Thyrotoxic Periodic Paralysis Research Articles

Rhabdomyolysis Induced by Nonstrenuous Exercise in a Patient with Graves’ Disease

Hyperthyroidism can result in several musculoskeletal conditions such as thyrotoxic periodic paralysis, thyrotoxic myopathy, and thyroid ophthalmopathy. Rhabdomyolysis has been rarely reported to be associated with hyperthyroidism. We describe a 33-year-old man who presented with bilateral thigh pain and dark brown urine after regular squatting. He had a past medical history of hyperthyroidism but stopped taking it 2 months prior to admission. He was found to have rhabdomyolysis, myoglobinuria, and thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins (TSI) and high radioiodine uptake confirmed a diagnosis of Graves' disease. He received aggressive fluid resuscitation and sodium bicarbonate intravenously along with monitoring fluid and electrolyte. Methimazole was also resumed. The patient responded to treatment and rhabdomyolysis gradually resolved. Therefore, nonstrenuous exercise can potentially induce rhabdomyolysis in patients with hyperthyroidism. Although hyperthyroidism is not widely recognized as a cause of rhabdomyolysis, it should be considered in the differential diagnosis of rhabdomyolysis.

Thyrotoxicosis with periodic paralysis

This case report is intended to highlight the importance of suspecting thyrotoxicosis in cases of periodic flaccid paralysis to facilitate its early diagnosis. Thyrotoxic periodic paralysis is a complication of thyrotoxicosis, more common among males in Asia. It presents as acute flaccid paralysis with associated hypokalemia. The features of thyrotoxicosis may be subtle or absent. We report a case of 33-year-old male patient with periodic flaccid paralysis. Hypokalemia secondary to thyrotoxicosis was diagnosed as the cause of the paralysis. The patient was treated with intravenous and oral potassium therapy. The patient showed complete recovery after this management and was discharged after 24 h with no residual paralysis. Thus, in cases of recurrent or acute flaccid muscle paralysis, it is important to consider thyrotoxicosis as one of the possible causes and take measures accordingly.

Thyrotoxic Periodic Paralysis: Clinical Challenges

Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. The underlying hyperthyroidism is often subtle causing difficulty in early diagnosis. Factors like high-carbohydrate meal exercise, steroid, and stress can precipitate an attack of TPP. Evidence is building up showing role of genetic mutations in Kir2.6 channel in the pathogenesis of TPP. Loss of function of Kir2.6 together with increased activity of Na+/K+ ATPase may trigger a positive feed-forward cycle of hypokalemia. Biochemical hyperthyroidism with normal urinary potassium excretion and ECG changes are characteristic of TPP. Treatment with low-dose potassium supplements and nonselective beta-blockers should be initiated upon diagnosis, and the serum potassium level should be frequently monitored to prevent rebound hyperkalemia.

Thyrotoxic Periodic Paralysis in a Pediatric Patient

Thyrotoxic periodic paralysis is a reversible metabolic disorder that is characterized by acute muscle weakness and hypokalemia. It predominantly affects males of Asian descent. We describe the youngest such patient yet reported, a 13-year-old Asian male with a history of transient attacks of weakness who presented to our emergency department with weakness in his extremities and mild tachycardia. Laboratory test results initially revealed marked hypokalemia and later confirmed associated hyperthyroidism. Correction of the hypokalemia reversed the patient's weakness in the emergency department.

A possible association of hypokalaemic periodic paralysis, autoimmune thyroiditis and neuromyotonia

Acute hypokalemic periodic paralysis (HPP), a clinical syndrome characterised by acute systemic weakness and low serum potassium (K+), is a rare but treatable cause of acute limb weakness. Hypokalemia can be caused by K+ loss via the kidneys or extra renal routes mainly the gut, or due to transcellular potassium shifts where extracellular K+ will move into the cell. In the latter situation, although there is hypokalaemia, there is no deficit of K+ in the body. The main causes for intracellular shift of K+ are familial hypokalemic periodic paralysis, thyrotoxic periodic paralysis, barium poisoning, insulin excess and alkalosis. Although the association between thyrotoxicosis and HPP is known, HPP with hypothyroidism is extremely rare. We report a case of hypokalemic periodic paralysis associated with hypothyroidism and neuromyotonia.

