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Biomedical subjects

W Langsteger

Publications and source records attributed to W Langsteger.

At least 37 records · Page 2Linked to original sources
PubMed1995

Intraoperative radiation therapy in advanced thyroid cancer.

An intraoperative radiation therapy (IORT)-protocol was designed for poorly differentiated non-anaplastic thyroid carcinoma. Out of 155 cases of differentiated thyroid tumours, 12 showed marked vascular/capsular invasion. Five entered the study (three primarily local invasive tumours, two local recurring). IORT was administered after tumour surgery (4-10 GY) and combined with post-operative percutaneous irradiation. The tumour control rate in the thyroid bed was achieved in all five patients, 1/5 developed mediastinal nodes and 1/5 with primary mediastinal tumour extension showed tumour progression. No specific complications occurred.

Adenocarcinoma, Follicular↗
PubMed1995

Changes in thyroid hormone parameters after acute myocardial infarction.

Abnormalities in circulating thyroid hormone levels are very common in systemic nonthyroidal illnesses, such as acute myocardial infarction. In this study, thyroid parameters were determined in a series of 16 consecutive infarction patients treated by thrombolysis. Blood samples were taken before therapy as well as 2, 4, 6, 8, 12 and 72 h following admission. Total and free serum thyroxin and triiodothyronine decreased and reverse T3 increased significantly showing no major variations up to 72 h, whereas thyroid-stimulating hormone values remained almost unchanged during the observation period. Subjects with CK-MB levels of more than 150 ng/ml (n = 10) revealed similar changes in thyroid parameters in comparison to those with lower values (n = 6; NS). Thus, although hormone modifications very often occur following acute infarction, thyroid status may not serve as a marker for the extent of left ventricular dysfunction in the early phase of myocardial infarction.

Aged↗
PubMed1995

Evaluation of the Cobas Core system for use in routine diagnosis of thyroid disorders.

The aim of this clinical study was to evaluate the TSH, FT4, FT3, T3, and T4 assays designed for use on the Cobas Core Immunoassay Analyzer. Performance of these enzyme immunoassays (EIAs) was compared with well established and routinely used radioimmunoassays (RIA) or immunoradiometric assay (IRMA). In the first part of the study, the between-run and within-run data as well as the linearity of the Cobas Core assays was carried out, showing a very high precision; most coefficients of variation (CVs) were below 8%. In the second part of the study, serum samples from patients with different thyroid diseases were evaluated, and the results compared with those obtained by RIA or by IRMA. All results were highly comparable with the clinical aspects of all investigated thyroid disorders, and the data of TSH, FT4, T3 and T4 were completely in concordance with those assessed by RIA or IRMA methods; however, only the FT3 assays had a moderately correlation. In contrast to RIA methods, Cobas Core EIAs provided precise results in patients with thyroid hormone transport protein anomalies or T4/T3 autoantibodies; moreover, elevated serum concentrations of thyroxine binding globulin (TBG) did not affect measurement of total thyroid hormone concentrations.

Adult↗
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

Coexistence of papillary and medullary carcinoma of the thyroid gland-mixed or collision tumour? Clinicopathological analysis of three cases.

We present three thyroid carcinomas displaying medullary and papillary components. In two cases the papillary component was characterized by typical papillae with a fibrovascular core; in one a follicular variant of papillary carcinoma was found. The papillary component was dominant in two and the medullary in one case. One tumour showed clear-cut borders between the two components, the others displayed an intermingled pattern. Both tumour components were seen in lymph node metastases with immunostaining with antibodies to calcitonin, chromogranin A, carcinoembryonic antigen, other neuroendocrine markers and thyroglobulin. At least two of our cases are true mixed carcinomas probably arising from a common stem cell.

Adult↗
PubMed1994

Familial dysalbuminaemic hyperthyroxinaemia and inherited partial TBG deficiency: first report.

