Test Normal Value Clinical Significance

values increases in prostatic cancer , some

Acid Phosphatase liver diseases , hyper para thyroidism ,
0.1 - 5.0 U/dl hemolytic anemia,sickle cell crisis
(ACP)
Values are decreased in Down syndrome

Increases in some liver and bone diseases ,

Alkaline phospatase hyper para thyroidism , pregnancy
4 -13 U/dl
(ALP) Decreases in cretinism , growth retardation
,scurvy , achondroplasia

In amniotic fluid and maternal blood values

increase with the faulty development of the
fetal nervous system especially neural tube
Alpha feto protien Non pregnant
defect such as spina bifida
adult
(AFP) <25 ng /ml
In non pregnant adult values increases in
liver cancer ,cirrhosis , chronic active
hepatitis

Alanin amino transferase(ALT)

Increases in liver diseases , liver damage due
5 - 40 U/L
Serum glutamic - pyrudic to toxic drugs
transaminase (SGPT )
Incease in miocardial infraction ,liver
Aspartate amino
disease ,trauma to skeletal muscles, sever
transferase(AST)
burn
5-40 U/L
Serum glutamic -
Decrease in beriberi ,uncontrolled diabetes
oxaloacetic transaminas(SGOT)
mellitus with acidosis

Increase in liver disease ,heart failure ,

Ammonia 20 - 120 mg/dl Emphysema ,pneumonia ,corpulmonale
,erithroblastosis fetalis

Increase in acute pancreatitis ,momps

,obstruction of pancreatic duct
Amylase 25 -125 U/Lit
Decrease in hepatitis , cirrhosis , toxemia of
pregnancy
 Conjugated : Increase in conjugated bilirubin probably
<0.5 mg/dl results from lived dysfunction or biliary
Unconjugated : obstruction
Bilirubin
0.2 - 1.0 mg/dl
Newborn : Increase in unconjugated bilirubin probably
1.0 - 12.o mg/dl results from excessive hemolysis of RBCs

Increase in kidney disease ,shock

,dehydration ,diabetes ,acute myocardial
Blood urea and nitrogen (BUN infraction
8 - 26 mg/dl
)
Decrease in liver failure ,impaired
absorbtion ,over hydration

Increase in cancer ,hyperparathyroidism ,

Total Addison's disease ,hyperthyroidism , Paget's
9 - 11 mg/dl disease
Calcium ( Ca / Ca2+)
Ionized
4.5 - 5.5 mg/dl Decrease in hypoparathyrodism ,chronic
renal failure ,osteomalacia ,rickets ,diarrhea

Arterial Increase in severe vomiting ,emphysima

19 - 24 mEq/l ,eldosteronism
Carbon dioxide (CO2) Venous
22 - 26 mEq/l Decrease in severe diarrhea ,starvation ,acute
renal failure

Increase in hypoventilation ,obstructive lung

Arterial
disease ,emphysema
Carbon dioxide partial pressure 35 - 40 mm Hg
(pCO2) Venous
Decrease in hyper ventilation ,hypoxia and
45 mm Hg
pregnancy

Increase in carcinoma of colon ,recrom

,breast, ovary ,liver and
Cacinoembrionic antigen (CEA) <3 ng /ml
pancreas,inflammatoy bowel
disease,cirrhosis ,chronic cigarette smoking
Increases in myxedema ,diabetes
Carotene beta 40 - 200 mg/dl mellitus,excessive dietary intake
Decrease in fat mal absorbtion ,liver disease
 ,poor dietary intake
Increase in dehydration ,Cushing's syndrome
,anemia
Chloride ion (Cl-) 95 - 103 mEq / Lit
Decrease in severe vomiting ,severe burns
,diabetic acidosis ,fever
Increase in diabetes mellitus ,cardio vascular
disease , nephrosis , hypothyroidism
Decrease in liver disease ,hyperthyroidism ,
Cholesterol Total <200 mg/dl
fat mal absorption ,pernicious anemia ,severe
infections ,terminal stages of cancer

HDL Cholesterol >40 mg/dl

LDL Cholesterol <130 mg/dl
8AM - 10 AM
5 - 23 Increase in hyperthyroidism , obesity , stress
microgram/dl ,Cushing's syndrome
Cortisol(Hydro cortisone)
4PM - 6PM Decrease in hypothyroidism ,liver disease
3 -13 ,Addison's disease
microgram/dl
Male
0.1 - 0.4 mg/dl Increase in muscular dystrophy , damage to
Creatine
Female muscle tissue ,nephritis and pregnancy
0.2 - 0.7 mg/dl
Male Increase in myocardial infarction ,
Creatine kinase (CK)
55 - 170 U/Lit progressive muscular dystrophy , myxedema
or
Female , convulsions , hypothyroidism pulmonary
Creatine phospho kinase (CPK)
30 - 135 U/Lit edema
Increase in impaired renal function ,
gigantism ,acromaegaly
Creatinine 0.5 - 1.2 mg/dl
Decrease in muscular dystrophy

Newborns
60 - 90 %
Increase in thalassemia ,sickle cell anemia ,
Before age 2
Fetal hemoglobin leakage of fetal blood into maternal blood
0-4%
stream
Adults
0-2%
Increase in obstruction of bile duct ,cirrhosis
Gamma - glutamyl transferase of liver , metastatic cancer of liver
5 - 40 IU/Litr
(GGT) ,congestive heart failure , alcoholism , coli
lithiasis
Fasting Increase in diabetes mellitus ,acute stress ,
70 - 110 mg /dl hyperthyroidism , chronic liver disease
Glucose ,nephritis
Random Decrease in Addison's disease
80 - 120 mg/dl ,hypothyroidism ,cancer of pancreas
 Immunoglobulin Increase in infections of all type, liver
800 - 1801 mg/dl
IgG disease , severe malnutrition
Increase in liver cirrhosis , chronic infections
Immunoglobulin , auto-immune disorders
113 - 563 mg/dl
IgA Decrease in immunologic deficiency states

Immunoglobulin
Increase in trypanosomiasis
IgM 54 - 222 mg/dl
Decrease in lymphoid aplasia
Immunoglobulin
0.5 - 3 mg/dl Increase in chronic infections , myelomas
IgD
Immunoglobulin Increase in hay fever ,asthma , anaphylactic
0.01 - 0.4 mg/dl
IgE shock
Increase in liver disease , various anemia

