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Technical Briefs |
1
Department of Laboratory Medicine, National Taiwan University Hospital, and
2
Department of Laboratory Medicine, Taipei City Psychiatric Center, Taipei 100, Taiwan, Republic of China
aaddress correspondence to this author at: Department of Laboratory Medicine, College of Medicine, and National Taiwan University Hospital, No. 7 Chung-Shan South Road, Taipei 100, Taiwan; fax 886-2-2322-4263, e-mail kstsaimd@ha.mc.ntu.edu.tw
Estrogen (1)(2)(3)(4)(5) may increase hepatic production of
thyroxine-binding globulin (TBG) and decrease TBG clearance
(6), thus increasing serum total thyroxine
(tT4) (3)(4) and, to a
lesser extent, total triiodothyronine (tT3)
(3)(4). As a result, increased
tT4 and tT3 are seen in
states of excessive estrogen and/or progestin, such as pregnancy,
estrogen replacement therapy (HRT) (5), and oral
contraceptive usage (1). This phenomenon may cause problems
in clinical diagnoses when tT4 or
tT3 is used for these patients. On the other
hand, estrogen has been shown to increase thyroid-stimulating hormone
(TSH) and to decrease free thyroxine (fT4)
through a mild inhibitory effect on the thyroid gland (4).
Compound that are analogs of estrogens, such as tamoxifen, have
been shown to increase TSH without decreasing fT4
(7)(8). Recently, a new category of therapeutic
agents, collectively termed selective estrogen receptor modulators
(SERMs), has
References
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