Focus | Clinical
36 Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 © The Royal Australian College of General Practitioners 2021
Kiernan Hughes, Creswell Eastman
Background
Hypothyroidism and hyperthyroidism
arecommonly encountered in clinical
practice. General practitioners have a
central role in the long-term management
of these conditions.
Objective
The aim of this review is to provide an
overview of the causes of thyroid function
disorders and guidance on management.
Discussion
Optimal management of hypothyroidism
relies on an understanding of the potential
risks and benefits of therapy versus
observation. If levothyroxine (LT4)
replacement is commenced in a person
with subclinical hypothyroidism on the
basis of the presence of possibly relevant
hypothyroid symptoms, consideration
should be given to ceasing LT4 if no
symptomatic benefit is observed. Thyroid
stimulating hormone levels below the
reference range are associated with atrial
fibrillation and osteoporosis, and should
be avoided. Treatment modalities for
hyperthyroidism include antithyroid
medications, radioactive iodine therapy
and thyroidectomy. Each is satisfactory,
but none is ideal. A patient-centred choice
oftreatment modality should be
individualised, taking into consideration
theunderlying pathology, age, sex, patient
preference and availability of expert thyroid
surgical care. Long-term management of
patients with hyperthyroidism requires
careful consideration of the likely
outcomes of treatment including
theriskof hypothyroidism.
HYPOTHYROIDISM AND HYPERTHYROIDISM
are commonly encountered problems in
clinical practice. General practitioners are
well placed to be the primary clinicians
overseeing the long-term management
of patients with thyroid function
abnormalities.
What are the causes of
hypothyroidism?
The diagnosis of hypothyroidism relies
on conirmation by laboratory testing.
Primary hypothyroidism, caused by failure
of the thyroid gland, is characterised by
a decreased serum free thyroxine (FT)
level with an appropriately elevated serum
thyroid stimulating hormone (TSH)
level. Secondary hypothyroidism is a rare
condition caused by hypothalamic or
pituitary disease and characterised by a
low serum FT level without an increased
TSH level, which is low or even normal.
Causes of hypothyroidism are listed
in Box. Globally, iodine deiciency
remains the most common cause of
hypothyroidism.
Hashimoto’s thyroiditis
(autoimmune thyroiditis) is the most
common cause of primary hypothyroidism
in Australia and most iodine-suficient
areas of the world.
Hashimoto’s thyroiditis
is characterised by gradual thyroid failure,
with or without goitre formation, due to
autoimmune-mediated destruction of
the thyroid gland. The exact prevalence
of primary hypothyroidism in Australia is
unknown, but it is probably similar to that
found in the USA, where hypothyroidism
has been documented in .% of the
population, with .% being clinical and
.% being subclinical.
Approximately
–% of the Australian population have
evidence of thyroid autoimmunity based
on the presence of circulating thyroid
autoantibodies,
but prevalence may
varywith age, sex and ethnicity.
Approach to management of
subclinical hypothyroidism
Subclinical hypothyroidism, deined
biochemically as an elevated TSH level
accompanied by a normal FT level,
is a very common inding in general
practice. It is useful to measure thyroid
peroxidase antibodies (anti-TPO) to
identify underlying Hashimoto’s disease
as the cause. People with Hashimoto’s
thyroiditis have an increased risk of other
autoimmune conditions including coeliac
disease, vitamin B deiciency and
Addison’s disease.
Most people with subclinical
hypothyroidism will have minimal or no
speciic symptoms. It can be challenging
to determine the extent to which mild
thyroid dysfunction is causing a patient’s
symptoms because of the high rate of
some complaints (eg cold intolerance,
weight gain, constipation, fatigue, hair loss
and dry skin) in the general population.
As subclinical hypothyroidism
progresses to overt hypothyroidism at
a rate of approximately % per year,
Thyroid disease
Long-term management of
hyperthyroidism and hypothyroidism
Focus | Clinical
Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 37© The Royal Australian College of General Practitioners 2021
Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
asymptomatic patients with subclinical
hypothyroidism can usually be observed
with annual thyroid function tests (TFTs).
Most guidelines recommend
levothyroxine (LT) treatment if TSH is
>mIU/L.
A lower TSH threshold is
appropriate in younger individuals and
during pregnancy. A TSH >.mIU/L
should prompt consideration of the need
for LT therapy during pregnancy, and
international guidelines recommend LT
replacement when TSH is >.mIU/L and
the patient is anti-TPO positive.
