Treatment of type II amiodarone-induced thyrotoxicosis by either iopanoic acid or glucocorticoids: a prospective, randomized study.
Amiodarone-induced thyrotoxicosis (AIT) may occur either in the presence of underlying thyroid disease (type I AIT) or in apparently normal thyroid glands (type II AIT). Type II AIT, a destructive thyroiditis, often favorably responds to glucocorticoids. Iopanoic acid (IopAc) is an iodinated cholecystographic agent that inhibits deiodinase activity and reduces the conversion of T(4) toT(3). It has recently been reported that cholecystographic agents restore euthyroidism in patients with type II AIT. We describe the results of a prospective randomized study conducted in 12 patients with type II AIT treated with either iopanoic acid (group A, n = 6) or glucocorticoids (group B, n = 6). Serum free T(3) levels normalized rapidly in both groups after 7 d, from 0.75 +/- 0.20 ng/dl (11.5 +/- 3.1 pmol/liter) to 0.46 +/- 0.10 ng/d (7.1 +/- 1.7 pmol/liter), P < 0.01, and from 0.58 +/- 0.10 ng/dl (9.0 +/- 1.2 pmol/liter) to 0.34 +/- 0.03 ng/dl (5.2 +/- 0.5 pmol/liter), P < 0.003, in groups A and B, respectively (P = NS). Serum free T(4) levels reduced at 6 months in group B [from 2.70 +/- 0.32 ng/dl (35.1 +/- 4.1 pmol/liter) to 1.0 +/- 0.04 ng/dl (13.4 +/- 0.6 pmol/liter), P < 0.0001] but not in group A (from 2.90 +/- 0.6 ng/dl (38.0 +/- 7.5 pmol/liter) to 2.30 +/- 0.4 ng/dl (35.6 +/- 6.1 pmol/liter, P = 0.39; P = 0.005 group B vs. group A). All patients in both groups became euthyroid and had their amiodarone-induced destructive thyroiditis cured as defined by normalization of both serum free T(4) and free T(3) levels, during both drugs therapy. However, patients in group B were cured more rapidly than patients in group A (43 +/- 34 d vs. 221 +/- 111 d, respectively, P < 0.002). This study shows that, albeit both drugs are effective, glucocorticoids are probably the drug of choice for more rapidly curing type II AIT.
Bogazzi
Fausto
F
Department of Endocrinology and Metabolism, University of Pisa, Italy. fbogazzi@hotmail.com
Bartalena
Luigi
L
Cosci
Chiara
C
Brogioni
Sandra
S
Dell'Unto
Enrica
E
Grasso
Lucia
L
Aghini-Lombardi
Fabrizio
F
Rossi
Giuseppe
G
Pinchera
Aldo
A
Braverman
Lewis E
LE
Martino
Enio
E
D000368:Aged; D000638:Amiodarone / Q000009:adverse effects*; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D007453:Iodide Peroxidase / Q000037:antagonists & inhibitors; D007480:Iopanoic Acid / Q000627:therapeutic use*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D011446:Prospective Studies; D013971:Thyrotoxicosis / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy*; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D000889:Anti-Arrhythmia Agents; D004791:Enzyme Inhibitors; D005938:Glucocorticoids; D014284:Triiodothyronine; D007453:Iodide Peroxidase; D007480:Iopanoic Acid; D000638:Amiodarone; D013974:Thyroxine; D011241:Prednisone