ThyroidChange, the United Voice of Thyroid Patients Worldwide, are encouraging thyroid patients to comment on their thoughts about the American Thyroid Associaton (ATA) and the American Association of Clinical Endocrinologists (AACE) treatment guidelines.
Although the guidelines are American, it may well help thyroid patients worldwide so Thyroid UK also encourages you to comment. ThyroidChange wrote an excellent letter to the ATA and the AACE which you can read here: irthyroidchange.org/response-...
ThyroidChange ask the following:
PLEASE tell the ATA and AACE how YOU feel about their treatment guidelines that encourage TSH only testing and treatment with Levothyroxine (T4) only.
WE NEED CHANGE NOW!
Please write something that explains how their emphasis on the TSH test and Levothyroxine (T4) only treatment has impacted your life and health. Write as LITTLE or AS MUCH as you want. JUST WRITE!
Tell these organizations the consequences of their guidelines.
The way to do this is to post your comment on the first link and then copy & paste it on the other 3 links:
The fundamentals of thyroid hormone control are, even 120 or so years after the start of various forms of hormone replacement therapy, not fully understood.
One particular problem area is the TSH test.
The theory of the feedback loop controlling thyroid hormone production clearly has some fundamental validity. But when you go further in trying to use it to screen for, diagnose or manage thyroid disorders, the sometimes subtle issues start to show themselves and result in inappropriate care.
1. The TSH distribution is not a Gaussian distribution (also called “normal”). It only even approximates a Gaussian distribution when, first, it is log transformed. And second, when its skew is entirely discounted. A typical TSH reference range used today might be 0.4 to 4.0. The chances of anyone having a TSH of, say, 10, are almost infinitesimal when you apply standard statistical techniques applicable to Gaussian distributions. And yet, a value of 10, or very much higher, is not uncommon. The 2.5% cut-offs at top and bottom are entirely artificial and do not reflect the reality for individuals.
2. The range of TSH values within which an individual is likely to stay is very much smaller than the full range of the 0.4 to 4.0 sort of reference range. Maybe a person would remain between 1.0 and 1.5, even over a year of monthly tests. So if they ever have a value of, say, 0.8 or 2.2, they are out of their personal range. Applying the distribution characteristics of a population to an individual simply is not tenable.
3. No account is taken of the well documented circadian changes in TSH, nor of its pulsatile release. That people have TSH taken at random times can mislead significantly.
4. Even now, a number of TSH tests are distorted by the presence of macro-TSH (antibody-bound TSH). So the TSH result from two different assay techniques can vary dramatically.
5. There is little to no understanding of the impact of the varying glycosylation levels of TSH. Likely there will not be any such understanding until these levels can routinely be measured and analysed.
6. Once a patient has suffered significant hypothyroidism, they may have a somewhat enlarged pituitary. In turn, any slight inadequacy of thyroid hormone which can increase TSH a little in many people, can send it very high. If not recognised, the patient might have too large an increase in thyroid hormone dose, ending up over-dosed. Once that is detected, their dose will be reduced, and so on.
7. If a patient has any impairment of their pituitary whatsoever, then it is likely not going to react properly to changes in thyroid hormone level. There seems to be no way in which it can accurately be determined that an individual is not suffering from this. So dosing by TSH will inevitably under-dose them. The usual approach might detect obvious secondary hypothyroidism, but not cases where there is a modest element of pituitary mis-function.
8. Issues such as pituitary resistance to thyroid hormone and peripheral resistance to thyroid hormone are extensively recorded. However there seems no way for the standard TSH model to be used successful in either condition.
9. No-one has yet incorporated the extensive innervation of the thyroid fully into a TSH model.
10. Using TSH alone will tend to miss situations in which other issues are affecting thyroid hormone. For example, iron deficiency anaemia seems to be fairly common in hypothyroid people. That in turn seems to affect the ability to process thyroid hormone.
11. TSH will only be produced as expected if the hypothalamus is producing the required level of TRH. This is almost never checked. Again, even a subtle impairment could be enough to render TSH unreliable.
12. TSH testing has demonstrated a massive improvement in sensitivity and that has, rightly, been praised. People appear, however, to have confused this extraordinary sensitivity with its fundamental meaning.
13. Little or no account is taken of the impact of various substances on TSH. Suppression from Glucocorticoids, Salicylate or Furosemide, Octreotide and Dopamine. Increased TSH from Dopamine antagonists, Amphetamine, IL-2 or Theophylline treatments. Though little seems to be known about the impact of unusual levels of endogenous forms of these and other substances.
I have always felt that one way of checking the appropriateness of using TSH would be to get a panel of endocrinologists to view a set of thyroid function tests. (I write “panel” but I intend that each person would make their own, independent assessments not that they would make joint assessments.) These would be TSH, fT4 and fT3. In each case the fT4 and fT3 values would be hidden and the experts asked to provide a ‘best guess’. Given some reasonable conditions to avoid “impossible” situations such as within a very short time of a change of dose, such a panel should achieve a high degree of agreement with actual test results. If the expert panel did not agree with themselves, and with the actual results, then questions would need to be answered.
Obviously this could be made ever more sophisticated by adding elements. For example, it might be possible to get a series of results for these patients and what medications they were prescribed. Then get the experts to predict what impact they would have had.
TSH might be better legitimised after it has been demonstrated that the levels do indeed reflect the underlying FT4 and FT3 levels in the individual. But even that, in my view, can only be justified if additional tests are readily available should there be any reason to question TSH as otherwise any change could easily be missed. Far better, though, would be always to perform a true thyroid panel consisting of at least TSH, FT4 and FT3 – and maybe others?
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