NAME ROLE NORMAL DIFF
GGT (Gamma glutamyltransferase) 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. Normal results in females under age 45, range from 5 to 27 U/L; in females over age 45 and in males, levels range from 6 to 37 U/L.  A normal GGT level suggests such elevation stems from skeletal disease. Serum GGT values vary with the assay method used (colorimetric or kinetic). The sharpest increases in GGT levels indicate obstructive jaundice and hepatic metastasis. Elevations may indicate any acute hepatic disease, acute 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.
MCV (mean corpuscular volume) MCV = Hct/Hgb  Normal values: MCV: 80 to 95 femtoliter MCH: 27 to 31 picograms/cell MCHC: 32 to 36 grams/deciliter  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 

Uric Acid   4.1 to 8.8 mg/dl  Greater-than-normal levels of uric acid (hyperuricemia) may indicate: 
acidosis  gout  leukemia
alcoholism hypoparathyroidism nephrolithiasis
diabetes mellitus lead poisoning polycythemia vera
renal failure toxemia of pregnancy  purine-rich diet 
severe exercise     

Lower-than-normal levels of uric acid may indicate:
 
Fanconi's syndrome Wilson's disease  SIADH 
low purine diet     

Additional conditions under which the test may be performed: chronic gouty arthritis injury of the kidney and ureter 

Cholesterol   140 to 310 mg/dl optimal values: 140-220 mg/dl Note: mg/dl = milligrams per deciliter  atherosclerosis biliary cirrhosis familial hyperlipidemias high-cholesterol diet hypothyroidism myocardial infarction nephrotic syndrome uncontrolled diabetes 
Triglycerides   Normal values: 10 to 190 mg/dl Note: mg/dl = milligrams per deciliter  cirrhosis familial hyperlipoproteinemia (rare) hypothyroidism low protein in diet and high carbohydrates poorly controlled diabetes nephrotic syndrome pancreatitis 
Alanine Aminotransferase (ALT, SGPT, GPT) Intracellular enzyme involved in amino acid and carbohydrate metabolism. Present in large concentrations in liver, kidney; smaller amounts in skeletal muscle and heart. Released with tissue damage.  Normal Range: Laboratory-specific U/L Increased in: Acute viral hepatitis (ALT>AST), biliary tract obstruction (cholangitis, choledocholithiasis), alcoholic hepatitis and cirrhosis (AST>ALT), liver abscess, metastatic or primary liver cancer; right heart failure, ischemia or hypoxia, injury to liver ("shock liver"), extensive trauma. Drugs causing cholestasis and other hepatotoxic drugs. 

Additional: ALT screening of donor blood used in blood banks to exclude non-A, non-B hepatitis.

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

Additional: Serum albumin gives an indication of severity in chronic liver disease. Useful in nutritional assessment if no impairment in production or increased loss.

Alkaline Phosphatase Alkaline phosphatases are found in liver, bone, intestine, placenta.  Normal Range: Method and age dependent  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. 

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).

ANA (Antinuclear Antibodies) Heterogeneous antibodies 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 fluorescein-conjugated polyvalent anti-human immunoglobulin.  Normal Range: < 1:20  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 (30-50%), 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

ANCA (antineutrophil
cytoplasmic antibodies),
P-ANCA (perinuclear)
C-ANCA (cytoplasmic)		 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. P-ANCA is found in some lupus patients. Normal Range: none present
Anti-Cardiolipin
(Anti-Phospholipid)		 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. Normal Range for anti-IgG: 0 - 20 GPL
Normal Range for anti-IgM: 0 - 10 MPL.		 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

Anti-DNA  IgG or IgM antibodies directed against host double-stranded DNA.  Normal Range: < 1:10 titer increased in: Systemic lupus erythematosus (60-70%, specificity 95%). Anti-ds-DNA antibody is not found in drug-induced lupus. 

Additional: High titers are seen only in SLE. Titers of anti-ds-DNA correlate well with disease activity and with occurrence of glomerulonephritis.

