Discussions that mention thyroxine

Endocrine Disorders board


Hello Ladies and Gentlemen,

Speak up boys! We need a male perspective. I promise not to bite! Until we get men on board.. you all will just have to listen to the ladies nag and gripe! ;)

I am starting week TWO as promised! First things first we learned in week one that getting treatment is never easy and you can not give up. You must keep fighting if you have a family history of hypoT and your symptoms indicate it may be endocrine in nature. So keep this thread in mind and continue to share your woes and what is or is not working for you. Getting treatment is hard enough, getting competent and optimal care is even harder.

I am including a summary of things learned in week One. The general points are as follows (THE MG's THYROID SCHOOL – Fondly taken from Apple):

BASICS:

What is normal TSH range versus optimal?
Optimal is 50-80% of normal range. This statistic comes from the N A C B where they determined 85 – 90 % of non-dysfunctional thyroid MALES had TSH levels between 0.89-1.1. Women of child bearing years need to have Fts in the 60-80% range of normal. Women after menopause tend to need slightly lower Ft values in the 40-70% range. (This is just my MFM and 2 Obs knowledge on this.. trying to dig up a public access postable journal article on this information) Many MDs do not know how to determine where you are in the normal range. So here is the formula you need to know and come to love.

Given the following formate:
Free T or Total T value (lower limit - upper limit)
0.85 (0.8-1.8)
Your percentage is calculated as follows:
[Your FT value - lower limit]/[upper limit - lower limit]*100 = %
[0.85 - 0.8]/[1.8-0.8]*100 = 5%
Optimal care is when your TSH is around 1 on a T4 supplement alone with Ft's are in the 50-80% range of normal. T3 supplementation such as cytomel or Armour results in TSH suppression and as a result you must gauge thyroid supplementation on your T4 and T3 hormone levels and symptoms alone.

Here is a summary of the A A C E and N A C B statements on the latest normal TSH range.
November 2002: The National Academy of Clinical Biochemistry (NACB), part of the Academy of the American Association for Clinical Chemistry (AACC) was first to issue new laboratory medicine practice guidelines. This is their job so it is to be expected they alter the requirements MDs use for the diagnosis and monitoring of thyroid disease. The particular statements of interest in the 2002 guideline announcement are:
"It is likely that the current upper limit of the population reference range is skewed by the inclusion of persons with occult thyroid dysfunction. . . . In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L because >95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/L. . . . A serum TSH result between 0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard L-T4 replacement dose for primary hypothyroidism."

Non-US Mds may turn their nose up at this information.. but it is always worth a shot. This announcment and research was then picked up and reviewed by the A A C E. Based on the N A C B's findings, in January 2003, the American Association of Clinical Endocrinologists (A A C E) made the following important announcement that all the MDs should get.. but haven't yet:
"Until November 2002, doctors had relied on a normal TSH level ranging from 0.5 to 5.0 to diagnose and treat patients with a thyroid disorder who tested outside the boundaries of that range. Now A A C E encourages doctors to consider treatment for patients who test outside the boundaries of a narrower margin based on a target TSH level of 0.3 to 3.0. The A A C E believes the new range will result in proper diagnosis for millions of Americans who suffer from a mild thyroid disorder, but have gone untreated until now."

It has now been 8 years since the original N A C B guidelines release, many laboratories have not yet adopted these new guidelines for a normal range, and many physicians are either unaware of the A A C E announcement or refuse to change their procedures until the labs revise their standards. Many of the people on this board can tell you that you can not trust or expect your MD to know this fact. Let them know you know!

An article that may help:
"Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range: randomized double blind placebo controlled crossover trial."
[url]http://www.ncbi.nlm.nih.gov/pubmed/11668132?dopt=Abstract[/url]
Hashimoto's Facts – [I need to work up a Graves Facts list too]:
Do antibodies correspond to your level of TSH?
My personal non-MD opinion and answer:
Not necessarily. The TSH and antibodies production mechanisms are not directly linked. My layman's explanation on the matter is the TSH (thyroid stimulating hormone). This is the pituitary function call to the thyroid that screams out.. HEY! I NEED MORE T4, MAKE IT NOW! The thyroid then responds by activating its production enzymes.. TPO and TG. Now the thyroid begins to produce more T4 so the TSH will decrease. In the case of Hashimoto's your immune system sees the TPO and TG as a threat to your system. So every time the TPO and Tg are activated, TPOAb and TGAb are produced to attack and destroy the thyroid. How long and how high the antibodies go is up to your body. Prophylactic treatment of my Hashimoto's may have saved my adrenal glands and no telling how many years of dysfunction symptoms. Studies indicate this may be true in others as well. Here is a national institute of health study on the matter.

