Thursday, October 15, 2015

A Lesson in Blood

Salutations, reader!  It has been a little while since I've posted anything of substance, so I decided to post a little update on what has been going on with me, and segue into a discussion on something I know you all want to know about: my blood.

Blood?  Not now, Charlie.

Things have been good over the last month or so. Got to see two shows at the Hollywood Bowl, went up to San Francisco to visit my sister and her family, and things have been fairly quiet at work, which is nice for a change.

On Monday (Sept 21st), I had my 3-month post-surgery blood draw.  After surgery, the start of my levothyroxine medication, the administration of Thyrogen, and the radioactive iodine treatment, this was the first time that my endocrinologist could get a clean, unadulterated read on my blood levels, since all of that stuff can temporarily tweak them.

I'll run through each of the important levels that my doctor has been monitoring, and their importance.

Thyroid Stimulating Hormone (TSH)

TSH is one of the most important factors, in terms of preventing the recurrence of thyroid cancer.  In my "LID Week 1 Post-Mortem" post from July, I went over what it was, but allow me to recap it.

TSH is part of what can be described as a negative feedback loop.  The pituitary gland is what produces TSH and releases it into the blood.  It does this when it cannot detect enough thyroid hormone in the bloodstream.  The TSH "wakes up" any thyroid cells in the body and stimulates them to begin convert iodine into thyroid hormone (T4).  TSH really serves no other purpose to the body, other than to cause thyroid cells to produce T4.

If you understand this meme, then I hate you for liking System of a Down.

I have been taking levothyroxine (synthetic T4) this whole time in order to replace the thyroid cells that I used to have that produced T4 themselves.  Therefore, the primary purpose of taking my hormone meds every morning is to ensure that I have enough thyroid hormone to regulate my metabolism and energy.  The secondary purpose however, is to ensure my pituitary gland doesn't think I need more T4 in my system, and therefore to ensure that it does not release TSH.

Why is that important?  Well, at this point, especially after taking the radioactive iodine (RAI), it is assumed that I have little to no more thyroid cells left in my body.  But what if I did have a few cells?  Well, then any TSH would stimulate them to produce T4.  Not a big deal, I could always use a little more T4.  But what if those remaining cells are cancerous?  No bueno, man.

So the second point of taking synthetic T4 is to keep TSH low, and therefore make sure that my pituitary gland is not stimulating any cancerous thyroid cells left in my body.  If a leftover cancerous cell isn't getting stimulated, it's far less likely to grow and become problem.

My blood reading this week was 0.43 mcIU/mL.  I know what you're thinking: "Solid number, Walter, I wish mine was as good."  Don't be jealous.  For those of you not in the thyroid-know, I'll explain.  "Standard range" for someone without thyroid cancer is 0.3-4.7.  Great, so I'm at least within normal range.  The norm for cancer patients is different, though.   According to current American Thyroid Association (ATA) guidelines, latest publication in 2009, the target range depends on the risk.  For high-risk or intermediate-risk patients, the target is below 0.1.  For low-risk patients like myself, regardless of whether or not RAI was administered, the target is 0.1-0.5.

It's important to note that TSH is not really considered a way to detect thyroid cancer.  TSH is typically normal when someone has it.  For example, before my surgery, my TSH measured between 0.5-0.7, well within the normal limits.

Great, I was within my target range!


Thyroglobulin, and Thyroglobulin Antibodies

The second vital reading is Thyroglobulin (Tg), along with Thyroglobulin Antibodies (Tg AB).  While TSH is more of a cancer preventing measurement, Tg is how you monitor recurrence of cancer.  So, it's kind of a big deal.

I'm Thyroglobulin Burgundy?

All thyroid cells produce Tg.  Therefore, prior to a thyroidectomy, measuring Tg is essentially useless.  For most, Tg won't really tell you anything about the presence of cancer, or its staging/severity.  From what I've read, the only time it may help is if a Tg reading is off the charts (above the standard rage of 3.0 - 40.0 ng/mL), which can indicate significant spread to several other organs.  However, as I said, in most cases this isn't even measured before the thyroid is removed, since all thyroid cells, cancerous or not, produce Tg.

After surgery however, this measure becomes absolutely key.  Once the thyroid is removed, it can be seen a direct measure of cancer activity in the body.  After RAI, it is assumed that one's Tg measure will be extremely low, perhaps even undetectable.  This makes sense because the RAI should have destroyed every last thyroid cell, cancerous or not.  Therefore, by monitoring this number through regular follow-up, any increase in the amount becomes immediately suspicious of cancer recurrence, which necessitates follow-up via physical inspection, ultrasound, whole body scan, or some other method.

In cases where people did not receive RAI, establishing a "zero" baseline becomes a bit harder.  Since residual thyroid tissue is always left over after a thyroidectomy, the number never becomes close to zero.  Therefore, doctors have to establish a baseline amount, and then monitor for spikes in the figure after that.  Even then, spikes may not indicate cancer.  Following up on Tg levels without RAI can be a bit more nuanced and have grey area; however, this alone is not reason enough to favor doing RAI over skipping it, according to several medical articles that I've read.

