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Review Article
Department of Nephrology, Nouvel Hpital Civil, Strasbourg, 2Department of Nephrology, Hopital Civil,
Colmar, and 3Department of Nephrology, Clinique Sainte Anne, Strasbourg, France
mainly results from plasma removal of cytokines, putative antibodies, and thyroid hormones and their bound
proteins. TPE has a transitory effect and thus should be
associated with other thyroid blockers. When there are
threatening symptoms, TPE should be done early, without
waiting for the efficiency of conventional treatment, since it
is the fastest method known for the improvement of the
clinical condition. We also suggest starting TPE in case of
neurologic symptoms because of very slow and incomplete
regression. The Burch and Wartofsky score seems to be
a helpful tool in establishing the diagnosis of thyroid
storm and for deciding on when to initiate TPE. Key
Words: Endocrinology, Plasma exchange, Thyroid storm.
storm using the following parameters: body temperature, central nervous system involvement,
gastrointestinalhepatic dysfunction, heart rate, and
the presence or absence of congestive heart failure
and/or atrial fibrillation. The severity of each
symptom correlates with a number of points, with a
maximum score of 140.A score of 2544 is considered
high risk for an imminent storm, and a score >45 is
defined as being diagnostic of thyroid storm.
The three most common treatments for hyperthyroidism are antithyroid drugs, radioactive iodine, and
thyroidectomy. TPE is an alternative treatment that
has been proposed since the 1970s for hyperthyroidism and, more precisely, for the thyroid storm, whatever the etiology (3). TPE has been shown to have a
clear benefit in the thyroid storm induced by Graves
disease, the most common cause of hyperthyroidism
and found especially in the life-threatening forms. Its
efficiency here can be explained by the rapid decline
of plasma hormones and antibodies responsible for
Graves disease (4). Its use was also reported in cases
of amiodarone-induced hyperthyroidism, inefficiency
or toxicity of conventional treatments (such as
leukopenia due to propylthiouracil), Hashimotos
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C Muller et al.
TABLE 1.
Authors
Review of the literature: black citations concern systemic manifestations, blue citations concern
ophthalmologic manifestations
Number
of cases
Median number of
TPE/median volume
replacement per patient
Indication
Ashkar et al.
1970 (3)
Herrmann 1973 (15)
6/3 L
Cardiac symptoms
5/2.65 L
1/5 L
Neurological symptoms
1
1
2/2.5 L
1/4 L
3/8.1 L
Before surgery
Cardiac, neurological and
ophthalmological
symptoms after surgery
Cardiac and neurological
symptoms
3/8.4 L
Shigematsu 1982
(21)
1/3.8 L
1/4.8 L
Resistance to conventional
antithyroid drugs,
agranulocytosis
Thyroid hormone
intoxication
Patte et al.
1983 (23)
2/3.4 L
Newcomer 1983
(24)
1/4 L
2/7.2 L
Cardiac and
ophthalmological
symptoms
3.5/2.63.8 L
per exchange
Thyrotoxicosis
Schlienger et al.
1985 (27)
2.75/40 mL/kg
Thyrotoxicosis
Braithwaite 1986
(28)
3/5.5 L
2/6 L
Binimelis et al.
1987 (30)
3.25/3.84.5 L
Thyrotoxicosis after
thyroid iodine
irradiation and
conventional drugs
Hematological symptoms
and before surgery
Thyrotoxicosis with
neurological and cardiac
symptoms
Thyrotoxicosis
De Rosa et al.
