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Biomedical subjects

B Grubeck-Loebenstein

Publications and source records attributed to B Grubeck-Loebenstein.

At least 91 records · Page 5Linked to original sources
PubMed1988

Pathogenetic relevance of HLA class II expressing thyroid follicular cells in nontoxic Goiter and in Graves' disease.

HLA class II expressing thyroid follicular cells are found not only in classical thyroid autoimmune diseases, such as Graves' disease, but also in presumably nonautoimmune thyroid disorders such as nontoxic goiter. In this study the immunostimulatory function of the HLA class II expressing thyroid follicular cells derived from patients with nontoxic goiter and with Graves' disease was compared by assessing their capacity to stimulate allogeneic and autologous peripheral blood mononuclear cells, as well as cultured intrathyriodal T lymphocytes. Proliferation of allogeneic peripheral blood mononuclear cells was stimulated by thyroid follicular cells from both nontoxic goiter and Graves' disease thyroids, thus demonstrating that thyroid follicular cells from both disorders are capable of presenting alloantigens. In contrast the proliferation of autologous peripheral blood mononuclear cells was more efficiently stimulated by thyroid follicular cells from Graves' disease than from nontoxic goiter. Cultured intrathyroidal T lymphocytes proliferated specifically in response to autologous HLA class II+ thyroid follicular cells in Graves' disease, but not in nontoxic goiter. The responses were dose dependent and HLA class II restricted. Thyroid autoantigen presentation by HLA class II expressing thyroid follicular cells thus only occurs in Graves' disease, suggesting that HLA class II expression on thyroid follicular cells is an essential feature, but by itself not sufficient for the induction of autoimmunity. Additional factors, the possible nature of which is discussed must also be involved.

Adult↗
PubMed1986

Thyroid growth-stimulating immunoglobulins in goitrous disease: relationship to thyroid-stimulating immunoglobulins.

Thyroid growth stimulating immunoglobulins (TGI) were assayed in IgG concentrates prepared from human plasma using a cytochemical bioassay (CBA) based on the measurement of changes in glucose-6-phosphate dehydrogenase (G6PD) activity in guinea pig thyroid follicular cells. TGI was present in all 8 patients studied who had goitrous Graves' disease, in 9 who had toxic diffuse goitres with asymmetric uptake on scintigram and/or symptomatic ophthalmopathy and in 4:8 who had toxic uninodular goitre with autonomously functioning nodules. TGI were also present in 34:54 (64%) of patients who had non-toxic goitres. In contrast, TGI were undetectable in 4 patients who had Graves' disease without palpable goitre and in all 18 euthyroid non-goitrous volunteers. Maximum increases in G6PD activity occurred at an IgG concentration of 50 micrograms/ml in all patients who had goitrous Graves' disease and in 5:7 who had diffuse non-toxic goitres. In contrast, IgG concentrates from 20:27 patients with nodular goitres caused maximum increases in G6PD activity at an IgG concentration of 500 micrograms/ml. A comparison of the prevalence of TGI with that of thyroid stimulating immunoglobulins (TSI), also measured by CBA, in 63 patients showed that although both stimulators were present in 8 patients who had goitrous Graves' disease they were only simultaneously present in 18:43 (42%) who had non-toxic goitres of various aetiologies. Thyrotrophin receptor antibodies (TRAb) were present in 11/44 (25%) of non-toxic goitrous patients but there was no significant correlation with IgG stimulators in such patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

The prevalence of immunological abnormalities in endemic simple goitre.

Thyroid growth stimulating immunoglobulins microsomal antibodies and antibodies against thyroglobulin were determined in patients with simple goitre (n = 20) and controls (n = 6) living in an iodine deficient area. In addition, lymphocytic infiltration of thyroid tissue, the amount of the various lymphocyte subsets (Leu 4+, Leu 3a+, and Leu 2a+ T-cells as well as B1+ B cells) in the thyroid gland, as well as the expression of the histocompatibility antigen HLA-DR on thyrocytes and intrathyroidal T-lymphocytes were examined. Goitrous patients were subdivided into two groups according to their individual iodine supply estimated by iodine excretion values, and immunological parameters were compared between patients with low (group A, iodine excretion less than 70 micrograms/24 h) and with higher (group B, iodine excretion greater than 100 micrograms/24 h) iodine supply. Thyroid growth stimulating immunoglobulins and antithyroid antibodies were equally prevalent in the two patient groups, but were absent in controls. Lymphocytic infiltration of thyroid tissue was present to a comparable extent in patients of groups A and B, but to a distinctly lower degree in control persons. Intrathyroidal T-lymphocyte subsets did not differ between patients and controls. B-lymphocytes, germinal centres as well as DR+ thyrocytes were detected in goitrous patients of both groups, but never in control persons. Thus, immunological abnormalities frequently occur in patients with simple goitre and do not depend upon individual iodine supply.

Adolescent↗
PubMed1985

[Current data on iodide excretion in the Vienna region].

