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Subclinical hypothyroidism
There is a consensus forming that subclinical
hypothyroidism (raised serum TSH but normal
thyroid hormone concentrations) represents the
mildest form of thyroid failure, and as such
should usually be treated with thyroxine. Those
favouring therapy are most influenced by the
knowledge that between 25–50% of such patients
feel better when taking thyroxine,31 and by the
inexorable progression to overt thyroid failure of
approximately 5% each year in those who possess
antithyroid peroxidase antibodies; a risk which
increases with higher serum TSH concentrations
32 .
As hyperlipidaemia is common in overt hypothyroidism
it was anticipated that treatment of subclinical
hypothyroidism with thyroxine would
improve the lipid profile. However, most patients
with subclinical hypothyroidism do not have
increased serum total cholesterol and triglyceride
concentrations and no substantial reduction
occurs after restoration of serum TSH to normal.
Arecent meta-analysis of the effectiveness of therapy
of subclinical hypothyroidism on serum
lipids showed a median decrease in serum total
cholesterol and LDL-cholesterol of only 5%,33 and
smaller studies have suggested that thyroxine has
no effect on lipid concentrations unless serum
TSH is greater than 10 mU/l. Although associations
have been recognised between autoimmune
thyroid disease 34 and subclinical hypothyroidism
35 and myocardial infarction, the link
does not seem to be through hyperlipidaemia.
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A raised serum TSH concentration does not necessarily
imply hypothyroidism and, if there is no
obvious reason for the elevation such as previous
treatment of hyperthyroidism with surgery or
iodine-131, or the presence of other organ specific
autoimmune diseases (pernicious anaemia,
insulin-dependent diabetes mellitus, Addison’s
disease, vitiligo) it is sensible to repeat the measurement
in 3–6 months. Furthermore, serum
TSH concentrations are not normally distributed
within the population and there is a significant
tail of values between the upper limit of the reference
range of 3.5–5.0 mU/l and 8–10 mU/l
which is not associated with evidence of thyroid
disease, particularly in men.
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Figure 1 summarises the current views of the
management of subclinical hypothyroidism.36
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