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   Abstract
  Introduction
  Case Report
  Discussion
  Conclusion
   References
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  Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 25  |  Issue : 2  |  Page : 103-105
 

Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome


1 Department of Internal Medicine, Division of Endocrinology and Metabolism, Faculty of Medicine, Selcuk University, Konya, Turkey
2 Department of Medical Genetics, Faculty of Medicine, Selcuk University, Konya, Turkey
3 Department of Internal Medicine, Faculty of Medicine, Selcuk University, Konya, Turkey

Date of Web Publication16-Jul-2014

Correspondence Address:
Dr. S Baldane
Department of Internal Medicine, Division of Endocrinology and Metabolism, Faculty of Medicine, Selcuk University, Postal code: 42075, Konya
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-4065.140719

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  Abstract 

A 35-year-old male patient was admitted with fatigue and muscle weakness. He had been on methimazole due to thyrotoxicosis for 2 weeks. Laboratory tests showed overt hyperthyroidism and hypokalemia. Potassium replacement was started with an initial diagnosis of thyrotoxic hypokalemic periodic paralysis. Later on, despite the euthyroid condition and potassium chloride treatment, hypokalemia persisted. Further investigations revealed hyperreninemic hyperaldosteronism. The patient was considered to have Gitelman's syndrome (GS) and all genetic analysis was done. A c. 1145C>T, p.Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3, exon 9 was detected and GS was confirmed.


Keywords: Gitelman′s syndrome, hypokalemic paralysis, thyrotoxicosis


How to cite this article:
Baldane S, Ipekci S H, Celik S, Gundogdu A, Kebapcilar L. Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome. Indian J Nephrol 2015;25:103-5

How to cite this URL:
Baldane S, Ipekci S H, Celik S, Gundogdu A, Kebapcilar L. Hypokalemic paralysis due to thyrotoxicosis accompanied by Gitelman's syndrome. Indian J Nephrol [serial online] 2015 [cited 2019 Feb 19];25:103-5. Available from: http://www.indianjnephrol.org/text.asp?2015/25/2/103/140719



  Introduction Top


Hypokalemic paralysis is a rare metabolic myopathy consisting of hypokalemia and acute systemic muscle weakness. The most common cause of hypokalemic paralysis is primary or familial hypokalemic periodic paralysis. However, sporadic cases could be secondary to thyrotoxicosis, renal tubular acidosis, primary hyperaldosteronism, Gitelman's syndrome (GS), barium intoxication or diarrhea. [1]

We have identified, for the first time in an adult, a case of hypokalemic paralysis associated with thyrotoxicosis and accompanied by GS. The aim of this report is to emphasize that hypokalemic paralysis could present with combined etiologies.


  Case Report Top


A 35-year-old male patient was admitted to another hospital with complaints of weakness, fatigue and sweating. Laboratory tests revealed overt hyperthyroidism [Table 1]. Thyroid Doppler ultrasonography documented increased perfusion of the thyroid gland. Therefore, methimazole (20 mg/day) treatment was started.
Table 1: Laboratory findings of the patient


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On the 15 th day of treatment, the patient presented to our clinic with extreme fatigue and difficulty in moving his limbs. Physical examination revealed body temperature of 37.2°C, heart rate of 88 beats/min, blood pressure of 120/80 mmHg and respiratory rate of 20/min. Upon neurological examination, a bilateral motor deficit of 2/5 in the upper extremities and 3/5 in the lower extremities was detected. There were no pathological reflexes, and sensory tests were normal. The patient's laboratory examinations revealed ongoing overt hyperthyroidism and hypokalemia, with high levels of anti-thyroperoxidase, anti-thyroglobulin, anti-thyroid stimulating hormone and thyroid receptor antibody (TRAb) [Table 1]. Intravenous potassium chloride (KCl) treatment increased the plasma potassium level to 3.8 mEq/L, and the patient's complaints subsided. He was prescribed oral KCl (2,400 mg/day) with a diagnosis of thyrotoxic hypokalemic periodic paralysis (THPP).

During follow-up, oral KCl was continued. During the 4 th month of anti-thyroid treatment, euthyroid state was acheieved and the TRAb level was normalized; however, serum potassium levels were below 4 mEq/L. Investigations were performed to reveal the etiology of the hypokalemia, and metabolic alkalosis, hypokalemia, hypomagnesemia, hypocalciuria, and elevated renin and aldosterone levels were recorded [Table 1]. In the patient's past medical history, there was no evidence for drug use, including diuretics and laxatives. Due to the above findings, GS was considered. Molecular genetic analysis revealed a c. 1145C>T, p.Thr382Met homozygote missense mutation located on solute carrier family 12, member gene 3 (SLC12A3), exon 9. With the confirmed diagnosis of GS, spironolactone (50 mg/day) and magnesium oxide (250 mg/day) were added to the methimazole and oral potassium treatment.

