Within a few hours of this treatment, the patient experienced significant improvement in muscle strength and complete resolution of weakness in his arms and legs. Serial measurements of potassium levels normalized.
Further workup revealed that the patient’s thyroid-stimulating immunoglobulin (TSI) was 4.2 on the TSI index (normal, ≤ 1.3) and his thyroid peroxidase (TPO) antibody level was 133.4 IU/mL (normal, < 34 IU/mL). Ultrasonography showed decreased echogenicity of the thyroid gland, consistent with the acute phase of Hashimoto thyroiditis or Graves disease.
The patient was unaware that he had any thyroid disorder previously. He was a private-pay, undocumented immigrant and did not have a regular primary care physician. On discharge, he was referred to a local primary care physician as well as an endocrinologist. He was discharged on atenolol and methimazole.
DISCUSSION
A rare neuromuscular disorder known as periodic paralysis can be precipitated by a hypokalemic or hyperkalemic state; HPP is more common and can be either familial (a defect in the gene) or acquired (secondary to thyrotoxicosis; TPP).1,2 In both forms of periodic paralysis, patients present with hypokalemia and paralysis. Physicians need to look closely at thyroid lab test results so as not to miss the cause of the paralysis.
TPP is most commonly seen in Asian populations, and 95% of cases reported occur in males, despite the higher incidence of hyperthyroidism in females.3 TPP can be precipitated by emotional stress, steroid use, beta-adrenergic bronchodilators, heavy exercise, fasting, or high-carbohydrate meals.2-4 In our patient, heavy exercise and fasting likely were the triggers.
Continue to: The pathophysiology for the hypokalemia...