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Most patients with primary hypothyroidism
require lifelong treatment with thyroxine. There
are, however, well-recognised situations in which
the thyroid failure is transient. For example, during
the recovery phase of subacute or painless
thyroiditis (including postpartum thyroiditis)
patients may have asymptomatic or mild
hypothyroidism for a few weeks which does not
usually justify treatment. Hypothyroidism
caused by chronic autoimmune thyroiditis may
remit spontaneously, particularly if excessive
iodine intake has been implicated, as in treatment
with the antidysrhythmic drug, amiodarone. It is
often not appreciated that hypothyroidism may
be transient if it occurs within 6 months of subtotal
thyroidectomy or iodine-131 for hyperthyroidism.
If thyroxine therapy is required at an
early stage a suboptimal dose of 75 µg daily
should be prescribed. Measurement of serum T 4
and TSH at 6 months will indicate whether continued
treatment with a higher dose is required
(raised serum TSH) or whether the thyroxine can
be discontinued (low or normal TSH) and thyroid
function reassessed 4–6 weeks later.
Goitre suppression Thyroxine in a dose sufficient to suppress serum TSH may be necessary to achieve maximum goitre shrinkage in patients with Hashimoto’s thyroiditis.37 Although thyroxine is often prescribed in an attempt to decrease the size of the thyroid in patients with diffuse or nodular goitre and to prevent regrowth after surgery, there are conflicting views on its effectiveness, reflecting the complexity of the causes of the disorder. However, what is established is that the natural history of multinodular goitre is the slow progression to hyperthyroidism over a period of approximately 20 years as autonomously functioning nodules increase in size and number. It follows, therefore, that in any patient with a nodular goitre and a low serum TSH concentration, thyroxine therapy is inadvisable since it may induce hyperthyroidism. In what is usually an elderly population this may have serious consequences such as the development of atrial fibrillation complicated by systemic embolism. Combination therapy with antithyroid drugs Although most patients with Graves’ disease are readily controlled with an antithyroid drug alone, there are circumstances when a “block and replace” regime with thyroxine combined with carbimazole (methimazole) or propylthiouracil is appropriate. In some patients thyroid function, while taking an antithyroid drug diligently, fluctuates between hyper- and hypothyroidism due to variation in the concentrations or ratios of stimulating and blocking TSH-receptor antibodies. Good control can only be achieved in this circumstance using combination therapy. In addition, in patients with significant ophthalmopathy it is essential to maintain as good control of thyroid function as possible and this is often most readily achieved by a “block and replace” regime, which may have the added advantage of the immuno-suppressive action of sustained high dose antithyroid drug therapy. Despite earlier claims, combination therapy does not lead to an increased remission rate in patients with Graves’ disease either given for a period of 18 months or more, or when the regime is applied unconventionally such that thyroxine alone is continued after the antithyroid drug is stopped.38,39 Non-thyroidal illness The biochemical changes of low serum TSH and T 3 associated with illness or starvation are often considered teleologically as an adaptive response to spare calories and protein. However, it is not clear whether severe illness can, in some circumstances, cause the potentially detrimental entity of “tissue hypothyroidism”.40 Although the present consensus is that thyroid hormone treatment is not indicated in patients with significant nonthyroidal illness, this has become a controversial issue. For example, there are studies which have shown improvements in cardiac output and systemic vascular resistance in patients with chronic cardiac failure following treatment with intravenous T 3 , 41 but there is, as yet, no evidence that intervention improves survival. Triiodothyronine in doses as high as 60 µg daily, which would produce symptoms of hyperthyroidism in normal individuals, have been employed in psychiatric practice in the treatment of depressed patients who respond unsatisfactorily to standard therapies, and to hasten the response to antidepressants, but the results are inconclusive.42 “Hypothyroidism” despite normal tests of thyroid function There is a vociferous lobby of patients, supported by some doctors with an eccentric view of thyroid physiology, that hypothyroidism can exist in the presence of normal tests of thyroid function. Known in North America as Wilson’s syndrome, affected patients complain of a variety of non-specific symptoms, such as fatigue, weight gain and low mood and make extravagant claims for the efficacy of thyroid hormone therapy. Their belief is that the reference ranges for serum T 4 and TSH are so wide that what are considered normal values may not be normal for them. Their stance does not take into account the fact that the pituitary thyrotroph is very sensitive to minor changes in thyroid hormone concentrations within the normal range 2 and, for example, a reduction in free T 4 from 20 to 14 pmol/l would be associated with a significant increase in serum TSH. For Wilson’s syndrome to exist would require a re-setting of the hypothalamic-pituitary-thyroid axis which has never been described. Furthermore, the only double- blind placebo-controlled trial of patients with symptoms which could be attributed to thyroid failure but with normal tests of thyroid function, not surprisingly, failed to show any benefit from thyroxine therapy.43 |
