American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules.

American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules are systematically developed statements to assist health care professionals in medical decision making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances.

American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules: executive summary of recommendations.

American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules are systematically developed statements to assist health care professionals in medical decision making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances.

American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules: Executive Summary of recommendations.

American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and European Thyroid Association medical guidelines for clinical practice for the diagnosis and management of thyroid nodules are systematically developed statements to assist health care professionals in medical decision making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances.

Optochiasmatic arachnoiditis with treatment by surgical lysis of adhesions, corticosteroids, and cyclophosphamide: report of a case.

A 24-year-old woman presented with progressive optochiasmatic arachnoiditis causing progressively worsening visual loss associated with headache and amenorrhea. Treatment with the standard initial therapy of dexamethasone, warfarin, and dipyridamole was unsuccessful at halting her disease process. Surgical lysis of adhesions led to a temporary improvement and then deterioration. A course of therapy with cyclophosphamide was initiated and her response to this therapy resulted in resolution of her headaches, return of her vision to normal, and resumption of her normal menstrual cycles.

Thyroid axis in patients with Cushing's syndrome.

Thyroid hormone values and serum thyrotropin (thyroid-stimulating hormone [TSH]) responses to the intravenous administration of 400 micrograms of protirelin were determined in ten patients with Cushing's syndrome and in ten matched normal subjects. In patients with Cushing's syndrome, the serum thyroxine (T4) level was mildly depressed and free T4 level was normal. The mean (+/- SD) concentrations of serum triiodothyronine (T3) and free T3 were both reduced in patients compared with normal subjects (P less than .001). At 20 and 60 minutes after protirelin administration, serum TSH levels were, respectively, 3.3 +/- 2.7 microU/mL and 2.6 +/- 2.3 microU/mL in patients with Cushing's syndrome and 12.3 +/- 5.4 microU/mL and 10.7 +/- 5.4 microU/mL in normal subjects (P less than .001). The reduced serum T3 and free T3 levels are due to a glucocorticoid suppressive effect on the peripheral conversion of T4 to T3. The protirelin test is of limited value in assessing the thyroid status because the response of TSH is frequently blunted or absent due to glucocorticoid excess.

Demonstration of steroid-producing gonadal tumors by external scanning with the use of NP-59.

Bilateral testicular Leydig cell tumors in a patient with Nelson's syndrome and a Leydig cell tumor of the ovary in a woman with a virilizing syndrome were successfully imaged with [6beta-131I]iodomethyl-19-norcholest-5(10)-en-3beta-ol (NP-59). Uptake by these tumors was comparable to uptake by adrenal glands in patients with funtioning adrenal tumors or bilateral hyperplasia. Scanning the gonads with NP-59 may be a helpful imaging procedure in localizing possible sites for exploratory surgery in certain cases of gonadal neoplasia.

Transient hyperthyroidism in patients with lymphocytic thyroiditis.

We have studied seven episodes of transient hyperthyroidism in three men and one woman, aged 19 to 38 years. No patient had fever or neck tenderness. All had palpable thyroid glands. Elevated serum thyroxine values persisted for 1 to 3 months. Thyroid131I uptake at 6 and 24 hours was low (1 to 3%). Erythrocyte sedimentation rates were normal or only slightly increased. Needle biopsy in four patients and a thyroidectomy specimen in one patient, all taken during the hyperthyroid phase, showed lymphocyte infiltration and extensive follicular disruption without oxyphilia. There was no evidence of granulomatous thyroiditis. Thyroglobulin antibodies were normal in all. In three patients, transient hypothyroidism followed the hyperthyroid episode. In two patients, the condition was recurrent. The findings are compatible with transient unregulated discharge of thyroid follicle content in some patients with lymphocytic thyroiditis. Recognition permits avoidance of unnecessary treatment with surgery, radioiodine, or antithyroid drugs.

Fluorescent thyroid scanning. A method based on stable iodine measurements.

Analysis by x-ray fluorescence allows in vitro determination of iodine content of the thyroid gland and a mapping of the regional distribution of iodine in the gland. The picture produced is similar to that of the conventional radioisotope thyroid scan. In 5 normal subjects and 70 patients with thyroid disease, the thyroid concentration of iodine varied between undetectable and 28 mg. With the exception of hypothyroid patients, who showed low thyroid levels of iodine, all patients showed iodine values overlapping the normal range. The fluorescent scan gave results similar to those of the isotope scan in most cases. Exceptions were noted in some hypothyroid patients, patients with flooded iodine pool, and patients receiving suppressive doses of exogenous thyroid hormone. Small cold nodules were best detected by the radionuclide scintigram. The value of the fluorescent scan is in its low radiation dose and in the possibility it affords of studying patients whose thyroid glands have reduced uptake of the radioactive tracer.

The significance of partial suppressibility of serum thyroxine by triidothyronine administration in euthyroid man.

Recent evidence indicates that triiodothyronine (T3) administration may not completely inhibit normal thyroid secretion. To further corroborate this observation, measurement of serum T4-RIA concentrations was performed on 15 normal controls (10 men, 5 women; ages 20-42) who were placed on 100 mug of T3 daily for a 5-week period. Decrements of 53%, 36%, and 28% from the baseline T4-RIA were noted at weeks 1, 2, and 3 respectively. At 3 weeks a nadir T4-RIA of 2.5 mug/100 ml was reached which did not significantly differ from the 4th (2.9 mug/100 ml) and 5th weeks (2.6 mug/100 ml). Further, seven euthyroid patients who had received replacement thyroid hormone for 1-16 were switched to T3 (75-100 mug/day) for 28 days. At the end of this period, their mean T4-RIA was 2.6 mug/100 ml. Similar T3 treatment studies were performed on 20 primary hypothyroid patients. After 4 weeks of T3 all 20 patients displayed a T4-RIA below the limits of assay detectability (less than 0.625 mug/100 ml) while all euthyroid subjects had values greater than 1.2 mug/100 ml. Suppression of T4-RIA with T3 was also noted in 4 patients with pituitary and 2 patients with hypothalamic hypothyroidism. Three days after cessation of T3 treatment in normal subjects, no significant rise in mean T4-RIA was seen (2.3 mug/100 ml). Subsequently, T4-RIA rose to 4.5 mug/100 ml on day 7 and 6.7 mug/100 ml on day 10 (74% of the presuppression value) in normals. A similar rise to 7.9 mug/100 ml 10 days after withdrawal from T3 was noted in the euthyroid subjects who had received long-term thyroid hormone replacement. In contrast, all primary hypothyroid patients had either a minimal or nondetectable elevation in T4-RIA while demonstrating a marked rise in TSH 10 days after T3 withdrawal. An absent or impaired rise in T4-RIA after T3 withdrawal was also noted in patients with pituitary and hypothalamic hypothyroidism. These observations indicated: 1) There is continued thyroidal T4 secretion in euthyroid subjects receiving 100 mug of T3 daily. 2) The hypothesis is advanced that an intact hypothalamic-pituitary-tyhroid axis may be required for continued T4 secretion while on T3. 3) The duration of prior suppression with thyroid hormone medication does not appear to influence this phenomenon.