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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 10  |  Issue : 2  |  Page : 79-81

A case report on thyrotoxic periodic paralysis from Dhaka, Bangladesh


1 Department of Internal Medicine, United Hospital Ltd., Dhaka, Bangladesh
2 Unit of Pharmacology, Faculty of Medicine and Defence Health, Universiti Pertahanan Nasional Malaysia (National Defence University of Malaysia), Kuala Lumpur, Malaysia

Date of Submission28-Jan-2020
Date of Acceptance21-Apr-2020
Date of Web Publication13-May-2020

Correspondence Address:
Mainul Haque
Faculty of Medicine and Defence Health, Universiti Pertahanan Nasional Malaysia (National Defence University of Malaysia), Kem Sungai Besi, Kuala Lumpur
Malaysia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AIHB.AIHB_7_20

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  Abstract 


Thyrotoxic periodic paralysis (TPP) is a disorder comprising acute hypokalaemia, intermittent muscle weakness and thyrotoxicosis. TPP is a rare manifestation of thyrotoxicosis predominantly seen in Asian people. We reported a patient who was brought to the emergency department with acute onset of weakness of her lower limbs. After a series of investigations, the patient was diagnosed as a case of thyrotoxicosis. The patient was placed on carbimazole, which prevented further attacks. The patient's improvement was satisfactory, and she is currently symptom free. Because of the presenting feature, its precipitating factor, the absence of a family history of periodic paralysis and the improvement of a clinical parameter after the starting of the antithyroid treatment, the condition was diagnosed as thyrotoxic periodic paralysis. The physician should concern about thyrotoxic periodic paralysis in people who present with weakness and features of thyrotoxicosis. A high prediction, early diagnosis and treatment of the condition can prevent severe complications, such as cardiac dysrhythmia.

Keywords: Bangladesh, Dhaka, report, thyrotoxic periodic paralysis


How to cite this article:
Jahan N, Begum A, Haque M. A case report on thyrotoxic periodic paralysis from Dhaka, Bangladesh. Adv Hum Biol 2020;10:79-81

How to cite this URL:
Jahan N, Begum A, Haque M. A case report on thyrotoxic periodic paralysis from Dhaka, Bangladesh. Adv Hum Biol [serial online] 2020 [cited 2022 Sep 27];10:79-81. Available from: https://www.aihbonline.com/text.asp?2020/10/2/79/284288




  Introduction Top


Thyrotoxic periodic paralysis is an endocrine disorder. It is one of the predominant causes of acquired periodic paralysis, in which episodes of weakness occur in association with low potassium. It is mainly seen in a person with thyrotoxicosis. TPP is most commonly seen in Asian males.[1] The pathogenesis of TPP is not fully understood, but Na-K-ATPase activity is raised in patients with both thyrotoxicosis and paralysis. Hyperthyroidism may result in increased adrenalin secretion and leads to activation of the Na+/K+-ATPase pump and results in cellular uptake of potassium.[2] The main precipitating factor is rest after vigorous physical activity, stress or diet containing high carbohydrates. Other precipitants of TPP include exposure to cold, concurrent infection, alcohol, intermittent corticosteroid therapy and menstruation.[3] In several cases, no noticeable precipitant features are recognised. The patient may present with weakness at any time of the day, but most of the cases present at night or early morning. TPP most commonly occurs in young individuals aged 20–40 years[4] as in our patient, who has transient, repeated episodes of muscle weakness with flaccid paralysis continued for hours. Proximal muscles are involved, sensitivity is intact and bone and tendon reflexes are decreased or absent. Features to consider differentials such as epidemiological background, family history and, especially, concurrent hyperthyroidism must, therefore, be searched. Many patients are primarily detected with paralysis, but unfortunately, delay in the diagnosis is frequent. Hence, all cases of acute weakness in young individuals should have high speculation for TPP. Rapid and specific treatment of thyrotoxicosis is necessary to prevent new attacks of muscle weakness.


