Gitelman's syndrome with silent thyroiditis.

Hypokalemic periodic paralysis is one of the most distinctive complications of hyperthyroidism and occurs in 8 to 34% of men and 0.2% of women with thyrotoxicosis in Asia. It is also complicated by other diseases with potassium defi ciency such as Bartter’s syndrome, Cushing’s syndrome, and Gitelman’s syndrome. Generally, hypokalemic periodic paralysis with hyperthyroidism is diagnosed by assessing thyroid function and observing clinical manifestations of thyrotoxicosis. A 34-year-old woman was admitted to a local hospital because of acute hypokalemic paralysis. She had never suffered from muscle weakness or paralysis before, and there was no family history of periodic paralysis or thyroid disease as far as she knew. Although diagnosed with Basedow’s disease because of her diffuse goiter and undetectable thyroid stimulating hormone (TSH) level, she was prescribed potassium orally without any treatment for the disease. After 3 months, she was admitted to our hospital for sustained hypokalemia and muscle weakness. The patient experienced no hypertension or weight loss during her illness. On physical examination, she had a hard diffuse goiter of the thyroid gland without any other symptom or sign of thyroid illness. She exhibited both hypokalemia (serum potassium level, 2.9 mEq/l; normal range, 3.6–5.0 mEq/l) and hypomagnesaemia (serum magnesium level, 1.6 mg/dl; normal range 1.9–2.5 mg/dl); but she had no chronic dermatitis characterized by thickening with a purple-red hue often associated with chronic hypomagnesaemia. Urinary excretion of potassium was 30 mEq/day, and urinary Na/K ratio was 5.25. The level of urinary calcium excretion was low (0.024 g/g creatinine). Arterial pH was 7.469 and base excess was 4 mmol/l, suggesting metabolic alkalosis. Her plasma renin level was high (75.2 pg/ml; normal range 3.22–36.3 pg/ml), while her plasma aldosterone level was normal (65.8 pg/ml; 35.7-240 pg/ml), as were her adrenocorticotropic hormone and cortisol levels. A computed tomography study of the abdomen showed no evidence of adrenal tumor. In order to demonstrate the lack of a response of renal thiazide-sensitive Na-Cl cotransporter to thiazide, we examined the effect of the administration of 8 mg trichlormethiazide on chloride clearance (C Cl = urinary chloride concentration × urine volume per min / serum chloride concentration). We found that chloride clearance was unchanged after thiazide administration (before, 1.30 ml/min; after 1.42 ml/min). On admission to our hospital, her TSH level was high (17.8 μU/ml; normal range, 0.56–3.91 μU/ml) with normal free triiodothyronine and free thyroxine levels. Anti-TSH receptor and anti-thyroid peroxidase antibodies were negative, but anti-thyroglobulin antibody was positive. An ultrasonographic study of the thyroid gland showed diffuse thyroid swelling with very low echogenecity. She was diagnosed as Gitelman’s syndrome with silent thyroiditis,