|
| |
Most patients have corrected themselves by increasing their serum thyroid hormones in the presence
of normal TSH (Hauffa, 1990; Weiss, 1999a). No treatment is necessary in these cases. When the
patient presents with hyperthyroid symptoms, especially tachycardia, beta-blockers can be used.
The thyroid hormone analogue 3,5,3'-triiodothyroacetic acid (TRIAC) has also been used successfully
to treat some symptoms of RTH such as increased TSH and goitre (Kunitake, 1989; Ueda, 1996;
Darendeliler, 1997; Radetti, 1999). This is due to the fact that TRIAC has a higher affinity for
the TRb then for the TRa, and is metabolized more rapidly then T3. Because of this it has a
limited effect on organs like the heart with a predominance of TRa. Similar treatment successes
with D-T4 (Schwartz, 1992; Pohlenz, 1996) have no clear explanation.
In cases where previous erroneous diagnosis has occurred resulting in post-surgical or post-
radiation hypothyroidism, treatment with thyroid hormone can be started. As an outcome for
successful therapy serum TSH can be used; required T4 doses can be as high as 1000 mg/day
(Weiss 1999a). In the case of ADHD in RTH children it was found that T3 treatment improved
symptoms (Weiss 1977).
In a recent report TRIAC was used to treat a fetus harboring a TR b-mutation in utero to reduce
fetal goitre (Asteria, 1999). Although treatment was successful up to a point, some controversy
has arisen due to the fact that repeated chordocentesis was necessary (with all risks attached to
it) and that we do not know enough about placental TRIAC transport and metabolism (Weiss, 1999a).
Here clearly much more clinical groundwork is needed.
|
|