Antinerythrocyte
antibodies (anti-RBC) 
also known as Coombs test		 The direct Coombs test measures the presence of 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. Normal Range: none present
Antineurofilament antibodies Limited studies have been done with this test. Antibodies against neurofilaments in blood serum. 60% of diffuse NP lupus patients have shown this antibody. Normal Range: non present
Anti-Cardiolipin
(Anti-Phospholipid)		 MPLAnticardiolipin 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. Normal Range for anti-IgG: 0 - 20 GPL
Normal Range for anti-IgM: 0 - 10 		 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.

Antinerythrocyte
antibodies (anti-RBC) 
also known as Coombs test		 The direct Coombs test measures the presence of 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. Normal Range: none present
Antineurofilament antibodies presentLimited studies have been done with this test. Antibodies against neurofilaments in blood serum. 60% of diffuse NP lupus patients have shown this antibody. Normal Range: non 
Antineuronal antibodies Most specifically, this is IgG neuron-reactive 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). Normal Range: non present
Anti-ribosomal P Antibodies to ribosomal P protein from blood serum. 80 - 90% positive in NP lupus that manifests with psychosis or depression. Normal Range: Negative
Anti-Ro/SS-A Autoantibody against acidic nuclear ribonucleoproteins that is found in patients with some connective tissue diseases, especially Sjogren's syndrome.  Normal Range: Negative 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 (50-60%) and SLE (10-15%). Patients with antibodies to SS-A may have a negative ANA test.

Aspartate Aminotransferase (AST, SGOT, GOT) U/LIntracellular enzyme involved in amino acid and carbohydrate metabolism. Present in large concentrations in liver, skeletal muscle, brain, red cells, and heart. Released into the bloodstream when tissue is damaged.  Normal Range: Laboratory-specific 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.

Bilirubin 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.  Normal Range: 0.1-1.2 Direct (conjugated to glucuronide) bilirubin, 0.1-0.4 mg/dL (< 7 µmol/L); Indirect (unconjugated) bilirubin, 0.2-0.7 mg/dL (< 12 µmol/L) mg/dL increased in: Acute or chronic hepatitis, cirrhosis, biliary tract obstruction, toxic hepatitis, congenital liver enzyme abnormalities (Dubin-Johnson, Rotor's, Gilbert's, Crigler-Najjar syndromes), fasting, hemolytic disorders. Hepatotoxic drugs. 

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. 

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.  Normal Range: 8-20 mg/dL 

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: Renal failure (acute or chronic), urinary tract obstruction, dehydration, shock, burns, CHF, gastrointestinal bleeding. Drugs with renal toxicity, eg, gentamicin. 

Decreased in: Hepatic failure, nephrotic syndrome, cachexia (low-protein and high-carbohydrate diets).

Aspartate Aminotransferase (AST, SGOT, GOT) Intracellular enzyme involved in amino acid and carbohydrate metabolism. Present in large concentrations in liver, skeletal muscle, brain, red cells, and heart. Released into the bloodstream when tissue is damaged.  Normal Range: Laboratory-specific U/L 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.

Bilirubin 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.  . Normal Range: 0.1-1.2 Direct (conjugated to glucuronide) bilirubin, 0.1-0.4 mg/dL (< 7 µmol/L); Indirect (unconjugated) bilirubin, 0.2-0.7 mg/dL (< 12 µmol/L) mg/dL increased in: Acute or chronic hepatitis, cirrhosis, biliary tract obstruction, toxic hepatitis, congenital liver enzyme abnormalities (Dubin-Johnson, Rotor's, Gilbert's, Crigler-Najjar syndromes), fasting, hemolytic disorders. Hepatotoxic drugs. 

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

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.  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. 

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.

C3 The classic and alternative complement 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 performed is an immunoassay (by radial immunodiffusion or nephelometry).  Normal Range: 64-166 mg/dL 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 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.

C4 C4 is a component of the classic complement pathway. Depressed levels usually indicate classic pathway activation.  Normal Range: 15-45 mg/dL increased in: Various malignancies: not clinically useful. 

Decreased by: Decreased synthesis, increased catabolism (SLE, rheumatoid arthritis, proliferative glomerulonephritis, hereditary angioedema), and increased loss (burns, protein-losing 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.

Calcium Level of ionized calcium is regulated by parathyroid hormone and vitamin D. Serum calcium equals the sum of ionized calcium plus complexed calcium and calcium bound to proteins (mostly albumin). Normal Range: 8.5-10.5 mg/dL 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. 

