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Carsten Kirkegaard - One of the best experts on this subject based on the ideXlab platform.
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Serum TSH and the response to radioiodine treatment of toxic Multinodular Goitre
2015Co-Authors: Ulrik Pedersen-bjergaard, Carsten KirkegaardAbstract:A retrospective analysis of data from 73 consecutive patients with toxic Multinodular Goitre treated with iodine-131 (131I) during a 2-year period was performed to investigate if serum TSH at the time of 131I treatment influences the outcome. The dose of 131I was calculated according to a model compensating for thyroid size estimated by palpation and 24-h 131I uptake. Serum TSH was determined by a third-generation assay with a functional sensitivity of 0.03 mU/l. A significantly more pronounced response to 131I treatment was observed in patients with TSH> 0.0 mU/l than in patients with TSH=0.0 mU/l (P 0.0006). This difference resulted in a threefold lower frequency of non-responders and a fivefold higher rate of early hypothyroidism in the group with detectable serum TSH. While the high frequency of hypothyroidism among patients with measurable serum TSH can be explained by destruction of normal thyroid tissue, the high frequency of treatment failure in the group with serum TSH 0.0 mU/l suggests that autonomous thyroid tissue may also be sensitized to a deleterious effect of 131I through stimulation by TSH. We conclude that serum TSH has a significant influence on the outcome of 131I treatment of toxic Multinodular Goitre. The results of 131I treatment may be improved by adjustment of the dose of 131I according to the serum TSH level, in addition to adjustment for Goitre size and 24-h 131I uptake. European Journal of Endocrinology 137 365–36
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Serum TSH and the response to radioiodine treatment of toxic Multinodular Goitre
European journal of endocrinology, 1997Co-Authors: Ulrik Pedersen-bjergaard, Carsten KirkegaardAbstract:A retrospective analysis of data from 73 consecutive patients with toxic Multinodular Goitre treated with iodine-131 ( 131 I) during a 2-year period was performed to investigate if serum TSH at the time of 131 I treatment influences the outcome. The dose of 131 I was calculated according to a model compensating for thyroid size estimated by palpation and 24-h 131 I uptake. Serum TSH was determined by a third-generation assay with a functional sensitivity of 0.03 mU/l. A significantly more pronounced response to 131 I treatment was observed in patients with TSH > 0.0 mU/l than in patients with TSH=0.0 mU/l (P o 0.0006). This difference resulted in a threefold lower frequency of non-responders and a fivefold higher rate of early hypothyroidism in the group with detectable serum TSH. While the high frequency of hypothyroidism among patients with measurable serum TSH can be explained by destruction of normal thyroid tissue, the high frequency of treatment failure in the group with serum TSH o 0.0 mU/l suggests that autonomous thyroid tissue may also be sensitized to a deleterious effect of 131 I through stimulation by TSH. We conclude that serum TSH has a significant influence on the outcome of 131 I treatment of toxic Multinodular Goitre. The results of 131 I treatment may be improved by adjustment of the dose of 131 I according to the serum TSH level, in addition to adjustment for Goitre size and 24-h 131 I uptake.
A. C. Nieuwenhuijzen Kruseman - One of the best experts on this subject based on the ideXlab platform.
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peripheral bone density in women with untreated Multinodular Goitre
Clinical Endocrinology, 1992Co-Authors: A. H. Mudde, F. J. L. Reijnders, A. C. Nieuwenhuijzen KrusemanAbstract:OBJECTIVES We wished to determine whether women with Multinodular Goitre and spontaneous subclinical hyperthyroidism have decreased bone density. DESIGN AND SUBJECTS Bone density was measured at the distal and proximal forearm. Data were expressed as Z-scores relative to the mean values out of 125 control subjects matched for age and menopause. The Z-scores of 23 women with subclinical hyperthyroid Goitre (TSH<0.1 mU/l and normal values for FT4 and total T3) and of 54 women with euthyroid Goitre were compared. MEASUREMENTS Bone density was measured by single photon absorptiometry. TSH was measured by IRMA, FT4 by RIA. RESULTS Relative to the euthyroid Goitre subjects the mean±SEM Z-scores of both the distal and proximal forearm density were lower (- 0.69±0.17 vs - 0.1 ± 0.18, P <0.05 and -0.5±0.18 vs 0.07±0.18, P <0.05, respectively). Median (range) FT4 in the subclinical hyperthyroid Goitre subjects was significantly higher than euthyroid Goitre subjects (15.6 (11–23.2) pmol/l vs 11.9 (8.3–18.3) pmol/l, P <0.001) although still within the normal range. FT4 correlated inversely with Z-scores of both distal and proximal forearm bone density in the subjects with subclinical hyperthyroidism (r= -0.42, P <0.05 and r= -0.43, P <0.05, respectively), but not in the euthyroid Goitre subjects. CONCLUSION These findings indicate that women with untreated Multinodular Goitre and subclinical hyperthyroidism have reduced bone density in the forearm.
