Guidelines for diagnosis and monitoring of thyroid disease

Clinical
Chemistry
188-192
42:1
(1996)
Guidelines
for diagnosis and monitoring
disease: nonthyroidal
illness
R.
JAN
On
the
basis
value,
and
of
cost,
assessment
specificity,
is at
function
in acutely
features
suggest
thyroid
dysfunction,
estimates
show
specificity
and
poor
disease.
When
critically
ill,
positive
disease
of both
improved
by using
elected
or
to
alter
testing
any
and
for
initial
clinical
be
TSH
thyroid
result
the
best
rather
should
than
apparent
either
diagnostic
therapy
either
based
tests
abnormal
results,
abnormality
and
dysfunction.
T4
of
the
T4
be
between
confirmed
Such
an
be-
miuiS:
thyroid
dysfunction
.
thyroxine
.
populations
unselected
in iodine-replete
[1]. Prevalence
is highest
dysfunction
is
likely
in older
to be
regions,
is estimated
of subclinical
responses
women.
at least
the
Unrecognized
as frequent
preva-
time
changes
Ewen
Alfred
Downie
Hospital,
Metabolic
Unit
Commercial
and
Monash
Rd.,
Melbourne,
University
Vie,
Department
Australia
21,
1995;
accepted
October
Il,
in the
will
that
an
be considered
patients.
Questions
the
factors
of
under
difference
(1 h), leading
these
to
critical
and
to
indicators.
and
generate
illness
involves
inhibition
axes
effects
the
normal
In the case of the
complicated
by
of medications.
axis
and
in peripheral
occur
in various
extensively
reviewed
briefly
of methodology
impair
of
[6]. These
further
diagnostic
that
large
intervals.
only
(TSH)
Many
to sampling
axis,
is
been
apparently
yield.
pituitary-thyroid
have
of
are used,
thyrotropin
uncertainty
reference
that
if this
intervals
to the
gonadal
major
thyroid
[2]. However,
between
response
evaluation
the
to be compelling
and TSH
create
of
and
associated
related
of doubtful
can compromise
the
here,
with
assessment
will
grades
on
elsewhere
emphasis
in hospi-
be summarized,
specificity
of various
of Medi3181.
Fax
613
‘Nonstandard
August
are
relations
and
illness
on factors
9276-3782.
Received
be
identify
features
nondiagnostic.’
[3, 5], due
iodothyronines
of
in particular
cine,
[2-4]
standard
in nutrition
[3, 7, 8] and
talized
1) is often
pituitary-
axis,
nonthyroidal
of
to have
prevalence
of T4 (1 week)
and
metabolism
thyroid
at the
is likely
seem
between
pituitary-adrenal
distort
The
to be 1-2%,
dysfunction
a high
hormonal
of the
pituitary-thyroid
lence of definite
thyroid
dysfunction
with a further
2-6%
showing
features
(Fig.
activity
general
changes
In
could
to
illness
reference
relation
abnormalities
diagnostic
The
triiodothy-
the
half-lives
nonspecific
activation
#{149}
thyrotropin
ronine
show
changes
pituitary-thyroid
INflEXING
standard
or uninterpretable
further
is commenced.
that
failure
clinical
testing
laboratory
conditions
discordant
relaof
illness
and
(T4)
the
another
would
but
nonspecific
of
of missing
will
non-steady-state
and
of
T4-TSH
Persistence
should
these
An
estimate
free
thyroxine
the
critical
widespread
individual
dysfunction,
in
maximum
intervention.
of
consequences
is adopted
approach
Diagnosis
on
for
reasons
therapeutic
presence
the
during
Thyroid
or free
alone.
in
serious
dysfunction
is
dysfunction
unreliability
disease
ill patient
methodology.
be
well-known
potentially
TSH
thyroid
testing
with
Whereas
to an important
to lead
thyroid
information
pituitary
of thyroid
any abnormality
therapy.
unrecognized
The
uns-
by
aim
identify,
is to
specificity,
and
acutely
analysis
value
for
and
thyroid
TSH
unlikely
be
the principal
that
chronic
less common.