Iron ,total 50 - 170 microgram/dl Decrease in iron deficiency anemia

Increase in iron deficiency anemia , blood loss

,pregnancy ,in women taking birth control pills
Iron-binding capacity , 300 - 420 microgram
total (TIBC) /dl
Decrease in many chronic diseases , wide spread
cancer , mal nutrition ,nephrotic syndrome
Negative
Increase in keto acidosis ,fever ,anorexia ,fasting
Ketone bodies ,starvation ,high fat diet ,low carbohydrate diet ,
Toxic level
following vomiting
20 mg/dl
Arterial
3 - 7 mg/dl
Increase during Muscular activity ,congestive
Lctic acid(Lactate)
heart failure ,shock ,severe hemorrhage
Venous
5 - 20 mg/dl
Increase in myocardial infarction ,liver
Lactic dehydrogenase
71 - 207 IU/litr disease,skeletal muscle necrosis , extensive
(LDH)
cancer
Increase in hyperlipidemia , diabetes mellitus
Lipids ,hypothyroidism
400 - 800 mg / dl
Total Decrease in fat mal absotbtion

Lipids
150 - 220mg/dl
Cholesterol
 Lipids
10 - 190 mg/dl
Triglycerides
Increase in cirrhosis ,congestive hear failure
,high protein diet
285 - 295 mOsm/kg
Osmolality
water
Decrease in aldosteronism ,diabetes insipidus
,hypercalcemia
Increase in polycythemya
Arterial
Oxygen (O2)
15 - 23 Volume %
Decrease in chronic obstructive lung disease
Increase in polycythemia , hyperventilation
Oxygen partial Arterial
pressure(pO2) 80 - 105 mm Hg Decrease in anemia , insufficient atmospheric
oxygen , hypoventilation
Increase in vomiting ,hyperventilation ,excessive
bicarbonate , lack of oxygen
Arterial
pH
7.35 - 7.45
Decrease in renal failure , diabetic ketoacidosis,
hypoxia , airway obstruction ,shock
Increase in renal failure hypoparathyroidism
Adults
,hypocalcemia , bone tumors , diabetic
2.5 - 4.5 mg/dl
Phosphorous , inorganic ketoacidosis ,acromagaly
(P)
Children
Decrease in hyperparathyroidism ,alcoholism
4-7 mg/dl
,rickets ,osteomalacia
Increase in dehydration ,shock , systemic lupus
erythematosus (SLE) , rheumatoid arthritis (RA)
, chronic infections , chronic liver disease
Protein , Total 6 - 7.8 g/dl
Decrease in insufficient protein intake
,hemorrhage, mal absorbtion , diarrhea , chronic
renal failure ,severe burns
Albumin 3.5 - 5.0 g/dl
Globulin 2.3 - 3.5 g/dl
Reversed A/G may indicate chronic liver disease
A/G ratio 1.5 : 1 to 2.5 : 1 , leukemia , Hodgkin's Disease ,Tuberculosis
(TB ),chronic hepetitis
Increase in dehydration ,aldosteronism , coma
,Cushing's disease ,diabetes insipidus
Sodium (Na+) 136 - 142 mEq/litr
Decrease in severe burns , vomiting ,diarrhea ,
Addison's disease ,nephritis , excessive sweating
, edema
Thyroid Hormone 80 - 200 ng/dl Increase in hyperthyroidism
 T3
(Triiodothyronine ) Decrease in hypothyroidism
Thyroid Hormone Increase in hyperthyroidism
T4 4 - 11microgram / dl
(Thyroxine ) Decrease in hypothyroidism
Thyroid stimulating
0.3 - 4.0 mU/Lit
hormone(TSH)
Increase in hypothyroidism
Thyroxine binding
10 -26 microgram /dl Decrease in hyperthyroidism
globulin (TBG )

Male Increase in impaired renal function , gout

4.0 - 8.5 mg/dl ,metastatic cancer , shock, starvation
Uric acid (urate)
Female Decrease in person treated with
2.7 - 7.3 mg/dl uricosuric drugs

Increase in Thrombocytopenia ,severe liver disease

Bleeding time 4 - 8 mints
,aplastic anemia

Female Under 50 yrs

Increase in pregnancy ,infection ,carcinoma
<20 mm/Hr
,tissue destruction , nephritis
Female over 50 years
Decrease in sickle cell anemia , congestive heart
30 mm/Hr
Erythrocyte failure
sedimentation rate
Male under 50 years
( ESR )
<15 mm/Hr

Male over 50 years

<20 mm/Hr

Male
13.5 - 18 g/ 100 ml Increase in polycythemia , congestive heart
failure , chronic obstructive pulmonary disease (
Female COPD ) , at high altitudes
Hemoglobin (Hb)
12 - 16 g /100 ml
Decrease in anemia , hyperthyriodism , liver
New born cirrhosis , severe hemorrhage
14 - 20 g / 100 ml
Male
40 - 54 %
Hematocrit Increase in polycythemia , severe dehydration ,
shock
Female
 38 - 47 %
Decrease in anemia , leukemia , cirrhosis ,
hyperthyroidism

Increase in cancer , trauma , heart disease

,cirrhosis
150000 - 400000
Platelet count
/cubic mm
Decrease in anemias ,allergic condition ,during
cancer chemotherapy

Increase in prothrombin & vitamin K deficiancy ,

Prothrombin time 11 - 15 seconds
liver disease , hypervitaminosis A

Male
4.5 - 6.5 million /
Increase in polycythemia , dehydration
cubic mm
Red blood cell count ,following hemorrhage ,
(RBC)
Female
Decrease in SLE ,anemia ,Addison's disease
3.9 - 5.6 million /
cubic mm
Increase in hemolytic anemia metastatic
carcinoma , leukemia
Reticulocyte count
0.5 - 2.0 %
(WB) Decrease in iron deficiency & pernicious
anemia ,radiation therapy ,kidney disease

Increase in acute infections ,trauma , malignant

disease , cardio-vascular disease
White blood cell count 5000 - 10000 /cubic
(WBC) Total mm
Decrease in diabetes mellitus , anemias
,following cancer chemotherapy

Neutrophils:
Neutrophils:60-70 % Increase in acute infections

Eosinophils: 2 - 4 % Eosinophils:
Increase in allergic reactions
WBC Differential count Basophils: 0.5 - 1 %
Basophils:
Lymphocytes:20-25% Increase in allergic reactions

Monocytes: 3 - 8 % Lymphocytes:
Increase during antigen - antibody reaction
 Monocytes:
Increase in chronic infections

Interpretation of Lab Test Profiles

The Analytes

Sodium

Increase in serum sodium is seen in conditions with water loss in

excess of salt loss, as in profuse sweating, severe diarrhea or
vomiting, polyuria (as in diabetes mellitus or insipidus), hypergluco- or
mineralocorticoidism, and inadequate water intake. Drugs causing
elevated sodium include steroids with mineralocorticoid activity,
carbenoxolone, diazoxide, guanethidine, licorice, methyldopa,
oxyphenbutazone, sodium bicarbonate, methoxyflurane, and
reserpine.

