unnecessary to fractionate total bilirubin. The
fractionation is unreliable by the diazo reaction and may
underestimate unconjugated bilirubin. Only conjugated
bilirubin appears in the urine and it is indicative of liver
disease; hemolysis is associated with increased
unconjugated bilirubin. Persistence of delta bilirubin in serum
in resolving liver disease means that total bilirubin does not
effectively indicate time course of resolution
Normal Range: 8-20 mg/dL increased in: Renal failure (acute or chronic), urinary tract
obstruction, dehydration, shock, burns, CHF, gastrointestinal
bleeding. Drugs with renal toxicity, eg, gentamicin.

protein metabolism, is
excreted by the kidney.
BUN is directly related to
protein intake and
nitrogen metabolism and
inversely related to the
rate of excretion of urea.
Urea concentration in
glomerular filtrate is the
same as in plasma, but
its tubular reabsorption is
inversely related to the
rate of urine formation.
The classic and
Normal Range: 64-166
alternative complement mg/dL
pathways converge at the
C3 step in the
complement cascade.
Low levels indicate
activation by one or both
pathways. Most diseases
with immune complexes
will show decreased C3
levels. Test as usually

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increased in: Acute or chronic hepatitis, cirrhosis, biliary

tract obstruction, toxic hepatitis, congenital liver enzyme
abnormalities (Dubin-Johnson, Rotor's, Gilbert's, CriglerNajjar syndromes), fasting, hemolytic disorders. Hepatotoxic
drugs.

Decreased in: Hepatic failure, nephrotic syndrome, cachexia

(low-protein and high-carbohydrate diets).
Additional: Urease assay method commonly used. BUN/Cr
ratio (normally 12:1-20:1) decreased in acute tubular
necrosis, advanced liver disease, low protein intake, following
hemodialysis. BUN/Cr ratio increased in dehydration, GI
bleeding, increased catabolism.
increased in: Many inflammatory conditions as an acute
phase reactant, active phase of rheumatic diseases
(rheumatoid arthritis, SLE, etc), acute viral hepatitis,
myocardial infarction, cancer, diabetes, pregnancy,
sarcoidosis, amyloidosis, thyroiditis.
Decreased by: Decreased synthesis (protein malnutrition,
congenital deficiency, severe liver disease), or increased
catabolism (immune complex disease, membranoproliferative
glomerulonephritis [75%], SLE, Sjogren's, rheumatoid
arthritis, disseminated intravascular coagulation, paroxysmal
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Laboratory tests

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levels. Test as usually

performed is an
immunoassay (by radial
immunodiffusion or
nephelometry).

C4

Calcium

C4 is a component of the Normal Range: 15-45

classic complement
mg/dL
pathway. Depressed
levels usually indicate
classic pathway
activation.

Level of ionized calcium is Normal Range: 8.5-10.5

regulated by parathyroid mg/dL
hormone and vitamin D.
Serum calcium equals the
sum of ionized calcium
plus complexed calcium
and calcium bound to
proteins (mostly albumin).

arthritis, disseminated intravascular coagulation, paroxysmal

nocturnal hemoglobinuria, autoimmune hemolytic anemia,
gram-negative bacteremia) and increased loss (burns,
gastroenteropathies).
Additional: Complement C3 levels may be useful in following
the activity of immune complex diseases. The best test to
detect inherited deficiencies is CH50. Levels can confirm
specific C3 defect.
increased in: Various malignancies: not clinically useful.
Decreased by: Decreased synthesis, increased catabolism
(SLE, rheumatoid arthritis, proliferative glomerulonephritis,
hereditary angioedema), and increased loss (burns, proteinlosing enteropathies). Congenital deficiency.
Additional: Low C4 accompanies acute attacks of hereditary
angioedema, and C4 is used as a first-line test for the
disease. C1 esterase inhibitor levels are not indicated for the
evaluation of hereditary angioedema unless C4 is low.
Congenital C4 deficiency occurs with an SLE-like syndrome.
Test as usually performed is an immunoassay and not a
functional assay.
increased in: Hyperparathyroidism, malignancies secreting
PTH-like substances (especially squamous cell carcinoma of
lung, renal cell carcinoma), vitamin D excess, milk-alkali
syndrome, multiple myeloma, Paget's disease of bone with
immobilization, sarcoidosis, other granulomatous disorders,
familial hypocalciuria, vitamin A intoxication, thyrotoxicosis,
Addison's disease. Drugs: antacids (some), calcium salts,
chronic diuretic use (eg, thiazides), lithium, others.
Decreased in: Hypoparathyroidism, vitamin D deficiency,
renal insufficiency, pseudohypoparathyroidism, magnesium
deficiency, hyperphosphatemia, massive transfusion,
hypoalbuminemia.

