A 66-year-old man developed a fever and had a syncopal attack during treatment with imipramine and amantadine for depression and Parkinson's disease. His muscular enzyme levels were very high, so he was diagnosed with incomplete syndrome malin and given hydration therapy. The electrocardiogram recorded an ST segment elevation like acute myocardial infarction in most leads, and the echocardiogram revealed left ventricular dysfunction with severe hypokinesis to dyskinesis of the anterior and apical wall regions, and hyperkinesis of the basal wall. One month from onset, the left ventricular contractility had not changed despite normal coronary arteries. Thallium-201((201)Tl) myocardial scintigraphy showed a perfusion defect and there was no accumulation of iodine-123((123)I) metaiodobenzylguanidine (MIBG) in the entire apex of the heart. Left ventricular function returned to normal and repeat (201)Tl scintigraphy showed recovery by the 4th month. However, there was still an absence of cardiac MIBG uptake. There are a number of reports from Japan of a syndrome demonstrating such reversible left ventricular dysfunction, called 'tako-tsubo cardiomyopathy', but the present case is the first to be associated with syndrome malin. A coronary microvascular abnormality and cardiac sympathetic denervation probably both play an important role in tako-tsubo cardiomyopathy.

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Thyroglobulin (Tg) can be detected in the circulation of normal subjects. Serum Tg is increased in patients with various thyroidal disorders including Graves' disease; however, little is known about Tg metabolism. Therefore, a kinetic study of human Tg was carried out in 13 normal men, 19-28 yr old, and 6 untreated hyperthyroid patients with Graves' disease, 3 men (22 to 25 yr old), and 3 women (21 to 63 yr old). Ten milligrams of Tg were injected as a bolus dose. Blood samples were collected before and 10 min, and 2, 4, 6, 8, 12 h and every 12 h up to 72 h after injection. Concentrations of serum Tg were measured by an RIA method developed in our laboratory. Anti-Tg antibody was not detected in any subject. Various indices of this kinetic study were calculated using single compartmental analysis. In 13 normal subjects, the mean serum concentrations of Tg were 17 +/- 12.6 (SD) ng/ml; mean half-life was 29.6 +/- 2.8 h; distribution volume was 11,210 +/- 3,076 ml/60 kg body weight; fractional decay was 2.40 +/- 0.22%/h; MCR was 268.9 +/- 87.8 ml/h X 60 kg; and release rate was 100.3 +/- 50.2 micrograms/day X 60 kg. Serum concentrations of Tg were increased in four of the six untreated hyperthyroid patients with Graves' disease. Their Tg half-lives and MCR were within the normal range. In the two patients who had normal serum concentrations of Tg, the Tg half-lives were shorter and MCR were greater than in normal subjects. The release rates of Tg were increased in all six of these patients. In summary, in hyperthyroid patients, Tg release is significantly greater than normal, whereas Tg metabolism is similar to that in normal subjects.