Response to editorial on thyroid function tests and hypothyroidism
The editorial in the BMJ 2003, 8th February, by Toft and Beckett is
disappointing in a number of regards. The opening paragraph encapsulates
the generalised and arrogant approach taken by Dr Toft together with so
many of his colleagues. His suggestion that patients with symptoms of
hypothyroidism, but normal blood tests, are a “vociferous minority” who
have psychosocial problems, is entirely misleading and quite insulting to
a great many patients. If he could be persuaded to take the trouble to
undertake a full clinical appraisal, including the invaluable basal
temperature test, suggested by Barnes as long ago as 1945 in the Lancet,
he would doubtless be able to make a diagnosis of hypothyroidism on
clinical grounds, and learn for himself the pitfalls of an uncritical
reliance on blood tests.
His second paragraph, concerning “misguided medical practitioners”
who in their alleged unwisdom actually try to solve their patients’
problems by using T3 as well as T4, or natural desiccated thyroid, is
again gratuitously insulting. These practitioners do not attempt to hit
some desired T4 or TSH level, but actually titrate the dosage to their
patients’ needs. A process called listening to the patient. Reliance on
the “sensitivity” of the TSH, expressly disregarding the clinical
response, is misplaced; the test approach must have a sensitivity of at
least 0.02 mu/l, which is difficult to reliably achieve and thus affords a
frequently seen cause for error.
He raises again the spectre of iatrogenic hyperthyroidism as a cause
of osteoporosis and atrial fibrillation. Although a theoretical
possibility, there is no evidence for this and I have never seen it in
many thousands of patients. It is particularly unlikely when patients
have been taught the value of self-monitoring.
Dr Toft refers to Pollock et al, who purported to demonstrate, in a
much criticised paper, that thyroxine helped a little in patients with
incontrovertible hypothyroidism but didn’t at all if they hadn’t. As with
the authors, Dr Toft confuses symptoms with a full clinical appraisal
providing a consequent diagnosis, which it is perfectly proper for an
experienced physician to make despite a normal TSH and T4. Neither this
paper nor Dr Toft’s comments have furthered understanding in any way.
Again, he refers to “the exquisite” sensitivity of the TSH which
leads him and his colleagues astray. He is right to point out that
pituitary or hypothalamic weakness, very much more common than he
believes, will provide a false low TSH; he would do well to remember that
a hypometabolic pituitary/hypothalamic axis is a commonly met cause of
unreliable TSH estimations.
However his observation that a replacement providing a higher than
normal T4 and suppressed TSH allows for greater patient well-being is to
be welcomed. Further is to be welcomed his consideration concerning the
addition of T3 to T4, if somewhat rather late in the day. Perhaps he
might in due course be persuaded that the use of T2 as well, as with
desiccated thyroid, confers additional advantage.
Dr Barry Durrant-Peatfield M.B., B.S., L.R.C.P, M.R.C.S.
Competing interests: No competing interests