BACKGROUND: Abnormalities of the serum thyroid hormone binding proteins are not uncommon but, when properly assessed, they do not present diagnostic difficulties. In contrast, the presence of two inherited defects of thyroid hormone transport, of the type presented in the family described here, may cause a major problem in diagnosis and has not been described previously. METHODS: All conventional thyroid function tests were carried out. In addition, thyroid hormone binding to serum proteins was assessed by agarose gel electrophoresis, and thyroxine binding globulin by immunoassays and by immunodiffusion. The affinity of TBG for thyroxine and its maximal binding capacity were assessed by Scatchard analysis. RESULTS: Tests carried out on 22 members of the family revealed familial dysalbuminaemic hyperthyroxinaemia in 10 family subjects. All five living siblings of the propositus had familial dysalbuminaemic hyperthyroxinaemia and two tested transmitted this trait to their children and grandchildren. This was not the case with the propositus. Partial thyroxine binding globulin deficiency only, inherited presumably from the propositus' mother, was found in two family members. Both thyroxine binding globulin deficiency and familial dysalbuminaemic hyperthyroxinaemia were detected in the propositus and in his male nephew, masking the typical laboratory abnormalities associated with each of these defects. CONCLUSIONS: Coexistence of two inherited defects of thyroid hormone transport proteins produce atypical thyroid function test abnormalities, which can be misinterpreted as thyroid hormone dysfunction.

Adult↗
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↗
PubMed1994

[Clinical aspects of autoimmune thyroid diseases].

AITD (autoimmune thyroid disease) comprise atrophic thyroiditis (AT), hypertrophic Hashimoto's thyroiditis (HT), and immunogenic hyperthyroidism (Graves' disease, GD). Combinations with other types of autoimmune disorders frequently occur and are called polyglandular autoimmune syndrome. Familial disposition may be documented by genetic markers: GD and AT are associated with HLA-B8 and DR3 respectively, while HT associates with DR5. Pathogenesis of the fore-mentioned 3 AITD may be explained on the one hand by an immunological balance and on the other hand by a predominance of either stimulating or destructive/blocking immune processes. In diagnosing AITD the determination of antibodies against thyroglobulin or thyroidal peroxidase have been in use for quite some times. Antibodies directed against TSH receptors (TRAb) are determined by means of a radioligand assay which will not distinguish between stimulating or blocking antibodies, so that clinical symptoms and thyroid function parameters are essential in evaluating hyper- oder hypothyroid function. TRAb are transferred via the placenta and should therefore be determined in patients with AITD within the 3rd trimester of pregnancy. The prevalence of AITD is far higher in iodine rich countries and is 4 times more frequent in women, with a general age peak between the 5th and 6th decade. The rare AT mostly presents as primary myxoedema and is discovered less frequently during the exploration of an unclear hypercholesterolemia. In HT we differentiate between the chronic fibrous and the juvenile oxiphilic variant. In the former fibrosis is predominant with plasmacellular infiltration producing extremely high titers of antibodies enabling diagnosis without fine needle biopsy (FNB). In the latter, the oxiphilic variant, titers of antibodies are mostly low or even missing so that a reliable diagnosis will require a FNB. However, two thirds of adolescent goitres are caused by HT.

Autoantibodies↗
PubMed1994

[Familial dysalbuminemic hyperthyroxinemia in long-term amiodarone treated patients].

A serum sample of an outpatient, under long-term amiodarone (AM) treatment was submitted for routine checkup of thyroid function parameters. It revealed the pattern of euthyroid dysalbuminemic hyperthyroxinemia. Since no results have been published so far covering the influence of amiodarone on the specific thyroxine binding proteins, we undertook a prospective study to investigate 28 amiodarone patients, comparing these with a series of age and sex matched euthyroid subjects. Not one amiodarone patient showed changed radio-T4 distribution against the normal group. Yet, in 3 relatives of the propositus, familial screening revealed the typical pattern of thyroid function tests and of T4 distribution in radio immune ice gel electrophoresis, respectively, proving familial dysalbuminemic hyperthyroxinemia syndrome. Thus, it is most likely that this syndrome has been prevalent already prior to the amiodarone administration and consequently amiodarone was of no influence on thyroxine transport protein patterns.