CH50

Chloride

Cholesterol

Additional: Need to know serum albumin to interpret calcium

level. For every decrease in albumin by 1 mg/dL, calcium
should be corrected upward by 0.8 mg/dL.
The quantitative assay of Normal Range: Laboratory- Decreased with: >50-80% deficiency of primary pathway
hemolytic complement
specific U/mL
complement components in congenital or acquired
activity depends on the
deficiency.
ability of the primary
complement pathway to
Normal in: Deficiencies of alternative pathway, complement
induce hemolysis of red
components.
cells sensitized with
optimal amounts of antiAdditional: This is a functional assay of biologic activity.
red cell antibodies. For
Sensitivity to decreased levels of complement components
precise titrations of
depends on exactly how the test is performed. It is used to
hemolytic complement,
detect congenital and acquired severe deficiency disorders of
the dilution of serum that
the primary complement pathway.
will lyse 50% of the
indicator red cells is
determined as the CH50.
This arbitrary unit
depends on the conditions
of the assay and is
therefore laboratoryspecific.
Chloride, the principal
Normal Range: 98-107
increased in: Renal failure, nephrotic syndrome, renal tubular
inorganic anion of
meq/L
acidosis, dehydration, overtreatment with saline,
extracellular fluid, is
hyperparathyroidism, diabetes insipidus, metabolic acidosis
important in maintaining
from diarrhea (loss of HCO3), respiratory alkalosis,
normal acid-base balance
hyperadrenocorticism. Drugs: acetazolamide
and normal osmolality. If
(hyperchloremic acidosis), androgens, hydrochlorothiazide,
chloride is lost (as HCl or
salicylates (intoxication).
NH4Cl), alkalosis ensues;
if chloride is ingested or
Decreased in: Vomiting, diarrhea, gastrointestinal suction,
retained, acidosis
renal failure combined with salt deprivation, overtreatment
ensues.
with diuretics, chronic repiratory acidosis, diabetic
ketoacidosis, excessive sweating, SIADH, salt-losing
nephropathy, acute intermittent porphyria, water intoxication,
expansion of extracellular fluid volume, adrenal insufficiency,
hyperaldosteronism, metabolic alkalosis. Drugs: aldosterone,
chronic laxative or bicarbonate ingestion, corticosteroids and
ACTH (alkalosis), diuretics.
Cholesterol level is
Normal Range: Desirable increased in: Familial or polygenic hyperlipoproteinemia,
determined by lipid
< 200 Borderline 200-239 familial dysbetalipoproteinemia, familial combined
metabolism, which is in High risk > 240 mg/dL
hyperlipidemia, hyperlipoproteinemia and
turn influenced by
hyperalphalipoproteinemia, hyperlipoproteinemias secondary
heredity, diet, and liver,
to hypothyroidism, uncontrolled diabetes mellitus, nephrotic
kidney, thyroid, and other
syndrome, chronic hepatitis, biliary cirrhosis, obstructive
endocrine organ functions.
jaundice, hypoproteinemia, glomerulonephritis, chronic renal

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endocrine organ functions.

Total cholesterol (TC) =
LDLC + HDLC + TG/5
(valid only if triglyceride
[TG] < 400). Since LDL
cholesterol (LDLC) is the
clinically important entity,
it is calculated as LDLC =
TC - HDLC - TG/5, and
this is valid only if
specimen is obtained
fasting (in order to obtain
relevant triglyceride and
HDL levels).

Creatinine

Differential
Neutophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Large unstained cells

Erythrocyte Sedimentation
Rate (Sed Rate, ESR)

Endogenous creatinine is
excreted by filtration
through the glomerulus
and by tubular secretion.
Clinically, creatinine
clearance is an
acceptable measure of
glomerular filtration rate
but sometimes
overestimates GFR. For
each 50% reduction in
GFR, serum creatinine
approximately doubles.
White blood cell
differentials are now done
on automated flow
cytometry instruments in
order to provide
reproducible data. 10,000
wbcs are classified on the
basis of size and
peroxidase staining as
neutrophils, monocytes or
eosinophils (which are all
peroxidase positive) and
as lymphocytes and large
unstained cells (which are
peroxidase negative).
These large unstained
cells (LUC), larger than
normal lymphocytes, may
be atypical lymphocytes,
myeloperoxidase deficient
cells or peroxidase
negative blasts. Basophils
are identified using two
angle light scattering,
based on their singular
resistance to lysis. There
will also be an indication
of more immature
neutrophils (commonly
called a left shift) based
on the ratio of
mono/polymorphonuclear
white cells (lobularity
index).

jaundice, hypoproteinemia, glomerulonephritis, chronic renal

failure, gout, malignancy (pancreas, prostate), pregnancy,
alcoholism, glycogen storage diseases types I, III, IV,
anorexia nervosa, GH deficiency, dietary excess. Drugs:
androgens, chlorpropamide, corticosteroids, oral
contraceptives, phenytoin, progestins, thiazides, others.
Decreased in: Acute hepatitis, alcoholic cirrhosis, Gaucher's
disease, hyperthyroidism, acute infections, anemia,
malnutrition, alphalipoprotein deficiency (Tangier disease),
malignancy (liver), severe acute illness, extensive burns,
COPD, rheumatoid arthritis, mental retardation, intestinal
lymphangiectasia, apolipoprotein deficiency.