Renal biopsy was recommended for proteinuria and a screening genetic analysis was proposed for the family members at risk, but they did not accept it.


  Discussion Top


Upon admission to our clinic, the patient was on methimazole treatment initiated previously due to thyrotoxicosis and he had overt hyperthyroidism and hypokalemia; therefore, THPP was considered the cause of the hypokalemic paralysis. However, during clinical follow-up, despite euthyroid status and potassium replacement, the hypokalemic condition persisted. GS was considered an accompanying condition requiring further examination, which revealed metabolic alkalosis, hypomagnesemia, hypocalciuria, and elevated renin and aldosterone levels. SLC12A3 gene analysis revealed the homozygote mutation, and the GS diagnosis was confirmed.

Thyrotoxic hypokalemic periodic paralysis is a disease characterized by recurrent episodic muscle weakness in the presence of hypokalemia and thyrotoxicosis. It occurs predominantly in males of Asian descent. [2] The thyrotoxic condition causes an ion channel defect leading to a rapid potassium shift to the intracellular space. In sporadic cases, Na + /K + -adenosine triphosphatase channel activation is responsible for this rapid shift, but in familial cases, the responsibility belongs to KCNE3 (voltage-gated potassium channel) gene mutation. [2] In this case, the THPP gene was not analyzed because the past family medical history did not reveal any thyroid disease.

Gitelman's syndrome is an autosomal recessive disorder characterized by hypokalemic metabolic alkalosis with hypocalciuria, hypomagnesemia and hyperreninemic hyperaldosteronism, observed in young adults. [3] GS was caused by mutation of the SLC12A3 gene encoding the thiazide-sensitive sodium chloride (Na + /Cl - ) co-transporter system in distal tubules. [3] To date, more than 170 mutations throughout the SLC12A3 gene in patients with GS have been identified. [4] The observed homozygous missense mutation in our case has been reported previously in patients with GS. [4],[5],[6]

Although in our case two simultaneous pathological mechanisms triggered hypokalemia, the patient's condition was not worse than expected with a single pathological condition. Clinical findings did not provide clues for a pathological condition other than thyrotoxicosis. In the medical literature, there is only one report describing hypokalemic paralysis, in a 16-year-old Japanese male patient, due to thyrotoxicosis accompanied by GS, [7] which differs from our case in the type of mutation. In our case, there was an SLC12A3 gene codon 382 (T382M) ACG > ATG homozygote mutation, while the Japanese case had an SLC12A3 gene 858 (L858H) CTC > CAC mutation.


  Conclusion Top


Patients with hypokalemic paralysis, investigations for etiology should be carried out and it is worthwhile to consider additional pathologies causing the hypokalemia, although thyrotoxicosis is in the foreground.

 
  References Top

1.
Lin SH, Lin YF, Halperin ML. Hypokalaemia and paralysis. QJM 2001;94:133-9.  Back to cited text no. 1
    
2.
Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge. J Clin Endocrinol Metab 2006;91:2490-5.  Back to cited text no. 2
    
3.
Knoers NV, de Jong JC, Meij IC, Van Den Heuvel LP, Bindels RJ. Genetic renal disorders with hypomagnesemia and hypocalciuria. J Nephrol 2003;16:293-6.  Back to cited text no. 3
    
4.
Vargas-Poussou R, Dahan K, Kahila D, Venisse A, Riveira-Munoz E, Debaix H, et al Spectrum of mutations in Gitelman syndrome. J Am Soc Nephrol 2011;22:693-703.  Back to cited text no. 4
    
5.
Balavoine AS, Bataille P, Vanhille P, Azar R, Noël C, Asseman P, et al. Phenotype-genotype correlation and follow-up in adult patients with hypokalaemia of renal origin suggesting Gitelman syndrome. Eur J Endocrinol 2011;165:665-73.  Back to cited text no. 5
    
6.
Berry MR, Robinson C, Karet Frankl FE. Unexpected clinical sequelae of Gitelman syndrome: Hypertension in adulthood is common and females have higher potassium requirements. Nephrol Dial Transplant 2013;28:1533-42.  Back to cited text no. 6
    
7.
Imashuku S, Teramura-Ikeda T, Kudo N, Kaneda S, Tajima T. Concurrence of thyrotoxicosis and Gitelman's syndrome-associated hypokalemia-induced periodic paralysis. Pediatr Rep 2012;4:e18.  Back to cited text no. 7
    



 
 
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