It is important to evaluate patients before they commence therapy with amiodarone. This should include clinical examination and a basal measurement of TSH and TPOAb, together with FT4 and FT3 if TSH is abnormal.
Lithium can cause hypothyroidism and hyperthyroidism in up to 10% of patients. Patients with positive TPOAb are particularly at risk. Patients taking lithium should have their TFT measured at 6 (if TPOAb positive) to 12 month intervals or earlier if goitre develops.
Sub Clinical Hypothyroidism
A TSH concentration above the reference range together with FT4 within the reference range defines subclinical (mild) hypothyroidism . Subclinical hypothyroidism requires to be confirmed 3-6 months after the initial results in order to exclude transient causes of a raised TSH. Subclinical hypothyroid patients who are TPOAb positive are more likely to have higher serum TSH and more likely to develop overt hypothyroidism but do not have increased mortality or increased incidence of ischaemic heart disease.
The decision on treatment of patients with subclinical hypothyroidism should be guided by repeated TSH measurements. When TSH is elevated but <10 mU/L there is no consistent evidence of an association with symptoms, secondary biochemical abnormalities (hyperlipidaemia), cardiac dysfunction or cardiac events. In patients with TSH >10 mU/L there is increasing evidence of progression to overt hypothyroidism and deterioration in hyperlipidaemia with the passage of time particularly in patients with elevated TPOAb. Subjects with subclinical hypothyroidism who are thyroid peroxidase antibody positive should have an annual thyroid function test.
Subjects with subclinical hypothyroidism who are thyroid peroxidase antibody negative should have repeat thyroid function testing approximately every 3 years.
Once a biochemical diagnosis of hyperthyroidism has been made, other tests may be needed to indicate the cause and specialist referral should be sought. Most cases of hyperthyroidism in the UK are due to Graves’ disease or toxic nodular goitre. In most cases the clinical picture indicates the cause (e.g. ophthalmopathy, diffuse goitre in Graves’ disease, nodular goitre in toxic nodular hyperthyroidism), in which case further investigations are not essential. If such clinical signs are absent, the presence of TSH-receptor antibodies is a more specific indicator of the diagnosis. Thyroid auto-antibodies are usually negative in toxic nodular hyperthyroidism.
Royal Devon & Exeter Hospital Chemical Pathology DeptSpecimen Labelling Procedure