Cation transport across lymphocyte plasma membranes in euthyroid and thyrotoxic men with and without hypokalaemic periodic paralysis

1990 ◽  
Vol 78 (2) ◽  
pp. 199-206 ◽  
Author(s):  
Vernon M. S. Oh ◽  
Elizabeth A. Taylor ◽  
Soo-Hwa Yeo ◽  
Kok-Onn Lee
Keyword(s):  
Plasma Membranes ◽  
Striated Muscle ◽  
Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Normal Number ◽  
Sodium Potassium Pump ◽  
86Rb Influx ◽  
Hypokalaemic Periodic Paralysis

1. To study potassium transport in hypokalaemic periodic paralysis in a model of striated muscle cells, we measured specific [3H]ouabain binding (the number of sodium-potassium pumps), sodium-potassium-pump-mediated (ouabain-sensitive) 86Rb+ influx and sodium-potassium-pump-independent (ouabain-resistant) 86Rb+ influx in lymphocytes in vitro. 2. The subjects comprised euthyroid and thyrotoxic men with hypokalaemic periodic paralysis between attacks, men with uncomplicated thyrotoxicosis, and healthy men matched for age and weight. 3. Thyrotoxic patients, both with and without periodic paralysis, had significantly more lymphocyte sodium-potassium pumps than normal, and a significantly greater sodium-potassium-pump-mediated 86Rb+ influx. Antithyroid treatment corrected this defect in patients with thyrotoxic periodic paralysis. Euthyroid patients with cryptogenic periodic paralysis had significantly increased sodium-potassium-pump-mediated 86Rb+ influx, but a normal number of sodium-potassium pumps. 4. Only untreated thyrotoxic and euthyroid patients with periodic paralysis showed a significant increase in sodium-potassium-pump-independent 86Rb+ influx (5.2 ± 2.8 and 4.5 ± 1.8 respectively, vs control 2.8 ± 1.0 pmol h−1 10−6 cells; mean ± sd; P < 0.001, P < 0.005). 5. We conclude that thyrotoxicosis increases the number and activity of sodium-potassium pumps and facilitates, but is probably not necessary for, periodic paralysis. Hypokalaemic periodic paralysis is associated with an increase in sodium-potassium-pump-independent potassium influx.

Thyrotoxic periodic paralysis and the sodium/potassium pump

1989 ◽  
Vol 12 (10) ◽  
pp. 810-815 ◽  
Author(s):  
Alexander Marx ◽  
Johann Peter Ruppersberg ◽  
Christian Pietrzyk ◽  
Reinhardt Rüdel
Keyword(s):  
Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Sodium Potassium Pump

HYPOKALÆMIC PERIODIC PARALYSIS STUDIED IN VITRO

Brain ◽  
1970 ◽  
Vol 93 (3) ◽  
pp. 445-474 ◽  
Author(s):  
W. W. HOFMANN ◽  
R. A. SMITH
Keyword(s):  
Periodic Paralysis ◽  
Hypokalaemic Periodic Paralysis

Effect of Extracellular Potassium Concentration on the Sodium-Potassium Pump Rate in Human Lymphocytes

1995 ◽  
Vol 88 (6) ◽  
pp. 695-700 ◽  
Author(s):  
George D. Webb ◽  
Elizabeth A. Taylor ◽  
M. S. OH Vernon ◽  
YEO Soh-Bee ◽  
L. NG Leong
Keyword(s):  
Potassium Concentration ◽  
Human Lymphocytes ◽  
Extracellular Potassium ◽  
Physiological Changes ◽  
Sodium Potassium ◽  
Extracellular Potassium Concentration ◽  
Pump Rate ◽  
Sodium Binding ◽  
Sodium Potassium Pump ◽  
86Rb Influx

1. The purpose of this study was to determine whether physiological changes in extracellular free [K+] cause significant changes in the Na+-K+ pump rate and intracellular free [Na+]. 2. The Na+-K+ pump rate was measured in human lymphocytes by determining ouabain-sensitive 86Rb+ influx at several concentrations of K+. The Na+-K+ pump rate increased within the physiological range of extracellular free [K+] (K1/2 = 1.5 mmol/l). 3. To test the hypothesis that elevation of extracellular free [K+] reduces intracellular free [Na+] rapidly, which in turn then slows the pump rate during experimental incubations, lymphocyte intracellular free [Na+] was measured using the fluorochrome sodium-binding benzofuran isophthalate. With larger elevations of extracellular free [K+], intracellular free [Na+] dropped more rapidly. Thus previous discrepancies among determinations of K1/2 may be the result of variations in incubation times, which can skew the pump rates measured during incubations in various extracellular free [K+] values. Steady-state intracellular free [Na+] varied inversely with extracellular free [K+].

scholarly journals An Unusual Case of Acute Muscle Weakness

2016 ◽  
Vol 15 (4) ◽  
pp. 209-211
Author(s):  
Suzanne R Harrogate ◽  
◽  
Edouard Mills ◽  
Asjid Qureshi ◽  
Jacob F de Wolff ◽  
...  
Keyword(s):  
Muscle Weakness ◽  
Unusual Case ◽  
Beta Blockers ◽  
Periodic Paralysis ◽  
Beta Blockade ◽  
Proximal Muscle ◽  
Thyrotoxic Periodic Paralysis ◽  
Potassium Supplementation ◽  
Leg Weakness ◽  
Hypokalaemic Periodic Paralysis

A previously healthy 35-year old man presented to hospital with acute leg weakness following an alcohol binge. On assessment, tachycardia, urinary retention and bilateral upper and lower limb proximal weakness with preserved peripheral power were noted. Biochemistry revealed marked hypokalaemia, which responded to intravenous replacement, and biochemical thyrotoxicosis, leading to the diagnosis of Thyrotoxic Periodic Paralysis (TPP). Anti-thyroid therapy and beta-blockers were commenced and his neurological symptomatology resolved as he became progressively euthyroid. TPP is a rare acquired subtype of hypokalaemic periodic paralysis, typically causing proximal muscle weakness associated with thyrotoxicosis. It is most common in young Asian males. Acute treatment requires cautious oral potassium supplementation, beta-blockade, and anti-thyroid therapy. TPP is prevented by maintaining euthyroidism; otherwise recurrence is likely.

