Clinical diagnosis of Graves’ or non-Graves’ hyperthyroidism compared to TSH receptor antibody test

Abstract

BackgroundTSH receptor antibody (TRAb) is considered the gold standard diagnostic test for the autoimmunity of Graves’ disease (GD), which is commonly diagnosed clinically.AimTo evaluate the true positive (sensitivity) and true negative (specificity) rates of clinical diagnosis of GD or non-GD hyperthyroidism compared to the TRAb test.SettingUniversity teaching hospital in North West England.ParticipantsPatients in the Endocrinology service who had a TRAb measurement between December 2009 and October 2015.MethodsElectronic patient records were studied retrospectively for a pre-TRAb clinical diagnosis of GD or non-GD hyperthyroidism. We examined descriptive statistics and binary classification tests; Fisher exact test was used to analyse contingency tables.ResultsWe identified 316 patients with a mean age of 45 (range, 17–89) years; 247 (78%) were women. Compared to the TRAb result, clinical diagnosis had a sensitivity of 88%, specificity 66%, positive predictive value 72%, negative predictive value 84%, false negative rate 12%, false positive rate 34%, positive likelihood ratio 2.6 and negative likelihood ratio 0.2 (P < 0.0001).ConclusionsClinicians were liable to both over- and under-diagnose GD. The TRAb test can help reduce the number of incorrect or unknown diagnoses in the initial clinical assessment of patients presenting with hyperthyroidism.

Diagnosing Graves’ Disease and Non-Graves Hyperthyroidism Using TSH Receptor Antibody Test versus Non-TSH Receptor Antibody Test Methods of Diagnosis

“…Lauren Bell et al have found that the TRAb result was the definitive diagnosis against which we evaluated the sensitivity and specificity of clinical diagnosis [7].…”

“…These findings suggest clinicians utilize a positive TRAb measurement over their clinical judgement to confirm a diagnosis of GD. A TRAb measurement in the initial clinical assessment of all patients could potentially prevent an incorrect diagnosis being made in the first place [7].…”

“…The diagnosis of GD is made on the basis of typical clinical features of hyperthyroidism, such as weight loss, fatigue, heat intolerance, tremor, palpitations and diffuse thyroid enlargement, plus specific clinical features of GD including orbitopathy, thyroid dermopathy (pretibial myxedema) and thyroid acropachy [7]. Serum analyses typically show suppressed thyroid-stimulating hormone (TSH; thyrotropin) and elevated thyroid hormones, tetraiodothyronine (T4; thyroxine) and triiodothyronine (T3) [8].…”

“…The autoimmune production of TSH receptor antibodies (TRAb) is central to the pathogenesis of GD [7]. More recent American Thyroid Association (ATA) guidelines place greater emphasis on the use of TRAb, particularly in monitoring the course of Graves' disease, but similarly recommend that its place is in the diagnosis of GD in those patients whose etiology of hyperthyroidism is unclear from their presentation and biochemistry [1].…”

Graves’ Disease: Pathophysiology, Genetics and Management

“…The RNASET2-FGFR1OP-CCR6 region at 6q27 and an intergenic region at 4p14 are two new susceptibility loci that had been found [20]. Moreover, thyroid-stimulating hormone receptor and major histocompatibility complex class II versions have strong associations with thyroid stimulating hormone receptor autoantibodies (TRAb)-positive GD [21]. Compared with healthy controls, GD patients have higher rate of peripheral blood mononuclear cell conversion into CD34 + fibrocytes.…”