Based
on the number of annual Pharmaceutical
Beneits Scheme prescriptions for LT
replacement therapy, it is likely that
approximately one million people are being
treated for hypothyroidism in Australia. It
is probable that the vast majority of these
patients are being treated for subclinical
hypothyroidism.
A recent systematic review concluded
that most non-pregnant individuals with
subclinical hypothyroidism do not beneit
from treatment.
This review has further
ignited debate regarding treatment
thresholds and highlighted concerns about
the potential for overtreatment.
Age-speciic local reference ranges
for TSH should be considered when
establishing a diagnosis of subclinical
hypothyroidism, particularly in older
people. Unfortunately, these reference
ranges are not generally available in
Australia. A recent placebo-controlled,
randomised, double-blind study failed
to ind any beneit from treatment of
subclinical hypothyroidism (mean baseline
TSH .mU/L) in elderly patients.
Most elderly patients with subclinical
hypothyroidism should be carefully
followed up with a ‘wait and see’ strategy,
generally avoiding replacement therapy.
Figure provides an algorithm to assist
in decision making for LT replacement
therapy for those with either overt or
subclinical hypothyroidism.
Goals of hypothyroidism treatment
The goals of therapy for hypothyroidism
include:
•
amelioration of hypothyroid symptoms
•
restoration of a euthyroid state
•
avoidance of overtreatment.
Restoration of a euthyroid state can be
readily accomplished in almost all patients
by oral administration of LT. The average
full replacement dose of LT in adults is
approximately . μg/kg body weight per
day. Mildly elevated levels of FT may
be seen if blood is taken in the irst few
hours after swallowing the medication. In
general, it is best to base dosing decisions
predominantly on TSH levels. Thyroxine
has a long half-life of approximately seven
days, and steady-state TSH concentrations
are therefore not achieved for at least
six weeks. Consequently, it is best not to
repeat TFTs sooner than this after initiating
LT therapy or changing the dose. The
long half-life also enables different doses
to be given on different days to provide
the required total weekly dose. In elderly
patients and those with known cardiac
disorders, it is better to go ‘low and slow’,
starting with –μg per day.
Because co-administration of food with
the medication can impair LT absorption,
the medication should be taken while
fasting at least minutes – and ideally
minutes – before breakfast. For patients
unable to comply, bedtime dosing can be
considered (three or more hours after the
evening meal). Care should also be taken
not to co-administer with supplements
such as iron and calcium, which may
reduce absorption. It is generally
appropriate to target a TSH level within
the reference range. The most common
cause of failure to achieve normal TSH
levels despite escalation of thyroxine
doses is non-adherence with therapy. If a
patient has ongoing symptoms suggestive
of hypothyroidism and the serum TSH is
conirmed by repeat measurement to be
at the upper limits or above the reference
range, it is reasonable to increase the dose
and to aim for a serum TSH value in the
lower half of the reference range. Some
studies have suggested psychological
wellbeing is better in patients with lower
serum TSH concentrations.
Combination thyroxine/triiodothyronine
(T/T) therapy may have a limited role in
the minority of patients who are dissatisied
with T monotherapy. Professional
guidelines support the use of liothyronine
(LT) in combination with LT for those
patients who have been properly screened
and unambiguously have not beneited
from LT. If the serum TSH level stays
within the reference range, replacing a
small fraction of the LT dose by LT once
or twice per day has not been associated
with adverse drug reactions.
Combination
therapy should generally be initiated under
specialist supervision with care to avoid
Box 1. Causes of hypothyroidism
19
• Autoimmune lymphocytic thyroiditis
(Hashimoto’s thyroiditis)
• Post-ablative therapy
– Radioiodine therapy
– Thyroidectomy
• Transient
– Subacute thyroiditis
– Postpartum thyroiditis
– Subtotal thyroidectomy
• Medication induced
– Thionamide (carbimazole,
propylthiouracil)
– Lithium
– Amiodarone
– Interferon
– Immune checkpoint inhibitors
– Medications that interfere with
thyroxine absorption (eg iron, calcium,
cholestyramine, sulcralfate)
• Iodine associated
– Iodine deficiency
– Iodine induced (eg contrast load,
Lugol’s iodine)
• Infiltrative
– Riedel’s thyroiditis
– Amyloid
– Haemochromatosis
– Scleroderma
• Neonatal/congenital
– Thyroid agenesis/ectopia
– Genetic disorders of thyroid
stimulating hormone (TSH),
TSHreceptor, thyroid peroxidase,
thyroglobulin, pendrin
– Transplacental passage of blocking
TSH receptor antibody
• Secondary
– Hypothalamic or pituitary disease
• Other
– Thyroid hormone resistance
– Factitious (eg falsely elevated TSH due
to heterophile antibodies)
Focus | Clinical
38 Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 © The Royal Australian College of General Practitioners 2021
Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
overtreatment. The European Thyroid
Association has published guidelines
with the intent of enhancing the safety of
combination therapy.
