Graves’ disease combined with acute myocarditis and thyrotoxic periodic paralysis in a male:a case report and review of the literature

Graves’ disease is the most common reason for hyperthyroidism which manifest as multi-system changes.Among these clinical manifestations acute myocarditis and thyrotoxic periodic paralysis are very rare and patients who are combined with both two haven’t been reported yet.The etiology may attribute to autoimmunity.

DECREMENTAL RESPONSE ON PROLONGED EXERCISE TEST IN A PATIENT WITH THYROTOXIC PERIODIC PARALYSIS

Paralysis of acute onset often presents a diagnostic challenge for the assessing physician because of a large number of differential diagnosis and overlap of clinical features among them. Thyrotoxic periodic paralysis is an uncommon cause of acute weakness. In addition to serological tests, electromyography findings during prolonged exercise test are very helpful in confirming the diagnosis. Only a few case reports of thyrotoxic periodic paralysis have been published from Middle East and none of them have described this specific electrophysiological data. A man in his 20s presented to us with acute onset weakness in both legs which was evaluated further and found to have hypokalemia. The work up for the etiology revealed thyrotoxic status and a final diagnosis of thyrotoxic periodic paralysis was established. The prolonged exercise test performed in this patient showed typical progressive decremental respsonse with nadir at 40 minutes after the exercise.

Upper extremity deep venous thrombosis secondary to thyrotoxic periodic paralysis with accompanying hyperphosphatemia and severe hypomagnesemia

Thyrotoxic periodic paralysis is a rare but life-threatening complication of hyperthyroidism. Characteristic features involve thyrotoxicosis, acute paralysis, and hypokalemia. Mild hypomagnesemia and hypophosphatemia are also present in most cases due to the resulting transcellular shift of electrolytes. Complications of thyrotoxic periodic paralysis reported in the literature have included cerebral venous thrombosis as well as lower extremity deep venous thrombosis. We present a patient with an unusual presentation of thyrotoxic periodic paralysis as reflected by hyperphosphatemia, upper extremity deep venous thrombosis and severe hypomagnesemia. This is the first reported case of upper extremity deep vein thrombosis in association with a peripherally inserted central catheter line secondary to thyrotoxicosis.

Making weight: acute muscle weakness and hypokalaemia exacerbated by thyrotoxicosis factitia in a bodybuilder

Summary A 32-year-old Caucasian male presented to the emergency department with a one-day history of acute severe bilateral lower limb weakness, three days after competing in a bodybuilding competition. He consumed large quantities of carbohydrate-rich foods following the competition. His past medical history was significant for anxiety, and family history was non-contributory. Examination was normal except for reduced power and hyporeflexia in both legs, despite his muscular physique. He was noted to have severe hypokalaemia (K+= 1.9 mmol/L). His thyroid function tests were consistent with thyrotoxicosis. He reported taking thyroxine and several other agents to facilitate muscle mass generation before the bodybuilding competition. His presentation was reminiscent of thyrotoxic periodic paralysis, albeit uncommon with Caucasian ethnicity. He also had transient hyperglycaemia at presentation with concomitant hyperinsulinaemia, which could be attributed to the carbohydrate load and may have exacerbated his hypokalaemia through a transcellular shift. Urine toxicology screen subsequently ruled out the use of diuretics but confirmed the presence of a long-acting beta agonist (clenbuterol) which, along with other substances, may have aggravated the hypokalaemia further. After 12 h of i.v. replacement, the potassium level normalised and leg weakness resolved. The patient agreed to stop taking thyroxine and beta agonists and was well during the clinic visit at one month follow-up. This case highlights the potential for thyrotoxicosis factitia to exacerbate hypokalaemia and muscle weakness from other causes in bodybuilders presenting with acute severe weakness, irrespective of ethnicity. Learning points In patients presenting with muscle weakness and hypokalaemia, early consideration of thyrotoxicosis is essential, even in the absence of a past history of thyroid disease or specific symptoms of thyrotoxicosis, in order to allow prompt initiation of appropriate treatment and to prevent recurrence. Bodybuilders may constitute a uniquely ‘at-risk’ group for thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia, especially where there is concomitant use of beta-adrenergic agonists, even in the absence of diuretic use. Although rare and usually described in patients of Asian or Polynesian ethnicity, this case highlights that thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia can also occur in patients with Caucasian ethnicity. We speculate that consuming large quantities of carbohydrates may induce hyperinsulinaemia, which could theoretically contribute to worse hypokalaemia, though mechanistic studies would be needed to explore this further.