We report here a case of alemtuzumab-induced thyroid disease in a female patient who showed a phase of thyrotoxicosis with positive anti-thyroglobulin (anti-Tg) and anti-thyroid peroxidase (TPO) antibodies, but a negative TSH receptor antibody, spontaneously followed by hypothyroidism.
Among the 21 candidate SNPs, no difference was found among areas with various water iodine, whereas, TG (rs2252696), TSHR (rs4903957), CTLA-4 (rs231775), CAPZB (rs1472565), PDE4D (rs27178), and HLA (rs2517532) were significantly associated with various subclinical thyroid diseases; in particular, the PDE4D (rs27178), ad hoc TT allele, was associated with all examined subclinical thyroid diseases.
Obtained TRAb levels were compared with a second-generation TRAb assay employing bovine TSH and a third-generation assay with human mAb M22 as TSHR-binding reagents by investigating 89 patients with GD, 56 with Hashimoto's thyroiditis (HT), 73 with non-autoimmune thyroid diseases, 17 with rheumatoid arthritis, and 100 healthy subjects.
Abnormal thyroid function studies and an elevated thyroid-stimulating hormone receptor antibody level confirmed the diagnosis of Graves thyrotoxicosis.
We reviewed thyroid disease management of patients younger than 18 years with thyrotropin receptor messenger RNA measurements identified from a prospective, institutional review board-approved registry during 2008 to 2010.
The objective of the study was to define a relation of the clinical appearance and the in vitro activity (IVA) of the TSHR mutations described by several authors for these thyroid disorders.
These results suggest that the polymorphisms (polymorphism in intron 1 at 81 bp upstream of exon 2; polymorphism in intron 4 at 135 bp upstream of exon 5; polymorphism in intron 4 at 365 bp upstream of exon 5; polymorphism in intron 5 at 69 bp upstream of exon 6; means polymorphism in intron 6 at 13 bp downstream of exon 6; polymorphism in intron 6 at 187 bp upstream of exon 7; E7+16: polymorphism in 16 bp of exon 7; polymorphism in 40 bp of exon 8) of the TSHR gene may not contribute to the pathogenesis of thyroid diseases.
The reference range and applications for TSHR mRNA were previously defined from 663 samples from patients with normal, benign, and malignant thyroid disease.
Involvement of functional polymorphisms in the TNFA gene in the pathogenesis of autoimmune thyroid diseases and production of anti-thyrotropin receptor antibody.
The prevalence of a positive family history of thyroid diseases was 1.9-fold higher in patients with nonsynonymous mutations in the TSH-R gene than in patients without any mutation (80 vs. 42%; P = 0.03).
However, the clinical spectrum of thyroid abnormalities due to mutant TSHRs is wide and ranges from severe hypoplasia to an almost normal sized and structured thyroid gland.
Detection of thyrotropin-receptor messenger ribonucleic acid (mRNA) and thyroglobulin mRNA transcripts in peripheral blood of patients with thyroid disease: sensitive and specific markers for thyroid cancer.
This can be shown by naturally existing germline and somatic mutations in the TSHR gene that cause various types of nonautoimmune and hereditary thyroid disease.
Lack of association of nonautoimmune hyperfunctioning thyroid disorders and a germline polymorphism of codon 727 of the human thyrotropin receptor in a European Caucasian population.
First evidence for the role of TSH receptor defects in the pathogenesis of congenital thyroid disorders was elucidated by the presence of activating germline mutations leading to congenital hyperthyroidism (Duprez et al., 1994).