Acute Colonic Pseudoobstruction: An Unusual Presentation of Thyrotoxic Periodic Paralysis

To the Editor: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder seen primarily in young Asian men. It is related to hypokalemia caused by hyperstimulation of the sodium/potassium pump by excess circulating thyroid hormone. The most classical presentation of TPP is an acute episode of proximal muscle weakness, but dysrhythmias, ventilatory failure, and death have been reported.1 We describe the case of an 81-year-old man with acute colonic pseudoobstruction due to hypokalemia related to thyrotoxicosis. This 81-year-old man presented in January 2004 at the emergency department for a first episode of acute abdominal distension. He had been hospitalized 8 years earlier for a myocardial infarction and atrial fibrillation. He lived at home with his wife. His treatment included aspirin (75 mg/d), an angiotensin-converting enzyme inhibitor, and digoxin. Initial electrolyte analysis showed severe hypokalemia, at 2.0 mmol/L. Natremia, urea nitrogen, and creatinemia were in the normal range. The electrocardiogram showed atrial fibrillation, with a ventricular rate of 92 beats per minute. A plain abdominal ray showed a gaseous distension of the right colon and of the rectum without sigmoid volvulus or fecal impaction. The diagnosis of acute colonic pseudoobstruction was made, and a colonoscopic exsufflation was performed. Kaliuresis was low (18 mmol/L). The patient was given 40 mEq potassium chloride intravenously. Because of the atrial fibrillation, thyroid function tests were performed, which showed latent hyperthyroidism with low thyroid-stimulating hormone (0.015 mUI/mL (normal range 0–15.4)) and normal peripheral hormones (T4, 19.4 pmol/L (normal range 10–25); T3, 5.23 pmol/L (normal range 4.5–9.2)). Clinically, the thyroid was normal. A second exsufflation was performed the day after admission. Kalemia was measured at 2.9 mm/L. The patient was given potassium supplementation orally (20 mEq/d). He was discharged on the tenth day. Kaliemia was 3.9 mmol/L. The abdomen was normal. A beta-blocker was added to his treatment because of the history of myocardial infarction, and potassium supplementation was stopped. The patient was rehospitalized 3 months later, in April 2004, with the same presentation: acute colonic pseudoobstruction and hypokalemia (1.9 mmol/L) with a low kaliuresis (11 mmol/L). Potassium supplementation was given intravenously initially and then orally. Two colonic exsufflations were necessary. The patient was discharged 10 days after admission. Kalemia was measured at 4.9 mmol/L. A third attack of acute colonic pseudoobstruction occurred 1.5 months later, in May 2004. Kalemia was measured at 2.5 mmol/L. The hypothesis of a relationship between hypokalemia and hyperthyroidism was formulated. Thyroid-stimulating hormone was undetectable (0.005 mUI/L (normal range 0.15–4), and free T4 was elevated (33 pmol/L (normal range 10–25)). Treatment with NeoMercazole (40 mg/d) was initiated. Radioactive iodine uptake was 30% at 4 hours, and the patient was treated with 7 milli Curie of 131 Iodine at the beginning of June 2004. Three months later, kalemia remained in the normal range, no colonic pseudoobstruction occurred, and thyroid function had normalized. This observation of TPP is unusual in two aspects: the age of the patient and the type of paralysis. TPP usually occurs in young Asian men. To our knowledge, it has never been described in an elderly person. The most frequent clinical presentation is recurrent attacks of flaccid weakness, predominantly involving the lower limbs. Bulbar, ocular, cardiac, and respiratory muscles are rarely involved. Smooth-muscle paralysis has never been described. The cardinal biochemical abnormality during an attack is hypokalemia, which is the result of an intracellular shift of potassium, the total body potassium store being normal.2 The relationship between thyrotoxicosis and hypokalemia is based on the fact that thyroid hormone has been shown to increase sodium/potassium ATPase activity in skeletal muscle, the liver, and the kidneys, resulting in increased intracellular transport of potassium in the setting of hyperthyroidism, but the pathogenic mechanisms of TPP are not totally explained. A defect in the neuromuscular junction, classically suggested, may explain the colonic paralysis observed.3 As in classical TPP, recurrent attacks of colonic pseudoobstruction occurred until correction of the hyperthyroid status. Hyperthyroidism must be excluded in older people who present with a hypokalemic colonic pseudoobstruction. Neither author had any financial support or sponsor. They both contributed to the diagnosis and to the writing of this letter.