scholarly journals Hypokalemic Periodic Paralysis Precipitated by Thyrotoxicosis and Renal Tubular Acidosis

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Ian Jackson ◽  
Yazan Addasi ◽  
Moeed Ahmed ◽  
Bashar Ramadan ◽  
Karson Kalian ◽  
...  

Background. Hypokalemic periodic paralysis is a rare neuromuscular disorder characterized by transient episodes of flaccid paralysis due to a defect in muscle ion channels. Most cases are hereditary, but it can be acquired. We present a case of acquired hypokalemic periodic paralysis associated with hyperthyroidism and renal tubular acidosis. Clinical Case. A 38-year-old female with a history of Graves’ disease presented to the emergency department with generalized weakness and associated nausea, vomiting, and weight loss. Examination was significant for diffuse weakness in all extremities. Labs showed hypokalemia, hyperthyroidism, and nonanion gap metabolic acidosis with a positive urine anion gap. She was treated for hypokalemic periodic paralysis and renal tubular acidosis. Potassium replacement, propranolol, methimazole, and sodium bicarbonate were initiated. Her potassium gradually corrected with resolution of her symptoms. Further investigation revealed a history of dry eyes, dry mouth, and recurrent dental carries. She had positive ANA, SS-A, and SS-B antibodies. She was diagnosed with Sjögren’s syndrome, which may have been associated with her Graves’ disease and thus contributed to both her RTA and hyperthyroidism. Conclusion. Early recognition and treatment of thyrotoxic periodic paralysis are important to prevent cardiac complications. Management includes potassium replacement with careful monitoring to prevent rebound hyperkalemia. The definitive treatment is to achieve euthyroid status.

2010 ◽  
Vol 57 (4) ◽  
pp. 347-350 ◽  
Author(s):  
Eun Joo IM ◽  
Jung Min LEE ◽  
Ji Hyun KIM ◽  
Sang Ah CHANG ◽  
Sung Dae MOON ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jilcy Joy Mathew ◽  
Ariana R Pichardo-Lowden

Abstract Background: Hypokalemic periodic paralysis (HPP) related to thyrotoxicosis, though rare, is more often seen in Asian males. Type 1 renal tubular acidosis (T1 RTA), which can also cause HPP, is typically managed with alkali therapy and potassium supplementation, though there are no well-established guidelines for management in pregnancy. Clinical Case: A 27-year-old Puerto Rican woman, at 32 weeks gestation, presented to the hospital with sudden onset muscle weakness, and was found to have 1/5 muscle strength in her lower extremities. She had no personal or family history of similar illness. Laboratory analysis revealed hypokalemia (potassium 2.0 mmol/L, range: 3.5 – 5); non-gap metabolic acidosis (sodium 137mmol/L, range 136 – 145; chloride 113 mmol/L, range 98- 107; and bicarbonate 8 mmol/L, range 22 – 29); and an arterial pH of 7.09. Urine studies demonstrated a urine pH of 6.5 and a urine sodium of 32 mmol/L which was diagnostic of T1 RTA in the context of her metabolic derangements. She was treated emergently with potassium and bicarbonate infusions, with improvement in her symptoms. Subsequent thyroid function testing revealed: a low TSH of 0.01 uIU/ml, normal free T4 of 1.66 (range: 0.9 - 1.7) ng/dl, normal free of T3 3.7 (range: 2.0 -4.4) pg/ml and elevated total T4 of 16.5 (range: 4.5 - 11.7) ug/dl. Renal ultrasound demonstrated medullary nephrocalcinosis. She was discharged on potassium and sodium citrate tablets. At 37 weeks, the patient was readmitted for induction of labor due to pre-eclampsia, and delivered a healthy male baby. Several months later, she presented to the Endocrinology clinic with symptoms of increased frequency bowel movements, palpitations and heat intolerance, which had been ongoing since pregnancy. On review, a metabolic panel prior to pregnancy had demonstrated non-gap acidosis and mild hypokalemia. Further testing demonstrated the following: TSH < 0.01 uIU/ml, Free T4 1.71 ng/dl, Free T3 4.8 pg/ml, TSI 280%, and a thyroid uptake scan with homogenous radiotracer uptake, with a 24-hour uptake of 40%. She was started on methimazole therapy, and continued on potassium and sodium citrate tablets with clinical and biochemical improvement. Conclusion: Thyrotoxicosis can augment hypokalemia in T1 RTA, and can increase the risk of HPP. Our patient had biochemical evidence of RTA prior to pregnancy, though without episodes of HPP, and we believe that her hyperthyroidism, triggered by pregnancy, may have been the additional insult that precipitated her paralysis. This is the first reported case of HPP related to co-existing thyrotoxicosis and T1 RTA in a pregnant individual. Reference:1. Tu ML, Fang YW, Leu JG, Tsai MH. An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report. BMC Nephrol. 2018;19(1):160. Published 2018 Jul 4. doi:10.1186/s12882-018-0971-9


F1000Research ◽  
2019 ◽  
Vol 7 ◽  
pp. 1154
Author(s):  
E. Dante Meregildo-Rodríguez ◽  
Virgilio E. Failoc-Rojas

