Endocrinology

MJA Practice Essentials

MJA Practice Essentials
Endocrinology

5: Diagnosis and management of hyperthyroidism

and hypothyroidism
Duncan J Topliss and Creswell J Eastman

Despite the development of highly sensitive laboratory tests, clinical assessment and judgement
remain paramount

THYROID
The Medical Journal ofisAustralia
DYSFUNCTION common. In the
ISSN: United States,
0025-729X 16 NSW.
hypothyroidism
February 2004is180
present in 4.6% of the population (clini-
4 186-193 Creswell J Eastman, AM, MD, FRACP, FRCPA, Director, and Clinical
Professor, Department of Medicine, University of Sydney, Sydney,
cal, ©The
0.3%;Medical
and subclinical, 4.3%)
Journal of Australia and
2003 wwwhyperthyroidism
.m j a . c o m .a u
NSW. Reprints: Associate Professor Duncan Topliss, Department of
in MJA Practice Essentials –Endocrinology Endocrinology and Diabetes, Alfred Hospital, Melbourne, VIC 3004.
1
1.3% (clinical, 0.5%; and subclinical, 0.7%). A long-term duncan. to pliss@med.mon ash.ed u.au
study in the United Kingdom found the incidence of
hyperthyroidism was 0.8 per 1000 women annually, and
2
hypothyroidism was 3.5 per 1000 women annually.

Diagnosis of thyroid
dysfunction
Thyroid function testing: Measurement of serum
thyroid stimulating hormone (TSH), using second- or
third-genera- tion assays, is a sensitive index of primary
3
thyroid disease.
Assay of free thyroxine (T4) and triiodothyronine (T3)
reliably eliminates the difficulties in interpretation of total
thyroid hormone levels caused by the common variations
in serum thyroid hormone-binding protein, best
exemplified by the oestrogen-induced rise in thyronine-
binding globulin which increases total thyroid hormone
levels. However, free hormone assays are still subject to
in-vitro and in-vivo artefacts in severe non-thyroidal
illness, severe disturbances of binding proteins, and
4
heparin therapy. Thus, if clinical assessment is not
concordant with thyroid function results, additional tests
and specialist opinion may be necessary. Interpretation
of thyroid function results is summarised in Box 1.
Antibody testing: The most common cause of
thyroid dysfunction in Australia is autoimmunity. The
most sensi- tive in-vitro index for this is measurement of
1
thyroid peroxi- dase antibody level, but this can
occasionally give false negative results (eg, in juvenile
autoimmune thyroiditis). In primary hypothyroidism, a
raised level of thyroid peroxidase antibody is evidence for
autoimmune chronic lymphocytic thyroiditis.
In hyperthyroidism, the role of routine antibody testing is
less clear. Diagnosis of Graves disease is usually possible

Series Editors: Donald J Chisholm and Jeffrey

D Zajac

Department of Endocrinology and Diabetes, Alfred

Hospital, Melbourne, VIC.
Duncan J Topliss, MD, FRACP, FACE, Director, and Associate
Professor, Department of Medicine, Monash University, Melbourne, VIC.
Institute of Clinical Pathology and Medical
Research, Westmead Hospital, Sydney,
186 MJA Vol 180 16 February 2004
ABSTRACT
■ The most common cause of hyperthyroidism in Australia
is Graves disease, caused by a defect in
immunoregulation in genetically predisposed individuals,
leading to production of thyroid-stimulating antibodies.
■ Each of the three modalities of therapy for Graves
disease
— thionamide drugs, subtotal or total thyroidectomy, and
radioactive iodine ablation — can render the patient
euthyroid, but all have potential adverse effects and
may not eliminate recurrences.
■ Hypothyroidism occurs in about 5% of the adult
population; most present with “subclinical”
hypothyroidism (mild thyroid failure), characterised by
raised levels of serum thyroid stimulating hormone (TSH)
but normal free thyroxine (T4).
■ The most common cause of hypothyroidism in Australia
is autoimmune chronic lymphocytic thyroiditis,
characterised by raised circulating levels of thyroid
peroxidase antibody.
■ Symptoms and signs of hypothyroidism are often mild or
subtle and, when there is clinical suspicion, thyroid
function tests are needed; if serum TSH level is raised,
free T4 and thyroid peroxidase antibody should be
measured.
■ Replacement therapy with thyroxine is the cornerstone
of therapy (1.6 g/kg lean body weight daily, taken on an
empty stomach); combination therapy with thyroxine and
liothyronine (T3) is promoted, but there is little evidence
of its clinical benefit.

MJA 2004; 180: 186–193

clinically, and measurement of thyroid peroxidase

antibody or TSH-receptor antibody may not contribute to
diagnosis or management. However, measurement of
TSH-receptor antibody has a role when the cause of
hyperthyroidism is obscure, in assessing the risk of
neonatal hyperthyroidism in pregnant women with a
history of Graves disease, and in assessing the risk of
relapse after a course of antithyroid drugs in Graves
disease.
Radionuclide scanning: Radionuclide thyroid scanning
is not routinely necessary for diagnosing Graves disease
or toxic multinodular goitre, but is useful when the cause
of hyperthyroidism is not apparent (eg, when no goitre
is palpable, when neck pain or tenderness suggests
subacute thyroiditis, or when a solitary “hot” nodule is
suspected).

187 MJA Vol 180 16 February 2004

Endocrinolo MJA Practice
gy Essentials

1: Interpretation matrix for thyroid function results*

High T4 Normal T4 Low T4

MJA Practice Endocrinolo
Essentials gy
High TSH In vivo or in vitro artefact Mild thyroid failure (primary) Primary hypothyroidism
Pituitary hyperthyroidism [TSHoma] (also termed subclinical hypothyroidism
Thyroid hormone resistance and diminished thyroid reserve)
Normal TSH As above Normal (in patients taking Pituitary or hypothalamic hypothyroidism
Sampling within 6 h of thyroxine dose thyroxine, TSH > 3 mU/L may Severe non-thyroidal illness
indicate subtle underreplacement)
Low TSH Hyperthyroidism Subclinical hyperthyroidism Subtle Pituitary or hypothalamic hypothyroidism
(for this diagnosis, TSH must be thyroxine overreplacement Thyroid Severe non-thyroidal illness
suppressed rather than just low) autonomy (multinodular goitre or
autonomous functioning thyroid nodule)
Non-thyroidal illness
T4 = serum free thyroxine. TSH = thyroid stimulating
hormone.
* The Health Insurance Commission restricts financial reimbursement to serum TSH alone, except in specified clinical circumstances, when additional
measurements of free T 4 and free triiodothyronine (T3) are sanctioned. We suggest that practitioners routinely request “thyroid function tests” and provide clear
clinical information to enable the laboratory to perform additional tests if justified. The information should include the suspected condition (especially if
hypopituitarism) and medications (eg, thyroxine, carbimazole or propylthiouracil, amiodarone or phenytoin).

Hyperthyroidi Management of Graves

sm disease
The terms hyperthyroidism and thyrotoxicosis are used The three modalities of therapy for Graves disease
interchangeably, irrespective of whether the disorder is are:
caused by endogenous overproduction or excessive inges- ■ blocking synthesis of thyroid hormone with antithyroid
tion of thyroid hormones. Causes of hyperthyroidism are drugs;
shown in Box 2. Most common in Australia are Graves ■ subtotal or “near-total” thyroidectomy; and
disease and toxic multinodular goitre. Management of ■ destruction of the thyroid by radioactive iodine (radio-
hyperthyroidism depends on the cause (particularly whether iodine ablation).
it is self-limiting, as in subacute thyroiditis), the size and While each modality is satisfactory in rendering the
nature of the goitre, intercurrent illnesses or medication 6
patient euthyroid, none is ideal, as all have a risk of
and, especially in Graves disease, patient preference. adverse effects and none but total thyroidectomy eliminates
the risk
Graves of recurrence. Although total thyroidectomy virtually elimi-
disease nates this risk, it is at the expense of a certain requirement
for thyroid hormone replacement. Selecting treatment for
Graves disease is caused by stimulation of the thyroid by an individual depends on many factors, not least being
antibodies which bind to TSH receptors and mimic the patient choice and physician bias. In the United States,
effect of prolonged TSH stimulation. These TSH-receptor radioiodine is the preferred primary modality, but, in
antibodies result from abnormal immunoregulation permit- Europe and Australia, antithyroid drug therapy is preferred
for patients with a first episode of Graves hyperthyroidism,
ahead of radioiodine and, lastly, surgery.7
ting generation and expansion of clone(s) of antibody-
Antithyroid drugs: Most patients with Graves
producing cells in genetically predisposed individuals with
5 disease
specific HLA-D subtypes. Spontaneous exacerbations and require short-term (several months) treatment with an
remissions of Graves disease can occur. The antithyroid drug (thionamide) before consideration of
environmental triggers are still not well characterised,
but postpartum exacerbation is common, and such a
history should be sought routinely when Graves disease is
2: Causes of hyperthyroidism
diagnosed. Excess
iodine can precipitate active Graves disease by providing ■ Graves disease ■ hCG-mediated
more substrate for hormone synthesis and possibly also by ■ Multinodular goitre (hyperemesis gravidarum,
■ Autonomously functioning trophoblastic disease)
disturbing immune function. Persistence or recurrence of
single thyroid nodule ■ Fetal and neonatal
Graves disease is more likely when there is a previous hyperthyroidism
(adenoma)
history ■ Thyroiditis (subacute, (TSH-receptor-antibody-
of recurrent disease, in the presence of a large goitre, when postpartum, lymphocytic) mediated)
T3 excess persists despite control of T 4 with thionamide ■ Factitious hyperthyroidism ■ Struma ovarii
therapy, and when TSH-receptor antibody persists during (thyroid hormone ingestion) ■ TSH-secreting pituitary
tumour
thionamide therapy. In addition to hyperthyroidism, other ■ Functioning thyroid
carcinoma (follicular ■ Partial (pituitary-selective)
autoimmune manifestations of Graves disease are Graves
carcinoma) thyroid hormone resistance
ophthalmopathy (Box 3) and Graves dermopathy (pretibial
myxoedema). Autoimmune thyroid disease is associated
with some other, less common, autoimmune diseases, including pernicious anaemia and Addison’s disease.
 Endocrinolo MJA Practice
gy Essentials
hCG = human chorionic gonadotropin. TSH = thyroid stimulating hormone.
3: Graves ophthalmopathy