ill subjects
acutely
patients.
of thyroid
combined
available
dysfunction
tion
T4,
suggest
the
disease-
prognostic
for any
risk
for
by
than
of nonspecific
individual
that
at increased
followed
with
for
features
abnormal
intervals
available
true
could
accept
Unrecognized
effect on outcome,
the detection
of transiently
abnormal
that result
from
nonthyroidal
illness
or medications
is
for
thyroid
much
influenced
previously
adverse
values
true
illness.
sensitivity
positively
lack
in
measurements
useful
ill
but
tested
for
triiodothyronine,
to yield
be readily
groups
should
fore
reference
knowledge
of
value
TSH
The
management
should
with
and
value
is
or
possible
the
for acute
is certainly
would
critically
thyrotropin
results,
predictive
wider
likely
and
function
predictive
abnormalities
currently
positive
thyroid
T4
populations.
related
not
free
of
increases
(T4)
Most
pa-
in severely
used
of abnormal
hypofunction
possibility
When
thyroid
the
hospitalized
the
thyroxine
hospitalization
routine
background
prevalence
have
for
dysfunction.
of both
a high
STOCKIGT
predictive
basis
or a patient’s
of thyroid
(TSH)
positive
no
clinical
unless
patients,
poor
present
of thyroid
tients,
likelihood
low
there
of thyroid
1995.
thyronine;
188
and
abbreviations:
FT4I,
free
thyroxine
TSH,
index.
thyrotropin;
T4,
thyroxine;
T3, triiodo-
Clinical
Chemistry
42,
No.
can
then
suggest
recovery,
B
D
and
/
samples
Changes
may
effects
quirks
vitro
to
Measure
active
Hormone
concentration
reflects
in vitro
low from
Reference
ranges
Normal
response
1. Relation between
normal
in the common
thyroid dysfunction.
a heparin-treated
generation
during
critical
prolonged
depends
on numerous
assumptions
Whereas
not
techniques
of free
value
potential
T4
estimation
of highly
in critically
sensitive,
ill subjects
and
third-generation
so
for
far
HORMONE
a valuable
acute
mone
action
which
show
and
[10].
block
on
Although
such
calorie-sparing
protein
synthesis
is beneficial
direct
benefit
from
adaptive
for
routine
present
occurs
harmful.
limited
therapy
documentation
there
low
T3
of
suggest
Immunoreactive
TSH
often
attributed
also
tends
in
to decrease
part
glucocorticoids
[14]
(either
endogenous
pamine
[15],
which,
even
therapy
profound
rapidly
reversible
to
or
exogenous),
in nonpressor
doses,
suppression
That
measured
immunoreactive
ical activity
in severe
illness also
of
serum
leads
T4
production;
in
processing,
take
total
account
of
that
T4 concentra-
illness
[7, 25, 26].
of studying
in an
body
TSH
attempt
to
of information
management
in feedback
has
decisions
relation,
predictable
for
inverse
in the
to
assay
sensitivity,
TSH
case
of primary
assumptions,
this
[28].
of alterations
when
of
relations
of pituitary-dependent
several
specificity
diseases
concordant
in the case
Subject
and
changes
e.g.,
relation
has high
However,
reflect
in critical
discordant
and T4 are considered
IN
HOSPITALIZED
of 364 consecutive
admissions,
DeGroot
and
population,
free
appropriate
prevalence,
probable
primary
a further
Mayor
thyroxine
apparent
[16].
findings
basis
and
produces
TSH
may show altered
biologremains
an important
possibility
to decreased
of
value
demonstrate
extreme
of a study
index
screening,
Crapo
[I).
nontogether.
after
ognized
primary
hypothyroidism
common
than
FT4I
those
that
in the general
was
study,
or TSH,
25%
but only
indicative
with
low
found
based
FT41
apparently
whereas
than
expected.
had
abnormalities
6%
the concordant
thyroid
had
low
normal
of
with
that
unrec-
much
more
the
prevalence
of either
T4 and TSH
dysfunction
or
the
hypothyroidism.
no higher
68%
cohort,
It is striking
of patients
showed
by
on
and TSH,
of their
subclinical
population,
their
would
as defined
was
of both
was
of primary
Vf41,
finding,”
in -5%
in <1%.
hospital
in
determination
conclusion
apparent
was
In
that,
assessment
showing
of hyperthyroidism
general
f2J suggested
or “case
hypothyroidism
6%
PATIENTS
acute
(FT.51)
This
Hyperthyroidism
changes
TSH
1).
proportion
Helfand
or do-
[17].
