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Lab Test Interpretation (monthly posting, 47K, version 2.1)

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Version: 2.1
Last-modified: September 10, 1997
Archive-name: pathology/lab-test-interpretation
Posting-Frequency: monthly (first Wednesday)
Maintainer: Ed Uthman <>

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                 Ed Uthman, MD <>
               Diplomate, American Board of Pathology

The various multiparameter blood chemistry and hematology profiles
offered by most labs represent an economical way by which a large
amount of information concerning a patient's physiologic status can be
made available to the physician. The purpose of this monograph is to
serve as a reference for the interpretation of abnormalities of each of
the parameters. 

     REFERENCE RANGES ("normal ranges") 

       Because reference ranges (except for some lipid studies) are
       typically defined as the range of values of the median 95% of
       the healthy population, it is unlikely that a given specimen,
       even from a healthy patient, will show "normal" values for all
       the tests in a lengthy profile. Therefore, caution should be
       exercised to prevent overreaction to miscellaneous, mild
       abnormalities without clinical correlate. 

     UNITS OF MEASUREMENT: America against the world 

       American labs use a different version of the metric system than
       does most of the rest of the world, which uses the Systeme
       Internationale (SI). In some cases translation between the two
       systems is easy, but the difference between the two is most
       pronounced in measurement of chemical concentration. The
       American system generally uses mass per unit volume, while SI
       uses moles per unit volume. Since mass per mole varies with the
       molecular weight of the analyte, conversion between American and
       SI units requires many different conversion factors. Where
       appropriate, in this paper SI units are given after American


       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. 


       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. 


       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,"

       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. 


       Increase in serum CO2 content for the most part reflects
       increase in serum bicarbonate (HCO3-) concentration rather than
       dissolved CO2 gas, or PCO2 (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

       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 "PCO2" component of blood gas analysis is a test
       of the ventilatory component of pulmonary function only. 


       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. 


       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).
       Generally, fasting blood glucose >140 mg/dL (7.8mmol/L) and/or
       2h postprandial glucose >200 mg/dL (11.1 mmol/L) demonstrated on
       several occasions is suggestive of diabetes mellitus; oral
       glucose tolerance test is usually not required for diagnosis. 

       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). 


       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." 


       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 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

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


       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. 


       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 phosphorous by interference with the


       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, Mg++ deficiency, prolonged anticonvulsant
       therapy, acute pancreatitis, massive transfusion, alcoholism,
       etc. Drugs producing hypocalcemiainclude most diuretics,
       estrogens, fluorides, glucose, insulin, excessive laxatives,
       magnesium salts, methicillin, and phosphates. 


       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


       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

       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. 


       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). 


       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] 


       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. 


       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. 


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

Drugs known to cause hepatocellular damage include the

    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. 


       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

       Decrease in serum total protein reflects decreases in albumin,
       globulin or both [see "Albumin" and "Globulin, A/G ratio,"


       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 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. 


       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


       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 "free 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 with 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. 

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. 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 should be taken with a large grain of salt substitute: 

                              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-a-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

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. 


       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: 

    A. Microcytic/hypochromic anemia (decreased MCV, decreased
              Iron deficiency (common) 
              Thalassemia (common, except in people of Germanic,
                 Slavonic, Baltic, Native American, Han Chinese, 
                 Japanese descent) 
              Anemia of chronic disease (uncommonly microcytic) 
              Sideroblastic anemia (uncommon; acquired forms more often
              Lead poisoning (uncommon) 
              Hemoglobin E trait or disease (common in Thai, Khmer,
                 Burmese,Malay, Vietnamese, and Bengali groups) 

    B. Macrocytic/normochromic anemia (increased MCV, normal MCHC)

              Folate deficiency (common) 
              B12 deficiency (common) 
              Myelodysplastic syndromes (not uncommon, especially in
                 older individuals) 
              Hypothyroidism (rare) 

    C. 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: 

           1. Normoregenerative normocytic anemias (appropriate
              reticulocyte response) 

                    Immunohemolytic anemia 
                    Glucose-6-phosphate dehydrogenase (G6PD) deficiency
                    Hemoglobin S or C 
                    Hereditary spherocytosis 
                    Microangiopathic hemolytic anemia 
                    Paroxysmal hemoglobinuria 

           2. 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 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 51chromium, 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. 


       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

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 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/uL
       gives 120 basophils, which is normal. However, 2% basophils in a
       WBC of 75,000/uL gives 1500 basophils/uL, which is grossly
       abnormal and establishes the diagnosis of chronic myelogenous
       leukemia over that of leukemoid reaction with fairly good


              Neutrophilia is seen in any acute insult to the body,
              whether infectious or not. Marked neutrophilia
              (>25,000/uL) 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/uL 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-Huet 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


              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. 


              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. 


       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/uL 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.


       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. 


       Tietz, Norbert W., Clinical Guide to Laboratory Tests,
       Saunders, 1983. 
       Friedman, RB, et al., Effects of Diseases on Clinical
       Laboratory Tests, American Association of Clinical Chemistry,
       Anderson, KM, et al., Cholesterol and Mortality, JAMA 257:
       2176­2180, 1987 


Many thanks to Michael Gayler, FIBMS, DMS, CertHSm (MLSO2, Department
of Chemical Pathology, Leicester Royal Infirmary)
<> for the excellent review and comments, and for
the labor of translating American to SI units. 


Please send all constructive comments regarding this FAQ to Ed Uthman,
MD <>. I am especially interested in correcting any
errors of commission or omission. 


This article is provided "as is" without any express or implied
warranties. While reasonable effort has been made to ensure the
accuracy of the information, the author assumes no responsibility for
errors or omissions, or for damages resulting from use of the
information herein. 

Copyright (c) 1994-97, Edward O. Uthman. This material may be reformatted
and/or freely distributed via online services or other media, as long as
it is not substantively altered. Authors, educators, and others are
welcome to use any ideas presented herein, but I would ask for
acknowledgment in any published work derived therefrom. Commercial use
is not allowed without the prior written consent of the author.

version 2.1, 9/10/97

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