Case Of Thyrotoxic Periodic Paralysis Research Articles

Thyrotoxic Periodic Paralysis in the Chinese Population: Clinical Features in 45 Cases

Thyrotoxic periodic paralysis (TPP) occurs predominantly in Asian males, but there are few reports about TPP in the mainland of the People's Republic of China. The purpose of this study was to report the clinical features of cases of TPP in mainland China. Forty-five cases of TPP, admitted to Zhongnan Hospital of Wuhan University during a 5-year period, were retrospectively reviewed. Patients typically presented with acute paralysis of the limbs, almost half (48.6%) initiated with legs, while the rest (51.4%) with both arms and legs. Twenty of 45 patients (44.4%) who had been diagnosed with hyperthyroidism suffered sudden attacks, while the remaining 25 patients were newly diagnosed with TPP. 16 patients had low potassium serum concentrations (1.44-3.00 mmol/L). There was a correlation between the lowest muscle strengths of the proximal and distal legs and serum potassium concentrations (Spearman correlation, r=0.556, P=0.049). TPP is not an uncommon disease in mainland China. Thyrotoxic patients need to improve medication compliance and follow-up. At the time of the TPP attack, a detailed interview and inquiry with a thorough physical examination usually provide clues to the diagnosis. Leg muscle strength evaluation may be useful to assess the severity of hypokalemia.

A Case of Thyrotoxic Periodic Paralysis with Rhabdomyolysis

Hyperthyroidism combined with rhabdomyolysis is extremely rare. There are only 6 reported cases of hyperthyroidism accompanied with rhabdomyolysis in the medical literature. Rhabdomyolysis is a syndrome involving the breakdown of skeletal muscle, and this causes myoglobin and intracellular protein to leak into the circulation. The causes of rhabdomyolysis include trauma, electrolyte abnormality, infection, drug, toxin and hypothyroidism. We report here on a patient who presented with thyrotoxic periodic paralysis and rhabdomyolysis with hypokalemia. He complained of lower leg paralysis along with muscle tenderness, and the laboratory findings showed elevated creatine kinase (CK) levels. After treatment by hydration, potassium replacement and drug medication, including propylthiouracil and beta-blocker, his CK levels were normalized and his symptoms were much improved. For patient with thyrotoxic periodic paralysis and muscle tenderness, the possibility of rhabdomyolysis should be clarified by examining the CK levels. (J Korean Endocr Soc

An Electrocardiogram Triad in Thyrotoxic Hypokalemic Periodic Paralysis

A 37-year-old Asian man presented to the emergency department with acute onset of bilateral lower-extremity weakness. Physical examination was notable for marked reduction in proximal muscle strength, with decreased deep tendon reflexes. Initial laboratory tests showed a potassium level of 1.3 mEq/L (normal range, 3.7 to 5.2 mEq/L), thyroid-stimulating hormone level <0.03 μIU/mL (normal range, 0.4 to 5.0 μIU/mL), total thyroxine of 21.8 μg/dL (normal range, 4.8 to 10.8 μg/dL), and free thyroxine level of 5.7 ng/dL (normal range, 0.8 to 1.8 ng/dL). The 12-lead ECG taken immediately after presentation was notable for sinus tachycardia, first-degree atrioventricular conduction delay, ST depressions, and prolonged T/U segments (Figure 1). Figure 1. Twelve-lead ECG shows …

Thyrotoxic periodic paralysis: a case report

Thyrotoxic periodic paralysis (TPP) is characterized by recurrent episodes of muscle weakness and hypokalemia associated with thyroid hyperactivity. Reported predominantly among individuals of Asian descent, TPP is a rare manifestation of hyperthyroidism in western populations. We describe a typical case of TPP in a 33-year-old portuguese male, who presented with acute tetraparesis associated with hypokalemia (K+ 2.6 mEq/L). The patient had a 8-week history of several episodes of paraparesis of variable intensity; these attacks were usually nocturnal, preceded by strenuous exercise and resolved spontaneously after a few hours. The presence of tachycardia, weight loss, and goiter led to the diagnosis of Graves's disease. The correction of the hyperthyroid function with metimazol and propranolol prevented further episodes of muscle weakness. Thyrotoxic periodic paralysis should be considered in the differential diagnosis of acute episodes of motor paralysis in young patients. The maintenance of a euthyroid status is an essential part of management as this prevents the paralytic episodes.

