Back to basics TSH question ...

[sy28]

Am I missing something? This follows my second Consultant's, second appointment. This is a basic question, I know, but if a patient's TSH is elevated above range, 0.04 - 4.00, is this solely judged as a marker for under-active thyroid or can it be interpreted as being significant for 'something else'? The reason for asking dates back to my original Hypothyroid diagnosis when TSH was measuring 5.1. Unfortunately, the consultant I am seeing is consistently reluctant to accept this result and questions whether I have a thyroid issue at all. I'm finding it difficult to believe what I'm hearing given I have above range Thyroid autoimmune antibodies present, positive DI02 genetic test result and blood test results indicating likely T4 conversion problem. I'm currently mulling over a letter for the consultant ... meanwhile, thanks for reading this post.

[SeasideSusie Remembering]

TSH can be temporarily elevated when we have a "non-thyroidal illness".

Before diagnosis, if you have an over range TSH and normal FT4 this is classed as "subclinical hypothyroidism". If at the same time you have raised antibodies, Dr Toft recommends starting Levo, he states this in the article he wrote for Pulse magazine (the magazine for doctors) where he states in answer to Question 2:

Question 2:

I often see patients who have an elevated TSH but normal T4. How should I be managing them?

Answer:

The combination of a normal serum T4 and raised serum TSH is known as subclinical hypothyroidism. If measured, serum T3 will also be normal. Repeat thyroid function tests in two or three months in case the abormality represents a resolving thyroiditisis.

But if it persists then antibodies to thyroid peroxidase should be measured. If these are positive - indicative of underlying autoimmune disease - the patient should be considered to have the mildest form of hypothyroidism.

In the absence of symptoms some would simply recommend annual thyroid function tests until serum TSH is over 10mU/l or symptoms such as tiredness and weight gain develop. But a more pragmatic approach is to recognise that the thyroid failure is likely to be come worse and try to nip things in the bud rather than risk loss to follow up.

Treatment should be started with levothyroxine in a dose sufficient to restore serum TSH to the lower part of it's reference range. Levothyroxine in a dose of 75-100mcg daily will usually be enough.

If there are no thyroid peroxidase antibodies, levothyroxine should not be started unless serum TSH is consistently greater than 10mU/l. A serum TSh of less than 10mU/l in the absence of antithyroid peroxidase antibodies may simply be that patient's normal TSH concentration.

If you don't have a copy of the article you can email Dionne at

[e-mail]

He has recently written a new article which says that T3 may be helpful for many patients

rcpe.ac.uk/sites/default/fi...

In particular:

….It is instructive to consider the history of thyroid hormone replacement in order to appreciate that many of our policies have, to some extent, been accidental rather than planned. Thyroid extract was first used some 125 years ago with good effect and remained in widespread use until the 1950s when a suitable synthetic LT4 preparation gradually supplanted it. The doses employed were 200–400 μg daily. Although T3 was discovered as the second thyroid hormone in 1952 it was not used to any extent therapeutically as patients seemed content with LT4 alone, long before the demonstration that circulating T3 was largely derived from deiodination of extrathyroidal T4. The seismic shift in the treatment of hypothyroidism, however, was the result of the development of sensitive assays for TSH which showed that, in order to restore serum TSH to normal, the dose of LT4 required was of the order of 75–150 μg daily. Higher doses caused suppression of TSH consistent with hyperthyroidism. The resultant dose reductions were tolerated by the majority of patients but this was the beginning of significant dissatisfaction with adequacy of the recommended treatment of primary hypothyroidism which remains problematic today. The previously high doses of LT4 would, by the law of mass action, have overcome any impaired D2 activity in affected patients. Little attention has been given to a study, important in retrospect, which showed that it was difficult to increase serum T3 into the hyperthyroid range with LT4 unless serum free T4 concentrations were markedly elevated at around 35–40 pmol/l. This was an elegant demonstration that exogenous subclinical hyperthyroidism was a different entity from endogenous subclinical hyperthyroidism, even although serum TSH was suppressed in both conditions. In other words, a low serum TSH concentration in patients taking LT4 did not necessarily indicate overtreatment.

In short, what he is saying is that for Levothyroxine to be effective, the patient needs a dosage between 200 and 400 mcg daily. But since the focus of the medical profession had shifted to the TSH, the medical profession has erroneously decided that the TSH has priority over the wellbeing of the patient.....

Hope that helps.

[MaisieGray]

I think the problem is, there are nuances to every factor you mention, and they need to be looked at in totality. Regarding your DIO2 result, it is not a diagnosis. It shows only that you have a particular common variation of that gene, which may not be expressed but even if it is, may affect you anywhere between not at all and disrupting your T4 to T3 conversion, and can depend also on whether you test heterozygous or homozygous positive ie whether you have only one allele or two. In terms of having above range thyroid antibodies present, not everyone with say, elevated TPO antibodies, necessarily goes on to develop hypothyroidism, but in any case they can be present for a long time before there is any measurable deterioration in thyroid function. Ditto, slightly elevated TSH levels, may be present along with in range thyroid hormone levels, as the thyroid gland can compensate for a while before it starts to fail to produce adequate levels of hormones. I believe there can unusually, also be cases of high TSH levels in association with being euthyroid, due to macromolecular complexes (macro-hormones and macro-enzymes with high molecular weight conjugating with immunoglobulins) that may cause artificially elevated biochemical test results - the science is very definitely above my intellectual pay grade, but I mention it to answer your question 'is an elevated TSH solely a marker for underactive thyroid'. Then of course, biotin supplementation can skew TSH results in either direction. Regarding test results showing poor(er) T4 to T3 conversion, at a lower level it's difficult to say what's an outer parameter of normal, and what's actually abnormal. So as I said, what one infers from these things, is often open to their magnitude, and the presence of other factors that can either reinforce or contradict them. So if you have for instance, a considerably elevated TSH, a flatlining FT4 level and stratospheric TPO antibodies, it's easier to make a definitive diagnosis than if the TSH is only mildly above the reference range, TPO Abs are high but still just in range, and FT4 is hovering around or just below midway in range. Presumably this Consultant is of the view that a TSH level below 10 always signifies euthyroidism; in which case you might want to refer to the CKS/NICE guidelines in which it states that where patients are symptomatic and have a TSH is between 4 and 10 mU/L and FT4 within the normal range, they can nevertheless be prescribed T4.