A: Asymmetrical proptosis, more marked in the right eye. Although unilateral proptosis sometimes occurs in Graves disease, further imaging
may be needed to exclude diagnoses such as orbital tumour. B: Patient attempting to look up, showing tethering of the left eye by swollen
inferior external ocular muscles, slight proptosis and lid retraction (with sclera visible above the iris of the left eye) and some infiltrative
swelling above the inner canthus of each eye. C: Marked bilateral proptosis with lid retraction and conjunctival injection indicating active
inflammatory ophthalmopathy.
longer-term or definitive active Graves disease, effect, as leukaemia, other
therapy. Prolonged thionamide i malignancies,
thionamide therapy (12– therapy can lower serum t reproductive
18 months in a first free T4 level below abnormalities or
8
episode ) has the normal, while free T3 level i congenital abnormalities
advantage of avoiding s in the offspring of
remains raised, and the 10
surgery with its inherent patient remains hyper- treated patients. It is
risks and destruction of thyroid. Thionamide dose r thus the default option for
the thyroid by should thus not be a definitive therapy in
radioiodine, and seems reduced on the basis of r adolescents and adults.
to give the best chance serum free T4 level alone. e More caution is
of sustained remission. recommended in children
Clinical assessment
Nonetheless, the risk of a because of the known
remains paramount,
relapse is greater than greater risk of inducing
guided by full thyroid n
50%. thyroid nodules and
function testing. d
Thionamide dose must carcinoma from external
Combined thionamide
be individualised, irradiation and other
and thyroxine therapy o
depending on radionuclide exposure in
(block– replace regimen) f
the initial severity of childhood.
is useful for patients with
disease and response, unstable hyper- Radioiodine therapy
a does not achieve
but an initial thyroidism, in whom b euthyroidism
divided dose of 10–30 small variations in
r immediately,
mg daily of carbimazole thionamide dose cause
u necessitating low-dose
is usually major fluctuations in
thyroid function, but does p thionamide therapy for
satisfactory. Response
t several months in many
should be assessed after not
patients. Occasionally,
2–4 weeks increase the
o early (usually transient)
and periodically likelihood of hypothyroidism occurs,
thereafter, with a long-term n
9 s with low serum free T4
minimum eventual fre- remission.
e levels without TSH
quency of every third Beta-blocker drugs are elevation, as TSH is
month. Initial high doses useful adjuncts for rapid t
. often suppressed for
should be sympto- weeks to months after
progressively reduced to matic relief in Radioiodine a b lat i on :
Ablative therapy with hyperthyroidism.
once-daily maintenance hyperthyroidism. Standard The likelihood of
doses of doses reduce heart radioiodine is
recommended for control of hyperthyroidism
2 rate, sweating and tremor, after a single radioiodine
patients with recurrent
. but do not influence treatment varies with the
hyperthyroidism
5 hypermetab- dose, continuing
or hyperthyroidism that
– olism or hormone immunological stimulus
persists after a prolonged
1 levels. Non-selective - of the thyroid, and thyroid
course of
0 blockers have respon- siveness to the
antithyroid drugs.
generally been radioiodine. Overall,
Reassuringly, several
m preferred for their control is achieved
large, long-term
g better effect on tremor. initially in about 75% of
studies have shown no
/ All patients should be cases. Eventual control
increased risk of thyroid
d warned about the rare through repeated doses,
cancer,
a but serious given after a minimum of
y complication of six months, is virtually
thionamide therapy, assured, but often at the
( agranulocytosis, with expense of permanent
B instructions to suspend hypothyroidism. The
o therapy while obtaining a probability of developing
hypothy- roidism
x white cell
increases with the dose of
count if fever, sore throat,
radioiodine and the
4 or other sepsis develops.
passage of time, so that
) We do
long-term follow-up and
. not recommend routine patient education is
Occasionally, in very blood testing for this side required in all cases.
T h yr oi d e ct om y : i
Thyroidectomy is c
generally undertaken
only after euthyroidism m
has been attained with u
thionamide l
therapy. The high rate t
of relapse after subtotal i
thyroidec- n
tomy has led many o
surgeons to recommend d
u
complete
l
thyroidectomy (termed a
total or near-total r
thyroidectomy),
but this inevitably
g
necessitates permanent o
thyroid hormone i
replacement therapy. t
Thyroidectomy offers r
rapid control e
without radiation
Toxic multinodular
exposure and reliably
goitre is almost always
removes a substan-
preceded by long-
tial goitre. It becomes
standing multinodular
the therapeutic choice
goitre and probably, in
when malig-
nancy is suspected or most
a large goitre is
causing local
compression. As with all
surgery, the individual
skill of the
surgeon is paramount,
and there should be no
role for the
o
c
c
a
s
i
o
n
a
l

e
x
p
o
n
e
n
t
.

T
o
x
patients, by episodes of subclinical hyperthyroidism. Hyper-
thyroidism is often precipitated by exposure to excessive
iodine from adventitious sources, such as medications and
radiocontrast media used in imaging procedures (see list
11
under Iodine-ind uced hyper thyroidism). The goitre may
compress or obstruct the trachea. Plain radiography of the
trachea may reveal this, but computed tomography is better,
provided no contrast is administered. Magnetic resonance
imaging best demonstrates the extent of the goitre but is not
directly available to the general practitioner. Oesophageal
symptoms occasionally require assessment by barium swal-
low. Venous obstruction, which is more common than
oesophageal obstruction, is assessed clinically (Box 5).
The initial choice of therapy for toxic multinodular goitre
is a thionamide to render the patient euthyroid. Spontane-
ous remission is not part of the natural history of this
condition and, unless there has been a specific precipitating
episode of iodine exposure, ablative therapy is indicated. In
the absence of obstruction, radioiodine is the treatment of
choice. Higher doses, and sometimes multiple treatments,
may be necessary for a satisfactory outcome. If obstruction
is present then thyroidectomy is indicated. Total
thyroidec- tomy also obviates the risk of regrowth of the
goitre.
Autonomously functioning thyroid
nodule
A single hyperfunctioning nodule, usually an adenoma, is an
uncommon cause of hyperthyroidism. If a single nodule is
detected on clinical or ultrasound examination in a hyper-
thyroid patient, the diagnosis should be confirmed by a
radionuclide scan. Radioiodine is the preferred treatment
after control of thyroid function by a short course of
thionamide. The risk of radiation-induced hypothyroidism
is small in this condition, in contrast to Graves hyperthy-
roidism, as the hyperfunctioning nodule suppresses the rest
12
of the thyroid. Lobectomy is still an acceptable choice.
Subacute
thyroiditis
Subacute thyroiditis is a self-limiting, postviral condition,
which can vary from a mild disorder to a debilitating
disease lasting up to a year. Thyroid pain and tenderness
are usual but not ubiquitous. Because the
hyperthyroidism results from leakage of preformed
hormone from damaged thyroid cells rather than increased
production, the circulating T3/T4 ratio is lower than in
Graves disease and toxic multinodular goitre. Thyroid
radionuclide uptake is reduced or absent. This finding is
often considered diagnostic of subacute thyroiditis, but
is also seen in patients ingesting large quantities of
iodine or taking suppressive doses of thyroxine. The
conditions can be differentiated by serum thyroglobulin
level, which is usually raised in subacute thyroiditis but low
in the others. Antithyroid antibodies can appear transiently
at modest levels.
Antithyroid drug therapy is inappropriate and ineffective.
Beta-blockers, aspirin, and non-steroidal anti-inflammatory
drugs provide symptomatic relief. Glucocorticoids, such as
prednisolone (20 mg per day), provide symptomatic
improvement in those who do not respond well to anti-
inflammatory drugs. The hyperthyroid phase is characteris-
tically followed by a hypothyroid phase (not usually
requir- ing treatment), then eventual return to
euthyroidism. Further episodes can occur.