Iodine excretion was investigated in 281 patients attending various medical outpatient departments in Vienna. In 64 consecutive patients determination of sodium excretion was performed additionally. 50% of the patients showed an iodine excretion of less than 92 micrograms/24 h, indicative of an insufficient supply of iodine. 25% had an iodine excretion of even less than 56 micrograms/24 h, which pointed to severe iodine deficiency. Iodine and sodium excretion were closely correlated, which indicates that table salt represents the most important source of iodine. Thus, the great deviation of iodine excretion among the population of one region demonstrated in this study is most likely due to varying salt intake. Iodine excretion did not differ in patients with simple goitre and controls, but was higher in polymorbid patients than in healthy persons. The apparent insufficiency of the iodine supply in the Vienna area favours an initiative for the legal augmentation of the iodine content of table salt.

Adolescent↗
PubMed1985

[Sonography of the thyroid gland with high-resolution real-time equipment].

The results of sonography of thyroid glands in 131 patients were compared with the findings on palpation and from scintigrams. High resolution sonography is the most accurate method of examination for demonstrating changes in the thyroid. In 40% cases sonography demonstrated lesions additional to the single abnormality found clinically. In 10% cases a suspected thyroid abnormality on palpation proved to be due to extra thyroid disease. Evaluation of the number, size and localisation of space-occupying lesions by means of sonography is superior to all other kinds of investigation. It is, however, not possible to determine whether a lesion is benign. An attempt has been made to define the usefulness of thyroid sonography and its place during routine diagnosis.

Female↗
PubMed1985

Immunological features of nonimmunogenic hyperthyroidism.

Blood lymphocyte subpopulations (Leu 4+ cells = pan-T cells, Leu 3a+ cells = helper/inducer cells, and Leu 2a+ cells = suppressor/cytotoxic cells), thyroid-stimulating immunoglobulins, microsomal antibodies and antibodies against thyroglobulin were determined in 10 patients with hyperthyroidism due to single autonomously functioning thyroid nodules (ATN), 11 patients with hyperthyroidism due to Graves' disease (GD) and in 20 normal subjects. Thyroidectomy was performed in 8 of the patients with ATN and in 6 of those with GD after 3 weeks of antithyroid drug treatment with methimazole. Lymphocytic infiltration of thyroid tissue, the amount of the various lymphocyte subsets (Leu 4+, Leu 3a+, and Leu 2a+ T cells as well as B+ B cells) in the thyroid gland, as well as the expression of the histocompatibility antigen HLA-DR on thyrocytes and intrathyroidal lymphocytes were examined. Blood Leu 4+ cells were reduced due to a lack of Leu 2a+ cells in patients with ATN and GD when compared to normal subjects. Thyroid-stimulating immunoglobulins were detected in all patients with ATN and GD, but in none of the normal subjects. Lymphocytic infiltration of thyroid tissue was present in patients with ATN and GD. The various lymphocyte subsets in the thyroid gland did not differ between the two patient groups. DR expression on thyrocytes was seen in 6 of the patients operated for ATN and in 5 of those who underwent surgery for GD. Infiltration with DR+-T lymphocytes was found in all thyroid glands investigated. Thus immunological findings usually classified as proof for the autoimmune origin of GD exist also in patients with ATN. An overlap in the pathogenetic background of both diseases seems possible.

Adult↗
PubMed1984

[Diagnosis and therapy of patients with simple goiter within the scope of a thyroid gland ambulatory care service].

Serum thyroxin, triiodothyronine, and basal and TRH-stimulated TSH concentrations, were determined in 285 patients with simple goitre. In addition, the efficiency of two years' therapy with a T4/T3 preparation (ratio 4:1) was investigated. Patients with goitres of larger size (stage II und III) presented with lower serum T4 and higher serum T3 concentrations than patients with smaller goitres (stage I) and controls. A decreased or elevated TSH response to TRH stimulation was more frequently found among patients with large goitres than among those with small ones. No reduction of goitre size was achieved by thyroid hormone medication in patients in whom TSH response to TRH had been decreased prior to therapy. In contrast, a reduction in goitre size was registered after two years' therapy in 84% of the patients in whom the TRH-TSH response was elevated and in 44% in whom it was normal. Small and/or diffuse goitres were more responsive to T4/T3 medication than large and/or nodular ones. These results suggest that TSH stimulation tests are of diagnostic value in patients with simple goitre and should at any rate be performed in patients with goitres of larger size before the commencement of thyroid hormone medication. The data also demonstrate that suppression of TSH secretion via administration of thyroid hormone influences thyroid growth only in a subgroup of the goitrous patients of our region.

Drug Combinations↗
PubMed1983

The effect of iodine containing contrast medium on thyroid function of patients undergoing coronary angiography.

Application of large amounts of iodine in the form of amidotricoic acid (Urografin) in 20 patients undergoing coronary angiography led to an increase in serum thyroxine (T4, p less than 0.005), triiodothyronine (T3, p less than 0.005) and plasma thyrotropin (TSH) in the basal state (p less than 0.05) as well as after TRH-stimulation (p less than 0.05), but not of serum 3,3',5'-triiodothyronine (reverse-T3, rT3) three weeks after contrast medium administration. Although TRH induced TSH stimulation had been subnormal prior to contrast medium application in five patients, T4 as well as T3 remained within the normal range in all patients. Neither preexisting iodine excretion nor the amount of contrast medium applied were related with the observed hormonal changes. We conclude, that application of relatively small as well as large amounts of amidotricoic acid leads to an increase of peripheral thyroid hormone concentrations, paralleled by a rise in basal and stimulated TSH secretion. These changes may be interpreted as physiological adaptation to augmented iodine supply in an area of moderate iodine deficiency.

