Diclofenac and Celecoxib inhibit T3

Caution, if you take either of these common Non-Steroidal Anti-Inflammatory (NSAID) drugs and have Thyroid T3-hormone issues, or problems in your blood vessels!

In my recent research I found a 2016 article with this title: “Evidence that diclofenac and celecoxib are thyroid hormone receptor beta antagonists.” (Zloh, et al, 2016) http://www.ncbi.nlm.nih.gov/pubmed/26792060

They analyzed the molecular structure of these drugs to confirm their “TRβ antagonistic properties.” They also measured “changes to Triiodothyronine (T3) induced vasodilation of rat mesenteric arteries” with these drugs.

They found these two drugs “significantly inhibited T3 induced vasodilation compared to controls.”

Inhibition of vasodilation is obviously NOT the effect you want if you have atherosclerosis or any problems with blood vessel spasms or constriction.

I was recently put on Diclofenac to resolve my chest arthritis AND at the same time, I was starting T3 therapy to resolve chest pain from vasoconstriction. Obviously the combination of these two therapies was contradictory.

In contrast, they tested naproxen and it did not have this TRβ inhibitory effect.


Zloh, M., Perez-Diaz, N., Tang, L., & Patel, P. (2016). Evidence that diclofenac and celecoxib are thyroid hormone receptor beta antagonists. Life Sciences, 146, 66–72. http://doi.org/10.1016/j.lfs.2016.01.013

Low-T3 syndrome and angina

When deprived of T3 hormone, the heart suffers

Low-T3 Syndrome—associated with angina or myocardial infarction: Although studies on Low-T3 syndrome usually focus on patients with “normal” thyroid glands and explicitly exclude patients with thyroid disease and/or on T4-therapy, the dysfunction of thyroid hormone equilibrium is also relevant to patients who suffer from Low-T3 while on T4-therapy despite having a normal TSH.

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Tingling sensation from electrode on heart monitor

When I was on a 48-hour holter monitor for my heart, I occasionally noticed a tingling electric-like sensation emanating from one of the electrodes into the skin under it. The little zaps pulsed for about 1 minute and then faded away.  Both times it was the same electrode in the same location.

It was not a feeling of itching or skin irritation like an allergic reaction, but a distinct sensation of tingling like low-level electricity.  It was very distinct from the deeper chest pains I have been recording in my heart monitor log.

My husband (who is an expert in electronics) suggested that even a little moisture, possibly secreted by sweat, or by the skin having an allergic reaction to contact with the electrode, might have caused this.

After the electrodes were taken off, the most reddened skin appeared under the electrode that tingled the most.

I can’t find anything about this online through random Google searches and I don’t have time to research it further right now.  I wonder if anyone else has experienced this.

Hypothyroidism and Angina: Research

Although it is more common to consider angina in relation to hyperthyroidism, several articles have reported angina appearing in hypothyroid patients when treated with exogenous thyroid hormones (T4). They recommended gradual increases in T4 dosage, but mentioned that a satisfactory dose may not be achievable, leaving patients to accept a compromise between hypothyroidism and angina.

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Thyrotoxicosis and angina

Commonly, research has connected “thyrotoxicosis” to angina or coronary vasospasm.  Hyperthyroidism is the usual cause of “thyrotoxicosis,” caused by toxic high levels of thyroid hormone, revealed by an abnormally low or undetectable TSH and/or high T4 and/or T3 level.  Reduction of T4/T3 levels and normalization of TSH led to resolution of their heart symptoms.

My question in reviewing these articles was “To what degree did these articles on thyrotoxicosis point to T3 as a factor in angina?” This is an important question to ask since T3 has a much more powerful effect on cells than T4.

Other research has pointed to the opposite type of thyroid dysfunction, hypothyroidism, as significantly associated with coronary vasospasm or variant angina, but has not studied T3 levels of its subjects, leading to similar questions about T3 levels and angina (Lee et al, 2015).  So, is it HIGH T3, or LOW T3, or both, that is associated with vasospasm/angina?

In addition, these articles remind us that not all thyrotoxicosis is the same, since various causes of hyperthyroidism vary in their T3 and T4 levels in serum.  Research (Carle, et al, 2013) has found that Total T3 levels are much higher than T4 levels in Graves’ disease hyperthyroidism, yielding the highest T3:T4 ratio. The same study found that Total T3 levels are significantly higher in Graves’ compared to other forms of hyperthyroidism such as “painless thyroiditis” (tT3 over 5.0 nmol/L for Graves’ disease, vs. 2.5 to 3.77 nmol/L for nine other forms of hypothyroidism, where the tT3 reference interval was 1.2–2.7 nmol/l).

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