Decrease in sodium is seen in states characterized by intake of free

water or hypotonic solutions, as may occur in fluid replacement
following sweating, diarrhea, vomiting, and diuretic abuse. Dilutional
hyponatremia may occur in cardiac failure, liver failure, nephrotic
syndrome, malnutrition, and SIADH. There are many other causes of
hyponatremia, mostly related to corticosteroid metabolic defects or
renal tubular abnormalities. Drugs other than diuretics may cause
hyponatremia, including ammonium chloride, chlorpropamide,
heparin, aminoglutethimide, vasopressin, cyclophosphamide, and
vincristine.

Potassium

Increase in serum potassium is seen in states characterized by

excess destruction of cells, with redistribution of K+ from the intra- to
the extracellular compartment, as in massive hemolysis, crush
injuries, hyperkinetic activity, and malignant hyperpyrexia. Decreased
renal K+ excretion is seen in acute renal failure, some cases of
chronic renal failure, Addison's disease, and other sodium-depleted
 states. Hyperkalemia due to pure excess of K+ intake is usually
iatrogenic.

Drugs causing hyperkalemia include amiloride, aminocaproic acid,

antineoplastic agents, epinephrine, heparin, histamine, indomethacin,
isoniazid, lithium, mannitol, methicillin, potassium salts of penicillin,
phenformin, propranolol, salt substitutes, spironolactone,
succinylcholine, tetracycline, triamterene, and tromethamine.
Spurious hyperkalemia can be seen when a patient exercises his/her
arm with the tourniquet in place prior to venipuncture. Hemolysis and
marked thrombocytosis may cause false elevations of serum K+ as
well. Failure to promptly separate serum from cells in a clot tube is a
notorious source of falsely elevated potassium.

Decrease in serum potassium is seen usually in states characterized

by excess K+ loss, such as in vomiting, diarrhea, villous adenoma of
the colorectum, certain renal tubular defects, hypercorticoidism, etc.
Redistribution hypokalemia is seen in glucose/insulin therapy,
alkalosis (where serum K+ is lost into cells and into urine), and familial
periodic paralysis. Drugs causing hypokalemia include amphotericin,
carbenicillin, carbenoxolone, corticosteroids, diuretics, licorice,
salicylates, and ticarcillin.

Chloride

Increase in serum chloride is seen in dehydration, renal tubular

acidosis, acute renal failure, diabetes insipidus, prolonged diarrhea,
salicylate toxicity, respiratory alkalosis, hypothalamic lesions, and
adrenocortical hyperfunction. Drugs causing increased chloride
include acetazolamide, androgens, corticosteroids, cholestyramine,
diazoxide, estrogens, guanethidine, methyldopa, oxyphenbutazone,
phenylbutazone, thiazides, and triamterene. Bromides in serum will
not be distinguished from chloride in routine testing, so intoxication
may show spuriously increased chloride [see also "Anion gap,"
below].

Decrease in serum chloride is seen in excessive sweating, prolonged

vomiting, salt-losing nephropathy, adrenocortical defficiency, various
acid base disturbances, conditions characterized by expansion of
extracellular fluid volume, acute intermittent porphyria, SIADH, etc.
 Drugs causing decreased chloride include bicarbonate,
carbenoxolone, corticosteroids, diuretics, laxatives, and theophylline.

CO2 content

Increase in serum CO2 content for the most part reflects increase in
serum bicarbonate (HCO3-) concentration rather than dissolved CO2
gas, or PCO 2 (which accounts for only a small fraction of the total).
Increased serum bicarbonate is seen in compensated respiratory
acidosis and in metabolic alkalosis. Diuretics (thiazides, ethacrynic
acid, furosemide, mercurials), corticosteroids (in long term use), and
laxatives (when abused) may cause increased bicarbonate.

Decrease in blood CO2 is seen in metabolic acidosis and

compensated respiratory alkalosis. Substances causing metabolic
acidosis include ammonium chloride, acetazolamide, ethylene glycol,
methanol, paraldehyde, and phenformin. Salicylate poisoning is
characterized by early respiratory alkalosis followed by metabolic
acidosis with attendant decreased bicarbonate.

Critical studies on bicarbonate are best done on anaerobically

collected heparinized whole blood (as for blood gas determination)
because of interaction of blood and atmosphere in routinely collected
serum specimens. Routine electrolyte panels are usually not
collected in this manner.

The tests "total CO2" and "CO2 content" measure essentially the
same thing. The "PCO 2" component of blood gas analysis is a test of
the ventilatory component of pulmonary function only.

Anion gap

Increased serum anion gap reflects the presence of unmeasured

anions, as in uremia (phosphate, sulfate), diabetic ketoacidosis
(acetoacetate, beta-hydroxybutyrate), shock, exercise-induced
physiologic anaerobic glycolysis, fructose and phenformin
administration (lactate), and poisoning by methanol (formate),
ethylene glycol (oxalate), paraldehyde, and salicylates. Therapy with
diuretics, penicillin, and carbenicillin may also elevate the anion gap.
 Decreased serum anion gap is seen in dilutional states and
hyperviscosity syndromes associated with paraproteinemias.
Because bromide is not distinguished from chloride in some
methodologies, bromide intoxication may appear to produce a
decreased anion gap.

Glucose

Hyperglycemia can be diagnosed only in relation to time elapsed after

meals and after ruling out spurious influences (especially drugs,
including caffeine, corticosteroids, estrogens, indomethacin, oral
contraceptives, lithium, phenytoin, furosemide, thiazides, thyroxine,
and many more). Previously, the diagnosis of diabetes mellitus was
made by demonstrating a fasting blood glucose >140 mg/dL
(7.8mmol/L) and/or 2-hour postprandial glucose >200 mg/dL (11.1
mmol/L) on more than one occasion. In 1997, the American Diabetes
Association revised these diagnostic criteria. The new criteria are as
follows:

 Symptoms of diabetes plus a casual plasma glucose of

200 mg/dL [11.1 mmol/L] or greater.

OR

 Fasting plasma glucose of 126 mg/dL [7.0 mmol/L] or greater.

OR

 Plasma glucose of 200 mg/dL [11.1 mmol/L] or greater at 2

hours following a 75-gram glucose load.

At least one of the above criteria must be met on more than one
occasion, and the third method (2-hour plasma glucose after oral
glucose challenge) is not recommended for routine clinical use. The
criteria apply to any age group. This means that the classic oral
glucose tolerance test is now obsolete, since it is not necessary for
the diagnosis of either diabetes mellitus or reactive hypoglycemia.

