The choice of therapy involves multiple considerations (Table 23.2) [25]. The physician should carefully go over each treatment’s benefits and risks with the patient and make specific recommendations; ultimately however, the decision must respect the patient’s reasonable preferences.

Thionamides. This class of compounds shares the thionamide grouping which, by acting as a substrate for the thyroid peroxidase enzyme, confers the ability to inhibit competitively the organification and coupling steps in thyroid hormone synthesis. Propylthiuracil (PTU) and methimazole (MMI) are the two available drugs. PTU and MMI are almost completely adsorbed after oral administration. The half-life of MMI is 6–8 h and its action lasts 40 h. The half-life of PTU is 1–2 h and its action lasts 24 h [24, 25]. Thionamides can be used both in the primary treatment of hyperthyroidism and as a preparation for radiometabolic or surgical treatment. The initial dose is still a matter of debate: generally the initial dose of MMI is 10–30 mg per day in one or two oral administrations, while that of PTU is 100–300 mg per day every 6 h. Although both drugs are effective in controlling hyperthyroidism, MMI normalize thyroid activity more rapidly compared to PTU [26, 27]. As previously stated, the thionamide derivatives have no effect on the release of preformed thyroid hormones. Hence, an initial clinical effect is not noted until 1–2 weeks after initiation of thionidamide therapy and frequently a euthyroid state is not attained until after 6–8 weeks or longer. Beta-blockers can be used to attenuate symptoms in this period. When the serum thyroid hormone levels have been normalized, the patient is placed on a lower maintenance dose such as 5–10 mg of MMI or 50–100 mg of PTU daily. At this point, management may vary depending on the type of definitive therapy planned for the individual patient. In the case of Graves’ disease the duration of therapy should be between 12 and 18 months, since periods of treatments inferior to 12 months lead to a higher possibility of recurrence, while periods superior to 18 months do not lead to higher percentages of remission [28]. Followup visits should be arranged every 4–6 weeks during the initial stage and every 2–3 months thereafter, in order to adequately adjust the thionamide dosage.

Thionamides can be associated with a variety of side effects with different severity levels grouped as minor and major (Table 23.3) [24, 25, 28]. Minor side effects are found in 1–5 % of patients and include pruritis, urticaria, arthralgia, nausea sickness, and olfaction disorders (more frequent with MMI). Major side effects include agranulocitosis, hepatoxicity, aplastic anemia, and vasculitis and occur in approx 0.2–0.5 % of cases [25, 28]. Thus complete blood-cell count and liver function tests along with thyroid function evaluation should be assessed at each control during thionamide therapy.

Potassium perchlorate. This can be used in the treatment of thyrotoxicosis caused by the excess of exogenous iodine. The drug competitively inhibits the uptake of iodine by thyroid cells and accelerates its release. It should be noted that this drug can produce various side effects, among which the most important is bone-marrow depression [24, 25].

Lithium Carbonate. The anthyroidal effect of lithium has been known since 1960. It seems that lithium, similarly to iodine, blocks the release of thyroid hormone for a transitory period. Sometimes it has been used as an adjunctive therapy to radiometabolic therapy to prevent the increase of serum thyroid hormone concentration [24, 25].

Glucocorticoids. Glucorticoids are used in thyrotoxicosis due to subacute thyroiditis for its as an anti-inflammatory action and reduction in the peripheral conversion of T4 into T3 [24, 25].

Radioiodine is given orally as a single dose of ¹³¹I-labeled sodium iodide in liquid or capsule form. The mechanism of action of ¹³¹I is through the production of an intense radiation thyroiditis followed by progressive interstitial fibrosis and glandular atrophy resulting in destruction of the synthetic capacity of the thyroid. The cell necrosis induced by ¹³¹I occurs gradually and an interval of 6–12 weeks or longer must elapse before a hypothyroid or euthyroid state is achieved [24, 25]. Retreatment with radioiodine is necessary in 14 % of patients with Graves’ disease, in 10–30 % of patients with toxic adenoma, and in 6–18 % of patients with toxic nodular goiter [24, 25]. Moderately severe ophthalmopathy may be a contraindication to treatment with radioiodine since radioiodine may exacerbate the condition especially in subjects who smoke (Table 23.2).

Surgery is the gold standard in the presence of a large multinodular goiter. In addition, it should be the treatment of choice in certain circumstances such as in patients with Graves’ disease due to a very large diffuse goiter (greater that 60 gm) for which a sustained remission with thionamide therapy is unlikely [24, 25]. In the hands of an experienced neck surgeon, thyroid surgery is safe and highly effective. Possible adverse effects include recurrent nerve injury with phoniatric problems and the development of hypoparathyroidism.

So far, two studies have specifically evaluated the efficacy of anti-thyroid treatment in hyperthyroid patients with premature ejaculation. Carani et al. [11], in a series of 34 subjects with hyperthyroidism (Graves’ disease in 19, Plummer’s disease in six and toxic multinodular goiter in nine), showed that medical treatment was able to reduce the prevalence of PE from 50 to 15 % at the end of treatment, a figure similar to that found in the general population (14 %) [29]. Similar results were thereafter reported by Cihan et al. [5]. In a series of 43 hyperthyroid subjects (Graves’ disease in 17, Plummer’s disease in two and toxic multinodular goiter in 24) the rate of PE declined from 72.1 % at the baseline to 25 % after achieving euthyroidism. Interestingly, the same study also demonstrated that compared with other treatments the surgically treated group reported higher mean intravaginal ejaculatory latency time (IELT).

Hypothyroidism is one of the most common chronic endocrine disorders in the Western population, with annual incidence rates of two in 10,000 for males [30–32]. The diagnosis is confirmed by elevated basal serum TSH and reduced free triiodothyronine (FT3) and thyroxine (FT4). Subclinical manifestation is present in about 5 % of the total population and it is characterized by normal thyroid hormones (FT3 and FT4) and elevated TSH levels (between 5 and 10 mU/l). Table 23.4 summarizes the most important causes of hypothyroidism. The most common cause of hypothyroidism in developed countries is autoimmune thyroiditis. Radioiodine ablation or surgical thyroidectomy are also responsible for an important number of cases. Less often, hypothyroidism may be drug induced or be secondary to disorders of the pituitary and hypothalamus (central or secondary hypothyroidism). In some parts of the world, iodine deficiency remains highly prevalent, with all of the subsequent consequences of deficits. As mentioned above, primary hypothyroidism has been associated with DE and replacement therapy might improve the problem.