Normal Range: 0.6-1.2

mg/dL

Additional: It is important to treat the cause of secondary

hypercholesterolemia (hypothyroidism, etc). National
Cholesterol Education Program Expert Panel has published
clinical recommendations for cholesterol management.
increased in: Acute or chronic renal failure; urinary tract
obstruction, nephrotoxic drugs.
Decreased in: Reduced muscle mass, possible drug effect.
Additional: In alkaline picrate method, substances other than
Cr (eg, acetoacetate, acetone, b-hydroxybutyrate, aketoglutarate, pyruvate, glucose) may give falsely high
results. Therefore, patients with diabetic ketoacidosis may
have spuriously elevated Cr. Cephalosporins may spuriously
increase or decrease Cr measurement. Increased bilirubin
may spuriously decrease Cr.

Normal Range:
1.8-6.8 K/mL
0.9-2.9 K/mL
0.1-0.6 K/mL
0-0.4 K/mL
0-0.1 K/mL
0-0.2 K/mL

A left shift usually suggests infection (rarely leukemia). The

reproducibility of 100 cell manual differentials is notoriously
poor, because of statistical error in counting and observer
variation, however, review of blood smears is useful to visually
identify rare abnormal cells, blasts, nucleated rbcs,
morphologic abnormalities e.g., hypersegmentation, toxic
granulation, sickle cells, target cells, spherocytes, basophilic
stippling, and to look for rouleau (stacking of red cells due to
increased globulins) and clumped platelets. White blood cell
differential is unlikely to be abnormal with a normal wbc
count or to be changed if the total wbc count is unchanged.
Increased neutrophils: suggests infection (bacterial or early
viral, rarely leukemia), acute stress, acute and chronic
inflammations, tumor, drugs, DKA.
Decreased neutrophils: suggests aplastic anemia, druginduced neutropenia (e.g., chloramphenicol, phenothiazine,
antithyroid drugs, sulphonamide), folate or B12 deficiency,
Chediak-Higashi syndrome, malignant lymphoproliferative
disease, physiologic in children up to 4 years.
Increased lymphocytes: viral infection (especially, infectious
mononucleosis, pertussis), thyrotoxicosis, adrenal
insufficiency disease (ALL, CLL), chronic infection, drug and
allergic reactions, autoimmune disease.
Decreased lymphocytes: immune deficiency syndrome.
Comments:
Increased monocytes: inflammation, infection, malignancy,
TB, myeloproliferative disorders.
Decreased monocytes: depleted in overwhelming bacterial
infection.
Increased eosinophils: allergic states, drug sensitivity
reaction, skin disorders, tissue invasion by parasites,
periarteritis nodosa, hypersensitivity response to malignancy
(e.g. Hodgkin's disease), pulmonary infiltrative disease,
disseminated eosinophilic hypersensitivity disease.
Decreased eosinophils: acute and chronic inflammation,
stress, drugs: steroids.

Increased basophils: hypersensitivity reactions, drugs,

myeloproliferative disorders (CML, polycythemia vera),
myelofibrosis.
Erythrocytes in plasma Normal Range: Male: < 10 increased in: Infections (osteomyelitis, pelvic inflammatory
usually settle slowly.
Female: < 15
disease [75%]), inflammatory disease (temporal arteritis,
However, if they aggregate
polymyalgia rheumatica, rheumatic fever), malignant
for any reason (usually
neoplasms, paraproteinemias, anemia, pregnancy, chronic
because of plasma
renal failure, GI disease (ulcerative colitis, regional ileitis).
proteins called acute
phase reactants, eg,
Decreased in: Polycythemia, sickle cell anemia,
fibrinogen), they settle
spherocytosis, anisocytosis, hypofibrinogenemia,
rapidly. Sedimentation of
hypogammaglobulinemia, congestive heart failure,

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Laboratory tests

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rapidly. Sedimentation of
RBCs occurs because of
their greater density than
plasma. ESR measures
the distance in mm that
erythrocytes fall during 1
hour.