Lowered
not
critical
this
either
adequate
sensitivity
diagnostic
are
show
(Fig.
and
provide
[13],
TSH
TSH
or direct
at
illness,
nutrition
and
no
during
in severe
altered
T4
of possible
storage,
do
to the
[27],
indicators,
a high
On the
illness.
a change
is due
as a result
free
because
hormone
SCREENING/CASE-FINDING
basis
states
acids
pa-
effect
of
illness
is no
T4
state
illness
lowering
studies
[12],
this
Any
subnormal
to improve
or pituitary
diagnostic
short-term
chronic
measured
ill patients.
dysfunction,
steady
over-
in severe
confer
whether
Since
replacement
may
abnormalities
in
not
that
that
sample
in
gone
shown
these
is
hor-
those
does
free
thyroid
these
changes
resemble
and
prediction
been
thyroid
as
restriction,
[9] and
response
term,
thyroid
caloric
in
for T4-
RELATION
between
that
diminished
that
conversion
short
evidence
T4 therapy
it is uncertain
or
the
in
that
Supplementary
an
regarded
during
consumption
benefit,
ofT3
to
studies
oxygen
in T4-T3
ILLNESS
generally
at least
lead
mainly
DURING
[7, 8]. The
to illness
lowered
hypothyroidism
the
(T),
concentrations
rests
enzyme
hepatic
CHANGES
economy,
response
T3
subnormal
[11].
TSH
calorie-sparing
a normal
come
AND
triiodothyronine
affinity
of medications,
prognosis
even
critically
TSFI/T4
the
of serum
illness.
hospitalized
activity.
thyrotropin.-releasing
prognostic
Because
Lowering
true
the
assays
TSH.
THYROID
known
of which
of TSH
have
to
individual
most
a poor
some
refine
that may not be lustified
been
during
or effects
lowering
indicate
responses
illness.
direct
is dubious
acids
studies,
of illness
tions
a low
fatty
in lipase
All
for
T4 is an important
delnonstrated
subject
below).
incubation.
duration
relationship
free
of nonesterified
of fatty
Numerous
applicable
(see
specificity
of associated
long
binding
or methodolog-
in heparin-treated
increase
from
in protein
lack
has
et al. /24/
vitro
levels
TSH and T4 shows diagonal deviations
from
types
of primary (A, B) or secondary
(C, 0)
Fig.
This interpretation
normal
trophic-target
it has
increased
generation
or assay
Distinguish
in serum,
heparin-induced
hormone
level
heparin
half-life),
15].
estimates
on apparent
Although
Mendel
T4
methods
presence
in the
is often
[23/.
alterations
With
increased,
longer
[7, 15, 20-22],
T4
[18/.
hypothyroidism
from
free
free
of heparin
sites
T4
tients
conditions
result
origin
transiently
of its much
primary
particular
effect
binding
(because
of medications
of
artifact.
free
also
dysfunction
The
Steady-state
become
suggest
available
thyroid
Assumptions
may
of T4 [19],
ical
of central
concentrations
if T4 is still subnormal
currently
TSH
hypothyroidism
TSH
single
T4
189
1, 1996
(Fig.
TSH;
1). Of
of those
NACB
with
high
TSH,
uncertain
the group
or
In
have
setting
be lower.
higher
care
values
only
2%
showed
suggestive
of
primary
reference
interval
abnormal
values,
primary
patients
with
but
TSH,
TSH
values
whom
in 13%
CHOICE
OF
testing
of their
was
INITIAL
contentious
in
whether
the
TSH
appropriate
features,
convenience.
