A 35 year-old man who had been diagnosed as chronic
hepatitis C with mild abnormal liver function patient and was
treated with interferon at out-patient clinic. He complained
of intermittent muscle weakness that was more severe in the
proximal parts of the extremities one month prior to
admission. The muscle weakness was heralded by muscle aches
and cramping that usually occurred in the early morning, and
was not precipitated by large meals or strenuous exercise; but
it did resolve spontaneously. However, the attacks occurred
with increased frequency in the following two weeks, with
three to four episodes a day. Finally, he could not even get
out of the bed and therefore he was brought to the emergency
room for further treatment.
On arrival, the consciousness was clear. His body height
was 161 cm, body weight was 57kg. The body temperature was
37.2 oC, the blood pressure was 142/76 mmHg, and the pulse
rate was 120 bpm. A complete loss of the muscle power over
both thighs was found, while the arms could not resist the
gravity. The muscle power distal to the thighs and the arms
was intact. Fine tremors of both hands were also noted.
Neither muscle wasting, goiter, ophthalmopathy, nor
respiratory distress was found. There was no sensory defect or
focal neurological sign. Electrocardiogram showed sinus
tachycardia without flattened T wave or U wave.
<Laboratory and Image
Study>
1. CBC/DC & coagulation
profiles:
Date |
WBC K/£gL |
RBC M/£gL |
Hgb g/dL |
Hct % |
MCV fL |
Plt K/£gL |
During attack |
8.95 |
4.55 |
12 |
36 |
92.3 |
489 |
Free of attack |
8.54 |
4.71 |
12.3 |
36.7 |
92.2 |
423 |
2.
Biochemistry
Date |
BUN mg/dl |
Cre mg/dl |
Na mmol/l |
K mmol/l |
Cl mmol/l |
Ca mmol/l |
P mmol/l |
GOT U/l |
T-Bil mg/dl |
LDH U/l |
CPK mg/dl |
During attack |
20 |
1.2 |
142 |
2.5 |
106 |
2.3 |
0.9 |
105 |
0.6 |
250 |
115 |
Free of attack |
19 |
1.1 |
138 |
3.8 |
102 |
2.3 |
1.2 |
87 |
0.5 |
190 |
85 | 3.
Urine analysis:
Date |
Appearance |
Sp. gr |
pH |
Protein mg/dL |
Glu g/dL |
Ketones |
O.B |
Urobil EU/dL |
Bil |
During attack |
Y;C |
1.020 |
6.0 |
¡Ð |
¡Ð |
¡Ð |
¡Ð |
0.1 |
¡Ð |
Free of attack |
Y;C |
1.026 |
6.0 |
¡Ð |
¡Ð |
¡Ð |
¡Ð |
0.1 |
¡Ð |
Date |
Nitrite |
WBC |
RBC /HPF |
WBC /HPF |
EpithCell /HPF |
Cast /LPF |
Crystal |
Bact |
During attack |
¡Ð |
¡Ð |
3-5 |
0-1 |
3-5 |
¡Ð |
¡Ð |
¡Ð |
Free of attack |
¡Ð |
¡Ð |
0-1 |
0 |
3-5 |
¡Ð |
¡Ð |
¡Ð |
During attack:
Arterial blood gas: PH:7.36, PaCO2: 42.3, PO2: 95, HCO3-:
22.6 Spot urinary potassium to creatinine ratio [UK/UCre
(nmol/nmol)]: 3.3 Transtubular potassium concentration
gradient (TTKG): 2.6 Thyroid function test: TSH < 0.1
£gIU/mL, free T4: 20.84 ng/dl
<Course and
Treatment>
At Emergency department, serum and spot urine potassium,
creatinine and osmolality were all checked as well as thyroid
function test. Intravenous KCL supplement, oral propanolol 10
mg 1# tid and carbimazole 10 mg bid were prescribed since the
blood tests revealed hypokalemia and hyperthyroidism. He was
transferred to general ward under the impression of thyrotoxic
periodic paralysis later. However, symptoms of persistent
tachycardia and frequent episodes of muscle weakness persisted
even after potassium supplement and oral ƒÒ-blockers
administration. Muscle power recovered gradually hours later.
