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A 46-year-old man was sent to
emergent department in summer of 2000 because of paralysis of
both lower limbs on awakening while he tried to get out of bed
in the morning. He had suffered sleeping disturbance,
nervousness, and anxiety for about 10 years. Neither weight
loss nor palpitation was found. He denied heat intolerance and
excessive sweating. Two to three months prior to this episode,
he often felt thirsty and took a lot of soft sweet drink. One
day prior to an episode of paralysis, he didn't take strenuous
exercise. On arrival at the hospital, flaccid paralysis was
noted at both lower limbs. There was no stool or urinary
incontinence, swallowing difficulty, hoarseness, diplopia, or
respiratory difficulty. No sensory impairment was found. Other
physical examination was unremarkable. Biochemistry
examination revealed a serum potassium level of 1.9 mM. His
muscle power regained gradually about 4 hours later when
potassium supplement was given by vein. He was discharged from
the hospital on the same day when his serum potassium was 5
mM.
No more similar episode of
paralysis was noted after he took anti-thyroid agents at the
outpatient department. However, pre-tibial myxedema developed
later in early 2002. There were also goiter, exophthalmos, red
eyes, eyeball pain, and blurred vision. Chemosis at the right
eye and limitation of up-ward gaze were noted without eyelid
lags. The computed tomography (CT) of the orbital region
showed exophthalmos with increased muscle volume of the
bilateral superior and inferior rectus muscle. Thyrotropin
binding inhibition immunoglobulin (TBII, normal <12%) was
90.1% in Aug 2002. His eye problem became more severe, and
therefore, he was admitted for pulse therapy with steroids .
On admission, physical examination
revealed a well-developed man with clear consciousness and
good JOMAC. His body height was 166.3 cm and weight 82.2 kg.
The blood pressure was 130/80 mmHg, the temperature was
36.8°C, the pulse rate was 84 beats per minute and
respirations 20 breaths per minute. Bilateral injected
conjuctivae were found. The eye movement was limited while
gazing upward in bilateral eyes. The thyroid was grade III
enlargement. The chest, heart and abdomen were remarkable.
Pre-tibial myxedema was found at the lower limbs. No muscle
weakness was found.
< Lab data
>
| |
WBC |
Hb |
Hct |
MCV |
PLT |
Seg |
Lym |
| Oct, 2002 |
7430/ul |
15.2g/dl |
44.4% |
86.2fL |
273K/ul |
59% |
27.5% |
| |
T-Bil |
AST |
ALT |
BUN |
Cre |
Na |
K |
Ca |
LDH |
CPK |
| Oct, 2002 |
0.6 |
17 |
20 |
13 |
0.8 |
142 |
4 |
2.28 |
73 |
364 |
| |
RIA: T3
(μIU/ml) |
RIA: T4
(ng/dL) |
RIA: TSH
(μg/dL) |
| Aug, 2002 |
298 |
8.65 |
0.38 |
| July, 2003 |
159 |
2.72 |
12.9 |
| ( Reference value) |
80-200 |
4.5 –12 |
< 6.5 |
| Inhibition of TSH binding (%) |
| 90.1 (reference value: <12%) in Aug
2002
|
< 病例討論
>
Dunlap和Kepler首先在1931年描述甲狀腺週期性麻痺（thyrotoxic periodic
paralysis）。它是後天性低血鉀週期性麻痺的最常見的形式。患者以男性為主(男比女，20︰1)，特別是發生在亞洲人種。它通常在20到40歲的時候發生。它會有先行症狀，例如：肌肉痛和僵硬。發作常是突然地，影響的肌肉大多是近端，且有對稱性，特別是下肢的近端肌肉。病患可能還未出現其它甲狀腺功能異常的症狀。甲狀腺週期性麻痺常發生在早晨，發作之後在幾小時到2天後可自然地恢復。甲狀腺週期性麻痺並沒有家族史，誘發的因子有：費力的體力活動後，接著有一段時期的休息；攝取高的碳水化合物或酒精；冷；壓力和感染。肌肉無力的可能的原因是由於低血鉀或者低血磷。低血鉀的原因是由於鉀離子向細胞內移動。
在處理甲狀腺週期性麻痺發作，很重要的是防止低血鉀的併發症，例如︰心律不整和呼吸衰竭。鉀的補充並不會加速恢復，並且可能在恢復期間，併發高血鉀症。Propranolol的使用，能拮抗catecholamine對Na-K
ATPase的作用，並且抑制胰島素分泌，因此可以用來治療甲狀腺週期性麻痺。對防止甲狀腺週期性麻痺來說，應使用抗甲狀腺藥物來達到甲狀腺功能正常，因此在達到甲狀腺功能正常之前應該使用β阻斷劑。
家族性週期性麻痺應該與甲狀腺週期性麻痺作區別。家族性週期性麻痺是肌肉興奮性的問題的體顯性遺傳疾病。大約2/3的案例是家族遺傳，其他1/3的是偶發的。它是一種去極化麻痺。它會間歇性地無法保持骨骼肌休息電位。它通常在高加索人種發生。
< References
>
- Ahlawat SK, Sachdev A. Hypokalaemic
paralysis. Postgrad Med J. 1999;75(882):193-7.
- Lin YH, Lin YF, Halperin ML.
Hypokalaemia and paralysis. QJM. 2001;94(3):133-9.
- Manoukian MA, Foote JA, Grapo LM. Clinical and metabolic
features of thyrotoxic periodic paralysis in 24 episodes.
Arch Intern Med. 1999 22;159(6):601-6.
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Case Discussion
繼續教育考題