Desiccated thyroid
extract has been extensively used in the
past and is widely promoted on social
media sites, but it is not recommended
by any of the current specialist society
guidelines. Typically it has a T-to-T ratio
of : – providing much more T than the
physiological ratio of approximately : to
:. The result is that thyroid extract will
often produce supraphysiological T levels
that may be associated with harm; it is
contraindicated in pregnant patients or the
elderly with cardiac disorders.
Potential adverse eects of
excessive thyroid hormone
replacement
Because many symptoms of
hypothyroidism are nonspeciic,
patients often think that their LT dose
is inadequate, such as when they feel
excessively tired or gain weight. This
can lead to an individual requesting an
LT dose escalation or self-escalating
their dose, causing a suppressed serum
TSHlevel.
TSH levels of <. mIU/L have been
associated with osteoporosis and atrial
ibrillation in people aged >years
of age.
In one study, patients aged
>years with serum TSH levels
<.mIU/L, the majority of whom were
taking LT, had a threefold increase in
the risk of atrial ibrillation over a -year
observation period when compared with
euthyroid controls.
The risk for low bone density
and fractures is also elevated in
postmenopausal women taking excessive
LT. In a cohort of women aged >years,
women with a low TSH level (≤.mU/L)
had a threefold increased risk for hip
fracture (relative hazard: .; %
conidence interval [CI]: ., .]) and
a fourfold increased risk for vertebral
fracture (odds ratio: .; % CI: .,
.) when compared with women who
had normal TSH levels (.–.mU/L).
In another prospective cohort study of
>, women, there was an increased
incidence of major osteoporotic fracture
(hip, spine, humerus, forearm) in patients
with low TSH levels (<.mU/L; .%,
compared with .% in those with normal
TSH levels).
Potential adverse eects of
inadequate thyroid hormone
replacement
The adverse effects of thyroid hormone
deiciency are often nonspeciic and
may include cognitive impairment,
hyperlipidaemia and progression of
cardiovascular disease. Patients with overt
TSH 4.0 to 6.9 mU/L
Observe and
monitor as
TSH level
may be age
appropriate
Patient is diagnosed with subclinical hypothyroidism due to Hashimoto’s thyroiditis
TSH 7.0 to 9.9 mU/L
Consider therapeutic trial of LT4 if
symptomatic*
TSH ≥10.0 mU/L
Treat with LT4 if not
contraindicated
Age ≥65 years Age <65 years Age ≥65 years Age <65 years
Treat with LT4
Figure 1. Algorithm for thyroid hormone replacement in adults with subclinical hypothyroidism due to Hashimoto’s thyroiditis
9
*Patients who commence LT4 therapy for symptoms attributed to subclinical hypothyroidism should be reviewed after three or four months to assess
response to treatment once the serum TSH returns to the reference range. If symptoms have not improved then LT4 therapy should generally be
discontinued and the patient reviewed for other disorders.
LT4, levothyroxine; TSH, thyroid stimulating hormone
Reproduced with permission of Medicine Today from Hughes K, Eastman CJ, Hashimoto’s thyroiditis: How to spot the diagnosis and how to manage it,
Med Today 2017;18(9):27–32.
Focus | Clinical
Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 39© The Royal Australian College of General Practitioners 2021
Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
hypothyroidism should generally have the
LT dose adjusted to achieve a normal
TSH level to avoid these potential adverse
effects. In extreme situations, myxoedema
coma could eventuate.
