Effectiveness of prophylactic therapy on goiter recurrence in an area with low iodine intake--a sonographic follow-up study.

There is no agreement as to whether or not drug treatment after surgery for nodular goiter is effective in preventing recurrence of goiter. Data about recurrences in areas of marginally low iodine intake (like Germany) vary widely. Therefore, we performed a retrospective study in 104 patients who had been treated surgically because of benign uninodular or multinodular goiter. The mean follow-up period was 6.4 years (minimal 1 year) with at least three examinations. Thyroid ultrasound with volumetric analysis was recorded in each patient. Thirty-two patients did not receive any prophylaxis, 50 patients were treated with L-thyroxine, 17 patients with a combination of L-thyroxine and iodine and 5 patients with iodine alone. Recurrence of goiter was documented in 28.0% of the untreated patients and in 8.9% of the patients on prophylaxis (P < 0.05). The mean increase of thyroid volume was 7.3 ml versus 3.1 ml in patients without versus with prophylactic drug treatment (not significant). No significant correlation was found between the increase of thyroid volume and age of the patients, follow-up time, or initial thyroid volume, respectively. These data clearly demonstrate the effectiveness of prophylactic drug therapy to prevent recurrence of goiter after thyroid surgery in an iodine-deficient area.

[Immune activity and serum interleukin-2-receptor concentration in autoimmune thyroid diseases]. / Immunaktivität und Interleukin-2-Rezeptor-Konzentration im Serum bei autoimmunbedingten Schilddrüsenerkrankungen.

Serum interleukin-2 receptor (IL-2R) concentrations were compared in 55 patients with thyrotoxicosis (14 men, 41 women, mean age 43.5 +/- 17 years), 18 patients with Hashimoto's thyroiditis (5 men, 13 women, mean age 47 +/- 15 years) and 28 healthy subjects (12 men, 16 women, mean age 30 +/- 10 years). The patients with thyrotoxicosis were divided into three groups depending on the activity or stage of the disease: 17 patients with florid untreated hyperthyroidism, 23 euthyroid patients receiving treatment with antithyroid drugs and 15 patients with thyrotoxicosis in remission after completing one year's antithyroid treatment. The patients with untreated thyrotoxicosis had significantly higher IL-2R values than the euthyroid patients receiving treatment or those in remission (207 +/- 112 vs 139 +/- 66 and 91 +/- 26 U/ml, P < 0.05 and P < 0.01). The IL-2R values of patients with thyrotoxicosis in remission were, however, significantly lower than those of the 28 healthy subjects (126 +/- 34 U/l; P < 0.01) or the euthyroid patients receiving treatment (P < 0.05). The 18 patients with Hashimoto's thyroiditis had significantly lower serum IL-2R values (70 +/- 39 U/ml) than the healthy controls. These data show that the serum IL-2R level depends on the state of thyroid metabolism and on the activity phase of the thyrotoxicosis. The low serum levels of IL-2R in patients with Hashimoto's thyroiditis could signify a genetically determined decrease in IL-2R production or might be linked with the destruction of thyroid tissue by the chronic autoimmune process.

Factitious hyperthyroxinemia due to a monoclonal IgA in a case of multiple myeloma.

A clinically euthyroid 53-year-old woman with an IgA-lambda-secreting multiple myeloma presented with increased serum concentrations of thyroid hormones. Laboratory studies revealed increased total thyroxine (T4) and triiodothyronine (T3) concentrations, a high-normal free T4 concentration, and a normal basal thyrotropin (TSH) concentration with a normal response to thyroliberin (TRH). Her serum concentration of IgA was 11,040 mg/L (normal range 900-4500 mg/L) and immunoelectrophoresis revealed it to be monoclonal. This monoclonal IgA bound both T4 and T3, as determined by serum immunoelectrophoresis and direct binding studies. Immunoelectrophoresis in the presence of [125I]T4 or [125I]T3 localized the radiolabeled iodothyronines to a band corresponding exactly to the precipitin arc of the monoclonal IgA. We performed direct binding studies with IgA purified by affinity chromatography with the lectin jacalin. Purified IgA (50 micrograms) bound both [125I]T4 (12.3%) and [125I]T3 (2.7%) specifically and in a dose-dependent manner. Scatchard analysis of competitive-binding data utilizing [125I]T4 and unlabeled T4 revealed a Kd of 2.2 x 10(-7) mol/L. The binding capacity for T4 was approximately 7 mumol/L. Thus, in this case of IgA-secreting myeloma, the monoclonal IgA acts as an additional thyroid hormone-binding protein in serum that interferes in the T4 and T3 RIAs. This is the first report of a monoclonal IgA producing an apparent euthyroid hyperthyroxinemia.

