Is it possible to have hypo and hyperthyroid

Its outcome depends on the type of thyroiditis, as follows. Two main types of thyroiditis exist. The first, subacute thyroiditis, involves pain that begins at the front of the neck and shoots toward the ears.

Subacute thyroiditis is caused by a virus and often resolves on its own, without lasting problems. The second type, silent thyroiditis, is painless and appears to be an autoimmune disorder, in which the immune system attacks thyroid tissue.

Silent thyroiditis is most likely to occur in women during the months following pregnancy. For many people with silent thyroiditis, thyroid function returns to normal after the first episode. This type of thyroiditis can recur, though. If it does, over time people with silent thyroiditis may develop long-term hypothyroidism. If you're already being treated for a thyroid problem, and your thyroid function begins to shift between underactive and overactive, thyroiditis probably isn't the source of the problem.

More likely, your medication is to blame. People diagnosed with hyperthyroidism usually take the medication methimazole to prevent the thyroid from producing excess hormones. Therapeutic decisions should be taken according to clinical manifestations and thyroid function tests, independent of the bioassays results. A definitive treatment might be considered due to the frequent switches in thyroid function and the need for close monitoring of pharmacological treatment.

Although its prevalence is higher in adults, it is also the most frequent etiology of acquired thyroid dysfunction in pediatrics. In this population, it is most common in girls and generally occurs in early and mid-puberty 2. Autoimmune thyroid disease encompasses an ample spectrum of thyroid disorders from which Hashimoto's thyroiditis and Graves' disease are the most common presentations.

They represent the two ends of the autoimmune thyroid disease spectrum once they have opposite phenotypes and distinct immunologic mechanism.

At first, there is T-cell infiltration of the gland leading to its destruction and clinical signs of hypothyroidism; finally, the gland is chronically stimulated by agonist antibodies of thyroid-stimulating hormone TSH receptor, produced by local B cells, causing hyperthyroidism. However, there is an interrelationship between the various autoimmune thyroid disorders that could be explained by a common pathophysiological mechanism and antibody production.

The thyroid gland releases antibodies against specific antigens, more frequently against thyroglobulin, thyroid peroxidase and TSH receptor. TBAbs are found in a significant number In very few adult patients, both antibodies may be present simultaneously, leading to a rapid oscillation in thyroid function as TBAbs or TSAbs become dominant 5. This situation is even more uncommon in pediatric population 4.

The TRAbs activity may be estimated in vitro through bioassays. The more sophisticated ones involve chinese hamster ovary cells CHO cells transfected with the recombinant human TSH-receptor. Herein, we report a case of an adolescent with fluctuating thyroid function associated with elevated levels of antithyroglobulin, antithyroid peroxidase and TSH-receptor antibodies.

A previously healthy year-old girl, referred for evaluation, presented in the clinic with a slightly increased thyroid volume, and a subclinical hyperthyroidism observed in June , with no signs or symptoms table 1.

There was family history of thyroid disease. On first evaluation, in March , she presented a visible and palpable thyroid gland with no individualized nodules, no adenomegaly, and no exophthalmos. There were no other relevant findings in her physical exam. The TSH and free-thyroxine fT 4 serum levels were within the normal range, but she presented with elevated levels of antithyroid peroxidase antibodies Table 1.

She was started on levoT 4 LT 4 0. However, after 6 months of treatment in September , she developed subclinical hyperthyroidism, and LT 4 was slowly weaned off. In June , 4 months after the LT 4 cessation, she gained weight rapidly 2. She was again started on LT 4 at 0. On follow-up after 2 months of LT 4 treatment in August , she was noted to have a decrease in TSH and an increase in fT 4 , with no signs of hyperthyroidism apart from weight loss Table 1.

She maintained treatment with LT 4. Methimazol was started at a dose of 0. Thyroid function was controlled with this double therapeutic regimen for a period of time, but after 6 months she again developed hyperthyroidism that demanded another adjustment, with a decrease in LT 4 to 0. Bioassay descriptions for measurement of TRAbs biological activity 6, 7.

In this clinical case, there is an alternation between hyper- and hypothyroidism associated with elevated levels of antithyroglobulin, antithyroid peroxidase and TRAbs, with ultrasonographic and scintigraphic findings compatible both with thyroiditis and Graves' disease, respectively. A hyperthyroid state was evident at the early onset in June , with spontaneous remission, and after the beginning of LT 4 therapy in March , to reduce goiter volume. Effectiveness of LT 4 treatment in reducing goiter volume in euthyroid children and adolescents with autoimmune thyroid disease is not clear yet, although recent data supports its use 8, 9.

However, due to the possibility of LT 4 overtreatment as a cause of hyperthyroidism noticed in September , LT 4 was slowly weaned off until its cessation. After a period without treatment, she unexpectedly developed hypothyroidism in June , associated with elevated levels of TRAbs. Notice also that without any medication, TSH levels decreased significantly within 3 days and that at this point scintigraphic findings were compatible with Graves' disease.

LT 4 was restarted and, once again, a switch to hyperthyroidism was noted right after the beginning of LT 4 that was only reverted with the addition of methimazol.

Further therapeutic adjustments were needed, due to thyroid function fluctuation over time. This type of oscillation in thyroid function is extremely rare, especially in the pediatric age, and is only described in a few case reports in literature 4, 5.

The balance between both antibodies determines whether a patient has hypo- or hyperthyroidism These tablets contain a synthetic hormone identical to thyroxine, the hormone that the thyroid gland produces naturally. Rene explains that generally, thyroid replacement medication must be taken for life because the effects of hypothyroidism are irreversible. Hyperthyroidism is basically the opposite of hypothyroidism. It occurs when the thyroid is overactive, producing too much thyroid hormone.

Graves' disease , a common autoimmune condition that stimulates the thyroid hormones T4 and T3. Feeling wired or anxious. Sweating spells. Itchy red skin. More frequent bowel movements than usual. Methimazole or Propylthiouracil PTU are used to treat hyperthyroidism. They signal the thyroid to slow down T4 and T3 hormone production. It comes in a tablet and may be taken up to three times per day. Again, this is not a cure.

If anti-thyroid medications do not regulate the thyroid, surgery to remove all or part of the thyroid gland or radioactive iodine treatment are alternative options used to slow the production of thyroid hormones. This is especially true if you have an irregular heart rhythm, which can lead to a life-threatening condition such as stroke. It is beneficial to know your family history because hypothyroidism is often a genetic condition.