1991 (4)
3/6.3 L
Thyrotoxicosis with
ophthalmopathy, and
before surgery
Response
Clinical improvement in 4872 h and
diminution of TT3 by 2280%
Clinical and biological amelioration,
patients successfully treated by the last
plasma exchange; 40% decrease in TT3
and 56.6% decrease in TT4
Clinical improvement and biological
improvement with significant fall in the
free hormones (633 mg FT4 and 13.6 mg
T3)
Clinical improvement in 48 h
Clinical improvement in less than 24 h; 25%
decrease in TT4
Clinical and biological improvement with a
decrease of 18.5 mg and 10 mg of TT3 and
TT4, respectively
Clinical and biological improvement with
the extraction of 530 mg of T4 and 2.8 mg
of T3
Clinical improvement after TPE, but no
change observed in TT3 or TT4
Clinical improvement immediately after
TPE and biological improvement (43%
decrease in TT4 and 68% decrease in
TT3)
No amelioration, plasma exchange not well
tolerated, with underlying cardiac disease
threatening
Biological improvement (decrease of 64%
TT3 and 54% TT4) and clinical
improvement in 24 h
Clinical improvement in 48 h, biological
improvement (decreases of 8.5% FT4,
27.4% FT3, and 15% TT3, but no
decrease in TT4)
39% decrease in TT4 in the first case; 53%
decrease in TT4 immediately after TPE in
the second case, with 80% after a few
days
7/8 showed clinical improvement, biological
improvement with almost no
improvement in FT3 or FT4, but
amelioration with decreases of 43% of
TT3 and 37% of TT4
Clinical improvement with cure in four days
and biological improvement (decreases of
76% of T3, 56% of T4, and 39% of FT4)
Clinical and biological amelioration;
decreases of 25% of TT3 and 17% of TT4
Biological and clinical improvement; thyroid
hormone normalization in
approximately15 days; >50% decreases in
TT3 and TT4
Clinical and biological improvement:
approximately 63.5% decrease in FT3
and 57.8% in FT4; one relapse after one
week
Biological improvement with decreases of
51% FT3, 47% FT4, 60% TT3, and 53%
of TT4
Authors
Number
of cases
Median number of
TPE/median volume
replacement per patient
Continued
Indication
Response
Biological improvement: decreases of 75%
TT4, 75% FT4, 78% FT3 (nothing for
TT3); amiodarone rate decreased too, but
then it rose again after TPE stopped
Biological amelioration with decreases of
40% TT3, 31% FT3, 27.2% TT4, and
14.4% FT4
Controls were six euthyroid patients:
decreases in TT4 and TT3 blood levels
(39% and 47%, respectively), more marked
for TT3, related to the removal of TBG
(thyroxine-binding globulin); FT3 and FT4
remained unchanged (6% decrease in FT4)
Transient clinical improvement, decreases of
approximately 7075% FT3, and 30% FT4,
no range normalization; and decreases of
60% TT3 and 4045% TT4
No clinical or biological improvement;
decreases of 84% FT4 and 58.5% FT3
immediately after TPE, but with
subsequent rises afterwards
Failure of treatment due to the death of the
patient; at first biological amelioration of
TT3 and TT4 was experienced, but
afterwards the rate rose again to levels
higher than previously
Little effect on plasma level (0% and 33%
decreases in FT4, and 7% and 18%
decreases in FT3) and no effect on the
hyperthyroid state
Clinical and biological improvement, with a
subsequent relapse; no FT3, FT4, TT3, or
TT4 samples taken
5/22.5 L
3/3.5 L
Severe hyperthyroidism
and cardiac failure
11
2.9/ND
Thyroid storm or
persistent thyrotoxicosis
Aghini-Lombardi
et al. 1993 (35)
2/4 L
Thyrotoxicosis
Henderson et al.
1994 (36)
2/4 L
Thyroxine overdose
5/ND
Ligtenberg et al.
1999 (38)
ND/ND
Boers and
Colebatch
2001 (5)
3/21 L
Nieuwenhuis 2004
(39)
3/ND
Resistance to conventional
antithyroid drugs
with neurological
manifestations
Severe neurological
symptoms
2.3/7.5 L
Kokuho et al.
2004 (41)
Ozbey 2004 (42)
1/3.4 L
3/11.5 L
per exchange
3/7.5 L
Resistance to conventional
antithyroid drugs
Before surgery
3/ND
Resistance to conventional
antithyroid drugs and
heart failure
Preparation for surgery
3/6 L
2/6 L
Resistance to conventional
antithyroid drugs
2/ND
11
Resistance to conventional
antithyroid drugs, major
bleeding
Before surgery
3.3/
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C Muller et al.