  Case Report Top


A 22-year-old woman presented to the accident and emergency room with sudden-onset paralysis on October 23, 2019 (Hospital ID: 1000396971). The patient developed weakness of both lower limbs and unable to move her lower extremities after returning from work. She had no problem regarding respiration or swallowing. Her neck and facial muscle movements were regular. She denied any pain or tingling sensation. She had a history of heat intolerance, palpitation and weight loss. She gave no history of diarrhoea, fever, cough, chest pain and breathlessness. The patient was not on any medications and gave no history of taking alcohol or drugs or recent changes in diet or physical activity levels. She reported a history of similar type of attack 3 months back, which was resolved with potassium supplementation. The patient's family had no history of related episodes and no other significant illnesses.

On physical examination, the patient's heart rate was 112/min and blood pressure was 120/70 mmHg. Her appearance was healthy overall. Her skin was cold and dry, and the oral mucosa was moist. Jugular venous pressure was not elevated. There was no goitre, and lymphadenopathy was not found. The cardiac examination revealed tachycardia; the rhythm was regular and no murmurs. The study of the lungs and abdomen was insignificant. There were no deformities, no pedal edema detected and peripheral pulses were normal and similar bilaterally. The neurologic examination revealed flaccid paralysis of the lower limbs. The sensation was unaffected, but deep tendon reflexes were slightly reduced to 3 out of 4 in both lower limbs. There was no abnormality in cranial nerve function. Routine laboratory workup, liver enzymes and complete blood count were normal, and the potassium level was 3.5 (3.5–5 mmol/L). Electrocardiogram revealed sinus tachycardia with U-wave [Figure 1].
Figure 1: Initial electrocardiogram of the case showing sinus tachycardia with U-wave.

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Subsequently, the thyroid function test was done as guided by the history and clinical features. Thyroid-stimulating hormone was 0.01 μIU/L (normal, 0.55–4.78), FT4 was 2.58 ng/dl (normal, 0.70–1.48) and FT3 was 13.80 pg/ml (normal, 1.71–3.71). Tc-99m thyroid scan was done, which revealed goitre with the hyperthyroid state [Figure 2]. (Tc-99m uptake of radiotracer at 20 min is 6.0%, where the normal range is 0.3%–4.5%.) The treatment was started with propranolol 40 mg BID and carbimazole 20 mg/day and discharged on the 4th day with a confirmed diagnosis of TPP secondary to Graves' disease.
Figure 2: Tc-99m thyroid scan showing increased uptake.

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  Discussion Top


TPP is mostly seen in male Asian origin, including Chinese, Japanese, Vietnamese, Filipino and Koreans, and most of the cases of thyrotoxicosis associated with TPP are due to Graves' disease.[5] There are some precipitating factors such as diet containing high carbohydrates, vigorous exercise, stress and steroids. Most of the cases are of 20–40 years and do not have distinct features of hyperthyroidism. The presentation is usually characterised by repeated transient muscle weakness that varies from mild weakness to complete flaccid paralysis. Majority of the patients present in the emergency department in the evening or late night, for which TPP was initially described as nocturnal palsy or night palsy.[6] There is some possible mechanism for nocturnal preponderance for TPP. Plasma glucose and insulin rise higher in response to meals in the evening than in the morning in controls. The circadian rhythmicity of many hormones reaching their peak in the sleep also contributes to this.

The predominant defect in TPP is the intracellular entry of potassium with typical storage of potassium in the body.[7] Thyroid hormones cause entry of potassium into the cell by an increase in plasma membrane permeability to potassium by influencing the Na/K-ATPase activity.[8] It will create an upregulation in the β-adrenergic receptors in skeletal muscles, which causes a rise in the Na/K-ATPase activity.[7] These factors will transfer the potassium into the cell. There is also evidence of dilatation of the sarcoplasmic reticulum on electron microscopic section.[9]

TPP is mostly associated with HLA-DRw8 5 and A2BW22/AW19B17.[10] In familial periodic paralysis, the intracellular transfer of potassium is not dependent on Na/K-ATPase, and an increase in non-aldosterone mineralocorticoids is found. There is an excellent response to treatment with spironolactone.[11]

Most of the cases of hyperthyroidism associated with TPP are due to Graves's disease, although other conditions including thyroiditis, toxic multinodular goitre, toxic adenoma, TSH-secreting pituitary tumour, ingestion of T4 and inadvertent thyroid excess are also implicated.

