Robert Utiger, M.D. (1931-2008) is well known in endocrinology as the father of the TSH test.
Despite his trust in the TSH test, in his publications he acknowledged that TSH behaved very unnaturally in response to T3 levels in blood while dosing T3 thyroid medication.
What Utiger discovered in the 1970s and 1980s about the TSH reponse to T3-T4 combination dosing matters a lot to thyroid patients’ health and well being today because it provides a model of genuine evidence-based inquiry.
Even though Utiger loved his TSH test, he was more than willing to admit that TSH behaved unexpectedly and inconsistently. He didn’t seem to doubt his clinical assessment of a patient’s true hormone status when it conflicted with a deceptive TSH.
First I’ll go over how important Utiger has been to the history of thyroid science, drawing some facts I’ve learned from a biographical tribute by Joffe, Emerson & Braverman (2009) and things I’ve learned from browsing many of the thyroid science publications since the discovery of T3 hormone in 1952.
Then I’ll engage in a dialogue with Utiger across time, “interviewing” Utiger and responding to his publications’ statements.
This dialogue between us reveals the amazing things he learned about TSH’s abnormal, paradoxical, yet “exquisitely sensitive” response to T3 & T4 dosing at a ratio similar to desiccated thyroid, in which TSH was suppressed when euthyroidism was finally achieved.
Finally, I’ll show you where he put his foot down on the policy of testing TSH first, trusting it to have the first voice, and allowing it to have too powerful a voice, often the only voice in thyroid therapy, despite all he had learned.
ROBERT UTIGER KNEW THE TSH.
If anybody understood TSH like the back of his hand in the 1970s and 80s and 90s, it was Utiger.
His single-authored paper in 1965, “Radioimmunoassay of Human Plasma Thyrotropin,” is now considered an important landmark in the field.
He was author or co-author of a steady stream of articles studying TSH under many conditions such as health, fasting, non-thyroidal illness, thyroid failure, and thyroid hormone replacement.
As for thyroid replacement, he studied T3-based therapies then in common use — synthetic T3 monotherapy, desiccated thyroid, and synthetic T3-T4 combinations.
UTIGER KNEW TRH-AMPLIFIED TSH
Utiger wasn’t even held back by the technological limitations of the TSH test.
For much of his career, when the TSH test was in its early stages of development, it couldn’t be trusted to be reliable or precise at lower concentrations.
However, a TRH-stimulation test was soon developed that could “amplify” the TSH response to an immense degree.
Giving people an intravenous dose of TRH, the hormone secreted by the hypothalamus that stimulates TSH release in the pituitary, would produce very “amplified” and distinctive TSH responses to a hyperthyroid person, normal person, and hypothyroid person.
The TRH-stimulation test laid open Utiger’s eyes to TSH’s tiniest shifts and changes.
It was much like “zooming in” to a Google map can bring you to the image of someone’s front door today.
Even today, some thyroid scientists are calling for a return of this old-fashioned TSH-stimulation test because it reveals the true basis of the lower levels of TSH response that our current TSH testing technologies, for all their refinement, can’t reveal. (Beck-Beccoz et al, 2017).
If TRH-stimulated TSH testing can reveal the subtleties of central hypothyroidism, the TRH stimulation test can also reveal the distinctions between “thyroid hormone overdose” and a T3 dosing effect that elicits … a kind of central hypothyroidism.
Central hypothyroidism. What else would be a good way to consider TSH oversuppression, a failure to remain normalized when not hyper?
UTIGER’S BLIND SPOTS AND PARADIGM
Despite his insider knowledge of TSH, Utiger was limited.
For much of his early career, the field didn’t yet understand about how thyroid hormone conversion, transport, and receptor sensitivity worked. So we have to take Utiger’s interpretations in the context of what nobody in thyroid science knew yet.
In addition, Utiger is not the hero of thyroid patients who are poor converters of T4 hormone.