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.

CH50 The quantitative assay of hemolytic complement activity depends on the ability of the primary complement pathway to induce hemolysis of red cells sensitized with optimal amounts of anti-red cell antibodies. For precise titrations of hemolytic complement, the dilution of serum that 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 laboratory-specific.  Normal Range: Laboratory-specific U/mL Decreased with: >50-80% deficiency of primary pathway complement components in congenital or acquired deficiency. 

Normal in: Deficiencies of alternative pathway, complement components. 

Additional: This is a functional assay of biologic activity. Sensitivity to decreased levels of complement components depends on exactly how the test is performed. It is used to detect congenital and acquired severe deficiency disorders of the primary complement pathway.

Chloride Chloride, the principal inorganic anion of extracellular fluid, is important in maintaining normal acid-base balance and normal osmolality. If chloride is lost (as HCl or NH4Cl), alkalosis ensues; if chloride is ingested or retained, acidosis ensues.  Normal Range: 98-107 meq/L increased in: Renal failure, nephrotic syndrome, renal tubular acidosis, dehydration, overtreatment with saline, hyperparathyroidism, diabetes insipidus, metabolic acidosis from diarrhea (loss of HCO3), respiratory alkalosis, hyperadrenocorticism. Drugs: acetazolamide (hyperchloremic acidosis), androgens, hydrochlorothiazide, salicylates (intoxication). 

Decreased in: Vomiting, diarrhea, gastrointestinal suction, renal failure combined with salt deprivation, overtreatment 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 Cholesterol level is determined by lipid metabolism, which is in turn influenced by heredity, diet, and liver, kidney, thyroid, and other 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).  Normal Range: Desirable < 200 Borderline 200-239 High risk > 240 mg/dL increased in: Familial or polygenic hyperlipoproteinemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia, hyperlipoproteinemia and hyperalphalipoproteinemia, hyperlipoproteinemias secondary to hypothyroidism, uncontrolled diabetes mellitus, nephrotic syndrome, chronic hepatitis, biliary cirrhosis, obstructive 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. 

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.

Creatinine 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.  Normal Range: 0.6-1.2 mg/dL 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, a-ketoglutarate, 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.

Differential

Neutophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Large unstained cells

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). 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, drug-induced 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.

Erythrocyte Sedimentation Rate (Sed Rate, ESR) Erythrocytes in plasma usually settle slowly. However, if they aggregate for any reason (usually because of plasma proteins called acute phase reactants, eg, fibrinogen), they settle rapidly. Sedimentation of RBCs occurs because of their greater density than plasma. ESR measures the distance in mm that erythrocytes fall during 1 hour.  Normal Range: Male: < 10 Female: < 15 increased in: Infections (osteomyelitis, pelvic inflammatory disease [75%]), inflammatory disease (temporal arteritis, polymyalgia rheumatica, rheumatic fever), malignant neoplasms, paraproteinemias, anemia, pregnancy, chronic renal failure, GI disease (ulcerative colitis, regional ileitis). 

Decreased in: Polycythemia, sickle cell anemia, spherocytosis, anisocytosis, hypofibrinogenemia, hypogammaglobulinemia, congestive heart failure, microcytosis, drugs (high dose corticosteroids). Low value of no diagnostic significance. 

Additional: There is a good correlation between ESR and C-reactive 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.

Gamma-Glutamyl Transpeptidase (GGT) U/LGGT is an enzyme present in liver, kidney, and pancreas. It transfers C-terminal glutamic acid from a peptide to other peptides of L-amino acids. It is induced by alcohol intake and is an extremely sensitive indicator of liver disease, particularly alcoholic liver disease. Normal Range: Laboratory-specific  increased in: Liver disease: acute viral or toxic hepatitis, chronic or subacute hepatitis, cirrhosis, biliary tract obstruction (intrahepatic or extrahepatic), primary or metastatic liver neoplasm, alcoholic hepatitis, mononucleosis. Drugs (by enzyme induction): phenytoin, barbiturates, alcohol.

