WHAT DO THE LAB
RESULTS MEAN?
|
Interpretation
of Lab Test Profiles
Diplomate, American Board of Pathology
15 Nov 1998
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 Système 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 units.
The Analytes
- Sodium
- Increase in serum sodium is seen in conditions
with water loss in excess of salt loss, as in
profuse sweating, severe diarrhea or vomiting,
polyuria (as in diabetes mellitus or insipidus),
hypergluco- or mineralocorticoidism, and
inadequate water intake. Drugs causing elevated
sodium include steroids with mineralocorticoid
activity, carbenoxolone, diazoxide, guanethidine,
licorice, methyldopa, oxyphenbutazone, sodium
bicarbonate, methoxyflurane, and reserpine.
Decrease
in sodium is seen in states characterized by
intake of free water or hypotonic solutions, as
may occur in fluid replacement following sweating,
diarrhea, vomiting, and diuretic abuse.
Dilutional hyponatremia may occur in cardiac
failure, liver failure, nephrotic syndrome,
malnutrition, and SIADH. There are many other
causes of hyponatremia, mostly related to
corticosteroid metabolic defects or renal tubular
abnormalities. Drugs other than diuretics may
cause hyponatremia, including ammonium chloride,
chlorpropamide, heparin, aminoglutethimide,
vasopressin, cyclophosphamide, and vincristine.
- Potassium
- Increase in serum potassium is seen in states
characterized by excess destruction of cells,
with redistribution of K+
from the intra- to the extracellular compartment,
as in massive hemolysis, crush injuries,
hyperkinetic activity, and malignant hyperpyrexia.
Decreased renal K+
excretion is seen in acute renal failure, some
cases of chronic renal failure, Addison's disease,
and other sodium-depleted states. Hyperkalemia
due to pure excess of K+
intake is usually iatrogenic.
Drugs causing
hyperkalemia include amiloride, aminocaproic acid,
antineoplastic agents, epinephrine, heparin,
histamine, indomethacin, isoniazid, lithium,
mannitol, methicillin, potassium salts of
penicillin, phenformin, propranolol, salt
substitutes, spironolactone, succinylcholine,
tetracycline, triamterene, and tromethamine.
Spurious hyperkalemia can be seen when a patient
exercises his/her arm with the tourniquet in
place prior to venipuncture. Hemolysis and marked
thrombocytosis may cause false elevations of
serum K+ as well.
Failure to promptly separate serum from cells in
a clot tube is a notorious source of falsely
elevated potassium.
Decrease in serum potassium is seen usually in
states characterized by excess K+
loss, such as in vomiting, diarrhea, villous
adenoma of the colorectum, certain renal tubular
defects, hypercorticoidism, etc. Redistribution
hypokalemia is seen in glucose/insulin therapy,
alkalosis (where serum K+
is lost into cells and into urine), and familial
periodic paralysis. Drugs causing hypokalemia
include amphotericin, carbenicillin,
carbenoxolone, corticosteroids, diuretics,
licorice, salicylates, and ticarcillin.
- Chloride
- Increase in serum chloride is seen in dehydration,
renal tubular acidosis, acute renal failure,
diabetes insipidus, prolonged diarrhea,
salicylate toxicity, respiratory alkalosis,
hypothalamic lesions, and adrenocortical
hyperfunction. Drugs causing increased chloride
include acetazolamide, androgens, corticosteroids,
cholestyramine, diazoxide, estrogens,
guanethidine, methyldopa, oxyphenbutazone,
phenylbutazone, thiazides, and triamterene.
Bromides in serum will not be distinguished from
chloride in routine testing, so intoxication may
show spuriously increased chloride [see also
"Anion gap," below].
Decrease in
serum chloride is seen in excessive sweating,
prolonged vomiting, salt-losing nephropathy,
adrenocortical defficiency, various acid base
disturbances, conditions characterized by
expansion of extracellular fluid volume, acute
intermittent porphyria, SIADH, etc. Drugs causing
decreased chloride include bicarbonate,
carbenoxolone, corticosteroids, diuretics,
laxatives, and theophylline.