Gamma-Glutamyl
Transpeptidase (GGT)

Glucose

Hematocrit

Hemoglobin

Immunoglobulins (IG)

hypogammaglobulinemia, congestive heart failure,

microcytosis, drugs (high dose corticosteroids). Low value of
no diagnostic significance.

Additional: There is a good correlation between ESR and Creactive protein, but ESR is less expensive. Test is useful
and indicated only for diagnosis and monitoring of temporal
arteritis and polymyalgia rheumatica. The test is not
sensitive or specific for other conditions. ESR is higher in
women and older persons.
U/LGGT is an enzyme
Normal Range: Laboratory- increased in: Liver disease: acute viral or toxic hepatitis,
present in liver, kidney, specific
chronic or subacute hepatitis, cirrhosis, biliary tract
and pancreas. It transfers
obstruction (intrahepatic or extrahepatic), primary or
C-terminal glutamic acid
metastatic liver neoplasm, alcoholic hepatitis,
from a peptide to other
mononucleosis. Drugs (by enzyme induction): phenytoin,
peptides of L-amino acids.
barbiturates, alcohol.
It is induced by alcohol
intake and is an
Additional: Useful in follow up of alcoholics undergoing
extremely sensitive
treatment. Test sensitive to modest alcohol intake. Test
indicator of liver disease,
positive in 90% of patients with liver disease. Used to confirm
particularly alcoholic liver
hepatic origin of elevated serum alkaline phosphatase.
disease.
Normally, the glucose
. Normal Range: 60-115 increased in: Diabetes mellitus, Cushing's syndrome (10concentration in
mg/dL
15%), chronic pancreatitis (30%) Drugs: corticosteroids,
extracellular fluid is
phenytoin, estrogen, thiazides
closely regulated so that
a source of energy is
Decreased in: Pancreatic islet B cell disease with increased
readily available to tissues
insulin, insulinoma, adrenocortical insufficiency,
and no glucose is
hypopituitarism, diffuse liver disease, malignancy
excreted in the urine
(adrenocortical, stomach, fibrosarcoma), infant of diabetic
mother, enzyme deficiency diseases (galactosemia, etc).
Drugs: insulin, ethanol, propranolol, sulfonylureas,
tolbutamide, other hypoglycemic agents.

The hematocrit represents Normal Range: Male: 39the percentage of whole 49 Female: 35-45 Ageblood volume made up by dependent
erythrocytes. Laboratory
instruments calculate the
Hct from the erythrocyte
count and the MCV, ie,
Hct = RBC x MCV.

Hemoglobin is the major Normal Range:

protein of erythrocytes
Male: 13.6-17.5
and transports oxygen
Female: 12.0-15.5
from the lungs to
peripheral tissues. It is
measured by
spectrophotometry on
automated instruments
after hemolysis of red
cells and conversion of all
hemoglobin to
cyanmethemoglobin.

Additional: Diagnosis of diabetes mellitus is consistent with

a fasting plasma glucose >140 mg/dL on more than one
occasion. Hypoglycemia is defined as glucose <50 mg/dL in
men and <40 mg/dL in women.
increased in: Hemoconcentration (as in dehydration, burns,
vomiting), polycythemia, extreme physical exercise.
Decreased in: Anemia: macrocytic (liver disease,
hypothyroidism, vitamin B12 deficiency, folate deficiency),
normocytic anemia (early iron deficiency, anemia of chronic
disease, hemolytic anemia, acute hemorrhage) and
microcytic anemia (iron deficiency, thalassemia).
Additional: Conversion from hemoglobin to hematocrit is
roughly Hgb x3 = Hct. Hematocrit reported by clinical
laboratories is not a spun hematocrit. The spun hematocrit
may be spuriously high if the centrifuge is not calibrated, if
the specimen is not spun to constant volume, or if there is
"trapped plasma."
Hemoglobin is increased in: Hemoconcentration (as in
dehydration, burns, vomiting), polycythemia, extreme
physical exercise, heavy smoking (due to presence of
nonfunctional carboxyhemoglobin).
Hemoglobin is decreased in: Anemia: macrocytic (liver
disease, hypothyroidism, vitamin B12 deficiency, folate
deficiency), normocytic anemia (early iron deficiency, anemia
of chronic disease, hemolytic anemia, acute hemorrhage)
and microcytic anemia (iron deficiency, thalassemia).