Hypokalaemic periodic paralysis in rural northern India – most have secondary causes

Hypokalaemic periodic paralysis (HPP) is a life-threatening condition. Our aim was to study the clinical profile and laboratory parameters of HPP patients and to develop an algorithm to determine the causes of HPP. 84 patients presented with HPP over a 3 year period. 58 (69.0%) were found to have renal tubular acidosis (RTA). The other causes were idiopathic HPP (8 (9.5%)), acute gastroenteritis (4 (4.8%)), suspected primary hyperaldosteronism and familial HPP (2 each (2.4%)) and suspected Gitelman/Bartter Syndrome and thyrotoxic periodic paralysis (1 each (1.2%)). The number of cases peaks in the hot season. Over a third of the patients (35.7%) had recurrent episodes. 80% had secondary HPP and therefore a biochemical evaluation is mandatory. A simple algorithm was developed. Both health professionals and patients need further education regarding this problem in order to improve diagnosis and treatment and to improve compliance.

Thyrotoxic periodic paralysis and chorea: two uncommon neuromuscular complications in an adolescent with newly diagnosed Graves disease

Both thyrotoxic periodic paralysis (TPP) and choreoathetosis are unusual complications of childhood thyrotoxicosis. We hereby report a boy who presented with both TPP and choreoathetosis at the initial presentation of his Graves disease. A 14 year-old Thai boy presented with acute generalized proximal muscle weakness and myalgia for 5 hours. Detailed history revealed the increased appetite, heat intolerance and labile mood for 6 months. Physical examination revealed tachycardia, goiter and mild exopthalmos. Generalized proximal muscle weakness and hyporeflexia were noted. Abnormal movement including ballism and mild spooning of hands were also noted. The milk maid sign was positive. The abnormal movement was consistent with choreoathetosis. Labs showed serum T3 > 651 ng/dL, Free T4 > 7.77 ng/dL, TSH < 0.005 uU/mL, K 2.1 mmol/L and CPK 1555 U/L. Autoimmune profile showed high titer of the anti-microsomal antibodies of 1:25000. The final diagnosis of Graves disease with TPP and choreoathetosis were made. Methimazole and propranolol were started. Intravenous K was administered to correct hypokalemia. Serum K was normalized within 7 hours after K replacement. The patient was able to stand and walk normally on the 2nd day of admission. After 4 weeks of treatment with Methimazole, the thyroid function test was consistent with hypothyroidism, therefore the dose of Methimazole was decreased. The choreoathetosis resolved completely within 4 weeks. Our case report demonstrates the first pediatric patient with Graves disease who developed combined neuromuscular complications which were TPP and choreoathetosis. There has been a previous case report of a 21-year-old man with Graves disease who had both muscular complication and choreoathetosis. The muscular involvement in that patient was different from our patient. In that particular patient, he developed acute severe thyrotoxic myopathy which involved both bulbar and skeletal muscle. TPP is an alarming and potentially lethal complication of hyperthyroidism. It usually resolves completely after the normalization of serum K levels. Effective control of hyperthyroidism can prevent the recurrence of TPP. While, choreoathetosis usually resolves after the patient recovers from hyperthyroid state. We should always be aware of Graves disease in any children who present with either muscle weakness or choreoathetosis since the signs and symptoms of Graves disease itself might not be very obvious.