Management of hypothyroidism
during pregnancy
Thyroxine production increases early
in gestation by –% in response to
human chorionic gonadotrophin (hCG)
stimulation of the normal thyroid gland
and increased oestrogen-stimulated
synthesis of thyroid hormone–binding
proteins. Accordingly, patients with
hypothyroidism who are maintained
on LT therapy should increase the
dosage of their medication initially by
approximately % as soon as pregnancy
has been conirmed. This increase can
often be easily achieved with an extra
two daily doses each week. Regular
monitoring of serum TSH and FT levels
is recommended, particularly during the
irst half of gestation, to adjust the LT
dosage to maintain these parameters
within the normal pregnancy reference
range (.–.mIU/L). A therapeutic
and monitoring regimen should apply
to women diagnosed with either overt
or subclinical hypothyroidism during
pregnancy. Soon after delivery, the LT
dosage must be reduced to the original
prepartum replacement dosage.
What are the causes of
hyperthyroidism?
Common causes of hyperthyroidism are
listed in Table. Investigations to determine
the cause of thyrotoxicosis should routinely
include TSH, FT, FT and thyroid
antibodies including thyroid receptor
antibodies (TRAb). C-reactive protein
should be checked if subacute thyroiditis
is suspected (indicated by a painful, tender
thyroid). Thyroid uptake scans are useful
if the diagnosis is not clear based on
clinical features and bloods tests. Thyroid
sonography has a limited role in evaluation
of patients with thyrotoxicosis and is not
necessary as part of routine assessment.
Management of Graves’ disease
Graves’ disease has three different
treatment modalities:
•
antithyroid medications (thionamides)
that block the synthesis of thyroid
hormones
•
radioactive iodine ablation (I-)
•
thyroidectomy.
Each of these modalities of therapy is a
satisfactory treatment but none is ideal.
The advantages and disadvantages of
different types of treatment are listed
in Table. Individual patient factors
will influence the choice of therapy, and
management decisions should involve
discussion of the values and preferences
of the patient. Administration of
beta-blocker medication (eg propranolol,
atenolol, metoprolol) is recommended as
initial, short-term symptomatic therapy
Table 1. Common causes of thyrotoxicosis and main diagnostic features
Cause Aetiology Uptake scan finding
Laboratory thyroid
autoantibody results
Graves’ disease TRAb stimulate thyroid hormone
production and development of a
diuse goitre
Normal or diusely increased
isotope uptake
Presence of TRAb is diagnostic
Toxic multinodular goitre or
toxic adenoma
Autonomous nodules produce thyroid
hormone without TSH stimulation;
hyperthyroidism may be precipitated
or exacerbated by exposure to excess
amounts of iodine
Increased isotope uptake into
toxic nodules with reduced
uptake into surrounding
normal thyroid tissue
Typically, a gradual progression
towards the hyperthyroid state
over several years and thyroid
autoantibody negative
Painless thyroiditis or
postpartum thyroiditis
Release of preformed thyroid hormone
due to autoimmune destruction of
thyroid tissue
Reduced or absent isotope
uptake
Anti-TPO antibodies and/or
antithyroglobulin antibodies
are present
Painful, subacute thyroiditis Release of preformed thyroid hormone
due to virally mediated destruction of
thyroid tissue
Reduced or absent isotope
uptake
Anti-TPO and antithyroglobulin
antibodies usually not detected
and CRP/ESR elevated
Amiodarone-induced
thyrotoxicosis
Type 1 – iodine induced in people with
underlying autonomous nodules or
Graves’ disease; Type 2 – destructive
thyroiditis
Usually reduced or absent
isotope uptake, but often not
helpful
Nil characteristic laboratory
results; recommend checking
anti-TPO antibodies and TRAb
to look for competing causes
Exogenous thyroid hormone
excess: Iatrogenic, intentional
orfactitious
Excess ingestion of thyroid hormone Reduced or absent isotope
uptake
Nil characteristic laboratory
results
Anti-TPO, thyroid peroxidase antibodies; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; TRAb, thyroid receptor antibodies; TSH, thyroid
stimulating hormone
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40 Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 © The Royal Australian College of General Practitioners 2021
Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
in all patients with moderate-to-severe
symptomatic thyrotoxicosis.
Antithyroid medications are the
usual irst-line treatment for patients
with Graves’ disease and are generally
favoured because they allow the
possibility of achieving a durable
remission without the need for lifelong
thyroid hormone replacement. Patients
with mild hyperthyroidism, a minimally
enlarged thyroid and/or only modestly
elevated TRAb levels are particularly
good candidates for a trial of thionamide
therapy as they have the best chance
of achieving a durable remission. Most
individuals will need treatment for
–months, with treatment continuing
until the TRAb becomes undetectable.
