Three things came together. First, reading through some of diogenes' papers, second, noticing the old PR Larsen paper, third, that someone expressly mentioned taking aspirin in order to help with blood flow when performing a finger-prick blood sample. (I did try, but I could not find where on the forum it was mentioned!)
The effect of aspirin and other salicylates is definitely at the level which could affect blood test results. Therefore using it prior to a thyroid hormone test (TSH, T4 or T3) is probably a bad idea.
It isn't quite as clear whether there is sufficient reason to avoid aspirin entirely in all those with thyroid issues. I suspect that it is possibly safest to avoid. In particular, in someone who is significantly hyperthyroid - when the unbinding of more thyroid hormone could cause their free hormone levels to rise even further.
Variable effects of nonsteroidal antiinflammatory agents on thyroid test results.
Abstract
To investigate the effects of nonsteroidal antiinflammatory drugs (NSAIDs) on thyroid tests, 25 healthy subjects underwent a single-dose study and/or a 1-wk study. In the single-dose study, subjects received a single dose of one of six NSAIDs (aspirin, salsalate, meclofenamate, ibuprofen, naproxen, or indomethacin) at 0800 h. Total and free thyroid hormones and TSH were analyzed 0, 1, 2, 3, 4, and 8 h later. In the 1-wk study, subjects received one of six NSAIDs for 7 d. Thyroid hormones and TSH were analyzed at 0800 h each day. Total T(4) and total T(3) were measured by RIA, free T(4) and free T(3) were measured by equilibrium dialysis, and TSH was measured by immunometric assay. There were no changes in any hormones after a single dose or 1 wk of ibuprofen, naproxen, or indomethacin. Single-dose aspirin or salsalate decreased, whereas meclofenamate increased, various total and free thyroid hormone measurements. One week of aspirin or salsalate decreased total T(4), free T(4) (salsalate only), total T(3), free T(3), and TSH. These data confirm that aspirin, salsalate, and meclofenamate affect total and free thyroid hormone measurements and identify three NSAIDs that did not change thyroid tests. TSH remained within the normal range during acute or 1-wk administration of all of the NSAIDs.
This is an old paper - but every subsequent work seems to reference it!
Salicylate-induced increases in free triiodothyronine in human serum. Evidence of inhibition of triiodothyronine binding to thyroxine-binding globulin and thyroxine-binding prealbumin.
Larsen PR
The Journal of Clinical Investigation, 01 May 1972, 51(5):1125-1134
Addition of sodium salicylate to human serum at concentrations often obtained during aspirin therapy causes 100-200% increases in free triiodothyronine (T(3)) and free thyroxine (T(4)) as estimated by ultrafiltration. The increase in free T(3) was unexpected since previous data had suggested that salicylate inhibits binding of T(4) only to thyroxine-binding prealbumin (TBPA) and that T(3) is not bound to this protein. Using ultrafiltration techniques, we demonstrated binding of T(3) to TBPA. The affinity constant for T(3)-TBPA binding appears to be slightly greater than that for albumin-T(3) binding. While salicylate inhibits the binding of T(3) (and T(4)) to TBPA, it can be predicted that little change will be observed in the free T(3) (or free T(4)) without inhibition of thyroid hormone binding to thyroxine-binding globulin (TBG). Using a competitive-binding protein displacement technique, it has been shown that sodium salicylate, like diphenylhydantoin (DPH), inhibits the binding of T(3) and T(4) to TBG. The magnitude of the increase in free T(3) and free T(4) induced by salicylates suggests that interference with TBG binding is its major effect. Aspirin was administered orally to two normal subjects in quantities sufficient to obtain serum salicylate levels of 20-25 mg/100 ml. This resulted in a decrease of 20-30% in total serum T(3) and T(4) levels. This decrease in T(4) levels is similar in magnitude to that previously observed in subjects receiving DPH. Unlike what has been observed with DPH treatment, therapeutic salicylate levels are associated with increases of 50-75% in the unbound fraction of both T(3) and T(4) which persist throughout an 8-10 day treatment period.
Open access but full paper is in the form of a PDF scan:
I think if you are on long term therapy, such as aspirin, and your medication is continuous and your blood levels are constant, you can use the value you get with the aspirin therapy as a baseline and look for changes based on that. However for acute use, it is useful to know that FT4 can be depressed, so as you have mentioned perhaps not a good idea to take one before a thyroid function test! 😉
I have noticed that a lot of older papers are now behind a paywall, which is so wrong and why I ask? And very few of the newer papers are offered free, despite the authors having to pay now for publishing in an apparent effort to make them all freely available, so the public has access. Yeah, that one was a dead fish too, as the journals charge the authors AND if you want to access papers. Licence to print money...
