Therapeutic Advances in Endocrinology and Metabolism Review

Ther Adv Endocrinol

Endocrine and metabolic emergencies: Metab
(2010) 1(3) 139—145

thyroid storm DOI: 10.1177/

2042018810382481
! The Author(s), 2010.
Richard Carroll and Glenn Matfin Reprints and permissions:
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Abstract: Thyrotoxicosis is a common endocrine condition that may be secondary to a number

of underlying processes. Thyroid storm (also known as thyroid or thyrotoxic crisis) represents
the severe end of the spectrum of thyrotoxicosis and is characterized by compromised organ
function. Whilst rare in the modern era, the mortality rate remains high, and prompt consid-
eration of this endocrine emergency, with specific treatments, can improve outcomes.

Keywords: hyperthyroidism, thyroid storm, thyrotoxic crisis, thyrotoxicosis

Introduction form thyroxine (T4) and triiodothyronine (T3). Correspondence to:

Thyroid storm (also known as thyroid or thyro-
toxic crisis) is an uncommon condition reflecting
an extreme physiological state within the spec-
trum of thyrotoxicosis. The condition is rare,
however, mortality rates are high and may
approach 10—20%. Thyroid storm is most com-
monly seen in the context of underlying Graves’
hyperthyroidism but can complicate thyrotoxico-
sis of any aetiology. Clinical features represent
manifestations of organ decompensation, with
fever seen almost universally. Management is
supportive with cooling and fluids, alongside
measures taken to reduce thyroid hormone syn-
thesis, hormone release and inhibition of the
peripheral effects of excessive thyroid hormone.
In addition, the management of thyroid storm
should not disregard the search and appropriate
treatment of any precipitating factors.
Pathophysiology
Normal thyroid function is maintained by endo-
crine interactions between the hypothalamus,
anterior pituitary and thyroid gland [Matfin,
2009]. Iodide is transported across the basement
membrane of the thyroid cells by an intrinsic
membrane protein called the Na/I symporter
(NIS). At the apical border, a second iodide
transport protein called pendrin moves iodide
into the colloid, where it is involved in hormono-
genesis. Once inside the follicle, most of the
iodide is oxidized by the enzyme thyroid peroxi-
dase (TPO) in a reaction that facilitates combi-
nation with a tyrosine molecule to ultimately
Richard Carroll, MB ChB
Thyroxine is the major thyroid hormone secreted Hammersmith Hospital,
into the circulation (90%, with T3 composing Imperial College,
London, UK
the other 10%). There is evidence that T3 richard.carroll@
is the active form of the hormone and that T4 imperial.nhs.uk
is converted into T3 before it can act Glenn Matfin, MSc (Oxon),
MB ChB, FFPM, FACE,
physiologically. FACP, FRCP
Joslin Diabetes Center,
Harvard Medical School,
All of the major organs in the body are affected Boston, MA, USA; and
by altered levels of thyroid hormone. These Division of Endocrinology,
New York University
actions are mainly mediated by T3. In the cell, School of Medicine New
T3 binds to a nuclear receptor, resulting in tran- York, NY, USA
scription of specific thyroid hormone response
genes.
Thyrotoxicosis is the clinical syndrome that
results when tissues are exposed to high
levels of circulating thyroid hormone. In most
instances, thyrotoxicosis is due to hyperactivity
of the thyroid gland, or hyperthyroidism
[Weetman, 2009]. Graves’ disease, an autoim-
mune thyroid disease associated with thyroid-sti-
mulating hormone (TSH)-receptor stimulating
antibodies, is the most common form of thyro-
toxicosis leading to thyroid storm, whilst other
causes of thyrotoxicosis such as toxic multinodu-
lar goitre and toxic adenoma are less-frequent
causes.
Thyroid storm is an acutely exaggerated manifes-
tation of the thyrotoxic state. Many of the man-
ifestations of thyrotoxicosis are related to the
increase in oxygen consumption and use of met-
abolic fuels associated with the hypermetabolic
state, as well as to the increase in sympathetic