Additional: Useful in follow up of alcoholics undergoing treatment. Test sensitive to modest alcohol intake. Test positive in 90% of patients with liver disease. Used to confirm hepatic origin of elevated serum alkaline phosphatase.

Glucose Normally, the glucose concentration in extracellular fluid is closely regulated so that a source of energy is readily available to tissues and no glucose is excreted in the urine . Normal Range: 60-115 mg/dL increased in: Diabetes mellitus, Cushing's syndrome (10-15%), chronic pancreatitis (30%) Drugs: corticosteroids, phenytoin, estrogen, thiazides

Decreased in: Pancreatic islet B cell disease with increased insulin, insulinoma, adrenocortical insufficiency, hypopituitarism, diffuse liver disease, malignancy (adrenocortical, stomach, fibrosarcoma), infant of diabetic mother, enzyme deficiency diseases (galactosemia, etc). Drugs: insulin, ethanol, propranolol, sulfonylureas, tolbutamide, other hypoglycemic agents. 

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.

Hematocrit The hematocrit represents the percentage of whole blood volume made up by erythrocytes. Laboratory instruments calculate the Hct from the erythrocyte count and the MCV, ie, Hct = RBC x MCV.  Normal Range: Male: 39-49 Female: 35-45 Age-dependent 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 Hemoglobin is the major protein of erythrocytes and transports oxygen 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. Normal Range: 
Male: 13.6-17.5 
Female: 12.0-15.5 		 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.

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

Decreased in: IgG: Immunosuppressive therapy, genetic (severe combined immunodeficiency, Wiskott-Aldrich syndrome, common variable immunodeficiency). IgM: Immunosuppresive therapy. IgA: Inherited IgA deficiency (ataxia telangiectasia, combined immunodeficiency disorders). 

Additional: IgG deficiency is associated with recurrent and occasionally severe pyogenic infections. Most common form of multiple myeloma is the IgG type.

Iron Plasma iron concentration is determined by absorption from intestine; storage in intestine, liver, spleen, bone marrow; rate of breakdown or loss of hemoglobin; rate of synthesis of new hemoglobin.  Normal Range: 50-175 µg/dL 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).

Iron Binding Capacity Iron is transported in plasma complexed to the 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%.  Normal Range: 250-460 µg/dL 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.

Lactate Dehydrogenase (LDH) LDH is an enzyme that catalyzes the 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.  Normal Range: Laboratory-specific 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.

Magnesium Magnesium is primarily an intracellular cation (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.  Normal Range: 1.8-3 mg/dL 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.

Mean Corpuscular Hemoglobin (MCH) MCH calculated from 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. Normal Range: 26-34 pg increased in: Macrocytosis. 

Decreased in: Microcytosis (iron deficiency, thalassemia). Hypochromia (lead poisoning, sideroblastic anemia, anemia of chronic disease).

Mean Corpuscular Hemoglobin Concentration (MCHC) MCHC describes how fully 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.  Normal Range: 31-36 g/dL 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).

Mean Corpuscular Volume (MCV) Average volume of the red cell is measured by automated instrument, by electrical impedance or by light scatter.  Normal Range: 80-100 fL 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.

Partial Thromboplastin Time Patient's plasma is activated to clot in vitro by mixing it with phospholipid and an activator substance. Screens the intrinsic coagulation pathway and adequacy of all coagulation factors except XIII and VII. PTT is usually abnormal if level of any factor falls below 30-40% of normal.  Normal Range: 25-35 (range varies) Panic > = 60 seconds increased in: Deficiency of any individual coagulation factor except XIII and VII, nonspecific inhibitors (lupus-like anticoagulant), specific factor inhibitors, von Willebrand's disease (may also be normal), hemophilia A and B, disseminated intravascular coagulation. Drugs: heparin, warfarin. 

Decreased in: Hypercoagulable states, DIC. 

Comments: PTT is the best test to monitor adequacy of heparin therapy. Test not always abnormal in von Willebrand's disease. Test may be normal in chronic DIC. Very common cause of prolongation is spurious presence of heparin in sample. 

