Thyrotoxicosis Treatment- What do you need to know and doctors don’t have time to tell you?

Thyrotoxicosis or Hyperthyroidism is the clinical syndrome caused by an excess of circulating free thyroxine and free triiodothyronine, (FT3 and FT4) or both. It is common, affecting about 2% of women and 0.2% of men. (For more information about test- TSH, FT3, FT4- check here>>>>>

Causes

Of all the causes of thyrotoxicosis, Graves’ disease is the most common (70-80%); toxic thyroid adenoma, toxic multinodular goitre, and subacute thyroiditis are the second of importance when considering the causes for thyrotoxicosis.

Causes of Thyrotoxicosis

Common causes:

Graves’ disease

Toxic multinodular goiter

Toxic nodule

Thyroiditis

Subacute Postpartum Silent

Factitious hyperthyroidism (administration of thyroxine or triiodothyronine)

Rare

Exogenous iodide (Jod-Basedow phenomenon)

Radiographic contrast agents

Health food preparations

Drugs (amiodarone)

Iodinisation programmes

Neonatal hyperthyroidism

Excess secretion of thyroid stimulating hormone

Pituitary adenoma Pituitary resistance to thyroxine and triiodothyronine

Metastatic thyroid cancer

Struma ovarii

and some other not so typical reasons.

Clinical features of thyrotoxicosis

Thyrotoxicosis usually develops insidiously, and most patients have had symptoms for at least 3-6 months before presentation. Almost every system is affected, and patients may initially present to various medical specialists – for example, to a cardiologist with atrial fibrillation, or to a neurologist with myopathy.

When thyrotoxicosis is suspected, the diagnosis should be confirmed by measurement of thyroid stimulating hormone (TSH) and free thyroxine in the serum, which are usually present in low and high concentrations respectively.

The concentration of thyroid stimulating hormone may, however, be normal or increased if the cause of thyrotoxicosis is either a pituitary adenoma secreting thyroid stimulating hormone or resistance to thyroid hormone.

In the latter case the patient is clinically euthyroid. Estimation of total thyroxine concentration is not useful and may be misleading as various factors, including pregnancy, cirrhosis of the liver, and opiate drugs, alter the binding of thyroxine to thyroxine binding globulin.

When the concentration of thyroid stimulating hormone is low but that of thyroxine normal, serum concentration of free triiodothyronine should be measured to diagnose triiodothyronine (T3) toxicosis. Thyroxine (T4) toxicosis (raised concentration of free thyroxine, normal concentration of free triiodothyronine), which is unusual, may occur with high iodine intake, treatment with amiodarone, severe intercurrent illness, or starvation. Finally, euthyroid patients with Graves’ ophthalmopathy, severe non-thyroidal illness, large goitres, or those who have had recent treatment for thyrotoxicosis may have a suppressed concentration of thyroid stimulating hormone.

Thyrotoxicosis treatment

Antithyroid drugs: Carbimazole, Methimazole and Propylthiouracil constitute the thionamide group of antithyroid drugs. Propylthiouracil is considered the safest drug among all of them and it is even prescribed to pregnant women.

They inhibit the excess iodide and coupling of iodothyronines, thus reducing production of triiodothyronine and thyroxine.

Propylthiouracil also inhibits the peripheral conversion of thyroxine to triiodothyronine. In addition to blocking thyroid hormone biosynthesis, these drugs also lower concentrations of thyroid stimulating hormone receptor antibodies and increase activity of suppressor T cells, which suggests that they have immuno- suppressive effects.

Carbimazole is given once daily, which makes it the drug of first choice, eventually. Once patients are taking a maintenance dose, serum concentrations of free thyroxine and thyroid stimulating hormone (TSH) are measured every three months.

The duration of antithyroid treatment has been much studied and debated (6-24 months), but is usually 18 months, even though I know people on thyroid medication for years.

Beta Blockers

These are useful for treating some of the clinical features, such as tremor, palpitations, and anxiety. Propranolol (120-240 mg/day) is the most commonly used beta blocker, although any could be used. Once a euthyroid state has been reached, the b blocker is discontinued.

Summary  for Thyrotoxicosis Treatment/ Hyperthyroidism

• Graves’ disease is the commonest cause of thyrotoxicosis
  
• It is an autoimmune disease: the thyrotoxicosis is caused by the presence of thyroid stimulating antibodies
• Eyes and skin may be commonly affected
• Initial treatment is with carbimazole (methimazole) or propylthiouracil, together with the use of a blocker for the first 4-6 weeks

Patients should be warned of the side effects of antithyroid drugs, however they are not typical.