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Thyrotoxic Periodic Paralysis with Sensory Deficits in Young African American Male: A Case Report and Literature Review

Irsa Munir MD, Talha Mehmood MD, Kaiser Islam, Lina Soni, Samy I. McFarlane*

Department of Internal Medicine, State University of New York, Downstate Medical Center, Brooklyn, N.Y, U.S.A-11203

Abstract: Thyrotoxic periodic paralysis is a sporadic entity characterized by hypokalemia and paralysis in the setting of hyperthyroidism. TPP is most commonly described in young Asian males. Studies have shown an association with mutations affecting inward rectifying potassium channels. The pathophysiology involves Na⁺-K⁺- ATPase channel causing an increased intracellular shift of potassium ions in the hyperthyroid state and in the presence of another precipitating condition. Most cases of thyrotoxic periodic paralysis are defined in young Asian males of 20-40 years of age, here we present an interesting case of thyrotoxic periodic paralysis in 32-year-old African American male, who presented with sudden onset weakness in the bilateral lower extremity and left upper extremity. Interestingly, the patient also has sensory deficits, a feature not known to be associated with thyrotoxic periodic paralysis.

Keywords: thyrotoxic periodic paralysis, hypokalemia, african american

Received March 03, 2019; Revised April 09, 2019; Accepted June 26, 2019

Citation: Irsa Munir MD, Talha Mehmood MD, Kaiser Islam, Lina Soni, Samy I. McFarlane, Thyrotoxic Periodic Paralysis with Sensory Deficits in Young African American Male: A Case Report and Literature Review. American Journal of Medical Case Reports, 7 (7). 138-142. January 2019. doi:10.12691/ajmcr-7-7-5

1. Introduction

Thyrotoxic periodic paralysis is a sporadic entity that only occurs in association with thyrotoxicosis. It is different from hypokalemic periodic paralysis that has an autosomal dominant pattern of inheritance (one of the sub-types of familial periodic paralysis). The pathophysiology always involves increased ionic transport via Na K ATPase channel activity [1,2]. Certain ion channels defects are found to be associated with TPP. In one study, 10 out of 30 Caucasians or Brazilian patients with TPP had a mutation in gene encoding KCNJ18 (kir2.6), an inward rectifying potassium channel expressed in skeletal muscle [2,3]. Similar mutations have been found in another study in the patient population from Singapore with TPP [3]. Another novel gene is identified in population from Taiwan negatively regulating KCNJ2 (Kir2.1) expression [4]. All these channelopathies along with increased Na K ATPase activity have been shown to cause a positive feed-forward cycle of hypokalemia in the presence of hyperthyroid state and an additional precipitant accentuating the ion transport [1,2,5,6,7,8,9]. While most cases of TPP are described in young Asian males [1,2,5,8], in this report we present a very interesting case of TPP in a young 32-year-old African American male.

2. Case Presentation

A 32-Year-old male with no significant past medical history presented to the emergency department with complaints of sudden onset bilateral lower extremity weakness as well as weakness in the left upper extremity. Along with the motor weakness patient also had sensory deficits in right upper extremity with dysarthria and aphasia. On presentation, the patient was afebrile, tachycardic to 110 BPM, blood pressure was in 120/80 mmHg and respiratory rate was 14 Breaths/minute. Stroke code was initiated, and the patient was evaluated by neurology. Physical exam was unremarkable except for neurological exam which was significant for 1/5 strength in bilateral lower extremities, 2/5 strength in left upper extremity and sensory deficits in right upper extremity with complete loss of fine sensations. Further history taking revealed that the patient was drinking fifteen beers the night before. On review of systems, the patient reported having lost weight in the last year with periodic palpitations, episodes of diarrhea, sweating, insomnia and appetite changes. Patient denies any history of similar symptoms in the past. No recent history of infections, tick bites, vaccines, sick contact or travel.

Initial labs were significant for potassium of 2.5 mmol/L (3.5-5.0) on the comprehensive metabolic panel and venous blood gas shock panel with a potassium of 2.1 mmol/L and a pH of 7.326. His thyroid stimulating hormone (TSH) was <0.005 mIU/L (0.27-4.20) with a free Thyroxine of 3.94 ng/dl (0.7-1.9). Rest of the laboratory workup was found to be unremarkable. Endocrinology was consulted, and his constellation of symptoms was attributed to thyrotoxic periodic paralysis likely precipitated by heavy drinking the day before. Thyroid stimulating immunoglobulin and thyroid peroxidase antibody were sent which were subsequently found to be 18.20 IU/L (<1.3) and 1935 IU/ml (<35) respectively. CT scan head and CTA head and neck showed no evidence of acute pathology. The patient was given 40 mEq IV potassium along with 40 mEq oral potassium and his symptoms resolved. The patient was started on methimazole 20 mg twice a day and propranolol 20 mg three times a day. Serial basic metabolic panels were done to monitor rebound hyperkalemia in the setting of beta-blockade from propranolol. The patient was admitted to telemetry monitoring and potassium was monitored over the next 24 hours. The patient was discharged the next day with follow up appointments to the endocrine clinic. The patient was also counseled extensively on alcohol abstinence.