Thyrotoxic Periodic Paralysis as an Initial Presentation of Graves Disease

Thyrotoxic Periodic Paralysis as an Initial Presentation of Graves Disease

THYROTOXIC PERIODIC PARALYSIS: DIAGNOSIS, MANAGEMENT AND ROLE OF PROPRANOLOL IN TREATMENT

Background: Hypokalemia is commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. This condition mainly affects male patients of Asian descent. With increasing population mobility and admixture, TPP as the presenting feature of hyperthyroidism is more common in Western countries and Gulf area. TPP is an alarming and potentially lethal complication of hyperthyroidism characterized by muscle paralysis and hypokalemia due to a massive intracellular shift of potassium. A potassium supplement has been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective β-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium. Methods: We describe 7 patients who had an acute attack of TPP with characteristic hypokalemia. Results: After oral propranolol, 3 mg/kg, serum potassium concentrations increased promptly in all patients, and there was complete amelioration of paralysis. Only 3 patient needed short term K supplement for their sever hypokalemia and sever symptoms. No rebound hyperkalemia was detected. Conclusion: Given propranolol efficacy in this study, propranolol should be considered as a first-line therapy for TPP. Key words: Hypokalemia, TPP, hyperthyroidism, propranolol, periodic paralysis

A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants

BackgroundA comprehensive analysis has not been performed on patients with thyrotoxic periodic paralysis (TPP) characterized by acute hypokalemia and paralysis in the setting of thyrotoxicosis.PurposeThe aim of this study was to analyze the detailed symptomatology of thyrotoxicosis and precipitating factors for the attack in a large cohort of TPP patients.Patients and methodsA prospective observational study enrolled patients with TPP consecutively over 10 years at an academic medical center. Clinical features, including signs/symptoms of thyrotoxicosis and precipitating factors, were analyzed. The Wayne's index was used to assess the severity of thyrotoxicosis at presentation. Patients who agreed to receive an oral glucose-loading test after recovery were evaluated.ResultsAmong the 135 TPP patients (male:female, 130:5), 70% of paralytic attacks occurred in the morning, especially during the seasons of summer and fall. Two-thirds of patients did not have a known family or personal history of hyperthyroidism. Only 17% of TPP patients manifested overt signs/symptoms of thyrotoxicosis (Wayne's index >19). A clear precipitating factor, such as high carbohydrate load, acute upper respiratory tract infection, strenuous exercise, high-salt diet, or the use of steroids or bronchodilators, was identified in only 34% of TPP patients. A glucose load to stimulate insulin secretion induced acute hypokalemia (K+2.47±0.6 mmol/l) with reparalysis in only 18% (10/55) of TPP patients.ConclusionsMost TPP patients have only subtle clinical signs/symptoms of thyrotoxicosis and only a small fraction has clear precipitating factors. In addition to the effects of hyperinsulinemia, other insulin-independent mechanisms may participate in the pathogenesis of TPP.

The predisposition to thyrotoxic periodic paralysis (TPP) is due to a genetic variant in the inward-rectifying potassium channel,KCNJ2

The predisposition to thyrotoxic periodic paralysis (TPP) is due to a genetic variant in the inward-rectifying potassium channel,<i>KCNJ2</i>

Thyrotoxic Periodic Paralysis: Correct Hypokalemia with Caution

BackgroundThyrotoxic periodic paralysis is rare in Caucasian populations, but affects approximately 2% of East Asians with thyrotoxicosis (13% of males, 0.17% of females). The presentation is characterized by abrupt-onset hypokalemia and profound proximal muscular weakness, and commonly occurs after carbohydrate loading or exercise. ObjectivesTo raise awareness of this condition through the description of a typical case of thyrotoxic periodic paralysis; to remind readers that, despite intravascular hypokalemia, total body potassium is normal and that correction must be done with caution; to highlight the differences in treatment compared to familial hypokalemic periodic paralysis. Case ReportWe describe the presentation of a 36-year-old Filipino man with a background history of Graves disease. Over-administration of intravenous potassium was narrowly averted in this case. ConclusionIt may be important to check thyroid function in patients presenting with acute paralysis, especially those of Asian origin. In patients with thyrotoxic periodic paralysis, administration of potassium, with cardiac monitoring and a total dose of <50 mmol, limits the dysrhythmia risk. Patients are likely to benefit from the prescription of non-selective beta-blockers until they become euthyroid. In contrast to familial periodic paralysis, regular oral potassium supplementation is ineffective in thyrotoxic periodic paralysis, and acetazolamide precipitates, rather than prevents, attacks.

