• Users Online: 252
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
   Table of Contents      
LETTER TO THE EDITOR
Year : 2016  |  Volume : 2  |  Issue : 3  |  Page : 164-165

Thyrotoxic periodic paralysis


Department of Medicine, King George's Medical College, Lucknow, Uttar Pradesh, India

Date of Web Publication7-Oct-2016

Correspondence Address:
Dr. Manish Gutch
Department of Medicine, King George's Medical College, Lucknow, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2394-7438.191694

Rights and Permissions

How to cite this article:
Shobhit S, Annesh B, Manjari D, Durgesh P, Gutch M. Thyrotoxic periodic paralysis. MAMC J Med Sci 2016;2:164-5

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 2019 Sep 21];2:164-5. Available from: http://www.mamcjms.in/text.asp?2016/2/3/164/191694

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: Thyroid scan with 99Tc pertechnetate showed a mildly enlarged thyroid gland with diffuse homogeneous radiotracer uptake, suggestive of Grave's disease

Click here to view


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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Fontaine B, Vale-Santos J, Jurkat-Rott K, Reboul J, Plassart E, Rime CS, et al. Mapping of the hypokalaemic periodic paralysis (HypoPP) locus to chromosome 1q31-32 in three European families. Nat Genet 1994;6:267-72.  Back to cited text no. 1
[PUBMED]    
2.
Millikan CH, Haines SF. The thyroid gland in relation to neuromuscular disease. AMA Arch Intern Med 1953;92:5-39.  Back to cited text no. 2
[PUBMED]    
3.
McFadzean AJ, Yeung R. Periodic paralysis complicating thyrotoxicosis in Chinese. Br Med J 1967;1:451-5.  Back to cited text no. 3
[PUBMED]    
4.
Ko GT, Chow CC, Yeung VT, Chan HH, Li JK, Cockram CS. Thyrotoxic periodic paralysis in a Chinese population. QJM 1996;89:463-8.  Back to cited text no. 4
[PUBMED]    
5.
Jurkat-Rott K, Lerche H, Lehmann-Horn F. Skeletal muscle channelopathies. J Neurol 2002;249:1493-502.  Back to cited text no. 5
[PUBMED]    
6.
Wang W, Jiang L, Ye L, Zhu N, Su T, Guan L, et al. Mutation screening in Chinese hypokalemic periodic paralysis patients. Mol Genet Metab 2006;87:359-63.  Back to cited text no. 6
[PUBMED]    
7.
Gutch M, Agarwal A, Amar A. Hypokalemic quadriparesis: An unusual manifestation of dengue fever. J Nat Sci Biol Med 2012;3:81-3.  Back to cited text no. 7
[PUBMED]    
8.
Okinaka S, Shizume K, Iino S, Watanabe A, Irie M, Noguchi A, et al. The association of periodic paralysis and hyperthyroidism in Japan. J Clin Endocrinol Metab 1957;17:1454-9.  Back to cited text no. 8
[PUBMED]    
9.
Shizume K, Shishiba Y, Kuma K, Noguchi S, Tajiri J, Ito K, et al. Comparison of the incidence of association of periodic paralysis and hyperthyroidism in Japan in 1957 and 1991. Endocrinol Jpn 1992;39:315-8.  Back to cited text no. 9
[PUBMED]    
10.
Kelley DE, Gharib H, Kennedy FP, Duda RJ Jr., McManis PG. Thyrotoxic periodic paralysis. Report of 10 cases and review of electromyographic findings. Arch Intern Med 1989;149:2597-600.  Back to cited text no. 10
    
11.
Tassone H, Moulin A, Henderson SO. The pitfalls of potassium replacement in thyrotoxic periodic paralysis: A case report and review of the literature. J Emerg Med 2004;26:157-61.  Back to cited text no. 11
[PUBMED]    
12.
Chang CC, Cheng CJ, Sung CC, Chiueh TS, Lee CH, Chau T, et al. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: Focus on symptomatology and precipitants. Eur J Endocrinol 2013;169:529-36.  Back to cited text no. 12
[PUBMED]    
13.
Gennari FJ. Hypokalemia. N Engl J Med 1998;339:451-8.  Back to cited text no. 13
[PUBMED]    
14.
Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc 2005;80:99-105.  Back to cited text no. 14
[PUBMED]    
15.
Levey GS, Klein I. Catecholamine-thyroid hormone interactions and the cardiovascular manifestations of hyperthyroidism. Am J Med 1990;88:642-6.  Back to cited text no. 15
[PUBMED]    
16.
Ginsberg AM, Clutter WE, Shah SD, Cryer PE. Triiodothyronine-induced thyrotoxicosis increases mononuclear leukocyte beta-adrenergic receptor density in man. J Clin Invest 1981;67:1785-91.  Back to cited text no. 16
[PUBMED]    
17.
Lee KO, Taylor EA, Oh VM, Cheah JS, Aw SE. Hyperinsulinaemia in thyrotoxic hypokalaemic periodic paralysis. Lancet 1991;337:1063-4.  Back to cited text no. 17
[PUBMED]    
18.
Gutch M, Kumar S, Razi SM, Gupta A, Gupta KK, Nath M. A case of type I diabetes mellitus and autoimmune thyroiditis presents with hypokalemic paralysis. Trop J Med Res 2015;18:121-3.  Back to cited text no. 18
  Medknow Journal  


    Figures

  [Figure 1]



 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
References
Article Figures

 Article Access Statistics
    Viewed518    
    Printed8    
    Emailed0    
    PDF Downloaded13    
    Comments [Add]    

Recommend this journal