3. Initial Labs

Table 1. Complete Blood Count

Table 2. Basic Metabolic panel

4. Imaging

Figure 1: Head CT scan:

Figure 1. CT scan of the head showed no acute infarction, masses or hemorrhage. No acute intracranial abnormality is identified

Figure 2: CTA Head and Neck:

Figure 2. CTA HEAD: No large vessel occlusion, central high-grade stenosis, aneurysm, or vascular malformation. 2. There are dental caries including in the left first maxillary premolar with a periapical dentigerous cyst. CTA neck:1. No significant atherosclerotic disease of the carotid bifurcation/proximal ICA. No hemodynamically significant stenosis, according to NASCET criteria. 2. No evidence of dissection, pseudoaneurysm, or vascular malformation. Carotid Stenosis Reference Using NASCET Criteria Mild: <50% stenosis Moderate: 50-69% stenosis Severe: 70-94% stenosis Near occlusion: 95-99% stenosis Occluded: 100% stenosis

Figure 3. EKG showed sinus tachycardia with HR of 109 BPM and QTc of 431ms with no appreciable T wave changes

5. Case Discussion and Literature Review

TPP is a rare presenting feature of the thyrotoxic state. The pathophysiology involves up-regulation of Na-K ATPase leading to an increased intracellular shift of potassium ions in hyperthyroid state and most often in the presence of another precipitant [1,2,5,6,7,8,9]. At the same time, efflux of potassium ions cannot take place because of decreased outward Kir current as explained by certain mutations [2,3,4,9,13,14]. Hyperthyroidism also leads to increased adrenergic drive leading to up-regulation of Na-K ATPase [1,9]. Any precipitant that leads to increased catecholamine surge or hyperinsulinemia ultimately cause increase Na-K ATPase pump activity expressed on skeletal muscles, liver, and kidneys due to increasing B2 adrenergic receptor activity [1,10,11,12]. Increased B2 activity causes an increase in cyclic adenosine monophosphate that further leads to increase protein kinase A. Increase protein kinase A is responsible for phosphorylation thus increasing pump affinity for intracellular Na. At the same time, insulin and catecholamine inhibit inward rectifier potassium channels in skeletal muscles which are normally responsible for efflux of potassium [13,14]. Many mutations responsible for Periodic Paralysis are described in association with inward rectifier channels which explains why an additional mechanism to prevent efflux of potassium is also needed to produce the effect [2,3,4,9,13,14]. The activity of Na-K ATPase alone cannot define the pathophysiology.

Table 3. Demographics, laboratory values for TPP patients based on our literature review of 15 case reports

In the above-mentioned case, increased alcohol intake likely led to increased catecholamine secretion causing an intracellular shift of potassium [1,2,15]. Also, excessive alcohol intake results in hyperinsulinemia which along with hyperthyroidism and hyperadrenergic state leads to low serum potassium [1,10,11,12,13,14,16,18]. Hypokalemia leads to hyperpolarization of skeletal muscles groups thus making them non-responsive to neuronal impulses leading to loss of contractility.

Almost all cases of TPP are associated with muscle weakness, with the proximal muscle groups being affected more than the distal muscle groups. In the above-mentioned case, the patient also presented with sensory deficits, not typically linked with TPP. The complete resolution of symptoms with potassium supplementation and anti-thyroid regimen supports the diagnosis of thyrotoxic periodic paralysis in our reported case.

Acknowledgements

This work is supported, in part, by the efforts of Dr. Moro O. Salifu M.D., M.P.H., M.B.A., M.A.C.P., Professor and Chairman of Medicine through NIH Grant number S21MD012474.