4: Case report — hyperthyroidism At 6-week review, the patient was feeling much better, and her
pulse rate was 76 bpm. Free T4 level was 16 pmol/L; free T3, 4.8
Presentation: A 25-year-old woman presented with a 6-month pmol/L; and TSH, 0.03 mU/L. The carbimazole dose was reduced
history of tremor, heat intolerance, irritability and weight loss of 4 to 10 mg/
kg. She had a small, diffuse, non-tender goitre (less than twice
normal size), a pulse rate of 104 bpm, and slightly tremulous,
warm, moist hands but no proximal myopathy. She had no
personal or family history of thyroid disease. Fertility was not a
current issue.
Investigations: Serum free thyroxine (T4) level was 34 pmol/L
(reference range [RR], 9.3–23.8 pmol/L); free triiodothyronine
(T3) level was 12 pmol/L (RR, 1.8–6.0 pmol/L); thyroid stimulating
hormone (TSH) level was < 0.03 mU/L (RR, 0.4–4.7 mU/L); and
thyroid peroxidase antibody level was 250 U/mL (RR, < 35
U/mL).
Comment: Radionuclide thyroid scanning will not assist
management in the absence of a reasonable need to exclude
subacute thyroiditis and in the presence of goitre.
Management: Graves disease was diagnosed, and carbimazole
(10 mg twice daily) prescribed.
At 3-week review, the patient was feeling better, and free T4 level
was 20 pmol/L; free T3, 6.5 pmol/L; and TSH, still < 0.03 mU/L. The
carbimazole dose was reduced to 15 mg/day, and a further 3-
week review scheduled.
Comment: There was a clinical and biochemical response, but
free T3 level was still high. Dose reduction by 25%–50% was
necessary to avoid overshoot to hypothyroidism.
day as a single dose. The options for longer-term therapy were
now discussed in detail with the patient.
Comment: Serum TSH can remain suppressed for weeks to
months after euthyroidism is restored and therefore cannot be
used to guide acute antithyroid drug therapy. Carbimazole is
effective in a once- daily dose for maintenance, assisting
compliance. When patients are euthyroid and well, the longer-
term options for therapy should be discussed.
The patient elected to have a thionamide course. The dose
was reduced and maintained at 5 mg/day in subsequent visits,
with thyroid function monitoring every 2–3 months. After 18
months therapy was ceased.
Comment: Thyroid function should then be checked at
decreasing frequencies indefinitely (eg, at 1 month, then after a
further 2 months, 3 months, 6 months, and then annually) or if
symptoms develop.
Three years later, the patient wished to get pregnant and
enquired about possible thyroid problems. She was clinically
euthyroid.
Comment: Thyroid function should be checked, not only to
exclude subclinical hyperthyroidism, but also hypothyroidism,
which is part of the natural history of Graves disease and can
have a subtle adverse effect on fertility and fetal development. If
the patient is euthyroid without prior ablative therapy, then assay
of TSH-receptor antibodies is unnecessary, but may be useful in
predicting the risk of neonatal hyperthyroidism. Thyroid function
should be monitored, especially in the first trimester and
particularly post partum, and the patient should be reminded
about postpartum recurrence.
5: Venous obstruction caused by goitre

A: Pemberton’s sign in a man with a goitre extending through the thoracic inlet and obstructing venous drainage. (A1) At rest, he has
moderate puffiness of the face. (A2) After raising the arms briefly to further obstruct venous drainage, swelling increases and there is
marked suffusion of the face.
B: Woman with an obstructive, predominantly retrosternal, multinodular goitre, showing dilated anterior chest veins caused by
increased
collateral venous
flow.
P t the drug itself causes
o h thyroiditis in (type II amiodarone-
s y 5%–10% of users, induced hyperthyroidism,
t r typically after about 2 the most common form in
14
p o years of therapy Australia ). Although
a i type I may respond to
r d high-dose thionamide
t i therapy, and type II to
u s glucocorti- coid therapy,
m m
these conditions can be
Iodine can induce severe and treatment-
h resistant, and
hyperthyroidism in
y
patients with an thyroidectomy may be
p
e underlying needed.
r autonomously
t functioning thyroid
gland (caused, for 6: Severe primary
h
hypothyroidism
y example, by a nodule,
r multinodular goitre or
o Graves disease). It is
i characterised by
d suppressed serum TSH
i
level with normal
s
m circulating thyroid
hormone levels, and is
Hyperthyroidism in the most commonly found in
postpartum period is patients with longstanding
13
usually autoimmune, multinodular goitre. A
caused by either Graves history should be sought
disease or thyroiditis. It of recent exposure to
differs from postviral iodine from radiocontrast
thyroiditis, although it media and pharma-
may follow a similar ceuticals such as
transient course, and amiodarone, herbal and
may recur after vitamin prepara- tions,
subsequent pregnancies kelp and Cellasene (a A: A patient with
and progress to unrecognised severe
preparation marketed as
primary hypothyroidism
established a treatment for cellulite). who became severely
hypothyroidism. As radiocontrast media obtunded after surgery for
are clear precipitants, fractured neck of femur.
computed tomography Marked myxoedema is
I evident.
o should be performed
d without contrast in the B: Several months later,
i investigation of after therapy including
n euthyroid goitre and thyroid hormone
undiagnosed neck mass. replacement.
e
- The antiarrhythmic
i drug amiodarone has a
n 37% iodine content, with
d high tissue penetration
u and a half-life of
c months. The elemental
e
iodine load of about 9 mg
d
per day from a 200 mg
tablet can precipitate
h
hyperthyroidism if there
y
is pre-existing goitre (type
p
e I amiodarone-induced
r hyperthyroidism), while
MJA Vol 180 16 February 2004 191
191

7: Causes of
hypothyroidism
Autoimmune
lymphocytic thyroiditis
■ Atrophic thyroiditis
■ Classic Hashimoto’s disease
Post-ablative therapy
■ Radioiodine (RAI) therapy
■ Thyroidectomy
Transient
■ Subacute thyroiditis
■ Postpartum thyroiditis
■ Early post-ablative therapy
(RAI, subtotal thyroidectomy)
Drug-induced
■ Thionamide
■ Lithium
■ Amiodarone
■ Interferon
■ Drugs that interfere with
thyroxine absorption in
treated hypothyroidism (iron
salts, cholestyramine,
sucralfate)
Iodine-associated
■ Iodine-deficiency disease
■ Iodine-induced
Infiltrative
■ Reidel’s thyroiditis
■ Scleroderma
■ Amyloid disease
■ Haemochromatosis
Neonatal/congenital
■ Thyroid agenesis/ectopia
■ Genetic disorders of TSH, TSH
receptor, thyroid peroxidase,
thyroglobulin, pendrin
■ Transplacental passage of
blocking TSH-receptor
antibody
Secondary
■ Pituitary or hypothalamic
disease
Other
■ Thyroid hormone resistance
serum thyroglobulin are suppressed. No treatment strategy
is known to be particularly effective, but non-judgemental
explanation of the medical consequences and gradual dose
reduction with psychological suppor tive therapy, if
accepted, is recommended.
Rare forms of
hyperthyroidism
TSH-secreting pituitary tumours constitute less than 1% of
all pituitary tumours. Thyroid stimulation results in hyper-
thyroidism with a diffuse goitre, clinically similar to Graves
disease. The presence of high serum free T4 and T3 levels
with an unsuppressed serum TSH level suggests the diagno-
18
sis. Other clinical conditions that need to be distinguished
include the partial (pituitary) resistance form of inherited
19
thyroid hormone resistance syndrome, and anomalous
laboratory TSH results caused by heterophil antibodies
(common antibodies that interfere with assays using mouse
monoclonal antibodies; they are either generated directly
against mouse antigens after exposure to mice or cross-react
with these antigens).

TSH = thyroid stimulating hormone.

Hypothyroidi
sm
Subclinical
hyperthyroidism The most common cause of hypothyroidism is primary
failure of the thyroid gland. While secondary hypothy-
roidism from pituitary or hypothalamic dysfunction is rare,
it is vital to identify the site of dysfunction at the outset. As
“Subclinical” hyperthyroidism is a poor term for this condi-
advice. It may be severe, with weight loss, weakness, cardiac
tion, as the definition is biochemical rather than clinical, tachyarrhythmia and failure. When due to thyroxine inges-
and tion, serum free T4 level is elevated disproportionately to T3
clinical consequences are possible. It is characterised by level, but, when due to liothyronine (T3) ingestion, serum
chronically suppressed TSH levels but normal serum free T4 free T4 level is suppressed. Thyroid radionuclide uptake and
and T3 levels. The condition must be distinguished from
transient TSH suppression in acute illness or after drug
therapy (eg, high-dose glucocorticoids). It occurs com-
monly with multinodular goitre, a hyperfunctioning single
thyroid nodule and thyroxine overreplacement. Subclinical
hyperthyroidism is associated with an increased risk of atrial
15
arrhythmia in those aged over 60 years and loss of bone
16
mineral density in postmenopausal women. Antithyroid
therapy should be considered in patients with subclinical
hyperthyroidism at increased risk of complications, and
reduction of thyroxine dose in those taking replacement
therapy. Subclinical hyperthyroidism is intentionally
pro- duced by TSH-suppressive thyroxine therapy for
differenti- ated thyroid cancer, but it is unnecessary to
continue this therapy lifelong if likely eradication of
carcinoma has been
demonstrated.

Factitious
hyperthyroidism
This is the deliberate, usually surreptitious, excessive
17
inges- tion of thyroid hormone. It is often part of a wider
psychiatric condition and may be refractory to medical

192 MJA Vol 180 16 February 2004

serum TSH levels rise logarithmically in response to
declin-
ing thyroid hormone levels, the distinction between
primary
and secondary hypothyroidism is usually obvious.
The
situation can, however, be confounded by impaired
pituitary
response in concomitant severe non-thyroidal illness,
occa-
sionally in ageing, and in profound prolonged hypothy-
roidism. A modest TSH elevation (up to 15–20 mU/L)
in
the recovery phase from the severe sick euthyroid state
(eg,
after acute trauma, burns or infection), or on cessation of
20
dopamine infusion, can cause diagnostic confusion.
Hypothyroidism covers a wide spectrum of clinical and
biochemical disease, from clinically inapparent disease to
myxoedema coma (Box 6). The causes of
hypothyroidism are shown in Box 7.

