Hindawi Publishing Corporation

Journal of yroid Research

Volume 2014, Article ID 649502, 6 pages
http://dx.doi.org/10.1155/2014/649502

Review Article
Thyrotoxic Periodic Paralysis: Clinical Challenges

Abhishek Vijayakumar,1,2 Giridhar Ashwath,1 and Durganna Thimmappa1

1
Department of General Surgery, Victoria Hospital, Bangalore Medical College and Research Institute, Bangalore 560002, India
2
#128 Vijay Doctors Colony, Konanakunte, Bangalore, Karnataka 560062, India

Correspondence should be addressed to Abhishek Vijayakumar; abhishekbmc@yahoo.co.in

Received 1 December 2013; Accepted 18 January 2014; Published 20 February 2014

Academic Editor: Massimo Tonacchera

Copyright © 2014 Abhishek Vijayakumar et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of
hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. The underlying
hyperthyroidism is often subtle causing difficulty in early diagnosis. Factors like high-carbohydrate meal exercise, steroid, and stress
can precipitate an attack of TPP. Evidence is building up showing role of genetic mutations in Kir2.6 channel in the pathogenesis
of TPP. Loss of function of Kir2.6 together with increased activity of Na+ /K+ ATPase may trigger a positive feed-forward cycle of
hypokalemia. Biochemical hyperthyroidism with normal urinary potassium excretion and ECG changes are characteristic of TPP.
Treatment with low-dose potassium supplements and nonselective beta-blockers should be initiated upon diagnosis, and the serum
potassium level should be frequently monitored to prevent rebound hyperkalemia.