Lack
deficiencies,
is the
TSH
discrimination
found
preanalytical
true
free
may
give
of
case
factor
true
from
with
free
the
T4
on
assay
For
TSH
or high
but
tend
to give
concentrain the
that
inhibit
T4
T4
values
methods
free
dilution,
which
attenuates
[22/, thereby
failing to show
rise in free
T4.
are much
binding
With
more
of T4
of the
often
sample
give
one-step
free T4 in the
to analytical
between
free
T4
TSH
ASSAYS
The
concentration
euthyroid
artifacts,
and
falsely
due
calibrators
low
or
variations,
these
the
steady-state
of illness
difference
free
[30].
T4
from
in
mltJ/L.
33, figure
ref.
the
the effect
of
the true extent
mIU/L,
are
suppressed
TSH
ized
subjects
subjects
had
ill subjects
TSH
relation
between
Although
values
low
free
all
by
differsuch
When
[5, 35].
If the
yet,
lowering
such
creased
as
improve
few
effects
dopamine
TSH
upper
most
of the
little
establish
of severe
illness,
or the
assay.
on
latter
will
as
values
the
alone.
identify
in critically
of TSH
TSH
loss
clearly
0.1
that
had
the
assays
up
reference
in critical
hypothyroidism.
and
be based
than
increases
glucocorticoids,
critically
0.01
is impaired
limit
<0.1
TSH
should
12 mIUIL
[2], with
or
values
illness
TSH
seen
hospital-
all hyperthyroid
between
studies
of primary
from
et al. [34] found
available
the
the values
whereas
rather
of
separate
of a third-generation
TSH,
Thirdlimit
TSH
nonthyroidal
nonspecific
to 8 or
clearly
As
of
values
specificity
transient
to
almost
Franklyn
T4 and
currently
subjects
increased
basis
mIU/L,
with
between
sensitivity
from
that
had
sensitivity
to
would
<0.01
TSH
value
of samples
the
found
TSH
is a marked
assays.
able
of hyperthyroidism
hypothyroidism,
mIUIL
on
of TSH.
there
well
than
non-
subnormal
TSH
In an analysis
physio-
reflect
predictive
generally
of patients
a diagnosis
the
a functional
in
to free
rather
half-life
short
positive
high
true
often
between
2). Nevertheless,
Hence,
indicate
medications,
of the
on
et al. [33]
with
of
or
In contrast
of hyperthyroidism,
preselected
Spencer
primary
that
illness
dialysis
normal,
of hyperthyroidism
values
illness.
mIU/L,
low,
generally
and
0.0 1-0.02
proteins
[3, 31].
falsely
abbreviated
by equilibrium
third-generation
based
T4
hyper-
to protein
with
illness.
effects
those
assays,
in nonthyroidal
be
distinction
generation
the functional
methods
illness,
severe
occur
Abnormalities
and
below
In critical
estimates
a thirdmlU/L
<0.1
Data
also
may
the
in specificity
in vitro
to true
and
because
and
to the
to be due
may
nonthyroidal
the
as 4%
free
another
[30]
conditions,
In considering
many
to
with
values
artifacts.
illness
of binding
largely
using
0.01-0.02
therapy.
deviations
or
in critical
or
T4
with
responses
(Fig.
analog
presence
glucocorticoid
of TSH
mIU/L
likely
values
for TSH concentrations
estimates
patients
logical
were
many
to measure
subject
one-step
free
sound
two-step
than
that
before
T4,
TSH
sensitivity
permission.
coexists
low
more
vulnerable
raises
with
method-
proteins
theoretically
falsely
protein
or
[3, 31].
contrast,
attempt
free
establish
patients
free
binding
and
results
to
in euthyroid
are particularly
which
[24],
supranormal
thyroidism
Gc,
ref. 3, with
or
values
free T4 assays
of medications
two-step
high
of the competitor-induced
methods,
Various
from
validated
methods
effect
it is difficult
values
In general,
better
reasons
to effects
of the T4 pool
are
normal
con-
precision
ill subjects.
serum
functional
preselected
hyperthyroidism;
from
reduced
with
patients
methodological
estimates.
the
of
assay
hyperthyroidism
T4
and
methodological
and
depends
is
of cost
suppressed
hyperthyroidism
it is
in the absence
a matter
Hyper,
TSH
[32].