Primary
hypothyroidism
In Australia, the most common cause of hypothyroidism is
autoimmune chronic lymphocytic thyroiditis. It is more
common in women than men (ratio, five to one) and is
most common in the fifth and sixth decades, when the
prevalence of antithyroid antibodies in women is 10%.
Classic Hashi- moto’s disease, with an enlarged, firm,
bosselated thyroid gland, is less common than the
atrophic form. Both are characterised by the presence of
serum antithyroid antibod- ies. Whereas levels of
thyroglobulin and microsomal anti- bodies have
conventionally both been measured, the sensitivity and
specificity of thyroid peroxidase antibody assays make
this the only test now required.
Around the world, iodine deficiency still remains the
predominant cause of hypothyroidism. Mild iodine defi-

MJA Vol 180 16 February 2004 193

193
 8: Case report — subclinical
hypothyroidism
problems from hypothyroidism and that combined thyroxine and
Presentation: A 52-year-old woman presented with tiredness, liothyronine (T4/ T3) therapy is best.
increasing over the previous 6 months. She was Comment: The worth of therapy in these circumstances is
perimenopausal but did not have severe vasomotor symptoms. unresolved. In its favour are a possible reduction in symptoms,
She was not depressed, and there were no significant physical early prevention of progression to frank hypothyroidism, and
findings. possible prevention of accelerated vascular disease.
Investigations: Routine laboratory tests excluded anaemia and Against giving therapy is that symptoms very often do not
iron deficiency, but serum free thyroxine (T4) level was 11.9
change, and compliance is therefore poor, lipid profile generally
pmol/L (reference range [RR], 9.3–23.8 pmol/L); and thyroid does not improve when TSH is < 10 mU/L, there is no good
stimulating hormone (TSH) level was 8.2 mU/L (RR, 0.3–4.7 mU/L). evidence that vascular disease risk is reduced, and therapy
On review of specific symptoms, the patient felt her skin was a increases the risk
little dry and of subclinical hyperthyroidism and loss of bone mineral density
her mental concentration had deteriorated. She had in postmenopausal woman.
chronic constipation.
General recommendations for asymptomatic patients are:
Comment: This is a common problem. Symptoms are mild,
■ Patients with TSH < 10 mU/L and no antithyroid antibodies
non- specific and shared by many in the population who are
should be monitored, with therapy started if TSH level
not hypothyroid.
increases above 10 mU/L.
Repeat thyroid function tests confirmed earlier results, with free
■ Patients with TSH 5–10 mU/L and antithyroid antibodies
T4 ,
present could be treated, depending on patient preference.
12.2 pmol/L; and TSH, 7.6 mU/L. Thyroid peroxidase antibodies
The best therapy is thyroxine alone, adjusted for a TSH level of
were present at 1200 U/mL (RR, < 35 U/mL). Serum lipid tests
1–2 mU/L. Patients who choose not to be treated should have
showed cholesterol, 5.7 mmol/L (RR, < 5.5 mmol/L); high
annual monitoring.
density lipoprotein, 1.2 mmol/L (RR, > 1.0 mmol/L); and
triglycerides, The patient elected to have treatment (thyroxine, 100 g/day).
1.8 mmol/L (RR, < 2.0 mmol/L). After 4 months, her thyroid function results were normal (free
T4 ,
Comment: The patient has subclinical hypothyroidism (also
15.8 pmol/L; TSH, 1.9 mU/L), but she felt no different. She elected
known as mild thyroid failure or diminished thyroid reserve). In the
to discontinue treatment, but, as she was positive for thyroid
presence of circulating antithyroid antibodies (thyroid peroxidase
peroxidase antibodies, her GP recommended annual
or thyroid microsomal antibodies), the risk of progression to frank
thyroid function testing.
hypothyroidism is 5% per year. Hypothyroidism may be
contributing to the hyperlipidaemia and to accelerated coronary
disease.
The patient was convinced that hypothyroidism was the cause
of her symptoms. She had read on an Internet site about severe

ciency is re-emerging in Australia (possibly related to biochemically by a raised serum TSH level in the presence of
decreased consumption of iodised salt), but apparently not a serum free T4 level within the reference range. Because
21
yet to a level to cause hypothyroidism. Public health the T4 set point varies between individuals, it is possible
measures to address this issue are likely to be needed, for a serum free T4 level in the normal range for the
including monitoring of iodine intake in the population. population to be too low in a given individual. The risk of
More widespread use of iodised salt, both domestically and progression to frank hypothy- roidism increases with
in manufactured food, may be sufficient to deal with the increasing TSH levels (odds ratio for women, 8), significant
problem. titres of circulating autoantibody (odds ratio, 8) and even
2
more with both (odds ratio, 38).
Congenital
hypothyroidism
Congenital hypothyroidism has an incidence of about one
in
4000 births, with thyroid agenesis and ectopia the main
causes. Exposure of premature infants to iodine-containing
22
antiseptics can result in transient hypothyroidism.
Routine screening of all neonates by heel-prick blood
sampling enables detection and treatment by the 10th day
after birth.
Appropriate thyroxine therapy, progressively adjusted by
body weight, results in normal intellectual development.

Subclinical
hypothyroidism
Also known as mild thyroid failure and diminished thyroid
reserve, “subclinical” hypothyroidism is defined
 In general, treatment is recommended if serum TSH
level is more than 10 mU/L or progressively rising, or if
23
thyroid antibodies or dyslipidaemia are present (see case
report, Box 8).

Management of
hypothyroidism
Replacement thyroxine is the cornerstone of therapy for
hypothyroidism. A dose of 1.6 g per kg body weight daily
is the average required in adults. The principal determinant
of dose is lean body mass, so patients in old age may need
as little as 50 g/day. In patients with ischaemic heart
disease, a low initial thyroxine dose is recommended (12.5–
50 g/day) to avoid exacerbating angina, but in some
patients thyroxine replacement is impossible until
coronary artery bypass surgery has been performed, with
extreme attention to drug and fluid therapy.
As thyroxine has a half-life of 1 week, once-daily admin-
istration is fully adequate to maintain stable levels. It
should be taken on an empty stomach, separately from
24
other drugs. Dose should not be adjusted until after a
minimum of three to five half-lives to allow a steady state
to be attained. In primary hypothyroidism,
normalisation of serum TSH level is the best
biochemical marker of adequate therapy. Occasionally,
symptoms of hypothy- roidism appear to persist when
TSH level is at the upper end of the reference range, and
dose adjustment to achieve the mean normal TSH
1
level of 1–2 mU/L is recom- mended. In pregnancy,
the dose may need to be increased. Maintaining a
25
normal TSH level is important for fetal development.
MJA Practice Essentials
Combined thyroxine and liothyronine (T3) therapy is
being promoted, particularly on some Internet sites, for
patients whose symptoms persist despite apparently ade-
quate thyroxine therapy. There are few published data to
26
support this practice, and a recent Australian study
27
showed no benefit. Thus, it should be discouraged in the
absence of evidence of benefit, with thyroxine alone remain-
ing standard therapy.
In patients with hypothalamopituitary hypothyroidism,
serum TSH level is not a valid biochemical indicator of
adequate replacement, and it is usual to adjust the
thyroxine dose to achieve an approximate mean normal
serum level of free T4.
References
1. Hollowell JG, Staehling NW, Flanders WD, et al. Serum TSH, T4 and thyroid
antibodies in the United States population (1988-1994): National Health and
Nutrition Survey (NHANES III). J Clin Endocrinol Metab 2002; 87: 486-488.
2. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid
disorders in the community: a twenty-year follow-up of the Whickham Survey.
Clin Endocrinol (Oxf) 1995; 43: 55-68.
3. Spencer CA, Takeuchi M, Kazarosyan M. Current status and performance goals
for serum thyrotropin (TSH) assays. Clin Chem 1996; 42: 140-145.
4. Stockigt JR. Free thyroid hormone measurement. A critical appraisal. Endocrinol
Metab Clin North Am 2001; 30: 265-289.
5. Chen QY, Huang W, She JX, et al. HLA-DRB1*08, DRB1*03/DRB3*0101, and
DRB3*0202 are susceptibility genes for Graves disease in North American
Caucasians, whereas DRB1*07 is protective. J Clin Endocrinol Metab 1999; 84:
3182-3186.
6. Torring O, Tallstedt L, Wallin G, et al. Graves’ hyperthyroidism: treatment with
antithyroid drugs, surgery, or radioiodine — a prospective, randomized study. J
Clin Endocrinol Metab 1996; 81: 2986-2993.
7. Walsh JP. Management of Graves’ disease in Australia. Aust N Z J Med 2000; 30:
559-566.
8. Maugendre D, Gatel A, Campion L, et al. Antithyroid drugs and Graves’ disease
– prospective randomized assessment of long-term treatment. Clin Endocrinol
(Oxf) 1999; 50: 127-132.
9. McIver B, Rae P, Beckett G, et al. Lack of effect of thyroxine in patients with
Graves’ hyperthyroidism who are treated with an antithyroid drug. N Engl J Med
1996; 334: 220-224.
10. Graham GD, Burman KD. Radioiodine treatment of Graves’ disease. An assess-
ment of its potential risks. Ann Intern Med 1986; 105: 900-905.
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Endocrinology
11. Martin FI, Deam D. Hyperthyroidism in elderly hospitalised patients. Clinical
features and treatment outcomes. Med J Aust 1996; 164: 200-203.
12. Ross DS, Ridgway EC, Daniels GH. Successful treatment of solitary thyroid
nodules with relatively low-dose iodine-131, with low prevalence of hypothy-
roidism. Ann Intern Med 1984; 101: 488-490.
13. Fradkin JE, Wolff J. Iodide-induced thyrotoxicosis. Medicine (Baltimore) 1983;
62: 1-20.
14. Wong R, Cheung W, Stockigt JR, Topliss DJ. Heterogeneity of amiodarone-
induced thyrotoxicosis: evaluation of colour-flow Doppler sonography in predict-
ing therapeutic response. Intern Med J 2003; 33: 420-426.
15. Sawin CT, Geller A, Kaplan MM, et al. Low serum thyrotropin concentrations as a
risk factor for atrial fibrillation in older persons. N Engl J Med 1994; 331: 1249-
1252.
16. Schneider DL, Barrett-Connor EL, Morton DJ. Thyroid hormone use and bone
mineral density in elderly women. Effects of estrogen. JAMA 1994; 271: 1245-
1249.
17. Cohen JH 3rd, Ingbar SH, Braverman LE. Thyrotoxicosis due to ingestion of
excess thyroid hormone. Endocr Rev 1989; 10: 113-124.
18. Beck-Peccoz P, Brucker-Davis F, Persani L, et al. Thyrotropin-secreting tumors.
Endocr Rev 1996; 17: 610-638.
19. Wynne AG, Gharib H, Scheitnauer BW, et al. Hyperthyroidism due to inappropri-
ate secretion of thyrotropin in 10 patients. Am J Med 1992; 92: 15-20.
20. Hamblin PS, Dyer SA, Mohr VS, et al. Relationship between thyrotropin and
thyroxine changes during recovery from severe hypothyroxinemia of critical
illness. J Clin Endocrinol Metab 1986; 62: 717-722.
21. Eastman CJ. Where has all our iodine gone? Med J Aust 1999; 171: 455-456.
22. Smerdely P, Boyages SC, Waite K, et al. Topical iodine-containing antiseptics
and neonatal hypothyroidism in very-low-birthweight infants. Lancet 1989; 2:
661-664.
23. Ayala AR, Danese MD, Ladenson PW. When to treat mild hypothyroidism.
Endocrinol Metab Clin North Am 2000; 29: 399-415.
24. Chopra IJ, Baber K. Treatment of primary hypothyroidism during pregnancy: is
there an increase in thyroxine dose requirement in pregnancy? Metabolism 2003;
52: 122-128.
25. Haddow JE, Palomakei GE, Allan WC, et al. Maternal thyroid deficiency during
pregnancy and subsequent neuropsychological development of the child. N
Engl J Med 1999; 341: 549-555.
26. Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ Jr. Effects of thyroxine
as compared with thyroxine plus triiodothyronine in patients with hypothyroidism.
N Engl J Med 1999; 340: 424-429.
27. Walsh JP, Shiels L, Lim EM, et al. Combined thyroxine/liothyronine treatment
does not improve well-being, quality of life or cognitive function compared to
thyroxine alone: a randomized controlled trial in patients with primary
hypothyroidism. J Clin Endocrinol Metab 2003; 88: 4543-4550.
(Received 26 Jun 2003, accepted 8 Dec 2003)
193
Diagnosis dan manajemen dari hipertiroidisme dan
hipotiroidisme
Duncan J Topliss dan Creswell J Eastman
Meskipun perkembangan tes laboratorium yang sangat
sensitif, penilaian klinis dan penilaian tetap penting
TIROID DISFUNGSI umum. Di Amerika Serikat,
hipotiroidisme hadir dalam 4,6% dari populasi (cal clini-,
0,3%, dan subklinis, 4,3%) dan hipertiroidisme di
1,3% (klinis, 0,5%, dan subklinis, 0,7%). 1 Sebuah studi
jangka panjang di Inggris menemukan kejadian
hipertiroidisme adalah 0,8 per 1000 wanita per tahun,
dan hipotiroidisme adalah 3,5 per 1000 wanita
annually.2
Diagnosis disfungsi tiroid
Pengujian fungsi tiroid: Pengukuran serum thyroid
stimulating hormone (TSH), menggunakan tes tion kedua
atau ketiga genera, adalah indeks sensitif disease.3 tiroid
primer
Assay tiroksin bebas (T4) dan triiodothyronine (T3) andal
menghilangkan kesulitan dalam interpretasi kadar
hormon tiroid Total yang disebabkan oleh variasi umum
dalam protein hormon pengikat serum tiroid, terbaik
dicontohkan oleh kenaikan estrogen-induced di
thyronine-binding globulin yang meningkatkan kadar
hormon tiroid Total. Namun, tes hormon bebas masih
tunduk in-vitro dan in-vivo artefak di penyakit berat non-
thyroidal, gangguan parah protein yang mengikat, dan
MJA Vol 180 16 February 2004
heparin therapy.4 Jadi, jika penilaian klinis tidak sesuai
dengan hasil fungsi tiroid, tes tambahan dan opini
spesialis mungkin diperlukan. Interpretasi hasil fungsi
tiroid diringkas dalam Kotak 1.
Tes antibodi: Penyebab paling umum dari disfungsi tiroid
di Australia adalah autoimunitas. The tive paling sensi-
in-vitro indeks ini adalah pengukuran kadar antibodi Dase
peroxi- tiroid, 1 tapi ini kadang-kadang dapat
memberikan hasil negatif palsu (misalnya, di remaja
tiroiditis autoimun). Pada hipotiroidisme primer, tingkat
mengangkat tiroid peroksidase antibodi bukti untuk
autoimun tiroiditis limfositik kronis.
Pada hipertiroidisme, peran tes antibodi rutin kurang
jelas. Diagnosis penyakit Graves biasanya mungkin
Seri Editor: Donald J Chisholm dan Jeffrey D Zajac
Departemen Endokrinologi dan Diabetes, Rumah Sakit
Alfred, Melbourne, VIC.
Duncan J Topliss, MD, FRACP, WAJAH, Direktur, dan
Associate Professor, Department of Medicine, Monash
University, Melbourne, VIC.
Institut Patologi Klinik dan Penelitian Medis, Rumah Sakit
Westmead, Sydney, NSW.
Creswell J Eastman, AM, MD, FRACP, FRCPA, Direktur, dan
Klinis Profesor, Departemen Kedokteran, Universitas
Sydney, Sydney, NSW. Cetak ulang: Associate Professor
Duncan Topliss, Departemen Endokrinologi dan Diabetes,
Rumah Sakit Alfred, Melbourne, VIC 3004. duncan.
topliss@med.monash.edu.au
ABSTRAK
193