1. Introduction The etiology of hypokalemic paralysis can be generally

Association of periodic paralysis and thyrotoxicosis had been
documented by Rosenfeld as early as 1902 [1]. Thyrotoxic
periodic paralysis (TPP) is more commonly reported in
oriental Asians [2]. It has also been reported from the
western countries as a result of migration of different ethnic
populations [3]. TPP is characterized by acute onset of severe
hypokalemia and profound proximal muscle weakness in
patients with thyrotoxicosis [4]. TPP is commonly misdi-
agnosed in Western countries because of its similarities to
familial periodic paralysis. The neuromuscular presentations
of both are identical and physicians need to look for subtle
features of hyperthyroidism in the presence of hypokalemic
periodic paralysis. Early diagnosis not only aids in definitive
management with nonselective beta-blockers and correction
of hyperthyroidism, but also prevents the risk of rebound
hyperkalemia due to excessive potassium replacement.
2. Discussion
Hypokalemia-related medical emergencies vary from muscle
weakness to paralysis and are called hypokalemic paralysis.
classified into two groups: hypokalemic periodic paralysis,
due to shift of potassium into the intracellular space without a
total potassium deficit; and nonhypokalemic periodic paral-
ysis, due to a large potassium deficit via gastrointestinal or
renal loss. Among the hypokalemic periodic paralysis, famil-
ial hypokalemic periodic paralysis (FPP) is the most common
cause in Western countries, and thyrotoxic periodic paralysis
(TPP), characterized by the triad of acute hypokalemia
without total body potassium deficit, muscle paralysis, and
thyrotoxicosis, is the most common cause in Asia.
3. Epidemiology
The incidence of TPP in Chinese and Japanese thyrotoxic
patients has been reported at 1.8% and 1.9%, respectively [2],
whereas in North Americans a 0.1%–0.2% [5]. In the Chinese,
TPP occurs in 13% of male and 0.17% of female thyrotoxic
patients, in a series published in 1967 [4]. The male to
female ratio ranges from 17 : 1 to 70 : 1 despite the fact that
hyperthyroidism is more common in females (female-to-
male ratio of 9 : 1) [6].
2 Journal of Thyroid Research
4. Pathophysiology
The pathogenesis of TPP remains unclear. Sodium, chloride,
calcium, and potassium channels on cell membranes are
responsible for membrane excitability and muscle contrac-
tions. Disruption of any of these cellular transport mecha-
nisms, especially 3Na+ /2K+ ATPase pump, may cause abnor-
malities in muscle contractibility and paralysis.
The important role of Na+ -K+ ATPase pumps in the
pathogenesis of TPP is supported by the finding that their
activity in the skeletal muscle is significantly increased.
Thyroid hormone can stimulate Na+ -K+ ATPase in skeletal
muscle by genomic mechanism, acting on the thyroid hor-
mone responsive elements to upregulate the transcription
of the gene encoding Na+ /K+ ATPase and via nongenomic
mechanisms by enhancing the intrinsic activity or promoting
membrane insertion of the pump. Thyrotoxic patients with
PP have been found to have higher sodium pump activity
than those without paralytic episodes [7]. Catecholamine
can also increase Na+ /K+ -ATPase activity in skeletal muscle
[8]. The enhanced beta-adrenergic response in thyrotoxicosis
further increases Na+ /K+ -ATPase activity.
Hyperinsulinemia is also observed in acute attack of
TPP, and the release of insulin in response to oral glucose
challenge is exaggerated in TPP patients, supporting the idea
that insulin participates in the pathogenesis of hypokalemia
in TPP [9]. Insulin-response sequences are present in the
upstream region of Na+ /K+ -ATPase genes, and insulin has
been shown to stimulate Na+ /K+ -ATPase activity [10]. The
effect of insulin may account for the observation that a
high-carbohydrate diet can be a precipitating factor for TPP.
Sympathetic stimulation of insulin release in pancreas 𝛽-
cells provides additional rationale for using nonselective 𝛽-
blockers to treat acute hypokalemia and paralytic attack of
TPP.
Androgens have been reported to increase the expres-
sion and activity of the Na+ /K+ -ATPase [11, 12]. Testos-
terone enhances hypertrophy of myoblasts and thus causes
higher muscle-to-body mass ratio and total Na+/ K+ -ATPase
abundance in males. Catecholamines, a strong activator of
Na+/ K+ -ATPase activity, have been found to be released
more in males in response to experimental stress [13]. The
preponderance of TPP attacks in the morning may also stem
from higher plasma catechol-amines and sympathetic tone in
the late morning [14]. With respect to the seasonal variation,
increased outdoor activity with increased perspiration of
potassium and ingestion of sugar-containing cold beverages
may be responsible for the higher prevalence of TPP attacks
in the summer and fall.
Exercise releases potassium from the skeletal muscles,
whereas rest promotes influx of potassium. This explains why
paralytic attacks occur only during recovery from exercise
