PubMed Health⌕ Search

Biomedical subjects

G Semlitsch

Publications and source records attributed to G Semlitsch.

11 recordsLinked to original sources
PubMed2000

[Point mutation of thyrotropin receptors as the main cause of autonomously functioning thyroid nodules: experiences in the framework of our Styrian patients].

Autonomously functioning thyroid nodules are frequently associated with mutations of the thyrotropin receptor. We analyzed a part of exon 10 of the thyrotropin receptor gene (base pairs 1762-1976) by direct sequencing and found missense mutations in 5 of 14 cases (codons 629, 631, 632, 633). Histologically, 3 of the 14 nodules were adenomas whereas 11 were hyperplasias. Nodules with mutations did not show significant differences from nodules without mutations with respect to age, histology, size, additional (non-functional) nodules and clinical symptomatology. Our results confirm that thyrotropin receptor mutations are involved in the development of autonomously functioning thyroid nodules. In this context, the terms hyperplasia and neoplasia should be reevaluated.

Adenoma↗
PubMed2000

[Seasonal variations in the diagnosis of hyperthyroidism].

Seasonal variations in the frequency of thyrotoxicosis are known for a long time. Both, variations in the temperature and in the iodine supplementation are believed to affect the incidence of the diagnosis of hyperthyroidism. Seasonal variation of the incidence of hyperthyroidism was investigated before and after increase of salt iodination in 1990/1991. In the period from January 1987 to December 1995 hyperthyroidism was diagnosed for the first time on 4711 patients in our department. This population was subdivided according to etiology (Graves' disease, autonomous nodular goiter) and grade of hyperthyroidism (preclinical or clinical form). The so formed groups were divided according to the month of diagnosis into further 12 subgroups. Significant differences in month to month variation were found in the patients suffering from Graves' disease and autonomous nodular goiter with preclinical hyperthyroidism after increased iodine supplementation. The peak incidence of the diagnosis occurred in June, July, and August. Our results indicate that improved iodine supplementation may be the main cause of seasonal variations in the incidence of thyrotoxicosis.

Austria↗
PubMed2000

[Measurement of free triiodothyronine (FT3) using an electrochemiluminescence immunoassay in patients with autoantibodies to triiodothyronine].

Thyroid hormone autoantibodies may lead to abnormal values of free triiodothyronine (FT3) and free thyroxine (FT4) by interference with the radio immunoassay (RIA). We examined thyroid function in six patients with known triiodothyronine-binding autoantibodies using a RIA and an electro-chemiluminescence immunoassay (ECLIA). FT3 values measured by RIA were spuriously high, ECLIA measurement of FT3 led to correct values according to the patients' thyroid status. We conclude from these results that in patients with triiodothyronine-binding autoantibodies FT3 measurement by ECLIA is more useful than measurement by RIA.

Adult↗
PubMed2000

[Effect of aceclofenac on thyroid hormone binding and thyroid function].

Influences of non-steroidal anti-inflammatory drugs (NSAID) on concentrations of thyroid hormones are known for a long time. These effects could be explained with interference between NSAIDs and thyroid hormone binding. We investigated the effects of a single dose of aceclofenac on thyroid function and thyroid hormone binding in 18 healthy volunteers. Serum levels of free thyroid hormones (FT3, FT4) and thyrotropin (TSH) were measured with commercial available kids and thyroid hormone binding was estimated with a specially modified horizontal argarose-gel-electrophoresis prior to and 2 hours after receiving a single dose of aceclofenac. We found a significant decrease in T3 binding on TBG and a significant increase of albumin-bound T3. All other investigated thyroid hormone binding parameters, FT3 and FT4, showed no significant changes. We conclude that aceclofenac leads to a significant redistribution of T3 protein binding. These effects seem to be explained by T3 displacement from TBG induced by aceclofenac.

Adult↗
PubMed2000

[Increased occurrence of autoimmune thyroiditis in patients with chronic rheumatoid arthritis].

The frequent occurrence of both rheumatoid arthritis and autoimmune thyroiditis was already investigated with in part many conflicting results. We investigated a number of 792 patients (383 of them suffering from rheumatoid arthritis and 409 with osteoarthritis). In all patients antithyroid peroxidase and antithyroglobulin antibodies were determined. Patients with rheumatoid arthritis showed a significantly higher occurrence of circulating thyroid antibodies than those with osteoarthritis (9.1% versus 3.7%, p = 0.0016). We conclude that there exists a cumulate coincidence of both diseases. Patients suffering from rheumatoid arthritis should undergo a thyroid examination especially for the presence of autoimmune thyroiditis.

Aged↗
PubMed1997

Thyrotropin and thyroglobulin as an index of optimal iodine intake: correlation with iodine excretion of 39,913 euthyroid patients.

