Management of Primary Hypothyroidism: Statement by the British Thyroid Association Executive Committee

Statement by the British Thyroid Association Executive Committee

Onyebuchi Okosieme; Jackie Gilbert; Prakash Abraham; Kristien Boelaert; Colin Dayan; Mark Gurnell; Graham Leese; Christopher McCabe; Petros Perros; Vicki Smith; Graham Williams; Mark Vanderpump


Clin Endocrinol. 2016;84(6):799-808. 

In This Article


Based on the current literature and following review of the published positions of the ETA and ATA, and in line with the best principles of good medical practice, the BTA, ACB, BTF, RCP and SFE have agreed the following statement:

  1. It is important that high-quality, unbiased, evidence-based information about hypothyroidism is made available to patients and the public. We recognize the need to engage with patients and promote more research in hypothyroidism.

  2. The diagnosis of primary hypothyroidism is based on clinical features of hypothyroidism supported by biochemical evidence that is elevated serum TSH together with low free T4 (overt hypothyroidism) or normal free T4 (subclinical hypothyroidism). Primary hypothyroidism should not be diagnosed in individuals with normal serum TSH who otherwise have intact pituitary function (1/++0).

  3. The evidence in favour of narrowing the serum TSH reference range is not convincing and cannot justify the large increase in the number of healthy people that would require investigation (1/++0).

  4. A significant proportion of healthy subjects in the community have asymptomatic chronic autoimmune thyroiditis and a significant proportion have subclinical hypothyroidism. Spontaneous recovery has been described in subjects with subclinical hypothyroidism. It is more likely in those with negative antithyroid antibodies and serum TSH levels less than 10 mU/l, and within the first 2 years after diagnosis. The higher the serum TSH value, the greater the likelihood of development of overt hypothyroidism in subjects with chronic autoimmune thyroiditis.

  5. Synthetic L-T4 remains the treatment of choice in hypothyroidism with the aim of therapy being to restore physical and psychological well-being while maintaining normal laboratory reference range serum TSH levels (1/++0). After initiation of therapy, TSH should be monitored 6–8 weekly and the dose of L-T4 should be adjusted until a stable TSH is achieved, after which TSH can be checked 4–6 monthly, and then annually (1/+00).

  6. It is acknowledged that a proportion of individuals on L-T4 are not satisfied with therapy and have persistent symptoms despite a normal serum TSH. Such symptoms should be given due consideration and patients should be thoroughly evaluated for other potentially modifiable conditions (Box 1). In some cases, a retrospective review of the original diagnosis of hypothyroidism may be necessary. Symptom and lifestyle management support should be provided and further dose adjustments may be required (1/+00).

  7. Although fine tuning of serum TSH levels within the reference range may be indicated for individual patients, deliberate serum TSH suppression with high dose thyroid hormone replacement therapy (serum TSH <0·1 mU/L) should be avoided where possible as this carries a risk of adverse effects such as cardiac rhythm disorders including atrial fibrillation, strokes, osteoporosis and fracture (1/++0). As an exception, patients with a history of thyroid cancer may require deliberate suppression of serum TSH if there is a significant risk of recurrence.

  8. For the vast majority of patients on L-T4, brand or named supplier prescribing is not considered necessary (2/+00). The Medicines and Healthcare Products Regulatory Agency (MHRA) have recently made recommendations to ensure the quality and consistency of L-T4 tablets that are on the UK market. Rarely, patients may require a specific brand of L-T4 to be prescribed due to intolerance of generic preparations.

  9. Serum T3 should not be used as a therapeutic target in the management of hypothyroidism as the value of this approach is unproven (1/+00).

  10. L-T4/L-T3 combination therapy in patients with hypothyroidism should not be used routinely, as there is insufficient evidence to show that combination therapy is superior to L-T4 monotherapy (1/++0).

  11. Clinicians have an ethical responsibility to adhere to the highest professional standards of good medical practice rooted in sound evidence. This includes not prescribing potentially harmful therapies without proven advantages over existing treatments.

  12. If a decision is made to embark on a trial of L-T4/L-T3 combination therapy in patients who have unambiguously not benefited from L-T4, then this should be reached following an open and balanced discussion of the uncertain benefits, likely risks of over-replacement and lack of long-term safety data. Such patients should be supervised by accredited endocrinologists with documentation of agreement after fully informed and understood discussion of the risks and potential adverse consequences. Many clinicians may not agree that a trial of L-T4/L-T3 combination therapy is warranted in these circumstances and their clinical judgement must be recognized as being valid given the current understanding of the science and evidence of the treatments (2/+00).

  13. The serum TSH reference range in pregnancy is 0·4–2·5 mU/l in the first trimester and 0·4–3·0 mU/l in the second and third trimesters or should be based on the trimester-specific reference range for the population if available. These reference ranges should be achieved where possible with appropriate doses of L-T4 preconception and most importantly in the first trimester (1/++0). L-T4/L-T3 combination therapy is not recommended in pregnancy (1/+00).

  14. There is no convincing evidence to support routine use of thyroid extracts, L-T3 monotherapy, compounded thyroid hormones, iodine containing preparations, dietary supplementation and over the counter preparations in the management of hypothyroidism (1/+00).