[url]http://www.ncbi.nlm.nih.gov/pubmed/11327616[/url]
The acredited referreed publication on this matter:
"One-year prophylactic treatment of euthyroid Hashimoto's thyroiditis patients with levothyroxine: is there a benefit?" Thyroid, 2001 Mar;11(3):249-55

ALL that an MD can tell for certian is whether or not you have antibodies present. If you are positive in TPOAb or TGAb you have Hashimoto's. This means your immune system is attacking your thyroid and will kill it eventually. WHEN? Well that is as individual as you are. Depending on how many you have... the destruction of your thyroid could be near complete... just beginning.. or at its peak. Anything over 1000 is seen as BAD. When levels get this bad.. added AI side bonuses should be looked for.

Other common issues with Hashimoto's:
1) Hashimoto's is know for thyroid flares, oscillations between hyperT and hypoT states. Some MDs referr to this as Hashitoxicosis.. others say Hashitoxicosis is having Graves and Hashimoto's disease. What Hashitoxicosis means is you have hyper and hypo thyroid episodes and medicating will be a constant adjustment issue.
2) Mild to moderate “joint and muscle pain”. This particular symptom is also one of those that seems to linger in some patients, months or even years after starting treatment for their hypothyroidism, with hormone replacement medication.
3) Some patients actually experience a worsening of their joint/muscle pain, once beginning thyroid medication. I had this happen. I am not sure if it is the fact I went so hyper after adjusting to 75 mcgs or just a side bonus of being thyroid dysfunctional and my body not liking the fact i am trying to keep it normal. ;)
4)Most patients see improvement of rheumatic symptoms with hormone replacement therapy to treat their hypothyroidism but if relief is minimal, they may to be tested for co-morbid arthritis, including the autoimmune types.

How do I know when my thyroid is underattack and I need to watch for a Hashimoto's flare?
Well when I go hypoT because my t4 and t3 levels are not right for me.. my pitutary gland calls to my ever growing thyroid by way of a TSH shout out. "Hey, Thyroid.. need some more T4 get cooking!" The thyroid sighs and thinks about it.. then tries to do its job. In Hashimoto's patients and my case the thyroid activates the TPO enzymes begin to make and release T4. It is at this point my 2000 lazy and bored TPOAb and TGAb perk up and yell, "ATTACK!" Or whatever they scream as they charge and attack. It is at this point that my thyroid feels full and aches, it is a continual process that starts out more intense in the morning and lessens as my T4 supplementation takes away some of the burden. The throb, pulse, ache and swellen in that area just at the base of your throat bracketing your wind pipe is classic thyroiditis.

I hope this helps you help yourself. Now how did you all get treatment and how is it going?
MG
Dang it I typed a book and my internet browser crashed. *GRUMBLE* Here we go again..
Kassikoo,
I keep a daily log of my symptoms. I check off what I am experiencing and the severity of the symptom. It is by our symptoms that we are feeling hypoT or hyperT. So just incase.. we need to classify them and keep up with them in an organized objective manner so that you can show the MD. This is how I felt this morning.. this is me now... ETC. Here is my daily list that I check off and comment on. I keep it in a spreadsheet on my computer and keep a weekly hard copy on hand.
Symptom occurance Log
Hyperthyroidism only symptoms experienced
Diarrhea
Dyslexia (difficulty with reading, calculating, thinking)
Hypersensitivity to heat (heat intolerance)
Increased appetite
Increased frequency of stools (without diarrhea)
Increased sweating
Muscle weakness (arm triceps, leg quadriceps)
Palpitations (rapid, forceful or irregular heart beats)
Tachycardia (rapid heart beat)
Tremors (shaking hands)
Hyper/Hypothyroidism symptoms experienced
Morning Temperature
Morning BP&HR
Breathing Difficulties (shortness of breath)
Constipation
Constipation Aides Used
Eye problems (gritty, dry, achy, blurry, irritated, red eyes; light sensitivity; double vision)
Facial puffiness (eyes, lids too)
Fatigue (all the time, despite sleep sufficiency)
Fertility problems
Hair problems (coarse, dry texture) (hypothyroid hair loss: head and outer edge of eyebrow )
Hearing disabilities (tinnitus, ear ringing among them)
Low resistance to infections
Menstrual changes (flow, duration)
Mental challenges (forgetfulness, brain fog)
Migraines
Nail problems (dry, brittle)
PMS (premenstrual syndrome)
Sexual dysfunction (low drive)
Skin changes (dry, itchy, patchy)
Throat problems (swallowing difficulty)
Voice changes (hoarse, husky)
Weakness (overall, all the time)
Weight fluctuation (Gain hypo/loss hyper)
Hypothyroidism – Underactive thyroid symptoms experienced
Allergies (developing or worsening)
Cold body temperature (feeling cold too)
Dizziness (often accompanied with vertigo)
Mood changes
Muscle and joint aches (severe, especially hands and feet)
Sleep apnea (lapses of breath while sleeping) and snoring
Evening Temperature
Evening BP&HR

Now to the rebutle of "Thats rubbish and it takes weeks for it to change and do that so its very unlikely." Notice he used VERY unlikely. ;) This covers him incase you can prove him wrong.