Diagnosis of gestational diabetes mellitus (GDM) is slightly different.

The screening test, performed between 24 and 28 weeks of
gestation, is done by measuring plasma glucose 1 hour after a 50-
 gram oral glucose challenge. If the plasma glucose is 140 mg/dL or
greater, then the diagnostic test is performed. This consists of
measuring plasma glucose after a 100-gram oral challenge. The
diagnostic criteria are given in the table below.

Time Glucose (mg/dL) Glucose (mmol/L)

Fasting 105 5.8
1 hour 190 10.5
2 hours 165 9.2
3 hours 145 8.0

In adults, hypoglycemia can be observed in certain neoplasms (islet

cell tumor, adrenal and gastric carcinoma, fibrosarcoma, hepatoma),
severe liver disease, poisonings (arsenic, CCl4, chloroform,
cinchophen, phosphorous, alcohol, salicylates, phenformin, and
antihistamines), adrenocortical insufficiency, hypothroidism, and
functional disorders (postgastrectomy, gastroenterostomy, autonomic
nervous system disorders). Failure to promptly separate serum from
cells in a blood collection tube causes falsely depressed glucose
levels. If delay in transporting a blood glucose to the lab is
anticipated, the specimen should be collected in a fluoride-containing
tube (gray-top in the US, yellow in the UK).

In the past, the 5-hour oral glucose tolerance test was used to
diagnose reactive (postprandial) hypoglycemia, but this has fallen out
of favor. Currently, the diagnosis is made by demonstrating a low
plasma glucose (<50 mg/dL[2.8 mmol/L]) during a symptomatic
episode.

Urea nitrogen (BUN)

Serum urea nitrogen (BUN) is increased in acute and chronic intrinsic

renal disease, in states characterized by decreased effective
circulating blood volume with decreased renal perfusion, in postrenal
obstruction of urine flow, and in high protein intake states.

Decreased serum urea nitrogen (BUN) is seen in high

carbohydrate/low protein diets, states characterized by increased
anabolic demand (late pregnancy, infancy, acromegaly),
malabsorption states, and severe liver damage.
 In Europe, the test is called simply "urea."

Creatinine

Increase in serum creatinine is seen any renal functional impairment.

Because of its insensitivity in detecting early renal failure, the
creatinine clearance is significantly reduced before any rise in serum
creatinine occurs. The renal impairment may be due to intrinsic renal
lesions, decreased perfusion of the kidney, or obstruction of the lower
urinary tract.

Nephrotoxic drugs and other chemicals include:

antimony arsenic bismuth cadmium

copper gold iron lead
lithium mercury silver thallium
uranium aminopyrine ibuprofen indomethacin
naproxen fenoprofen phenylbutazone phenacetin
salicylates aminoglycosides amphotericin cephalothin
colistin cotrimoxazole erythromycin ampicillin
methicillin oxacillin polymixin B rifampin
sulfonamides tetracyclines vancomycin benzene
zoxazolamine tetrachloroethylene ethylene glycol
acetazolamide aminocaproic acid aminosalicylate boric acid
cyclophosphamide cisplatin dextran (LMW) furosemide
mannitol methoxyflurane mithramycin penicillamine
pentamide phenindione quinine thiazides
carbon
tetrachloride

Deranged metabolic processes may cause increases in serum creatinine,

as in acromegaly and hyperthyroidism, but dietary protein intake does not
influence the serum level (as opposed to the situation with BUN). Some
substances interfere with the colorimetric system used to measure
creatinine, including acetoacetate, ascorbic acid, levodopa, methyldopa,
glucose and fructose. Decrease in serum creatinine is seen in pregnancy
and in conditions characterized by muscle wasting.
BUN:creatinine ratio

BUN:creatinine ratio is usually >20:1 in prerenal and postrenal

azotemia, and <12:1 in acute tubular necrosis. Other intrinsic renal
disease characteristically produces a ratio between these values.

The BUN:creatinine ratio is not widely reported in the UK.

Uric acid

Increase in serum uric acid is seen idiopathically and in renal failure,

disseminated neoplasms, toxemia of pregnancy, psoriasis, liver
disease, sarcoidosis, ethanol consumption, etc. Many drugs elevate
uric acid, including most diuretics, catecholamines, ethambutol,
pyrazinamide, salicylates, and large doses of nicotinic acid.

Decreased serum uric acid level may not be of clinical significance. It

has been reported in Wilson's disease, Fanconi's syndrome,
xanthinuria, and (paradoxically) in some neoplasms, including
Hodgkin's disease, myeloma, and bronchogenic carcinoma.

Inorganic phosphorus

Hyperphosphatemia may occur in myeloma, Paget's disease of bone,

osseous metastases, Addison's disease, leukemia, sarcoidosis, milk-
alkali syndrome, vitamin D excess, healing fractures, renal failure,
hypoparathyroidism, diabetic ketoacidosis, acromegaly, and
malignant hyperpyrexia. Drugs causing serum phosphorous elevation
include androgens, furosemide, growth hormone, hydrochlorthiazide,
oral contraceptives, parathormone, and phosphates.

Hypophosphatemia can be seen in a variety of biochemical

derangements, incl. acute alcohol intoxication, sepsis, hypokalemia,
malabsorption syndromes, hyperinsulinism, hyperparathyroidism, and
as result of drugs, e.g., acetazolamide, aluminum-containing
antacids, anesthetic agents, anticonvulsants, and estrogens (incl. oral
contraceptives). Citrates, mannitol, oxalate, tartrate, and
phenothiazines may produce spuriously low phosphorus by
interference with the assay.

Calcium
 Hypercalcemia is seen in malignant neoplasms (with or without bone
involvement), primary and tertiary hyperparathyroidism, sarcoidosis,
vitamin D intoxication, milk-alkali syndrome, Paget's disease of bone
(with immobilization), thyrotoxicosis, acromegaly, and diuretic phase
of renal acute tubular necrosis. For a given total calcium level,
acidosis increases the physiologically active ionized form of calcium.
Prolonged tourniquet pressure during venipuncture may spuriously
increase total calcium. Drugs producing hypercalcemia include
alkaline antacids, DES, diuretics (chronic administration), estrogens
(incl. oral contraceptives), and progesterone.

Hypocalcemia must be interpreted in relation to serum albumin

concentration (Some laboratories report a "corrected calcium" or
"adjusted calcium" which relate the calcium assay to a normal
albumin. The normal albumin, and hence the calculation, varies from
laboratory to laboratory). True decrease in the physiologically active
ionized form of Ca++ occurs in many situations, including
hypoparathyroidism, vitamin D deficiency, chronic renal failure,
magnesium deficiency, prolonged anticonvulsant therapy, acute
pancreatitis, massive transfusion, alcoholism, etc. Drugs producing
hypocalcemia include most diuretics, estrogens, fluorides, glucose,
insulin, excessive laxatives, magnesium salts, methicillin, and
phosphates.

