Lingual thyroid carcinoma: a case report and review of the literature.

Ectopic thyroid tissue may reside anywhere along its embryologic path of descent. Most ectopias manifest as simple thyroglossal duct cysts in conjunction with a normally developed thyroid gland in its usual thyroid cervical bed. Lingual thyroid is a rare developmental abnormality characterized by the failure of the thyroid gland, or remnants, to descend from its embryologic site of origin at the foramen cecum to its usual pretracheal position. Carcinoma arising in a lingual thyroid is even more unusual with fewer than 30 cases reported in the literature. We report the second case of lingual papillary thyroid carcinoma and review the clinical features, natural history, diagnosis, and treatment of lingual thyroid carcinoma.

Short-term effects of coronary angiographic contrast agents on thyroid function.

OBJECTIVE: To determine the effect of two iodine-containing contrast agents used for coronary angiography on subsequent thyroid hormone concentrations. METHODS: We prospectively studied thyroid function in 56 patients, with no previous history of thyroid disease and normal findings on thyroid examinations, who underwent nonemergent cardiac catheterization. Thyroid hormone concentrations were assessed at baseline and at day 1 and day 7 after administration of a radiographic iodinated contrast agent (Renografin or Omnipaque). RESULTS: Use of Omnipaque and Renografin was not associated with significant changes in thyroid-stimulating hormone, total thyroxine, triiodothyronine resin uptake, free thyroxine index, or total triiodothyronine. Three patients had slightly increased thyroid-stimulating hormone concentrations at 7 days after angiography. CONCLUSION: Administration of iodinated contrast agents for cardiac catheterization does not result in hyperthyroidism in patients with previously normal findings on thyroid examination.

Effect of desuppression on nodular thyroid disease.

OBJECTIVE: To ascertain the clinical effect of discontinuation of thyroxine (T4) suppression therapy in patients with solitary thyroid nodules or multinodular goiters (MNGs). METHODS: After long-term T4 suppression therapy was discontinued (desuppression) in 63 patients (45 with solitary or dominant nodules and 18 with MNGs), we conducted a prospective follow-up for a mean of 18 months in an effort to detect any thyroid-related changes. RESULTS: A dominant nodule developed in 4 of 18 patients with MNGs. Fine-needle aspirations showed benign lesions in these four patients, but two were referred for thyroidectomy because of substantial nodule growth (both lesions proved to be benign). Of the 45 patients with solitary or dominant thyroid nodules, 4 were lost to follow-up, and 9 had clinically significant nodule enlargement and underwent thyroidectomy. One patient had clinically significant papillary carcinoma, and one had microscopic papillary carcinoma. CONCLUSION: These data on effect of discontinuation of T4 suppression therapy suggest that (1) about 20% of patients with MNGs will ultimately have thyroid nodule enlargement and (2) about 20% of patients with a solitary or dominant nodule will have nodule enlargement, of which approximately 20% will have papillary carcinoma.

Use of a gonadotropin-releasing hormone agonist in the evaluation of postmenopausal virilization due to ovarian hyperthecosis. A case report.

BACKGROUND: Hyperthecosis in a postmenopausal woman is a very rare cause of virilization, and only five cases have been reported previously. CASE: A woman presented with a nine-year history of increasing hirsutism and a mild virilization beginning in the perimenopausal period. Initial androgen metabolite concentrations suggested attenuated late-onset adrenal hyperplasia, but a trial of dexamethasone treatment was ineffective. Subsequent use of leuprolide acetate resulted in a biochemical and clinical improvement in the signs and symptoms. CONCLUSION: This case is unique because gonadotropin-releasing hormone agonist administration was utilized as both a diagnostic and therapeutic modality.

Thionamides alter the efficacy of radioiodine treatment in patients with Graves' disease.

Thionamides are often used acutely to control the symptoms of thyrotoxicosis associated with Graves' disease before definitive treatment with radioiodine. Several reports have suggested that pretreatment with thionamides reduces the efficacy of radioiodine therapy in patients with Graves' disease, but other data refute this. This study retrospectively reviewed the records of 95 patients with Graves' disease treated with radioiodine. Pretreatment with thionamides resulted in significantly greater (2 1/2-fold) treatment failure rate than in patients not pretreated with thionamides but given a comparable dose of radioiodine. Higher serum thyroxine concentration at the time of diagnosis was also an independent factor associated with radioiodine treatment failure.

Sternoclavicular septic arthritis due to haemophilus influenzae.

We have reported a case of septic sternoclavicular arthritis illustrating a rare complication of infection with a relatively common pathogen, Haemophilus influenze. Early identification of the infecting organism and appropriate antibiotic therapy are essential to prevent further morbidity from the complications of this unusual pyoarthritis.

The phosphorylation of adrenal proteins in response to adrenocorticotropic hormone.

The phosphorylation of rat adrenal protein components in response to adrenocorticotropin has been studied in adrenal quarters, isolated cells, and in vivo. In adrenal quarters, adrenocorticotropic hormone (ACTH)-stimulated phosphorylation or dephosphorylation of proteins was not affected by the presence of protein synthesis inhibitors despite a total inhibition of steroidogenesis. (The term dephosphorylation refers to an apparent decrease in the labeling of a particular protein with 32P at various times after the addition of ACTH. This may be due to enzymatic removal of phosphate or protein degradation or complexation of this protein with another cellular component.) Studies with isolated cell preparations identified several proteins that are phosphorylated or dephosphorylated in response to hormone. These changes in phosphorylation were also observed in adrenal quarters and correlated well with ACTH-stimulated steroidogenesis as determined by temporal analysis and dose-response studies of corticosterone production. In vivo injection of male hypophysectomized rats with [32P]phosphate and ACTH demonstrated changes in the labeling of six adrenal proteins. Many of the proteins phosphorylated in vivo were also demonstrated to be phosphorylated in both in vitro systems. Finally, the injection of a physiological dose of ACTH appeared to selectively activate the type I cAMP-dependent protein kinase within the microsomal fraction as determined by the binding of a photoaffinity-labeled reagent. These results suggest that alterations in phosphorylation of adrenal proteins in response to ACTH is proximal to or independent of the obligatory role of protein synthesis in acute steroidogenesis.

On the mechanism of action of adrenocorticotropic hormone. The role of ACTH-stimulated phosphorylation and dephosphorylation of adrenal proteins.

The regulatory role of phosphorylation of adrenal proteins as it relates to the mechanism of action of adrenocorticotropic hormone (ACTH) has been studied. ACTH, cyclic AMP, or cyclic GMP were added to rat adrenal quarters which had been preincubated with [32P]phosphate. 32P-labeled proteins in subcellular fractions were identified after separation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. The addition of ACTH consistently resulted in the phosphorylation and dephosphorylation of specific adrenal proteins and produced characteristic phosphorylation patterns (autoradiographs) for each subcellular fraction which were very different from control. The changes in phosphorylation of proteins preceded corticosterone production. Also, the degree of phosphorylation of these specific proteins followed a dose-response relationship with ACTH which correlated well to the dose-response for corticosterone production. When cAMP was added to adrenal quarters, the resulting phosphorylation changes were identical to those induced by ACTH. When cGMP was added to adrenal quarters, the resulting phosphorylation patterns were very similar to those produced by control incubations. ACTH or cAMP stimulated corticosterone production 6-fold when compared to control or cGMP-treated tissue. These results suggest that tropic action of ACTH is mediated by cAMP by both phosphorylation and dephosphorylation of specific adrenal proteins.