A study of thyroglobulin and peroxidase activity in the thyroid tissue of patients with non-endemic non-toxic nodular goitre

Mories, Teresa; Miralles, José Manuel Pavía; Reglero, Ángel; Felipe, Stela Mirla da Silva; Corrales, J. J.; García, L

doi:10.1042/cs0800301

Cited by 9 publications

(4 citation statements)

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“…Thyroid hormones and autoantibodies Thyroid hormones and TSH levels were measured in the serum of all patients by RIA and by an amplified immunoradiometric assay (for TSH), according to pre¬ viously described techniques , Mories et al 1991. For the determination of serum TBII levels, the ability of antibodies to block the binding of ,25I-labelled TSH to porcine thyroid membranes was measured by a radioreceptor assay using a commercial kit (TRAK Assay; Henning, Berlin, Germany).…”

Section: Patientsmentioning

confidence: 99%

Serial analysis of the effects of methimazole therapy on circulating B cell subsets in Graves' disease

Corrales

Órfão²,

López³

et al. 1996

Journal of Endocrinology

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The immunosuppressive effects of antithyroid drug therapy are well recognized; however, the cellular mechanisms underlying their action remain largely unknown. In the present paper we have prospectively analyzed the in vivo effects of methimazole treatment on a large number of circulating B cell subsets, involved in the effector phase of the immune response, in a group of 18 hyperthyroid patients with Graves' disease (GD). The patients were sequentially studied before (day 0) and 7, 14, 30, 90 and 180 days after methimazole therapy. The results were compared with both a group of 19 age- and sex-matched healthy controls and a group of 20 untreated/euthyroid GD patients in long-term remission. The combination of flow cytometry and three colour immunofluorescence revealed a clear increase (P < 0.001) in the numbers of circulating total B cells (CD19+) due to a significant increase (P < 0.001) in the CD5+, FMC7+, CD5+/ FMC7+ and CD23+ B cell subsets in hyperthyroid GD patients with respect to both healthy individuals and to GD patients in long-term remission. The absolute numbers of all these B cell subsets analyzed before treatment, although abnormal, were not statistically different from those observed during the whole period of therapy. When comparing the percentages of these B cell subsets during treatment, significant changes (P < 0.001) were only observed in the proportion of CD5+, CD5+/FMC7+ and CD5- B cells at the end of the follow-up period with respect to those found both before and during the first month of therapy. Whereas CD5+ and CD5+/FMC7+ B cells decreased (P < 0.001) after 3 months of therapy, CD5- B cells showed a significant increase (P < 0.001) at the end of therapy. It is remarkable that the percentage of CD5+, CD5+/FMC7+, CD5- and CD23+ B cell subsets were abnormal during the whole period of treatment and that they never reached normal values. These results show that, in vivo, GD patients treated with methimazole exhibited an abnormal but rather stable pattern of B cell distribution, similar to that present in hyperthyroid untreated GD patients, except for the CD5+ and CD5- B cell populations. Our findings suggest that in vivo methimazole therapy would not directly have an important influence on circulating B cell subsets.

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Section: Patientsmentioning

confidence: 99%

Serial analysis of the effects of methimazole therapy on circulating B cell subsets in Graves' disease

Corrales

Órfão²,

López³

et al. 1996

Journal of Endocrinology

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show abstract

“…Thyroid hormones and TSH concentrations were measured in the serum of all patients by RIA and by an amplified immunoradiometric assay (for TSH), according to previously described techniques (Corrales et al 1991, Mories et al 1991. For the determination of serum TBII concentrations, the ability of antibodies to block the binding of 125 I-labelled TSH to porcine thyroid membranes was measured by a radioreceptor assay using a commercial kit (TRAK-Assay, Henning, Berlin, Germany).…”

Section: Thyroid Hormones and Autoantibodiesmentioning

confidence: 99%

Methimazole therapy in Graves' disease influences the abnormal expression of CD69 (early activation antigen) on T cells

