methimazole and Hypokalemic-Periodic-Paralysis

Topics: Adrenergic beta-Antagonists; Adult; Antithyroid Agents; Humans; Hypokalemic Periodic Paralysis; Male; Methimazole; Potassium Chloride; Propranolol; Thyrotoxicosis

Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with recurrent episodes of muscle weakness and hypokalaemia due to hyperthyroidism. Diagnosis is often delayed or misdiagnosed due to its rarity in the western world and subtle features of hyperthyroidism on initial presentation. Here we present the case of a 25-year-old man who presented to the emergency department (ED) with sudden onset weakness of bilateral upper and lower extremities. His labs revealed hypokalaemia with elevated T4 and suppressed thyroid-stimulating hormone and he was diagnosed with thyrotoxic periodic paralysis. He was treated with potassium repletion, atenolol and methimazole with complete reversal of his paralysis within the next day. Unfortunately, he failed to keep the follow-up appointment after discharge, ran out of his methimazole and landed up in the ED again.

Topics: Adrenergic beta-1 Receptor Antagonists; Adult; Antithyroid Agents; Atenolol; Humans; Hypokalemia; Hypokalemic Periodic Paralysis; Male; Methimazole; Potassium; Thyrotoxicosis; Thyrotropin; Thyroxine

Topics: Adult; Anti-Arrhythmia Agents; Antithyroid Agents; Humans; Hypokalemic Periodic Paralysis; Male; Methimazole; Metoprolol; Muscle Strength; Potassium; Tachycardia, Sinus; Thyroid Gland; Thyroid Hormones; Thyrotoxicosis; Treatment Outcome; Ultrasonography

Topics: Adult; Antithyroid Agents; Biomarkers; Electrocardiography; Graves Disease; Humans; Hypokalemic Periodic Paralysis; Male; Methimazole; Potassium Chloride; Thyrotoxicosis; Treatment Outcome; Turkey

A 26-year-old Hispanic man with no significant medical history presented to our emergency room with gradual onset weakness of his lower extremities. He was haemodynamically stable and examination revealed loss of motor function in his lower limbs up to the level of hips. Laboratory data revealed hypokalaemia. The patient was started on potassium supplementation and he recovered his muscle strength. Differential diagnosis included familial hypokalaemic periodic paralysis and thyrotoxic periodic paralysis (TPP). Further investigations revealed a low thyroid-stimulating hormone and high free thyroxine levels. Radio iodine 123 scan revealed an enhanced homogeneous uptake in the thyroid suggesting Graves' disease. Thyroid stimulating antibodies were also found to be elevated. The patient was started on methimazole and propranolol and he never had another attack of TPP even at 1 year follow-up.

Topics: Adult; Diagnosis, Differential; Graves Disease; Hispanic or Latino; Humans; Hypokalemia; Hypokalemic Periodic Paralysis; Immunoglobulins, Thyroid-Stimulating; Iodine Radioisotopes; Male; Methimazole; Muscle Strength; Muscle Weakness; Potassium; Propranolol; Thyroid Gland; Thyrotoxicosis; Thyrotropin; Thyroxine

Topics: Graves Disease; Humans; Hypokalemic Periodic Paralysis; Intracellular Fluid; Ion Transport; Male; Methimazole; Middle Aged; Potassium; Radionuclide Imaging; Recurrence; Thyrotoxicosis

Acute bilateral lower extremity paralysis is a medical emergency frequently caused by spinal cord pathology. A few systemic diseases including metabolic and endocrine abnormalities, however, can also present with lower extremity paralysis. In such cases, an abnormal electrocardiogram can immediately point to a likely systemic etiology. In this report, we present 2 patients with a near carbon-copy presentation where previously healthy Hispanic men woke up in the morning not being able to get out of bed because of severe lower extremity weakness. In both cases, abnormal electrocardiograms on presentation pointed to the most likely diagnosis, which was quickly confirmed by simple laboratory testing. The appropriate evaluation and management of such patients are discussed.

Topics: Adrenergic beta-Antagonists; Adult; Antithyroid Agents; Diagnosis, Differential; Electrocardiography; Humans; Hypokalemic Periodic Paralysis; Lower Extremity; Male; Methimazole; Potassium; Propranolol

11β hydroxylase deficiency (OHD) is one of the main causes of congenital adrenal hyperplasia. There have been only a few reported cases of nonclassic 11β OHD, a milder form of the disease. It is difficult to detect occult nonclassic 11β OHD because patients present with no or mild symptoms. We herein present a case of thyrotoxic periodic paralysis (TPP) with Graves' disease leading to the discovery of a hidden nonclassic 11β OHD. In this case, increased levels of thyroid hormone seem to have induced symptoms of occult nonclassic 11β OHD and aggravated TPP.

Topics: Adrenal Hyperplasia, Congenital; Diagnosis, Differential; Drug Therapy, Combination; Graves Disease; Humans; Hypokalemic Periodic Paralysis; Male; Methimazole; Mutation; Polymerase Chain Reaction; Polymorphism, Genetic; Potassium; Propranolol; Risk Assessment; Severity of Illness Index; Steroid 11-beta-Hydroxylase; Thyrotoxicosis; Tomography, X-Ray Computed; Treatment Outcome; Young Adult

Periodic paralysis in the setting of hypokalemia can be the result of several underlying conditions, requiring systematic evaluation. Thyrotoxic periodic paralysis (TPP), a curable cause of hypokalemic periodic paralysis, can often be the first manifestation of thyrotoxicosis. Because the signs and symptoms of thyrotoxicosis can be subtle and clouded by the clinical distress of the patient, the diagnosis of the underlying metabolic disorder can be overlooked. The authors report a case of TPP in a young Chinese man in whom the diagnosis of thyrotoxicosis was initially missed. This case illustrates the lack of awareness of TPP among many physicians, delay in the diagnosis of TPP and the importance of performing thyroid function testing in all cases of periodic paralysis.