Characterization of insulin-like growth factor receptors in human thyroid tissue.

We have characterized the binding of 125I-IGF-I and 125I-IGF-II to plasma membranes purified from human thyroid tissue. IGF binding was time- and temperature-dependent. At 4 degrees C, maximal specific binding of 125I-IGF-I was 17.3 +/- 2.5% and of 125I-IGF-II was 8.8 +/- 2.0% (mean +/- SD/60 micrograms membrane protein). 125I-IGF-I binding was inhibited completely by unlabeled IGF-I, IGF-II, insulin, and the type-I IGF receptor monoclonal antibody, alpha IR-3. 125I-IGF-II was inhibited completely by unlabeled IGF-II and nearly completely by IGF-I. 125I-IGF-II binding also was inhibited significantly by insulin, suggesting that much or all of the IGF-II was bound to the type-I IGF receptor. Scatchard analysis revealed a single class of binding sites with a Kd of 6.0 +/- 4.2 x 10(-10) M for IGF-I binding and 5.7 +/- 1.3 x 10(-10) M for IGF-II binding. IGF-I binding was inhibited by a variety of salts in a dose-dependent manner, calcium and magnesium salts being more effective than sodium or potassium salts. Affinity crosslinking of 125I-IGF-I and -II showed clear evidence only for type-I IGF receptors. Thus, a crude plasma membrane fraction of human thyroid tissue expresses predominantly type-I IGF receptors.

[Side effects of antithyroid therapy of hyperthyroidism. A study of 1256 continuously treated patients]. / Nebenwirkungen der antithyreoidalen Therapie der Hyperthyreose. Eine Untersuchung an 1256 fortlaufend betreuten Patienten.

Side effects of antithyroid treatment were retrospectively analysed in 1256 patients with hyperthyroidism. Overall rate of side effects was 14.3%. Skin reactions were the most frequent ones (5.6%), followed by arthropathies (1.6%). The incidence of agranulocytosis was 0.14%. Median duration of all side effects was 1.5 months. In half the cases the side effects were controllable so that treatment was continued, although at a changed dosage. The rate of cross-reaction between carbimazole and thiamazole, on the one hand, and propylthiouracil, on the other, was 13.8% and 15.2%, respectively. The side effects became apparent after a mean of one month's treatment, almost always (in 97.1%) within the first year of treatment. There was a significant dose dependence for an initial thiamazole dose of over 20 mg (relative side effect risk of 2.3), and for an initial dose of over 30 mg for carbimazole (relative side effect risk of 1.6). Although most side effects were not dangerous, in normal instances the lowest possible dosage should be administered to control hyperthyroid metabolism. Long-term treatment with low doses seem to be without problems.

Metabolism of GnRH in man: influence of estrogens.

UNLABELLED: To clarify the influence of estrogens on the metabolism of gonadotropin-releasing hormone (GnRH), we studied the metabolic clearance rate (MCR) of GnRH (MCRGnRH), and the serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol and testosterone (total and free fraction) in 9 sexually mature men and 7 women under basal conditions and after treatment with the antiestrogen tamoxifen (2 X 10 mg/day p.o.) for 7 days. In women, the medication was started on day 7 +/- 1 of their menstrual cycles. To calculate the MCR, synthetic GnRH was continuously infused (1.53 micrograms/min) and its serum levels were measured by a radioimmunoassay. During tamoxifen treatment we observed a small but significant decrease in the MCR in men (455 +/- 48 to 357 +/- 46 ml/min/1.86 m2), whereas the known cyclic increase in the MCR in women was blunted (1,769 +/- 147 to 1,558 +/- 119 ml/min/1.86 m2). There was a small but significant increase in LH levels in women (8.3 +/- 2.1 to 11.5 +/- 2.5 mU/ml). LH and testosterone levels in men, and FSH and estradiol levels in both sexes did not change significantly. CONCLUSION: (1) estrogens regulate the MCRGnRH either directly or by changing gonadotropin levels, but the effect is only slight; (2) an enhanced metabolism of GnRH may contribute to the feedback of estrogens on the secretion of gonadotropins, and (3) the sex-specific difference of the MCR is presumably not caused by estrogens.