Corrales

López²,

Ciudad³

et al. 1997

Journal of Endocrinology

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At present, the in vivo response of T, B and natural killer (NK) cells to antithyroid drug therapy remains largely unknown. In the present study, we have prospectively analyzed the in vivo effects of methimazole treatment on a large number of circulating T and NK cell subsets, some of them expressing cell surface activation antigens involved in the very early phase of the immune response, in a group of 17 hyperthyroid, untreated patients with Graves' disease (GD). As one of the first events during T cell activation is the expression of interleukin (IL) receptors, we also studied the binding of IL-2 and IL-6 to T cells. Patients with Graves' disease were sequentially studied at diagnosis/before treatment (day 0) and 7, 14, 30, 90 and 180 days after methimazole therapy. The results were compared with both a group of 19 age- and sex-matched control volunteers and a group of 20 untreated/euthyroid patients with Graves' disease in long-term remission. The combination of flow cytometry and three-color immunofluorescence revealed a clear (P < 0.01) decrease in the percentage of NK cells before and during the whole course of therapy with respect to both controls and patients with Graves' disease who were in long-term remission. Before therapy, a marked increase (P < 0.001) in the ratio of B to NK cells was also observed; thereafter, a slight decrease in this ratio was observed, although normal values were detected only in patients in long-term remission. Expression of the CD69 early activation antigen in the hyperthyroid untreated patients with Graves' disease was clearly increased (P < 0.01) with respect to both controls and patients with Graves' disease who were in long-term remission. This abnormal CD69 expression was found to be significantly reduced (P < 0.001) by methimazole therapy, and this represents a new effect of the drug. Expression of the low-affinity receptor for IL-2 (CD25)--another early T cell activation marker--was not altered in Graves' disease, but the binding of IL-2 and IL-6 to T cells exhibited a progressive and parallel increase during the first 30 days of therapy, decreasing thereafter. Our results show that methimazole therapy downregulates the abnormally high expression of the CD69 early activation antigen on T cells, being less effective on inducing changes in other T cell activation markers and in NK cells.

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“…Thyroid hormone and TSH levels were measured by RIA (T3 and T4) and by an amplified immunoradiometric technique that included the use of monoclonal antibodies (TSH) according to previously described techniques {Corrales, Tabernero, Miralles and Hernandez 1991; Mories, Miralles, Reglero, Felipe, Corrales and Garcia 1991). Antithyroglobulin and antimicrosomal antibodies were determined by a hemagglutination technique using kits from Wellcome Reagents (Dartford UK).…”

Section: Thyroid Hormones Tsh and Antibody Serum Levelsmentioning

confidence: 99%

The Relationship Between Hyperthyroidism and the Distribution of Peripheral Blood T, NK and B-Lymphocytes in Multinodular Goiter

Corrales¹,

Órfão²,

Miralles³

et al. 1994

Horm Metab Res

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Peripheral blood T, NK and B-cell subsets were analyzed in 18 patients with nontoxic multinodular goiter (NMG) and 11 patients with toxic multinodular goiter (TMG) in order to evaluate whether hyperthyroidism modifies the distribution of these cell populations. As a control group, 26 age and sex-matched healthy individuals were included in the study. Lymphoid subsets were analyzed with flow cytometry by double staining immunofluorescence techniques using a large panel of monoclonal antibodies. No differences were found in the absolute or relative numbers in any of the cell populations analyzed in both groups--NMG and TMG--, with the exception of a significant decrease in CD19+ cells in TMG. However, patients with multinodular goiter showed important abnormalities in the distribution of T, NK and B lymphocytes with respect to the control subjects. The pattern of abnormalities detected was characterized by a marked increase in the absolute and relative counts of activated T-lymphocytes (CD3+/HLA-DR+), cytotoxic T-cells (CD57+/CD8+) and of cells expressing NK-related antigens. None of these alterations were related to the serum levels of T3, T4 or TSH. Our results point to the existence of important abnormalities in the distribution of several lymphoid subsets in multinodular goiter, regardless of whether the subjects are euthyroid or hyperthyroid.

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A study of thyroglobulin and peroxidase activity in the thyroid tissue of patients with non-endemic non-toxic nodular goitre

Cited by 9 publications

References 0 publications

Serial analysis of the effects of methimazole therapy on circulating B cell subsets in Graves' disease

Serial analysis of the effects of methimazole therapy on circulating B cell subsets in Graves' disease

Methimazole therapy in Graves' disease influences the abnormal expression of CD69 (early activation antigen) on T cells

The Relationship Between Hyperthyroidism and the Distribution of Peripheral Blood T, NK and B-Lymphocytes in Multinodular Goiter

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