http://tae.sagepub.com 139
Therapeutic Advances in Endocrinology and Metabolism 1 (3)
nervous system activity that occurs. The detailed
pathophysiology of thyroid storm is not fully
understood, but is thought to be related to
increased numbers of beta1-adrenergic receptors
being exposed to increased catecholamine levels
in states of stress. Displacement of free thyroid
hormones by circulating inhibitors of binding
in systemic illness (e.g. cytokines) may also play
an important role.
Aetiology
Thyroid storm is most commonly associated with
underlying Graves’ disease, although has been
reported with autonomous thyroid nodular dis-
ease. Traditionally, the condition was experi-
enced frequently following thyroidectomy for
thyrotoxic state (due to manipulation of the
hyperactive thyroid gland during surgery), but
modern treatments aimed at reducing preopera-
tive thyroid output and hormone stores have
dramatically reduced this complication.
Regardless of the underlying aetiology of thyro-
toxicosis, the rare transition to a state of thyroid
storm usually requires a second superimposed
insult. Most commonly this is infection, although
trauma, surgery, myocardial infarction (MI),
diabetic ketoacidosis (DKA), pregnancy and
parturition have been reported as causes. The
administration of large quantities of exogenous
iodine (such as with iodinated contrast agents
or amiodarone) can provide the substrate for
significant thyroid hormone production and
secretion if there are areas of autonomous thyroid
tissue within the gland (i.e. Jod-Basedow phe-
nomenon). Abrupt cessation of thionamide
therapy (i.e. antithyroid drugs such as pro-
pylthiouracil [PTU], methimazole and carbima-
zole) usually due to poor patient adherence or
other issues has been associated with worsening
thyrotoxicosis and rarely descent into thyroid
storm. Biological agents such as interleukin-2
and a-interferon have been reported to induce
thyroid storm when used to treat infectious dis-
ease, certain cancers and disorders of immune
function.
Diagnostic considerations
The diagnosis of thyroid storm must be made on
the basis of suspicious but nonspecific clinical
findings. If the diagnosis of thyroid storm is
strongly suspected, waiting for the results of
tests may cause a critical delay in the initiation
140
of effective life-saving treatment. Furthermore,
biochemical markers of thyroid function are not
discernably different from thyrotoxic states with-
out thyroid storm. Serum thyroid hormone levels
(i.e. free T3 [FT3] and free T4 [FT4]) are ele-
vated with suppressed TSH levels (with the rare
exceptions being states of thyroid hormone resis-
tance or TSH secreting pituitary adenomas)
confirming the diagnosis of thyrotoxicosis.
As noted previously, in most situations thyroid
storm occurs in the context of a superimposed
insult with an underlying predisposition to thyro-
toxicosis. Therefore, an immediate search should
begin for precipitating factors such as infection or
other causes. Pregnancy should be excluded
urgently in any woman of childbearing age with
urinary or plasma assessment of human chorionic
gonadotropin (HCG) levels and an ECG and
cardiac enzymes should be procured to exclude
acute coronary syndromes (ACS). Other investi-
gations should be promptly performed as per
clinical circumstances.
Clinical signs and features
Thyroid storm by definition represents the
extreme in the spectrum of thyrotoxicosis where
decompensation of organ function can occur.
Therefore any of the classical signs and symp-
toms of a thyrotoxic state may be seen. The scor-
ing system suggested by Burch and Wartofsky
(Table 1) illustrates the typical features of end
organ dysfunction that may be seen when thyro-
toxicosis is severe enough as to be termed thyroid
storm [Burch and Wartofsky, 1993]. Fever is
almost universal (>39 C or 102 F) and when
present in an unwell patient with known thyro-
toxicosis, should prompt immediate consider-
ation of thyroid storm. Associated profuse
sweating contributes to excessive insensible
water and electrolyte loss leading to dehydration.
Cardiac decompensation, usually in the context
of high-output cardiac failure, is manifested as
evidence of peripheral oedema or pulmonary
congestion with respiratory compromise when
severe. Tachyarrhythmias are common and
usually atrial in origin, unless there is a predispo-
sition to ventricular arrhythmias secondary to pri-
mary cardiac disease. Neurological dysfunction
may be severe enough as to cause profound delir-
ium or psychosis. Liver dysfunction, secondary
to either the presence of cardiac failure with
hepatic congestion or hypoperfusion, or a direct
effect of the excess thyroid hormone itself, is
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 R Carroll and G Matfin

Table 1. Diagnostic criteria for thyroid storm.

