Metabolic clearance of thyrotropin-releasing hormone in the rat in hypothyroid and hyperthyroid states: comparison with serum degradation in vitro.
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Animals↗
Biomedical subjects
P D Papapetrou
Publications and source records attributed to P D Papapetrou.
Hypothalamic hypothyroidism causing spastic paraplegia: recovery following thyroid medication.
A 63-year-old woman with longstanding spastic paraplegia and neurological evidence of long tract disturbance was found to have hypothyroidism, partial diabetes insipidus, hyperprolactinemia, and gonadotropin deficiency of hypothalamic origin. Replacement therapy with thyroxine and prednisone induced complete remission of the neurological abnormalities. The association of spastic paraplegia with hypothalamic insufficiency has not been reported previously. The possibility of hypothalamic disease should be considered in cases of spastic paraplegia of unknown cause.
Brain Diseases↗
Cortisol secretion in Nelson syndrome: Persistence after "total" adrenalectomy for Cushing syndrome.
In two patients who were severely pigmented (Nelson syndrome) following bilateral adrenalectomy for Cushing syndrome, symptoms of hyper-cortisolism developed while they were receiving only physiologic steroid replacement. Cortical assays proved that endogenous cortisol production had not been obliterated. Even after total adrenalectomy, steroid measurement should be performed to guard against adrenocortical excess.
17-Hydroxycorticosteroids↗
Thyrotoxicosis due to "silent" thyroiditis.
3 patients (2 male, 1 female) presented with symptoms of thyrotoxicosis associated with elevated blood-levels of thyroid hormone and a markedly depressed thyroidal uptake of 131-I. The male patients (aged 59 and 47) each had a cardiac arrhythmia, but did not have any thyroid pain or swelling. The female with a goitre had no discomfort in the neck. Thyrotoxicosis factitia was excluded by history. The subsequent course of their disease was typical of subacute thyroiditis. The elevated thyroid-hormone levels spontaneously fell to normal over a few weeks. In 1 patient, however, chemical hypothyroidism developed. These patients could have been diagnosed as having hyperthyroidism, rather than subacute thyroiditis, since thyroid pain--and swelling in 2 of the cases--was absent. The correct diagnosis was suspected only after finding a thyroidal uptake of 131-I near zero. The thyroidal uptake of 131-I is still important as a routine diagnostic aid in thyroid disease.
Adult↗
Relation between thyroid iodine content and the accumulation and oxidation of [35-S] Methimazole in the rat.
The thyroid accumulation and oxidation of a single intraperitoneal dose of [35-S] methimazole has been studied in iodine-deficient, normal and iodine-treated rats. A highly significant positive linear correlation was found between the thyroid oxidation of methimazole to sulfate and intrathyroidal iodine content. A single dose of potassium iodide given intraperitoneally (ip) to rats 1 h before administration of [35-S] methimazole (1 mg/kg ip) increased the thyroid accumulation and oxidation of methimazole. Conversely, the thyroids of rats maintained on a low iodine diet for 21 days showed a markedly reduced capacity to accumulate and oxidize methimazole. The level of oxidation found in the iodine-deficient, normal and iodide-treated groups was 0.21, 4.15 and 12.6 nmol sulfate/g thyroid respectively. The animals maintained on the low iodine diet for 21 days showed significant increases in thyroid weight and thus the decrease in methimazole oxidation occurred in spite of increased stimulation by endogenous TSH. These results show that the intrathyroidal iodine content is a critical factor in the metabolism of methimazole in the thyroid.
Animals↗