To all thyroid patients who have been tyrannized by the TSH and forced into the dungeons of chronic underdose, this is a sobering thought: Utiger was one of the key researchers involved in promoting and advocating for today’s TSH-first testing policy and its utility in guiding T4 monotherapy, which was leaving T3 therapies behind as TSH advanced alongside it.
Utiger had a strong influence through his publications and as he sat on key medical association committees. He was so revered for his knowledge that he rose to prominence among endocrinologists. He served as the co-editor of “Werner and Ingbar’s The Thyroid,” a major foundational text for advanced study in thyroidology, from its sixth edition in 1991 through its ninth edition in 2005. He also served as editor of several journals in the field of thyroid science.
Utiger helped to shape what our thyroid patients campaign calls the “TSH-T4 paradigm,” and he shaped many policy decisions about our therapy and testing.
BUT UTIGER EXPRESSED DOUBTS.
However, even while Utiger advocated for the utility of the TSH test, he expressed misgivings and qualifications about it. (Utiger, 1988) That’s where this short story will conclude, and I’ll foreshadow it for you.
His doubts about even the technological advancements in TSH testing were likely based on some of his early research. His early research showed the diversity of TSH response under many circumstances.
At the same time, his respect for the TSH sometimes led to pronouncements filled with (over)confidence and optimism about the TSH’s pseudo-omniscience and benign power, which many people thought he implied with his favorite phrase, “exquisite sensitivity.”
Have those doubts, cautions, and misgivings about TSH been heard? Have they been misinterpreted or overlooked in favor of emphasizing his advocacy for his beloved test?
LET’S INTERVIEW UTIGER.
Utiger’s not alive anymore to answer for himself. So let’s interview a few of Utiger’s research studies. Here’s some questions I have in mind:
Did you find that orally dosing T3 oversuppressed the TSH far more than naturally secreted and converted T3?
Can a given Free T3 level in a healthy person result in a normal TSH, while a similar Free T3 level in a T3-dosing thyroid patient suppresses the TSH or lowers it significantly?
Did you find that in T3-based therapy, TSH appeared to calibrate mainly to a higher T3 level while completely ignoring a very low concurrent T4 level in a thyroid patient’s blood?
If you found a TSH-oversuppressive T3 dosing effect, how did you try to explain it?
In a 1972 study, Utiger learned that using a 1:4 ratio of T3:T4 in therapy exaggerated the TSH-suppressive effect of small amounts of thyroid hormone as one got closer to an euthyroid dosage.
He and his co-author Peter J. Snyder, in fact, thought this erratic behavior of the TSH was very puzzling and surprising.
The study’s aim was to measure the effects of what they considered very “small” quantities of combined T3 and T4 dosing on TSH.
They put normal, healthy people AND 11 hypothyroid people through several rounds of thyroid hormone dosing plus TRH-stimulated TSH testing.
The medication they used was a brand available then, called “Liotrix,” which came in three strengths. One combined 15mcg of T3 + 60 mcg T4; the next 22.5 + 90, and the strongest was 30 + 120. Therefore, the ratio in this medication was 1 microgram of T3 for every 4 micrograms of T4 (1:4).
This medication ratio was roughly an imitation of the ratio of 1:4.2 (T3:T4) found in desiccated thyroid preparations.
What did they think was surprising about their results?
I’ll let Snyder and Utiger speak, and I’ll interject conversationally with them:
NORMAL T3 & T4, BUT ABNORMALLY LOW TSH
SNYDER & UTIGER: “The data presented here demonstrate that the chronic administration of small quantities of exogenous T3 + T4 to normal subjects and to patients with partially treated, primary hypothyroidism results in marked inhibition of TRH-induced TSH release.
Marked inhibition occurs even when the serum T3 and T4 levels are not increased above the normal range.”