Clinical feature Scoring points
Thermoregulatory dysfunction
Temperature  F ( C)
99—99.9 (37.2—37.7) 5
100—100.9 (37.8—38.2) 10
101—101.9 (38.3—38.8) 15
102—102.9 (38.9—39.4) 20
103—103.9 (39.5—39.9) 25
104 (40) 30

Cardiovascular dysfunction
Tachycardia (beats per minute)
<99 0
99—109 5
110—119 10
120—129 15
130—139 20
140 25
Congestive heart failure
Absent 0
Mild (Pedal oedema) 5
Moderate (Bibasal rales or crackles) 10
Severe (Pulmonary oedema) 15
Atrial fibrillation
Absent 0
Present 10

Central nervous system dysfunction

Absent 0
Mild (Agitation) 10
Moderate (Delirium, psychosis, extreme lethargy) 20
Severe (Seizures, coma) 30

Gastrointestinal-hepatic dysfunction
Absent 0
Moderate (Diarrhoea, nausea/vomiting, abdominal pain) 10
Severe (Jaundice) 20

Previous episode of thyroid storm

Absent 0
Present 10
Total
>45 Highly likely thyroid storm
25—44 Suggestive of impending storm
<25 Unlikely to represent storm

Adapted from Burch and Wartofsky [1993].

characterized by abnormal liver function bio- Acute intervention

chemistry. Jaundice may be noted, and abdomi-
nal pain is often seen accompanied by nausea and
vomiting, and diarrhoea.
Elderly patients often present atypically
(so-called apathetic thyroid storm), with apathy,
stupor, cardiac failure, coma and minimal signs
of thyrotoxicosis.
Once thyroid storm is recognized the patient
should be managed in an appropriate location
such as an Acute Medical Unit (AMU),
high-dependency area or intensive care unit. As
with all acute medical patients, prompt assess-
ment and management of the ABCDEs should
occur (i.e. airway; breathing; circulation; disabil-
ity, i.e. conscious level; and examination).

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Therapeutic Advances in Endocrinology and Metabolism 1 (3)

General supportive care positive pressure ventilation (NIPPV) or intubated

Supportive care includes cooling measures, appro-
priate intravenous (IV) fluid resuscitation, electro-
lyte replacement and nutritional support.
Antipyretics can be administered to relieve the dis-
tress of profound pyrexia, but salicylates (e.g. aspi-
rin) should be avoided as they are associated with
displacement of thyroid hormone binding from
thyroid binding globulin (TBG) (Table 2).
Tachyarrhythmias, if associated with haemody-
namic instability (e.g. hypotension), should be
managed as an urgent matter with cardioversion
by defibrillation. Otherwise, appropriate antiar-
rhythmic therapy and treatment of the underlying
condition and complications would be warranted.
Ventilatory support, either with noninvasive
ventilation, should be performed if required based
on arterial blood gas (ABG) analysis and other
assessments. Occasionally patients will be severely
agitated limiting further intervention, and in these
situations a sedative such as haloperidol or a ben-
zodiazepine can be given, mindful of the possible
deleterious respiratory effects of these agents.
Chlorpromazine 50—100 mg orally or intramuscu-
lar (IM) every 6 hours as needed, has the addi-
tional benefit of reducing body temperature
through effects on central thermoregulation.
Nutritional support is important (including vita-
min replacement, e.g. thiamine) and includes
close monitoring of glucose levels (as liver glyco-
gen stores are depleted during thyroid storm).

Table 2. Medical management of thyroid storm.

Medication Dose Notes
Inhibition of hormone synthesis
Propylthiouracil (PTU) 600 mg loading dose, followed by Additional inhibition of peripheral
200—250 mg PO q4-6h deiodination However, recent warning
from FDA regarding severe liver
toxicity with PTU makes either
carbimazole or methimazole
first-choice thionamide
Carbimazole (or methimazole) 20—30 mg PO q4-6h
Inhibition of hormone release
SSKI (Potassium Iodide) 5 drops PO q6-8h Administer at least 1 hour
after thionamide
Lugol’s Solution 5—10 drops PO q6-8h Administer at least 1 hour
In UK, 1 ml PO q6h after thionamide
Iapanoic Acid 1000 mg IV q8h for 24 h, followed Administer at least 1 hour after
by 500 mg bd thionamide, infrequently available
Inhibition of peripheral effects of excess thyroid hormone
Propranolol 1—2 mg/min IV q15min up to IV dose initially if haemodynamically
max 10 mg 40—80 mg PO q4-6h unstable
Esmolol 50 mg/kg/min IV — may increase by Short acting
50 mg/kg/min q4min
as required to a max of 300 mg/kg/min.
Metoprolol 100 mg PO q6h Cardioselective; use if known
Diltiazem 60—90 mg PO q6-8h airways disease
Use if beta-blockers contraindicated
IV formulation available
Supplementary management
Hydrocortisone 100 mg IV q6h
Dexamethasone 2 mg IV q6h
Acetaminophen (commonly known 1 g PO q6h Care if significant hepatic dysfunction
as paracetamol or Tylenol)
Additional therapies
Lithium Carbonate 300 mg PO q8h Monitor for toxicity
Potassium perchlorate 1 g PO od Associated with aplastic anaemia
and nephritic syndrome
Cholestyramine 4 g PO q6-12h