■ Penyebab paling umum dari hipertiroid di Australia
adalah penyakit Graves, yang disebabkan oleh cacat
dalam immunoregulation pada individu cenderung
genetik, menyebabkan produksi antibodi thyroid-
stimulating.
■ Setiap tiga modalitas terapi untuk penyakit Graves
- Thionamide obat, subtotal atau total tiroidektomi, dan
radioaktif iodine ablasi - dapat menjadikan eutiroid
pasien, tetapi semua memiliki efek samping potensial
dan
mungkin tidak menghilangkan kambuh.
■ Hipotiroidisme terjadi pada sekitar 5% dari populasi
orang dewasa; kebanyakan hadir dengan "subklinis"
hipotiroidisme (kegagalan tiroid ringan), yang ditandai
dengan peningkatan kadar serum thyroid stimulating
hormone (TSH) tapi tiroksin bebas normal (T4).
■ Penyebab paling umum dari hipotiroidisme di Australia
adalah autoimun tiroiditis limfositik kronis, yang ditandai
dengan mengangkat tingkat sirkulasi antibodi
peroksidase tiroid.
■ Gejala dan tanda hipotiroidisme sering ringan atau
halus dan, ketika ada kecurigaan klinis, tes fungsi tiroid
diperlukan; jika kadar serum TSH dinaikkan, T4 bebas
dan tiroid peroksidase antibodi harus
diukur.
■ Terapi Penggantian dengan tiroksin adalah batu
penjuru
g / kg berat badan ramping harian, diambil pada waktu
perut kosong);terapi (1,6 terapi kombinasi dengan
tiroksin dan liothyronine (T3) dipromosikan, tapi ada
sedikit bukti manfaat klinis.
MJA Vol 180 16 February 2004
MJA 2004; 180: 186-193
klinis, dan pengukuran tiroid peroksidase antibodi atau
antibodi TSH-reseptor mungkin tidak berkontribusi
diagnosis atau manajemen. Namun, pengukuran antibodi
TSH-reseptor memiliki peran ketika penyebab
hipertiroidisme tidak jelas, dalam menilai risiko
hipertiroidisme neonatal pada ibu hamil dengan riwayat
penyakit Graves, dan dalam menilai risiko kambuh
setelah kursus obat antitiroid di penyakit Graves.
Radionuklida scanning: radionuklida scanning tiroid tidak
rutin diperlukan untuk mendiagnosis penyakit Graves
atau goiter multinodular toksik, tetapi berguna ketika
penyebab hipertiroidisme tidak jelas (misalnya, ketika
tidak ada gondok bisa diraba, ketika sakit leher atau nyeri
menunjukkan subakut tiroiditis, atau ketika soliter
"panas" nodul dicurigai).
1: Interpretasi matriks untuk fungsi tiroid menghasilkan *
Tinggi T4 normal T4 rendah T4
TSH tinggi Dalam vivo atau artefak vitro
Hipertiroidisme hipofisis [TSHoma]
Resistensi hormon tiroid
TSH yang normal Seperti di atas
Sampling dalam waktu 6 jam dari dosis tiroksin
Rendah TSH Hipertiroidisme
(Untuk diagnosis ini, TSH harus
193
ditekan bukan hanya rendah)
Kegagalan tiroid ringan (primer)
(Juga disebut hipotiroidisme subklinis dan berkurang
cadangan tiroid)
Normal (pada pasien yang memakai tiroksin, TSH> 3
mU / L dapat menunjukkan underreplacement halus)
Hipertiroidisme subklinis tiroksin Halus tiroid
overreplacement otonomi (goiter multinodular atau
otonom fungsi nodul tiroid) penyakit Non-thyroidal
Hipotiroidisme primer
Hipofisis atau hipotiroidisme hipotalamus
Parah penyakit non-thyroidal
Hipofisis atau hipotiroidisme hipotalamus
Parah penyakit non-thyroidal
T4 = serum tiroksin bebas. TSH = thyroid stimulating
hormone.
* Komisi Asuransi Kesehatan membatasi penggantian
keuangan serum TSH saja, kecuali dalam keadaan klinis
tertentu, ketika pengukuran tambahan T4 bebas dan
triiodothyronine bebas (T3) yang disetujui. Kami
menyarankan bahwa praktisi secara rutin meminta "tes
fungsi tiroid" dan memberikan informasi klinis yang jelas
untuk memungkinkan laboratorium untuk melakukan tes
tambahan jika dibenarkan. Informasi harus mencakup
kondisi yang dicurigai (terutama jika hipopituitarisme)
dan obat-obatan (misalnya, tiroksin, karbimazol atau
propylthiouracil, amiodaron atau fenitoin).
MJA Vol 180 16 February 2004
Hipertiroidisme
Istilah hipertiroidisme dan tirotoksikosis digunakan
secara bergantian, terlepas dari apakah gangguan ini
disebabkan oleh kelebihan produksi endogen atau tion
cuka garam berlebihan hormon tiroid. Penyebab
hipertiroidisme yang ditampilkan dalam Kotak 2. Paling
umum di Australia penyakit Graves dan gondok
multinodular toksik. Manajemen hipertiroidisme
tergantung pada penyebab (terutama apakah itu
membatasi diri, seperti dalam subakut tiroiditis), ukuran
dan sifat dari gondok, penyakit penyerta atau obat dan,
terutama pada penyakit Graves, keinginan pasien.
Penyakit Graves
Penyakit Graves disebabkan oleh stimulasi tiroid oleh
antibodi yang mengikat reseptor TSH dan meniru efek
dari TSH stimulasi berkepanjangan. Antibodi TSH-
reseptor ini hasil dari immunoregulation normal izin-
Manajemen penyakit Graves
Tiga modalitas terapi untuk penyakit Graves adalah:
■ menghalangi sintesis hormon tiroid dengan antitiroid
obat;
■ subtotal atau "dekat-total" tiroidektomi; dan
■ penghancuran tiroid dengan yodium radioaktif (radio
yodium ablasi).
Meskipun setiap modalitas yang memuaskan di
rendering eutiroid pasien, 6 tidak ideal, karena semua
memiliki risiko efek samping dan tidak ada tapi
193
tiroidektomi total menghilangkan risiko
kekambuhan. Meskipun tiroidektomi total akhiri hampir
mengeliminasi risiko ini, itu adalah dengan
mengorbankan kebutuhan tertentu untuk penggantian
hormon tiroid. Memilih pengobatan untuk seorang
individu tergantung pada banyak faktor, tidak sedikit
menjadi pilihan pasien dan bias dokter. Di Amerika
Serikat, radioiodine adalah modalitas utama yang
disukai, tapi, di Eropa dan Australia, terapi obat antitiroid
lebih disukai untuk pasien dengan episode pertama dari
Graves hipertiroidisme,
7 Graves dermopathy (miksedema pretibial). Penyakit
ting generasi dan perluasan clone (s) dari antibodi sel
memproduksi pada individu genetik cenderung dengan
HLA-D subtypes.5 eksaserbasi spontan spesifik dan
remisi penyakit Graves dapat terjadi. Pemicu lingkungan
masih tidak baik ditandai, tapi postpartum eksaserbasi
adalah umum, dan sejarah tersebut harus dicari secara
rutin ketika penyakit Graves didiagnosis. Kelebihan
menjelang radioiodine dan, terakhir, operasi.
Obat antitiroid: Kebanyakan pasien dengan penyakit
Graves
memerlukan jangka pendek (beberapa bulan)
pengobatan dengan
obat antitiroid (thionamide) sebelum pertimbangan
2: Penyebab hipertiroidisme
yodium dapat memicu penyakit Graves aktif dengan
menyediakan
lebih substrat untuk sintesis hormon dan mungkin juga
MJA Vol 180 16 February 2004
oleh
fungsi kekebalan tubuh mengganggu. Kegigihan atau
kambuhnya
Penyakit Graves adalah lebih mungkin bila ada riwayat
penyakit berulang, dengan adanya goiter yang besar,
ketika
T3 kelebihan berlanjut meskipun kontrol T4 dengan
terapi thionamide, dan ketika antibodi TSH-reseptor
berlanjut selama terapi thionamide. Selain
hipertiroidisme, manifestasi autoimun lain dari penyakit
Graves adalah Graves ophthalmopathy (Kotak 3) dan
tiroid autoimun terkait
■ penyakit Graves
■ Multinodular gondok
■ mandiri berfungsi nodul tiroid tunggal (adenoma)
■ Tiroiditis (subakut, postpartum, limfositik)
■ hipertiroidisme tiruan
(Tiroid hormon pencernaan)
■ Berfungsi karsinoma tiroid (karsinoma folikular)
■ hCG-dimediasi (hiperemesis gravidarum, penyakit
trofoblas)
■ janin dan hipertiroidisme neonatal
(TSH-reseptor-antibodi dimediasi)
■ Struma ovarii
■ TSH-mensekresi tumor hipofisis
■ parsial (pituitary-selektif)
resistensi hormon tiroid
dengan beberapa, kurang umum, penyakit autoimun
lainnya, termasuk anemia pernisiosa dan penyakit
Addison.
193