A Case of Thyrotoxic Periodic Paralysis at a Remote EMEDS Unit Supporting Operation Enduring Freedom.

A Case of Thyrotoxic Periodic Paralysis at a Remote EMEDS Unit Supporting Operation Enduring Freedom.

Paralysie périodique thyréotoxique À propos d'un cas chez un sujet africain

Thyrotoxic periodic paralysis is an unusual disease, more commonly reported among Asian populations. Its pathophysiology remains unclear. Hypokalemia is most probaly due to influx of potassium in muscle cells. This influx can depend or not on membrane cells Na-K-ATPase pumps. We report the case of a black African male patient. Thyrotoxic periodic paralysis cases have rarely been reported in black populations in Europe (up to now cases reports were only in black Americans). The symptomatic treatment of thyrotoxic periodic paralysis is a medical emergency. Only an etiologic treatment can prevent the recurrence of attacks.

Thyrotoxic periodic paralysis

A case of thyrotoxic periodic paralysis is reported in a Hispanic man with an unusual recurrence six weeks after radioactive iodine treatment. Thyrotoxic periodic paralysis has now been well characterized in the literature: it occurs primarily in Orientals with an overwhelming male preponderance and a higher association of specific HLA antigens. Clinical manifestations include onset after high carbohydrate ingestion or heavy exertion, with progressive symmetric weakness leading to flaccid paralysis of the extremities and other muscle groups, lasting several hours. If hypokalemia is present, potassium administration may help abort the attack. Although propranolol can be efficacious in preventing further episodes, the only definitive treatment is establishing a euthyroid state. The pathophysiology is still controversial, but reflects altered potassium and calcium dynamics as well as certain morphologic characteristics within the muscle unit itself.

A propos d'un cas de paralysie periodique thyrotoxique (PPT): etude electromyographique (EMG)

The authors report on a case of thyrotoxic periodic paralysis characterized by attacks of flaccid tetraplegia with hypokalemia in a patient with Basedow disease, the cure of which led to the disappearance of the neurological symptomatology. The EMG investigations, performed in the course of a spontaneous paralytic attack, showed the same abnormalities as in the few similar published cases: discordance between the rich interferential recordings and the weakness of the movements; low amplitude of the electrodetection tracings; reduced amplitude of the evoked muscle action potentials on nerve stimulation. These myogenic patterns are related to the aspect of the muscle biopsy which, when performed during the paralytic phase, shows a vacuolization of the muscular fibers. The pathophysiological underlying mechanisms of the thyrotoxic periodic paralysis still remain hypothetic.

Studies in thyrotoxic periodic paralysis

A new case of thyrotoxic periodic paralysis (TPP) is described. Prior to treatment by subtotal thyroidectomy, paralysis was induced by a variety of measures which acutely decreased the serum potassium concentration. The magnitude of the potassium ion shifts was not consistent with the degree of clinical paralysis, nor did the serum potassium concentrations rise as the clinical attacks cleared. Hypokalemia was not, therefore, the sole cause of paralysis. Aldosterone excretion seemed to be normal. EMG studies revealed that the paralytic attacks were caused by an acute myopathy, and the muscle biopsy showed a prominent vacuolar myopathy during paralysis. The vacuoles developed from the sarcoplasmic reticulum (SR) and were absent or much less notable between attacks. Glycogen masses, degenerative changes and other microscopic findings seem to be secondary phenomena; some degree of vacuolization is the only consistent histologic finding in all cases studied thus far. A small but significant increase of the muscle water content in an affected muscle was found in the present case during induced paralysis. Although it is tempting to attribute paralysis to SR distension by fluid, this mechanism of paralysis in TPP is unproven and may also be a secondary phenomenon. The EMG studies indicated a depression of sarcolemmal excitability during paralysis, which should be investigated when possible in the future by means of microelectrode recording of the muscle membrane potential. A systemic factor appears to trigger paralysis in TPP. The only endocrine abnormality is hyperthyroidism and the attacks recur after thyroid treatment if an excess of hormone is administered. The level of circulating hormone should be studied in future cases in relationship to spontaneous and induced paralytic attacks.