PO, oral; IV, intravenous; q4-6h, every 4—6 hours; q6h, every 6 hours; q8h, every 8 hours; q4min, every 4 minutes; q15min, every 15 minutes;
od, once daily; bd, twice daily.

142 http://tae.sagepub.com

Thyroid-specific therapy
The immediate goals when treating thyroid storm
are to decrease thyroid hormone synthesis, pre-
vent thyroid hormone release, decrease periph-
eral action of circulating thyroid hormone to
reduce heart rate and support the circulation,
and to treat the precipitating condition [Nayak
and Burman, 2006]. The therapeutic options
for thyroid storm are the same as those for
uncomplicated thyrotoxicosis, except that the
drugs are given in higher doses and more
frequently. When treating thyroid storm, one
should consider the five ‘Bs’: Block synthesis
(i.e. antithyroid drugs); Block release (i.e.
iodine); Block T4 into T3 conversion (i.e. high-
dose propylthiouracil [PTU], propranolol,
corticosteroid and, rarely, amiodarone); Beta-
blocker; and Block enterohepatic circulation
(i.e. cholestyramine).
An antithyroid drug (i.e. thionamide) should be
administered immediately to prevent the forma-
tion of further thyroid hormone by inhibiting the
iodination of tyrosine residues by TPO enzymes.
PTU or carbimazole (or methimazole) can be
used, but PTU was traditionally preferred
because of its more rapid onset of action and
the additional benefit of inhibition of peripheral
deiodinase enzyme-mediated conversion of T4
into T3. PTU should be administered orally or
via a nasogastric (NG) tube in the unresponsive
patient with a loading dose of 600 mg followed by
a dose of 200—250 mg every 4—6 hours.
Carbimazole (or methimazole) is administered
at a dose of 20—30 mg every 4—6 hours. Both
agents can be administered rectally if needed.
However, the US Food and Drug
Administration (FDA) have recently released an
advisory on PTU for its liver toxicity potential
[Food and Drug Administration, 2010]. As no
head-to-head trial has demonstrated clear supe-
riority of PTU over either carbimazole or methi-
mazole in thyroid storm (or thyrotoxicosis, where
the latter agents are generally preferred over
PTU), many experts now recommend using
either carbimazole or methimazole in all thyro-
toxic patients (unless other compelling reasons
exist for using PTU such as pregnancy), and
achieving T4 into T3 conversion inhibition
solely with beta-blockers and corticosteroids
[Food and Drug Administration, 2010;
Malozowski and Chiesa, 2010].
Iodine should be administered at least 1 hour
after the thionamide to block the release of
http://tae.sagepub.com
R Carroll and G Matfin
preformed thyroid hormone. This apparent par-
adox makes use of the acute Wolff—Chaikoff
effect, whereby large doses of iodine suppress
thyroid hormone release. The effect lasts for up
to 2 weeks, because escape from this effect occurs
and is therefore unsuitable as a long-term thera-
peutic option. The thionamide should be admin-
istered prior to iodine administration so as to
prevent undesired tyrosine residue iodination
and enrichment of thyroid hormone stores. The
minimal time required between thionamide
administration and iodine treatment is debated
with 1—6 hours commonly prescribed. Iodine is
administered in the various formulations, includ-
ing saturated solution of potassium iodide
(SSKI) 5 drops orally every 6—8 hours (equalling
250 mg iodide with 1 drop containing 50 mg
iodide). Alternatively, 5—10 drops of Lugol’s
solution orally every 6—8 hours can be used. In
the UK, many experts prescribe 1 ml of Lugol’s
solution orally every 6 hours. Iapanoic acid, an
iodinated contrast agent, although rarely avail-
able now, is effective at a dose of 1g IV
8-hourly for the first 24 hours of treatment fol-
lowed by 500 mg twice daily.
Beta-blockade should be instigated immediately
(unless contraindicated) so as to block the adre-
nergic consequences of thyroid hormone excess.
Propranolol (i.e. non-cardiac specific beta-
blocker) has traditionally been used and has the
advantage of being suitable for IV administration
and is also relatively short acting. IV propranolol
at a dose of 1—2 mg/min can be administered
every 15 minutes until adequate haemodynamic
control is achieved or a maximum dose of 10 mg
is used, followed by 40—80 mg orally every
4—6 hours. Caution is warranted in patients
with heart failure, although beta-blockade may
be beneficial when tachycardia is a significant
precipitant to decompensated cardiac function.
Esmolol, a short-acting beta-blocker, can be
used as an alternative if a deleterious cardiac
effect is anticipated and is given IV at a rate of
50 mg/kg/min and increased as per response.
Contraindications to propranolol use include a
history of asthma or reversible chronic obstruc-
tive pulmonary disease (COPD), and a cardiose-
lective beta-blocker such as metoprolol or
