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Biomedical subjects

H Schleusener

Publications and source records attributed to H Schleusener.

At least 55 records · Page 3Linked to original sources
PubMed1983

HLA-DR3 and HLA-DR5 associated thyrotoxicosis--two different types of toxic diffuse goiter.

One hundred fifty patients with toxic and scintigraphically diffuse goiter were HLA typed (A, B, C, DR). One group consisted of 101 patients with concomitant Graves' ophthalmopathy and/or TSH-binding inhibiting antibodies (TBIAb). Forty nine patients had neither ophthalmopathy nor TBIAb. The former group showed a higher prevalence of HLA-B8 and DR3 compared to a normal control group. The latter group showed a higher frequency of HLA-DR5, whereas the HLA-B8 and DR3 antigens were slightly below normal prevalence. These data indicate an immunogenetic heterogeneity in patients with toxic diffuse goiter. A group of 47 hyperthyroid patients with single autonomous thyroid adenoma had no increased prevalence of any HLA-antigens. Patients with long term remission did not show an altered prevalence of any of the HLA antigens compared to controls. In contrast, patients with Graves' ophthalmopathy and/or TBIAb activity who relapsed had a significantly higher prevalence of HLA-B8 DR3, whereas patients without TBIAb and eye signs who relapsed had a significantly higher prevalence of HLA-DR5 than the control group.

Graves Disease↗
PubMed1982

Circulating TSH-binding inhibiting immunoglobulins in myasthenia gravis.

Using a radioligand receptor assay the sera of 46 patients with myasthenia gravis (MG) were tested for the presence of circulating TSH-binding inhibiting immunoglobulins (TBII). In addition thyroid function was evaluated on the basis of T3, T4, TBG and TSH radioimmunoassays including the TRH stimulation test. Circulating antimicrosomal and antithyroglobulin thyroid antibodies were measured by haemagglutination techniques. Two patients had concomitant Graves' disease (GD), 5 were euthyroid with autonomously functioning thyroid tissue due to non-immunogenic multinodular goitre and 39 myasthenic patients were euthyroid with normal pituitary thyroid axis. Only 1 patient with GD had strongly positive TBII-activity and 3 euthyroid MG patients were TBII borderline-positive.

Adolescent↗
PubMed1981

[Clinical importance of the estimation of thyrotropin displacing antibodies (author's transl)].

In 69 hyperthyroid patients with diffuse uptake in the scintigram, thyrotropin displacing antibodies (TDA) were measured before, during and after thyrostatic treatment. In a further 42 patients antibody activity was investigated before and 6-12 weeks after radio-iodine treatment, and in 29 patients it was measured before and after subtotal thyroidectomy. Persistence of demonstrable TDA during and after the end of drug treatment was in all cases indicative of recurrence of hyperthyroidism. On the other hand, disappearance of TDA activity was not a guarantee for prolonged remission as five patients had a recurrence despite loss of TDA activity. In a further nine patients hyperthyroidism reappeared with recurrence of TDA after varyingly long periods of remission. Thyrostatic treatment should be performed until disappearance of antibodies. Prolonged demonstration of TDA should lead to surgical intervention. Besides the usefulness in establishing the diagnosis of immunogenic hyperthyroidism (Graves' disease) TDA estimation may be of some prognostic value in the use of thyrostatics. In contrast, after radio-iodine treatment or operation the functioning capacity of the remaining thyroid tissue seems to be more relevant for the success of treatment than the possibly longer acting antibodies.

Antibodies↗
PubMed1981

Mitogenic response of peripheral blood lymphocytes from patients with Graves' disease incubated with solubilized thyroid cell membranes containing TSH receptor and with thyroglobulin.

Transformation of peripheral blood lymphocytes (PBL) in response to solubilized TSH receptor and to human thyroglobulin (hTG) was carried out in patients with Graves' disease (GD). Mean stimulation index (SI) in response to solubilized TSH receptor was significantly increased only in hyperthyroid GD patients (SI = 3.0 +/- 1.8 SD, n = 13, p less than 0.025) when compared to normal subjects (SI = 1.5 +/- 0.8 SD,n = 14). All other subgroups of GD patients (i.e., euthyroid GD patients after treatment as well as those with/without ophthalmopathy or TSH-displacing antibody [TDA]) showed a tendency to elevated mean SI, which, however, was never significantly increased. In contrast, patients who were suspected of having a "disseminated autonomy" showed a tendency to decreased mean SI compared to GD patients. The mitogenic response of PBLs induced by solubilized TSH receptor could be suppressed by incubation of antigen and PBLs with bTSH. Control experiments with purified protein derivate of tuberculin(PPD) as stimulating antigen revealed, however, that bTSH itself suppresses the mitogenic response of PBLs and that the decrease of SI in this experiment is not due to blockage of the antigenic determinants of the TSH receptor protein. Human thyroglobulin (hTG) produced no significant increase in the SI of PBLs. Only 9 out of 47 GD patients showed an SI higher than the mean of normals + 2 SD. All those patients, however, who showed an elevated SI ( greater than 2.0) also revealed an increased SI with solubilized TSH receptor.

