Iopanoic acid rapidly controls Type I amiodarone-induced thyrotoxicosis prior to thyroidectomy

被引:33
作者
Bogazzi, F
Aghini-Lombardi, F
Cosci, C
Lupi, I
Santini, F
Tanda, ML
Miccoli, P
Basolo, F
Pinchera, A
Bartalena, L
Braverman, LE
Martino, E
机构
[1] Univ Pisa, Dept Endocrinol & Metab, I-56100 Pisa, Italy
[2] Univ Pisa, Surg Clin, I-56100 Pisa, Italy
[3] Univ Pisa, Dept Oncol, I-56100 Pisa, Italy
[4] Univ Insubria, Chair Endocrinol, Varese, Italy
[5] Boston Med Ctr, Sect Endocrinol Diabet & Nutr, Boston, MA USA
关键词
amiodarone; hyperthyroidism; iopanoic acid;
D O I
10.1007/BF03343984
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Amiodarone-induced thyrotoxicosis (AIT) may develop either in apparently normal thyroid glands (Type 11 AIT) or in the presence of sub-clinical thyroid abnormalities (either autonomous goiter or latent Graves' disease; Type I AIT). Mixed forms also occur. While Type I AIT is due to iodine-induced excess thyroid hormone synthesis, Type 11 AIT is a form of amiodarone (possibly iodine) -induced destructive thyroiditis. Type I AIT is usually treated by combined thionamide and potassium perchlorate therapy, but may be resistant to therapy. On the other hand, Type 11 AIT often responds favorably to gluco-corticoids and may not require further therapy once euthyroidism has been restored. Not infrequently, however, AIT (especially Type 1) is resistant to conventional treatment, and several weeks or months may elapse before euthyroidism is restored. Thyroidectomy has been carried out in Type I AIT patients, but thyroid surgery in thyrotoxic patients, especially those with underlying cardiac problems, carries a high surgical risk. In this study we describe 3 patients with Type I AIT, who were successfully treated with a short course of iopanoic acid (IOP), an oral cholecystographic agent, which is rich in iodine and is a potent inhibitor of 5'-deiodinase, resulting in a marked decrease in the peripheral tissue conversion of T-4 to T-3, in preparation for thyroid surgery. Euthyroidism was rapidly restored in 7-12 days, allowing a subsequent safe and uneventful thyroidectomy in all cases. These patients were then treated with L-T-4 for their hypothyroidism and amiodarone was safely re-instituted. We suggest that IOP is the drug of choice in the rapid restoration of euthyroidism prior to definitive thyroidectomy in patients with drug resistant Type I AIT. (C)2002, Editrice Kurtis.
引用
收藏
页码:176 / 180
页数:5
相关论文
共 20 条
[1]   TREATMENT OF AMIODARONE IODINE-INDUCED THYROTOXICOSIS WITH PLASMAPHERESIS AND METHIMAZOLE [J].
AGHINILOMBARDI, F ;
MARIOTTI, S ;
FOSELLA, PV ;
GRASSO, L ;
PINCHERA, A ;
BRAVERMAN, LE ;
MARTINO, E .
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, 1993, 16 (10) :823-826
[2]   RAPID PREOPERATIVE PREPARATION IN HYPERTHYROIDISM [J].
BAEZA, A ;
AGUAYO, J ;
BARRIA, M ;
PINEDA, G .
CLINICAL ENDOCRINOLOGY, 1991, 35 (05) :439-442
[3]   Effects of amiodarone administration during pregnancy on neonatal thyroid function and subsequent neurodevelopment [J].
Bartalena, L ;
Bogazzi, F ;
Braverman, LE ;
Martino, E .
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, 2001, 24 (02) :116-130
[4]  
BARTALENA L, 2001, J CLIN ENDOCR METAB, V81, P2930
[5]   Color flow Doppler sonography rapidly differentiates type I and type II amiodarone-induced thyrotoxicosis [J].
Bogazzi, F ;
Bartalena, L ;
Brogioni, S ;
Mazzeo, S ;
Vitti, P ;
Burelli, A ;
Bartolozzi, C ;
Martino, E .
THYROID, 1997, 7 (04) :541-545
[6]   Oral cholecystographic agents and the thyroid [J].
Braga, M ;
Cooper, DS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (05) :1853-1860
[7]  
BRENNAN MD, 1987, SURGERY, V102, P1062
[8]   Refractory amiodarone-associated thyrotoxicosis: An indication for thyroidectomy [J].
Claxton, S ;
Sinha, SN ;
Donovan, S ;
Greenaway, TM ;
Hoffman, L ;
Loughhead, M ;
Burgess, JR .
AUSTRALIAN AND NEW ZEALAND JOURNAL OF SURGERY, 2000, 70 (03) :174-178
[9]   Clinical review 120 - Amiodarone-induced thyrotoxicosis [J].
Daniels, GH .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (01) :3-8
[10]   Amiodarone induces cytochrome c release and apoptosis through an iodine-independent mechanism [J].
Di Matola, T ;
D'Ascoli, F ;
Fenzi, G ;
Rossi, G ;
Martino, E ;
Bogazzi, F ;
Vitale, M .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (11) :4323-4330