TP.CA: I notice your tone here, “marked inhibition,” means, in context, that the inhibition is exaggerated given the fact that quantities are “small” and serum T3 and T4 are “normal.” You seem like someone who knows the behavior of TSH when it’s normal, and you’re saying it’s a “marked” inhibition.
I want to know what you think is so striking about this TSH inhibition result and what makes it a significant degree of inhibition:
SNYDER & UTIGER: “One striking example of this inhibition is the ability of 15 + 60, when administered to normal subjects for 3-4 wk, to cause a 76% reduction in the TSH response to 400 μg TRH and an 87% reduction in the response to 25 μg TRH.”
TP.CA. So let me get this straight — you reduced TRH from 400 to 25 μg — that’s a reduction of 16x, but the TSH response only changed by 9% (from 76% to 87%)?
What is so special about the 15μg T3 + 60μg T4 dose causing almost equally strong TSH suppression despite such different levels of TRH amplification?
SNYDER & UTIGER: “This degree of inhibition is especially significant considering that
(a) this dosage of T3 + T4 is less than a replacement dosage, as documented by its failure in the primary hypothyroid patients to lower baseline TSH levels to normal (Table IV); and that
(b) this dosage of T3 + T4 causes only a small rise in the serum T3 level, not above the normal range, and no measurable change in the serum T4 levels (Figs. 2 and 3).”
TP.CA: Okay, then it’s about the dose being so small, and having such a tiny rise in serum T3 levels, and hardly any change in T4, yet it has such a powerful an effect on TSH.
This certainly looks like TSH is being oversensitive to T3 dosing. The TSH-suppressive effect has very little to do with excess thyroid hormone in the pills or in the blood.
The TSH is curling up inside its shell over this threateningly tiny increase in serum T3 within the normal reference range.
What else did you find, this time in your hypothyroid patients?
SNYDER & UTIGER: “Another striking example of this inhibition is the ability of an increase of only 7.5 + 30 in the dosage administered to patients with partially-treated primary hypothyroidism to reduce the serum TSH response to TRH from above normal or in the upper normal range to below normal (Fig. 4).”
TP.CA: Whoa. So this tiny change makes the amplified version of TSH go from above normal to below normal. That must be a long way for a little dosing to move it, since you’re so surprised by it.
With a tiny change in dose, you brought hypothyroid people from being only “partially-treated” to supposedly _fully_ treated … and the end result was a suppressed TSH.
Was this the same in all 11 of your hypo patients?
VARIABLE T3-DOSING TSH THRESHOLD
SNYDER & UTIGER: “Although in three of the patients this obliteration of the response occurred when the dose was raised from 15 + 60 to 22.5 + 90 and in the other three patients the obliteration occurred when the dose was raised from 22.5 + 90 to 30 + 120, the abrupt change from a supranormal or high-normal response to a subnormal response occurred uniformly with an increase in dosage of only 7.5 + 30.”
“The mean increases in serum T3 and T4 levels associated with these six abrupt changes in TSH response, moreover, were only 25 ng/100 ml and 1.3 μg/ 100 ml.”
TP.CA: This means, then, that for each individual, the point at which their TSH suppresses abnormally will differ.
But for each individual it only takes the addition of the same small amount of dosing, and a corresponding small increase in serum levels, to see TSH drop fast.
I’ve heard them say the TSH test is sensitive, but this is really oversensitive. Hypersensitive.
And it’s interesting that you would be just fine with leaving these people’s TSH suppressed because you know they’d be only “partially treated” without it.
But nowadays people panic when they see a low TSH. They would rather leave the patient partially treated than suppress the TSH and treat the patient.
Why doesn’t anyone notice today that the TSH is being oversuppressed by T3 thyroid hormone dosing? At times, this TSH test can be so oversensitive that it’s unfair to us as T3-dosing thyroid patients!
What did you conclude from these observations?
NORMAL TSH IS EXTREMELY SMALL?
SNYDER & UTIGER: “One implication of the data presented here is that the ranges of serum T3 and T4 concentrations in which TSH response to TRH is normal must be very small.”