- CO2 content
- Increase in serum CO2
content for the most part reflects increase in
serum bicarbonate (HCO3-)
concentration rather than dissolved CO2 gas, or PCO 2 (which accounts
for only a small fraction of the total).
Increased serum bicarbonate is seen in
compensated respiratory acidosis and in metabolic
alkalosis. Diuretics (thiazides, ethacrynic acid,
furosemide, mercurials), corticosteroids (in long
term use), and laxatives (when abused) may cause
increased bicarbonate.
Decrease in blood CO2 is seen in metabolic
acidosis and compensated respiratory alkalosis.
Substances causing metabolic acidosis include
ammonium chloride, acetazolamide, ethylene glycol,
methanol, paraldehyde, and phenformin. Salicylate
poisoning is characterized by early respiratory
alkalosis followed by metabolic acidosis with
attendant decreased bicarbonate.
Critical studies on bicarbonate are best done
on anaerobically collected heparinized whole
blood (as for blood gas determination) because of
interaction of blood and atmosphere in routinely
collected serum specimens. Routine electrolyte
panels are usually not collected in this manner.
The tests "total CO2"
and "CO2
content" measure essentially the same thing.
The "PCO 2"
component of blood gas analysis is a test of the
ventilatory component of pulmonary function only.
- Anion gap
- Increased serum anion gap reflects the presence
of unmeasured anions, as in uremia (phosphate,
sulfate), diabetic ketoacidosis (acetoacetate,
beta-hydroxybutyrate), shock, exercise-induced
physiologic anaerobic glycolysis, fructose and
phenformin administration (lactate), and
poisoning by methanol (formate), ethylene glycol
(oxalate), paraldehyde, and salicylates. Therapy
with diuretics, penicillin, and carbenicillin may
also elevate the anion gap.
Decreased serum
anion gap is seen in dilutional states and
hyperviscosity syndromes associated with
paraproteinemias. Because bromide is not
distinguished from chloride in some methodologies,
bromide intoxication may appear to produce a
decreased anion gap.
- Glucose
- Hyperglycemia can be diagnosed only in relation
to time elapsed after meals and after ruling out
spurious influences (especially drugs, including
caffeine, corticosteroids, estrogens,
indomethacin, oral contraceptives, lithium,
phenytoin, furosemide, thiazides, thyroxine, and
many more). Previously, the diagnosis of diabetes
mellitus was made by demonstrating a fasting
blood glucose >140 mg/dL (7.8mmol/L) and/or 2-hour
postprandial glucose >200 mg/dL (11.1 mmol/L)
on more than one occasion. In 1997, the American Diabetes
Association revised these diagnostic criteria.
The new
criteria are as follows:
-
- Symptoms of diabetes plus a casual plasma
glucose of 200 mg/dL [11.1 mmol/L]
or greater.
OR
- Fasting plasma glucose of 126 mg/dL
[7.0 mmol/L] or greater.
OR
- Plasma glucose of 200 mg/dL [11.1 mmol/L]
or greater at 2 hours following a 75-gram
glucose load.
At least one of the above criteria must be met
on more than one occasion, and the third method (2-hour
plasma glucose after oral glucose challenge) is
not recommended for routine clinical use. The
criteria apply to any age group. This
means that the classic oral glucose tolerance
test is now obsolete, since it is not necessary
for the diagnosis of either diabetes mellitus or
reactive hypoglycemia.
Diagnosis of gestational
diabetes mellitus (GDM) is slightly different.
The screening test, performed between 24 and 28
weeks of gestation, is done by measuring plasma
glucose 1 hour after a 50-gram oral glucose
challenge. If the plasma glucose is 140 mg/dL
or greater, then the diagnostic test is performed.
This consists of measuring plasma glucose after a
100-gram oral challenge. The diagnostic criteria
are given in the table below.
| Time |
Glucose (mg/dL) |
Glucose (mmol/L) |
| Fasting |
105 |
5.8 |
| 1 hour |
190 |
10.5 |
| 2 hours |
165 |
9.2 |
| 3 hours |
145 |
8.0 |
In adults, hypoglycemia can be
observed in certain neoplasms (islet cell tumor,
adrenal and gastric carcinoma, fibrosarcoma,
hepatoma), severe liver disease, poisonings (arsenic,
CCl4, chloroform,
cinchophen, phosphorous, alcohol, salicylates,
phenformin, and antihistamines), adrenocortical
insufficiency, hypothroidism, and functional
disorders (postgastrectomy, gastroenterostomy,
autonomic nervous system disorders). Failure to
promptly separate serum from cells in a blood
collection tube causes falsely depressed glucose
levels. If delay in transporting a blood glucose
to the lab is anticipated, the specimen should be
collected in a fluoride-containing tube (gray-top
in the US, yellow in the UK).
