Periodic Paralysis Syndromes: A T3 Thyrotoxicosis Etiology Presentation and Review of Literature

Abstract

DescriptionPeriodic paralysis is a group of muscle diseases that are related to transmembrane ion channels. Dysfunction of these channels causes an increase in sodium-potassium (Na-K) adenosine triphosphatase (ATPase) activity that pushes potassium into the cells that result in serum hypokalemia that manifests as muscle weakness. Beta-adrenergic stimulation and insulin sensitivity might also play a role.Periodic paralysis is divided into hereditary and acquired forms. Thyrotoxic periodic paralysis is an acquired form of periodic paralysis that manifests as muscle weakness, hypokalemia, and hyperthyroidism. The onset of the symptoms is mainly over the age of 20 and can be triggered by intense physical activity, stress, and excessive carbohydrate intake.This review presents the different types of this disease (hypokalemic, hyperkalemic, thyrotoxic, and Andersen-Tawil syndrome) while presenting a unique case of T3 thyrotoxicosis causing periodic paralysis.

Hypokalemic Hypophosphatemic Thyrotoxic Periodic Paralysis Associated with Bipolar Disorder Therapy

“…Another player in the increased activity of the Na/K-ATPase channels is thyroid hormone-responsive elements (TREs), which are involved in transcribing a subunit of the Na/K-ATPase channel and are stimulated by elevated levels of thyroid hormone [6]. Although hyperthyroidism has a higher incidence in women, TPP is more frequently seen in men.…”

“…Although hyperthyroidism has a higher incidence in women, TPP is more frequently seen in men. This disparity could be due to the stimulation effect testosterone has and the inhibition effect estrogen and progesterone have on the activity of Na/K-ATPase channels [6][7][8].…”

“…The intracellular shift of potassium seen in TPP occurs due to the increase in beta-adrenergic stimulation from elevated circulating thyroid hormone. This causes activation of Na/K-ATPase channels in skeletal muscle membranes, causing a large intracellular potassium shift leading to hypokalemia, hyperpolarization, and eventually periodic paralysis [ 1 , 6 ]. This phenomenon can be precipitated by a high-carbohydrate diet, which increases adrenergic activity and insulin release, ultimately leading to Na/K-ATPase activity [ 6 ].…”

“…This causes activation of Na/K-ATPase channels in skeletal muscle membranes, causing a large intracellular potassium shift leading to hypokalemia, hyperpolarization, and eventually periodic paralysis [ 1 , 6 ]. This phenomenon can be precipitated by a high-carbohydrate diet, which increases adrenergic activity and insulin release, ultimately leading to Na/K-ATPase activity [ 6 ]. Another player in the increased activity of the Na/K-ATPase channels is thyroid hormone-responsive elements (TREs), which are involved in transcribing a subunit of the Na/K-ATPase channel and are stimulated by elevated levels of thyroid hormone [ 6 ].…”

“…This phenomenon can be precipitated by a high-carbohydrate diet, which increases adrenergic activity and insulin release, ultimately leading to Na/K-ATPase activity [ 6 ]. Another player in the increased activity of the Na/K-ATPase channels is thyroid hormone-responsive elements (TREs), which are involved in transcribing a subunit of the Na/K-ATPase channel and are stimulated by elevated levels of thyroid hormone [ 6 ]. Although hyperthyroidism has a higher incidence in women, TPP is more frequently seen in men.…”