Adult↗
PubMed1993

[Hemorheologic effects of ginkgo biloba extract EGb 761. Dose-dependent effect of EGb 761 on microcirculation and viscoelasticity of blood].

METHOD: In a randomized open clinical trial involving 42 patients with pathological visco-elasticity values, the effect of a single intravenous injection of 50, 100, 150 or 200 mg of the Ginkgo biloba extract EGb 761, commercially available as Tebonin p.i. on the microcirculation of the skin (Doppler flowmetry) and the visco-elasticity of whole blood was investigated. RESULTS: A dose-dependent significant increase in the microcirculation was found. In the case of visco-elasticity, this dose-dependence was less marked. The present study thus confirms the positive effect of EGb 761 on the microcirculation and whole-blood visco-elasticity in patients with pathological visco-elasticity values, already found in earlier studies, and shows it to be dependent on the dose employed.

Aged↗
PubMed1993

The impact of geographical, clinical, dietary and radiation-induced features in epidemiology of thyroid cancer.

Cancer of the thyroid accounts for less than 1% of all cancers recognised each year, but the incidence is rising. Much of the early work of the epidemiology and aetiology of thyroid cancer was based on the assumption that thyroid cancer can be treated as an entity. The recognition that two distinct types of endocrine cell occur within the thyroid has made it clear that any discussion of the aetiology and epidemiology of thyroid malignancies must take into account the histological classification of these tumours. Moreover, there are difficult problems to be considered when comparing thyroid cancer incidence across tumour registries, because of a lack of standardisation or morbidity data collection, difficulties in histological diagnosis, varying rates of diagnosis of occult papillary carcinoma, and prevalence and techniques of autopsies. So far only a relatively small proportion of thyroid cancer cases can be explained with adequate certainty as regards epidemiology and aetiology. As in cancer in general, the aetiology and epidemiology of thyroid cancer in detail remains unknown in the majority of cases.

Adult↗
PubMed1993

Expression of various MHC class II molecules and of intracellular adhesion molecule-1 (ICAM-1) on focal clusters of dendritic cells in iodine deficiency goitres.

Thyroid sections from 18 consecutive euthyroid patients undergoing surgery for iodine deficiency goitre were investigated by means of immunohistochemistry and immunofluorescence, evaluating the expression of MHC class II antigens (HLA-DR, -DP, -DQ, and RFD1) and intercellular adhesion molecule-1 on the formerly described clusters of dendritic cells, as well as on thyrocytes. Eleven of 18 iodine deficiency goitres contained clusters of dendritic cells. These clusters appeared to express only HLA-DR in two cases; in nine of 12 cases they showed a differential expression of class II molecules in the following frequency: HLA-DR > DQ and/or -DP > RFD1. These dendritic cells also were ICAM-1+. In four of 18 iodine deficiency goitres, thyroid epithelial cells showed MHC class II expression in several combinations, but were ICAM-1-. In normal thyroids and in nodular goitres from inhabitants of the endemic area not having an actual iodine deficiency, only sparse clusters of dendritic cells were found; these cells were only HLA-DR+. Follicle lining cells were negative for the MHC class II molecules. In normal thyroids from an area with sufficient iodine supply, no clusters of dendritic cells were seen. The few dendritic cells observed were lying isolated in the interstitium and only positive for HLA-DR and ICAM-1; epithelial cells were negative for the studied markers. These data show clusters of dendritic cells in thyroids of inhabitants of an endemic area. When goitre is accompanied by iodine deficiency at the moment of operation, there appears to be activation of these dendritic cells and of thyroid epithelial cells.

Adult↗
PubMed1993

The effect of treatment with levothyroxine or iodine on thyroid size and thyroid growth stimulating immunoglobulins in endemic goitre patients.