hCG = human chorionic gonadotropin. TSH = thyroid
stimulating hormone.
3: Graves ophthalmopathy
A: proptosis asimetris, lebih jelas pada mata kanan.
Meskipun proptosis unilateral kadang-kadang terjadi
pada penyakit Graves, pencitraan lanjut mungkin
diperlukan untuk menyingkirkan diagnosis seperti tumor
orbital. B: Pasien berusaha untuk mencari, menunjukkan
penarikan dari mata kiri bengkak dengan rendah otot
eksternal mata, sedikit proptosis dan retraksi (dengan
sklera terlihat di atas iris mata kiri) dan beberapa
infiltratif pembengkakan di atas kantus dalam setiap
mata. C: Ditandai proptosis bilateral dengan retraksi dan
injeksi konjungtiva menunjukkan aktif ophthalmopathy
inflamasi.
jangka panjang-atau terapi definitif. Terapi thionamide
lama (12-18 bulan di episode8 pertama) memiliki
keuntungan menghindari operasi dengan risiko dan
penghancuran tiroid melekat dengan radioiodine, dan
tampaknya memberikan kesempatan terbaik remisi
berkelanjutan. Meskipun demikian, risiko kambuh lebih
besar dari 50%.
Dosis Thionamide harus individual, tergantung pada
MJA Vol 180 16 February 2004
keparahan awal penyakit dan respon, tetapi awal
dosis dibagi 10-30 mg sehari-hari karbimazol biasanya
memuaskan. Respon harus dinilai setelah 2-4 minggu
dan setelah itu secara berkala, dengan fre- akhirnya
minimum
quency setiap bulan ketiga. Dosis tinggi awal harus
semakin dikurangi menjadi dosis pemeliharaan sehari
sekali
2,5-10 mg / hari (Kotak 4).
Kadang-kadang, pada penyakit Graves yang sangat aktif,
thionamide
Terapi dapat menurunkan serum T4 bebas di bawah
normal, sementara tingkat T3 bebas tetap mengangkat,
dan pasien tetap tiroid hiper. Dosis Thionamide harus
demikian tidak dikurangi atas dasar serum tingkat T4
bebas saja. Penilaian klinis tetap penting, dipandu oleh
pengujian fungsi tiroid penuh. Gabungan thionamide dan
terapi tiroksin (blok-ganti rejimen) berguna untuk pasien
dengan hipertiroidisme yang tidak stabil, di antaranya
variasi kecil dalam thionamide dosis menyebabkan
fluktuasi besar dalam fungsi tiroid, tetapi tidak
meningkatkan kemungkinan remission.9 jangka panjang
Obat beta blocker yang tambahan yang berguna untuk
sympto- cepat
lega matic di hipertiroidisme. Dosis standar mengurangi
jantung
tingkat, berkeringat dan tremor, tetapi tidak
mempengaruhi hypermetab-
olism atau hormon tingkat. -blocker memilikiNon-
selektif
umumnya lebih disukai untuk efek mereka lebih baik
pada tremor.
Semua pasien harus diperingatkan tentang jarang namun
serius
193
komplikasi terapi thionamide, agranulositosis, dengan
instruksi untuk menangguhkan terapi sementara
mendapatkan sel putih
menghitung jika demam, sakit tenggorokan, atau sepsis
lainnya berkembang. Kami melakukan
tidak merekomendasikan tes darah rutin untuk efek
samping ini, sebagai
sangat jarang dan onset mendadak.
Radioiodine ablation: terapi ablatif dengan radioiodine
adalah
dianjurkan untuk pasien dengan hipertiroidisme
berulang
atau hipertiroidisme yang bertahan setelah kursus lama
obat antitiroid. Meyakinkan, beberapa jangka panjang-
besar,
penelitian telah menunjukkan tidak ada peningkatan
risiko kanker tiroid,
leukemia, keganasan lainnya, kelainan reproduksi atau
kelainan bawaan pada keturunan diperlakukan
patients.10 Dengan demikian pilihan default untuk terapi
definitif pada remaja dan orang dewasa. Lebih hati-hati
dianjurkan pada anak-anak karena diketahui risiko yang
lebih besar menginduksi nodul tiroid dan karsinoma dari
iradiasi eksternal dan paparan radionuklida lainnya di
masa kanak-kanak.
Terapi radioiodine tidak mencapai euthyroidism segera,
memerlukan terapi thionamide dosis rendah untuk
beberapa bulan pada banyak pasien. Kadang-kadang,
awal (biasanya sementara) hipotiroidisme terjadi,
dengan serum rendah tingkat T4 bebas tanpa elevasi
TSH, seperti TSH sering ditekan selama berminggu-
minggu sampai berbulan-bulan setelah hipertiroidisme.
Kemungkinan kontrol hipertiroidisme setelah
MJA Vol 180 16 February 2004
pengobatan radioiodine tunggal bervariasi dengan dosis,
terus stimulus imunologi tiroid, dan tiroid siveness jawab
untuk radioiodine tersebut. Secara keseluruhan, kontrol
dicapai awalnya di sekitar 75% kasus. Kendali akhirnya
melalui dosis berulang, diberikan setelah minimal enam
bulan, yang hampir dipastikan, tetapi sering dengan
mengorbankan hipotiroidisme permanen. Probabilitas
mengembangkan roidism meningkat hypothy- dengan
dosis radioiodium dan berlalunya waktu, sehingga jangka
panjang tindak lanjut dan pendidikan pasien diperlukan
dalam semua kasus.
Tiroidektomi: Tiroidektomi umumnya dilakukan
setelah euthyroidism telah dicapai dengan thionamide
Terapi. Tingginya tingkat kekambuhan setelah thyroidec-
subtotal
tomy telah menyebabkan banyak ahli bedah untuk
merekomendasikan lengkap
tiroidektomi (disebut Total atau nyaris total tiroidektomi),
tapi ini pasti memerlukan hormon tiroid permanen
terapi penggantian. Tiroidektomi menawarkan kontrol
yang cepat
tanpa paparan radiasi dan terpercaya menghilangkan
substansial yang
Tial gondok. Ini menjadi pilihan terapi ketika malig-
nancy dicurigai atau gondok besar yang menyebabkan
lokal
kompresi. Seperti semua operasi, keterampilan individu
dari
Dokter bedah adalah yang terpenting, dan harus ada
peran untuk
eksponen sesekali.
Beracun gondok multinodular
Beracun gondok multinodular hampir selalu didahului
193
dengan gondok multinodular lama dan mungkin, di
sebagian besar
pasien, dengan episode hipertiroidisme subklinis.
Hipertiroidisme sering dipicu oleh paparan yodium yang
berlebihan dari sumber adventif, seperti obat-obatan
dan media radiocontrast digunakan dalam prosedur
pencitraan (lihat daftar di bawah Iodine-induced
hyperthyroidism) .11 gondok dapat menekan atau
menghalangi trakea. Radiografi polos trakea dapat
mengungkapkan ini, tapi computed tomography lebih
baik, tidak memberikan kontras yang diberikan. Magnetic
resonance imaging terbaik menunjukkan tingkat gondok
tapi tidak langsung tersedia untuk dokter umum. Gejala
esofagus kadang-kadang membutuhkan penilaian oleh
barium swal- rendah. Obstruksi vena, yang lebih umum
daripada obstruksi esofagus, dinilai secara klinis (Kotak
5).
Pilihan awal terapi untuk goiter multinodular toksik
adalah thionamide untuk membuat eutiroid pasien.
Spontane- remisi ous bukan bagian dari sejarah alam
kondisi ini dan, kecuali telah ada episode pencetus
spesifik paparan yodium, terapi ablatif diindikasikan.
Dengan tidak adanya obstruksi, radioiodine adalah
pengobatan pilihan. Dosis yang lebih tinggi, dan kadang-
kadang beberapa perawatan, mungkin diperlukan untuk
hasil yang memuaskan. Jika obstruksi hadir maka
tiroidektomi ditunjukkan. Jumlah tomy thyroidec- juga
menyingkirkan risiko pertumbuhan kembali gondok.
Mandiri berfungsi nodul tiroid
MJA Vol 180 16 February 2004
Sebuah hiperfungsi nodul tunggal, biasanya adenoma,
merupakan penyebab umum dari hipertiroid. Jika nodul
tunggal terdeteksi pada pemeriksaan klinis atau USG
pada pasien tiroid hiper, diagnosis harus dikonfirmasi
oleh scan radionuklida. Radioiodine adalah pengobatan
pilihan setelah kontrol fungsi tiroid oleh kursus singkat
thionamide. Risiko radiasi hipotiroidisme kecil dalam
kondisi ini, berbeda dengan Graves hipertiroidisme,
sebagai nodul hiperfungsi menekan sisa Lobektomi
thyroid.12 masih merupakan pilihan yang dapat diterima.
Subakut tiroiditis
Tiroiditis subakut adalah, kondisi postviral membatasi
diri, yang dapat bervariasi dari gangguan ringan sampai
penyakit yang melemahkan berlangsung sampai satu
tahun. Sakit tiroid dan nyeri yang biasa tapi tidak di
mana-mana. Karena hasil hipertiroidisme dari kebocoran
hormon preformed dari sel tiroid rusak daripada
meningkatkan produksi, beredar rasio T3 / T4 lebih
rendah dari pada penyakit Graves dan gondok
multinodular toksik. Serapan radionuklida tiroid
berkurang atau tidak ada. Temuan ini sering dianggap
diagnostik subakut tiroiditis, tetapi juga terlihat pada
pasien menelan jumlah besar yodium atau mengambil
dosis supresif tiroksin. Kondisi dapat dibedakan oleh
tingkat tiroglobulin serum, yang biasanya dibesarkan di
subakut tiroiditis tetapi rendah di lain. Antibodi antitiroid
dapat muncul secara sementara di tingkat sederhana.
Terapi obat antitiroid adalah tidak pantas dan tidak
efektif. Beta-blocker, aspirin, dan obat anti-inflamasi non-
steroid memberikan bantuan gejala. Glukokortikoid,
193
seperti prednisolon (20 mg per hari), memberikan
perbaikan gejala pada mereka yang tidak merespon
dengan baik untuk anti-inflammatory drugs. Tahap
hipertiroid adalah characteris- tically diikuti oleh fase
hipotiroid (biasanya tidak requir- ing pengobatan),
kemudian akhirnya kembali ke euthyroidism. Episode
selanjutnya dapat terjadi.
4: Laporan Kasus - hipertiroidisme
Presentasi: Seorang wanita 25 tahun disajikan dengan
sejarah 6-bulan tremor, intoleransi panas, mudah marah
dan penurunan berat badan dari 4 kg. Dia memiliki kecil,
difus, goiter non-tender (kurang dari dua kali ukuran
normal), denyut nadi dari 104 bpm, dan sedikit gemetar,
hangat, tangan lembab tetapi tidak ada miopati
proksimal. Dia tidak memiliki riwayat pribadi atau
keluarga dari penyakit tiroid. Kesuburan bukan masalah
saat ini.
Investigasi: Serum tiroksin bebas (T4) tingkat adalah 34
pmol / L (kisaran referensi [RR], 9,3-23,8 pmol / L);
triiodothyronine (T3) tingkat bebas adalah 12 pmol / L
(RR, 1,8-6,0 pmol / L); merangsang tiroid
Hormon (TSH) tingkat adalah <0,03 mU / L (RR, 0,4-4,7
mU / L); dan tingkat antibodi peroksidase tiroid adalah
250 U / mL (RR, <35 U / mL).
Komentar: radionuklida scanning tiroid tidak akan
membantu manajemen dalam ketiadaan kebutuhan yang
wajar untuk mengecualikan subakut tiroiditis dan di
hadapan gondok.
Manajemen: penyakit Graves didiagnosis, dan
MJA Vol 180 16 February 2004
karbimazol
(10 mg dua kali sehari) yang ditentukan.
Pada 3 minggu review, pasien merasa lebih baik, dan
tingkat T4 bebas adalah 20 pmol / L; T3 bebas, 6,5 pmol /
L; dan TSH, masih <0,03 mU / L. Dosis karbimazol
dikurangi menjadi 15 mg / hari, dan selanjutnya 3 minggu
ulasan dijadwalkan.
Komentar: Ada respon klinis dan biokimia, tetapi tingkat
T3 bebas masih tinggi. Pengurangan dosis sebesar 25%
-50% yang diperlukan untuk menghindari overshoot
untuk hipotiroidisme.
Pada 6 minggu review, pasien merasa jauh lebih baik, dan
denyut nadi nya 76 bpm. Tingkat T4 bebas adalah 16
pmol / L; T3 bebas, 4,8 pmol / L; dan TSH, 0,03 mU / L.
Dosis karbimazol dikurangi menjadi 10 mg /
hari sebagai dosis tunggal. Pilihan untuk terapi jangka
panjang yang sekarang dibahas secara rinci dengan
pasien.
Komentar: Serum TSH dapat tetap ditekan selama
beberapa minggu atau bulan setelah euthyroidism
dipulihkan dan karena itu tidak dapat digunakan untuk
memandu terapi obat antitiroid akut. Karbimazol efektif
dalam dosis harian sekali-untuk pemeliharaan,
membantu kepatuhan. Ketika pasien eutiroid dan baik,
pilihan jangka panjang untuk terapi harus didiskusikan.
Pasien terpilih untuk memiliki kursus thionamide. Dosis
dikurangi dan dipertahankan pada 5 mg / hari dalam
kunjungan berikutnya, dengan fungsi tiroid pemantauan
setiap 2-3 bulan. Setelah 18 bulan terapi berhenti.
Komentar: fungsi tiroid kemudian harus diperiksa pada
penurunan frekuensi tanpa batas (misalnya, pada 1
193
bulan, kemudian setelah lebih 2 bulan, 3 bulan, 6 bulan,
dan kemudian setiap tahun) atau jika timbul gejala.
Tiga tahun kemudian, pasien ingin hamil dan bertanya
tentang masalah tiroid mungkin. Dia klinis eutiroid.
Komentar: fungsi tiroid harus diperiksa, tidak hanya
untuk mengecualikan hipertiroidisme subklinis, tetapi
juga hipotiroidisme, yang merupakan bagian dari sejarah
alam penyakit Graves dan dapat memiliki efek buruk
pada kesuburan halus dan perkembangan janin. Jika
pasien eutiroid tanpa terapi ablatif sebelumnya, maka uji
antibodi TSH-reseptor ini tidak perlu, tetapi mungkin
berguna dalam memprediksi risiko hipertiroidisme
neonatal. Fungsi tiroid harus dipantau, terutama pada
trimester pertama dan terutama setelah melahirkan, dan
pasien harus diingatkan tentang postpartum kambuh.
5: obstruksi vena yang disebabkan oleh gondok
A: Tanda Pemberton di seorang pria dengan goiter
memperluas melalui cerukan dada dan menghalangi
drainase vena. (A1) Pada saat istirahat, ia memiliki
bengkak moderat wajah. (A2) Setelah menaikkan
sebentar lengan untuk lebih menghalangi drainase vena,
pembengkakan meningkat dan ada ditandai suffusion
wajah.
B: Wanita dengan obstruktif, terutama retrosternal,
gondok multinodular, menunjukkan dada anterior
melebar pembuluh darah yang disebabkan oleh
peningkatan
MJA Vol 180 16 February 2004
aliran vena kolateral.
Postpartum hipertiroidisme
Hipertiroidisme pada periode postpartum biasanya
autoimun, yang disebabkan oleh salah satu penyakit
Graves atau tiroiditis. Ini berbeda dari tiroiditis postviral,
meskipun mungkin mengikuti kursus sementara yang
sama, dan mungkin kambuh setelah kehamilan dan
kemajuan untuk mendirikan hipotiroidisme berikutnya.
Yodium-induced hyperthyroidism
Yodium dapat menyebabkan hipertiroidisme pada pasien
dengan mendasari mandiri berfungsi kelenjar tiroid
(disebabkan, misalnya, oleh nodul, gondok multinodular
atau penyakit Graves). Hal ini ditandai dengan tingkat
TSH serum ditekan dengan tingkat sirkulasi hormon tiroid
normal, dan ini paling sering ditemukan pada pasien
dengan multinodular lama goitre.13 sejarah A harus
dicari dari paparan baru untuk yodium dari media
radiocontrast dan Ceuticals Pharma seperti amiodarone,
herbal dan vitamin tions persiapan, rumput laut dan
Cellasene (persiapan dipasarkan sebagai pengobatan
untuk selulit).
Media radiocontrast adalah pencetus jelas, computed
tomography harus dilakukan tanpa kontras dalam
penyelidikan gondok eutiroid dan massa leher tidak
terdiagnosis.
The amiodaron obat antiaritmia memiliki kandungan
yodium 37%, dengan penetrasi jaringan tinggi dan paruh
bulan. Beban yodium unsur dari sekitar 9 mg per hari
193
dari tablet 200 mg dapat memicu hipertiroidisme jika pengobatan dikenal sangat efektif, tetapi tidak
ada sudah ada gondok (tipe I amiodaron-induced menghakimi
hyperthyroidism), sedangkan obat itu sendiri
menyebabkan tiroiditis di Tiroiditis limfositik autoimun
5% -10% dari pengguna, biasanya setelah sekitar 2 tahun ■ Atrophic tiroiditis
terapi ■ penyakit Klasik Hashimoto
Terapi pasca-ablatif
■ terapi Radioiod (RAI)
(Tipe II amiodaron-induced hyperthyroidism, bentuk ■ Tiroidektomi
yang paling umum di Australia14). Meskipun tipe I dapat Sementara
menanggapi dosis tinggi terapi thionamide, dan tipe II ■ subakut tiroiditis
untuk glucocorti- terapi coid, kondisi ini dapat menjadi ■ Postpartum tiroiditis
parah dan treatment- tahan, dan tiroidektomi mungkin ■ terapi pasca-ablatif Awal
diperlukan. (RAI, tiroidektomi subtotal)
Obat-induced
■ Thionamide
6: hipotiroidisme primer parah ■ Lithium
■ Amiodarone
■ Interferon
■ Obat yang mengganggu penyerapan tiroksin di
A: Seorang pasien dengan hipotiroidisme primer yang diperlakukan hipotiroidisme (garam besi, cholestyramine,
belum diakui berat yang menjadi parah obtunded setelah sucralfate)
operasi untuk leher patah tulang paha. Miksedema
ditandai jelas. TSH = thyroid stimulating hormone.
B: Beberapa bulan kemudian, setelah terapi termasuk
penggantian hormon tiroid.
Hipertiroidisme subklinis

