MAMC Journal of Medical Sciences

: 2016  |  Volume : 2  |  Issue : 3  |  Page : 164--165

Thyrotoxic periodic paralysis

Shakya Shobhit, Bhattacharjee Annesh, Dwivedi Manjari, Pushkar Durgesh, Manish Gutch 
 Department of Medicine, King George's Medical College, Lucknow, Uttar Pradesh, India

Correspondence Address:
Dr. Manish Gutch
Department of Medicine, King George«SQ»s Medical College, Lucknow, Uttar Pradesh

How to cite this article:
Shobhit S, Annesh B, Manjari D, Durgesh P, Gutch M. Thyrotoxic periodic paralysis.MAMC J Med Sci 2016;2:164-165

How to cite this URL:
Shobhit S, Annesh B, Manjari D, Durgesh P, Gutch M. Thyrotoxic periodic paralysis. MAMC J Med Sci [serial online] 2016 [cited 2020 Jan 17 ];2:164-165
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Full Text

Dear Sir,

Hypokalemic periodic paralysis (HPP) occurs with a prevalence of one in 100,000.[1] Periodic paralysis is a rare complication of hyperthyroidism.[2] Thyrotoxic periodic paralysis (TPP) is characterized by acute onset of profound muscle weakness and severe hypokalemia in patient with thyrotoxicosis.[3] This condition might be precipitated in the presence of certain factors such as high-carbohydrate meal, exercise, stress, high-salt diet, alcohol, or steroids. Although hyperthyroidism itself is more common in women, TPP is mostly reported in men, with the male:female ranging from 17:1-70:1.[4] Hypokalemia in TPP results from an intracellular shift of potassium induced by the thyroid hormone sensitization of Na+ /K+ -ATPase rather than depletion of total body potassium.

A 20-year-old male presented to the emergency unit with complaints of acute onset weakness in all four limbs while trying to get up early in the morning; he was unable to walk or stand unassisted. He had no symptoms before going to bed the previous night. There was no history of any precipitating factor such as drug or alcohol intake; there was no significant change in either diet or activity levels. He had suffered from similar episodes of weakness thrice in the past, for which he was hospitalized and recovered completely following treatment. There was no history suggestive of sensory abnormalities, fever, diarrhea, weight loss, palpitations, or heat intolerance. Family history was unrewarding.

On examination, the patient was conscious and afebrile. His vitals were stable, with a pulse rate of 82/min, bilaterally regular, and symmetrical. There was no evidence of tremors, goiter, or any eye and nail-bed changes. Neurologic examination revealed power of 1/5 in the upper limbs across all joints and 0/5 in both lower limbs across all joints with decreased tone and diminished deep tendon reflexes. Rest of the neurological examination and that of other organ systems were within normal limits.

Investigations revealed a normal hemogram, liver, and renal functions while serum K+ was on the lower side (2.7 meq/l), with normal levels of serum Na+ and Ca+ 2 (ionic). Hypokalemia was also reflected in the prominent U-waves in electrocardiogram. Intravenous potassium infusion was started which resulted in gradual improvement of the patient's weakness.

On further evaluation, thyroid profile revealed FT3-12.51 pmol/L, FT4-45.30 pmol/L, and thyroid-stimulating hormone 0.005 mIU/ml. Antithyroid peroxidase antibody titer was raised (113.4 IU/ml). Thyroid scan with99 Tc pertechnetate showed a mildly enlarged thyroid gland with diffuse homogeneous radiotracer uptake, suggestive of Grave's disease [Figure 1]. Tablet propranolol 40 mg and tablet methimazole 20 mg once daily were added to his treatment regimen. Subsequently, his weakness improved and serum potassium normalized. The patient is regularly followed up, and compliance to therapy is ensured. There were no further episodes of limb weakness since the initiation of antithyroid medications.{Figure 1}

HPP may occur sporadically in the form of familial hypokalemic paralysis, a poorly understood disorder that may occur spontaneously or as the result of autosomal dominant inheritance.[1] This form of periodic paralysis is felt to be the result of disordered cellular potassium regulation, perhaps due to sodium or calcium channel abnormalities.[5],[6] The association of thyrotoxicosis with periodic paralysis was discovered first in 1902.[7] It is the most common form of HPP and is seen primarily in Asian males occurring in 1.9% of Japanese hyperthyroid patients overall, and in up to 8% of hyperthyroid Japanese men.[8],[9] In patients who develop HPP, however, the symptoms of hyperthyroidism are often quite mild and may be overlooked.[10],[11] TPP usually presents in young adult males 20-40 years of age. Recurrent transient episodes of muscle weakness ranging from mild weakness to complete flaccid paralysis are the usual presenting complaints. Precipitating factors include high-carbohydrate loads, strenuous exercise, trauma, acute upper respiratory infections, high-salt diet, emotional stress, exposure to cold, alcohol ingestion, menstruation, and use of drugs such as corticosteroids, epinephrine, acetazolamide, and nonsteroidal anti-inflammatory drugs. Precipitating factors can be traced in only 34% of patients.[12] The proximal muscles are affected more severely. Attacks usually occur at night.[11] On neurological examination during an episode, hyporeflexia/areflexia muscle weakness with decreased muscle tone is typically seen without any involvement of sensory system and autonomic functions. Extreme cases with severe hypokalemia may present with respiratory muscle weakness requiring ventilator support or fatal arrhythmias.

TPP is not related to the etiology, severity, and duration of thyrotoxicosis although Grave's disease is most commonly associated. Family history of periodic paralysis is frequently absent. Pathogenesis of TPP remains unclear. Transcellular distribution of potassium is maintained by the Na+ /K+ -ATPase activity in the cell membrane, and it is mainly influenced by the action of insulin and beta-adrenergic catecholamines.[13] Hypokalemia in TPP results from an intracellular shift of potassium and not total body depletion. Hyperthyroidism may result in a hyperadrenergic state, which may lead to the activation of the Na+ /K+ -ATPase pump and result in cellular uptake of potassium.[13],[14],[15] Thyroid hormones may also directly stimulate Na+ /K+ -ATPase activity and increase the number and sensitivity of beta-receptors.[13],[16] Patients with TPP have associated hyperinsulinemia during episodes of paralysis, accounting for precipitation of the attacks after high-carbohydrate meals.[17] Paralytic episodes can be induced in these patients by administering insulin and glucose but only when they are hyperthyroid.[14]

Treatment of TPP includes prevention of this shift of potassium by using nonselective beta-blockade, correcting the underlying hyperthyroid state, and replacing potassium. Although acute paralytic episodes are treated with potassium replacement, the administration of prophylactic potassium or acetazolamide do not benefit these patients since potassium levels are normal between episodes; on the contrary, it may result in dangerous hyperkalemia.[18] The attainment of a euthyroid state prevents further episodes of TPP.

TPP is the most common cause of HPP in the Asian population. A high index of suspicion is required since the early recognition is rendered difficult by minimal clinical features of associated hyperthyroidism. Treatment consists of emergent correction of hypokalemia and management of underlying thyrotoxic state.

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