3-I in this situation, in order to combine it with an RAIU measurement.
Thyroid Ultrasound- US exam of the thyroid is sometimes of value in diagnosis. For example, if a possible nodule is detected on physical exam. It also may confirm hypoechogenicity if the diagnosis is actually Hashimoto’s thyroiditis, or intense vascularity of Graves’ disease if a color Doppler flow exam is done.
Determination of antibody titers provides supporting evidence for Graves’ disease. More than 95% of patients have positive assays for TPO (microsomal antigen), and about 50% have positive anti-thyroglobulin antibody assays. In thyroiditis the prevalence of positive TG antibody assays is higher. Positive assays prove that autoimmunity is present, but they do not prove thyrotoxicosis. However, patients with causes of thyrotoxicosis other than Graves’ disease usually have negative assays. During therapy with antithyroid drugs the titers characteristically go down, and this change persists during remission. Titers tend to become more elevated after RAI treatment.
Antibodies to TSH-Receptor-
Thyrotrophin receptor antibody assays (TRAb) have become readily available, and a positive result strongly supports the diagnosis of Graves’ disease(11.1). Determination of TRAb is not required for the diagnosis, but the implied specificity of a positive test provides security in diagnosis, and for this reason the assay is now widely used. The assay is valuable as another supporting fact in establishing the cause of exophthalmos, in the absence of thyrotoxicosis, and high maternal levels predict fetal or neonatal thyrotoxicosis. Measurement of TRAb (TSH-R binding antibodies), any antibody that binds to the TSH-R, is generally available.Assays for Thyroid Stimulating Antibodies (TSAb,TSI) are less available, but are more specific for the diagnosis. Using current tests, both are positive in about 90% of patients with Graves disease who are thyrotoxic. “Second generation” assays becoming available use monoclonal anti-TSH-R antibodies and biosynthetic TSH-R in coated tube assays, are reported to reach 99% specificity and sensitivity(11.11,11.12,16). Although rarely required, serial assays are of interest in following a patient’s course during antithyroid drug therapy, and a decrease predicts probable remission(11.2).
Other Assays Rarely Used-
General availability of assays that can reliably measure suppressed TSH has made this the gold standard to which other tests must be compared, and has effectively eliminated the need for most previously used ancillary tests. There are only rare causes of confusion in the TSH assay. Severe illness, dopamine and steroids, and hypopituitarism, can cause low TSH, but suppression below 0.1 µ/ml is uncommon and below 0.05 µ/ml is exceptional, except in thyrotoxicosis. Thyrotoxicosis is associated with normal or high TSH in patients with TSH producing pituitary tumors and selective pituitary resistance to thyroid hormone. If TSH, FT4, TRAb, and other test noted above do not establish the diagnosis, it may be wise to do nothing further except to observe the course of events. In patients with significant thyroid hyperfunction, the symptoms and signs will become clearer, and the laboratory measurements will fall into line. Measurement of BMR, T3 suppression of RAIU, TRH testing, and response to KI are of historical interest.
DIFFERENTIAL DIAGNOSIS of THYROTOXICOSIS
Graves’ disease must be differentiated from other conditions causing thyrotoxicosis. (Table -4).
Thyrotoxicosis factitia-Thyrotoxicosis may be caused by taking T4 or its analogs, most commonly due to administration of excessive replacement hormone by the patient’s physician.Hormone may be taken surreptitiously by the patient for weight loss or psychologic reasons. The typical findings are a normal or small thyroid gland, an131-I uptake of zero, a low serum TG, and, of course, a striking lack of response to antithyroid drug therapy. The problem can easily be confused with “painless thyroiditis”, but in thyrotoxicosis factitia, the gland is typically small.
Toxic nodular goite