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D E Zantut-Wittmann

Publications and source records attributed to D E Zantut-Wittmann.

6 recordsLinked to original sources

99mTc-sestamibi thyroid uptake in euthyroid individuals and in patients with autoimmune thyroid disease.

PURPOSE: We investigated the biokinetics of (99m)Tc-sestamibi in the thyroid of euthyroid volunteers (EVs) and in patients with autoimmune thyroid diseases and determined the best time interval between (99m)Tc-sestamibi injection and calculation of uptake. METHODS: Forty EVs, 30 patients with Graves' disease (GD), 15 patients with atrophic Hashimoto's thyroiditis (AHT) and 15 patients with hypertrophic Hashimoto's thyroiditis (HHT) underwent (99m)Tc-sestamibi thyroid scintigraphy. Dynamic images were acquired for 20 min, and static images were obtained 20 min, 60 min and 120 min post injection. Five-, 20-, 60- and 120-min uptake, time to maximal uptake (T(max)) and T(1/2) of tracer clearance were calculated. Thyroid hormones and antibodies were measured. (99m)Tc-pertechnetate uptake was investigated in GD patients. RESULTS: T(max) was approximately 5 min in all four groups. The mean T(1/2) value for EVs was similar to the GD value and lower than the HHT and AHT values. The mean (+/-SD) 5-min uptake was 0.13% (+/-0.05%) for EVs. The 5-min uptake in GD was higher than that in EVs(P<0.001) and correlated with free thyroxine (r=0.54) and with (99m)Tc-pertechnetate uptake (r=0.68). Uptake in HHT was higher than that in AHT (P=0.0003) and EVs (P=0.002). Uptake in AHT was lower than uptake in EVs (P=0.0001). CONCLUSION: Five minutes is the optimal time interval between (99m)Tc-sestamibi injection and calculation of thyroid uptake. Five-minute uptake differentiates euthyroid individuals from GD patients. There is a high correlation between (99m)Tc-sestamibi and (99m)Tc-pertechnetate uptake in GD. The reduced (99m)Tc-sestamibi uptake in AHT patients is probably due to glandular destruction and fibrosis. Inflammatory infiltrate and high mitochondrial density in thyrocytes possibly explain the increased uptake in GD and HHT.

Adolescent↗

Antithyroid drugs inhibit in vivo HLA-DR expression in thyroid follicular cells in Graves' disease.

Antithyroid drugs have been reported to reduce the expression of HLA-DR in thyrocytes in Graves' disease, but only circumstantial evidence has been provided about their in vivo immunologic effects. This present study was designed to examine the in vivo immunologic effect of antithyroid drugs on thyroid follicular cells. The study was conducted on 25 patients who had Graves' disease in remission or in activity and who were or were not receiving treatment (7 in overt thyrotoxicosis, 6 patients in remission, and 12 patients under medication). HLA-DR expression in thyroid biopsies was verified by immunohistochemistry. The follicular cells of all patients in overt thyrotoxicosis expressed HLA-DR whereas those of patients in remission were negative for HLA-DR. HLA-DR was also not expressed in all patients under medication, but this did not correlate with the clinical evolution after thyroid drug withdrawal. In conclusion, antithyroid drugs inhibit follicular cell HLA-DR expression in Graves' disease, when thyrotoxicosis is controlled. This suggests that additional mechanisms not involving HLA-DR play a role in thyroid autoimmune disease.

Adult↗

Thyroid suppression test with L-thyroxine and [99mTc] pertechnetate.

OBJECTIVE: The thyroid suppression test is still used in some centres as an adjunt in the diagnosis of autonomous functioning thyroid nodules. With the purpose of minimizing the disadvantages of the original T3 suppression test, we have evaluated the efficacy of a method using L-thyroxine as TSH suppression agent and [99 mTc] pertechnetate as radiopharmaceutical. DESIGN: Open nonrandomized prospective study MATERIALS AND METHODS: A control group of 15 normal volunteers (11 males, 4 females; 21-35 years, mean 26.4 years) and a patient group of 20 patients (18 females, 2 males; 27-83 years, mean 53.6 years) divided into 4 subgroups, were studied: 7 patients with autonomous functioning nontoxic nodules, 3 with autonomous functioning toxic nodules, 7 with Graves disease and 3 with nonautoimmune diffuse toxic goitre. Baseline thyroid uptake and imaging were begun 20 minutes after an intravenous injection of 370 MBq (10 mCi) of [99 mTc] pertechnetate. This was followed by a single daily intake of 2 microg/kg of L-thyroxine, for 10 days. Thyroid imaging and uptake were then repeated. RESULTS: In the control group [99 mTc] pertechnetate uptake after L-thyroxine suppression had a mean reduction of 75.8 +/- 7.69% (58-87%) in comparison to the baseline level. All subjects were euthyroid by clinical and laboratory criteria and none complained of side-effects, despite significant suppression of TSH levels. In the patient group, thyroid uptake after suppression decreased in 10 patients (maximum reduction 39%), was unchanged in 2 patients and increased in the remaining 8 patients. CONCLUSION: The method described was efficient for demonstration of autonomous thyroid tissue, since none of the patients showed significant reduction of thyroid uptake after L-thyroxine suppression compared with the control group. This test was as effective as the original T3 suppression test, but more convenient to the patient: no side-effects, ease of hormonal intake, low dosimetry and short stay in the nuclear medicine laboratory.

