Possibly more questions than answers, but also possibly of some interest.
Thyroglobulin Antibodies are Associated with Symptom Burden in Patients with Hashimoto’s Thyroiditis: A Cross-Sectional Study
Ana Barić, Luka Brčić, Sanda Gračan, Veselin Škrabić, Marko Brekalo, Marta Šimunac
Published online: 17 Oct 2018
ABSTRACT
Background: Hashimoto’s thyroiditis (HT) is the most common form of autoimmune thyroid disorders characterized by lower production of thyroid hormones and positivity to autoantibodies to thyroglobulin (TgAb) and/or thyroid peroxidase (TPOAb). We performed a comprehensive phenotypic characterization of patients with HT, with specific focus on thyroid autoimmunity, to get better understanding of disease manifestation.
Methods: We collected information on thyroid-specific phenotypes (TSH, T3, T4, fT4, TgAb, TPOAb, thyroid volume) and other clinical phenotypes (age, body surface area, number of hypothyroidism symptoms, blood pressure) from 290 patients with HT without levothyroxine (LT4) therapy with the aim to test for correlations between thyroid-specific and clinical phenotypes.
Results: Our key and novel finding is the existence of significant positive correlation between TgAb levels and the number of symptoms (r = 0.25, p = 0.0001) in HT patients without LT4 therapy that remained significant after adjustment for TPOAb, T3, TSH levels and thyroid volume (β = 0.66, SE = 0.3, p = 0.0299). Increased TgAb levels are significantly associated with fragile hair (p = 0.0043), face edema (p = 0.0061), edema of the eyes (p = 0.0293) and harsh voice (p = 0.0349).
Conclusions: Elevated TgAb levels are associated with symptom burden in HT patients, suggesting a role of thyroid autoimmunity in clinical manifestations of HT. Based on these results, we recommend screening for TgAb antibodies in HT patients with symptom burden. We also suggest that further work on understandings of symptoms appearance due to their autoimmune or hypothyroid causation is needed.
At last, perhaps the possible destructive nature of elevated thyroid antibodies is starting to be recognised.
Some live quite happily with thyroid antibodies, but for others, they can cause immense irregularities within the immune system leading to inflammation and awful symptoms.
Thyroid antibodies do matter because it is the amount that our genetic makeup and present health state can tolerate, and that is so variable from person to person.
But even now I ask, in what way are Thyroglobulin (and Thyroid Peroxidase) antibodies destructive?
Yes - the worse the lymphocytic destruction of the thyroid, the higher the antibodies are likely to be. Therefore, high antibody levels certainly seem to be indicative of worse health. But I struggle to seem them as causative. That could very well be my ignorance.
I think we can all appreciate that TSH Receptor antibodies (at least the stimulating sort), affect health by their direct effect on the thyroid. They are like super-TSH and result in the thyroid producing and releasing too much thyroid hormone with all the effects that has. But I don't think anyone has identified a way on which the antibodies, or even the antibody-antigen complex formed when the antibody attaches to its target, impact on our health.
I really, really don't know. And it would be so very helpful to have certainty on this issue (as some many other thyroid issues).
Because this self attack by the immune system causes bodily inflammation mainly due to a reaction from cytokines such as interleukin-1 & interleukin-6, and that is why people see weird symptoms such as achy joints, a sore/hoarse throat, or the eye edema as sited in your article, that doctors will not agree are related.
And inflammation can cause massive irregularities on thyroid metabolism and physiology by suppressing the HPT axis, decreasing both the number & sensitivity of thyroid hormone receptors, & decreasing T4 - T3 conversion.
TNF is an inflammatory protein (cytokine) involved in systemic inflammation made chiefly of macrophages (type of white blood cell) and its primary role is in the regulation of immune cells. When high it reduces blood levels of TSH, T4, T3 and TRH.
Patients get shunted off for all sorts of invasive investigations, when measuring the level of reactive proteins in relation to the amount & type of antibodies present might possibly give a fair indication of the symptom causation.
Thyroid hormone replacement replaces those missing hormones but does nothing to address the decreased function in the hypothalamus/pituitary gland, receptors, etc
How true! I diagnosed myself with hypothyroidism years and years before a doctor finally told me that I had it. Nearly every one sent me for a 24-hour urine collection and who-knows-how-many more blood tests. One told me that I had a "male pattern output of cortisol"--but offered no treatment aimed at relieving my symptoms.
Fascinating study. I feel encouraged / supported by its findings, imagining the far-off day when doctors might treat the symptoms and not the TSH levels.
Could we see a day dawning where TSH is not the <be all and end all> measure of how a hypothyroid patient is doing? Or are you all there already?
On the basis of this study, I would be asking for my (TgAB) levels to be measured by the GP every time I had a TSH blood test.
What other implications for medical practice does anyone see following on from this paper’s conclusions?
Thanks for posting this helvella , very interesting to read about a link between thyroglobulin antibodies TgAb and Hashimoto's. I recently tested positive for TgAb but my GP said it wasn't linked to Hashimoto's and only useful to know when treating thyroid cancer. I'm learning a lot from all the info posted on this forum!
Very good article 🤗 Puffy face, eyes and a voice like I’ve smoked a thousand fags has always been some of my more prominent symtoms when I’m under medicated. To hear that TgAb might be a marker for this is interesting but for me optimal medications sorts me out and ofcourse there are never any tests to see a rise or fall in these antibodies to make any correlations.
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