I am a physician who practice in El Paso, TX. I just got a patient complaining of fatigue with the following thyroid panel results:
TSH – 2.04 uIU/mL T4 Total – 8.55 ug/dL (4.87 – 11.72) T Uptake – 43.3 % (32 – 51) Free Tiroxine Index – 9.26 ug/dL (5.93 – 13.13) T3 Total – 1.03 ng/ml (0.58 – 1.59) T3 Free – 2.90 pg/ml (1.7 – 3.7) T4 Free – 1.37 ng/dL (0.70 – 1.48) Thyroglobulin Autoantibodies – 14 U/mL (Reference range <60) Thyroid Peroxidase Autoantibodies – 19 U/mL (Reference range <60) Reverse T3 – 741 pg/ml (90 – 350)
All of the above tests were within range except Reverse T3 (normal ranges-90 to 350 pg/mL). I also read in some articles that TSH levels above 2.0 could be a sign of hypothyroidism. Do you colleagues think that a T3 thyroid replacement will benefit my patient in his fatigue?. Also any idea of why he got high Reverse T3 values?. He is currently taking the following drugs:
Amytriptiline: 125mg daily Pherpenazine: 4mg daily Indera (propanolol): 20mg daily
As fas as depression, he is now very stable and no showing signs or symptoms of depression.
I would appreciate your feedback regarding this patient.
Thanks in advance,
Roberto Meza M.D., El Paso, TX
The explanation of the situation is possibly as follows. Even to the more recent stringent criteria his TSH is normal as well. The increase in rT3 may be caused by the use of propranolol. I patch the abstract of a study that we did, below. It shows, see attachment, that in healthy subjects the effect of propranolol on parameters of serum T3 and serum T4 is moderate but huge on serum rT3. I assume that, because the dose of propranolol that your patient is using is low, only rT3 falls out of range, but not T3 and T4 parameters. However the situation is not completely comparable as our subjects were healthy young men treated for the purpose of the study with 200 micrgr. T4/day, and 3 times daily with 80 mgr propranolol. Furthermore the dose of propranolol that your patient is using is so low as compared to our subjects that I am surprised that rT3 is affected to such an extent. It may be that your patient also has a mild non-thyroidal illness where there is an early rise of rT3. Maybe, that a combination of these 2 factors explains the hormone profile of your patient. At any rate I am pretty sure that the thyroid function of your patient is normal and does not explains his complaints
Am J Physiol. 1988 Jul;255(1 Pt 1):Three-compartmental analysis of effects of D-propranolol on thyroid hormone kinetics. van der Heijden JT, Krenning EP, van Toor H, Hennemann G, Docter R.
Tracer thyroxine (T4), 3.3′,5-triiodothyronine (T3), and 3,3′,5′-triiodothyronine (rT3) kinetic studies were performed in normal T4 substituted subjects before and during oral D-propranolol treatment to determine whether changes in thyroid hormone metabolism in a propranolol-induced low-T3 syndrome result from inhibition of 5′-deiodination or inhibition of transport of iodothyronines into tissues. Data were analyzed according to a three-compartmental model of distribution and metabolism. T4 plasma appearance rate decreased by 16% (P less than 0.01), reflecting a decreased intestinal absorption of orally administered T4 during propranolol. Serum T4 and free T4 levels increased significantly by 14%, whereas T4 metabolic clearance rate (MCR) was lowered by 26% (P less than 0.001). No changes were observed in size of the three T4 compartments or in fractional and mass transfer rates of T4 from plasma to the rapidly (REP) and slowly (SEP) equilibrating pools. Serum T3, free T3, T3 plasma pool, T3 mass transfer rate to REP and SEP, and the T3 pool masses were all significantly decreased during propranolol to a similar extent as the T3 plasma production rate (PR). T3 MCR decreased by 14% (P less than 0.05). Serum total and free rT3 increased, whereas the rT3 MCR was substantially lowered during propranolol (P less than 0.001). The rT3 plasma pool, rT3 REP and SEP, and the mass transfer rates to REP and SEP increased, whereas no alterations were observed in rT3 PR and fractional transfer rates of rT3 to