atenolol could be used in these patients.
Alternatively, the calcium-channel blocker,
diltiazem can be used at a dose of 60—90 mg
orally 6—8-hourly or the appropriate dose by
IV. If anticoagulation is required for atrial fibril-
lation (or other indications), thyrotoxic patients
143
Therapeutic Advances in Endocrinology and Metabolism 1 (3)
are very sensitive to warfarin and should be mon-
itored closely.
Corticosteroids inhibit peripheral conversion of
T4 into T3 and have been shown to improve out-
comes in patients with thyroid storm. Adrenal
axis dysfunction in the context of thyrotoxicosis
of any degree is documented, and responds to
exogenous steroid therapy. Hydrocortisone
100 mg 6-hourly should be administered IV or
IM and continued until resolution of the thyroid
storm. Alternatively, dexamethasone 2 mg IV
every 6 hours can be used. Treatment should
be tapered appropriately based on the required
duration of steroid therapy.
Lithium carbonate, at a dose of 300 mg every
8 hours, can be used when there is a contraindi-
cation or previous toxicity to thionamide therapy.
Lithium inhibits thyroid hormone release from
the gland and reduces iodination of tyrosine
residues, but its use is complicated by the toxic-
ity that can ensue. Potassium perchlorate com-
petitively inhibits iodide transport into the
thyrocyte but has traditionally been associated
with aplastic anaemia and nephritic syndrome.
Several studies however have demonstrated its
use when used over short periods in the treat-
ment of amiodarone-induced thyrotoxicosis
[Erdogan et al. 2003]. A suggested dose is 1 g
daily and, similarly to iodide therapy, should be
combined with a thionamide. Cholestyramine 4 g
orally two to four times each day has been used in
the management of thyrotoxicosis due to reduced
reabsorption of metabolized thyroid hormone
from the enterohepatic circulation [Tsai et al.
2005].
Thyroidectomy is occasionally employed in
the management of thyroid storm refractory to
medication [Nayak and Burman, 2006], but is
associated with a risk of storm exacerbation if
preoperative thyroid hormone levels are high.
Treatment of precipitating illness
Management of thyroid storm should not disre-
gard the search for and treatment of precipitating
factors. An active search should be made for
infection and antibiotics chosen on the basis of
likely pathogens or microbial cultures. Other
likely precipitants such as trauma, MI, DKA,
and other underlying processes should be
managed as per standard care.
144
Maintenance therapy
Through adequate rehydration, repletion of
electrolytes, treatment of comorbid disease
such as infection and the use of specific thera-
pies (antithyroid drugs, iodine, beta-blockers
and corticosteroids), a marked improvement in
thyroid storm usually occurs within 24—72
hours. Once haemodynamic, thermoregulatory
and neurological stability has been achieved
attention should switch to maintenance therapy.
Escape from the Wollf—Chaikoff effect is usually
seen between 10 and 14 days after commence-
ment of iodine therapy, and therefore continua-
tion of iodine therapy beyond this point is
unlikely to be beneficial and could exacerbate
the situation. Furthermore, future treatment
with radioactive iodine (RAI) is delayed if thy-
roid iodine stores are saturated. Corticosteroid
therapy should be stopped as soon as possible,
but beta-blockade should be used whilst the
patient remains thyrotoxic.
The antithyroid treatment should be continued
until euthyroidism is achieved, at which point
a final decision regarding antithyroid drugs,
surgery or RAI therapy can be made.
Emerging treatments
Thyroid storm can occasionally be refractory
despite the above measures, and other treatment
options should be considered. Plasmapharesis,
with removal of thyroid hormone, has been used
successfully both in the thyrotoxic state and to
prepare those with thyrotoxicosis for surgery
[Ezer et al. 2009]. However, plasmapharesis
needs to be repeated several times as only about
20% of the T4 pool and even less of the T3 pool
can be removed each session. Charcoal haemoper-
fusion has also been demonstrated to be useful in
thyrotoxic states [Kreisner et al. 2010]. There is
great interest in the role of biological agents in
treatment of immune-mediated thyrotoxic states.
Rituximab (an anti-CD20 monoclonal antibody
which depletes B lymphocytes in circulation),
and various other emerging therapies have shown
promise in the treatment of Graves’ opthalmopa-
thy, but the role of these agents in the manage-
ment of the thyrotoxic state is less clear [Abraham
and Acharya, 2010; Bahn, 2010].
Conclusions
Thyroid storm is a rare endocrine emergency
but is associated with high mortality. It most
commonly occurs in the context of underlying
Graves’ thyrotoxicosis, but is frequently
http://tae.sagepub.com