Iron

Serum iron may be increased in hemolytic, megaloblastic, and

aplastic anemias, and in hemochromatosis, acute leukemia, lead
poisoning, pyridoxine deficiency, thalassemia, excessive iron therapy,
and after repeated transfusions. Drugs causing increased serum iron
include chloramphenicol, cisplatin, estrogens (including oral
contraceptives), ethanol, iron dextran, and methotrexate.

Iron can be decreased in iron-deficiency anemia, acute and chronic

infections, carcinoma, nephrotic syndrome, hypothyroidism, in
protein- calorie malnutrition, and after surgery.

Alkaline phosphatase (ALP)

Increased serum alkaline phosphatase is seen in states of increased

osteoblastic activity (hyperparathyroidism, osteomalacia, primary and
 metastatic neoplasms), hepatobiliary diseases characterized by some
degree of intra- or extrahepatic cholestasis, and in sepsis, chronic
inflammatory bowel disease, and thyrotoxicosis. Isoenzyme
determination may help determine the organ/tissue responsible for an
alkaline phosphatase elevation.

Decreased serum alkaline phosphatase may not be clinically

significant. However, decreased serum levels have been observed in
hypothyroidism, scurvy, kwashiokor, achrondroplastic dwarfism,
deposition of radioactive materials in bone, and in the rare genetic
condition hypophosphatasia.

There are probably more variations in the way in which alkaline

phosphatase is assayed than any other enzyme. Therefore, the
reporting units vary from place to place. The reference range for the
assaying laboratory must be carefully studied when interpreting any
individual result.

Lactate dehydrogenase (LD or "LDH")

Increase of LD activity in serum may occur in any injury that causes

loss of cell cytoplasm. More specific information can be obtained by
LD isoenzyme studies. Also, elevation of serum LD is observed due
to in vivo effects of anesthetic agents, clofibrate, dicumarol, ethanol,
fluorides, imipramine, methotrexate, mithramycin, narcotic
analgesics, nitrofurantoin, propoxyphene, quinidine, and
sulfonamides.

Decrease of serum LD is probably not clinically significant.

There are two main analytical methods for measuring LD: pyruvate-
>lactate and lactate->pyruvate. Assay conditions (particularly
temperature) vary among labs. The reference range for the assaying
laboratory must be carefully studied when interpreting any individual
result.

Many European labs assay alpha-hydroxybutyrate dehydrogenase

(HBD or HBDH), which roughly equates to LD isoenzymes 1 and 2
(the fractions found in heart, red blood cells, and kidney).

ALT (SGPT)
 Increase of serum alanine aminotransferase (ALT, formerly called
"SGPT") is seen in any condition involving necrosis of hepatocytes,
myocardial cells, erythrocytes, or skeletal muscle cells. [See
"Bilirubin, total," below]

AST (SGOT)

Increase of aspartate aminotransferase (AST, formerly called

"SGOT") is seen in any condition involving necrosis of hepatocytes,
myocardial cells, or skeletal muscle cells. [See "Bilirubin, total,"
below] Decreased serum AST is of no known clinical significance.

GGTP (GAMMA-GT)

Gamma-glutamyltransferase is markedly increased in lesions which

cause intrahepatic or extrahepatic obstruction of bile ducts, including
parenchymatous liver diseases with a major cholestatic component
(e.g., cholestatic hepatitis). Lesser elevations of gamma-GT are seen
in other liver diseases, and in infectious mononucleosis,
hyperthyroidism, myotonic dystrophy, and after renal allograft. Drugs
causing hepatocellular damage and cholestasis may also cause
gamma-GT elevation (see under "Total bilirubin," below).

Gamma-GT is a very sensitive test for liver damage, and unexpected,

unexplained mild elevations are common. Alcohol consumption is a
common culprit.

Decreased gamma-GT is not clinically significant.

Bilirubin

Serum total bilirubin is increased in hepatocellular damage (infectious

hepatitis, alcoholic and other toxic hepatopathy, neoplasms), intra-
and extrahepatic biliary tract obstruction, intravascular and
extravascular hemolysis, physiologic neonatal jaundice, Crigler-Najjar
syndrome, Gilbert's disease, Dubin-Johnson syndrome, and fructose
intolerance.

Drugs known to cause cholestasis include the following:

aminosalicylic androgens azathioprine benzodiazepines

 acid
carbamazepine carbarsone chlorpropamide propoxyphene
estrogens penicillin gold Na thiomalate imipramine
meprobamate methimazole nicotinic acid progestins
oral
penicillin phenothiazines
contraceptives
erythromycin
sulfonamides sulfones
estolate

Drugs known to cause hepatocellular damage include the following:

acetaminophen allopurinol aminosalicylic acid amitriptyline

androgens asparaginase aspirin azathioprine
carbamazepine chlorambucil chloramphenicol chlorpropamide
dantrolene disulfiram estrogens ethanol
ethionamide halothane ibuprofen indomethacin
iron salts isoniazid MAO inhibitors mercaptopurine
methotrexate methoxyflurane methyldopa mithramycin
nicotinic acid nitrofurantoin oral contraceptives papaverine
paramethadione penicillin phenobarbital phenazopyridine
phenylbutazone phenytoin probenecid procainamide
propylthiouracil pyrazinamide quinidine sulfonamides
tetracyclines trimethadione valproic acid

Disproportionate elevation of direct (conjugated) bilirubin is seen in

cholestasis and late in the course of chronic liver disease. Indirect
(unconjugated) bilirubin tends to predominate in hemolysis and
Gilbert's disease.

Decreased serum total bilirubin is probably not of clinical significance

but has been observed in iron deficiency anemia.

Total protein

Increase in serum total protein reflects increases in albumin, globulin,

or both. Generally significantly increased total protein is seen in
volume contraction, venous stasis, or in hypergammaglobulinemia.
 Decrease in serum total protein reflects decreases in albumin,
globulin or both [see "Albumin" and "Globulin, A/G ratio," below].

Albumin

Increased absolute serum albumin content is not seen as a natural

condition. Relative increase may occur in hemoconcentration.
Absolute increase may occur artificially by infusion of hyperoncotic
albumin suspensions.

Decreased serum albumin is seen in states of decreased synthesis

(malnutrition, malabsorption, liver disease, and other chronic
diseases), increased loss (nephrotic syndrome, many GI conditions,
thermal burns, etc.), and increased catabolism (thyrotoxicosis, cancer
chemotherapy, Cushing's disease, familial hypoproteinemia).

