Whither TSH Receptor Blocking Antibodies in the Treatment of Graves' Disease?

Thyroid ◽  
2008 ◽  
Vol 18 (7) ◽  
pp. 695-696 ◽  
Author(s):  
Basil Rapoport ◽  
Sandra M. McLachlan
1992 ◽  
Vol 37 (2) ◽  
pp. 135-140 ◽  
Author(s):  
Z. Kraiem ◽  
B. Y. Cho ◽  
O. Sadeh ◽  
M. H. Shong ◽  
P. Plckerill ◽  
...  

Thyroid ◽  
2008 ◽  
Vol 18 (11) ◽  
pp. 1239-1239 ◽  
Author(s):  
Bernard Rees Smith ◽  
Jadwiga Furmaniak ◽  
Jane Sanders

2020 ◽  
Vol 13 (11) ◽  
pp. e236465 ◽  
Author(s):  
Preethi Padmanaban ◽  
Rohit Jain

We report a case of a 21-year-old young woman who was initially diagnosed with hyperthyroidism secondary to Graves’ disease and spontaneously switched to hypothyroidism in a year. While most autoimmune hypothyroidism is due to Hashimoto’s disease, in her case, we suspect that her hypothyroidism is due to a switch of antibody dominance from thyroid stimulating hormone (TSH) receptor-stimulating antibody (TS Ab) to TSH receptor-blocking antibody (TB Ab). Switching from dominant TS Ab activity to dominant TB Ab activity is a rare phenomenon. Optimal management of this condition is not known. Loss of follow-up and medication non-adherence has made medical management in this young woman of reproductive age further challenging.


2004 ◽  
Vol 89 (1) ◽  
pp. 352-356 ◽  
Author(s):  
Waldemar B. Minich ◽  
Cornelia Lenzner ◽  
Andreas Bergmann ◽  
Nils G. Morgenthaler

We developed a coated tube assay to discriminate TSH-receptor-stimulating autoantibodies [thyroid-stimulating antibodies (TSAb)] from those autoantibodies blocking TSH binding without intrinsic activation [thyroid-blocking antibodies (TBAb)]. The wild-type TSH receptor in the TSH binding-inhibitory assay was exchanged for a chimeric receptor where a TSAb epitope (amino acids 8–165) was replaced by comparable LH-R residues. Binding of 125I-labeled TSH to this chimera could be inhibited by sera containing TBAb up to 95%. Sera from 316 patients with Graves’ disease and 17 with autoimmune thyroid disease were grouped according to their bioassay activity. At the decision threshold, the chimera A assay had a sensitivity of 78.0% for TBAb with a specificity of 90.2%. In detail, 19 of 22 (86.4%) TBAb sera and 15 of 23 (65.2%) TSAb/TBAb sera were positive but only 32 of 216 (14.0%) TSAb sera and 5 of 72 (6.9%) bioassay negative sera. There was a weak but significant positive correlation (r = 0.46) between the chimera assay and the bioassay for TBAb. This is the first report of a coated tube assay for the determination of TBAb employing an adaptation of the TSH binding-inhibitory format, which could be a useful alternative to the bioassay.


2021 ◽  
Vol 30 (2) ◽  
pp. 79-84
Author(s):  
Keisuke Nagasaki ◽  
Akie Nakamura ◽  
Takeru Yamauchi ◽  
Hotaka Kamasaki ◽  
Yosuke Hara ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A913-A914
Author(s):  
Michelle N Lee ◽  
Jeffrey A Colburn

Abstract Disclaimer: The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. Government. Introduction: The most common cause of hypothyroidism is Hashimoto’s thyroiditis, a destructive autoimmune injury to the thyroid gland. Rarely, autoimmune hypothyroidism can be caused by thyroid-stimulating hormone (TSH) receptor blocking antibodies (TSHRab), and can be difficult to differentiate clinically from Hashimoto’s. Grave’s disease is the most common etiology of hyperthyroidism, and is typically caused by activation from TSHRab acting as an agonist for the TSH receptor. Patients with autoimmune thyroiditis, whether from TSHRab or Hashimoto’s, have been infrequently reported to convert to Grave’s disease1–3. Presentation: We present four cases whom initially presented with typical symptoms of hypothyroidism, were diagnosed with autoimmune hypothyroidism and started on levothyroxine. All four cases were later found to be hyperthyroid and ultimately diagnosed and treated for Grave’s disease. Conclusion: Primary hypothyroidism can rarely transition to a hyperthyroid state, although these cases may be underreported. The mechanism isn’t well understood, but is hypothesized to be from a switch of a predominance of TSH receptor blocking antibodies (TBAb) to that of thyroid stimulating antibodies (TSAb)1. Assays using competitive binding for TSH receptor antibodies will not differentiate between blocking and stimulating antibodies4. A high index of suspicion is needed to diagnose these individuals. References: 1. McLachlan SM, Rapoport B. Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: Potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa. Thyroid. 2013;23(1). doi:10.1089/thy.2012.03742. Takasu N, Matsushita M. Changes of TSH-stimulation blocking antibody (TSBAb) and thyroid stimulating antibody (TSAb) over 10 years in 34 TSBAb-positive patients with hypothyroidism and in 98 TSAb-positive graves’ patients with hyperthyroidism: Reevaluation of TSBAb and TSAb in TSH-receptor-antibody (TRAb)-positive patients. J Thyroid Res. 2012;2012. doi:10.1155/2012/1821763. Gonzalez-Aguilera B, Betea D, Lutteri L, et al. Conversion to graves disease from hashimoto thyroiditis: A study of 24 patients. Arch Endocrinol Metab. 2018;62(6). doi:10.20945/2359-39970000000864. Li Y, Kim J, Diana T, Klasen R, Olivo PD, Kahaly GJ. A novel bioassay for anti-thyrotrophin receptor autoantibodies detects both thyroid-blocking and stimulating activity. Clin Exp Immunol. 2013;173(3). doi:10.1111/cei.12129


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