I've certainly found a number of papers which used to be open access are now behind paywalls. And when they offer access to what you might know are a sentence or two of actual text (typically a comment letter) and want to charge the same as for a huge great paper...
Officially, papers produced under things like US government grants have to be open access.
I've started making sure I actually download papers while the going is good. It's the only way. But it sure does help when they are already offered as PDFs rather than having to deal with .xml and such like and printing to PDF.
SIR,-Whilst examining the effects of salicylates on thyroid function tests we investigated a group of fourteen patients with rheumatoid arthritis who had been taking aspirin 3 g daily for over a year. We were surprised to find total thyroxine (T4) values with a mean of 98 nmol/l spread throughout the normal range (mean 98 nmol/l) but free T4 values significantly depressed with a mean of 11•2 pmol/l (normal range mean 16•1 pmol/l) (p<0•001, t test). Our literature survey led us to expect the total T4 to be depressed with FT4 values normal. In view of this contradiction we did further tests. Triiodothyronine (T3) uptake values (normal range mean 30%) were normal (mean 29%) and the mean FT4 index (FTI) was similarly little affected (28 compared with the normal mean of 31). Thyroxine binding globulin (TBG) levels were all above the mean of the normal range, and the mean value of 27 mg/l was significantly greater than normal (21 mg/l) by t test (p<0•01). The results are summarised in the table.
'Amerlex' kits (Amersham International) were used to measure FT4, total T4, and TSH; T3 uptake was measured by Amersham’s 'MAA' kit and TBG by the Corning kit.
The combination of normal T4 with significantly raised TBG concentrations for this group of patients predicts a reduced FT4 value and leads us to believe that the depression in FT4 more accurately reflects thyroid status than does FTI or T4. In fact the increase in mean TBG (29%) is almost exactly reflected by the fall in mean FT4 (30%). We measured thyroid stimulating hormone concentrations on the four patients with lowest FT4 values (6•7-9•9 pmol/l) but no increase was detected, perhaps reflecting an inhibition of the pituitary response to thyrotrophin releasing hormone by aspirin.
The T3 uptake test (and hence FTI) does not correct for the rise in TBG levels presumably because aspirin is bound to binding proteins thus competing with the binding of T3 tracer and producing an erroneously raised uptake result. TBG and thyroxine binding prealbumin bind T4 much more strongly than does T3 (10-20 fold), so the direct measurement of FT 4 is unlikely to be affected. The changes in TBG levels may be related to aspirin's effect on the liver.
The reason for the discrepancies between our results and previous work is that earlier workers considered only short term (7-day) effects of aspirin on healthy volunteers. The long term effects of drugs may differ considerably from the short term ones.
We thank Dr J. Giddings of the coagulation unit, haematology department,
Heath Hospital, Cardiff for serum samples.
Clinical Reagents Development Department, Medical Products Division, Amersham International plc, Amersham, Buckinghamshire HP7 9LL
In general, the newer DOACs (direct oral anticoagulants) are preferred to aspirin (classed as an anti-platelet) - where there could be a choice. I suspect many who were once on aspirin have been moved across to DOACs though there will be some who have not.
And combining aspirin with a DOAC is definitely to be avoided where possible.
Oh really? I wonder why (not) 'my' GP hasn't mentioned this? I've been taking aspirin for 12 years and I wonder whether it's been affecting my use of T4?
For a long time, the DOACs were considerably more expensive. I believe that the prices have dropped a bit but can still be up to £60 a month (just checked BNF - Apixaban, Rivaroxaban, Edoxaban).
And there are contra-indications such as anti-phospholipid syndrome.
It is not all plain sailing but they do avoid the negative effects of aspirin.
Check out the very relevant link posted earlier by Tina_Maria
The list of main concerns related to NSAID use does not include any threats to thyroid function. However, there are two studies that suggest NSAIDs may influence it.
In one study published in the journal Life Sciences, researchers used computer and chemistry methods (not human participants) to analyze how three commonly prescribed NSAIDs interact with thyroid hormone receptors in the body. The NSAIDs studied were Voltaren (diclofenac), Aleve (naproxen), and Celebrex (celecoxib).4"
But nothing about aspirin. So, as usual with all these studies, one contradicts another! You can go crazy trying to reconcile all these 'studies'. I tried to find something on aspirin and levothyroxine interactions and found this reference which is totally useless!
If you are on long-term aspirin, skipping the dose on one day will not make a big change in your plasma levels of aspirin, as the half-life of aspirin is 5 days, so after 10 days you will still have 25% of the aspirin in your blood.
However, if you are on long term therapy, you just have the thyroid results you get with your aspirin as your baseline and adjust your thyroid medication accordingly. So if you are on long-term aspirin and that affects your T4 levels (usually somewhat reduced), you may need a bit of extra LT4 to compensate?
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