Tg antibodies could still be possible, but also you might just be sero-negative. I was initially diagnosed as sero-negative (hashimoto’s but no antibodies showing up) your TSH and low T4 are demonstrative of overt hypothyroidism. Do you know your T3? 😊
You will definitely need your T3, that is the active hormone. T4 is just the storage form. Yes, about 12 years after onset I had some antibodies show up but nothing dramatic.
I've had two lots of antibody tests, once privately, once by NHS, both negative, done 4 years apart. So I can only conclude my hypothyroidism isn't caused by Hashimotos. Some with Hashis apparently don't have antibodies.
There are other causes of hypo, problems with pituitary gland, pregnancy can be anothercause, lack of iodine in the diet. It's much rarer to have non autoimmune hypothyroid.
Ultimately though the treatment is the same, irrespective of the cause. Replacement thyroid hormones, either by Levothyroxine via NHS or NDT, or just replacement T3. Or a combination. It's very hard to get NDT on NHS or T3 for that matter. However your TSH is over 10 so you should be offered Levothyroxine. Was this your first abnormal blood test?
How many times have you been tested for TPOab? One negative result does not totally rule out Hashi's because antibodies fluctuate. Or, as Hidden says, your TgAb could be high. But, even if that's negative, there's a certain percentage of Hashi's people that never even have over-range antibodies, and they are diagnosed by ultrasound of the thyroid.
If it turns out that you don't have Hashi's - and not all hypos do - there's not much chance of finding out why. There are so many possibilities. Could be a pituitary problem - although that would have showed up on diagnosis - or an accident, like whiplash. Or endocrin-disrupters in cleaning and beauty products. Or eating disorders. Or certain medications, like lithium. But, whatever the cause, as the treatment is always the same, doctors really aren't interested in finding out why. And, in any case, the chances of being able to reverse it are minimal. So, one has to ask: does it really matter?
And, even if you do find you have Hashi's, there then arises they question: why did I develop Hashi's? And, your chances of finding an answer to that are pretty slim, too, because there are many, many possible causes. But, once again, whatever the cause, the treatment is the same, so...
Hashimoto's isn't ruled out. A percentage of Hashi's people never show positive antibodies so you could still have it. get GP to retest when you can and if you do any private bloods.
I was diagnosed hypo back in 1975, 2 years after first becoming unwell and a clueless doctor. I have had quite a few antibody tests over the years, all private and many part of a test bundle, each time antibodies very low in range. I don't have Hashi's and I've never had the swings that Hashi's causes.
Although Hashi's is the most common cause of hypothyroidism. Other causes, as listed by Dr Peatfield in his book "Your Thyroid and How to Keep It Healthy:
Genetic - thyroid gland may not develop properly in the womb, may be totally inactive or partially inactive.
Environment - iodine deficiency, selenium deficiency, environmental poisons such as mercury, fluoride (not naturally occurring fluoride but the toxic waste fluoride added to toothpastes, water, etc).
But what difference would it make? If there is no known way of treating the actual cause, it wouldn't actually make much difference!
That isn't to say you shouldn't look, and try to identify causes and contributory factors. Just that it is likely more important to consider what to do.
Thyroid hormone therapy not only preserved renal function better, but was also an independent predictor of renal outcome in chronic kidney disease patients with subclinical hypothyroidism.
Standard starter dose of levothyroxine is 50mcg
Bloods should be retested 6-8 weeks after each dose increase
Likely to need several further increases in levothyroxine over coming months
This was very informative . Thank you. I will definitely test for anti TG. i do not take any supplements so i will test for vitamins listed. Hopefully my GFR will improve as I dont have diabetes or hypertension. Thanks again
Vitamin D deficiency is frequent in Hashimoto's thyroiditis and treatment of patients with this condition with Vitamin D may slow down the course of development of hypothyroidism and also decrease cardiovascular risks in these patients. Vitamin D measurement and replacement may be critical in these patients.
Vitamin D insufficiency was associated with AITD and HT, especially overt hypothyroidism. Low serum vitamin D levels were independently associated with high serum TSH levels.