Yodium terkait
■ penyakit Iodine-kekurangan
■ Iodine-induced
7: Penyebab hipotiroidisme Infiltratif
■ tiroiditis Reidel dunia
serum thyroglobulin ditekan. Tidak ada strategi ■ Scleroderma
MJA Vol 180 16 February 2004 193
■ penyakit amiloid
■ Hemokromatosis
Neonatal / kongenital
■ tiroid agenesis / ectopia
■ Gangguan genetik dari TSH, TSH reseptor, peroksidase
tiroid, tiroglobulin, Pendrin
■ transplasental berlalunya memblokir antibodi TSH-
reseptor
Sekunder
■ hipofisis atau penyakit hipotalamus
Lain
■ Tiroid resistensi hormon
Penjelasan dari konsekuensi medis dan pengurangan
dosis bertahap dengan terapi tive suppor psikologis, jika
diterima, dianjurkan.
Bentuk yang jarang dari hipertiroidisme
Tumor hipofisis TSH-mensekresi merupakan kurang dari
1% dari semua tumor hipofisis. Hasil stimulasi tiroid pada
hipertiroidisme dengan goiter difus, secara klinis mirip
dengan penyakit Graves. Kehadiran serum tinggi gratis T4
dan T3 tingkat dengan tingkat serum TSH unsuppressed
menunjukkan diagno- sis.18 kondisi klinis lain yang perlu
dibedakan meliputi parsial (pituitary) bentuk resistensi
dari tiroid mewarisi sindrom resistensi hormon, 19 dan
laboratorium anomali hasil TSH yang disebabkan oleh
antibodi heterophil (antibodi umum yang mengganggu
tes menggunakan antibodi monoklonal tikus, mereka
baik dihasilkan secara langsung terhadap antigen tikus
setelah paparan tikus atau bereaksi silang dengan
antigen tersebut).
MJA Vol 180 16 February 2004
Hypothyroidism
Penyebab paling umum dari hipotiroidisme adalah
kegagalan utama dari kelenjar tiroid. Sementara
hipotiroidisme sekunder dari hipofisis atau disfungsi
hipotalamus jarang, sangat penting untuk
mengidentifikasi situs disfungsi pada awalnya. Sebagai
"Subklinis" hipertiroid adalah istilah yang buruk bagi-
kondisi ini
tion, seperti definisi adalah biokimia daripada klinis, dan
konsekuensi klinis yang mungkin. Hal ini ditandai dengan
kronis ditekan kadar TSH serum yang normal namun T4
bebas dan tingkat T3. Kondisi ini harus dibedakan dari
TSH penindasan sementara pada penyakit akut atau
setelah terapi obat (misalnya, glukokortikoid dosis tinggi).
Hal ini terjadi Kendala ini com- dengan gondok
multinodular, sebuah hiperfungsi tunggal nodul tiroid
dan tiroksin overreplacement. Hipertiroidisme subklinis
dikaitkan dengan peningkatan risiko aritmia atrium pada
mereka yang berusia lebih dari 60 years15 dan hilangnya
kepadatan mineral tulang pada pascamenopause
women.16 terapi antitiroid harus dipertimbangkan pada
pasien dengan hipertiroidisme subklinis pada
peningkatan risiko komplikasi, dan pengurangan tiroksin
dosis di mereka yang memakai terapi pengganti.
Hipertiroidisme subklinis sengaja yang diproduksi oleh
terapi tiroksin TSH-penekan untuk diferensiasi kanker
tiroid diciptakan, tetapi tidak perlu untuk melanjutkan
terapi ini seumur hidup jika kemungkinan
pemberantasan karsinoma telah
ditunjukkan.
193
 hipotiroidisme ditunjukkan pada Box 7.

