School of Medicine and Health Sciences Poster Presentations

Title

Thyrotoxic Periodic Paralysis

Document Type

Poster

Keywords

Thyrotoxic; Paralysis; Hypokalemia

Publication Date

Spring 2017

Abstract

Thyrotoxic periodic paralysis (TPP) is characterized by abrupt onset of hypokalemia and paralysis secondary to thyrotoxicosis (1). The hypokalemia is a result of intracellular shift of potassium due to sensitization of the sodium/potassium (Na+-K+) ATPase. TPP is most commonly seen in people of asian decent, and over 95 percent of TPP cases occur in men. We present a case of TTP presenting in an african american female.

41 year old women of African American descent with a past medical history of Grave’s disease on methimazole, sickle cell trait, and bilateral kidney stones status post lithotripsy presented with worsening bilateral leg cramping and generalized weakness of 2 days duration. She denies localized weakness, numbness, or change in sensation. Denies fever, chills, rash, nausea, vomiting, abdominal pain, change in bowel habit, or urinary symptoms. Her endocrinologist reduced the dose of methimazole four weeks prior. Patient had two prior episodes of hypokalemia and weakness in the past year. Found to have decreased potassium of 2.7 mmol/L and a decreased thyroid stimulating hormone level of 0.81.

Hypokalemic periodic paralysis is composed of a class of disorders with episodic muscle weakness associated with hypokalemia from acute shift of potassium into cells. Hypokalemic periodic paralysis may be familial caused by a mutation in the Cav1.1 skeletal muscle voltage-gated Ca2+ channel or the Nav1.4 Na+ channel. Nonfamilial periodic paralysis such as thyrotoxic periodic paralysis (TPP) and sporadic periodic paralysis (SPP), which are caused by sporadic mutations and are more common among Asians and Hispanics. The incidence of TTP is 10-20 times higher in asian populations compared to non-asian populations where the incidence is 0.1%–0.2%.

In TTP, there is an increase in the activity of Na+-K+ ATPase pumps in skeletal muscle. Both thyroid hormone and b2-adernergic agonists can increase Na+-K+ATPase activity by up-regulating its production and increasing the production of intracellular cAMP, respectively. TPP is also known to occur predominately among males despite a higher incidence of thyrotoxicosis in women, suggesting the potential role of androgen on Na+–K+ ATPase activity. Episodes are found to be aggravated with exercise and stress possibly due to an increase in beta-adrenergic response. These episodes can be prevented by treating the patient’s thyroid disease hence preventing hyperthyroid states and with the use of propranolol to reduce the beta-adrenergic activity. Moreover, potassium supplementation and spironolactone have been shown to decrease these episodes.

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Comments

Poster to be presented at GW Annual Research Days 2017.

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Thyrotoxic Periodic Paralysis

Thyrotoxic periodic paralysis (TPP) is characterized by abrupt onset of hypokalemia and paralysis secondary to thyrotoxicosis (1). The hypokalemia is a result of intracellular shift of potassium due to sensitization of the sodium/potassium (Na+-K+) ATPase. TPP is most commonly seen in people of asian decent, and over 95 percent of TPP cases occur in men. We present a case of TTP presenting in an african american female.

41 year old women of African American descent with a past medical history of Grave’s disease on methimazole, sickle cell trait, and bilateral kidney stones status post lithotripsy presented with worsening bilateral leg cramping and generalized weakness of 2 days duration. She denies localized weakness, numbness, or change in sensation. Denies fever, chills, rash, nausea, vomiting, abdominal pain, change in bowel habit, or urinary symptoms. Her endocrinologist reduced the dose of methimazole four weeks prior. Patient had two prior episodes of hypokalemia and weakness in the past year. Found to have decreased potassium of 2.7 mmol/L and a decreased thyroid stimulating hormone level of 0.81.

Hypokalemic periodic paralysis is composed of a class of disorders with episodic muscle weakness associated with hypokalemia from acute shift of potassium into cells. Hypokalemic periodic paralysis may be familial caused by a mutation in the Cav1.1 skeletal muscle voltage-gated Ca2+ channel or the Nav1.4 Na+ channel. Nonfamilial periodic paralysis such as thyrotoxic periodic paralysis (TPP) and sporadic periodic paralysis (SPP), which are caused by sporadic mutations and are more common among Asians and Hispanics. The incidence of TTP is 10-20 times higher in asian populations compared to non-asian populations where the incidence is 0.1%–0.2%.

In TTP, there is an increase in the activity of Na+-K+ ATPase pumps in skeletal muscle. Both thyroid hormone and b2-adernergic agonists can increase Na+-K+ATPase activity by up-regulating its production and increasing the production of intracellular cAMP, respectively. TPP is also known to occur predominately among males despite a higher incidence of thyrotoxicosis in women, suggesting the potential role of androgen on Na+–K+ ATPase activity. Episodes are found to be aggravated with exercise and stress possibly due to an increase in beta-adrenergic response. These episodes can be prevented by treating the patient’s thyroid disease hence preventing hyperthyroid states and with the use of propranolol to reduce the beta-adrenergic activity. Moreover, potassium supplementation and spironolactone have been shown to decrease these episodes.