A Case of Thyrotoxic Periodic Paralysis

Hypokalemic periodic paralysis is an uncommon manifestation of thyrotoxicosis and the condition is most commonly reported in young Asian men. Patient often presents with acute onset symmetrical flaccid muscle paralysis and proximal limb muscles may be more severely involved compared to distal muscles. Thyroid swelling as well as features of thyrotoxicosis may not be overt. A very high index of suspicion is often required for the diagnosis of thyrotoxic periodic paralysis. Treatment of throtoxicosis prevents further episodes of paralysis. We report a case of thyrotoxic periodic paralysis in a young male.Bangladesh Journal of Medical Science Vol. 12 No. 03 July ’13 Page 320-321 DOI: http://dx.doi.org/10.3329/bjms.v12i3.12719

Coexisting atrial fibrillation and paralysis as a result of hypokalemia in a Caucasian man with Graves' disease

A 29-year-old Caucasian man with a history of Graves' disease for 6 weeks presented to our emergency department at midnight with muscle weakness. He had woken up after 1–2 hours of sleep with weakness in his lower extremities. Electrocardiography (ECG) showed atrial fibrillation. His potassium level was 2.6 mEq/L. His ECG was monitored, and potassium chloride mixed with a normal saline infusion (20 mEq/L) was given for 1 hour. After his potassium level returned to normal (4.63 mEq/L), clinical improvement was noted. The ECG showed sinus rhythm. Clinicians should consider thyrotoxic periodic paralysis in patients with hypokalemia and paralysis, even though it is rare in Caucasians.

Episodes of Paralysis in Chinese Men with Thyrotoxic Periodic Paralysis Are Associated with Elevated Serum Testosterone

The strong predilection for thyrotoxic periodic paralysis (TPP) to occur in males suggests androgen may contribute to its pathogenesis. We therefore sought to determine if serum total and free testosterone (TT and FT) concentrations differed among patients with TPP during episodes of paralysis, patients with TPP between episodes of paralysis, and patients with Graves' disease (GD) not having TPP. A total of 105 Chinese men were included in the study, and were divided into three groups. Group 1 consisted of men with TPP who were studied during episodes of paralysis; group 2 consisted of men with TPP who were studied between episodes of paralysis; group 3 consisted of men with GD not having TPP. Patients in each were different persons. Serum electrolytes, free triiodothyronine (FT3), free thyroxine (FT4), TT, and FT were measured. Multiple regression analyses and analysis of covariance were performed to analyze the relationship of serum parameters, group status, and age. One multiple regression analysis was used to determine if serum TT concentrations were associated with age, FT3, FT4, or group status. This analysis indicated that age, FT4 level, and group status were significantly and independently associated with serum TT concentrations. With regard to group status, patients in group 1 had serum TT concentrations 0.92 ng/mL higher than patients in group 3 (p=0.033). As to FT4 level, TT concentrations increased by 0.016 ng/mL for each additional pmol/L of FT4 (p=0.002). Another multiple regression analysis was used to determine if serum FT concentrations were associated with age, FT3, FT4, group status, or serum TT concentrations. This analysis revealed that serum TT concentrations and group status were significantly and independently associated with serum FT concentrations. In terms of group status, patients in group 1 had serum FT concentrations of 2.11 pg/mL greater on average than patients in group 3 (p=0.006). We infer that episodes of paralysis in Chinese men with TPP are associated with elevated serum testosterone. We also found serum TT and FT concentrations of men with GD are both affected by group status; serum TT rather than FT concentrations are associated with thyroid function.

Thyrotoxic Periodic Paralysis in Chinese Patients

Thyrotoxic periodic paralysis (TPP) is a complication of thyrotoxicosis mainly observed in male Asian patients. It was proposed that patients with TPP tend to have lower thyroid hormone levels. We aimed to prove this observation and to assess whether a lower I dose is feasible for prompt control of TPP. A total of 123 male TPP patients were enrolled in this study in a 7-year period. Baseline characteristics were compared with 70 thyrotoxic patients without periodic paralysis (nTPP). Different I doses were given to 90 TPP patients with a median follow-up of 11 months, and the outcome was evaluated. The serum thyroid hormone levels, including total T3 and T4, and free T3 and T4, in TPP patients were slightly less elevated compared with those in nTPP patients. Patients who received lower radioactivity of I had an unsatisfactory overall remission rate of 28.6%. Longer time to remission (P = 0.004; hazard ratio, 1.846; 95% confidence interval, 1.216-2.798) was also observed in patients with lower dose. The serum thyroid hormone levels of TPP patients are lower than those of nTPP patients. Median/high dose of I is necessary to achieve rapid control of thyrotoxicosis.