In the past, the 5-hour oral glucose tolerance
test was used to diagnose reactive (postprandial)
hypoglycemia, but this has fallen out of favor.
Currently, the diagnosis is made by demonstrating
a low plasma glucose (<50 mg/dL[2.8 mmol/L])
during a symptomatic episode.
- Urea nitrogen (BUN)
- Serum urea nitrogen (BUN) is increased in acute
and chronic intrinsic renal disease, in states
characterized by decreased effective circulating
blood volume with decreased renal perfusion, in
postrenal obstruction of urine flow, and in high
protein intake states.
Decreased serum urea
nitrogen (BUN) is seen in high carbohydrate/low
protein diets, states characterized by increased
anabolic demand (late pregnancy, infancy,
acromegaly), malabsorption states, and severe
liver damage.
In Europe, the test is called simply "urea."
- Creatinine
- Increase in serum creatinine is seen any renal
functional impairment. Because of its
insensitivity in detecting early renal failure,
the creatinine clearance is significantly reduced
before any rise in serum creatinine occurs. The
renal impairment may be due to intrinsic renal
lesions, decreased perfusion of the kidney, or
obstruction of the lower urinary tract.
Nephrotoxic
drugs and other chemicals include:
| antimony |
arsenic |
bismuth |
cadmium |
| copper |
gold |
iron |
lead |
| lithium |
mercury |
silver |
thallium |
| uranium |
aminopyrine |
ibuprofen |
indomethacin |
| naproxen |
fenoprofen |
phenylbutazone |
phenacetin |
| salicylates |
aminoglycosides |
amphotericin |
cephalothin |
| colistin |
cotrimoxazole |
erythromycin |
ampicillin |
| methicillin |
oxacillin |
polymixin B |
rifampin |
| sulfonamides |
tetracyclines |
vancomycin |
benzene |
| zoxazolamine |
tetrachloroethylene |
ethylene |
glycol |
| acetazolamide |
aminocaproic acid |
aminosalicylate |
boric acid |
| cyclophosphamide |
cisplatin |
dextran (LMW) |
furosemide |
| mannitol |
methoxyflurane |
mithramycin |
penicillamine |
| pentamide |
phenindione |
quinine |
thiazides |
carbon
tetrachloride |
Deranged metabolic processes
may cause increases in serum creatinine, as in
acromegaly and hyperthyroidism, but dietary
protein intake does not influence the serum level
(as opposed to the situation with BUN). Some
substances interfere with the colorimetric system
used to measure creatinine, including
acetoacetate, ascorbic acid, levodopa, methyldopa,
glucose and fructose. Decrease in serum
creatinine is seen in pregnancy and in conditions
characterized by muscle wasting.
- BUN:creatinine ratio
- BUN:creatinine ratio is usually >20:1 in
prerenal and postrenal azotemia, and <12:1 in
acute tubular necrosis. Other intrinsic renal
disease characteristically produces a ratio
between these values.
The BUN:creatinine ratio
is not widely reported in the UK.
- Uric acid
- Increase in serum uric acid is seen
idiopathically and in renal failure, disseminated
neoplasms, toxemia of pregnancy, psoriasis, liver
disease, sarcoidosis, ethanol consumption, etc.
Many drugs elevate uric acid, including most
diuretics, catecholamines, ethambutol,
pyrazinamide, salicylates, and large doses of
nicotinic acid.
Decreased serum uric acid
level may not be of clinical significance. It has
been reported in Wilson's disease, Fanconi's
syndrome, xanthinuria, and (paradoxically) in
some neoplasms, including Hodgkin's disease,
myeloma, and bronchogenic carcinoma.
