Biochemical tests are important in diagnosis

Editor—Like Gordon R B Skinner and colleagues, we recognise that the clinical diagnosis of hypothyroidism is a challenge for general practitioners1; recent reviews of the published literature make it clear that the non-specific nature of the signs and symptoms of hypothyroidism means that biochemical tests of thyroid function (specifically serum thyroid stimulating hormone) are an essential component of the diagnosis.2 3 4 5

There were several shortcomings in the letter from Skinner and colleagues. The clinical criteria of hypothyroidism used are neither stated nor referenced. The method of selecting patients is not stated; as a result the letter wrongly implies that for every four to five patients with biochemical evidence of hypothyroidism there are 75 who are clinically hypothyroid but biochemically euthyroid. No recognition is given to the natural history of primary hypothyroidism which requires an increase in thyroid stimulating hormone to maintain thyroid hormone production in a failing gland. Consequently, the authors wrongly place equal weight on the measurement of thyroid stimulating hormone and free thyroxine as diagnostic tests of hypothyroidism especially at the early (subclinical) stage.

New objective scientific evidence is always a useful addition to current knowledge and understanding. Therefore, there may be merit in a short term incremental trial of thyroxine in a cohort of patients who are clinically hypothyroid but biochemically euthyroid, provided that objective criteria are used for patient definition and assessment during treatment; the trial is blind and placebo controlled with crossover; appropriate biochemical measurements are made before and during the trial; and it is recognised that no evidence will be obtained about the likely success of continued treatment or of any long term side effects of such treatment.

Threshold of thyroid stimulating hormone should be higher before treatment is started

Editor—A P Weetman summarised the available data on hypothyroidism. I am, however, concerned about the suggestion that all patients with thyroid antibodies and with a normal thyroxine concentration but raised thyroid stimulating hormone concentration (whatever its value) should be treated with thyroxine.1 The Whickham survey reported that only 55% of such patients developed hypothyroidism after 20 years of follow up.2 The recommendation to treat patients with a thyroid stimulating hormone just above the upper limit of normal assumes that the patient's hypothalamopituitary axis would not secrete more thyroid stimulating hormone despite sensing the body's need for more thyroxine. It also assumes that the doctor (in most cases the general practitioner) would know the particular concentration of thyroid stimulating hormone to aim for in a particular patient. This is debatable3; patients are frequently referred to my clinic for assessment of the correct dose of thyroxine.

I would suggest a threshold of thyroid stimulating hormone of, for example, 10 mU/l or a compelling clinical indication before starting thyroxine treatment in this group. Patients not given thyroxine treatment should be followed up every six to 12 months indefinitely.