ABSTRACT:Cerebrovascular accidents due to Moyamoya disease, a disorder characterized by arterial stenosis at the base of the brain accompanied by typical net-like collateral vessels, occurred in two young Japanese women with Graves' disease when they were in thyrotoxicosis. In one patient, a second attack of cerebral infarction occurred with the recurrence of thyrotoxicosis. Association of Moyamoya disease and Graves' thyrotoxicosis is rare and the pathegenetic relationship is discussed.
Serum fructosamine was measured in patients with Graves' disease and primary hypothyroidism. Fructosamine levels and fructosamine per albumin ratio were significantly lower in patients with Graves' disease than in normal subjects, while they were significantly higher in patients with primary hypothyroidism. Fructosamine levels were normalized by treatment in the euthyroid state in patients with Graves' disease. Along with the normalization of thyroid stimulating hormone levels, fructosamine levels returned to the normal range in patients with primary hypothyroidism with treatment. There were significant correlations between fructosamine levels and free triiodothyronine levels, free thyroxine levels, thyroid stimulating hormone levels, hemoglobin A1C levels, albumin levels, and creatine phosphokinase levels. We concluded that it was useful to measure serum fructosamine as an indicator of peripheral metabolic function in patients with thyroid diseases.
We studied the secretion capacity of TSH-beta in 63 patients with various pituitary disorders, carrying out the observation of TSH-beta changes after TRH administration. Serum TSH-beta concentrations were measured by radioimmunoassay according to the modified method of Kourides. Serum TSH concentrations were measured by immunoradiometric assay, and serum concentrations of free thyroid hormones were measured by radioimmunoassay. Basal TSH-beta concentrations were below 0.39 ng/ml in 17 patients with Acromegaly, below 0.56 ng/ml in 5 patients with Prolactinoma, below 0.68 ng/ml in 4 patients with Cushing's disease, below 0.48 ng/ml in 12 patients with non-functioning tumor, below 6.4 ng/ml in 16 patients with SITSH, and below 0.45 ng/ml in 9 patients with other pituitary diseases. TSH-beta changes after TRH administration differed from TSH changes in 4 patients (25%) with Acromegaly, in 2 patients (67%) with Prolactinoma, in 5 patients (71%) with non-functioning tumor, in one patient (33%) with Cushing's disease, in 4 patients (100%) with Rathke's cleft cyst, in one patient with suprasellar meningioma, and in one patient with suprasellar arachnoid cyst. 2 patients (67%) with Prolactinoma, 3 patients (43%) with non-functioning tumor, all 6 patients with non-neoplastic SITSH, and one patient with Rathke's cleft cyst showed exaggerated TSH-beta changes after TRH administration. In patients with some pituitary disorders, we thought the secretion and synthesis of TSH and TSH-beta differed from that of normal subjects. We concluded that it was necessary to investigate the mechanism of secretion of TSH-beta in patients with pituitary disorders.
A 28-year-old female with a 12-year history of goiter is presented. She had both clinical and laboratory evidence of hyperthyroidism, and her serum TSH was persistently and markedly elevated after treatment with antithyroid drugs. A TRH stimulation test resulted in no further rise in serum TSH after cessation of medication. Menses were regular and serum prolactin levels were normal. Serum LH and FSH responses to LHRH stimulation test were normal. No other evidence of pituitary or peripheral endocrine deficiencies existed. She underwent a subtotal thyroidectomy followed by 131I therapy three years later. A pituitary adenoma with sphenoidal and suprasellar extension was completely removed by transphenoidal approach. On light microscopy, it was mostly composed of chromophobic cells with occasional calcification showing sinusoidal pattern. On electron microscopy, most of the cells contained fine granules, which suggested thyrotroph. The immunoperoxidase technique revealed TSH beta in the cytoplasm of some adenoma cells. Three days postoperatively the patient's serum TSH levels returned to normal. TRH stimulation test produced a normal response in serum TSH. The patient was diagnosed hypothyroid by laboratory findings and is currently on thyroid replacement therapy. The patient became pregnant and delivered twice prior to the operation for pituitary adenoma. The previously reported TSH secreting adenomas associated with hyperthyroidism were reviewed.
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