Abstract #1038809: Hypokalemic Periodic Paralysis as Initial Presentation for Graves’ Disease

AbstractPeriodic paralysis associated with hyperthyroidism and hypokalemia is an uncommon disorder reported primarily in Asian males and rarely in children. We report three Hispanic adolescent males who were seen with Graves’ disease (GD) and THPP.The method used was chart review.Two of these boys presented with episodes of paralysis and were diagnosed with GD. The third was initially seen with hyperthyroidism and developed weakness and paralysis when his disease progressed because of therapeutic noncompliance. Hypokalemia was documented in two of the three patients with the third not seen during paralysis. Intravenous KTHPP is considered uncommon except in Asian males and rare in childhood and adolescence. Its occurrence in these three Hispanic boys suggests that it may occur more frequently in the young and in the USA than has been suspected, especially with the changing national demographics. We believe that our experience should raise the awareness of THPP among pediatric care providers.

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SAT-LB81 Carbohydrate Crash: A Rare Case of Thyrotoxic Periodic Paralysis

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.2253 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Rani Sittol ◽

Juliann Allen ◽

Jason Lofters ◽

Dan Ran-Castillo ◽

Karlene Williams

Keyword(s):

Lower Limb ◽

Periodic Paralysis ◽

Initial Presentation ◽

Western World ◽

Hypokalemic Periodic Paralysis ◽

Diagnostic Challenge ◽

The West ◽

Thyrotoxic Periodic Paralysis ◽

Hand Tremor ◽

Endocrine Society

Abstract IntroductionThyrotoxic Hypokalemic Periodic Paralysis (TPP) is an uncommon diagnosis in the western world and may be the initial presentation of hyperthyroidism. CaseA healthy 37 year old Asian male was visiting the US when he had sudden onset lower limb weakness after carbohydrate rich meal on Saturday night. He reported hand tremors for 1 month and a 10kg weight loss. On examination he was anxious with a fine hand tremor, BP 158/80mmHg, and HR 106bpm. He had grade 2/5 power to lower limb proximal muscles and brisk reflexes. Thyroid and eyes were normal. Laboratory results significant for potassium (K) 3.2mmol/l, TSH 0.005 (0.270-4.4uiu/ml), FT4 2.6 (0.8-2.2ng/dl), FT3 12.4 (2.77-5.27 pg/ml) and TSH Receptor antibody was 23.9% (<16%). Thoracolumbar MRI was normal. Repletion of K resulted in total resolution of paresis. He was given propranolol and methimazole and chose to complete workup in China.Clinical LessonTPP results in paralysis due to hypokalemia and hyperthyroidism and can be the initial presentation of hyperthyroidism. It is most common in Asian males 20-40 years with incidence 1.9%, but only 0.2% in the west. Proximal muscles are affected more. Attacks may be precipitated by carbohydrate load, rest after exercise, or stress. Patients tend to present on weekends between 2100-0900hrs. It is hypothesized that K metabolism is diurnal, with influx to muscle at night or at rest. Once euthyroid, TPP will not recur unlike familial hypokalemic periodic paralysis which is recurrent and of earlier onset. The underlying reason remains unclear. It may be related to the action of thyroxine on Na/K-ATPase pump. TPP is usually associated with Graves’ disease, but other causes of hyperthyroidism have been reported. TPP is a treatable rare illness in Asians, and very uncommon in the West. Physicians must be aware of its subtleties, as it may be confused with other more common conditions.ReferencesChang-Hsun Hsieh, Shi-Wen Kuo, Dee Pei, Yi-Jen Hung, Sandra Chyi-Fan, Ling-I Wu, Chih-Tsueng He, Tsao-Chin Yang, Wei-Cheng Lian, and Chien-Hsing Lee, Thyrotoxic periodic paralysis: an overview, Ann Saudi Med. 2004 Nov-Dec; 24(6): 418-422. doi:10.5144/0256-4947.2004.418Annie W. C. Kung, CLINICAL REVIEW: Thyrotoxic Periodic Paralysis: A Diagnostic Challenge, The Journal of Clinical Endocrinology and Metabolism 91(7):2490-2495, Copyright © 2006 by The Endocrine Society doi: 10.1210/jc.2006-0356

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SUN-518 Graves’ Disease Newly Diagnosed in the Setting of Hypokalemic Periodic Paralysis in an HIV+ Patient

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.812 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Emily V Nosova ◽

Emily Japp ◽

Sheldon T Brown ◽

Alan J Cohen ◽

Pietra D Greenberg

Keyword(s):

African American ◽

Case Report ◽

Thyroid Disease ◽

Sudden Onset ◽

Periodic Paralysis ◽

Graves Disease ◽

Thyroid Function Tests ◽

Hypokalemic Periodic Paralysis ◽

10Mg Daily ◽

First Case

Abstract Relevance: A rare yet distinct cause of sudden onset paralysis is severe hypokalemia associated with thyrotoxicosis. This is thought to be associated with mutations in genes encoding cellular potassium channels. We report a case of acute onset paralysis with profound hypokalemia and a new diagnosis of Graves’ thyrotoxicosis in a previously asymptomatic African American, HIV+ man on highly active antiretroviral therapy (HAART) for over 8 years. Clinical case: A 49-year-old man with hypertension and HIV presented with acute paralysis of his bilateral upper and lower extremities. His initial potassium was 1.8 mEq/L (3.5-5.0). Prior to sudden onset loss of motor strength, he denied any preceding palpitations, tremor, anxiety, diaphoresis, hyper-defecation, weight loss, heat or cold intolerance, neck pain, increase in neck girth or difficulty swallowing, proptosis or other ocular symptoms. He has no family history of thyroid disease. He had an enlarged palpable thyroid without nodules and no audible bruit. There was no periorbital edema or proptosis, and no signs of dermopathy. A thyroid ultrasound showed a hyperemic and diffusely enlarged thyroid gland without nodules. Labs included a TSH of 0.007 mCU/mL (0.43-3.8), Free T4 2.1 ng/dL (0.71-1.85), Total T3 229.6 ng/dL (58-194), and thyrotropin receptor antibody 2.6 IU/L (0-1.75). The CD4+ count was 146 in 2010 with a slow gradual rise to 673 in 2019, and HIV viral load was undetectable. There were no offending medications or supplements identified. With aggressive potassium repletion, the serum potassium improved to 4.6 mEq/L and he regained normal strength within several hours. He was started on Methimazole 10mg daily and propranolol 10mg TID. At one month, the thyroid function tests normalized. Methimazole 10mg daily was continued and propranolol was tapered off. He remains euthyroid. Genetic testing is pending. Conclusions: Graves’ disease is the most common thyroid disease triggered by immune reconstitution in HIV + individuals on HAART. The incidence of thyroid disease in HIV patients on HAART is higher in women and Africans with a 1.5-2 fold increase compared with the general population [Muller et. al, Eur Thyroid J 2019;8:173-185]. Despite a higher incidence of hyperthyroidism in women, over 95% of cases of hypokalemic periodic paralysis have been reported in men, with a 10-fold higher incidence among Asians compared to Westerners. There has been one prior case report of Thyrotoxic Periodic Paralysis in an HIV + patient and this was in a Polynesian male (Brown JD et al. Hawaii Med J 2007). To our knowledge, this is the first case report of an African American HIV+ patient with this disorder. An association with mutations in the Kir2.6 gene (encodes a potassium channel, is expressed in skeletal muscle, and is transcriptionally regulated by thyroid hormone) has been proposed [Ryan et. al, Cell 2010 January 8; 140(1):88-98].

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