- Inorganic phosphorus
- Hyperphosphatemia may occur in myeloma, Paget's
disease of bone, osseous metastases, Addison's
disease, leukemia, sarcoidosis, milk-alkali
syndrome, vitamin D excess, healing fractures,
renal failure, hypoparathyroidism, diabetic
ketoacidosis, acromegaly, and malignant
hyperpyrexia. Drugs causing serum phosphorous
elevation include androgens, furosemide, growth
hormone, hydrochlorthiazide, oral contraceptives,
parathormone, and phosphates.
Hypophosphatemia
can be seen in a variety of biochemical
derangements, incl. acute alcohol intoxication,
sepsis, hypokalemia, malabsorption syndromes,
hyperinsulinism, hyperparathyroidism, and as
result of drugs, e.g., acetazolamide, aluminum-containing
antacids, anesthetic agents, anticonvulsants, and
estrogens (incl. oral contraceptives). Citrates,
mannitol, oxalate, tartrate, and phenothiazines
may produce spuriously low phosphorus by
interference with the assay.
- Calcium
- Hypercalcemia is seen in malignant neoplasms (with
or without bone involvement), primary and
tertiary hyperparathyroidism, sarcoidosis,
vitamin D intoxication, milk-alkali syndrome,
Paget's disease of bone (with immobilization),
thyrotoxicosis, acromegaly, and diuretic phase of
renal acute tubular necrosis. For a given total
calcium level, acidosis increases the
physiologically active ionized form of calcium.
Prolonged tourniquet pressure during venipuncture
may spuriously increase total calcium. Drugs
producing hypercalcemia include alkaline antacids,
DES, diuretics (chronic administration),
estrogens (incl. oral contraceptives), and
progesterone.
Hypocalcemia must be interpreted
in relation to serum albumin concentration (Some
laboratories report a "corrected calcium"
or "adjusted calcium" which relate the
calcium assay to a normal albumin. The normal
albumin, and hence the calculation, varies from
laboratory to laboratory). True decrease in the
physiologically active ionized form of Ca++ occurs in many
situations, including hypoparathyroidism, vitamin
D deficiency, chronic renal failure, magnesium
deficiency, prolonged anticonvulsant therapy,
acute pancreatitis, massive transfusion,
alcoholism, etc. Drugs producing hypocalcemia
include most diuretics, estrogens, fluorides,
glucose, insulin, excessive laxatives, magnesium
salts, methicillin, and phosphates.
- Iron
- Serum iron may be increased in hemolytic,
megaloblastic, and aplastic anemias, and in
hemochromatosis, acute leukemia, lead poisoning,
pyridoxine deficiency, thalassemia, excessive
iron therapy, and after repeated transfusions.
Drugs causing increased serum iron include
chloramphenicol, cisplatin, estrogens (including
oral contraceptives), ethanol, iron dextran, and
methotrexate.
Iron can be decreased in iron-deficiency
anemia, acute and chronic infections, carcinoma,
nephrotic syndrome, hypothyroidism, in protein-
calorie malnutrition, and after surgery.
- Alkaline phosphatase (ALP)
- Increased serum alkaline phosphatase is seen in
states of increased osteoblastic activity (hyperparathyroidism,
osteomalacia, primary and metastatic neoplasms),
hepatobiliary diseases characterized by some
degree of intra- or extrahepatic cholestasis, and
in sepsis, chronic inflammatory bowel disease,
and thyrotoxicosis. Isoenzyme determination may
help determine the organ/tissue responsible for
an alkaline phosphatase elevation.
Decreased
serum alkaline phosphatase may not be clinically
significant. However, decreased serum levels have
been observed in hypothyroidism, scurvy,
kwashiokor, achrondroplastic dwarfism, deposition
of radioactive materials in bone, and in the rare
genetic condition hypophosphatasia.
There are probably more variations in the way
in which alkaline phosphatase is assayed than any
other enzyme. Therefore, the reporting units vary
from place to place. The reference range for the
assaying laboratory must be carefully studied
when interpreting any individual result.