TP.CA Hold it right there. At a certain point, a tiny increase in serum T3 and T4 within the normal reference range can be suddenly too much for the TSH to respond normally to.
In therapy today, with T4 dosing alone, we’re used to seeing the TSH response as something fairly linear — as we increase T4 doses and blood concentrations TSH gradually falls.
But when you add T3 dosing to the mix, you are seeing something odd. It’s not gradual.
It’s not a continuous TSH-T3 inverse relationship that goes in a straight diagonal line on a graph.
There’s a tipping point within the normal T3 range at which you are at an obviously insufficient dose, and then you add a tiny bit more T3, and TSH suddenly crashes.
That makes it very hard to achieve a “normal” TSH response while on thyroid therapy, since dosages can so easily make a person’s TSH leap nimbly over the lower boundary.
What does this TSH abnormality mean, practically, for treated hypothyroid patients taking a preparation that includes a 1:4 ratio of T3:T4?
AN EUTHYROID STATE AND LOW TSH CAN COEXIST
SNYDER & UTIGER: “Therefore, a replacement dosage of thyroid hormone, one sufficient to maintain a hypothyroid patient in a euthyroid state with a serum TSH level that is not elevated, is generally also a suppressive dosage, capable of suppressing TSH secretion below normal.”
TP.CA. My jaw is dropping here. Only the first half of that sentence is something we can all take for granted.
Sure, we all know that the main goal in hypothyroid therapy is to make sure that serum TSH is “not elevated” above reference range anymore.
But the second half of your sentence says that in order to maintain a hypothyroid person in a truly “euthyroid” state using a 1:4 ratio T3-T4 combination like you have done here in 1972, (when this dose ratio ruled over thyroid therapy), it has to be a dosage “capable of suppressing TSH secretion below normal.”
So the patient group “Stop the Thyroid Madness” is in agreement with you that “optimal” dosing of desiccated thyroid may often suppress the TSH!
Wow, just wow.
What else can we learn from you, dear Utiger?
How about the question of the TSH-suppressive effects of higher levels of endogenous T3 versus dosed T3?
TSH RESPONSE TO T3 LEVELS IN “OVERFEEDING”
TP.CA: Later on, in 1982, Utiger, you were single author of a research paper that compared TSH response to T3 dosing with the T3-elevations induced by overfeeding.
I see that you picked up the narrative right where you left us in your 1972 article as you introduced the opening puzzle or problem to be solved by research.
UTIGER: “Basal thyrotropin (TSH) secretion and the TSH response to thyrotropin-releasing hormone (TRH) are both very sensitive to small variations in serum thyroid hormone concentrations when these changes are due to changes in the availability of serum thyroxine (T4) and triiodothyronine (T3) such as occur in patients with thyroid disease or following exogenous thyroid hormone administration.”
TP.CA: Aha, you’ve summarized it well, that people who have thyroid disease and people on thyroid therapy are special populations in whom the TSH overreacts to tiny changes in T3 and T4 concentrations.
These populations are not equivalent to normal-thyroid healthy populations in their TSH response.
What else have you learned about abnormalities in TSH response, in your research betweeen 1972 and 1982?
UTIGER: “Basal and TRH-stimulated TSH secretion is NOT similarly sensitive to altered serum T3 concentrations occurring as a result of altered extrathyroidal T3 production.
Patients who are starved or who have various nonthyroidal illnesses have substantial decreases in serum T3 concentrations. Their basal and TRH-stimulated TSH concentrations, which might be expected to increase, are unchanged or decreased.”
TP.CA: Utiger, now you’re saying that under certain circumstances the TSH response is abnormally dull because it can’t rise when it should.
That would make TSH not a very “specific” test, because these people have a lot less thyroid hormone. Their normal TSH is supposed to rule out hypothyroidism.
Can you make up your mind?
