• Annals of Clinical Neurophysiology
• /
• v.17 no.2
• /
• pp.98-100
• /
• 2015

• Annals of Clinical Neurophysiology
• /
• v.10 no.2
• /
• pp.119-122
• /
• 2008

Thyrotoxic periodic paralysis (PP) is the most common acquired form of PP in Asian populations, and its cardinal and biochemical abnormality is hypokalemia. We describe a 39-year-old man who had acute bilateral limb motor weakness and paresthesia, and showed normokalemia during attack. Thyroid studies showed subclinical thyrotoxic Goiter. Control of the hyperthyroidism nearly eliminated his PP. Regardless of normokalemia, our patient might be a case of hypokalemic PP because of improvement from anti-thyroid medication.

• Clinical and Experimental Pediatrics
• /
• v.51 no.7
• /
• pp.771-774
• /
• 2008

Familial hypokalemic periodic paralysis (hypoPP) is a rare inherited channelopathy that often presents with episodic weakness accompanied by hypokalemia. Thus far, mutations in the gene encoding two ion channels (CACNL1A3, L-type calcium channel alpha-1 subunit and SCN4A, a sodium channel type IV alpha subunit) have been identified. Several cases of familial hypoPP in children have been reported in Koreans, but there are only a few cases with identified mutations. We report a 12-year-old boy and his affected mother with hypoPP who has a heterozygous G to A substitution at codon 1239 in exon 30 of the CACNL1A3 gene that causes a change from arginine to histidine (Arg1239His, CACNL1A3). This mutation is common among Caucasians; however, it has not yet been reported in Koreans. The patients were treated with oral acetazolamide and potassium replacement and were instructed to avoid precipitating factors. After the medication and lifestyle modification, the paralytic attacks significantly decreased.

• The Journal of Korean Medicine
• /
• v.32 no.5
• /
• pp.134-138
• /
• 2011

Glycyrrhetinic acid, which is a component of licorice, can cause hypermineralocorticoidism through the inhibition of $11{\beta}$-hydroxysteroid dehydrogenase. So, a high dose intake of licorice can lead to hypermineralocorticoidism with potassium loss and depression of the renin-angiotensin-aldosterone system. We report a 73-year-old man with muscle weakness of proximal lower limbs with hypokalemia (Serum $K^+$: 1.4 mEq/L) due to taking self-prescribed licorice without OMD's diagnosis. He boiled 60~100g licorice / day in water and drank it intermittently for 1 month due to arthralgia and swelling of both his knees. Patient's serum renin activity and aldosterone level were far beyond the normal range. He also had metabolic alkalosis with pH 7.552. After quitting the licorice, hypokalemia and muscle weakness of proximal lower limbs gradually improved within 1week.

• Journal of Life Science
• /
• v.20 no.3
• /
• pp.457-461
• /
• 2010

Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant disorder characterized by reversible flaccid paralysis and intermittent hypokalemia. Although it has been reported that decreased activity in the $K_{ATP}$ channels of the skeletal muscle cell membrane plays a role in the pathogenesis of HOKPP, a clear mechanism has not yet been established. This study aimed to investigate the molecular biological mechanism underlying the decreased activity of $K_{ATP}$ channels in the skeletal muscles of familial HOKPP patients by studying the levels of the $K_{ATP}$ channel subunit Kir6.2. We found that when cells obtained from healthy individuals (normal cells) and HOKPP patients (patient cells) were treated with 4 mM potassium buffer, there was no quantitative change in the KCNJ11 mRNA levels and no difference in the Kir6.2 protein expression in the cytosol and cell membrane. On the other hand, when 1 mM potassium buffer was used, normal cells showed decreased expression of KCNJ11 mRNA as well as decreased expression of Kir6.2 protein in the cell membrane. However, patient cells treated with the same buffer showed no quantitative change in the levels of KCNJ11 mRNA or in the levels of Kir6.2 protein in the cytosol and cell membrane. Thus, in HOKPP patients, the Kir6.2 protein cannot be transported from the cell membrane to the cytosol, leading to closure of the $K_{ATP}$ channels, induction of depolarization, and subsequently, to the paralytic symptoms observed in the patient. Our findings thus provide new insights into the pathogenesis of HOKPP.

• Journal of Yeungnam Medical Science
• /
• v.4 no.1
• /
• pp.133-137
• /
• 1987

Myopathy in primary aldosteronism is relatively rare disease in Korea. A 42-year-lod woman with hypokalemic periodic paralysis, proximal muscle weakness and hypertension was found to have myopathy associated with adenoma in the right adrenal gland. She showed marked elevation of muscle enzymes and myopathic pattern in EMG.

• Journal of Yeungnam Medical Science
• /
• v.16 no.2
• /
• pp.228-236
• /
• 1999

Background: Thyrotoxic periodic paralysis is an uncommon illness characterized by intermittent flaccid paralysis of skeletal muscle, usually accompanied by hypokalemia, in patient with hyperthyroidism. However, the pathophysiology of thyrotoxic periodic paralysis remains largely unexplained and controversial. This report describes the clinical and biochemical findings in 19 patients with thyrotoxic periodic paralysis who were examined at the Yeungnam University Medical Center(YUMC) during the past decade. Methods: The medical records of 997 YUMC patients, seen between 1986 and 1996, with diagnosis of hyperthyroidism were reviewed. Nineteen patients out of 997 hyperthyroidism patients were diagnosed, and examined by history, physical examination, serum electrolyte value, and thyroid function test during paralysis. On the basis of these results, comparisons were made on age, sex, precipitating factors, timing, affected limbs, prognosis, serum potassium and serum phosphate and thyroid hormone levels. Results: The prevalence of periodic paralysis in hyperthyroidism was 1.9 percent and the male to female prevalence ratio was 30:1 and in all patients, the development of perodic paralysis was correlated with hyperfunctional state of the thyroid gland. Eleven cases of periodic paralysis were associated with hypokalemia and their thyroid hormone levels were significantly more increased than those of the patients without hypokalemia. Interestingly, our study shows the recurrence of paralysis after treatment. Conclusion: Although the precise pathophysiology of the disease is as yet undefined and controversial, it occurs primarily in Asians with an overwhelming male preponderance and prevalence of 2 percent in hyperthyroidism. The interactive roles of thyroid hormone, Na-K pump, and genetically inherited defect in the cellular membrane potential of the skeletal muscle can be speculated. Further investigation will be needed to firmly establish the mechanism of thyrotoxic periodic paralysis.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.21 no.2
• /
• pp.151-155
• /
• 2023

Licorice is a perennial herb belonging to the legume family that mainly grows in northeastern China, Mongolia, Siberia, and other regions. It is used in traditional medicine in the form of dried roots in the East and the West. The main active component of licorice, glycyrrhizin, is known to produce mineralocorticoid effects when consumed chronically, which can lead to apparent mineralocorticoid excess syndrome. Herein, we present the case of a 72-year-old woman who was admitted to the emergency room with severe generalized weakness and difficulty keeping her neck upright, which had developed after daily consumption of licorice-infused water for the past 2 months. Blood tests revealed metabolic alkalosis and severe hypokalemia, and an electrocardiogram showed ventricular bigeminy. The patient was treated with daily potassium and spironolactone supplements, leading to a significant improvement in muscle strength after a week. One week later, the patient was discharged, showing rare ventricular premature contractions on electrocardiography, but with no specific complaints. Chronic licorice ingestion leading to hypokalemia and muscle weakness can be life-threatening, necessitating the discontinuation of the causative agent, close monitoring, and cautious supplementation of potassium and spironolactone as treatment.