>
>Dear All
>
>1. Patients on adequate thyroxine replacement (i.e normal/lowish TSH +
>normal/highish FT4) tend to have lowish FT3, is there any explanation?
I always assumed it was because the thyroid can produce both T4 and T3 which
adds to the T3 that is formed by peripheral conversion. With replacement it
is only the latter which circulates.
>
>2. In determining optimal replacement dose, should normalisation of TSH be
>the sole determinant, even if the patient still has clinical symptoms of
>hypothyroidism?
You may have noticed that in the new GP contract that there are quality
points for testing for TFTs in patients on T4, but there are no targets to
achieve. This is because their advisors felt there was insufficient evidence
to be dogmatic about this.
>
>3. If FT3 is the active hormone, should we be monitoring it for determining
>adequacy of replacement?
There was a vogue for measuring total T3 at one point, but it seems to have
disappeared.
>
>4. Is there any merit in using combination of T3 + T4 as replacement in
>hypothyroid patients?
The original New England Journal paper advocating its use has since had its
study design roundly criticised.
>
>5. Since T4 half life is > 7 days, why should it be taken daily?
One of our endocrinologists gives a weekly supervised dose of 1 mg T4 in
patients who appear unresponsive to T4. I do not know of one where the TSH
did not subsequently fall!
>
Eric
Dr. Eric S. Kilpatrick MD, FRCPath
Consultant in Chemical Pathology
Hull Royal Infirmary
Anlaby Rd
Hull HU3 2JZ
Tel: 01482-607708
Fax: 01482-607752
>thanks
>
>Mohammad
>
>
>
>Dr. M A Al-Jubouri
>Consultant Chemical Pathologist
>
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