So, what were my numbers?  Well, my doctor felt that the 3-month point was too early to get a reliable Tg reading on my blood due to potential interference from the Thyrogen shots and the RAI, so we skipped it this time around.  However, here are the numbers I have seen from previous draws:

First blood draw, post-surgery: 1.3 ng/mL
- 3.5 weeks of levothyroxine
- I've seen many studies try to predict what level of post-thyroidectomy Tg can be indicative of recurrence of the cancer down the road.  I've seen as low as 1.3, but have also seen 4.2 and >50.  It's all over the place, man.  None of my doctors seemed to be alarmed by my level, so I guess it was fine.

Post-Thyrogen, pre-RAI: 8.8 ng/mL
- On the morning of my RAI treatment, after 2 days of Thyrogen injections
- Oh no, it went up!  This is fine.  Because Thyrogen increases TSH to ungodly levels, that much TSH causes any existing thyroid cells to be in overdrive.  As a result, they release way more Tg.  This was my first "stimulated Tg" reading, as opposed to my previous reading, which was "unstimulated."  Stimulated Tg becomes more important down the road if cancer recurrence is suspected, otherwise this should be the only time I get a stimulated Tg reading.

5 days post-RAI: 12.9 ng/mL
- 5 days after taking my RAI dose
- Up slightly again!  This makes sense though, because: A) my TSH is still slightly elevated from the Thyrogen in the prior week, and B) the RAI was actively destroying my thyroid cells at this point.  When thyroid cells die, they release Tg.

So, we'll see what my Tg reading is 3 months from now, to establish a true post-RAI baseline.

Tg AB, on the other hand, only means something if it is on the high side. The presence of Tg AB can interfere with Tg readings, and make them less reliable, particularly if they are found in high quantities.  Tg AB may be present as the result of the body's defense against thyroid cancer, or against other thyroid disorders like Hashimoto's disease where thyroid cells or the organ itself is malfunctioning.

In any case, if Tg AB is high, then it makes the Tg measurement less valuable, since Tg AB causes interference with lab readings of Tg.  If high Tg AB values persist after a thyroidectomy and subsequent RAI, it could suggest the presence of residual thyroid cancer, or underlying thyroid disease like Hashimotos'.

The acceptable range of Tg AB is <4.0 IU/mL.  The three times mine has been measured, I have been at 0.9.  So, all good there!

Free T4

T4, as I described earlier, is the primary thyroid hormone.  Levothyroxine pills (or their brand name equivalents) are synthetic T4 hormone.  The thyroid primarily produces T4 over T3, in about an 80/20 ratio.

As the thyroid takes in iodine and converts it into T4, it then releases it into the bloodstream, where it circulates around the entire body.  Most of the T4 molecules bind themselves to cellular receptors in specific organs, such as the liver, kidney, and muscles.  In these organs, one iodine molecule is released, effectively converting the T4 into T3.  From there, T3 circulates to the rest of the organs and tissues in the body, which regulates the body's overall metabolism of carbohyrdrates, proteins, and fats, as well as the stimulation of growth and development, both physically and mentally.  Important stuff!

When I said that most of the T4 molecules produced by the thyroid get bound to organs, I wasn't kidding.  About 99% of T4 gets bound to organs or various transport proteins, but that remaining 1% ends up floating freely in the bloodstream, essentially homeless.  This is Free T4, which can be measured in a blood draw.  It can be seen as the concentration of "available" T4 that can be taken in by any organs that need a fresh supply.  By measuring this Free T4, doctors can assess if the patient is getting an adequate supply of synthetic T4 from their pills, and adjust as needed.  Many endocrinologists believe that the measurement of free T4 is more important than free T3.

I've only had my free T4 measured twice.  The acceptable range is 0.8 - 1.6 ng/dL.  My values have been 2.1 right after my surgery, and 1.7 more recently.  Therefore, everything looks good here!

Free T3

T3 is another thyroid hormone that is created by the thyroid in smaller quantities.  As discussed above, the primary source of T3, is the body itself, which creates T3 by converting T4.  T3 is also available as a synthetic pill (generic name Cytomel), but I'm not currently on it, so I can't really speak about it with much authority.  In addition, my doctor isn't currently measuring my Free T3, so I don't have any blood readings to share with you either.

T3 is the primary "active ingredient" in stimulating your metabolism.  Much research suggests that T4's main reason to exist is to be converted into T3 so that the rest of the body can use it.  I have read of patients who have been diagnosed as "poor converters" of T4 to T3, and as a result experience symptoms of hypothyroidism despite being on an adequate does of T4.  In those cases, I know some people end up taking a tandem of T4 and T3 pills.  I don't appear to be in that boat so far, so all good to me.

I know.  No more medical jargon for today.

And so, in summary, all my blood tests have been pretty much on the money so far.  Hopefully everything stays that way!  I hope you all are doing well!

-W

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