A case of type 2 diabetes manifested by hypokalemic periodic paralysis

Hypokalemic periodic paralysis may be precipitated by stress, rest after exercise, or events that lower serum potassium levels, such as carbohydrate ingestion or the use of insulin or diuretics. In healthy subjects, insulin activates ATPase, which elicits potassium influx and transient hypokalemia;however, hypokalemia is compensated by ATP channel activation. Recently, we encountered a 49-year-old male patient with type 2 diabetes mellitus and hyperinsulinemic hypokalemic periodic paralysis. The patient had no family history of muscle weakness or diabetes mellitus. At the time of the attack, plasma glucose was 142.4 mg/dL, plasma insulin was 116.86 IU/mL, serum potassium was 2.08 mEq/L, and thyroid hormone, renin, aldosterone, ACTH, and cortisol levels were normal. Symptoms improved rapidly upon potassium replacement. Oral glucose tolerance testing revealed high glucose and insulin levels at 2 h, and serum potassium and phosphate levels decreased from 5.1 to 4 mEq/L and 3.6 to 2.0 mg/dL, respectively.