TABLE 1.
Authors
Number
of cases
Muller 2011
Glinoer and
Schrooyen
1987 (11)
Glinoer et al.
1988 (12)
11
Median number of
TPE/median volume
replacement per patient
4.6/2.5 L
per exchange
4/510 L
4/8.510 L
Dandona et al.
1979 (7)
Glinoer 1981 (47)
34/23 L
4/10 L
4/8 L
Kuzuya and
Degroot
1982 (10)
Sawers et al.
1981 (8)
Yamamoto et al.
1982 (9)
15/ND
3/ND
4/5 L
Continued
Indication
Resistance to conventional
drugs, cardiac and
neurological symptoms
Severe ophthalmopathy
with no response to
traditional treatment
Severe Graves
ophthalmopathy
Ophthalmological
symptoms
Ophthalmological
symptoms
Ophthalmological
symptoms
Ophthalmological
symptoms
Ophthalmological
symptoms
Severe ophthalmological
symptoms
Response
Biological and clinical amelioration: mean
decreases of 55% FT4 and 26% FT3
immediately after TPE sessions
Clinical improvement in 91% of the
patients; four relapsed at six months
8/9 clinical improvement; three relapses one
year after treatment, successfully treated
again by TPE
Clinical amelioration in 48 h
Clinical amelioration in 15 days
Clinical improvement, but three relapsed at
six months
No clinical improvement
Clinical improvement with adjuvant
immunosuppressive therapy
Clinical improvement soon after the end of
TPE, but with a further increase in pain
two weeks later
TIA, transient ischemic attack; FT3, free triiodothyronine; FT4, free thyroxine; ND, not determined; TPE, therapeutic plasma exchange;
TT3, total triiodothyronine; TT4, total thyroxine.
Patient 3
An 85-year-old woman was admitted for hyperthyroidism on September 2002. She had a history of
giant cell arteritis, polymyalgia rheumatica, hypertension, and valvular and ischemic cardiomyopathy with
conduction and rhythm impairment. A multinodular
goiter with hyperthyroidism had been treated with
radioactive iodine in 1992 with stable hormonal
levels thereafter.
One month before admission, an aortic valve
replacement and a mitral valvuloplasty were performed because of recurrent pulmonary edema. In
the postoperative days, the patient became asthenic
and blood tests revealed a high FT4 at 42.3 pmol/L
and a low TSH concentration at 0.005 mU/L. Despite
the introduction of carbimazole, she presented with
tachycardia (120 beats/min) and severe amyotrophia.
Propranolol was introduced; however, her clinical
status worsened with the onset of confusion, requiring admission to the ICU nine days later.
In the ICU, she was found to be thin with mild
exophthalmia. She presented with atrial fibrillation,
tachypnea (50/min), with rales in the right lung.
Her blood pressure was 130/80 mm Hg. Neurologic
examination found an isolated confusion. Biologically, there was no acidosis or electrolyte imbalance.
FT4 was increased to 80 pmol/L and FT3 to
14.3 pmol/L; TSH was undetectable; thyroid antibod 2011 The Authors
Therapeutic Apheresis and Dialysis 2011 International Society for Apheresis
527
FIG. 1. Free triiodothyronine (FT3) and free thyroxine (FT4) serum concentrations during hospitalization
in the intensive care unit for each patient. B, before
a session of therapeutic plasma exchange (TPE);
and A, after TPE. RR: FT3: 3.16.2 pmol/L; FT4:
921.9 pmol/L.
treatment with carbimazole was switched for propylthiouracil with a tapering dose (Fig. 1). No radical
treatment was performed.
In this case, TPE was justified by the high score, the
failure of one months conventional therapy, and the
appearance of precarious respiratory and cardiac
states. In this elderly patient with severe cardiomyopathy, TPE allowed a favorable outcome without
complications.
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DISCUSSION
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