Phosphorous The plasma concentration of inorganic phosphate is determined by parathyroid gland function, action of vitamin D, intestinal absorption, renal function, bone metabolism, and nutrition.  Normal Range: 2.5-4.5 mg/dL increased in: Renal failure, massive blood transfusion, sarcoidosis, neoplasms, adrenal insufficiency, acromegaly, hypoparathyroidism, hypervitaminosis D, phosphate infusions or enemas, osteolytic metastases to bone, leukemia, milk-alkali syndrome, healing bone fractures, pseudohypoparathyroidism, diabetes mellitus with ketosis, malignant hyperpyrexia, cirrhosis, lactic acidosis, respiratory acidosis. Drugs: eg, anabolic steroids, ergocalciferol, furosemide, hydrochlorothiazide and others. 

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.

Platelet Count Platelets are released from megakaryocytes in bone marrow, and they are important for adequate hemostasis. Platelet counting is done by flow cytometer based on size discrimination using either electrical impedance or electro-optical systems.  Normal Range: 150-450 X 10 3/uL increased in: Myeloproliferative disorders: polycythemia vera, CML, essential thrombocythemia, myelofibrosis, after bleeding, postsplenectomy, reactive thrombocytosis secondary to inflammatory diseases. 

Decreased in: Decreased production: bone marrow suppression or replacement, chemotherapeutic agents, other drugs, eg, ethanol. Increased destruction or removal: splenomegaly, DIC, platelet antibodies (ITP, posttransfusion purpura, neonatal isoimmune thrombocytopenia, drugs (eg, quinidine, cephalosporins).

Potassium Normal Range: 3.5-5.0 meq/L Potassium is 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. 

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. 

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.

Protein 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. Normal Range: 6-8 g/dL increased in: Polyclonal or monoclonal gammopathies, marked dehydration. Drugs: anabolic steroids, androgens, corticosteroids, epinephrine. 

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.

Prothrombin Time PT screens the extrinsic pathway of the 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. Normal Range: 11-15 seconds 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.

Rheumatoid Factor  Heterogeneous autoantibodies usually of the IgM class that react against the Fc region of human IgG.  Normal Range: Negative (<1:16) Positive in: Rheumatoid arthritis (75-90%), Sjogren's (80-90%), 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. 

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.

Sodium Sodium is the predominant extracellular cation. Serum sodium level is primarily determined by the volume status of the individual. Hyponatremia can be divided into hypovolemia, euvolemia, and hypervolemia categories. Normal Range: 135-145 meq/L 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 Uric acid is an end product of nucleoprotein metabolism and is excreted by the kidney. An increase in serum uric acid concentration occurs with increased nucleoprotein synthesis or catabolism (blood dyscrasias, therapy of leukemia) or decreased renal excretion (eg, with use of thiazide diuretics or renal failure).  Normal Range: Males: 2.4-7.4 Females 1.4-5.8 mg/dL increased in: Renal failure, gout, myeloproliferative disorders (leukemia, lymphoma, myeloma, polycythemia vera), psoriasis; glycogen storage disease (type I); Lesch-Nyhan syndrome (X-linked hypoxanthine-guanine phosphoribosyltransferase deficiency); lead nephropathy. Drugs: antimetabolite and chemotherapeutic agents, diuretics, ethanol, nicotinic acid, salicylates (low dose). 

Decreased in: SIADH, xanthine oxidase deficiency, low-purine diet. Fanconi's syndrome, neoplastic disease (various, causing increased renal excretion), liver disease. Drugs: salicylates (high dose), allopurinol (xanthine oxidase inhibitor). 

Additional: Sex and age affect uric acid levels. The incidence of hyperuricemia is greater in some racial groups (eg, Filipinos) than others (Whites).

White Blood Count (WBC, Leukocyte count) Measure of the total number of leukocytes in whole blood. Counted on automated instruments using light scattering or electrical impedance after lysis of RBCs. WBCs are distinguished from platelets by size.  Normal Range: 3.4-10 K/µL increased in: Infection, inflammation, hematologic malignancy, leukemias (AML, ALL, CML, CLL), lymphoma. Drugs: corticosteroids. 

Decreased in: Aplastic anemia (decreased production), B12 or folate deficiency (maturation defect), sepsis (decreased survival). Drugs: phenothiazines, chloramphenicol, aminopyrine. 

Additional: Spurious increase: with high number of nucleated red cells.