Additional: Hypertriglyceridemia and very high WBC counts

can cause false elevations of Hgb.
IgG makes up about 85% Normal Range: IgA: 78-367 increased in: IgG: Polyclonal: Autoimmune diseases (eg,
of total serum
mg/dL IgG: 583-1761
SLE, RA), sarcoidosis, chronic liver diseases, some
immunoglobulins and
mg/dL IgM: 52-335 mg/dL parasitic diseases, chronic or recurrent infections.
predominates late in
Monoclonal: Multiple myeloma (IgG type), lymphomas or
immune responses. It is
other malignancies. IgM: Polyclonal: Isolated infections such
the only immunoglobulin
as viral hepatitis, infectious mononucleosis, early response
to cross the placenta. IgM
to bacterial or parasitic infection. Monoclonal: Waldenstrom's
antibody predominates
macroglobulinemia, lymphoma. IgA: Polyclonal: Chronic liver
early in immune
disease, chronic infections (especially of the GI and
responses. Secretory IgA
respiratory tracts). Monoclonal: Multiple myeloma (IgA).
plays an important role in
host defense mechanisms
Decreased in: IgG: Immunosuppressive therapy, genetic
by blocking transport of
(severe combined immunodeficiency, Wiskott-Aldrich
microbes across mucosal
syndrome, common variable immunodeficiency). IgM:
surfaces.
Immunosuppresive therapy. IgA: Inherited IgA deficiency
(ataxia telangiectasia, combined immunodeficiency
disorders).

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Laboratory tests

Iron

Iron Binding Capacity

Lactate Dehydrogenase
(LDH)

Magnesium

Mean Corpuscular
Hemoglobin (MCH)

10/7/2013

Plasma iron concentration Normal Range: 50-175

is determined by
g/dL
absorption from intestine;
storage in intestine, liver,
spleen, bone marrow; rate
of breakdown or loss of
hemoglobin; rate of
synthesis of new
hemoglobin.

Iron is transported in
Normal Range: 250-460
plasma complexed to the g/dL
metal-binding globulin,
transferrin, which is
synthesized in the liver.
Total iron binding capacity
is calculated from
transferrin levels
measured
immunologically. Each
molecule of transferrin has
two iron-binding sites, so
its iron binding capacity is
1.47 mg/g. Normally,
transferrin carries an
amount of iron
representing about 16?
60% of its capacity to
bind iron, ie, % saturation
of iron binding capacity is
16-60%.
LDH is an enzyme that Normal Range: Laboratorycatalyzes the
specific
interconversion of lactate
and pyruvate in the
presence of NAD/NADH.
It is widely distributed in
body cells and fluids and
since its RBC/plasma
ratio is high, it is
spuriously elevated in
plasma/serum following
hemolysis.

Magnesium is primarily an Normal Range: 1.8-3

intracellular cation
mg/dL
(second most abundant,
60% found in bone). In
extracellular fluid, it
influences neuromuscular
response and irritability. A
magnesium deficit may
exist with little or no
change apparent in serum
level.

MCH calculated from

Normal Range: 26-34 pg
measured values of Hb
and RBC; ie, MCH =
Hb/RBC. A low MCH can
mean hypochromia or
microcytosis or both. A
high MCH is evidence of
macrocytosis.

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Additional: IgG deficiency is associated with recurrent and

occasionally severe pyogenic infections. Most common form
of multiple myeloma is the IgG type.
increased in: Hemochromatosis, hemosiderosis (eg, multiple
transfusions, excess iron administration), hemolytic anemia,
pernicious anemia, aplastic or hypoplastic anemia, viral
hepatitis, lead poisoning, thalassemia. Drugs: dextran,
estrogens, ethanol, oral contraceptives.
Decreased in: Iron deficiency, nephrotic syndrome, chronic
renal failure, many infections, active hematopoiesis,
remission of pernicious anemia, hypothyroidism, malignancy
(carcinoma), postoperative state, kwashiorkor, drugs.
Additional: Used in evaluation of iron deficiency (see TIBC
and Ferritin).
increased in: Iron deficiency anemia, late pregnancy, infancy,
hepatitis. Drugs: oral contraceptives.
Decreased in: Hypoproteinemic states (eg, nephrotic
syndrome, starvation, malnutrition, cancer), chronic
inflammatory disorders, chronic disease, chronic liver
disease.
Additional: Increased % transferrin saturation with iron: in
iron overload (iron poisoning, hemolytic anemia, sideroblastic
anemia, thalassemia, hemochromatosis, pyridoxine
deficiency, aplastic anemias). Decreased % transferrin
saturation with iron: in iron deficiency (usually saturation
<16%). Transferrin levels can also be used to assess
nutritional status.

