Graves' disease

Related article: Hashimoto's


Thyroid markers

BACKGROUND: T helper type 1 (Th1), Th2, and Th17 cells produce interferon (IFN)-gamma, interleukin (IL)-4, and IL-17A, respectively. We reported that IFN-gamma and IL-4 gene polymorphisms, which are related to higher IFN-gamma and lower IL-4 production, respectively, are more frequent in patients with severe Hashimoto's disease (HD) than in those mild HD. We now aim to investigate the proportion of peripheral Th1, Th2, and Th17 cells in patients with autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body thyroid disease (AITD).

METHODS: We studied 17 patients with HD who developed hypothyroidism and were treated with l-thyroxine, referred to as severe HD; 17 untreated patients with HD who were euthyroid, referred to as mild HD; 18 euthyroid patients with Graves' disease (GD) who remained positive for anti-thyrotropin receptor antibody (TRAb) despite being treated with anti-thyroid drugs for more than 5 years, referred to as intractable GD; and 17 patients with GD who were euthyroid and negative for TRAb for more than 2 years after cessation of anti-thyroid drugs, referred to as GD in remission; and 10 control subjects without AITD. By the definitions in this study Th1 cells were CD4(+)IFN-gamma(+)IL-4(-)IL-17A(-) cells, Th2 cells were CD4(+)IFN-gamma(-)IL-4(+)IL-17A(-) cells, and CD4(+)IFN-gamma(-)IL-4(-)IL-17A(+) cells were Th17 cells.

RESULTS: The proportion of peripheral Th1 cells was higher in patients with severe HD than in patients with mild HD (p < 0.05), and the proportion of peripheral Th2 cells was lower in patients with severe HD than in patients with mild HD (p < 0.001). Therefore the Th1/Th2 ratio was higher in severe than in mild HD patients (p < 0.001). The proportion of peripheral Th17 cells in patients with AITD was higher than in control subjects and the proportion of these cells in patients with intractable GD was higher than in patients with GD in remission (p < 0.05).

CONCLUSIONS: The peripheral Th1/Th2 cell ratio is related to the severity of HD, and the proportion of Th17 cells is related to the intractability of GD. We hypothesize that these patterns of peripheral Th cell subsets may be expressed within the thyroid.

Nanba, T., M. Watanabe, et al. (2009). “Increases of the Th1/Th2 cell ratio in severe Hashimoto's disease and in the proportion of Th17 cells in intractable Graves' disease.” . 1)

Evidence of infectious cause

AUTOIMMUNE DISEASE ASSOCIATED WITH IRIS Graves Disease Several different autoimmune processes have been described in patients initiating ART, although a clear association with IRIS has yet to be defined for many. It is widely accepted that Graves disease occurring after ART initiation is a manifestation of IRIS. This occurs late in the course of immune restoration, with a median time to onset after ART initiation of 21 months. In one study the median CD4 count before initiation of therapy in patients who developed Graves disease was 10 cells/mm, indicating severe immunodeficiency at the time of ART initiation in this population.”

Distinguishing between manifestations of IRIS and active infection is of paramount importance and poses a diagnostic challenge to the provider in the acute care setting. Presentations of IRIS are often atypical for the precipitating pathogen, and novel presentations are likely. Of the diseases associated with IRIS, mycobacteria and cryptococcal infections are commonly encountered, as are dermatologic symptoms in general. 2)

Patient posted

photosensitivity_Constant but have graves active phase.Have dry eyes and increasing double vision(graves). difficult to post due to vision but optic nerve intact and no undue inner eye inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. per opthamologist seen on 01/31. Use eye drops.



Regarding the thyroid. Having had both issues of hyper and hypo thyroid I would probably force my doc to run the following tests to see if I really had auto immune thyroid issues before he/she labeled me as such.

I would suggest that you try and get the following tests done to see exactly what type of thyroid issues you are dealing with.

Thyroid Antibodies: anti-TPO and TgAb will help discern Hashimotos. You need both. You could add TSI (thyroid stimulating immunoglobulins) for the Graves antibodies–some have all three.

I would also have them check the TRab (Thyrotropin Receptor Ab) sometimes this is called the TBII test. This will help show if there are any blocking antibodies for Graves, which can trick the results into thinking you are hypothyroid. The TSI are the stimulating antibodies and the TRab are the blocking antibodies in Graves (hyper thryoid). From the looks of your labs it is possible that you do have hashimotos but I'd want to know the whole story. Your Free T4 is in mid range which can be argued as the best indicator of how well the thyroid is working. I also would like to see the Free T3 as well to see how well your body converts T4 into T3 which is the usable form of the hormone.

They may say you don't have graves you have hashimotos but people can have both. It is also possible that you have/had a nodule on your thyroid that is responsible for the hyper experiences but the hypo situations most of the time. This could be diagnosed with a thyroid ultrasound.


Also test mineral status, as Selenium and Iodine are essential for thyroid hormone synthesis and function.3)

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===== References =====

Nanba T, Watanabe M, Inoue N, Iwatani Y. Increases of the Th1/Th2 cell ratio in severe Hashimoto's disease and in the proportion of Th17 cells in intractable Graves' disease. Thyroid. 2009 May;19(5):495-501. doi: 10.1089/thy.2008.0423.
[PMID: 19415997] [DOI: 10.1089/thy.2008.0423]
Beatty GW. Immune reconstitution inflammatory syndrome. Emerg Med Clin North Am. 2010 May;28(2):393-407, Table of Contents. doi: 10.1016/j.emc.2010.01.004.
[PMID: 20413021] [DOI: 10.1016/j.emc.2010.01.004]
Guastamacchia E, Giagulli VA, Licchelli B, Triggiani V. Selenium and Iodine in Autoimmune Thyroiditis. Endocr Metab Immune Disord Drug Targets. 2015;15(4):288-92. doi: 10.2174/1871530315666150619094242.
[PMID: 26088475] [DOI: 10.2174/1871530315666150619094242]
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