References

[1]   | Tella, Sri Harsha, and Anuhya Kommalapati. “Thyrotoxic periodic paralysis: an underdiagnosed and under-recognized condition.” Cureus 7.10 (2015).
[2]   | Vijayakumar, Abhishek, Giridhar Ashwath, and Durganna Thimmappa. “Thyrotoxic periodic paralysis: clinical challenges.” Journal of thyroid research 2014 (2014).
[3]   | Ryan, Devon P., et al. “Mutations in potassium channel Kir2. 6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis.” Cell 140.1 (2010): 88-98.
[4]   | Song, I-Wen, et al. “Novel susceptibility gene for nonfamilial hypokalemic periodic paralysis.” Neurology 86.13 (2016): 1190-1198.
[5]   | Kung, Annie WC. “Thyrotoxic periodic paralysis: a diagnostic challenge.” The Journal of Clinical Endocrinology & Metabolism 91.7 (2006): 2490-2495.
[6]   | McFadzean, A. J., and Rose Yeung. “Periodic paralysis complicating thyrotoxicosis in Chinese.” British Medical Journal 1.5538 (1967): 451.
[7]   | Finsterer, J. “Primary periodic paralyses.” Acta Neurologica Scandinavica 117.3 (2008): 145-158.
[8]   | Hagel, Stefan, et al. “Chest pain and paralysis after pulse prednisolone therapy an unusual case presentation of thyrotoxic periodic paralysis: a case report.” Cases journal 2.1 (2009): 7501.
[9]   | Lin, Shih-Hua, and Chou-Long Huang. “Mechanism of thyrotoxic periodic paralysis.” Journal of the American Society of Nephrology (2012): ASN-2012010046.
[10]   | Manoukian, Mariam Avakian, Julie A. Foote, and Lawrence M. Crapo. “Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes.” Archives of Internal Medicine 159.6 (1999): 601-606.
[11]   | Lee, Kok Onn, et al. “Hyperinsulinaemia in thyrotoxic hypokalaemic periodic paralysis.” The Lancet 337.8749 (1991): 1063-1064.
[12]   | Chan, A., et al. “Hyperinsulinaemia and Na+, K+-ATPase activity in thyrotoxic periodic paralysis.” Clinical endocrinology. 41.2 (1994): 213-216.
[13]   | Ruff, Robert L. “Insulin acts in hypokalemic periodic paralysis by reducing inward rectifier K current.” Neurology 53.7 (1999): 1556-1556.
[14]   | Puwanant, Araya, and Robert L. Ruff. “INa and IKir are reduced in Type 1 hypokalemic and thyrotoxic periodic paralysis.” Muscle & nerve 42.3 (2010): 315-327.
[15]   | Ireland, M. A., et al. “Acute effects of moderate alcohol consumption on blood pressure and plasma catecholamines.” Clinical science (London, England: 1979) 66.6 (1984): 643-648.
[16]   | Kim, Soo-Jeong, and Dai-Jin Kim. “Alcoholism and diabetes mellitus.” Diabetes & metabolism journal 36.2 (2012): 108-115.
[17]   | Lulsegged, Abbi, Christina Wlodek, and Michela Rossi. “Thyrotoxic periodic paralysis: case reports and an up-to-date review of the literature.” Case reports in endocrinology 2011 (2011).
[18]   | Belayneh, Dereje K., and Thomas Kellerth. “Thyrotoxic hypokalemic periodic paralysis in an African male: a case report.” Clinical case reports 3.2 (2015): 102-105.
[19]   | Naqi, Muniba, et al. “A 20-year-old Chinese man with recurrent hypokalemic periodic paralysis and delayed diagnosis.” BMJ case reports 2012 (2012): bcr0120125541.
[20]   | Zumo, Lawrence A., Christian Terzian, and Timothy Brannan. “Thyrotoxic hypokalemic periodic paralysis in a Hispanic male.” Journal of the National Medical Association 94.5 (2002): 383.
[21]   | Oh, Sang Bo, et al. “Thyrotoxic periodic paralysis associated with transient thyrotoxicosis due to painless thyroiditis.” Journal of Korean medical science 27.7 (2012): 822-826.
[22]   | Thethi, Tina K., et al. “Case of thyrotoxic periodic paralysis in a caucasian male and review of literature.” Case reports in medicine 2014 (2014).
[23]   | Barahona, M. J., et al. “Thyrotoxic periodic paralysis: a case report and literature review.” Clinical medicine & research. (2009): cmr-2009.
[24]   | Lam, Lien, Rajasree J. Nair, and Leslie Tingle. “Thyrotoxic periodic paralysis.” Baylor University Medical Center Proceedings. Vol. 19. No. 2. Taylor & Francis, 2006.
[25]   | Meseeha, Marcelle, et al. “Thyrotoxic periodic paralysis: a case study and review of the literature.” Journal of community hospital internal medicine perspectives 7.2 (2017): 103-106.
[26]   | Hegde, Swati, Mohammed Aslam Shaikh, and Thejaswi Gummadi. “Hypokalaemic periodic paralysis in a patient with subclinical hyperthyroidism: a rare case.” Journal of clinical and diagnostic research: JCDR 10.1 (2016): OD14.
[27]   | Hakami, Osamah, Maswood M. Ahmad, and Naji Al Johani. “A Case of Nonfatal Ventricular Arrhythmia Due to Thyrotoxic Periodic Paralysis in a Saudi Patient as an Initial Presentation of Graves’ Disease.” Clinical Medicine Insights: Case Reports9 (2016): CCRep-S34560.
[28]   | Sehmer, Benjamin, and Terra Arnason. “Pop-provoked paralysis: silent Graves’ disease presenting as thyrotoxic periodic paralysis.” BMJ case reports 2012 (2012): bcr2012006292.
[29]   | Jung, Se Yong, et al. “A case of thyrotoxic periodic paralysis as initial manifestation of Graves' disease in a 16-year-old Korean adolescent.” Annals of pediatric endocrinology & metabolism 19.3 (2014): 169.