We present two cases of Graves' disease whose initial thyroidal scintiscan with 99mTcO4- (Case 1) and 123I (Case 2) showed unilateral diffuse uptake of radioisotopes. Initial diagnosis was possibility of malignancy in Case 1 and Graves' disease or Plummer's disease in Case 2. Both cases underwent right hemithyroidectomy. Histopathology of the resected thyroid gland in both showed hyperplastic columnar epithelium and infiltrative lymphocytes which was compatible with Graves' disease. Twenty seven (Case 1) and eight months (Case 2) after operation, both presented with thyrotoxic symptoms associated with enlarged left lobe, increased serum free thyroid hormone concentrations, suppressed TSH concentration, increased thyroidal 123I uptake in the remaining left lobe, and positive thyrotropin receptor antibodies. Both cases were successfully treated with methimazole. It was concluded that initial radioisotope uptake as well as scintigram in rare subgroup of patients with Graves' disease could be similar with that of non-autoimmune autonomous goiter (Plummer's disease).

A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. Diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range.

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The authors aimed at developing a simplified method for the measurement of plasma free (unbound) steroids with ultrafiltration using Grace MPS device, and its clinical application. In this method, the movement of free steroids from plasma into ultrafiltrate was monitored with [14C]glucose added to the plasma. Plasma free steroids (cortisol, testosterone, estradiol and prednisolone) were measured as follows: Plasma was incubated with [14C]glucose (1.2 X 10(4) dpm/5 microliters) for 30 min at 37 degrees C. A 0.5 ml of aliquot was transferred to MPS device containing a single YMT membrane, and centrifuged at 1100 x g, at 37 degrees C, for 30 min in a 45 degree fixed angle head with the special temperature controller. After centrifugation, [14C] in 30 microliters of plasma and ultrafiltrate were counted. For the calculation of plasma free level, steroid concentration of ultrafiltrate measured directly by radioimmunoassay (RIA) was multiplied by the ratio of [14C]glucose (dpm) in plasma to [14C]glucose (dpm) in ultrafiltrate. For RIA of cortisol, testosterone and estradiol, commercially available kits were used, and for prednisolone, anti-prednisolone antibody developed in our laboratory was utilized. Since plasma free cortisol level showed a parallel increase with rise in temperature, strict temperature control during ultracentrifugation was required. On the other hand, the duration of centrifugation and the sample volume applied to MPS did not show any significant effect on the estimated values. Intraassay and interassay variations were 4.4% and 6.1% in free cortisol, 6.3% and 8.7% in free testosterone, 8.5% and 9.2% in free estradiol, and 8.8% and 9.9% in free prednisolone, respectively. The correlations between the plasma free steroid levels obtained by ultrafiltration (y) and equilibrium dialysis (x) were as follows, respectively: free cortisol; y = 1.16x + 0.017 (r = 0.95, n = 10), free testosterone; y = 1.17x-0.027 (r = 0.92, n = 10), free estradiol; y = 1.33x + 8.55 (r = 0.98, n = 12), free prednisolone; y = 1.03x + 1.00 (r = 0.98, n = 7). The mean plasma free cortisol levels and percent free fractions (%FF) were 1.16 +/- 0.40 (+/- SD) micrograms/dl and 10.9 +/- 3.0% in 10 control patients, 4.4 +/- 1.6 micrograms/dl and 15.6 +/- 3.3% in 8 patients with Cushing's syndrome, and 1.45 +/- 0.48 micrograms/dl and 5.9 +/- 2.4% in 11 normal pregnant women (10-40 weeks of pregnancy), respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

A rare occurrence of the association of parathyroid adenoma in a case of thyroid papillary carcinoma is described. The patient was incidentally found to have parathyroid adenoma which was preoperatively diagnosed to be a metastatic lymph node. Analysis of her serum obtained before operation showed an elevation of serum parathyroid hormone (PTH) concentration without hypercalcemia. Since the association of hyperparathyroidism is high in patients with thyroid diseases, examination of not only serum levels of calcium and PTH but also careful interpretation of computed tomography (CT) and/or nuclear magnetic imaging (MRI) is necessary in the diagnosis of co-existing asymptomatic hyperparathyroidism. (Internal Medicine 31: 459-462, 1992) Key words: serum PTH, normal serum calcium, computed tomography (CT), nuclear magnetic imaging (MRI) Intr oductionIt has been reported that thyroid disease is common in patients with hyperparathyroidism, and vice versa (1). Parathyroid adenoma is clinically recognized in patients presenting with either hypercalcemia or it may be a part of multiple endocrine neoplasia (MEN) type I and type Ha (2). There have also been sporadic reports of the coexistence of hyperparathyroidism and nonmedullary thyroid carcinoma (3-8). Thus, the presence of hyper parathyroidism has to be kept in mind in patients with thyroid carcinoma. In such cases, hypercalcemia is a virtually inevitable laboratory finding and therefore, is an important laboratory finding in the diagnosis of hyperparathyroidism. Except for such conditions, it is very rare to find parathyroid adenoma. We have recently encountered a case of nonmedullary thyroid carcinoma (papillary carcinoma) associated with parathyroid adenoma which was initially diagnosed to be a metastatic lymph node of thyroid malignancy. She had neither radiologic abnormalities such as subperi osteal bone resorption nor symptoms associated with hyperparathyroidism. Since the elevated concentration of PTH normalized after operation, we speculate that the patient had asymptomatic hyperparathyroidism, namely parathyroid adenoma with the preclinical stage of hyperparathyroidism. Materials and MethodsSerum concentrations of free T3 (FT3) and free T4 (FT4) were measured by analog method radioimmuno assay (RIA) kits (Amerlex FT3 and FT4, Amersham International, Tokyo,.7pg/ml and 0.80-2.10ng/dl, respectively. Serum TSH levels were measured by an immunoradiometric assay (IRMA) kit (Spac TSH, Daiichi Isotope Lab, Tokyo, with normal range of 0.1-5.0/^U/ml). Titers of anti-thyroglobulin (Tg) and anti-microsomal antibodies were measured by hemagglutination kits (Serodia-ATG, Serodia-AMC, Fujirebio Inc., Tokyo). Titers of serum anti-TSH receptor antibodies (TRAb) were measured using a commercially available radioreceptor assay kit (Baxter, Tokyo, normal range less than 10%). Serum calcitonin was measured by a double antibody RIA kit (Calcitonin kit Daiichi, Daiichi Isotope Lab, Tokyo, normal range, less that 100pg/ml) and an IRMA kit ELSA-hCT, CSI diagnostic, Osaka, normal r...