Globulin, A/G ratio

Globulin is increased disproportionately to albumin (decreasing the

albumin/globulin ratio) in states characterized by chronic inflammation
and in B-lymphocyte neoplasms, like myeloma and Waldenström's
macroglobulinemia. More relevant information concerning increased
globulin may be obtained by serum protein electrophoresis.

Decreased globulin may be seen in congenital or acquired

hypogammaglobulinemic states. Serum and urine protein
electrophoresis may help to better define the clinical problem.

T3 uptake

This test measures the amount of thyroxine-binding globulin (TBG) in

the patient's serum. When TBG is increased, T3 uptake is decreased,
and vice versa. T3 Uptake does not measure the level of T3 or T4 in
serum.

Increased T3 uptake (decreased TBG) in euthyroid patients is seen in

chronic liver disease, protein-losing states, and with use of the
following drugs: androgens, barbiturates, bishydroxycourmarin,
chlorpropamide, corticosteroids, danazol, d-thyroxine, penicillin,
phenylbutazone, valproic acid, and androgens. It is also seen in
hyperthyroidism.
 Decreased T3 uptake (increased TBG) may occur due to the effects
of exogenous estrogens (including oral contraceptives), pregnancy,
acute hepatitis, and in genetically-determined elevations of TBG.
Drugs producing increased TBG include clofibrate, lithium,
methimazole, phenothiazines, and propylthiouracil. Decreased T3
uptake may occur in hypothyroidism.

Thyroxine (T4)

This is a measurement of the total thyroxine in the serum, including

both the physiologically active (free) form, and the inactive form
bound to thyroxine-binding globulin (TBG). It is increased in
hyperthyroidism and in euthyroid states characterized by increased
TBG (See "T3 uptake," above, and "FTI," below). Occasionally,
hyperthyroidism will not be manifested by elevation of T4 (free or
total), but only by elevation of T3 (triiodothyronine). Therefore, if
thyrotoxicosis is clinically suspect, and T4 and FTI are normal, the
test "T3-RIA" is recommended (this is not the same test as "T3
uptake," which has nothing to do with the amount of T3 in the patient's
serum).

T4 is decreased in hypothyroidism and in euthyroid states

characterized by decreased TBG. A separate test for "T4" is available,
but it is not usually necessary for the diagnosis of functional thyroid
disorders.

FTI (T7)

This is a convenient parameter with mathematically accounts for the

reciprocal effects of T4 and T3 uptake to give a single figure which
correlates with free T4. Therefore, increased FTI is seen in
hyperthyroidism, and decreased FTI is seen in hypothyroidism. Early
cases of hyperthyroidism may be expressed only by decreased
thyroid stimulation hormone (TSH) with normal FTI. Early cases of
hypothyroidism may be expressed only by increased TSH with
normal FTI. Currently, the method of choice for screening for both
hyper- and hypothyroidism is serum TSH only. Modern
methodologies ("ultrasensitive TSH") allow accurate determination of
the very low concentrations of TSH at the phyisological cutoff
between the normal and hyperthyroid states.
ASSESSMENT OF ATHEROSCLEROSIS RISK: Triglycerides, Cholesterol,
HDL-Cholesterol, LDL-Cholesterol, Chol/HDL ratio

All of these studies find greatest utility in assessing the risk of

atherosclerosis in the patient. Increased risks based on lipid studies are
independent of other risk factors, such as cigarette smoking.

Total cholesterol has been found to correlate with total and cardiovascular
mortality in the 30-50 year age group. Cardiovascular mortality increases
9% for each 10 mg/dL increase in total cholesterol over the baseline value
of 180 mg/dL. Approximately 80% of the adult male population has values
greater than this, so the use of the median 95% of the population to
establish a normal range (as is traditional in lab medicine in general) has
no utility for this test. Excess mortality has been shown not to correlate with
cholesterol levels in the >50 years age group, probably because of the
depressive effects on cholesterol levels expressed by various chronic
diseases to which older individuals are prone.

HDL-cholesterol is "good" cholesterol, in that risk of cardiovascular disease

decreases with increase of HDL. An HDL-cholesterol level of <35 mg/dL is
considered a coronary heart disease risk factor independent of the level of
total cholesterol. One way to assess risk is to use the total cholesterol/HDL-
cholesterol ratio, with lower values indicating lower risk. The following chart
has been developed from ideas advanced by Castelli and Levitas, Current
Prescribing, June, 1977. It is not commonly cited in current literature, but I
have never seen a specific refutation of its validity either.

Total cholesterol (mg/dL)

150 185 200 210 220 225 244 260 300
------------------------------------------------------
25 | #### 1.34 1.50 1.60 1.80 2.00 3.00 4.00 6.00
30 | #### 1.22 1.37 1.46 1.64 1.82 2.73 3.64 5.46
35 | #### 1.00 1.12 1.19 1.34 1.49 2.24 2.98 4.47
HDL-chol 40 | #### 0.82 0.92 0.98 1.10 1.22 1.83 2.44 3.66
(mg/dL) 45 | #### 0.67 0.75 0.80 0.90 1.00 1.50 2.00 3.00
50 | #### 0.55 0.62 0.66 0.74 0.82 1.23 1.64 2.46
55 | #### 0.45 0.50 0.54 0.60 0.67 1.01 1.34 2.01
60 | #### 0.37 0.41 0.44 0.50 0.55 0.83 1.10 1.65
65 | #### 0.30 0.34 0.36 0.41 0.45 0.68 0.90 1.35
over 70 | #### #### #### #### #### #### #### #### ####
The numbers with two-decimal format represent the relative risk of
atherosclerosis vis-à-vis the general population. Cells marked "####"
indicate very low risk or undefined risk situations. Some authors have
warned against putting too much emphasis on the total-chol/HDL-chol ratio
at the expense of the total cholesterol level.

Readers outside the US may find the following version of the table more
useful. This uses SI units for total and HDL cholesterol:

Total cholesterol (mmol/L)

3.9 4.8 5.2 5.4 5.7 5.8 6.3 6.7 7.8
------------------------------------------------------
0.65 | #### 1.34 1.50 1.60 1.80 2.00 3.00 4.00 6.00
0.78 | #### 1.22 1.37 1.46 1.64 1.82 2.73 3.64 5.46
0.91 | #### 1.00 1.12 1.19 1.34 1.49 2.24 2.98 4.47
HDL-chol 1.04 | #### 0.82 0.92 0.98 1.10 1.22 1.83 2.44 3.66
(mmol/L) 1.16 | #### 0.67 0.75 0.80 0.90 1.00 1.50 2.00 3.00
1.30 | #### 0.55 0.62 0.66 0.74 0.82 1.23 1.64 2.46
1.42 | #### 0.45 0.50 0.54 0.60 0.67 1.01 1.34 2.01
1.55 | #### 0.37 0.41 0.44 0.50 0.55 0.83 1.10 1.65
1.68 | #### 0.30 0.34 0.36 0.41 0.45 0.68 0.90 1.35
over 1.81 | #### #### #### #### #### #### #### #### ####

Triglyceride level is risk factor independent of the cholesterol levels.