Is TSH sometimes very sensitive or is TSH sometimes abnormally dull?
Or does TSH have a problem with T3 hormone — it overreacts to tiny increases in T3 but is entirely apathetic to an isolated shortfall in T3?
Or is TSH just altogether untrustworthy because there are too many exceptions to its rules?
Sigh. What else did you observe about TSH’s dullness?
UTIGER: “Conversely, subjects fed excess calories have a rise in serum T3 concentrations, but no change in basal or peak serum TSH concentrations after TRH.”
TP.CA — I see. Overeating can cause T3 to rise, but you’re puzzled that T3 rises in blood without dropping the TSH like it does in T3-T4 combination therapy.
But what puzzles you today, sir? What’s your current research question?
UTIGER: “However, it is not known if the increments in serum T3 concentrations produced by overnutrition are sufficient T3 when produced by administration of exogenous T3, to alter TSH secretion.
Data indicating that comparable rises in serum T3 concentrations produced by overfeeding and exogenous T3 administration affect TSH secretion differently are reported herein.”
TP.CA — Now you’ve set up the competition. Which will win the race to suppress TSH more, overfeeding or T3 monotherapy dosing?
You’re taking T4 dosing out of the picture, because the T4 in the T3 + T4 combination might have been causing TSH oversensitivity in your 1972 study.
Now you’re comparing “TSH changes to T3 dosing” with “TSH changes to the same amount of elevated serum T3 in overfeeding.”
I’m curious what both T3 monotherapy and overfeeding do to the T4 level, because we all know that T4 needs to be considered when you want to understand TSH response.
UTIGER: To summarize, I found that in overfeeding, T3 increased while T4 stayed the same. However, in T3 dosing, T3 increased to a similar degree while T4 levels declined a little.
TP.CA: And now, how did the TSH respond to those similar T3 rises but the difference of the T4 decrease in the monotherapy?
UTIGER: “There were no significant changes in mean basal serum TSH concentrations during the overfeeding period. The serum TSH responses to TRH in the control test and after overfeeding were similar.”
“In contrast, after T3 administration the serum TSH response to TRH was lower at all time points.”
TP.CA: My doctor will not be surprised by this, though. Both the healthy controls and the overfed people had less TSH suppression than the people who dosed T3.
My doctor will always blame the T3 medication for being so unnatural and offending the TSH. My doctor never questions the TSH. She won’t stop to think critically about whether the TSH’s behavior was inappropriate or not in the context of serum T3 or T4 changes.
But you did point out that T4 fell a bit lower in those who dosed T3 and that was the only difference.
If T4 fell, the TSH should have risen, not remained continually oversuppressed by T3 dosing “at all time points.” That’s the puzzling part, right?
How did you interpret these results of T3 dosing’s more powerful TSH suppression despite T4’s concurrent fall?
UTIGER: “These results again demonstrate the exquisite sensitivity of the thyrotrophs to small increases in serum thyroid hormone concentrations occurring as a result of administration of small doses of thyroid hormones or of thyroid diseases.”
TP.CA: Hm, so you are praising the “exquisite sensitivity” of TSH, even when it appears to be a form of hypersensitivity to T3 dosing.
Isn’t this abnormally “exquisite sensitivity” a flaw?
It sounds like TSH can’t tolerate T3 dosing even when serum levels are the same and T4 drops.
TSH is consistently lower when it gets T3 in pill form. The pituitary and hypothalamus prefer to receive T3 only through natural means.
Isn’t that an unfair prejudice against people who can’t secrete T3 from a thyroid plus are so inefficient at extrathyroidal T4-T3 conversion that they can’t supply the bloodstream with enough T3? What if a pill is their only way of getting enough T3 in blood?
UTIGER: “In this study very similar increases in serum T3 concentrations resulting from increased extrathyroidal T3 production or from T3 administration also had different effects on TSH secretion.”