Adult↗

Autoimmune and non-autoimmune thyroid diseases have different patterns of cellular HLA class II expression.

CONTEXT: Surface HLA-DR antigen is usually only expressed by antigen-presenting cells (APC). In autoimmune thyroid disease, follicle cells function as APC, thus expressing HLA-DR. However, non-autoimmune thyroid diseases may also express surface class II antigens. OBJECTIVE: To evaluate the presence and pattern of HLA class II expression in autoimmune and non-autoimmune thyroid disorders. DESIGN: Retrospective: histopathological and immunohistochemical analysis. LOCATION: Referral center, university hospital. SAMPLE: Ten histologically normal thyroids, 11 Graves' disease, 7 Hashimoto's thyroiditis, 10 atoxic multinodular goiter and 3 toxic adenomas were analyzed by immunohistochemistry, using a monoclonal antibody anti-HLA-DR. MAIN MEASUREMENTS: The presence of these antigens in thyroid follicular cells and their relation to inflammatory infiltrate was evaluated. The pattern of HLA-DR expression in thyroid follicular cells was analyzed: membrane, cytoplasmic or both. RESULTS: Although HLA-DR antigens were sparsely present in one of the 8 normal thyroids, in 6 of the 9 atoxic multinodular goiter and in 2 of the 3 toxic adenomas a net positivity could be seen in large areas. In all 5 Hashimoto's thyroiditis and in 7 of the 10 Graves' disease cases. This expression occurred in follicle cells either in contact with inflammatory cells or not. In non-autoimmune thyroid disease, HLA-DR positivity was essentially cytoplasmic, whereas in Graves' disease and Hashimoto thyroiditis it was mainly in cell membranes. CONCLUSIONS: It is suggested that the HLA class II expression on the surface of follicle cells could be related to auto-antigen presentation to the immune system by these cells, leading to inflammation.

Antibodies, Monoclonal↗

Evidence of integrity of the follicular basement membrane in Hashimoto's thyroiditis.

The basement membrane as an antigenic structure in autoimmune diseases has been a matter of controversy. The purpose of our study was to determine possible structural changes in the follicular basement membrane (FBM) in thyroid autoimmune and non-autoimmune diseases. Immunohistochemical staining for collagen IV and laminin showed that the continuity of the FBM was preserved in toxic adenoma (three cases), atoxic multinodular goiter (nine cases) as well as in autoimmune disease. Integrity of the FBM was observed in all 11 cases of Graves' disease and Hashimoto's thyroiditis (seven cases) studied. In some instances, the FBM was thinned in areas of contact with inflammatory infiltrate. We conclude that the auto-antibodies, and possibly other factors present in autoimmune thyroid diseases, do not significantly alter the integrity of the FBM.

Adenoma↗

Alteration of the follicular basement membrane in non-obese diabetic mice with spontaneous autoimmune thyroiditis.

The follicular basement membrane (FBM) prevents thyroglobulin from escaping to the peri-follicular space, where it can act as an antigen to induce experimental thyroiditis. Laminin, a component of the FBM, is responsible for directing cell migration and stimulates greater adhesion of activated T lymphocytes. Our purpose was to study the expression of laminin in the thyroid of NOD mice, which have a propensity for autoimmune diseases, including thyroiditis. Thirty NOD mice between 3 and 42 weeks old were studied. Eight had thyroiditis and 22 showed no inflammatory infiltration. An immunohistochemical examination using the streptavidin-biotin-peroxidase technique was conducted on paraffin-embedded tissue sections, with a polyclonal antilaminin antibody. Antigen retrieval was achieved through pepsin digestion and microwave irradiation in citrate buffer. Staining for laminin was restricted to the basement membrane. In thyroids with no infiltration, laminin was shown as a fine, continuous brown line in the basement membrane. In 6 out of the 8 cases of thyroiditis, clearcut interruption and destruction of the FBM was observed, particularly when the follicles were located in lymphocyte infiltrated areas or when there was fibrosis. There were significant alterations in the pattern of the FBM with extensive areas of discontinuity in the distribution of laminin. Such discontinuities could facilitate antigen exposure, especially thyroglobulin, which may contribute to autoimmune thyroiditis in NOD mice.

Animals↗