The thyroid hormone status would play a role in the maintenance of vitamin D sufficiency, and its immunomodulatory role would influence the presence of autoimmune thyroid disease. The positive correlation between free T4 and vitamin D concentrations suggests that adequate levothyroxine replacement in HT would be an essential factor in maintaining vitamin D at sufficient levels.
Our results indicated that patients with hypothyroidism suffered from hypovitaminosis D with hypocalcaemia that is significantly associated with the degree and severity of the hypothyroidism. That encourages the advisability of vit D supplementation and recommends the screening for Vitamin D deficiency and serum calcium levels for all hypothyroid patients.
Same applies to low B12 - extremely common in hypothyroid patients
All patients who are hypothyroid should have B12 tested
There is a high (approx 40%) prevalence of B12 deficiency in hypothyroid patients. Traditional symptoms are not a good guide to determining presence of B12 deficiency. Screening for vitamin B12 levels should be undertaken in all hypothyroid patients, irrespective of their thyroid antibody status. Replacement of B12 leads to improvement in symptoms, although a placebo effect cannot be excluded, as a number of patients without B12 deficiency also appeared to respond to B12, administration.
Levothyroxine can decrease serum homocysteine level partly; still its combination with folic acid empowers the effect. Combination therapy declines serum homocysteine level more successfully.
None of my family have ever had antibodies but 5 of us have thyroid problems. Two without a thyroid the rest just on medication. My partner has antibodies but no symptoms apart from a high TSH reading. I have been tested many times, so has my sister both have no antibodies.
My TPO is normal, but my TgAb is high. When I was only tested for TPO I was told I did not have Hashimoto's. Fortunately, I knew already that I do because TgAb had been tested before and was high. Just to be on the safe side I tested for it again privately and it was still high. So, contrary to what I was told, I was not in remission (sadly). You should not rule out Hashi just yet. Most importantly, I would think, is to get your hormone levels in order for now, though.
Furthermore, the Hashimoto's had been diagnosed by ultrasound which showed significant destruction of the thyroid and consequent atrophy. So, to be "diagnosed" with no Hashi was just based on that specific doctor's complete lack of knowledge. This is a good place to come to and collect as much knowledge as you can because many doctors sure don't have it.
I am interested in your comments regarding Hashimotos and atrophied thyroid. It has, for many years, been my understanding that Hashimotos cause destruction of the gland but not any atrophy and that most Hashi patients retain full sized thyroid gland throughout adult life.
Indeed in my case it was believed my thyroid was destroyed by radiation therapy in the early 1950s. I had a scan about 10 years ago and was told I had the smallest thyroid he had ever seen. I was diagnosed sixty years ago and at the time of the scan I was advised it confirmed no Hashimotos. I have always had negative antibodies. There was some discussion of Ords if any autoimmune cause, however they decided the originally suggested cause was correct.
Where can I learn more about Hashimotos as the cause of atrophy please. It makes no difference to me now but I’d be interested to learn more. Thank you.
Ord's is actually the correct term for thyroiditis causing atrophy, but I have learned to just use the term "Hashimoto's", which is already enough of a challenge for many doctors I encountered (let alone most "ordinary" people). Hashimoto's is thyroiditis with a goiter. So, I too, have Ord's.
I questioned why you called atrophied thyroid Hashimotos it seems you just prefer to use the wrong terminology. Had you said the scan you had confirmed autoimmune thyroiditis that would have been clearer in my opinion.
There really was no need for you to go to the trouble of providing a link to confirm something I had known for many years.
You are absolutely right. Thank you for the correction. I'm hoping to be more precise with my words in the future. It certainly is a very worthy goal.
As far as the link goes, I apologize for misinterpreting your post and providing information that you have been aware of for many years. While it merely reiterates knowledge you already have, I hope that the link may be at least of some use to somebody else, as I perceive it as very comprehensive.
Thanks again for taking the time to set me on the right path. All my very best wishes for health and happiness.
I had subacute thyroiditis supposedly caused by a virus. My antibodies are normal and I’m on levothyroxine, for all the good it does.
I often wonder if the advice given to those with Hashi’s is relevant, such as gluten free diet etc
My t3 has never gone above the bottom range despite my t4 being slightly over the top range. Also there is little information regarding the cause, although mine started a few days after my first flu jab. Doctors dismiss this as a cause but my own research shows there are some links
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