Triglycerides are important as risk factors only if they are not part of the
chylomicron fraction. To make this determination in a hypertriglyceridemic
patient, it is necessary to either perform lipoprotein electrophoresis or
visually examine an overnight- refrigerated serum sample for the presence
of a chylomicron layer. The use of lipoprotein electrophoresis for routine
assessment of atherosclerosis risk is probably overkill in terms of expense
to the patient.

LDL-cholesterol (the amount of cholesterol associated with low-density, or

beta, lipoprotein) is not an independently measured parameter but is
mathematically derived from the parameters detailed above. Some risk-
reduction programs use LDL-cholesterol as the primary target parameter
for monitoring the success of the program. The "desirable" level for LDL-
cholesterol is less than 100 mg/dL.
A detailed statement on this subject is "Primary Prevention of Coronary
Heart Disease: Guidance From Framingham", Circulation 97:1876-1887,
1998. The full text is available online, courtesy of the American Heart
Association.

Triglycerides

Markedly increased triglycerides (>500 mg/dL) usually indicate a

nonfasting patient (i.e., one having consumed any calories within 12-
14 hour period prior to specimen collection). If patient is fasting,
hypertriglyceridemia is seen in hyperlipoproteinemia types I, IIb, III,
IV, and V. Exact classification theoretically requires lipoprotein
electrophoresis, but this is not usually necessary to assess a patient's
risk to atherosclerosis [See "Assessment of Atherosclerosis Risk,"
above]. Cholestyramine, corticosteroids, estrogens, ethanol,
miconazole (intravenous), oral contraceptives, spironolactone, stress,
and high carbohydrate intake are known to increase triglycerides.
Decreased serum triglycerides are seen in abetalipoproteinemia,
chronic obstructive pulmonary disease, hyperthyroidism, malnutrition,
and malabsorption states.

RBC (Red Blood Cell) count

The RBC count is most useful as raw data for calculation of the
erythrocyte indices MCV and MCH [see below]. Decreased RBC is
usually seen in anemia of any cause with the possible exception of
thalassemia minor, where a mild or borderline anemia is seen with a
high or borderline-high RBC. Increased RBC is seen in erythrocytotic
states, whether absolute (polycythemia vera, erythrocytosis of chronic
hypoxia) or relative (dehydration, stress polycthemia), and in
thalassemia minor [see "Hemoglobin," below, for discussion of
anemias and erythrocytoses].

HEMOGLOBIN, HEMATOCRIT, MCV (mean corpuscular volume), MCH

(mean corpuscular hemoglobin), MCHC (mean corpuscular hemoglobin
concentration)

Strictly speaking, anemia is defined as a decrease in total body red cell

mass. For practical purposes, however, anemia is typically defined as
hemoglobin <12.0 g/dL and direct determination of total body RBC mass is
almost never used to establish this diagnosis. Anemias are then classed by
MCV and MCHC (MCH is usually not helpful) into one of the following
categories:

 Microcytic/hypochromic anemia (decreased MCV, decreased MCHC)

o Iron deficiency (common)
o Thalassemia (common, except in people of Germanic,
Slavonic, Baltic, Native American, Han Chinese, Japanese
descent)
o Anemia of chronic disease (uncommonly microcytic)
o Sideroblastic anemia (uncommon; acquired forms more often
macrocytic)
o Lead poisoning (uncommon)
o Hemoglobin E trait or disease (common in Thai, Khmer,
Burmese,Malay, Vietnamese, and Bengali groups)
 Macrocytic/normochromic anemia (increased MCV, normal MCHC)
o Folate deficiency (common)
o B12 deficiency (common)
o Myelodysplastic syndromes (not uncommon, especially in older
individuals)
o Hypothyroidism (rare)
 Normochromic/normocytic anemia (normal MCV, normal MCHC) The
first step in laboratory workup of this broad class of anemias is a
reticulocyte count. Elevated reticulocytes implies a normo-
regenerative anemia, while a low or "normal" count implies a
hyporegenerative anemia:
o Normoregenerative normocytic anemias (appropriate
reticulocyte response)
 Immunohemolytic anemia
 Glucose-6-phosphate dehydrogenase (G6PD) deficiency
(common)
 Hemoglobin S or C
 Hereditary spherocytosis
 Microangiopathic hemolytic anemia
 Paroxysmal hemoglobinuria
o Hyporegenerative normocytic anemias (inadequate reticulocyte
response)
 Anemia of chronic disease
 Anemia of chronic renal failure
 Aplastic anemia*
*Drugs and other substances that have caused aplastic anemia include the
following:

amphotericin sulfonamides phenacetin trimethadione

silver chlordiazepoxide tolbutamide thiouracil
carbamazepine chloramphenicol tetracycline oxyphenbutazone
arsenicals chlorpromazine pyrimethamine carbimazole
acetazolamide colchicine penicillin aspirin
mephenytoin bismuth promazine quinacrine
methimazole chlorothiazide dinitrophenol ristocetin
indomethacin phenytoin gold trifluoperazine
carbutamide perchlorate chlorpheniramine streptomycin
phenylbutazone primidone mercury meprobamate
chlorpropamide thiocyanate tripelennamine benzene

The drugs listed above produce marrow aplasia via an unpredictable,

idiosyncratic host response in a small minority of patients. In addition, many
antineoplastic drugs produce predictable, dose-related marrow
suppression; these are not detailed here.

POLYCYTHEMIA

Polycythemia is defined as an increase in total body erythrocyte mass. As

opposed to the situation with anemias, the physician may directly measure
rbc mass using radiolabeling by 51Cr, so as to differentiate polycythemia
(absolute erythrocytosis, as seen in polycythemia vera, chronic hypoxia,
smoker's polycythemia, ectopic erythropoietin production,
methemoglobinemia, and high O2 affinity hemoglobins) from relative
erythrocytosis (as seen in stress polycythemia and dehydration). Further
details of the work-up of polycythemias are beyond the scope of this
monograph.

