Neonatal Thyroid Function after Propylthiouracil Therapy for Maternal Graves' Disease

1981 ◽  
Vol 304 (9) ◽  
pp. 525-528 ◽  
Author(s):  
Robert G. Cheron ◽  
Michael M. Kaplan ◽  
P. Reed Larsen ◽  
Herbert A. Selenkow ◽  
John F. Crigler
2004 ◽  
Vol 18 (2) ◽  
pp. 289-302 ◽  
Author(s):  
Michel Polak ◽  
Isabelle Le Gac ◽  
Edith Vuillard ◽  
J. Guibourdenche ◽  
J. Leger ◽  
...  

2016 ◽  
Vol 22 ◽  
pp. 305-306
Author(s):  
Sheela Metgud ◽  
Anup Kumar ◽  
Erin Drever ◽  
Tahira Yasmeen

2008 ◽  
Vol 47 (04) ◽  
pp. 153-166 ◽  
Author(s):  
I. Weber ◽  
W. Eschner ◽  
F. Sudbrock ◽  
M. Schmidt ◽  
M. Dietlein ◽  
...  

SummaryAim: This study was performed to analyse the impact of the choice of antithyroid drugs (ATD) on the outcome of ablative radioiodine therapy (RIT) in patients with Graves' disease. Patients, material, methods: A total of 571 consecutive patients were observed for 12 months after RIT between July 2001 and June 2004. Inclusion criteria were the confirmed diagnosis of Graves' disease, compensation of hyperthyroidism and withdrawal of ATD two days before preliminary radioiodine-testing and RIT. The intended dose of 250 Gy was calculated from the results of the radioiodine test and the therapeutically achieved dose was measured by serial uptake measurements. The end-point measure was thyroid function 12 months after RIT; success was defined as elimination of hyperthyroidism. The pretreatment ATD was retrospectively correlated with the results achieved. Results: Relief from hyperthyroidism was achieved in 96 % of patients. 472 patients were treated with carbimazole or methimazole (CMI) and 61 with propylthiouracil (PTU). 38 patients had no thyrostatic drugs (ND) prior to RIT. The success rate was equal in all groups (CMI 451/472; PTU 61/61; ND 37/38; p=0.22). Conclusion: Thyrostatic treatment with PTU achieves excellent results in ablative RIT, using an accurate dosimetric approach with an achieved post-therapeutic dose of more than 200 Gy.


1990 ◽  
Vol 32 (2) ◽  
pp. 141-152 ◽  
Author(s):  
ROBIN H. MORTIMER ◽  
SHIRLEY A. TYACK ◽  
JOHN P. GALLIGAN ◽  
DONALD A. PERRY-KEENE ◽  
YONG M. TAN

1993 ◽  
pp. 199-209 ◽  
Author(s):  
François Delange ◽  
Pierre Bourdoux ◽  
Michael Laurence ◽  
Lilia Peneva ◽  
Paul Walfish ◽  
...  

2011 ◽  
Vol 5 (1) ◽  
pp. 9 ◽  
Author(s):  
Atsushi Fukao ◽  
Junta Takamatsu ◽  
Sumihisa Kubota ◽  
Akira Miyauchi ◽  
Toshiaki Hanafusa

Author(s):  
Nami Suzuki ◽  
Akiko Kawaguchi ◽  
Jaeduk Yoshimura Noh ◽  
Ran Yoshimura ◽  
Kentaro Mikura ◽  
...  

Abstract Background Thyroid stimulating hormone (TSH) receptor antibody (TRAb) is detected in the serum of patients with Graves’ disease (GD). This study aims to investigate the prevalence of euthyroid individuals showing positive results for TRAb and to clarify the clinical course of thyroid function and TRAb levels in these subjects. Objective Subjects were female patients who newly visited our hospital for a screening test prior to fertility treatment and showed normal thyroid function and volume without nodules between 2014 and 2017. After excluding subjects with a history of thyroid disease, 5,622 subjects were analyzed. Results Forty-seven of the 5,622 subjects showed positive results for TRAb (reference range, < 2.0 IU/L) at the initial visit. Median initial TRAb was 2.9 IU/L (range, 2.0 -14.7 IU/L) and median follow-up was 18.3 months (range, 0- 66.5 months). Six of the 47 subjects (12.8%) developed GD and median duration until development was 6.6 months (range, 1.2 -13.2 months). Median TRAb values initially and at diagnosisof GD for those 6 patients were 3.7 IU/L (range, 2.7 -5.1 IU/L) and 7.2 IU/L (range 3.6 -21.4 IU/L), respectively. TRAb results turned negative for 20 of the 47 subjects, but remained positive despite normal thyroid function in 13 of the 47 subjects. Conclusion GD developed over time in 12.8% of euthyroid young female patients showing positive TRAb within a median of 6.6 months. A positive result for TRAb itself did not mean development of GD, so other factors must be essential for the pathogenesis of GD.


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