Hyperthyroidism etiology

Thyroid-associated ophthalmopathy (TAO) is present in 90% of patients with the classical triad of Graves disease (goiter, ophthalmopathy, dermopathy) but these features may follow independent courses and successful control of the hyperthyroidism improves TAO in less than 5% cases. Immunosuppression has been used since theories of the etiology of TAO include the presence of circulating antibodies to both thyroid and ocular muscle fibers, and of thyroglobulin-antithy-roglobulin complexes with high affinity for extraocular muscles. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. 

Thyroid disorders can be divided into two primary categories conditions that increase thyroid function (hyperthyroidism) and conditions that decrease thyroid function (hypothyroidism).8 There are several different types of hyperthyroidism and hypothyroidism, depending on the apparent etiology, symptoms, and age of onset of each type. The types of hyperthyroidism and hypothyroidism are listed in Table 31-1. Although we cannot review the causes and effects of all the various forms of thyroid dysfunction at this time, this topic is dealt with elsewhere exten-sively.6,8,56 74... 

There are numerous thyroid gland function tests, each designed to determine the etiology of thyroid dysfunction. In general, though, when hypothyroidism is present, circulating T3 and T4 levels are down and TSH is up. The opposite is true of hyperthyroidism. In addition, free (non-protein-bound) T4 and TBG may be determined to clarify inconclusive results. In hyperthyroidism, free T4 is increased but total T4 may be normal. It is the free serum T4 that has been correlated with clinical symptoms rather than total T4. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. Nonpharmacologic interventions include cardiac rehabflitation and restriction of fluid intake (maximum 2 L/day from all sources) and dietary sodium (approximately 2 to 3 g of sodium per day). 

The first step in the management of chronic heart failure is to determine the etiology (see Table 14—1) and/or any precipitating factors. Treatment of underlying disorders such as anemia or hyperthyroidism may obviate the need for treatment of heart failure. Patients with valvular diseases may derive significant benefit from valve replacement or repair. Revascularization or anti-ischemic therapy in patients with coronary disease may reduce heart failure symptoms. Drugs that aggravate heart failure (see Table 14—3) should be discontinued, if possible. 

The thyroid gland seems to be well adapted to incidents of iodine intake in very high amounts. Still, there is evidence showing that increased intake of iodine may induce clinically relevant problems in some susceptible subjects. These effects are optimally identifiable at population level, as individual responses vary depending on many other factors that are difficult to control. One of the main undesirable consequences of increased iodine intake in a population is a higher incidence of hyperthyroidism. This chapter discusses the epidemiology and etiology of iodine-induced hyperthyroidism (IIH), which follows normalization of iodine supply. 

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