Hyperthyroidism: An Update

Graves’ disease is caused by a complex interaction of genetic and environmental risk factors andits natural course has been one of repeated episodes of relapse and remission of hyperthyroidism formany years. In this autoimmune disease, unregulated stimulation of TSH receptors of the thyrocytes byTSH receptor antibodies (TRAb) causes hyperthyroidism. These circulating IgG antibodies are thepathological hallmark, present in every patient with Graves’ disease.Three forms of current therapeutic approaches available for Graves’ hyperthyroidism, i.e.antithyroid drugs (ATD), radioiodine and surgery, have not been able to re-establish normal lifelongthyroid function in all patients. Conventional ATD treatment of 12-18 months duration restoreseuthyroidism with a 50% risk of relapse upon discontinuation of drugs. Radioiodine and surgery causeablation or removal of thyroid tissue at the expense of development of another disease, hypothyroidism,which is definitely for the rest of the patient’s life. It is northworthy that despite the limitations of theavailable treatment, several studies have shown an association of hyperthyroidism and mortality.The choice of treatment for each Graves’ patient has always been a dilemma. Antithyroids havebeen the first choice for treatment of Graves’ disease in Europe, Japan and Latin America for decadesand the most recent data showed that ATD is possibly the most common treatment in the United Statesfor Graves’ hyperthyroidism.Can we predict relapse in Graves’ disease Many clinical studies have attempted to identify riskfactors predicting relapse in patients with Graves’ hyperthyroidism, reporting many factors to beassociated with decreased remission rates of hyperthyroidism following antithyroid drug withdrawal.Thyroid volume TSH receptor antibodies (TRAb), smoking, postpartum period, biochemically severedisease, Graves’ ophthalmopathy and prolonged treatment have impact on risk of relapse, whileassociations of age, gender and family history remin uncertain. Overall, identified markers are notstrong enough to predict recurrence in a single patient, because each marker has limited power.Graves’ disease is caused by a complex interaction of genetic and environmental risk factors andits natural course has been one of repeated episodes of relapse and remission of hyperthyroidism formany years. In this autoimmune disease, unregulated stimulation of TSH receptors of the thyrocytes byTSH receptor antibodies (TRAb) causes hyperthyroidism. These circulating IgG antibodies are thepathological hallmark, present in every patient with Graves’ disease.Three forms of current therapeutic approaches available for Graves’ hyperthyroidism, i.e.antithyroid drugs (ATD), radioiodine and surgery, have not been able to re-establish normal lifelongthyroid function in all patients. Conventional ATD treatment of 12-18 months duration restoreseuthyroidism with a 50% risk of relapse upon discontinuation of drugs. Radioiodine and surgery causeablation or removal of thyroid tissue at the expense of development of another disease, hypothyroidism,which is definitely for the rest of the patient’s life. It is northworthy that despite the limitations of theavailable treatment, several studies have shown an association of hyperthyroidism and mortality.The choice of treatment for each Graves’ patient has always been a dilemma. Antithyroids havebeen the first choice for treatment of Graves’ disease in Europe, Japan and Latin America for decadesand the most recent data showed that ATD is possibly the most common treatment in the United Statesfor Graves’ hyperthyroidism.Can we predict relapse in Graves’ disease Many clinical studies have attempted to identify riskfactors predicting relapse in patients with Graves’ hyperthyroidism, reporting many factors to beassociated with decreased remission rates of hyperthyroidism following antithyroid drug withdrawal.Thyroid volume TSH receptor antibodies (TRAb), smoking, postpartum period, biochemically severedisease, Graves’ ophthalmopathy and prolonged treatment have impact on risk of relapse, whileassociations of age, gender and family history remin uncertain. Overall, identified markers are not.strong enough to predict recurrence in a single patient, because each marker has limited power.