Carbimazole is the favoured thionamide
as it has less hepatotoxicity than
propylthiouracil (PTU). However, PTU
is preferred during the irst trimester of
pregnancy and in treatment of thyroid
storm because it inhibits conversion of T
to T. PTU may also be used for people
with adverse reactions to carbimazole.
Agranulocytosis is a rare but serious
adverse effect of thionamide medications.
Before commencing thionamides,
all patients should have baseline full
blood examination and liver function
tests performed. Any patient taking
thionamides who develops fever, sore
throat or other signs of sepsis should have
an urgent assessment of white cell count
and liver function. It is worth discussing
the risk of agranulocytosis when
prescribing thionamides so patients are
aware to attend for a blood test if infective
symptoms develop.
Long-term thionamide medication has
generally been discouraged because of
challenges with compliance and potential
side effects; however, some patients
and clinicians express a preference for
thionamide, wanting to avoid permanent
hypothyroidism from either radioactive
iodine ablation or thyroidectomy.
A course of antithyroid medication is
recommended to achieve euthyroidism
before the patient is treated deinitively
with either radioiodine or thyroidectomy.
Deinitive treatment with radioiodine
is generally considered in the following
settings:
•
failure to achieve a durable remission
despite prolonged or recurrent courses
of thionamide therapy
•
recurrent Graves’ disease
•
individuals who are unable to tolerate
thionamides because of adverse effects.
The cure rate (achieving euthyroid or
hypothyroid state) following the oral
administration of a Mbq dose of
radioactive iodine is approximately %
at months. Radioiodine typically takes
–months to induce a hypothyroid
state, and some individuals will need
more than one dose. There is lingering
concern about possible adverse effects
of I- ablation on fertility in women
and a potential small increased risk of
malignancy associated with radiation
exposure. Radioiodine carries the risk of
exacerbating Graves’ orbitopathy and so
is best avoided in patients with signiicant
thyroid eye disease. Corticosteroids
should be given prophylactically at the
time of radioiodine therapy to reduce the
risk of a flare of orbitopathy in individuals
with mild orbitopathy.
Thyroidectomy is generally the
preferred option in the following settings:
•
moderate-to-severe Graves’
orbitopathy
•
women who desire a pregnancy within
the next –months
•
large goitres causing compressive
symptoms or goitres with signiicant
retrosternal extension
•
where thyroid malignancy is suspected
•
when patients are fearful of taking
radioactive medication.
Thyroidectomy should only be performed
by a high-volume surgeon as complication
rates are lower in the hands of an
experienced surgeon.
None of the available therapeutic
options for the management of Graves’
disease has been able to re-establish
normal thyroid function in all patients.
Regardless of the treatment chosen, up
to % of patients report not feeling fully
recovered after their treatment, mostly
because of persistent fatigue and eye
Table 2. Advantages and disadvantages of Graves’ disease treatment options
Treatment Advantages Disadvantages
Thionamides • Allows possibility of a durable remission and
preservation of endogenous thyroid function
• Low cost
• Side eects – rash, pruritus, gastrointestinal, agranulocytosis
and hepatitis, usually occurring early in the course of therapy
• Risk of birth defects if pregnant
• Frequent monitoring required
Radioiodine • Permanent resolution of hyperthyroidism
• Low cost
• Permanent hypothyroidism in most cases
• Radiation exposure to salivary glands
• Potential adverse eects on fertility
• Risk of exacerbation of Graves’ orbitopathy
Thyroidectomy • Rapid, permanent resolution of hyperthyroidism
• May help improve Graves’ orbitopathy
• Provides relief of compressive symptoms if large
goitre is present
• Permanent hypothyroidism
• Risks of surgery and anaesthesia
• Risk of hypoparathyroidism and recurrent laryngeal nerve injury
• High cost in comparison to other treatments
Focus | Clinical
Reprinted from AJGP Vol. 50, No. 1–2, Jan–Feb 2021 41© The Royal Australian College of General Practitioners 2021
Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
symptoms.
Weight loss is a common
feature of hyperthyroidism, and many
patients gain considerable weight after
treatment of their hyperthyroidism.