increased in: Tissue necrosis, especially in acute injury of

cardiac muscle, RBCs, kidney, skeletal muscle, liver, lung,
skin. Commonly elevated in various carcinomas and in
Pneumocystis carinii and B cell lymphoma in AIDS. Marked
elevations occur in hemolytic anemias, vitamin B12
deficiency anemia, folate deficiency anemia, polycythemia
vera, acute (but not chronic) hepatitis, cirrhosis, obstructive
jaundice, renal disease, musculoskeletal disease, CHF.
Drugs causing hepatotoxicity or hemolysis.
Decreased in: Clofibrate, fluoride (low dose).
Additional: LDH is elevated after myocardial infarction (2-7
days), in liver congestion (eg, in CHF) and in Pneumocystis
carinii pneumonitis. LDH is not a useful liver function test and
it is not specific enough for the diagnosis of hemolytic or
megaloblastic anemias. Its main diagnostic use is in
myocardial infarction in which the CKMB elevation has
passed. With the availability of specific LD1 measurements,
the total LD level may no longer be useful.
increased in: Dehydration, tissue trauma, renal failure;
hypoadrenocorticism; hypothyroidism. Drugs: aspirin
(prolonged use), lithium, magnesium salts, progesterone,
triamterene, vitamin D (renal failure).
Decreased in: Chronic diarrhea, enteric fistula, starvation,
chronic alcoholism, chronic liver disease, total parenteral
nutrition with inadequate replacement, hypoparathyroidism
(especially post-parathyroid surgery), high-dose vitamin D
and calcium therapy, acute pancreatitis, delirium tremens,
chronic glomerulonephritis, hyperaldosteronism, diabetic
ketoacidosis, SIADH, pregnancy. Drugs: albuterol,
amphotericin B, calcium salts, cisplatin, citrates (blood
transfusion), cyclosporine, diuretics, ethacrynic acid.
Additional: Mg2+ concentration is determinated by intestinal
absorption, renal excretion, and exchange with bone and with
intracellular fluid.
increased in: Macrocytosis.
Decreased in: Microcytosis (iron deficiency, thalassemia).
Hypochromia (lead poisoning, sideroblastic anemia, anemia
of chronic disease).

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Laboratory tests

Mean Corpuscular
Hemoglobin Concentration
(MCHC)

Mean Corpuscular Volume

(MCV)

10/7/2013

MCHC describes how fully Normal Range: 31-36 g/dL

the erythrocyte volume is
filled with hemoglobin and
is calculated from
measurement of
hemoglobin (Hb), mean
corpuscular corpuscular
volume (MCV) and red cell
count (RBC); ie, MCHC =
Hb/MCV x RBC.
Average volume of the red Normal Range: 80-100 fL
cell is measured by
automated instrument, by
electrical impedance or by
light scatter.

increased in: Marked spherocytosis. Spuriously increased in

autoagglutination, hemolysis (with spuriusly high Hb or low
MCV or RBC), lipemia. Cellular dehydration syndromes,
xerocytosis.
Decreased in: Hypochromic anemia (iron deficiency,
thalassemia, lead poisoning), sideroblastic anemia, anemia
of chronic disease. Spuriously decreased in high WBC (with
spuriously low Hgb or high MCV or RBC).
increased in: Liver disease, megaloblastic anemia (folate,
B12 deficiencies), reticulocytosis, newborn. Drugs:
phenytoin. Spurious increase in autoagglutination, high
WBC.
Decreased in: Iron deficiency, thalassemia; decreased or
normal in anemia of chronic disease.

Additional: MCV can be normal in combined iron and folate

deficiency. In patients with two red cell populations
(macrocytic and microcytic), MCV may be normal.
Patient's
plasma
is
Normal
Range:
25-35
increased in: Deficiency of any individual coagulation factor
Partial Thromboplastin Time
activated to clot in vitro by (range varies) Panic > = 60 except XIII and VII, nonspecific inhibitors (lupus-like
mixing it with phospholipid seconds
anticoagulant), specific factor inhibitors, von Willebrand's
and an activator
disease (may also be normal), hemophilia A and B,
substance. Screens the
disseminated intravascular coagulation. Drugs: heparin,
intrinsic coagulation
warfarin.
pathway and adequacy of
all coagulation factors
Decreased in: Hypercoagulable states, DIC.
except XIII and VII. PTT is
usually abnormal if level of
Comments: PTT is the best test to monitor adequacy of
any factor falls below 30heparin therapy. Test not always abnormal in von
40% of normal.
Willebrand's disease. Test may be normal in chronic DIC.
Very common cause of prolongation is spurious presence of
heparin in sample.
The
plasma
concentration
Normal
Range:
2.5-4.5
increased in: Renal failure, massive blood transfusion,
Phosphorous
of inorganic phosphate is mg/dL
sarcoidosis, neoplasms, adrenal insufficiency, acromegaly,
determined by parathyroid
hypoparathyroidism, hypervitaminosis D, phosphate infusions
gland function, action of
or enemas, osteolytic metastases to bone, leukemia, milkvitamin D, intestinal
alkali syndrome, healing bone fractures,
absorption, renal function,
pseudohypoparathyroidism, diabetes mellitus with ketosis,
bone metabolism, and
malignant hyperpyrexia, cirrhosis, lactic acidosis, respiratory
nutrition.
acidosis. Drugs: eg, anabolic steroids, ergocalciferol,
furosemide, hydrochlorothiazide and others.