“These results provide further evidence that nutritional or other nonthyroidal factors alter the ability of thyroid hormones to regulate TSH secretion by as yet unknown mechanisms.”
TP.CA That’s interesting. Earlier you said that TSH is exquisitely sensitive to thyroid hormones even in small quantities.
Now you are saying TSH’s sensitivity can be interfered with by its exquisite sensitivity to yet unknown factors in addition to thyroid hormones.
And — oh no, that’s your final sentence. You’re going to leave us with “unknown mechanisms?”
You’re so humble here, Utiger. You’re so willing to admit that there are “yet unknown” things that suppress TSH in the case of T3 dosing.
You can’t yet explain it, but you are forced to admit the truth that something about T3 dosing, something you can’t yet explain, over-suppresses TSH.
UTIGER’S (GUARDED) ADVOCACY FOR TSH TESTING
But here’s one thing I don’t understand, dear Utiger.
In spite of all you learned as a researcher about TSH’s abnormal response to T3 dosing in the context of T3-T4 combination therapy and T3 monotherapy, and all you admitted about what was yet unknown about TSH oversuppression, why did you advocate for the TSH-first testing policy six years later, in 1988?
UTIGER: “Until recently, it was not possible to distinguish subnormal from normal serum TSH concentrations reliably. The sensitivity of the available TSH assays was about 0.5 to 2 μU/ml, such that serum TSH concentrations were undetectable in some normal subjects.
Now, as a result of recent developments in immunoassay technology, the sensitivity of TSH assays has been improved considerably, as has their specificity. …
The sensitivity of these assays is such that serum TSH concentrations as low as 0.01 to 0.02 μU/ml can be detected.
TP.CA “Oh no, Utiger, did you get seduced by technology? Did you forget that your TRH-stimulation test was also a new and exciting technology at one time?”
No, you didn’t forget.
I think you might have decided to put aside some of what you learned about the T3 dosing effect because at that point, fewer people were dosing with T3 hormone. By 1988, most doctors had decided to change their patients’ medication to T4 monotherapy. I believe this move was partly because they felt that TSH responded more “normally” to T4 dosing. They seem to have deserted T3 dosing for the sake of fitting the medication to their preferred test.
I’m going to let you speak out the rest of your reasoning by yourself, even if you say some things that I don’t want you to say!
Dear reader — Let’s notice all of Utiger’s back and forth — all his misgivings, all his cautions and doubts, and where he ends up. This good man is having an internal battle trying to figure out all the complex pros and cons.
UTIGER: “serum TSH concentrations are also undetectable in patients with various types of thyroid autonomy or patients receiving moderate to large doses of exogenous thyroid hormone who seem clinically euthyroid and whose serum T4 and T3 concentrations are within the normal range—that is, patients with subclinical hyperthyroidism.
These observations attest to the considerable sensitivity of the thyrotrophs to small increases in serum T4 and T3 concentrations.
From a practical perspective, I do not think that the distinction between undetectable and subnormal serum TSH concentrations in and of itself should be overvalued.
It depends on assay sensitivity vis-á-vis the lower limit of the normal range.
Moreover, although a greater reduction in TSH secretion reflects a greater increase in thyroid hormone production (or a larger exogenous thyroxine dosage) and a higher probability of symptoms and signs of hyperthyroidism, the presence or absence of the latter depends not only on the magnitude of the increase in thyroid hormone availability but also on the vulnerability of the individual patient.
Patients with overt (symptomatic) hyperthyroidism need not have undetectable serum TSH concentrations, and patients with subclinical (asymptomatic) hyperthyroidism may have undetectable serum TSH concentrations.
In physiologic terms, a clinically euthyroid patient who has a chronically subnormal serum TSH concentration has too much thyroid hormone.
Does this mean that some treatment of patients with subclinical hypothyroidism is indicated? This issue will be considered subsequently.