OBJECTIVE: We assessed the effect of levothyroxine or iodine on thyroid size and on thyroid growth stimulating immunoglobulins in endemic goitre patients. DESIGN: Levothyroxine or iodine was given orally in an open randomized prospective study (100 and 200 micrograms respectively). PATIENTS: Thirty-seven euthyroid patients with diffuse iodine deficiency goitres and thyroid growth stimulating immunoglobulins were studied. MEASUREMENTS: Thyroid size, thyroid growth stimulating immunoglobulins (mitosis arrest assay), basal TSH, free T3, free T4, thyroid anti-microsomal antibodies, antithyroglobulin antibodies, anti-TSH receptor antibodies and urinary iodine excretion were measured. RESULTS: Thyroid size decreased significantly in both groups, in the levothyroxine group more than in the iodine treated group. Thyroid growth stimulating immunoglobulins levels also decreased significantly in both groups. Between groups there was no statistically significant difference. A statistically significant correlation between thyroid growth stimulating immunoglobulins reduction profiles and goitre size reduction could not be established. TSH levels became suppressed in the levothyroxine group while the T4 values rose; in the iodine treated group TSH levels stayed constant as did T4. None of the patients developed thyroid microsomal or thyroglobulin auto-antibodies and/or hyperthyroidism during the treatment. CONCLUSIONS: Levothyroxine as well as iodine was effective in reducing thyroid size as well as thyroid growth stimulating immunoglobulins levels in endemic goitre patients. Since in both groups TSH levels were not related to thyroid size reduction, other factors than TSH suppression must be responsible for the observed thyroid size reduction. Iodine itself by virtue of its antiproliferative action on thyrocytes may have had a direct action on the goitre reduction during iodine treatment; however, the levothyroxine dose, containing less iodine, had a similar effect. A complicated picture hence emerges with regard to factors involved in the shrinkage of iodine deficiency goitre during thyroxine or iodine therapy. These findings indicate that TSH and thyroid growth promoting immunoglobulins are not the only influences on the size of endemic goitres, although it cannot be excluded that these two factors contribute to influence the pathogenetic process.

Antibodies↗
PubMed1993

[Iodine content of infant food in Austria].

An adequate iodine supplementation is essential for the normal and intellectual development in premature birth and in newborns. The ceric arsenite reaction method modified by the authors was applied to examine whether a sufficient iodine content in milk samples of four manufacturers ensured the iodine supply of bottlefed preterms and fullterms. Only very few of 23 preparations examined contained the required iodine content recommended by the Food and Drug Nutrition Board of the National Academy of Sciences, the National Research Council of the United States, the European Society of Pediatric Gastroenterology and Nutrition, and the German Society of Nutrition. It could be demonstrated that the majority of the commercially available baby food-milk preparations contained insufficient quantities of iodine. To assure a sufficient iodine supply in this bottlefed group it would be necessary to add a varied quantity of iodine to formula milk or to prepare baby food with iodine containing mineral water. Moreover, manufacturers might use milk from cows fed with iodinated salt. The results show clearly that an improvement in iodine content of commercial baby food is essential for the cerebral development of solely bottlefed newborns.

Austria↗
PubMed1993

[Prevention of iodine-induced hyperthyroidism after coronary angiography].

Coronary angiography (CA) is followed by an iodine load of 15 to 20 mg for the thyroid and may be the cause of iodine-induced hyperthyroidism. 60 consecutive patients hospitalized for CA without any thyroid history were examined and 56 had thyroid diseases with normal thyroid function. 33 patients still showed a significant decrease of 20 min Technetium uptake (TcU) and an increase of urine iodine excretion because of iodine excess 12 weeks after CA. 3 patients developed latent hyperthyroidism. 27 patients received medication of 1 g natrium-perchlorate and 60 mg methimazole 24 hours before and on the day of CA. These patients showed normal TcU and urine iodine excretion 4 and 12 weeks after CA. 1 out of these 27 patients developed overt hyperthyroidism but had PTCA without premedication 2 weeks after CA. Since Iodine excess leads to iodine-induced hyperthyroidism even in euthyroids a prophylaxis with perchlorate and methimazole is generally recommended in patients with CA.

Adult↗