Thyrotoxic hypokalemic periodic paralysis as the presenting symptom of silent thyroiditis

Silent thyroiditis is a rare cause of thyrotoxic periodic paralysis. The objective was to present a case of silent thyroiditis presenting as periodic paralysis. A 23-year-old man presented with recurrent acute flaccid predominantly proximal weakness of all four limbs. He had a similar episode 3 weeks back. On examination he was found to have hypokalemia secondary to thyrotoxicosis. Clinically there were no features of thyrotoxicosis or thyroiditis. He was initially treated with intravenous and later oral potassium supplementation and propranolol. At 8 weeks of follow-up his thyroid profile became normal and his propranolol was stopped. He had no further recurrence of paralysis. He was diagnosed as a case silent thyroiditis presenting as thyrotoxic periodic paralysis. In cases of recurrent or acute flaccid muscle paralysis, it is important to suspect thyrotoxicosis, even if asymptomatic. Definitive treatment of thyrotoxicosis prevents recurrence.

Three cases of thyrotoxic periodic paralysis due to painless thyroiditis

We present three cases of thyrotoxic periodic paralysis (TPP) due to painless thyroiditis presenting as acute quadriparesis. All responded to potassium supplementation and propranolol. TPP may be due to thyrotoxicosis of any etiology, commonly Grave's disease. The absence of clinical signs of thyrotoxicosis can delay diagnosis and treatment. Thyroid function tests should be a routine evaluation in all cases of hypokalemic periodic paralysis.

Clinical and biochemical spectrum of hypokalemic paralysis in North: East India

Background:Acute hypokalemic paralysis, characterized by acute flaccid paralysis is primarily a calcium channelopathy, but secondary causes like renal tubular acidosis (RTA), thyrotoxic periodic paralysis (TPP), primary hyperaldosteronism, Gitelman’s syndrome are also frequent.Objective:To study the etiology, varied presentations, and outcome after therapy of patients with hypokalemic paralysis.Materials And Methods:All patients who presented with acute flaccid paralysis with hypokalemia from October 2009 to September 2011 were included in the study. A detailed physical examination and laboratory tests including serum electrolytes, serum creatine phosphokinase (CPK), urine analysis, arterial blood gas analysis, thyroid hormones estimation, and electrocardiogram were carried out. Patients were further investigated for any secondary causes and treated with potassium supplementation.Result:The study included 56 patients aged 15-92 years (mean 36.76 ± 13.72), including 15 female patients. Twenty-four patients had hypokalemic paralysis due to secondary cause, which included 4 with distal RTA, 4 with Gitelman syndrome, 3 with TPP, 2 each with hypothyroidism, gastroenteritis, and Liddle’s syndrome, 1 primary hyperaldosteronism, 3 with alcoholism, and 1 with dengue fever. Two female patients were antinuclear antibody-positive. Eleven patient had atypical presentation (neck muscle weakness in 4, bladder involvement in 3, 1 each with finger drop and foot drop, tetany in 1, and calf hypertrophy in 1), and 2 patient had respiratory paralysis. Five patients had positive family history of similar illness. All patients improved dramatically with potassium supplementation.Conclusion:A high percentage (42.9%) of secondary cause for hypokalemic paralysis warrants that the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.

Thyrotoxicosis presenting first time as hypokalemic paralysis

Thyrotoxicosis has varied manifestations, from its usual to rare presentations. Thyrotoxicosis presenting as acute quadriplegia is a very rare phenomenon and is attributed to hypokalemia. Thyrotoxic hypokalemic periodic paralysis is known but rare manifestation and as a first presentation is relatively unknown. Here, we present a case of young male in whom thyrotoxicosis presented for the first time as hypokalemic paralysis.