A second benefit is that TRH stimulation tests are obsolete. Because the degree of suppression of TSH secretion can now be measured directly, the primary need for TRH stimulation testing —that is, to determine whether basal TSH secretion is low or normal—no longer exists.
The fact that a few patients with subnormal or undetectable basal serum TSH concentrations have small serum TSH responses to TRH is neither surprising nor clinically important. …
The greatest potential problem is that the ability to measure very low serum TSH concentrations will lead to unnecessary intervention.
Consider the problem of subclinical thyroid disease—that is, patients who are clinically euthyroid and have normal serum T4 and T3 concentrations but abnormal serum TSH concentrations.
Most patients with low serum TSH concentrations will have overt or subclinical hyperthyroidism, but some will be euthyroid, because of transient TSH deficiency accompanying nonthyroidal illness (adaptive hypothyroidism), or hypothyroid, because of permanent TSH or TRH deficiency.
Moreover, when chronically inhibited by hyperthyroidism, serum TSH may remain low for weeks or months after effective antithyroid treatment.
Although most patients with normal serum TSH concentrations will have normal thyroid function, a few will be hypothyroid, because of TSH or TRH deficiency, and a few will be hyperthyroid, because of excess TSH secretion.
Finally, almost all patients with elevated serum TSH concentrations will have overt or subclinical hypothyroidism, but a few will be hyperthyroid because of excess TSH secretion. …
Suffice it to say that the TSH-first strategy, applied intelligently in light of the clinical findings and complemented by measurements of serum T4 and occasionally T3 concentrations, will allow accurate diagnosis, just as does the older strategy.
In comparison with serum thyroxine [T4] measurements, TSH measurement alone is clearly better for confirmation of a diagnosis of hyperthyroidism, for assessment of patients receiving thyroxine [T4] therapy and of patients with nonthyroidal illness, and for obtaining the strongest possible evidence against any possible thyroid dysfunction.
The penalty, however, is the identification of the rather large groups of patients with subclinical hyperthyroidism and subclinical hypothyroidism. These patients will likely undergo additional tests. In contrast, had only serum thyroxine [T4] been measured in such patients, the normal result would preclude the need for additional tests.
In practice, much depends on the testing philosophy of those ordering the tests and the physician’s confidence in his clinical judgment, but it is difficult to envision not measuring serum thyroxine [T4] in a seemingly clinically euthyroid patient with a low or high serum TSH concentration.
My conclusion is that the use of initial serum TSH measurements for evaluation of suspected thyroid disease has both strengths and weaknesses.
It is clearly superior for assessment of certain patients, but as a general test in an ambulatory setting, TSH measurements will identify too many patients in whom the unwary or overzealous may undertake unnecessary further testing and even treatment.”
- Written by Tania S. Smith, with the assistance of TP.ca editorial & writing team member S. F.
Beck-Peccoz, P., Rodari, G., Giavoli, C., & Lania, A. (2017). Central hypothyroidism—A neglected thyroid disorder. Nature Reviews. Endocrinology, 13(10), 588–598. https://doi.org/10.1038/nrendo.2017.47
Joffe, H. V., Emerson, C. H., & Braverman, L. E. (2009). Dr. Robert David (“Bob”) Utiger, 1931–2008. Thyroid, 19(1), 81–82. https://doi.org/10.1089/thy.2008.1562
Snyder, P. J., & Utiger, R. D. (1972). Inhibition of thyrotropin response to thyrotropin-releasing hormone by small quantities of thyroid hormones. Journal of Clinical Investigation, 51(8), 2077–2084. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292364/
Utiger, R. D. (1982). Differing thyrotropin responses to increased serum triiodothyronine concentrations produced by overfeeding and by triiodothyronine administration. Metabolism: Clinical and Experimental, 31(2), 180–183.
Utiger, R. D. (1988). Thyrotropin Measurements: Past, Present, and Future. Mayo Clinic Proceedings, 63(10), 1053–1056. https://doi.org/10.1016/S0025-6196(12)64925-8