Cell Membrane↗
PubMed1980

Binding of thyrotrophin to low molecular weight fragments of human thyroid membranes.

The LATS absorbing activity from thyroid homogenates which is associated with the soluble thyroid fraction (4S-LAA) binds TSH in addition to LATS. This may indicate that 4S-LAA originates from the receptor sites for TSH at the thyroid cell surface. The affinity of 4S-LAA for TSH is much lower than that of thyroid membranes suggesting that 4S-LAA represents incomplete receptor sites or receptor sites which are altered in their structure.

Absorption↗
PubMed1979

TSH-receptor antibodies, HLA B8 and thyroid autoantibodies in patients with Graves' disease in therapeutically induced euthyroidism.

The prevalence of TSH-receptor antibodies and of thyroid autoantibodies was studied in 48 HLA-typed patients with Graves' disease, who were in an euthyroid state after antithyroid therapy with methimazole. TSH-receptor antibodies, which were found in 35% of the patients, did not correlate with the positivity of HLA B8. By contrast the persistence of thyroid microsomal antibodies was significantly associated with HLA B8.

Antibodies↗
PubMed1978

Relationship between thyroid status and Graves' disease-specific immunoglobulins.

The prevalence of TSI in Graves' disease was investigated with a radioligand receptor assay using human thyroid membranes and highly purified labeled porcine TSH or bovine TSH in 110 patients before treatment and in 39 patients after successful treatment with antithyroid drugs. In 11 patients, the assay was performed before, during, and after therapy. The results in the radioligand receptor assay were compared to thyroid function tests (TRH test, free T4 index, serum %3 level, and thyroid suppression test). Normal IgG inhibits nonspecifically, but dose dependently, the binding of [125I]TSH to thyroid membranes. IgG samples from patients were only considered to be positive if they reduced the binding of the labeled hormone below the mean value minus 2 SD of the controls. TSI activity was found in 50% of the patients with untreated diffuse toxic goiter, in 3 out of 27 cases who regained suppressible thyroid function, and in 5 out of 12 cases who were off therapy for more than 6 weeks and showed normal TRH tests and normal hormone levels but in whom the suppression test was not performed. Our data cannot prove the hypothesis that only humoral antibodies are responsible for the thyroid stimulation in Graves' disease, but of course they cannot exclude it; furthermore, they suggest the existence of antibodies which bind to the human thyroid cell membrane without necessarily stimulating thyroid cellular activity.

Antigen-Antibody Complex↗
PubMed1978

[Kinetics of the temperature dependence of thermal activation and inactivation of bacterial endospores as a consequential reaction].

Reaction kinetics explains the thermal activation and destruction of bacterial endospores as a consequent reaction with the activation rate constant k 1 of the resting spores N 0 and the destruction rate constant k 2 of the heat-activated spores N ++: (formula see text). If one takes also into account the activated spores already present in a suspension, one obtains, at constant temperature, destruction curves that become straight lines when plotted semi-logarithmically or correspond to the convex and concave curves often described in the literature. The D value of destruction must be calculated from the k value of the slowest reaction. Experiments with endospores of Bac. subtilis showed that k 1 greater than k 2 at temperatures less than 100 degrees C, and k 2 greater than k 1 at temperatures greater than 135 degrees C. In case of further confirmation of this theory, far-reaching conclusions might be drawn as to the calculation of the sterilization of F value.

Bacillus subtilis↗
PubMed1975

Different effects of oral doses of triiodothyronine or thyroxine on the inhibition of thyrotrophin releasing hormone (TRH) mediated thyrotrophin (TSH) response in man.

Since contradicting results about the existence of T3 or T3 and T4 receptors in pituitary tissue have been reported, the influence of L-triiodothyronine (L-T3) or L-thyroxine (L-T4) on TRH stimulated TSH release was investigated. Oral administration of 50 mug L-T3 caused an increasing inhibition of TSH response to 400 mug TRH from 64% 2 h after L-T3 intake to 29% after 24 h, while serum T3 peaks up to 5.45 ng/ml occurred between 2 to 4 h after L-T3 ingestion and became normal after 8 to 10 h. This delay in the T3 action on TRH inhibition agrees with the postulate that T3 induces the synthesis of an inhibiting protein which is blocking TSH liberation. Oral administration of 1000 mug L-T4 induced increments of serum T4 up to 221 ng/ml between 6 to 24 h after intake; however, a TRH inhibition of 62% did not become evident before 48 h. At this time T3 levels had risen to the upper normal range. These results support the theory that T3 is responsible for the regulation of TSH secretion. An intra-pituitary conversion from T4 to T3 seems more likely the cause of the TRH inhibition rather than the peripheral T4-T3 conversion or a direct action by T4 binding sites in the pituitary.

Administration, Oral↗