Patients should be counselled regarding
the risk of weight gain; appropriate early
dietary modiication may help to minimise
weight gain.
Management of toxic nodules
Toxic nodules are a common cause
of mild hyperthyroidism, generally
progressing slowly over many years.
In the early stages, a subnormal TSH
level is frequently the only biochemical
abnormality. Risks of osteoporotic
fractures and atrial ibrillation increase,
particularly in the elderly, as the TSH
levels falls below .mIU/L; therefore,
this is a common threshold for considering
treatment (even when the FT and
FT concentrations remain within the
reference range). Exposure to large iodine
loads, as occurs with iodinated contrast,
may precipitate a transient increase in
severity of hyperthyroidism. Diagnosis is
usually conirmed by the appearance on a
radionuclide scan (Figure).
Radioiodine is generally the preferred
treatment for toxic nodules as it provides
the best chance of achieving the euthyroid
state without the need for medication.
Surgery is preferable in patients with
very large goitres and/or signiicant
compressive symptoms and for those who
do not want to have radiation therapy.
Long-term thionamide therapy is an
option, particularly in elderly people or in
individuals who prefer to avoid radiation
or surgery. Percutaneous ethanol therapy
or laser therapy are available in some
parts of the world, but their availability in
Australia is very limited currently.
Management of thyroiditis
Thyroiditis may have multiple different
causes, including autoimmune
(egpainless lymphocytic and postpartum
thyroiditis), viral (eg subacute thyroiditis)
and medication induced (egamiodarone).
Thyrotoxicosis associated with thyroiditis
is typically self-limited. Antithyroid
(thionamide) medication therapy is
generally ineffective and inappropriate.
Beta-blockers are indicated for
symptomatic relief in patients with
signiicant palpitations, tachycardia
and tremor. Corticosteroids may have
a role in people with persistent, painful
subacute thyroiditis and in people with
type destructive thyroiditis associated
with amiodarone therapy.
Hyperthyroidism associated with
thyroiditis is attributable to the release
of preformed thyroid hormone from the
inflamed thyroid. The thyrotoxic phase
may be followed by a hypothyroid phase,
so monitoring of thyroid function tests
is prudent. The hypothyroid phase is
usually transient; therefore, thyroxine
replacement may not be required. If
LT is considered necessary, it can
usually be weaned within – months.
The rate of permanent hypothyroidism
associated with thyroiditis will depend
on the underlying cause. Females
with a history of thyroiditis should be
encouraged to have TSH checked prior
to attempting conception and during
the irst trimester of pregnancy as they
are at risk of developing hypothyroidism
during pregnancy.
Conclusion
Thyroid function disorders are commonly
encountered in general practice.
Long-term management requires an
understanding of the range of causes and
beneits from a shared decision-making
approach, with discussion about potential
risks and beneits of therapy.
Key points
•
Thyroid function abnormalities are
commonly encountered in general
practice, occurring much more often
in females than males, with close to
a million people being treated for
hypothyroidism.
•
Treatment of established
hypothyroidism should be with LT,
in preference to other forms of thyroid
hormone replacement, with goals of
ameliorating symptoms, achieving
the euthyroid state and avoiding
overtreatment.
•
Decisions about who and when to treat
for hypothyroidism can be challenging
and may beneit from a shared decision-
making approach with discussion about
potential risks and beneits of therapy.
•
Hyperthyroidism, even when
subclinical, carries long-term risks of
osteoporosis and atrial ibrillation,
particularly in the elderly, and generally
should not be left untreated.
•
Choice of treatment modality for
hyperthyroidism should be patient
centred and dependent on underlying
pathology, patient preference and
availability of expert surgical care.
Authors
Kiernan Hughes MBBS (Hons), MSc, FRACP,
Consultant Endocrinologist, St Vincent’s Hospital,
NSW
Creswell Eastman AO MBBS, MD, FRACP, FRCPA,
FAFPHM, Principal, Sydney Thyroid Clinic, NSW;
Professor, Sydney Medical School, University of
Sydney, NSW
Competing interests: None.
Funding: None.
Provenance and peer review: Commissioned,
externally peer reviewed.
Correspondence to:
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. Graves’ disease; . Multinodular goitre;
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A
C
B
D
Sternal notch
Sternal notch
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Thyroid disease: Long-term management of hyperthyroidism and hypothyroidism
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