and resumption of exercise can abort an attack. Overall, it
appears that patients with TPP have an underlying predispo-
sition for activation of Na/K-ATPase activity, either directly
by thyroid hormone or indirectly via adrenergic stimulation,
insulin, or exercise. Traditional views regarding mechanism
of paralysis are shown in Figure 1.
↑ Adrenergic response T4 Increased insulin release
↑ Na/K ATPase
Disrupted ion channels
Intracellular potassium shif
Hypokalemia
Hyperpolarization
Periodic paralysis
Figure 1: Mechanism of paralysis in TPP.
Activation of Na+ /K+ ATPase cannot be the only mech-
anism for TPP, because only a minority (∼2%) of patients
with hyperthyroidism develop hypokalemic paralysis. The
increased Na-K ATPase activity in muscle may be compen-
sated by increased potassium efflux preventing development
of hypokalemia. It was seen that the total intracellular pota-
ssium content measured in the diaphragm muscle of a
thyrotoxic mouse is unchanged from the normal [15].
Additional factors such as decreased potassium efflux
might cause clinically significant hypokalemia. Studies have
shown that the outward Kir current is decreased in inter-
costal muscle fibers of both patients with TPP and familial
hypokalemic periodic paralysis [16]. Moreover, insulin and
catecholamine not only activate Na+ /K+ ATPase but also
inhibit Kir channels [17].
Recent studies have shown that mutations in the gene
encoding Kir2.6, a skeletal muscle-specific Kir channel, are
associated with TPP and predispose these patients to acute
paralytic attacks. A study by Ryan et al. [18] showed that the
prevalence of Kir2.6 mutation was up to 33% in Caucasians
and Brazilians with TPP. Thyroid hormone upregulates the
transcription of Kir2.6 through an upstream thyroid hor-
mone responsive element in the promoter region of channel
gene. Cheng et al. [19] found three additional loss-of-function
mutations in Kir2.6 channels in patients with TPP as well as
sporadic periodic paralysis. Cheng et al. also reported that
Kir2.6 forms functional homotetramer and heterotetramer
with Kir2.1, another Kir channel in the skeletal muscle. Kir2.6
mutants exert a dominant negative effect on both WT Kir2.1
and Kir2.6 channels.
Evidence is building up showing role of genetic mutations
in Kir2.6 channel in the pathogenesis of TPP. Loss of function
of Kir2.6 together with increased activity of Na+ /K+ ATPase
may trigger a positive feed-forward cycle of hypokalemia,
Journal of Thyroid Research
leading to paradoxical depolarization with consequent inac-
tivation of Na+ channel and muscle inexcitability [20].
The central to pathophysiology of skeletal muscle paraly-
sis in hypokalemic periodic paralysis is paradoxical depolar-
ization. The resting membrane potential should hyperpolar-
ize when extracellular K+ decreases. However, muscle fibers
from patients with hypokalemic periodic paralysis depolar-
ize under low extracellular K+ concentrations (<3 mEq/L).
This hypokalemia-induced paradoxical depolarization of the
resting membrane potential leads to inactivation of Na+
channels, rendering them unexcitable.
In familial Hypokalemic periodic paralysis paradoxical
depolarization is caused by mutations in the voltage sensor
of Nav1.4 and Cav1.1 channels giving imbalance between
inward leak current and outward K current. In TPP, reduced
outward K+ current because of loss-of-function mutations
of Kir2.6 causes a similar imbalance between inward leak
current and outward K+ current, and it results in paradoxical
depolarization.
5. Clinical Features
Patients are usually young adult males 20–40 yr of age. The
attack is characterized by recurrent, transient episodes of
muscle weakness that range from mild weakness to complete
flaccid paralysis. Neurologic examination during an attack
demonstrates weakness, usually affecting proximal more than
distal muscles, and the legs more than the arms. Mild myalgia
is a complaint in less than half of patients [21]. Decreased
muscle tone with hyporeflexia or areflexia is typical, although
normal or hyperactive reflexes may be seen in some cases.
Sensory function is not affected. The muscles affected may
be asymmetrical and bowel and bladder function are never
affected. In one series, tachycardia (mean heart rate =
105 bpm) was noted at presentation and distinguished these
patients from those with familial hypokalemic periodic par-
alysis [22]. Exceptional cases of bulbar weakness and res-
piratory weakness requiring ventilatory support have been
reported in TPP [23]. In severe cases of hypokalemia, even
fatal, arrhythmias (sinus arrest, second degree atrioventricu-
lar [AV] block, ventricular fibrillation, and ventricular tachy-
cardia) have been seen. Patients may experience recurrent
episodes of weakness that last from a few hours up to 72 h,
with complete recovery in between the attacks. Table 1 shows
some salient features of TPP.
As with hypokalemic PP, attacks in thyrotoxic PP may be
