THYROTOXIC PERIODIC PARALYSIS IN A PATIENT ABUSING THYROXINE FOR WEIGHT REDUCTION

Abstract

Thyrotoxic periodic paralysis is a rare endocrine disorder most prevalent among individuals of Asian descent that presents as proximal muscle weakness, hypokalemia, and signs of hyperthyroidism. We present an unusual patient with previous normal thyroid function who had abused thyroxine as antiobesity pills and developed periodic paralysis affecting the upper and lower limbs.

• Hypokalemia
• Thyrotoxic periodic paralysis
• Hyperthyroidism
• Thyroxine

INTRODUCTION

Thyrotoxic periodic paralysis (TPP), an acute complication of thyrotoxicosis, is common in Oriental men [[1]]. TPP attacks occur only when thyrotoxicosis is present. Attacks can be induced by insulin and carbohydrate administration in hyperthyroid patients with a history of TPP, but not in patients who have become euthyroidic after treating TPP. Paralytic attacks can recur with relapse into a thyrotoxic state, and can be induced by exogenous thyroid hormone [[2]].

We report here a patient who presented with hypokalemic TPP when she abused thyroxine for weight reduction.

CASE REPORT

A 36–year-old native Taiwanese female was admitted to the emergency room with a chief complaint of an inability to move her lower extremities. She had no family or personal history of periodic paralysis. The only relevant information in her history was body weight gain in the last two years, and she had normal thyroid function (TSH 1.69 mU/L, normal 0.35–5.5) at the time.

Two weeks before admission, the patient had started taking thyroxine (Eltroxin 0.1 mg/tab b.i.d.) by herself as a weight-reducing agent. The midnight prior to admission, she awoke with “muscle aches” in both thighs. Upon awakening in the morning, she experienced intense weakness of her lower extremities and mild weakness of her upper extremities.

At the time of admission, the initial physical examination revealed no exophthalmos, lid lag, or thyroid enlargement, but she was unable to move her arms or legs nor lift her head from the bed. Flaccid quadriparesis was noted with abolition of all the deep tendon reflexes. Her sensory system was intact. A lumbar puncture was performed, suspecting Guillain-Barré syndrome, but CSF study showed a normal pattern.

Serum potassium was 1.6 meq/L (normal 3.0–4.8), phosphate 0.7 meq/L (normal 2.4–4.7); CBC, BUN, creatinine, CPK, and other general laboratory studies were normal. EKG revealed sinus tachycardia and a prolonged QT interval (no μ waves were seen) of 0.48 seconds (normal is less than 0.35). Muscle weakness was completely resolved approximately six hours after initiation of KCl therapy. Thyrotoxicosis was considered because of the presence of hypokalemic periodic paralysis and the patients history of thyroxine abuse.

Thyroid function test results showed thyroxine 6.5 μg/dL (normal 4.8–12.5), triiodothyronine by radioimmunoassay 100 ng/dL (normal 60–181), free T4 0.74 ng/dL (normal 0.84–1.83), and serum TSH 0.003 mU/L. Immunologic tests (anti-smooth muscle antibody, ANA, anti-mitochondrial antibody, and thyroid stimulating immunoglobulins) were negative. A ¹³¹I scan of the thyroid gland showed decreased uptake (1%) after 24 hours. TRH (500 μg Relefact TRH, Hoechst) evoked a normal response of TSH with a peak level of 14.9 mU/L 30 minutes after intravenous administration of TRH (95% CI of normal peak TSH levels: 2.8–22.5 mU/L).

Laboratory data repeated 10 days after discharge revealed normal thyroid function (free T4 1.45 ng/dL, and TSH 1.2 mU/L).

DISCUSSION

The rapid onset of areflexic weakness is usually due to Guillain-Barré syndrome, but other important causes include metabolic derangements, periodic paralysis, botulism, and poliomyelitis. We report a case clinically mimicking Guillain-Barré syndrome, and discuss the diagnostic difficulties when TPP is often thought to be Guillain-Barré syndrome, spinal cord compression, familial periodic paralysis, or sporadic periodic paralysis [[3]].

Rosenfeld first reported association between hypokalemic periodic paralysis and thyrotoxicosis in 1902 [[4]]. Although the majority of causes of TPP are sporadic, there is a 5% crossover between TPP and the more common familial hypokalemic periodic paralysis that is transmitted in an autosomal dominant fashion. It is about 17 to 76 times more common in men than women. The paralysis usually follows ingestion of a carbohydrate meal, heavy exercise, or both [[5]].

Ohno and Miyoshi [[6]] reported 123 cases of thyrotoxicosis due to abuse of thyroid medication, without mentioning any neuromuscular symptoms. Perhaps this may be explained by the fact that the patients were all female; the incidence of periodic paralysis in thyrotoxic Oriental women is much lower than in men. Most persons who abuse thyroid medication, whether because of a psychiatric disorder or simply in a misguided attempt to lose weight, are women, and as long as this is true, periodic paralysis will continue to be a rare complication of self-induced hyperthyroidism.

Hyperthyroidism must be differentiated from nonhyperthyroid thyrotoxic states. Common to the majority of nonhyperthyroid conditions is a low radioactive iodine (RAI) uptake (<8 to 10%), which is evidence that the thyroid gland itself is not actively synthesizing and secreting thyroid hormone. Mechanisms include liberation of thyroid hormone from the thyroid (thyroiditis), ectopic hormone production from thyroid tissue in abnormal locations (lingual goiter, struma ovarii, metastatic thyroid carcinoma), and ingestion of pharmacologic preparations, or food containing thyroid hormone [[7]]. Our patient's radioactive iodine uptake after 24 hours was 1%, and the TRH test revealed normal hypothalamus-pituitary axis. This suppression was secondary to exogenous thyroxine.

Oral and intravenous potassium repletion has been reported to correct symptoms in both familial and thyrotoxic periodic paralysis. Rendering the patient euthyroidic will prevent further attacks. In our case, typical attacks of periodic paralysis were precipitated by administration of thyroxine, and the patient had complete recovery following potassium therapy without further attacks.

Several lessons should be learned from this patient. First, on the basis of the case presented, we suggest that hypokalemia should be excluded in any patient presenting with a typical Guillain-Barré syndrome. Second, low radioactive iodine uptake in an obese woman should raise the suspicion of exogenous ingestion of thyroid hormone. Finally, for the management of acute muscle paralysis of TPP, treatment with potassium chloride is preferred.

In conclusion, we described a young woman who suffered from TPP after abusing thyroxine for weight reduction. This attack subsided soon after intravenous potassium repletion and the withdrawal of the thyroxine. The diagnosis should always be considered when dealing with patients with acute muscle weakness especially if they are young, with severe paralysis, and in those who have a history of using drugs for weight reduction who also have suppressed TSH and low radioactive iodine uptake.