Hipertiroidisme buatan
Ini adalah disengaja, biasanya diam-diam, tion cuka
garam berlebihan tiroid hormone.17 Hal ini sering bagian
dari kondisi kejiwaan yang lebih luas dan mungkin
refraktori untuk nasihat medis. Ini bisa berat, dengan
penurunan berat badan, kelemahan, takiaritmia jantung
dan kegagalan. Ketika karena tiroksin cuka garam tion,
serum tingkat T4 bebas meningkat tidak proporsional
dengan tingkat T3, tetapi, ketika karena liothyronine (T3)
menelan, serum tingkat T4 bebas ditekan. Serapan
radionuklida tiroid dan
kadar serum TSH meningkat logaritmik dalam
menanggapi declin-
ing kadar hormon tiroid, perbedaan antara primer
dan hipotiroidisme sekunder biasanya jelas. Itu
Situasi bisa, bagaimanapun, akan dikacaukan oleh
gangguan hipofisis
respon dalam bersamaan penyakit non-thyroidal parah,
occa-
Hipotiroidisme primer
Di Australia, penyebab paling umum dari hipotiroidisme
adalah tiroiditis limfositik kronis autoimun. Hal ini lebih
sering terjadi pada wanita daripada pria (rasio, 5-1) dan
paling sering terjadi pada dekade kelima dan keenam,
ketika prevalensi antibodi antitiroid pada wanita adalah
10%. Penyakit klasik Hashi- moto, dengan, perusahaan,
bosselated kelenjar tiroid membesar, kurang umum
daripada bentuk atrofi. Keduanya ditandai dengan
adanya serum ies antibodi antitiroid. Sedangkan tingkat
tiroglobulin dan mikrosomal antibodi telah konvensional
keduanya telah diukur, sensitivitas dan spesifisitas tes
antibodi peroksidase tiroid membuat satu-satunya tes
sekarang diperlukan.
Di seluruh dunia, kekurangan yodium masih tetap
menjadi penyebab utama hipotiroidisme. Mild defisiensi
yodium
❏

sionally di penuaan, dan di hypothy- berkepanjangan

mendalam
roidism. Sebuah TSH elevasi sederhana (hingga 15-20
mU / L) di
tahap pemulihan dari negara eutiroid sakit parah
(misalnya,
setelah trauma akut, luka bakar atau infeksi), atau
penghentian infus dopamin, 20 dapat menyebabkan
kebingungan diagnostik.
Hypothyroidism mencakup spektrum yang luas dari
penyakit klinis dan biokimia, klinis dari penyakit tanpa
gejala untuk miksedema koma (Kotak 6). Penyebab
MJA Vol 180 16 February 2004 193