precipitated by events that are associated with an increased
release of epinephrine or insulin, both of which cause move-
ment of potassium into cells and low potassium blood levels.
Precipitating factors include high carbohydrate loads, stren-
uous exercise, trauma, acute URI, high-salt diet, emotional
stress, exposure to cold, alcohol ingestion, menstruation, and
use of drugs such as corticosteroids, epinephrine, acetazo-
lamide, and nonsteroidal anti-inflammatory drugs. In a large
study by Chang et al. [24] in 2013 one hundred and thirty five
patients of TPP were followed up for 10 years. It was found
that only 34% had identifiable precipitants. TPP patients with
and without known precipitating factors had no significant
differences in their clinical and biochemical findings. A high
3
Table 1: Clinical features of TPP.
Clinical manifestations of thyrotoxic periodic paralysis
General
Male predominance; initiation at age 20 to 40
Periodic flaccid paralysis of proximal muscles, mainly of
lower extremities
Negative family history of similar symptoms
Hypertension
Subtle clinical features of hyperthyroidism
Laboratory findings
Hypokalemia, hypophosphatemia, and mild hypomagnesemia
Normal acid-base balance
Low potassium excretion rate (low urinary potassium-
creatinine ratio and low TTKG)
Hypercalciuria and hypophosphaturia
Abnormal thyroid function tests (low TSH; elevated free and
total T4 and T3; increased T3 uptake)
Electrocardiographic abnormalities
Sinus tachycardia
Hypokalemic changes: prominent U wave, prolonged PR
interval, increased
P-wave amplitude, widened QRS complexes
First-degree atrioventricular block
Atrial and ventricular arrhythmias
Electromyography: low-amplitude compound muscle action
potential with no change after epinephrine.
TTKG indicates transtubular potassium gradient (a semiquantitative
index of the activity of the potassium secretory process calculated as
[urine K/(urine osmolality/plasma osmolality)]/plasma K); TSH: thyroid-
stimulating hormone; T4: serum thyroxine; T3: triiodothyronine.
carbohydrate or strenuous exercise was identified as precip-
itant in only 12 and 7%, respectively. Though high carbohy-
drate meal has been associated with an attack of TPP, stan-
dardization of glucose meal test for diagnosis is not available.
It was found that only 10 of the 55 (18%) patients developed
hypokalemia after glucose loading of 2 g/Kg. Also in a
recent study none of the 51 cases of TPP developed symptoms
after glucose loading test [25]. Although attacks of weakness
may occur at any time of the day, a high frequency of attacks
at night or early in the morning has been reported in TPP.
A seasonal variation has also been suggested, with more
frequent attacks in summer months.
Most patients with TPP have only mildly elevated serum
thyroid hormone levels and only about 10% of patients may
have mild thyrotoxic symptoms [6]. Using the Wayne’s index,
a reliable quantitative score of hyperthyroid severity, it was
found that only 17% of TPP patients had toxic thyrotoxicosis
(score > 19), supporting the notion that most TPP patients
have equivocal symptoms [24].
Although the majority of cases of thyrotoxicosis associ-
ated with TPP are due to Graves’ disease, TPP can appear
with thyrotoxicosis of any origin. Patients with TPP have
been reported with thyroiditis [26, 27], toxic adenoma [28],
toxic nodular goiter [29], TSH-secreting pituitary adenoma
4 Journal of Thyroid Research
Table 2: Differential diagnosis of hypokalemic paralysis.
Type of potassium Imbalance
Transcellular shift
Renal loss of potassium
Gastrointestinal loss of potassium
[30, 31], ingestion of T4 or T3 [32, 33], inadvertent iodine
excess [34], subacute thyroiditis of de Quervain [35], amio-
darone therapy [36], radiation thyroiditis with Graves’ disease
[37], and nutraceuticals containing tiratricol [38].
During an attack of paralysis or weakness serum, potas-
sium level is usually less than 3.0 mmol/liter and can be as low
as 1.1 mmol/liter. Occasionally if the patient is at the recovery
stage of the paralysis, serum potassium can be normal. In
addition to hypokalemia, there may be hypophosphatemia
and hypomagnesemia. Mild to moderate hypophosphatemia
in the range of 0.36–0.77 mmol/liter has been reported in two
thirds of cases [39]. Serum phosphate level returns to normal
without supplementation when the patient recovers from the
weakness. Serum creatine phosphokinase of muscle origin is
elevated in about two thirds of patients, particularly among
those whose attacks are precipitated by exercise. The compli-
cation of rhabdomyolysis may occur in a severe attack.
Electrocardiographic findings may be characteristic of
hypokalemia, with increased P-wave amplitude, prolonged
PR interval, widened QRS complexes, decreased T-wave
amplitude, and U waves. Unlike hypokalemia from other
causes, sinus tachycardia predominates in patients with TPP.
Other electrocardiographic abnormalities include atrioven-
tricular block, atrial fibrillation, ventricular fibrillation, and