Let's get technical.. but I will try to do it in the engineering spirit of KISS.
Basic pharmokinetic reactivity of T4 and T3.. known and observed and documented for any to find. Heck your own T4 and T3 medication inserts should have this...
T4 is slowly eliminated from your system. The major pathway of thyroid hormone metabolism is through sequential deiodination. This means your liver strips an iodine off the T4 molecule making T3. Approximately eighty-percent of circulating T3 is derived from peripheral T4 by monodeiodination. This is why we need a 4:1 ratio of T4 to T3 in our system. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80% of the daily dose of T4 is deiodinated to yield equal amounts of T3 and reverse T3 (rT3). Occasionally our inherent mechanisms do this improperly causing too much to be turned into rT3.. or not enough to be converted at all OR in the case of adrenal insufficiency.. too much T3 to be made. But I digress and need to get back on point. "it takes weeks.. ;)"
From the FDA database of pharmokinetic information:
Hormone********* Ratio in Thyroglobulin *****Biologic Potency *****t1/2 (days) *****Protein Binding (%)2
Levothyroxine (T4) *****10 - 20 *************** 1 ********************* 6-7 *************99.96
Liothyronine (T3) **********1 ******************* 4 ********************* ≤ 2 ************* 99.5

Now if you have too much in your system your will be driven hyperT and burn of T4 with a half-life rate of 3 to 4 days. If you are hypo the T4 half-life is longer, 9 to 10 days, because your body needs every last molecule and rations it accordingly. The same holds true for T3.. but the rate is even more dramatic. Instead of a 2 day half-life you burn it up in 12-24 hours if you are hyperT.

Now it does take 2 weeks for your blood to equilibrate to a new dose of T4. It takes another 2-4 weeks depending on your personal metabolism and body to determine if that dosage increase is enough to suit you. It takes 7 days for T3 to equilibrate when given a steady dose and then another 2-3 weeks for your body to say YEAH or NEAH!

So how can you spike? How can you have a flare? Well unfortunately our body under the influence of an AIT such as Hashimoto's.. IS NOT STEADY! We do not produce hormone at rate X at time T daily. It coughs and hacks and vomits T4 out with every wave of antibody attack!

Thyroid hormones are stored extracellularly in the colloid inside the follicle in the form of ioidinated bound protiens.. like thyroglobulin. This is why when we decide to kill off our source of thyroid hormones for whatever dysfunctional reason.. we generate thyroiglobulin antibodies as well as TPOAbs. Kill the carrier and the creator. SO what happens when this tissue is destroyed? Does the bound T4 suddenly blip out of existance? NOOOOO.. it is suddenly released. What happens then? Well as a result of sudden tissue destruction your T4 blood level temporarily spikes. How high? Well that depends on the amount stored and amount destroyed. Back to point. Like when you up a dose of meds this sudden added hormone causes your body to begin to work more. Dormant starved process will activate.. or in the case of a stabilized individual they will flare hypert in an effort to burn off excess T4 in the system. Now remember.. 80% of the T4 is converted to T3.. so you get the physical bonuses of Hypersensitivity to heat (heat intolerance), Increased appetite, Increased frequency of stools (with or without diarrhea), Increased sweating, Muscle weakness (arm triceps, leg quadriceps),
Palpitations (rapid, forceful or irregular heart beats), Tachycardia (rapid heart beat), Tremors (shaking hands).. the most common feeling is a hot flash. If you have a massive dump you get increased body temp, heart rate, BP, and some of the other mess.

So it may take a couple of weeks for the blood to attain or show a new level, but with every T4 dump you will get a temporary short lived T3 spike and flare. Because it is inconsistent we physically percieve it as a hyperT spike. It goes back to needing to treat the symptoms as well as the labs. It is also a known fact that the TSH fluxuates through out the day. Hence when the N A C B is reviewing the normal TSH range. They take readings at 8 am and 6 pm.

In normal thyroid functioning people and euthroid treated patients with out AIs I will grant your MD his point. But if he is a normal functioning thyroid patient. Ask him what taking a single mcg cytomel or single 25 mcg synthroid would make him feel. He would spike in a day and go back to normal in another day or two.

Whew! Okay.. did I explain it well enough?
MG