precipitated by a secondary event such as infec-
tion or MI. Prompt recognition of the condition
with timely intervention is crucial, and manage-
ment of the patient in an AMU, high-dependency
or intensive care unit is essential. Treatment is
based on immediate blockade of thyroid hor-
mone synthesis, prevention of the release of
further thyroid hormone from thyroid stores,
and alleviation of the peripheral effects of thyroid
hormone excess. A search for a precipitant for the
thyroid storm is critical and should be treated
promptly. Maintenance therapy takes into
account disease-specific factors and patient
preference, with measures taken to prevent a
recurrence of thyroid storm.
Funding
This article received no specific grant from
any funding agency in the public, commercial,
or not-for-profit sectors.
Conflict of interest statement
None declared.
References
Abraham, P. and Acharya, S. (2010) Current
and emerging treatment options for Graves’ hyper-
thyroidism. Therapeut Clin Risk Managem 6: 29—40.
Bahn, R. (2010) Graves’ opthalmopathy. N Engl J Med
362: 726—738.
Burch, H.B. and Wartofsky, L. (1993) Life-threatening
thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin
North Am 22: 263—277.
http://tae.sagepub.com
R Carroll and G Matfin
Erdogan, M.F., Gulec, S., Tutar, E., Baskal, N. and
Erdogan, G. (2003) A stepwise approach to the treat-
ment of amiodarone-induced thyrotoxicosis. Thyroid
13: 205—209.
Ezer, A., Caliskan, K., Parlakgumus, A., Belli, S.,
Kozanoglu, I. and Yildirim, S. (2009) Preoperative
therapeutic plasma exchange in patients with thyro-
toxicosis. J Clin Apharesis 11: 111—114.
Food and Drug Administration (2010)
Propylthiouracil tablets. http://www.fda.gov/Safety/
MedWatch/SafetyInformation/ucm209256.htm
(accessed 2 August 2010).
Kreisner, E., Lutzky, M. and Gross, J. (2010)
Charcoal hemoperfusion in the treatment of levothyr-
oxine intoxication. Thyroid 20: 209—212.
Malozowski, S. and Chiesa, A. (2010)
Propylthiouracil-Induced Hepatotoxicity and Death.
Hopefully, Never More. J. Clin. Endocrinol. Metab 95:
3161–3163.
Matfin, G. (2009) Disorders of endocrine control
of growth and metabolism, In: Porth, C.M. and
Matfin, G. (eds). Pathophysiology: Concepts of
Altered Health States, 8th edn, Wolters Kluwer
Health: Philadelphia, PA.
Nayak, B. and Burman, K. (2006) Thyrotoxicosis and
thyroid storm. Endocrinol Metab Clin N Am
35: 663—686.
Tsai, W.C., Pei, D., Wang, T., Wu, D.A., Li, J.C., Wei,
C.L. et al. (2005) The effect of combination therapy
with propylthiouracil and cholestyramine in the treat-
ment of Graves’ hyperthyroidism. Clin Endocrinol
(Oxf) 62: 521—524. Visit SAGE journals online
http://tae.sagepub.com
Weetman, A. (2009) Thyrotoxicosis. Medicine
37: 430—435.
145