Thyroxine should be tried in clinically hypothyroid but biochemically euthyroid patientsBMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7096.1764 (Published 14 June 1997) Cite this as: BMJ 1997;314:1764
- Gordon R B Skinner, Clinical virologista,
- R Thomas, General practitionerb,
- M Taylor, General practitionerc,
- M Sellarajah, General practitionerd,
- S Bolt, General practitionere,
- S Krett, General practitionerf,
- A Wright, General practitionerg
- a Harborough Banks, Old Warwick Road, Lapworth, Warwickshire B94 6LD
- b Old Road Surgery, Llanelli, Carmarthenshire SA15 3HR
- c 9 East Street, Prittlewell, Southend on Sea, Essex SS2 6LQ
- d 115 Humberstone Road, Pype Hayes, Erdington B24 0PY
- e Westcotes Health Centre, Leicester LE3 0LP
- f 118 Station Road, Hendon, London NN4 3FN
- g 57 Chorley New Road, Bolton BL1 4QR
Editor—We wish to question present medical practice, which considers abnormal serum concentrations of free thyroxine and thyroid stimulating hormone–those outside the 95% reference interval–to indicate hypothyroidism but incorrectly considers “normal” free thyroxine and thyroid stimulating hormone concentrations to negate this diagnosis.1 It is unusual for doctors to start thyroxine replacement in clinically hypothyroid but biochemically euthyroid patients.
The free thyroxine and thyroid stimulating hormone concentrations in 80 patients considered to be hypothyroid on established criteria indicated that only five patients had free thyroxine concentrations (just) below the reference interval of 10-19 pmol/l (values of 9.4, 9.8, 9.8, 9.9, and 9.9 pmol/l) and only four patients had thyroid stimulating hormone values above the reference interval of 0.5-5.5 mU/l (values of 5.6, 8.4, 11.8, and 30.1 mU/l); moreover in these 80 patients the mean (SE) concentration of free thyroxine was 12.9 (0.2) pmol/l and the mean concentration of thyroid stimulating hormone was 2.2 (0.4) mU/l; both of these values lie well within the normal reference intervals. While we accept that there will be subjective variation in the evaluation of clinical diagnostic criteria and that the long term response to thyroid replacement is a prerequisite of our proposition, exclusion of hypothyroidism on the grounds of hormone concentrations measured in the laboratory seems wrong.
We contend that an incremental three month trial of thyroxine treatment in clinically hypothyroid but biochemically euthyroid patients is a safe and reasonable strategy. The dangers of osteoporosis and cardiac catastrophe–particularly during a three month trial–are sometimes quoted, but these worries are unfounded and condemn many patients to years of hypothyroidism with its pathological complications and poor quality of life. We urge that the question of clinical hypothyroidism in biochemically euthyroid patients should be subjected to a formal clinical trial.