Although, not frequent, YES, it is possible.
Before going into details let's briefly summarise and distinguish the two conditions.
Hashimoto's disease is an autoimmune condition causing hypothyroidism. A state, which you probably know, cause a decrease in thyroid hormones production.
Diagnosis is done via blood test, detecting an increase in Thyroid Stimulating Hormone (TSH), with or without low T4 (thyroid hormone), and presence of autoantibodies.
Most common autoantibody is antibodies against thyroid peroxidase (TPO antibodies), an enzyme normally found in the thyroid gland that plays an important role in the production of thyroid hormones.
Why is your TSH increasing?
TSH is released by your pituitary gland (in the brain) to stimulate your thyroid hormonal production. When your T4 and T3 levels decrease, your brain senses it and makes more TSH with the aim of stimulating more your thyroid.
TPO antibodies act by destroying thyroid tissues and lead to a decrease amount of circulatory T4. This will cause an increase in TSH.
Is Hashimoto's constantly active?
The answer is NO.
Hashimoto's works in relapse and remitting patten. Meaning, you will likely experience flares.
According to a scientific paper (1) Hashimoto's can be divided into 3 stages:
The early stage has hyperthyroidism state as there is excessive thyroid hormone secretion into circulation due to partial destruction thyroid cells.
In the second stage, the thyroid has normal function (euthyroid).
The third and final stage, includes hypothyroidism.
Hashimoto’s hyperthyroidism (stage one) usually has mild and transient hyperthyroidism. Thus, most patients in hyperthyroid state remain unrecognised. The fact, they stay unrecognised is important when we talk about overlapping of Grave's. We must differentiate between Grave's and transient Hashimoto's hyperthyroidism.
Graves' disease is an autoimmune condition causing hyperthyroidism. A state, which you probably know, cause an increase in circulating thyroid hormones.
Diagnosis is done via blood tests detecting a decrease in TSH, FT4, and antiTSH, antiTg, antiTPO.
Moreover, Radioactive Iodine Uptake is another test that together with ultrasound and blood tests cam help your physician in the diagnosis.
Radioactive Iodine Uptakes works on the principle that thyroid glad uses iodine to function. In case of hyperthyroidism, your thyroid works more than it should. This results in an increase in signal.
Why is your TSH decreasing?
Same idea as for Hashimoto's but in this case your thyroid is producing more T4 and T3. As a consequence, less TSH is produced.
Is there a difference between Hashimoto's autoantibodies and Graves' ones?
Yes. In fact, in Hashimoto's autoantibodies destroy the gland. In case of Graves, autoantibodies overstimulate your thyroid rather than destroying it.
Both conditions can give goitre or multi nodular goitre. Assessed with ultrasound.
Association of Graves' disease with Hashimoto's disease:
In 15-20% of the cases Graves' disease can cause Hashimoto's. The opposite, Hashimoto's turning into Graves' instead it is a very rare event, with only very few cases mentioned in literature (about 1.2%).
The reason behind it is not very clear in fact there are mainly assumptions that need to be further confirmed by research (I will put the links to the articles).
Graves' patients suspending antithyroid therapy due to remission are at risk of developing Hashimoto's.
The basic idea stands in autoimmunity further going crazy and converting the activity of your autoantibodies before causing Hashimoto's and now Graves', and vice versa.
Here I add some citations from the articles about shifting between these two diseases:
In 10 to 15% of Graves’ hyperthyroidism cases, Hashimoto’s thyroiditis may occur after remission by anti-thyroid treatment. We assume that it is due to the expansion of immune response of autoantibodies that stimulate TSH receptor. Subsequently, it produces autoantibodies against TPO and TG causing lymphocytic infiltration and defect on thyroid cells; finally, hypothyroid occurs. (1)
Several mechanisms have been postulated behind the conversion from Hashimoto's to Graves' Disease. One of them is the presence of different autoantibodies that include thyroid stimulating antibodies and thyroid blocking antibodies. Another possible explanation for this transition is that the autoimmune tissue damage, initially severe enough to cause thyroid hypo-function, recovers sufficiently to allow subsequent stimulation by TSAb (thyroid stimulating autoantibodies) (2).
The shifting from Hashimoto's to Graves' Disease have nothing to do with Levothyroxine dosage. Rather it seems to be mainly related with autoimmunity and tissue damage.
Lastly, a possible effect of Helicobacter pilory infection has been suggested in thyroid autoimmunity because of *cross autoantigens reaction between the bacteria capsid and gastric cells*. As a matter of fact, H.pilory is a bacterial infection that cause gastritis and can be associated with gastric cancer.
**Cross reactivity refers to the bacteria stimulating an immune response. This response, however, will generate an attack to the thyroid.
Why is this important?
Continuous monitoring of thyroid function in patients with Graves’ disease, despite remission, after being treated with anti-thyroid agents.
To what it concerns Hashimoto's turning into Graves', we cannot be certain due to the little percentage. For this reason, more research is needed to assess guidelines. However, keep monitoring your thyroid and pay attention to your symptoms.
Is it possible to be hyperthyroid and hypothyroid at the same time?
No. You can shift between the two stages and this must be carefully assessed by your physician. You need to regularly check your blood tests and thyroid.
Last point to assess: If you suffer from Graves' and Hashimoto's and you are being treated for hepatitis C. Then, it maybe your treatments causing your thyroid conditions (3).
Let us know about you:
Have you been diagnosed with both conditions?