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Peripheral bone density in women with untreated Multinodular Goitre.
Clinical endocrinology, 1992Co-Authors: A. H. Mudde, F. J. L. Reijnders, A. C. Nieuwenhuijzen KrusemanAbstract:OBJECTIVES We wished to determine whether women with Multinodular Goitre and spontaneous subclinical hyperthyroidism have decreased bone density. DESIGN AND SUBJECTS Bone density was measured at the distal and proximal forearm. Data were expressed as Z-scores relative to the mean values out of 125 control subjects matched for age and menopause. The Z-scores of 23 women with subclinical hyperthyroid Goitre (TSH
Frédérique Savagner - One of the best experts on this subject based on the ideXlab platform.
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Multinodular Goitre is a gateway for molecular testing of DICER1 syndrome.
Clinical endocrinology, 2019Co-Authors: Isabelle Oliver-petit, Anne‐isabelle Bertozzi, Solange Grunenwald, Marion Gambart, Patricia Pigeon‐kerchiche, Jean-louis Sadoul, Philippe Caron, Frédérique SavagnerAbstract:Background DICER1 syndrome is an autosomal dominant disorder that predisposes individuals to develop benign or malignant tumours from infancy to adulthood. There is low-to-moderate penetrance of tumour development, which is sex- and age-dependent. Multinodular Goitre (MNG) is among the most highly penetrant phenotype of the disorder, especially in females. Patients and methods We report a series of eight families referred for childhood-onset of MNG or DICER1-related tumours with familial history of MNG in relatives. No additional families with these criteria stated were identified during the same date. We screened DNA samples from the probands and members of their family (40) for constitutional DICER1 variants using Next Generation Sequencing tools. Results Germline pathogenic DICER1 gene variants were identified in all probands and several of their relatives: 64% presented with MNG/thyroidectomy as the phenotypic expression of the syndrome. DICER1 gene variants were identified in the RNAseIII and the PAZ domains. All tumour tissues studied presented clonal pathogenic variants in hotspot regions. Early identification of DICER1 variant carriers has permitted diagnosis and therapeutic scheme correction for two patients and cascade testing in relatives. Conclusions Multinodular Goitre is uncommon in children. Childhood-onset MNG, multiple occurrences of the disease within the same family, or its association with rare benign or malignant tumours should raise suspicions of anomalies in the DICER1 gene, as proposed by recent international recommendations. Early detection of DICER1 pathogenic variants has important consequences in terms of therapeutic strategy, early tumour screening, and genetic counselling.
Yoshio Ban - One of the best experts on this subject based on the ideXlab platform.
