Graves Basedow’s disease is the most frequent cause of hyperthyroidism with incidence between 1.5 and 3% of the population. Graves Basedow’s disease mainly affects the female sex, with a male/female ratio of 1:5-1:10. It can occur at any age, but is more frequent between 30 and 40 years and over 60 years.


The symptoms at the beginning of the disease are nuanced. Psychic disorders are often interpreted with difficulty. The patient can thus complain of excessive emotional reactions, anxiety, difficulty sleeping, irritability, concern for negligible reasons, cognitive disorders, easy mental fatigue, up to develop real depressive pictures.

Graves Basedow’s disease presents the typical symptoms of hyperthyroidism: fine distal tremors, tachycardia, arrhythmias (up to atrial fibrillation), weakness, intolerance to heat with copious sweating, redness of the face and neck, menstrual disorders up to amenorrhea, decreased libido and fertility, bowel movements with frequent diarrheal episodes, increased thyroid volume (goiter), shortness of breath, brittleness of the nails, weight loss despite increased appetite. Hyperphagia can in some cases lead to weight gain by offsetting the commonplace that hyperthyroids necessarily lose weight.

Eye protrusion (exophthalmos) and paralysis of extrinsic eye muscles with diplopia (double vision) and squint fortunately affect a small percentage (5-10%) of patients with Graves Basedow’s disease. In most patients the ocular symptoms are limited to eyelid retraction (reversible), lacrimation, photophobia (intolerance to light), a feeling of sand in the eyes and mild periorbital edema. Eye symptoms are related to TSH receptor antibodies that not only overstimulate the thyroid hormone production and release but also bind to periorbital tissues causing inflammation



The neck of the patient suffering from Graves Basedow’s disease may show a swelling due to goiter by volumetric increase of the thyroid gland. The thyroid ultrasound confirms the presence of diffuse goiter and hypoechoic gland (darker than normal) due to lymphocytic infiltration (Fig. 2). A characteristic ultrasound appearance is thyroid hypervascularization detectable with color doppler or microVessels study that detects fast and slow vascular flows. This ultrasound picture is called “thyroid hell” (Fig. 3). Graves Basedow’s disease is a manifestation of chronic autoimmune thyroiditis and in some ways the ultrasound aspects of Graves Basedow’s disease resemble this

Many symptoms may remain nuanced in the elderly patient, except asthenia, cardiovascular and myopathic symptoms (muscle suffering), which tend to become accentuated. The natural history of Graves Basedow’s disease does not generally have a uniform course, the alternation of remissions and relapses is characteristic. In 30-40% of cases the disease goes into stable remission or evolves into hypothyroidism. Probably this type of evolution is manifested in a higher percentage of cases because the few patients who do more than 2 years of antithyroid therapy may have a tendency to turn off hyperthyroidism.



The origin of Basedow’s disease is on an autoimmune basis and is influenced by an important genetic and hereditary component. In the serum of the patients it is possible to find abnormal auto-antibodies directed against enzymatic components (antibodies to Thyroperoxidase) or against Thyroglobulin (antibodies to Thyroglobulin), a protein that contains the preformed thyroid hormones. Characteristic of Graves Basedow’s disease are antibodies directed against the TSH receptor. TSH is the pituitary hormone that stimulates the synthesis of thyroid hormones; the binding of these antibodies to the TSH receptor reproduces the stimulating effects of TSH on thyroid activity. Hyperthyroidism therefore results from functional hyperactivation of the thyroid, with increased circulation of both thyroid hormones (FT4 and FT3) and blocking of TSH, almost always undetectable given the well-known negative feedback effect exerted by thyroid hormones on TSH (elevated thyroid hormones reduce TSH levels). Still quite obscure remains the reason that triggers this auto-antibody attack.


In order to diagnose Basedow’s disease, in addition to the clinical examination of the patient (research of the symptoms and risk factors listed above), it is essential to measure bood thyroid hormones, TSH and TSH antithyroid and antireceptor antibodies, associated with ultrasound images of the thyroid with ecocolordoppler to investigate its vascularity or, more modernly, with microV. Doppler microV displays slow flows and capillary flows, and the thyroid typically glows in color with the picture of the “thyroid inferno”. Thyroid scintigraphy is no longer needed to make a diagnosis.


The therapy of Graves Basedow’s disease aims to reduce the amount of circulating thyroid hormones and for this purpose makes use of thyrostatic drugs, the thionymides, with immunosuppressive action. These drugs are represented by Metimazole, propylthiouracil (preferred in pregnancy). Beta blocker propranolol is used in the early stages to dominate cardiovascular symptoms.

The drug therapy of Graves Basedow’s disease must be prolonged at gradually decreasing doses and – with a dosage calibrated on the individual patient based on the aggressiveness of the disease – prolonged until the clinical hormonal remission of hyperthyroidism syndrome. Destructive treatment of the thyroid with radioactive iodine or (only in extreme situations) with thyroidectomy is reserved for forms not manageable with drug therapy. Treatment of severe ocular symptoms is with local or systemic corticosteroids In the early stages have given promising results biological drugs such as rituximab or infliximab. Corrective or orbit decompressive surgeries are reserved for the most severe cases.

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