Platelet Count

Potassium

Decreased in: Hyperparathyroidism, hypovitaminosis D

(rickets, osteomalacia), malabsorption (steatorrhea);
malnutrition, starvation or cachexia; GH deficiency, chronic
alcoholism, severe diarrhea, vomiting, nasogastric suction,
severe hypercalcemia (any cause), acute gout, osteoblastic
metatases to bone, severe burns (diuretic phase), respiratory
alkalosis, hyperalimentation with inadequate phosphate
repletion, carbohydrate administration (intravenous), renal
tubular acidosis and other renal tubular defects, diabetic
ketoacidosis (during recovery), acid-base disturbances,
hypokalemia, pregnancy, hypothyroidism; prolonged use of
thiazides, glucose infusion, salicylates (toxicity). Drugs: eg,
phosphate-binding antacids, anticonvulsants, estrogens,
isoniazid, oral contraceptives.
Platelets are released
Normal Range: 150-450 X increased in: Myeloproliferative disorders: polycythemia vera,
from megakaryocytes in 10 3/uL
CML, essential thrombocythemia, myelofibrosis, after
bone marrow, and they
bleeding, postsplenectomy, reactive thrombocytosis
are important for adequate
secondary to inflammatory diseases.
hemostasis. Platelet
counting is done by flow
Decreased in: Decreased production: bone marrow
cytometer based on size
suppression or replacement, chemotherapeutic agents, other
discrimination using either
drugs, eg, ethanol. Increased destruction or removal:
electrical impedance or
splenomegaly, DIC, platelet antibodies (ITP, posttransfusion
electro-optical systems.
purpura, neonatal isoimmune thrombocytopenia, drugs (eg,
quinidine, cephalosporins).
Normal Range: 3.5-5.0
Potassium is
meq/L
predominantly an
intracellular cation whose
plasma level is regulated
by renal excretion. Plasma
concentration determines
neuromuscular and
muscular irritability.
Elevated or depressed
potassium concentrations
interfere with muscle
contraction.

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Laboratory tests

10/7/2013

increased in: Massive

hemolysis, severe tissue
damage, rhabdomyolysis,
acidosis, dehydration,
acute or chronic renal
failure, Addison's disease,
renal tubular acidosis type
IV (hyporeninemic
hypoaldosteronism),
hyperkalemic familial
periodic paralysis. Drugs:
potassium salts,
potassium-sparing
diuretics (spironolactone,
triamterene), non-steroidal
anti-inflammatory drugs,
beta-blockers, ACE
inhibitors.
Decreased in: Low
potassium intake,
prolonged vomiting or
diarrhea, renal tubular
acidosis (types I, II),
hyperaldosteronism,
Cushing's syndrome,
osmotic diuresis (eg, of
hyperglycemia), alkalosis,
familial periodic paralysis,
diuretic therapy.

Protein

Prothrombin Time

Rheumatoid Factor

The plasma protein

concentration is
determined by the
nutritional state, hepatic
function, renal function,
and various disease
states and hydration. The
plasma protein
concentration determines
colloidal osmotic
pressure.

Additional: Spurious K+
can occur with hemolysis
of sample, delayed
separation of plama from
erythrocytes, prolonged fist
clenching during blood
drawing, tourniquet placed
for prolonged periods, and
very high white cell or
platelet counts.
Normal Range: 6-8 g/dL increased in: Polyclonal or monoclonal gammopathies,
marked dehydration. Drugs: anabolic steroids, androgens,
corticosteroids, epinephrine.

PT screens the extrinsic Normal Range: 11-15

pathway of the
seconds
coagulation system. It is
performed by adding
calcium and tissue
thromboplastin to a
sample of citrated,
platelet-poor plasma and
measuring the time
required for fibrin clot
formation. It is most
sensitive to deficiencies in
the vitamin K-dependent
clotting factors II, VII, and
X. It is also sensitive to
deficiencies of factor V. It
is insensitive to fibrinogen
and not affected by
heparin. It is used to
monitor warfarin therapy.
Heterogeneous
Normal Range: Negative
autoantibodies usually of (<1:16)
the IgM class that react
against the Fc region of
human IgG.