T4 estimation
finding
arising
between
due
influence
of sample
binding competitors
methods
For
accuracy,
analytical
artifacts.
heparin
ences
of
studies.
illness,
of free
is largely
in critically
normal,
a fraction
[3, 30]. These
are
test.
associated
Classification
second-generation
illness,
step
In
form
illness
and
low,
dependent
factors
or some
limiting
T4 values
nonthyroidal
[3, 30],
two
ASSAYS
For
assay
low
all of
prevalence
in the
1-0.1
at the
found
almost
The
2.
generation
hospitalized
modified
range.
T4
isolate
values.
of
choice
of
in severe
subnormal
FREE
the
typical
centrations
patients,
(12-14%)
presence
initial
of clinical
assays,
T4
similar
in
receiving
study
et al. [26]
care
of
ASSAY
is done
more
intensive
had
higher
patients
0.0
<0.01
mlU /L
Fig.
TSH
12%
Mayor’s
Rothwell
total
values
the
much
of
and
TSH
indicative
was
exclusion
[2],
subnormal
TSH
When
concordance
DeGroot
admission
showed
increased
tions
after
to
found
relation
mIU/L,
Mortality
200
mIU/L,
0.3-5
TSH-T4
0.2-8
showed
is
In
et al. /26]
range
dysfunction.
none
of nonspe-
abnormalities
a concordant
to
that
studied.
Rothwell
the
TSH
be limited
prevalence
are
outside
dysfunction.
low
of hospital
or TSH
extended
In contrast
time
of T4
thyroid
was
thyroid
dopamine.
the
best
8%
for
of either
where
patients,
TSH
remains
suggested
might
populations
care
had
It
is appropriate
[29]
disease
prevalence
intensive
intensive
although
Ross
for thyroid
will
22%
the
study,
care
when
values.
if any,
abnormalities
this
ambulatory
consecutive
If
to
programs
A much
Ff41
nondiagnostic
abnormalities
found
that
normal
investigation,
response
case-finding
to the
had
further
who
T4.
cific
70%
what
Symposium
illness,
ill
to
20
interval
specificity
of sensitivity.
whether
influence
can
the
TSH-
of medications
normalize
Subnormal
the
in-
T4 values
Clinical
Table
1. Increased
Previous
risk of thyroid
illness.
dysfunction
1, 1996
invaluable
However,
disease(s)
Biological
Irradiation of head and neck
Contrast
agent exposure
Severe
Amiodarone
Hypothermia
could
Interleukin-2
head injury
generally
resolved
identify
only
by
subnormal
T4
transiently
during
such
serial
and
cases,
but
sampling,
substantially
recovery
uncertainty
because
the
increased
from
may
be
combination
TSH
of
may
drug-induced
occur
hypothyroxin-
[5].
the
Because
steady-state
therapy
REFERENCE
in
specified
in
to confirm
in
doubt
Fig.
1,
critically
a persistent
ill
abnormality
we are concerned
related
disease,
abnormalities
and
free
patients
per
T4
free
T4
is of
reference
interval
for
threefold
upwards
and
of sensitivity
loss
0.1-12
mIU/L
underlying
value
can
improved
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be
relation
T4.
he
a
of the
in critically
or
than
two-
so that
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with
range
the
quite
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ill patients
disease,
compatible
ill
halving
be extended
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thyroid
for true
for
Since
[33],
clinical
Hence,
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direct
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of illness-
predictive
reference
TSH
of unrecog-
diagnosis
documentation
positive
less
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than
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6. Reichlin
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function.
of thyroid
groups
thyroid
of
has
cancer
dysfunction
patients
dysfunction,
transient,
been
of
chronic
10-15%
In
in some
will
in acute
psychiatric
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usually
14.
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routine
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These
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