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This patient has Graves disease.
Graves’ disease is a pathology of autoimmune origin, characterized by increased thyroid hormone levels, due to antibodies against thyroglobulin and thyroid peroxidase. Thyroid stimulating immunoglobulins (TSIs) bind to the thyrotropin receptors and activate them. The excess hormones cause thyroid follicular hypertrophy and hyperplasia. The result is the characteristic goitre, enlarged gland which can often been as well as felt.
There is a known association with other autoimmune conditions, such as rheumatoid arthritis, and screening of one with the other is advised.
Following are some signs and symptoms associated with Graves’ Disease:
• Lethargy and weakness, with fatigue
• Increased sweating; Backache and an increased risk of fractures
• Involuntary movements, weakness especially in proximal limbs, easily fatigability, periodic paralysis in some cases
• Palpitations, exertional breathlessness, chest tightness
• Diarrhoea due to increased gut motility
• Increased lacrimation, foreign body sensation in the eye, photophobia, ocular pain, double vision and loss of sight
• Increased thirst and urination
• Heat intolerance, uncontrolled diabetes
• Amenorrhea and/or oligomenorrhea, increased breast mass in males as well as sterility
• Irritability, apprehensive and depressed mood, disturbed sleep
• Hot clammy skin; increased risk of nail infection; loss of hairs; swelling around the eyes
• Tachycardia sinus or atrial fibrillation
• Weight reduction
• Fine tremor, hyperreflexia, hyperkinesis
• Palmar erythema, onycholysis
The key clinical sign is found in Graves’ ophthalmopathy. The signs of ophthalmopathy is adequate to confirm the diagnosis of Graves’ disease in a patient with hyperthyroidism and a diffuse goitre. See below.
Thyroid hormone levels of free T3 and free T4 are initially carried out in a suspected case and are usually above reference range although the asymptomatic disease may show these levels to be well within the range but thyrotropin is decreased.
• Raised Free T4 levels
• Elevated triiodothyronine T3
• Low TSH (thyroid stimulating hormone)
75% of Graves’ will also have positive anti-thyroid peroxidase (TPO) antibodies.
It is of debate whether further testing is required of thyrotropin-receptor antibodies with positive clinical signs and basic thyroid function tests. However, if further investigations are required:
Isotope imaging (with technetium or radioactive iodine) may help to determine Graves’ disease from other causes of thyrotoxicosis.
The pathophysiology of the disease is that B and T lymphocytes attack the following 4 thyroid antigens:
• thyroid peroxidase
• sodium-iodide symporter
• thyrotropin receptor
Thyrotropin seems to be the chief auto-antigen causing the hyperthyroidism associated with Graves’ disease. The antibody and cell mediated thyroid antigen specific immune reaction are markedly seen.
Treatment can be divided into medical and surgical and radiological.
Medical – symptomatic relief
• Beta-adrenoceptor blockers for tachycardia, remor and anxiety. The most common one used is propranolol
Medical – definitive treatment
• Carbimazole or propylthiouracyl commonly
• Usual duration of treatment is around 12-18 months
• Can also conduct block-and-replace where the thyroid gland is completely suppressed and levothyroxine replacement is given
• With propylthiouracyl, the risk of agranulocytosis has to be monitored for
Radiological – radioiodine
• Treatment of choice in relapsed Graves’ disease
Surgery – thyroidectomy
• Infrequently used
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