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Decreased in: Protein-losing gastroenteropathies, acute

burns, nephrotic syndrome, severe dietary protein deficiency,
chronic liver disease, malabsorption syndrome,
agammaglobulinemia.
Additional: The serum total protein consists primarily of
albumin and globulin. Hypoproteinemia usually means
hypoalbuminemia, since albumin is the major serum protein.
Globulin is calculated as total protein minus albumin.
increased in: Liver disease, vitamin K deficiency,
intravascular coagulation, circulating anticoagulant, massive
blood volume replacement. Drugs: warfarin.
Additional: In liver disease, the PT reflects the hepatic
capacity for protein synthesis. PT responds rapidly to altered
hepatic function because the serum half-lives of factors II and
VII are short (hours). Routine preoperative measurement of
PT is unnecessary unless there is clinical history of a
bleeding disorder. Efforts to standardize and report the
prothrombin time as an INR (International Normalized Ratio)
depend on assigning reagents an International Sensitivity
Index (ISI) so that INR = [PT patient/PT normal]ISI. However,
assignment of incorrect ISI by reagent manufacturers has in
fact caused a greater lack of standardization.

Positive in: Rheumatoid arthritis (75-90%), Sjogren's (8090%), scleroderma, dermatomyositis, SLE (30%),
sarcoidosis, Waldenstrom's macroglobulinemia. Drugs:
methyldopa, others. Low titer can be found in healthy older
patients (20%). 1-4% of normals and in a variety of acute
immune responses (eg, viral infections, infectious
mononucleosis, and viral hepatitis), chronic infections
(tuberculosis, leprosy, subacute bacterial endocarditis) and
chronic active hepatitis.

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Laboratory tests

Sodium

Uric Acid

White Blood Count (WBC,

Leukocyte count)

10/7/2013

Sodium is the
Normal Range: 135-145
predominant extracellular meq/L
cation. Serum sodium
level is primarily
determined by the volume
status of the individual.
Hyponatremia can be
divided into hypovolemia,
euvolemia, and
hypervolemia categories.

Additional: It can be useful in differentiating rheumatoid

arthritis from other chronic inflammatory arthritides. However,
a positive RF test is only one of several criteria needed to
make the diagnosis of rheumatoid arthritis.
increased in: Dehydration (excessive sweating, severe
vomiting or diarrhea), polyuria (diabetes mellitus, diabetes
insipidus), hyperaldosteronism, inadequate water intake
(coma, hypothalamic disease). Drugs: steroids, licorice, oral
contraceptives.
Decreased in: Congestive heart failure, cirrhosis, vomiting,
diarrhea, excessive sweating (with replacement of water but
not salt); salt-losing nephropathy, adrenal insufficiency,
nephrotic syndrome, water intoxication, SIADH. Drugs:
thiazides, diuretics, ACE inhibitors, chlorpropamide,
carbamazepine.

Additional: Spurious hyponatremia produced by severe

lipemia and hyperproteinemia if sodium analysis involves a
dilution step. Sodium falls about 1.6 mmol/L for each 100
mg/dL increase in blood glucose. Hyponatremia in a
normovolemic patient with urine osmolality higher than
plasma osmolality suggests the possibility of SIADH,
myxedema, hypopituitarism, or reset osmostat.
Uric acid is an end
Normal Range: Males: 2.4- increased in: Renal failure, gout, myeloproliferative disorders
product of nucleoprotein 7.4 Females 1.4-5.8 mg/dL (leukemia, lymphoma, myeloma, polycythemia vera),
metabolism and is
psoriasis; glycogen storage disease (type I); Lesch-Nyhan
excreted by the kidney.
syndrome (X-linked hypoxanthine-guanine
An increase in serum uric
phosphoribosyltransferase deficiency); lead nephropathy.
acid concentration occurs
Drugs: antimetabolite and chemotherapeutic agents,
with increased
diuretics, ethanol, nicotinic acid, salicylates (low dose).
nucleoprotein synthesis or
catabolism (blood
Decreased in: SIADH, xanthine oxidase deficiency, lowdyscrasias, therapy of
purine diet. Fanconi's syndrome, neoplastic disease (various,
leukemia) or decreased
causing increased renal excretion), liver disease. Drugs:
renal excretion (eg, with
salicylates (high dose), allopurinol (xanthine oxidase
use of thiazide diuretics or
inhibitor).
renal failure).
Additional: Sex and age affect uric acid levels. The incidence
of hyperuricemia is greater in some racial groups (eg,
Filipinos) than others (Whites).
Measure of the total
Normal Range: 3.4-10 K/L increased in: Infection, inflammation, hematologic
number of leukocytes in
malignancy, leukemias (AML, ALL, CML, CLL), lymphoma.
whole blood. Counted on
Drugs: corticosteroids.
automated instruments
using light scattering or
Decreased in: Aplastic anemia (decreased production), B12
electrical impedance after
or folate deficiency (maturation defect), sepsis (decreased
lysis of RBCs. WBCs are
survival). Drugs: phenothiazines, chloramphenicol,
distinguished from
aminopyrine.
platelets by size.
Additional: Spurious increase: with high number of nucleated
red cells.

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