A response to Dr Anthony Toft's article, "‘Thyroid hormone replacement – a counterblast to guidelines" has been published today in the Letters to the Editor section of the Journal for the Royal College of Physicians.
The authors refute Dr Toft's comments that their 2010 paper was flawed and also state, "Evidence-based guidelines describe a
foundation of knowledge, but should not be the ceiling of clinical practice."
They also state, " Far from restricting the development of evidence-based guidelines, we need to be educated to use them constructively and to ensure they are not misinterpreted or misused by people who do not have a patient-focused agenda."
Thyroid UK completely agrees with the authors and looks forward to any training that may be set up for doctors to understand that guidelines are not meant to be used as a one size fits all solution to diagnosis and treatment.
The problem of interpreting the results in the papers is as usual: shoehorning, diagnosing by category instead of individually, mixing up statistical likelihood of a patient group with actual likelihood for the individual. One simply cannot use evidence-based medicine in this generalised way - the statistical analysis is wrongly based and by mixing up patients, simply causes undue alarm to the individual say with a TSH of <0.01 who may NOT be prone to bone fractures, as opposed to another who may. TSH of <0.01 for one person may represent overdosing, but adequate dosing for another.
There is a statistical association between very low TSH levels and cardiovascular disease and fractures academic.oup.com/jcem/artic... . However, this is what I would call a 'random' association - in general these patients have a very low TSH by chance, patients rarely get a careful clinicial assessment when thyroid hormone is titrated. These patients have been prescribed hormone on the basis of diagnosis and treatment by blood test rather than assessing clinical need by examination of the patient's signs and symptoms.
It is interesting to note that a later study by Leese press.endocrine.org/doi/10.... found no increased risk for patients receiving liothyronine. Although liothyronine is inherently more hazardous (it bypasses deiodinase protective mechanisms) it would seem the extra care taken by doctors willing to prescribe liothyronine more than makes up for any potential risk.
The surveys tell you what happens if TSH is suppressed at 'random', either by need (to prevent cancer returning) or by accident. When TSH is suppressed on careful clinical grounds there appears to be no additional risk with the benefit of making the patient well and avoiding risks associated with clinical hypothyroidism.
From a 'lay' perspective - I was alarmed to think that two of the 'good guys' were arguing! But having looked back - it all looks understandable. Phew. I was worried for a moment.
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Endo wants me to stop taking Levothyroxine in order to qualify for CCG approval of T3
The American Thyroid Association's New Guidelines
Follow up to follow up of Referral letter **