Both anti-microsomal antibody (AMA) and TSH receptor antibody
(TSHr Ab) were significantly elevated. The thyroid
ultrasonography showed a hypoechoic heterogeneous pattern,
which suggested autoimmune thyroid disease and a
99mTc-pertechnetate thyroid scan also revealed the diffuse
enlargement of the thyroid gland with an increased rate of
tracer uptake (5.28%; normal range 0.4-2.4 %). These findings
were all compatible with typical Graves¡¦ disease. The patient
was treated with carbimazole 10 mg bid and higher dose of
propranolol (40 mg tid). The frequency of the attacks declined
gradually, and he was discharged with a diagnosis of
interferon-induced TPP. The post-treatment course was smooth
without recurrence.
<Analysis>
The Patient was diagnosed as hypokalemia and
hyperthyroidism. He denied history of binge drinking or heavy
meal prior to these attacks. There were also no
gastrointestinal symptoms such as vomiting and diarrhea.
Besides, he also denied the use of diuretics or laxatives. The
spot urinary UK/UCre was 3.3 and the TTKG was 2.6, which
rendered renal or gastrointestinal potassium wasting less
likely. Thyrotoxic periodic paralysis was the final diagnosis
that was proved by thyroid function test, immunological exams
and imaging studies.
Thyrotoxic periodic paralysis (TPP) is manifested as
recurrent episodes of hypokalemia and muscle weakness which
lasts from hours to days. It is most common in adults aged
20-40 years. The incidence of the disorder is relatively
higher among Asians, especially in male. Hyperinsulinemia, a
carbohydrate or salt load, and exercise are important in
precipitating paralytic attacks. It is one of clinical
periodic paralysis diseases. Periodic paralysis is a group of
genetic diseases including hypokalemic or hyperkalemic type.
Both forms may be inherited or occur without a family history.
If inherited, they often occur in an autosomal dominant
fashion. The periodic paralysis has been associated with
thyrotoxicosis from various etiologies. The pathogenesis of
TPP is uncertain, but there is evidence for a decrease in the
activity of the calcium pump, whereas hyperkalemic periodic
paralysis is related to sodium channel. It involves attacks of
muscle weakness or paralysis alternating with periods of
normal muscle function. Attacks usually begin after symptoms
of hyperthyroidism have developed. The frequency of attacks
varies from daily to yearly. Episodes of muscle weakness may
last for a few hours or may persist for several days. Serum
potassium level decreases, but not necessarily below normal,
during attacks. Patients experience urinary retention with
elevated urine levels of sodium, potassium, and chloride. A
concomitant decrease in serum phosphorous level also occurs.
Creatine phosphokinase (CPK) level rises during
attacks.Potassium will remain normal between attacks and the
total body potassium is not decreased. Weakness most commonly
affects the proximal muscle group of the arms and legs. The
muscles associated with respiration can sometimes be affected
and this can be fatal.
Arrhythmias can also occur. Although muscle strength is
initially normal between attacks, repeated attacks may
eventually cause progressive and persistent muscle weakness.
Risk factors include a family history of periodic paralysis
and hyperthyroidism.
The best treatment is a rapid reduction in thyroid hormone
levels and £]-blocker. Potassium should also be given during
the attack. Oral potassium supplement is preferred, but if the
weakness persisted, intravenous potassium may be necessary
with caution. For patients with hypokalemic periodic
paralysis, administering potassium may stop an attack.
However, taking regular doses of potassium will not prevent
future attacks. Diet with low carbohydrates and salt may be
recommended to prevent attacks. Acetazolamide, a medication
that is effective in attack prevention with familial periodic
paralysis, is usually not effective with thyrotoxic periodic
paralysis.
<Reference>
1. J Emerg Med. 2005 Feb;28(2):201-9 2. J Emerg
Med. 2004 Feb;26(2):157-61 3. Thyroid. 2002
Jan;12(1):77-80. 4. Arch Intern Med 2004, 164, (14),
1561-6 5. Mayo Clin Proc. 2005 Jan;80(1):99-105. 6.
Harrison¡¦s principles of internal medicine 15 edition
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