INTRODUCCION
Graves’ disease affects approximately 0.5% of the population and is the underlying cause of 50 to 80% of cases of hyperthyroidism. The hyperthyroidism of Graves’ disease is the result of circulating IgG antibodies that bind to and activate the G-protein–coupled thyrotropin receptor.1 This activation stimulates follicular hypertrophy and hyperplasia, causing thyroid enlargement, as well as increases in thyroid hormone production and the fraction of triiodothyronine (T3) relative to thyroxine (T4) in thyroid secretion (from approximately 20% to as high as 30%). Thyroid-function testing in Graves’ disease typically reveals a suppressed serum thyrotropin level and elevated levels of serum T4 and T3. A suppressed serum thyrotropin level with normal serum levels of T4 and T3 is referred to as subclinical hyperthyroidism. Graves ophthalmopathy is clinically apparent in approximately 30 to 50% of patients with Graves’ disease, but it is detected in more than 80% of patients who undergo assessment by means of orbital imaging. Manifestations of ophthalmopathy, which vary in severity and have a course that is typically independent of the thyroid disease, can include proptosis, periorbital edema and inflammation, exposure keratitis, photophobia, extraocular muscle infiltration, and eyelid lag (which can also occur with augmented adrenergic stimulation).
TIPO: REVISION
FORMATO: PDFDESCARGAR DIRECTA: DOWNLOAD
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