Effect of Aldosterone on the Human Erythrocyte Sodium-Potassium Pump in vitro

1983 ◽  
Vol 64 (2) ◽  
pp. 183-186 ◽  
Author(s):  
N. Stern ◽  
F. Beck ◽  
J. Sowers
Keyword(s):  
Atpase Activity ◽  
Human Erythrocyte ◽  
Erythrocyte Membranes ◽  
Ouabain Binding ◽  
Physiological Concentration ◽  
Sodium Potassium ◽  
Human Erythrocyte Membranes ◽  
Erythrocyte Sodium ◽  
Sodium Potassium Pump

1. The effects of aldosterone in vitro on the Na+,K+-dependent ATPase activity of isolated human erythrocyte membranes and on rubidium (86Rb) uptake and [3H]ouabain binding of intact erythrocytes were studied. 2. ATPase activity was nearly doubled (0.061 ± 0.006 to 0.110 ± 0.01 μmol of Pl h−1 mg−1 of protein) by the addition of a physiological concentration of aldosterone (2.7 × 10-10 mol/l). Higher concentrations had no greater effect. 3. Aldosterone had no significant effect on 86Rb uptake or [3H]ouabain binding. 4. Erythrocytes contain aldosterone at concentrations similar to that in plasma. The effect of aldosterone on ATPase is probably maximal.

scholarly journals A Case of Recurrent Paralysis and Low Potassium: Is It the Thyroid?

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A909-A909
Author(s):  
Justin Do ◽  
Hoveda Mufti
Keyword(s):  
Radioactive Iodine ◽  
Rare Complication ◽  
Periodic Paralysis ◽  
Definitive Treatment ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Potassium Atpase ◽  
Hispanic Male ◽  
Hyperthyroid Patients

Abstract Introduction: Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that is characterized by episodes of hypokalemia and acute weakness. Although hyperthyroidism is more common in females, over 95% of cases of TPP have been observed in males, especially in Asian males with an incidence of 2% among hyperthyroid patients. In non-Asian populations, the incidence in hyperthyroid patients is estimated to be around 0.1 to 0.2% [1]. We describe a case of TPP seen in a Hispanic male. Case Report: A 36-year-old Hispanic male with no past medical history presents with weakness in all extremities and difficulty breathing after consuming a carbohydrate heavy meal the night prior. He reports a recent, similar episode evaluated in another ER, which resolved after given potassium supplementation. He denied any vomiting, diarrhea, polyuria, diaphoresis, use of insulin or other medications, or any family history of paralysis. His labs were significant for hypokalemia of 1.9, TSH of &lt;0.005 (0.358-3.740), free T4 of 2.22 (0.76-1.46), and total T3 of 2.7 (0.60-1.81). Thyroid stimulating immunoglobulin was 0.12 (0.0-0.55). His symptoms improved and potassium levels normalized following the administration of potassium chloride. He was discharged on propranolol and advised to follow up for further workup of his hyperthyroidism with radioactive iodine uptake scan. Discussion: Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with cardiac arrhythmias and respiratory failure. Hyperthyroidism increases response to β-adrenergic stimulation, which increases activity of the sodium-potassium ATPase and causes hyperpolarization of skeletal muscle [2]. Hyperthyroid patients are prone to episodes of paralysis due to their increased susceptibility to the hypokalemic action of insulin, which activates the sodium-potassium ATPase pump, and epinephrine, which stimulates β-adrenoreceptors. Management of an acute attack of TPP includes potassium administration. In cases where paralysis and hypokalemia are not reversed, intravenous propranolol has been shown to resolve the attack by blocking the β-adrenergic receptors. Definitive treatment of TPP includes managing the hyperthyroid state with medical therapy, radioactive iodine therapy, or surgery. Until the euthyroid state is reached, a β-blocker can prevent episodes of acute paralysis. Avoidance of carbohydrate heavy meals, exercise, and stress are recommended as these factors can potentially exacerbate hypokalemia. In patient with acute paralysis, it is important to consider the diagnosis of TPP as this condition can be prevented once euthyroidism is achieved. Diagnosis and management will lead to prevention of morbidity and mortality associated with the hypokalemia. References: 1.Vijayakumar A, et al. J Thyroid Res. 2014;2014:649502. 2.Layzer RB. Annals of Neurology. 1982;11(6):547–552.

Thyrotoxic periodic paralysis and polymorphisms of sodium-potassium ATPase genes

2006 ◽  
Vol 64 (2) ◽  
pp. 158-161 ◽  
Author(s):  
Annie W. C. Kung ◽  
K. S. Lau ◽  
William M. W. Cheung ◽  
Vivian Chan
Keyword(s):  
Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Potassium Atpase
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