Thyrotoxicosis is common, about 1 in 100 people have it, it is six times more common in women than men. There are two main causes in the UK:
The immune system making antibodies that stimulate the thyroid and the patient becomes hyperthyroid - this is Graves' thyrotoxicosis.
There is benign nodularity in the thyroid - a multinodular goitre.
The following conditions are less common, but still not rare, their treatment is completely different and thus them being diagnosed and distinguished from Graves' thyrotoxicosis is critically important - a single nodule can cause thyrotoxicosis and in some people a viral inflammation of the thyroid can cause sudden hyperthyroidism.
Graves' thyrotoxicosis
In Graves' disease the body makes antibodies that stimulate the TSH receptor causing thyroid over-reactivity and the production of excess thyroid hormones - thyroxine (T4) and liothyroinine (T3). These hormones attach to thyroid hormone receptors all round the body causing the symptoms of thyrotoxicosis. Robert Graves was a Dublin physician who wrote one of the first descriptions of this form of thyrotoxicosis.
The features of Graves' disease are: Hyperthyroidism with a smoothly enlarged fleshy enlargement of the thyroid - a goitre.
The antibodies can also attach to other parts of the body causing the other features of Graves' disease.
The muscles of the eyes - causing protrusion of the eye, Graves' ophthalmopathy, or thyroid eye disease (TED); much more common in cigarette smokers.
The skin - most commonly on the leg, over the shin, called pre-tibial myxoedema, or Graves' dermopathy; rare.
The nails and the bones of the wrist - causing digital clubbing and pain at the wrist - thyroid acropachy; very rare.
The diagnosis of Graves' disease is supported by the presence of thyroid antibodiesin the bloodstream. Very commonly anti thyroid peroxidase antibodies (anti-TPO Ab) are elevated, most UK Hospital laboratories measure these and the result comes back quickly. Antibodies agains the TSH-receptor (TRAb) are also elevated, they define Graves' disease, but they are not measured in every Hospital and the result tends to come back a fews days to a fortnight after being taken. They should be measured to diagnose and monitor the patient's condition, they are very useful to predict the course of therapy and whether the patient is more likely to relapse after treatment.
Graves' disease may rarely not be associated with thyrotoxicosis, the patient might not be thyrotoxic or hyperthyroid and the thyroid function tests (TFT) might be completely normal but the patient still have TED, dermopathy or acropachy.
The mainstay of treatment for Graves' thyrotoxicosis is antithyroid medication - carbimazole and propylthiouracil (PTU) these are discussed in the resources page. The patient can expect to be treated for 12 - 18 months before making a decision on stopping, to see whether they are cured, or whether they will relapse. Factors that favour Graves' thyrotoxicosis relapsing are high titre of TRAb, male sex, large goitre, difficult to control thyrotoxicosis and extra-thyroidal Graves' disease. If it does relapse off treatment it is not a problem to take carbimazole or PTU again and many patients are controlled on small doses for many years or decades.
What if the patient relapses after a course of treatment?
Many endocrinologists used to say that a patient who had relapsed would need definitive, or permanent, therapy for Graves', usually guaranteeing cure of the thyrotoxicosis; these treatments were radioactive iodine (RAI) or surgical thyroidectomy- discussed in patient resources. Some patients are treated with RAI as first line therapy, it is a respected strategy in many units around the world, much more rarely is surgery used as a primary treatment; surgery carries more risk in a thyrotoxic patient, and there is a small but predictable risk of damaging the nerves controlling the voice box or the parathyroid glandsthat control calcium and phosphate balance across the body.
However many endocrinologist did not agree with a permanent treatment, that would usually leave the patient dependent on thyroid hormone therapy for life, and would choose to maintain patients on low doses of carbimazole (or PTU) for life, as long as the patient tolerated these drugs and it was the patient's informed preference. Long-term antithyroid medication has generally been a strategy I have supported in the majority of patients and this has now become a more accepted strategy internationally, with support from the American Thyroid Association.
Gender, family plans, pregnancy, breastfeeding, child care responsibilities and co-existing medical conditions all have to be taken into account before deciding on what is best by each individual patient.
General Practitioners in the UK are generally reluctant to manage hyperthyroidism themselves, particularly Graves' thyrotoxicosis. It is usual that patients are referred to an endocrinologist, though some GPs will have experience of managing the condition and local practice varies.
It is important is that the patient sees someone experienced in the diagnosis and management of thyroid disease, who is able to accurately diagnosis the condition, counsel the patient on treatment options and supervise treatment appropriately AND that the patient and doctor have a relationship based on mutual trust.
Hyperthyroidism, if not treated well, is associated with ill-health, and before effective treatment used to shorten patients' lives, and it still retains the potential to do so even with modern treatment. It is a serious condition.