asystole [40, 41].
TPP must be differentiated from other causes of hypo-
kalemic periodic paralysis. (Table 2) Workup for other
causes of hypokalemia include urinary potassium excretion
(>30 mEq indicates urinary loss), arterial blood gas for
acidosis, urinary potassium to creatinine ratio which is <13
in TPP.
Cause
Drugs (tocolytics, theophylline toxicity, chloroquine
toxicity, insulin overdose)
Thyrotoxic periodic paralysis
Familial periodic paralysis
Sporadic periodic paralysis
Barium poisoning
Drugs: diuretics
Primary hyperaldosteronism
Pseudohyperaldosteronism: licorice ingestion
Bartter’s syndrome, Gitelman’s syndrome
Renal tubular acidosis
Other: nephrotic syndrome, acute tubular necrosis, diabetic
ketoacidosis, and ureterosigmoidostomy.
Celiac disease
Tropical sprue
Infectious diarrhea: Salmonella enteritis, Strongyloides enteritis, and
Yersinia enterocolitis
Short bowel syndrome
6. Treatment
Management of TPP includes correction of hypokalemia and
treatment of the underlying hyperthyroid state. Traditionally,
patients are given intravenous or oral potassium to hasten
muscle recovery and prevent cardiopulmonary complica-
tions; however, there is a danger of rebound hyperkalemia
due to release of potassium and phosphate from the cells on
recovery.
One prospective study compared treatment with intra-
venous potassium chloride to normal saline infusion and
found a shorter recovery time with use of potassium (6.3 vs.
13.5 hours) [42]. In a retrospective case series, patients who
received intravenous potassium recovered more quickly than
those who received oral supplementation [43]. There may be a
delayed response of a few hours following potassium admin-
istration [44]. Required doses of potassium supplementation
are variable and range from 10 to 200 mEq. Rebound hyper-
kalemia occurred in approximately 40% of patients with TPP,
especially if they received >90 mEq of potassium chloride
within the first 24 hours. There is a positive correlation
between the dose of potassium chloride administered and
the degree of rebound hyperkalemia. Patients receiving a
total dose of ≤50 mEq of potassium chloride rarely develop
rebound hyperkalemia. Lower doses of potassium chloride
may be effective while lowering the patient’s risk of hyper-
kalemia. Thus KCl supplementation should be given at a slow
rate unless there are cardiopulmonary complications. Use of
potassium supplements is not useful for prophylaxis against
further paralytic attacks and should not be given to patients
between attacks.
Journal of Thyroid Research
Nonspecific beta-adrenergic blockers like propranolol
have also been proposed as an alternative treatment to
ameliorate the paralysis without rebound hyperkalemia and
raise the serum levels of potassium and phosphate. High-dose
oral propranolol (3-4 mg/kg orally) alone has been reported
to rapidly abort the paralysis [45].
Propranolol, but not the selective beta1-blocker metopro-
lol, also effectively prevented recurrence of paralytic attacks
or inhibited paralysis induced by a carbohydrate load. At a
dose of 40 mg four times a day, propranolol prevented paral-
ysis in carbohydrate-induced TPP in about two thirds of cases
by inhibiting the activity of Na/K-ATPase [46]. Because TPP
does not recur once the patient’s euthyroid adequate control
of hyperthyroidism is the mainstay of therapy. The cause for
the hyperthyroidism should be identified. Definitive treat-
ment with radioactive iodine or thyroidectomy should be
given to patients with hyperthyroidism due to Graves’ disease,
multinodular goiter, or toxic adenoma. Patients should avoid
precipitating factors including heavy carbohydrate intake,
high-salt diet, alcohol ingestion, and undue exertion until
thyrotoxicosis is under control. The use of nonselective beta-
blockers is important during early treatment with antithyroid
drugs or after radioactive iodine when a euthyroid status
is not yet achieved. In contrast to familial hypokalemic PP,
carbonic anhydrase inhibitors have not been shown to be of
benefit in thyrotoxic PP and may even increase the frequency
of attacks [47].
7. Conclusion
TPP has to always be kept in mind while evaluating a
case of hypokalemic paralysis. TPP has been increasingly
documented in Asian and Hispanic populations in the USA.
The subtleness of underlying hyperthyroidism often delays
diagnosis. Biochemical hyperthyroidism with normal uri-
nary potassium excretion and ECG changes clinches to dia-
gnosis of TPP. Treatment with low-dose potassium supple-
ments and nonselective beta-blockers should be initiated
upon diagnosis, and the serum potassium level should be
frequently monitored to prevent rebound hyperkalemia.
Increased awareness among physicians about this disorder
will result in early diagnosis, appropriate treatment, and the
prevention of rebound hyperkalemia.
Conflict of Interests
The authors declare that there is no conflict of interests
regarding the publication of this paper.
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