AOL BES 3-1772 DiS Caetston OF FF a Conmterd. ~795. 077 Medical Research Center Brookhaven ; National Reprinted from REPOSITORY THE JOURNAL OF CLINICAL ENDOCRINOLOGY AND Labo owtery7, No. 12, December, 1907, Upton, L. L, New York Lv L Kec GR DS SLiEayggaowbolt slang Printed in the US -bes oy No. MENS — Two Panel Discussions on HyperthyroidismER Ie p) ' fice NOY Em. i Sidney C. Werner, Moderator - II. Etiology and Treatmentof Hyperthyroidism in the Adult antithyroid medication and finally arrived at the hospital hyperthyroid and with evident joint involvement. DR. SIDNEY C. WERNER, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, Moderator: The second panel on hyperthyroidism is composed of the following members: Doctors Robert Conard, Carl R. Feind, Ernest Gould, David Hsia, Sidney H. Ingbar, Joseph P. Kriss, Stuart Lindsay, Farahe Maloof, J. Maxwell McKenzie, Louis Sokoloff and Kenneth Sterling. Following the pattern of the first panel (1), we shall present a patient. But the subsequent discussion will open with two ifferent problems: 1) the mechanism of ics of thyroid hormone, and 2) the etiology of toxic diffuse goiter. The patient was a 16}-year-old girl who arrived at the hospital with obvious hyperthyroidism of three years’ duration. She also had had joint pains and fever for these three years. The hyperthyroidism had been moreorless controlled with methimazole or with propylthiouracil given by various physicians. There were persistent efforts to make the diagnosis of rheumatic disease or of disseminated lupus erythematosus, but a numberof rheumatologists could find no tangible evidence of either. She had had a sore throat a few months before admission and received penicillin. After this, her joints had a flare-up of activity. She was irregular in taking her Received April 7, 1967; accepted August 2. 1 Sponsored by The American Thyroid Associa- tion, Inc., as part of the annual program, October 13, 1966, Chicago,Il. * Address reprint requests to Dr. Sidney C. Werner, Department of Medicine, Columbia Uni- versity College of Physicians and Surgeons, 630 West 168th Street, New York, N. Y. 10032. >The first of these two articles appeared in the Jovember 1967 issue of The Journal of Clinical Endocrinology and Metabolism. IO 5094 For the month prior to admission, her joint involvement had become worse; she had developed periumbilical pain associated with periods of fever to 103 F, A 24 hour radioactive iodine uptake three days after stopping the small amountof propylthiouracil she was taking was 75%. The admission findings were as follows: She was evidently hyperthyroid, looked sick, but had no eye signs. The joints, as well as the other systems, were negative to physical examination, except for a moderate-sized rather soft diffuse goiter with a bruit. She had a fever, 103 F. In the laboratory, 24 hour '!*'I uptake was 55%, PBI 9 uwg/100 ml. The erythrocyte sedimentation rate was 48 mm at one hour; a disseminated lupus erythematosus preparation was negative; and the antistreptolysin titer was negative. It was concluded that she had toxic diffuse goiter; and since the usual surveys for connective tissue or rheumatic disease were essentially negative, it was considered likely that the articular and other manifestations were due to a reaction to antithyroid drugs. This view was probably correct, inasmuch as she became well when propylthiouracil therapy was terminated. The arthralgia and fever subsided. At this point, it seemed reasonable to administer sodium iodide in preparation for surgery. Since she was 163 years old, 18\T therapy was eliminated from consideration. Sodium iodide was started, 0.1 g daily. However, within 24 hours, she developed a fever of 102 F, her joints became red and swollen, and she developed a vesicular 1763 LT