- Lactate dehydrogenase (LD or "LDH")
- Increase of LD activity in serum may occur in any
injury that causes loss of cell cytoplasm. More
specific information can be obtained by LD
isoenzyme studies. Also, elevation of serum LD is
observed due to in vivo effects of anesthetic
agents, clofibrate, dicumarol, ethanol, fluorides,
imipramine, methotrexate, mithramycin, narcotic
analgesics, nitrofurantoin, propoxyphene,
quinidine, and sulfonamides.
Decrease of serum
LD is probably not clinically significant.
There are two main analytical methods for
measuring LD: pyruvate->lactate and lactate->pyruvate.
Assay conditions (particularly temperature) vary
among labs. The reference range for the assaying
laboratory must be carefully studied when
interpreting any individual result.
Many European labs assay alpha-hydroxybutyrate
dehydrogenase (HBD or HBDH), which roughly
equates to LD isoenzymes 1 and 2 (the fractions
found in heart, red blood cells, and kidney).
- ALT (SGPT)
- Increase of serum alanine aminotransferase (ALT,
formerly called "SGPT") is seen in any
condition involving necrosis of hepatocytes,
myocardial cells, erythrocytes, or skeletal
muscle cells. [See "Bilirubin, total,"
below]
- AST (SGOT
- )
- Increase of aspartate aminotransferase (AST,
formerly called "SGOT") is seen in any
condition involving necrosis of hepatocytes,
myocardial cells, or skeletal muscle cells. [See
"Bilirubin, total," below] Decreased
serum AST is of no known clinical significance.
- GGTP (GAMMA-GT)
- Gamma-glutamyltransferase is markedly increased
in lesions which cause intrahepatic or
extrahepatic obstruction of bile ducts, including
parenchymatous liver diseases with a major
cholestatic component (e.g., cholestatic
hepatitis). Lesser elevations of gamma-GT are
seen in other liver diseases, and in infectious
mononucleosis, hyperthyroidism, myotonic
dystrophy, and after renal allograft. Drugs
causing hepatocellular damage and cholestasis may
also cause gamma-GT elevation (see under "Total
bilirubin," below).
Gamma-GT is a very
sensitive test for liver damage, and unexpected,
unexplained mild elevations are common. Alcohol
consumption is a common culprit.
Decreased gamma-GT is not clinically
significant.
- Bilirubin
- Serum total bilirubin is increased in
hepatocellular damage (infectious hepatitis,
alcoholic and other toxic hepatopathy, neoplasms),
intra- and extrahepatic biliary tract obstruction,
intravascular and extravascular hemolysis,
physiologic neonatal jaundice, Crigler-Najjar
syndrome, Gilbert's disease, Dubin-Johnson
syndrome, and fructose intolerance.
Drugs
known to cause cholestasis include the following:
| aminosalicylic 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 following:
| acetaminophen |
allopurinol |
aminosalicylic acid |
amitriptyline |
| androgens |
asparaginase |
aspirin |
azathioprine |
| carbamazepine |
chlorambucil |
chloramphenicol |
chlorpropamide |
| dantrolene |
disulfiram |
estrogens |
ethanol |
| ethionamide |
halothane |
ibuprofen |
indomethacin |
| iron salts |
isoniazid |
MAO inhibitors |
mercaptopurine |
| methotrexate |
methoxyflurane |
methyldopa |
mithramycin |
| nicotinic acid |
nitrofurantoin |
oral contraceptives |
papaverine |
| paramethadione |
penicillin |
phenobarbital |
phenazopyridine |
| phenylbutazone |
phenytoin |
probenecid |
procainamide |
| propylthiouracil |
pyrazinamide |
quinidine |
sulfonamides |
| tetracyclines |
trimethadione |
valproic acid |
Disproportionate elevation of
direct (conjugated) bilirubin is seen in
cholestasis and late in the course of chronic
liver disease. Indirect (unconjugated) bilirubin
tends to predominate in hemolysis and Gilbert's
disease.
Decreased serum total bilirubin is probably
not of clinical significance but has been
observed in iron deficiency anemia.
- Total protein
- Increase in serum total protein reflects
increases in albumin, globulin, or both.
Generally significantly increased total protein
is seen in volume contraction, venous stasis, or
in hypergammaglobulinemia.