Background: Hypokalemic periodic paralysis (HypoKPP) is characterized by transient episodes of flaccid muscle weakness. We describe the case of a teenaged boy with HypoKPP and hyperthyroidism due to Hashimoto's thyroiditis with initial manifestation of renal tubular acidosis. This combination is rare and little described previously in men. Case presentation: A 17-year-old boy was admitted after three days of muscular weakness and paresthesia in the lower limbs with an ascending evolution, leading to prostration. Decreased strength was found in the lower limbs without a defined sensory level, reduced patellar and ankle reflexes. Positive antithyroid antibodies were found. He received hydration treatment, IV potassium and levothyroxine, with which there was a clinical improvement. Other examinations led to the diagnosis of type 1 renal tubular acidosis. Conclusion: HypoKPP is a rare disorder characterized by acute episodes of muscle weakness. Type 1 renal tubular acidosis can occur as a consequence of thyroiditis, which is explained by the loss of potassium. This combination is unusually rare, and has not been described before in men. The etiopathogenesis of the disease as well as a dynamic explanation of what happened with the patient are discussed in this report.


CHEST Journal ◽  
2020 ◽  
Vol 158 (4) ◽  
pp. A720
Author(s):  
Ali Nayfeh ◽  
Noor Addasi ◽  
Karson Kalian ◽  
Bryan Krajicek

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A966-A967
Author(s):  
Bishow Chandra Shrestha ◽  
Chheki Sherpa ◽  
Swarup sharma Rijal ◽  
Vasudev Magaji ◽  
Vinita Singh

Abstract Background: Thyrotoxic periodic paralysis (TPP) is a rare but serious thyroid emergency characterized by hypokalemia, acute onset flaccid paralysis & thyrotoxicosis. Typically, seen in an Asian male with untreated hyperthyroidism symptoms, who awakens at night or in the early morning with flaccid ascending paralysis. This is precipitated by exercise, alcohol or carbohydrate rich meal. TPP is widely reported & studied in Asian population. Its prevalence is about 2 % in Asian hyperthyroid patients. However, incidence is 0.1-0.2% in non-Asian hyperthyroid patients. Clinical Case: 33-year-old Caucasian male with celiac disease and no thyroid disease sought emergency care for complaints of sudden onset severe weakness in all extremities. He reported 20-pound unintentional weight loss, intermittent palpitations and low-grade fever. He noticed leg cramps with numbness and unable to move his extremities. At initial evaluation, he had acute flaccid paralysis and tachycardia. Initial laboratory studies showed potassium at 1.9 mmol/l, Magnesium at 1.8, suppressed TSH <0.005 uIU/ml with elevations in free T4 at 2.43 ng/dl and total T3 at 1.9 ng/ml. CT and MRI head were normal. Patient’s aldosterone level was normal. The patient’s paralysis and hypokalemia resolved after potassium replacement. Thyroid stimulating immunoglobulin was elevated and increased vascularity suggestive of Grave’s disease noted on thyroid Ultrasound. Methimazole and propranolol were initiated. His neurological workup was negative. After resolution of paralysis and hypokalemia he was discharged home. Since our patient presented with severe hypokalemia, flaccid paralysis and hyperthyroidism, that resolved promptly with potassium replacement, hence likely diagnosis of thyrotoxic periodic paralysis. Discussion: Thyrotoxic periodic paralysis is potentially reversible and mostly seen with Graves’ disease among Asian population. Early diagnosis & treatment prevents life threatening complications. Differential diagnosis of TPP includes familial periodic paralysis, Guillain-Barre Syndrome & acute intermittent porphyria. Diagnosis is based on family history, characteristic presentation, hyperthyroidism with low serum potassium level. Possible mechanism is increased sodium-potassium ATPase activity in the skeletal muscle membrane leading to intracellular shift of potassium causing hypokalemia and muscle inexcitability. Treatment includes potassium replacement, nonselective beta-blocker and definitive treatment of hyperthyroidism, to prevent further episodes.


F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1154 ◽  
Author(s):  
E. Dante Meregildo-Rodríguez ◽  
Virgilio E. Failoc-Rojas

Background: Hypokalemic periodic paralysis (HypoKPP) is characterized by transient episodes of flaccid muscle weakness. We describe the case of a teenaged boy with HypoKPP and hyperthyroidism due to Hashimoto's thyroiditis with initial manifestation of renal tubular acidosis. This combination is rare and little described previously in men. Case presentation: A 17-year-old boy was admitted after three days of muscular weakness and paresthesia in the lower limbs with an ascending evolution, leading to prostration. Decreased strength was found in the lower limbs without a defined sensory level, reduced patellar and ankle reflexes. Positive antithyroid antibodies were found. He received hydration treatment, IV potassium and levothyroxine, with which there was a clinical improvement. Other examinations led to the diagnosis of type 1 renal tubular acidosis. Conclusion: HypoKPP is a rare disorder characterized by acute episodes of muscle weakness. Type 1 renal tubular acidosis can occur as a consequence of thyroiditis, which is explained by the loss of potassium. This combination is unusually rare, and has not been described before in men. The etiopathogenesis of the disease as well as a dynamic explanation of what happened with the patient are discussed in this report.


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