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Graves' disease is the most common cause of over-secretion of hormones from the thyroid gland. It is a multi-factor condition that occurs when a hereditary predisposition is combined with the effect of certain adverse factors.
The precise cause of Graves' disease has not been established, but numerous studies show that this is a pathology with an autoimmune origin. The adverse effect of external or internal factors disrupts the functioning of the immune system, which starts to manufacture antibodies against its own healthy tissues. The antibodies bind to thyroid-stimulating hormone (TSH) receptors, activating the cells of the thyroid, increasing the secretion of hormones and giving rise to the classic symptoms of the disease. The risk factors that have received most study are:
The disease is frequently triggered by intense stress (bereavement, for example) or an acute infection.
The significance of the hereditary factor was established by studying the family history of patients and analyzing the population statistics. It is now known that the close relatives (daughters, sons, brothers, sisters, parents) of a Graves' disease sufferer have a 9% risk of developing the disease. If one of a pair of identical twins has the disease, the other has a 60% chance of developing it too.
Genetic studies have identified ethnicity-dependent gene structures responsible for the disease: in Caucasian people, these are HLA-B8 and DRw3; in Japanese and Chinese people, HLA-Bw46 and HLA-Bw36. Studies of familial cases have identified a link between Graves' disease and another autoimmune condition of the thyroid that manifests as hyperthyroidism: autoimmune thyroiditis. Cases have been described of a progression of symptoms from those typical of Graves’ disease to thyroiditis and back.
Graves' disease is characterized by three main symptoms: goiter, ophthalmopathy and signs of thyrotoxicosis (hyperthyroidism).
(enlarged thyroid) can be a symptom of various diseases of the thyroid gland. In Graves' disease, the enlargement is even, with no obvious areas of hardening. The gland feels soft and healthy to the touch. There is no correlation between the size of the thyroid gland and the severity of the disease: often, a pronounced enlargement of the thyroid is accompanied by only mild initial symptoms of hypersecretion.
is caused by an elevated concentration of thyroid hormones in the body. The thyroid hormones are thyroxine (Т4) and triiodothyronine (Т3). Their synthesis is mainly regulated by the thyroid-stimulating hormone (TSH) produced in the pituitary gland. Like most hormones, they control, not just one single function, but a whole set of interrelated micro- and macro-processes.
The clinical manifestations of hyperthyroidism as therefore very varied:
irritability, weepiness, fits of aggression, insomnia, tremor (slight shaking) in the hands, weakness, fatigue.
increased heart rate, fluctuations in blood pressure with raised systolic (upper) and lowered diastolic (lower) readings.
stomach rumbling, frequent ill-formed stool, heightened appetite, nausea, heartburn with a bitter taste.
weight loss, weakness, osteoporosis, nail fragility, hair loss, unexplained increase in body temperature to subfebrile levels (37–37.5°).
reduced libido; menstrual cycle disruptions, infertility, miscarriage, stillbirth and premature birth in women; gynecomastia and erectile dysfunction in men.
with an overactive thyroid is another typical symptom of the disease. In its classic form, it manifests itself as exophthalmos, where patients have a distinctive appearance with bulging eyes. The eyeballs protrude (often asymmetrically) and patients complain of dry eyes, a sensation of sand, swollen eyelids, inability to stand bright light, and double vision.
are typical in severe cases of Graves' disease. These usually take time to develop, but with acute onset many complications can occur as initial symptoms:
Endocrine psychosis;
Atrial fibrillation, either permanent or paroxysmal;
Embolic complications;
Cardiovascular deficiency;
Thyrotoxic hepatosis;
Diabetes;
Adrenal deficiency;
Dystrophic processes in internal organs;
Cachexia (extreme exhaustion)
In especially severe cases, a life-threatening deterioration of symptoms known as a thyroid storm or thyrotoxic crisis can occur. Mental agitation, severe arrhythmia, extremely high blood pressure, renal deficiency, generalized edema, and fever can have unhappy consequences. Without urgent medical help or with inadequate treatment, the condition can have a fatal outcome.
Two scales are used to classify Graves' disease. The first describes the size of the thyroid gland (goiter measurements). The second describes the extent of thyrotoxicosis.
In terms of thyroid size, cases are divided into three groups:
The extent of hormonal damage is classified according to its severity:
The treatment of endocrine conditions entails intervention in the delicate system of humoral regulation. For this reason, a great deal of effort and considerable resources are needed to put together an optimal treatment program for these diseases.
Protect yourself with the trusty shield of early prevention! Take a DNA test for genetic predisposition to Graves' disease.
To confirm a diagnosis, the endocrinologist uses the following diagnostic methods:
measurement of weight and height;
TSH, free Т4 and free Т3 counts are analyzed;
helps establish the size of the thyroid and identify its structure – its homogeneity, the presence of nodules, tumors, or signs of inflammation (for differential diagnosis).
if signs of cardiovascular dysfunction are present;
helps differentiate Graves' disease from nodular thyroid diseases;
indicated where a tumorous process is suspected;
helps confirm or rule out autoimmune origin of hyperthyroidism;
both general and biochemical. Helps identify certain complications of the basal disease.
The first priority is to correct the hyperthyroidism; this is usually done by means of complex treatment. An additional goal of the treatment is to suppress the autoimmune reaction in order to stabilize the illness. It is equally important to prevent stable complications of the cardiovascular, digestive and nervous systems.
For the main treatment to be as effective as possible, diet and lifestyle adjustments are needed:
The main conservative therapy uses thyrostatics, medicines that block the synthesis of thyroid-stimulating hormones. The most popular drugs in this class are imidazole and thiouracil. In most cases, a correctly selected dosage of these will bring about a rapid regression of symptoms. A further advantage of thyrostatics is their ability to reduce immune cell activity.
Once the pathological symptoms have been halted and hormone levels normalized, the dosage of thyrostatics is reduced. Treatment is carried out under close medical supervision. These drugs are prescribed for long periods, up to 18 months. There is a recurrence within a year of stopping thyrostatics in about a half of cases.
are generally used during preoperative preparation. These iodine compounds have a thyrostatic effect, but, as the effect is short-lived, medicines of this class are not usually included in standard treatment protocols for Graves' disease.
are part of the array of symptomatic therapies designed to correct cardiovascular dysfunction. These drugs normalize blood pressure and correct arrhythmic symptoms.
are hormonal preparations analogous to adrenal cortex hormones. Glucocorticoids are usually prescribed for severe forms of the disease.
A rapid therapeutic effect can be achieved by surgical means: a full or partial thyroidectomy followed by hormone replacement therapy. Operative therapy is indicated where conservative measures are ineffective, where there is thyrostatic intolerance, or where the goiter is particularly large.
An operation is frequently resorted to with child patients, because the disease is often particularly severe in this patient group.
This treatment method is similar in effect to surgery and is less traumatic, but it takes longer. The patient drinks a radioactive iodine preparation that concentrates in the thyroid tissues and destroys them. After treatment, the level of thyroid-stimulating hormone falls below physiological values, so the patient is prescribed lifelong hormone replacement therapy.
Prevention of Graves' disease is non-specific.
The following are recommended to prevent the disease and its early onset:
As the condition has a clearly established genetic character, it is important to know your family history of Graves' disease. All patients in the risk group should be seen by an endocrinologist at least once a year.
A DNA test is the only examination that can identify a genetic predisposition to Graves' disease. The test results will give your doctor valuable information for compiling an individual program of preventive and diagnostic measures.
Don't wait until you are ill! Take a DNA test for genetic predisposition to Graves' disease – and begin prevention as soon as possible.