RDW (Red cell Distribution Width)

The red cell distribution width is a numerical expression which

correlates with the degree of anisocytosis (variation in volume of the
population of red cells). Some investigators feel that it is useful in
differentiating thalassemia from iron deficiency anemia, but its use in
this regard is far from universal acceptance. The RDW may also be
useful in monitoring the results of hematinic therapy for iron-
deficiency or megaloblastic anemias. As the patient's new, normally-
 sized cells are produced, the RDW initially increases, but then
decreases as the normal cell population gains the majority.

Platelet count

Thrombocytosis is seen in many inflammatory disorders and

myeloproliferative states, as well as in acute or chronic blood loss,
hemolytic anemias, carcinomatosis, status post-splenectomy, post-
exercise, etc.

Thrombocytopenia is divided pathophysiologically into production

defects and consumption defects based on examination of the bone
marrow aspirate or biopsy for the presence of megakaryocytes.
Production defects are seen in Wiskott-Aldritch syndrome, May-
Hegglin anomaly, Bernard-Soulier syndrome, Chediak-Higashi
anomaly, Fanconi's syndrome, aplastic anemia (see list of drugs,
above), marrow replacement, megaloblastic and severe iron
deficiency anemias, uremia, etc. Consumption defects are seen in
autoimmune thrombocytopenias (including ITP and systemic lupus),
DIC, TTP, congenital hemangiomas, hypersplenism, following
massive hemorrhage, and in many severe infections.

WBC (White Blood Cell) count

The WBC is really a nonparameter, since it simply represents the

sum of the counts of granulocytes, lymphocytes, and monocytes per
unit volume of whole blood. Automated counters do not distinguish
bands from segs; however, it has been shown that if all other
hematologic parameters are within normal limits, such a distinction is
rarely important. Also, even in the best hands, trying to reliably
distinguish bands from segs under the microscope is fraught with
reproducibility problems. Discussion concerning a patient's band
count probably carries no more scientific weight than a medieval
theological argument.

Granulocytes
Granulocytes include neutrophils (bands and segs), eosinophils, and
basophils. In evaluating numerical aberrations of these cells (and of
any other leukocytes), one should first determine the absolute count
by multiplying the per cent value by the total WBC count. For
instance, 2% basophils in a WBC of 6,000/µL gives 120 basophils,
which is normal. However, 2% basophils in a WBC of 75,000/µL
gives 1500 basophils/µL, which is grossly abnormal and establishes
the diagnosis of chronic myelogenous leukemia over that of
leukemoid reaction with fairly good accuracy.

Neutrophils

Neutrophilia is seen in any acute insult to the body, whether

infectious or not. Marked neutrophilia (>25,000/µL) brings up the
problem of hematologic malignancy (leukemia, myelofibrosis) versus
reactive leukocytosis, including "leukemoid reactions." Laboratory
work-up of this problem may include expert review of the peripheral
smear, leukocyte alkaline phosphatase, and cytogenetic analysis of
peripheral blood or marrow granulocytes. Without cytogenetic
analysis, bone marrrow aspiration and biopsy is of limited value and
will not by itself establish the diagnosis of chronic myelocytic
leukemia versus leukemoid reaction.

Smokers tend to have higher granulocyte counts than nonsmokers.

The usual increment in total wbc count is 1000/µL for each pack per
day smoked.

Repeated excess of "bands" in a differential count of a healthy patient

should alert the physician to the possibility of Pelger-Huët anomaly,
the diagnosis of which can be established by expert review of the
peripheral smear. The manual band count is so poorly reproducible
among observers that it is widely considered a worthless test. A more
reproducible hematologic criterion for acute phase reaction is the
presence in the smear of any younger forms of the neutrophilic line
(metamyelocyte or younger).

Neutropenia may be paradoxically seen in certain infections,

including typhoid fever, brucellosis, viral illnesses, rickettsioses, and
malaria. Other causes include aplastic anemia (see list of drugs
 above), aleukemic acute leukemias, thyroid disorders,
hypopitituitarism, cirrhosis, and Chediak-Higashi syndrome.

Eosinophils

Eosinophilia is seen in allergic disorders and invasive parasitoses.

Other causes include pemphigus, dermatitis herpetiformis, scarlet
fever, acute rheumatic fever, various myeloproliferative neoplasms,
irradiation, polyarteritis nodosa, rheumatoid arthritis, sarcoidosis,
smoking, tuberculosis, coccidioidomycosis, idiopathicallly as an
inherited trait, and in the resolution phase of many acute infections.

Eosinopenia is seen in the early phase of acute insults, such as

shock, major pyogenic infections, trauma, surgery, etc. Drugs
producing eosinopenia include corticosteroids, epinephrine,
methysergide, niacin, niacinamide, and procainamide.

Basophils

Basophilia, if absolute (see above) and of marked degree is a great

clue to the presence of myeloproliferative disease as opposed to
leukemoid reaction. Other causes of basophilia include allergic
reactions, chickenpox, ulcerative colitis, myxedema, chronic
hemolytic anemias, Hodgkin's disease, and status post-splenectomy.
Estrogens, antithyroid drugs, and desipramine may also increase
basophils.

Basopenia is not generally a clinical problem.

Lymphocytes

Lymphocytosis is seen in infectious mononucleosis, viral hepatitis,

cytomegalovirus infection, other viral infections, pertussis,
toxoplasmosis, brucellosis, TB, syphilis, lymphocytic leukemias, and
lead, carbon disulfide, tetrachloroethane, and arsenical poisonings. A
mature lymphocyte count >7,000/µL is an individual over 50 years of
age is highly suggestive of chronic lymphocytic leukemia (CLL).
Drugs increasing the lymphocyte count include aminosalicyclic acid,
griseofulvin, haloperidol, levodopa, niacinamide, phenytoin, and
mephenytoin.
 Lymphopenia is characteristic of AIDS. It is also seen in acute
infections, Hodgkin's disease, systemic lupus, renal failure,
carcinomatosis, and with administration of corticosteroids, lithium,
mechlorethamine, methysergide, niacin, and ionizing irradiation. Of all
hematopoietic cells lymphocytes are the most sensitive to whole-body
irradiation, and their count is the first to fall in radiation sickness.

Monocytes

Monocytosis is seen in the recovery phase of many acute infections.

It is also seen in diseases characterized by chronic granulomatous
inflammation (TB, syphilis, brucellosis, Crohn's disease, and
sarcoidosis), ulcerative colitis, systemic lupus, rheumatoid arthritis,
polyarteritis nodosa, and many hematologic neoplasms. Poisoning by
carbon disulfide, phosphorus, and tetrachloroethane, as well as
administration of griseofulvin, haloperidol, and methsuximide, may
cause monocytosis.

Monocytopenia is generally not a clinical problem.