Management

During periodic paralysis and marked hypokalaemia, immediate treatment with potassium chloride at a slow rate is warranted to prevent major cardiopulmonary fatality.[2] High-dose oral propranolol (3–4 mg/kg) alone has been reported to rapid resolution of the paralysis.[12] TPP does not occur when the patient becomes euthyroid, so adequate control of thyrotoxicosis is the primary concern of therapy. Carbimazole and propylthiouracil are the mainstays of treatment to control hyperthyroidism and symptoms. A cure for TPP may be considered when euthyroidism is maintained for at least 6 months. In our patient, the diagnosis of thyrotoxicosis was delayed due to the lack of any florid features of thyrotoxicosis. Thus, this case highlights the importance of suspecting thyrotoxicosis in cases of recurrent periodic flaccid paralysis, especially in Asian men to facilitate early diagnosis, and thyroid function test should form a routine part of the assessment of it.


  Conclusion Top


The condition may present as a severe attack, and unawareness with the syndrome could result in a grievous outcome. It can present with an atypical picture, and there is more chance to be missed at the initial stage. Therefore, a thyroid function test should be performed in all cases of periodic paralysis to confirm an early diagnosis of TPP and to start specific therapeutic intervention. Medication is given with the objective to achieve euthyroid level, as relapse of TPP usually stops with euthyroid condition. The success of therapeutic intervention of TPP case primarily dependent on patient's strict compliance with medication for his/her own health and better quality of life.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the way, the patient has given his consent for images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published, and outstanding efforts will be made to conceal the identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
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. 1
    
2.
Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc 2005;80:99-105.  Back to cited text no. 2
    
3.
Mellgren G, Bleskestad IH, Aanderud S, Bindoff L. Thyrotoxicosis and paraparesis in a young woman: Case report and review of the literature. Thyroid 2002;12:77-80.  Back to cited text no. 3
    
4.
Darrow M, Brammer WK, Rowley A. Thyrotoxic periodic paralysis: Two case studies. Arch Phys Med Rehabil 1995;76:685-7.  Back to cited text no. 4
    
5.
Vijayakumar A, Ashwath G, Thimmappa D. Thyrotoxic periodic paralysis: Clinical challenges. J Thyroid Res 2014;2014:649502.  Back to cited text no. 5
    
6.
Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge. J Clin Endocrinol Metabol 2006;91:2490-5.  Back to cited text no. 6
    
7.
Deitch S, Davis D. Hypokalemic thyrotoxic periodic paralysis. Am J Emerg Med 2001;19:85-6.  Back to cited text no. 7
    
8.
Kjeldsen K, Nørgaard A, Gøtzsche CO, Thomassen A, Clausen T. Effect of thyroid function on number of Na-K pumps in human skeletal muscle. Lancet 1984;2:8-10.  Back to cited text no. 8
    
9.
Pearson CM. The periodic paralyzes. Differential features and pathological observations in permanent myopathic weakness. Brain 1964;87:341-54.  Back to cited text no. 9
    
10.
Yeo PP, Chan SH, Lui KF, Wee GB, Lim P, Cheah JS. HLA and thyrotoxic periodic paralysis. Br Med J 1978;2:930.  Back to cited text no. 10
    
11.
Kodali VR, Jeffcote B, Clague RB. Thyrotoxic periodic paralysis: A case report and review of the literature. J Emerg Med 1999;17:43-5.  Back to cited text no. 11
    
12.
Lin SH, Lin YF. Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis. Am J Kidney Dis 2001;37:620-3.  Back to cited text no. 12
    


    Figures

  [Figure 1], [Figure 2]



 

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