Topics: Antithyroid Agents; Delayed Diagnosis; Diagnosis, Differential; Humans; Hypokalemic Periodic Paralysis; Male; Methimazole; Thyrotoxicosis; Young Adult

Thyrotoxic periodic paralysis (TPP) is an uncommon but potentially lethal manifestation of hyperthyroidism characterized by muscle paralysis and hypokalemia. We have reported 3 cases of TPP in male patients, which manifested with morning muscle weakness evolved into paralysis. In all patients were found severe hypokalemia, abnormalities on electrocardiogram, and Graves' hyperthyroidism. Intravenous potassium administration led to normalization of potassium levels, and resolution of neurological symptoms. In addition, beta blockers and methimazole were started. Two patients required total thyroidectomy for poor control of hyperthyroidism with antithyroid drug. In patients presenting with periodic paralysis or diffuse muscle weakness thyroid function should be investigated in order to find out the cases secondary to unknown hyperthyroidism and to start an early appropriate combined therapy. The correct management of TPP can prevent serious cardiopulmonary complications.

Topics: Adrenergic beta-Antagonists; Adult; Antithyroid Agents; Drug Therapy, Combination; Electrocardiography; Graves Disease; Humans; Hypokalemic Periodic Paralysis; Injections, Intravenous; Male; Methimazole; Potassium; Thyroidectomy; Treatment Outcome

Topics: Adult; Anti-Arrhythmia Agents; Antithyroid Agents; Anxiety; Arrhythmias, Cardiac; Dyspnea; Graves Disease; Humans; Hypokalemic Periodic Paralysis; Malaysia; Male; Methimazole; Muscle Weakness; Neurologic Examination; Potassium; Propranolol; Propylthiouracil; Sleep Initiation and Maintenance Disorders; Tremor; Weight Loss

Topics: Adult; Antihypertensive Agents; Antithyroid Agents; Emergencies; Follow-Up Studies; Genetic Predisposition to Disease; Graves Disease; Humans; Hypokalemic Periodic Paralysis; Jews; Male; Methimazole; Potassium; Prevalence; Propranolol; Recurrence; Thyrotoxicosis; Time Factors; Treatment Outcome

Thyrotoxic hypokalemic periodic paralysis (THPP) is a very rare complication of thyrotoxicosis in whites, but is more frequently reported in individuals of Asian descent. Hypokalemia, with associated flaccid paralysis, and signs of hyperthyroidism, are the hallmark. We have reported a case of a 28-yr-old white man with Graves' disease presenting with a 2-wk history of episodic flaccid quadriplegia. Physical examination disclosed a resting tachycardia and symmetrical, proximal weakness involving both arms and legs. Electrocardiogram and electrolyte analysis showed a severe hypokalemia, and thyroid function tests revealed hyperthyroidism. The patient was diagnosed as having Graves' hyperthyroidism and THPP. Paralysis resolved with potassium supplements. He was treated with propranolol and, subsequently, methimazole. He had no further episodes of hypokalemic paralysis. To the best of the author's knowledge, and after a Medline search, THPP has not been described previously in a Turkish man.

Topics: Adult; Antithyroid Agents; Electrocardiography; Graves Disease; Humans; Hypokalemia; Hypokalemic Periodic Paralysis; Male; Methimazole; Potassium Chloride; Thyrotoxicosis; Water-Electrolyte Balance

Hypokalemic Periodic Paralyses comprise diverse diseases characterized by acute and reversible attacks of severe muscle weakness, associated with low serum potassium. The most common causes are Familial Hypokalemic Periodic Paralysis (FHypoKPP), an autosomal dominant disease, and Thyrotoxic Hypokalemic Periodic Paralysis (THypoKPP), secondary to thyrotoxicosis. Symptoms of paralysis are similar in both diseases, distinguished by thyrotoxicosis present in THypoKPP. FHypoKPP is caused by mutations in ionic channel genes calcium (CACN1AS), sodium (SCN4A) and potassium (KCNE3). Since both diseases are similar, we tested the hypothesis that THypoKPP could carry the same mutations described in FHypoKPP, being the paralysis a genetically conditioned complication of thyrotoxicosis. In 15 patients with THypoKPP, using target-exon PCR, CSGE screening, and direct sequencing, we excluded known mutations in CACN1AS and SCN4A genes. On the other hand, we were able to identify the R83H mutation in the KCNE3 gene in one sporadic case of THypoKPP, a man who had been asymptomatic until developing thyrotoxicosis caused by Graves' disease; we confirmed the disease-causing mutation in 2 of 3 descendants. R83H was recently found in two FHypoKPP unrelated families, in which the mutant decreased outward potassium flux, resulting in a more positive resting membrane potential. We, therefore, identified the first genetic defect in THypoKPP, a mutation in the KCNE3 gene.

Topics: Adult; Antithyroid Agents; Genetic Predisposition to Disease; Humans; Hypokalemic Periodic Paralysis; Iodine Radioisotopes; Male; Membrane Potentials; Methimazole; Mutation; Pedigree; Polymerase Chain Reaction; Potassium Channels; Potassium Channels, Voltage-Gated; Potassium Chloride; Thyrotoxicosis