Adult↗
PubMed1983

Thyroid function in adrenocortical insufficiency during withdrawal and re-administration of glucocorticoid substitution.

The regulatory function of glucocorticoids on thyroid hormone concentrations was studied in patients with adrenocortical insufficiency (ACI, n = 8) and in healthy subjects (n = 6). In patients with ACI withdrawal of glucocorticoid substitution for 84 h led to an increase in serum concentrations of total triiodothyronine (TT3) from 110 +/- 20 to 133 +/- 22 ng/dl and a decrease of serum reverse-T3 (rT3) from 23 +/- 6 to 18 +/- 6 ng/dl, whereas subsequent administration of dexamethasone (0.5 mg po q.i.d. for 3 days) induced a fall in TT3 (129 +/- 22 to 88 +/- 16 ng/dl) and a rise in rT3 (17 +/- 5 to 37 +/- 11 ng/dl) concentrations. Serum levels of total thyroxine (TT4) were unchanged by either withdrawal or re-administration of glucocorticoids. Basal plasma thyrotrophin (TSH) concentrations were unchanged by glucocorticoid withdrawal and fell from 2.2 +/- 1.5 to 1.1 +/- 0.8 mU/l during subsequent dexamethasone therapy. In healthy subjects a decrease of TT3 (89 +/- 8 to 69 +/- 8 ng/dl) and an increase in rT3 (19 +/- 5 to 32 +/- 8 ng/dl) concentrations were seen after stimulation of endogenous cortisol production by prolonged infusion of ACTH1-24 (0.5 mg, t = 8 h on 2 consecutive days), whereas concentrations of TT4 remained unchanged. During subsequent administration of dexamethasone serum level of both. TT3 and rT3 returned to basal levels. Thus, changes in thyroid hormone concentrations are induced by alterations of substitution therapy in patients with ACI. In healthy subjects the application of 2 mg dexamethasone/day following prolonged maximal stimulation of endogenous cortisol by iv ACTH may represent a state of relative glucocorticoid deficiency, thus explaining the observed hormonal changes, which are inverse to those generally induced in healthy man by endogenous or exogenous glucocorticoids.

Adrenal Insufficiency↗
PubMed1982

[Endemic goiter in Austria. Is iodine deficiency the primary cause of goiter?].

In spite of government-regulated iodide admixture to table salt, the incidence of goiter is still high in Austria. Iodine excretion and thyroid function were therefore investigated in 80 patients suffering from ordinary goiter in whom thyroid size and resulting symptoms had increased lately. 25 euthyroid non-goitrous subjects served as controls. 48% of the goitrous patients investigated presented with iodine excretion of less than 70 micrograms/24 h, suggesting an insufficient iodine supply. Thyroid I131 uptake, basal and TRH-stimulated plasma TSH concentrations, and serum T3 levels were higher, whereas serum T4 levels were lower in these patients than in goitrous patients with higher iodine excretion and non-goitrous controls. Iodine deficiency thus appears to be of pathogenetic relevance in about half of the goitrous Austrian population. Other factors enhancing goiter development seem to assume particular importance in goitrous patients with a sufficient iodine supply.

Adolescent↗
PubMed1982

Adrenergic mechanisms and blood pressure regulation in diabetes mellitus.

Changes in blood pressure (BP) and plasma norepinephrine (NE) following various stimuli of the sympathetic, nervous system were studied in six healthy subjects and in 17 diabetic patients. The latter were subdivided in three groups: (1) six patients with neither peripheral neuropathy nor autonomic dysregulation, (2) six patients with severe peripheral neuropathy without autonomic dysregulation, and (3) five patients with autonomic dysregulation, three of whom suffered also from peripheral neuropathy. The following procedures were performed: (1) cold pressor test (2 min), (2) mechanical irritation of the skin by suction (0.75 kg/cm2, 10 min), (3) orthostasis (10 min), and (4) i.v. infusion of NE (50, 100, 200 ng kg-1 min-1 for 15 min each). Both the stimulated endogenous plasma NE levels and BP response to exogenous NE were the same in normal subjects, in diabetic controls and in diabetics with peripheral neuropathy without autonomic dysregulation. In contrast, diabetics with postural hypotension showed a less pronounced release of NE to standing (P less than 0.05), but not to cold pressor test and mechanical skin irritation. Furthermore, they showed increased vasoreactivity to the highest dose (P less than 0.05), but not to the lower doses of exogenous NE. Thus NE release and adrenergic BP regulation seem to be altered only in diabetics with clinical signs of autonomic dysregulation. These alterations can only be evaluated when patients are exposed to stimuli of higher intensity, such as orthostasis or infusion of a high NE dose.

Adult↗