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Toxic Multinodular Goitre in a patient with generalized resistance to thyroid hormone who harbours the R429Q mutation in the thyroid hormone receptor β gene
Clinical endocrinology, 2001Co-Authors: Matsuo Taniyama, Naofumi Ishikawa, Naoko Momotani, Koichi Ito, Yoshio BanAbstract:The association of resistance to thyroid hormone (RTH) due to a receptor defect with toxic Multinodular Goitre or with carcinoma of the thyroid has not been previously reported. Previous histopathological studies of the thyroid gland in patients with RTH have revealed changes similar to Multinodular Goitre, probably due to continuous stimulation by TSH. We report here a case of generalized resistance to thyroid hormone associated with a Multinodular Goitre, which became toxic. The patient was a 46-year-old Japanese woman who noticed a Goitre although she had no symptoms of thyrotoxicosis. Initial examination revealed elevated serum thyroid hormone levels and a normal TSH level. Ultrasonography disclosed a Multinodular Goitre with cystic lesions. Three years later, the patient complained that the Goitre had become larger and that she had developed symptoms of thyrotoxicosis such as palpitation and hyperhydrosis. Progressive hyperthyroxinaemia with relatively suppressed TSH, increased radioiodine uptake and negative anti-TSH receptor antibodies led to the diagnosis of toxic Multinodular Goitre. Subtotal thyroidectomy was performed, and pathological examination revealed a micropapillary carcinoma within the Multinodular Goitre. Occurrence of thyroid carcinoma should be considered in RTH because its incidence is high in Multinodular Goitre. Molecular examination revealed the R429Q mutation in the thyroid hormone receptor β gene, which is one of the mutations usually manifesting as the pituitary resistance phenotype. That thyrotoxic manifestations appeared only during toxic stage of Multinodular Goitre in this case suggests that the phenotype of this type of mutation can be dependent on the amount of thyroid hormone.
Ulrik Pedersen-bjergaard - One of the best experts on this subject based on the ideXlab platform.
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Serum TSH and the response to radioiodine treatment of toxic Multinodular Goitre
2015Co-Authors: Ulrik Pedersen-bjergaard, Carsten KirkegaardAbstract:A retrospective analysis of data from 73 consecutive patients with toxic Multinodular Goitre treated with iodine-131 (131I) during a 2-year period was performed to investigate if serum TSH at the time of 131I treatment influences the outcome. The dose of 131I was calculated according to a model compensating for thyroid size estimated by palpation and 24-h 131I uptake. Serum TSH was determined by a third-generation assay with a functional sensitivity of 0.03 mU/l. A significantly more pronounced response to 131I treatment was observed in patients with TSH> 0.0 mU/l than in patients with TSH=0.0 mU/l (P 0.0006). This difference resulted in a threefold lower frequency of non-responders and a fivefold higher rate of early hypothyroidism in the group with detectable serum TSH. While the high frequency of hypothyroidism among patients with measurable serum TSH can be explained by destruction of normal thyroid tissue, the high frequency of treatment failure in the group with serum TSH 0.0 mU/l suggests that autonomous thyroid tissue may also be sensitized to a deleterious effect of 131I through stimulation by TSH. We conclude that serum TSH has a significant influence on the outcome of 131I treatment of toxic Multinodular Goitre. The results of 131I treatment may be improved by adjustment of the dose of 131I according to the serum TSH level, in addition to adjustment for Goitre size and 24-h 131I uptake. European Journal of Endocrinology 137 365–36
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Serum TSH and the response to radioiodine treatment of toxic Multinodular Goitre
European journal of endocrinology, 1997Co-Authors: Ulrik Pedersen-bjergaard, Carsten KirkegaardAbstract:A retrospective analysis of data from 73 consecutive patients with toxic Multinodular Goitre treated with iodine-131 ( 131 I) during a 2-year period was performed to investigate if serum TSH at the time of 131 I treatment influences the outcome. The dose of 131 I was calculated according to a model compensating for thyroid size estimated by palpation and 24-h 131 I uptake. Serum TSH was determined by a third-generation assay with a functional sensitivity of 0.03 mU/l. A significantly more pronounced response to 131 I treatment was observed in patients with TSH > 0.0 mU/l than in patients with TSH=0.0 mU/l (P o 0.0006). This difference resulted in a threefold lower frequency of non-responders and a fivefold higher rate of early hypothyroidism in the group with detectable serum TSH. While the high frequency of hypothyroidism among patients with measurable serum TSH can be explained by destruction of normal thyroid tissue, the high frequency of treatment failure in the group with serum TSH o 0.0 mU/l suggests that autonomous thyroid tissue may also be sensitized to a deleterious effect of 131 I through stimulation by TSH. We conclude that serum TSH has a significant influence on the outcome of 131 I treatment of toxic Multinodular Goitre. The results of 131 I treatment may be improved by adjustment of the dose of 131 I according to the serum TSH level, in addition to adjustment for Goitre size and 24-h 131 I uptake.