Decrease in serum
total protein reflects decreases in albumin,
globulin or both [see "Albumin" and
"Globulin, A/G ratio," below].
- Albumin
- Increased absolute serum albumin content is not
seen as a natural condition. Relative increase
may occur in hemoconcentration. Absolute increase
may occur artificially by infusion of
hyperoncotic albumin suspensions.
Decreased
serum albumin is seen in states of decreased
synthesis (malnutrition, malabsorption, liver
disease, and other chronic diseases), increased
loss (nephrotic syndrome, many GI conditions,
thermal burns, etc.), and increased catabolism (thyrotoxicosis,
cancer chemotherapy, Cushing's disease, familial
hypoproteinemia).
- Globulin, A/G ratio
- Globulin is increased disproportionately to
albumin (decreasing the albumin/globulin ratio)
in states characterized by chronic inflammation
and in B-lymphocyte neoplasms, like myeloma and
Waldenström's macroglobulinemia. More relevant
information concerning increased globulin may be
obtained by serum protein electrophoresis.
Decreased
globulin may be seen in congenital or acquired
hypogammaglobulinemic states. Serum and urine
protein electrophoresis may help to better define
the clinical problem.
- T3 uptake
- This test measures the amount of thyroxine-binding
globulin (TBG) in the patient's serum. When TBG
is increased, T3
uptake is decreased, and vice versa. T3 Uptake does not
measure the level of T3
or T4 in serum.
Increased
T3 uptake (decreased
TBG) in euthyroid patients is seen in chronic
liver disease, protein-losing states, and with
use of the following drugs: androgens,
barbiturates, bishydroxycourmarin, chlorpropamide,
corticosteroids, danazol, d-thyroxine,
penicillin, phenylbutazone, valproic acid, and
androgens. It is also seen in hyperthyroidism.
Decreased T3
uptake (increased TBG) may occur due to the
effects of exogenous estrogens (including oral
contraceptives), pregnancy, acute hepatitis, and
in genetically-determined elevations of TBG.
Drugs producing increased TBG include clofibrate,
lithium, methimazole, phenothiazines, and
propylthiouracil. Decreased T3
uptake may occur in hypothyroidism.
- Thyroxine (T4)
- This is a measurement of the total thyroxine in
the serum, including both the physiologically
active (free) form, and the inactive form bound
to thyroxine-binding globulin (TBG). It is increased
in hyperthyroidism and in euthyroid states
characterized by increased TBG (See "T3 uptake," above,
and "FTI," below). Occasionally,
hyperthyroidism will not be manifested by
elevation of T4
(free or total), but only by elevation of T3 (triiodothyronine).
Therefore, if thyrotoxicosis is clinically
suspect, and T4
and FTI are normal, the test "T3-RIA" is
recommended (this is not the same test as "T3 uptake," which
has nothing to do with the amount of T3 in the patient's
serum).
T4 is
decreased in hypothyroidism and in euthyroid
states characterized by decreased TBG. A separate
test for "T4"
is available, but it is not usually necessary for
the diagnosis of functional thyroid disorders.
- FTI (T7)
- This is a convenient parameter with
mathematically accounts for the reciprocal
effects of T4
and T3 uptake to
give a single figure which correlates with free T4. Therefore, increased
FTI is seen in hyperthyroidism, and decreased FTI
is seen in hypothyroidism. Early cases of
hyperthyroidism may be expressed only by
decreased thyroid stimulation hormone (TSH) with
normal FTI. Early cases of hypothyroidism may be
expressed only by increased TSH with normal FTI.
Currently, the method of choice for screening for
both hyper- and hypothyroidism is serum TSH only.
Modern methodologies ("ultrasensitive TSH")
allow accurate determination of the very low
concentrations of TSH at the phyisological cutoff
between the normal and hyperthyroid states.
ASSESSMENT OF ATHEROSCLEROSIS RISK: Triglycerides,
Cholesterol, HDL-Cholesterol, LDL-Cholesterol, Chol/HDL
ratio
All of these studies find greatest utility in
assessing the risk of atherosclerosis in the patient.
Increased risks based on lipid studies are independent of
other risk factors, such as cigarette smoking.
Total cholesterol has been found to correlate with
total and cardiovascular
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