
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Diffuse toxic goiter (basal goiter disease) - Information Overview
Medical expert of the article
Last reviewed: 12.07.2025
Diffuse toxic goiter (Graves' disease, Basedow's goiter, Graves' disease) is the most common thyroid disease, which occurs due to increased production of thyroid hormones. In this case, as a rule, a diffuse increase in its size is noted. The disease is more common among the urban population aged 20 to 50 years, mainly in women.
Cause of diffuse toxic goiter
Currently, diffuse toxic goiter (DTG) is considered an organ-specific autoimmune disease. Its hereditary nature is confirmed by the fact that there are familial cases of goiter, thyroid antibodies are detected in the blood of relatives of patients, a high frequency of other autoimmune diseases among family members (type I diabetes, Addison's disease, pernicious anemia, myastenia gravis ) and the presence of specific HLA antigens (HLA B8, DR3). The development of the disease is often provoked by emotional stress.
The pathogenesis of diffuse toxic goiter (Graves' disease) is caused by a hereditary defect, apparently a deficiency of T-lymphocyte suppressors, which leads to mutation of prohibited clones of T-lymphocyte helpers. Immunocompetent T-lymphocytes, reacting with thyroid autoantigens, stimulate the formation of autoantibodies. The peculiarity of immune processes in diffuse toxic goiter is that autoantibodies have a stimulating effect on cells, leading to hyperfunction and hypertrophy of the gland, whereas in other autoimmune diseases autoantibodies have a blocking effect or bind the antigen.
Symptoms of Graves' disease
The pathogenesis of clinical symptoms is due to the influence of excess thyroid hormones on various organs and systems of the body. The complexity and multiplicity of factors involved in the development of thyroid pathology also determine the diversity of clinical manifestations of the disease.
In addition to cardinal symptoms such as goiter, exophthalmos, tremor and tachycardia, patients, on the one hand, experience increased nervous excitability, tearfulness, fussiness, excessive sweating, a feeling of heat, slight temperature fluctuations, unstable stool, swelling of the upper eyelids, and increased reflexes. They become quarrelsome, suspicious, overly active, and suffer from sleep disorders. On the other hand, adynamia and sudden attacks of muscle weakness are often observed.
What's bothering you?
Diagnosis of diffuse toxic goiter
If the clinical symptoms are sufficiently pronounced, the diagnosis is beyond doubt. Laboratory tests help to make a correct and timely diagnosis. Diffuse toxic goiter is characterized by an increase in the basal level of thyroid hormones and a decrease in TSH. Usually, the basal level of T3 is increased to a greater extent than the level of T4. Sometimes there are forms of the disease when T3 is higher, and thyroxine, total and free, are within normal fluctuations.
In doubtful cases, when T3 and T4 are slightly elevated and there is a suspicion of thyrotoxicosis, it is useful to perform a test with rifathiroin (TRH). The absence of an increase in TSH with the introduction of TRH confirms the diagnosis of diffuse toxic goiter.
What do need to examine?
How to examine?
What tests are needed?
Who to contact?
Treatment of diffuse toxic goiter
Currently, there are three main methods of treating diffuse toxic goiter: drug therapy, surgical intervention - subtotal resection of the thyroid gland, and treatment with radioactive iodine. All available methods of treating diffuse toxic goiter lead to a decrease in the elevated level of circulating thyroid hormones to normal values. Each of these methods has its own indications and contraindications and should be determined for patients individually. The choice of method depends on the severity of the disease, the size of the thyroid gland, the age of the patient, and concomitant diseases.
Drugs
Prognosis and working capacity
The prognosis of patients with diffuse toxic goiter is determined by the timeliness of diagnosis and the adequacy of the therapy. At the early stage of the disease, patients, as a rule, respond well to adequately selected therapy, and practical recovery is possible.
Late diagnosis of diffuse toxic goiter, as well as inadequate treatment, contribute to further development of the disease and loss of ability to work. The appearance of pronounced symptoms of adrenal cortex insufficiency, liver damage, heart failure complicate the course and outcome of the disease, make the prognosis for the ability to work and life of patients unfavorable.
The prognosis of ophthalmopathy is complex and does not always parallel the dynamics of thyrotoxicosis symptoms. Even when a euthyroid state is achieved, ophthalmopathy often progresses.
Proper employment of patients with diffuse toxic goiter helps to maintain their ability to work. By decision of the advisory and expert commission (AEC), patients should be exempted from heavy physical labor, night shifts, and overtime work. In severe forms of diffuse toxic goiter, their physical performance drops sharply. During this period, they are incapacitated and, by decision of the VTEK, can be transferred to disability. If the condition improves, it is possible to return to mental or light physical labor. In each specific case, the issue of ability to work is decided individually.