The recommendations for the dietary allowance of iodine are 150 micrograms per day for adolescents and adults. Thyrotropin (TSH) and thyroglobulin (Tg) can be used as surveillance indicators for assessing iodine deficiency disorders. We compared the relation between TSH and Tg, free triiodothyronine, and thyroxine serum levels with urinary iodine excretion in 2311 untreated euthyroid patients using our modified cericarsenite method. An adequate iodine intake may be assumed when TSH and Tg values are at the lower end of the normal range. Patients were grouped according to urinary iodine excretion and goiter size. In the group with an iodine excretion between 201 and 300 micrograms of iodine per gram of creatinine, the lowest TSH values and even low Tg levels could be shown. We conclude that an iodine intake of approximately 250 micrograms/day is associated with the lowest TSH stimulation to thyrocytes. In the groups separated according to thyroid size, significantly higher Tg levels were found in the patients with uninodular and multinodular goiter as a result of longstanding iodine deficiency, whereas actual urinary iodine excretion did not differ significantly. Additionally, iodine excretion of 39,913 euthyroid patients between 1984 was 1996 was examined. In Austria iodized salt (10 mg KI/kg) was introduced by law in 1963 and increased to 20 mg KI/kg salt in 1990. An initial increase of iodine excretion until 1993 was followed by a decrease in 1994 and 1995 without further changes in 1996. These results show that iodine intake has improved since 1984; however, in 1996 iodine excretion in one-third of the investigated patients was under 100 micrograms per gram of creatinine and more than 80% had less than 200 micrograms per gram of creatinine.

Adult↗
PubMed1997

[Iodine and thyroid hormone metabolism in pregnancy].

The influence of pregnancy on thyroid function as well as important interactions of pregnancy and thyroid disorders are of high clinical importance. During the last decade knowledge of these issues greatly influenced clinical aspects and basic science. Because of the increasing frequency of thyroid disorders during pregnancy, knowledge of these issues is important in order to diagnose, treat and manage all patients exposed to these problems.

Female↗
PubMed1997

[Point mutations of the thyrotropin receptor gene in autonomously functioning thyroid gland nodules: correlation with clinical findings and morphology].

Seventeen autonomously functioning thyroid nodules (AFTN) were analyzed for the most frequent mutations of the thyrotropin (TSH) receptor gene at codons 619, 631, 632 and 633. DNA was extracted from formalin-fixed, paraffin-embedded samples from both nodules and surrounding tissue after micro- or macrodissection. A fragment of the TSH receptor gene (bp 1762-1976) encoding the third cytoplasmic loop and the sixth transmembranous domain was amplified by PCR. Screening for mutations at codons 619, 631, 632 and 633 was performed by restriction enzyme analysis using Asp 718, Hph I, Taq I and EcoR I, respectively. For verification, cases with a mutated restriction site were cloned and sequenced. Mutations were found in 3 AFTNs (18%): in 2 cases at codon 632 and in 1 case at codon 631. The 2 cases with a mutation at codon 632 harbored additional mutations at codon 599 and 640, respectively, detected by sequencing. Normal thyroid tissue outside the AFTNs did not harbor mutant TSH-receptor. Mutations occurred in patients with clinical and subclinical hyperthyroidism. Mutations were associated both with total (2 cases) and partial (1 case) suppression of the surrounding thyroid tissue as noted on the scinti scan. AFTNs with TSH-receptor mutation occurred as single nodules. All 3 nodules with mutations were classified histologically as nodular hyperplasia according to the criteria of the WHO. Although the number of cases is small, our data suggest that AFTNs are clinically and morphologically heterogenous. Since the most common TSH-receptor mutations occur only in a small subset of AFTNs other molecular genetic alterations may be involved in the development of AFTNs.

Adenoma↗
PubMed1995

[TSH receptor double mutation in functional autonomic thyroid nodule].

TSH receptor stimulating antibodies (TSAb) are well known in the pathogenesis of Graves' disease. Recently mutations in the DNA coding for the TSH-receptor (TSHR) have been revealed in autonomously functioning thyroid nodules (AFTN). In this study we looked for mutations in 9 patients with AFTN. DNA was extracted separately from the nodules and the paranodular thyroid tissues. A fragment of the TSHR gene (bp 1762-1976) was amplified by PCR. The amplified DNA was digested with Hph I, Taq I, Kpn I and Eco RI, respectively, and the resulting fragments were analyzed by gel electrophoresis. Mutations were detected in the nodules of 3 of the 9 patients. In the nodules of 2 patients we found simultaneous mutations affecting the restriction sites of Hph I and Taq I. In the 3rd patient a mutation affecting the restriction site of Hph I was observed. The simultaneous occurrance of TSHR-mutations altering Hph I (Position 631) and Taq I (position 632) restriction sites in AFTN have not been described so far.

Adenoma↗
PubMed1994

Postpartum thyroiditis and familial dysalbuminemic hyperthyroxinemia.

Familial dysalbuminemic hyperthyroxinemia (FDH) is a syndrome associated with euthyroidism and increased binding of T4 to serum albumin. The combined occurrence of FDH and postpartum hyperthyroidism due to Graves' disease has only been reported in one patient. We now describe the first case of FDH and thyrotoxicosis due to postpartum silent thyroiditis. In a 19-yr-old woman, FDH, suspected on the basis of strikingly elevated analog free T4 (fT4) and total T4 values, but normal two-step fT4 and serum TSH values, was confirmed by [125I]T4 agarose-gel electrophoresis. When FDH and thyrotoxicosis, characterized by markedly elevated analog fT4, total T4, and two-step fT4 values and undetectable TSH values, coexist, the differential diagnosis may be confusing.

Adult↗