The predominant form of non-toxic goiter in Greece is now autoimmune thyroiditis.

Endemic non-toxic goiter (NTG) in Greece has been attributed primarily to iodine deficiency. Thirty years ago about 60% of the prepubertal boys and girls examined in endemic goiter regions presented with NTG and among them thyroid autoimmunity was rarely detected. Although iodine supplementation has corrected this deficiency during the past 30 years, new cases of NTG still appear. To evaluate the prevalence and type of NTG and the effect of iodine supplementation on them in Greece at present, we performed two cross-sectional clinical studies and a retrospective pathology one: (i) thyroid gland volume and urinary iodine excretion (UIE) were assessed in a representative sample of 1213 schoolchildren from previously endemic and non-endemic regions; (ii) serum thyroxine, tri-iodothyronine, TSH, thyroid autoantibodies (AAB) (anti-thyroid peroxidase and anti-thyroglobulin antibodies) and UIE (in 60 patients) were measured in 300 consecutive patients with NTG from Athens and Heraklion; and (iii) we compared the prevalence of autoimmunity among fine needle aspiration smears of benign thyroid pathologies performed by the same pathologist between 1985 and 1986 (975 cases) and between 1994 and 1995 (2702 cases). We found that 12. 5% of the schoolchildren examined in regions with a previous history of endemic goiter had NTG, whereas this percentage was only 1.7% in areas without such a history. In Athens (61.6%) and Heraklion (58. 5%) a substantial number of NTG patients were AAB positive and biochemically hypothyroid. UIE in Athens did not differ between patients with autoimmune goiter (ATG) and simple goiter. The prevalence of autoimmune stigmata in pathology smears has increased from 5.94% (years 1985-1986) to 13.91% (years 1994-1995) (P<0.05). We conclude that: (i) the persistence of endemic goiter in regional foci despite iodine deficiency correction suggests a possible role for a naturally occurring goitrogen; (ii) ATG is the predominant form of NTG in Greece nowadays; and (iii) the five-fold decrease in the prevalence of NTG during the past 30 years followed by the increase of ATG may support the relative character of the latter.

The medical treatment of non-toxic goiter: several questions remain.

In this review it is concluded that thyroxine (T4), triiodothyronine (T3) and iodine (KI), singly or in combination, are all effective in reducing the goiter size, but there is insufficient evidence to prove which is the best (possibly the combination of T4 + KI?). Higher doses are more effective than smaller, but also lead to more side-effects. Thus, the optimal dose has yet to be found. The suppression of the pituitary thyroid axis plays a major role in the treatment of non-toxic goiter, but it is not definite that this is the only mechanism responsible for the beneficial effect of the agents mentioned. In view of the lack of better evidence, it is simply suggested that non-toxic goiters in young persons should be initially treated aggressively with 200 micrograms of T4/day or more for some months. If the goiter shrinks then the dose should be gradually decreased. If the goiter persists, it is futile to continue with large doses for more than 6-12 months. One may continue with smaller doses, maintaining the serum TSH in the low-normal range. The treatment of benign thyroid nodules with thyroxine is controversial. Probably thyroxine is beneficial in about a third of the cases. For both non-toxic goiters and nodules, autonomy should be excluded before starting thyroxine treatment, and old age, cardiac disease and a poor general condition are contraindications.

Does coffee consumption protect against thyroid disease?

In a case-control, serially matched study, 70 patients with thyroid cancer, 55 with benign thyroid disease and 71 controls were interviewed in regard to a variety of socioeconomic, social and dietary characteristics. Statistical analysis revealed a strikingly negative (p less than 0.05) association between benign and malignant thyroid disease and consumption of coffee. After adjustment for possible confounding variables, the association remained statistically significant. The mechanism by which coffee consumption may play a protective role against development of benign or malignant thyroid neoplasms may be the stimulatory effect of caffeine on the intracellular cyclic AMP production, which is known to inhibit cell growth.

Thyroid hormone and immunological studies in endemic goiter.

Iodized oil (1 ml im) was given to 58 goitrous patients from a mildly iodine-deficient area in Greece. Goiter size, urinary iodine, and serum T4, T3RU, T3, rT3, TSH, thyroxine-binding globulin (TBG), and thyroid autoantibodies were measured before and 1, 3, and 6 months after the injection. Goiter size decreased. Serum T4 remained relatively constant, but TBG decreased and therefore T3RU and FTI increased. Serum T3 and rT3 initially decreased (P less than 0.001) and then increased at the sixth month (P less than 0.001), both showing roughly parallel changes. Serum TSH, initially normal (1.42 +/- 0.11 (SEM) mU/liter), decreased to 0.65 +/- 0.01 and 0.76 +/- 0.05 mU/liter at the third and sixth month (difference from baseline P less than 0.001). Thyroid autoantibodies, both against thyroglobulin and the microsomal antigen, were undetectable before treatment, but became positive in 42.8% of the patients 3 and 6 months later. Three patients developed transient hyperthyroidism. This occurred 3 or 6 months after treatment, and was associated with high titers of thyroid autoantibodies. These results indicate that: 1) transient hyperthyroidism may occur after the administration of iodized oil, possibly because of thyroid tissue necrosis and leakage of hormones, and 2) serum TBG decreases after iodized oil, a finding not previously reported and one whose cause is not known.

The toxic effect of small iodine supplements in patients with autonomous thyroid nodules.

In sixteen cases of toxic adenoma of the thyroid (autonomous hot nodule with complete suppression of the surrounding normal parenchyma) potassium iodide was given in doses of 100 microgram/day for one week, 200 microgram/day for another and 400 microgram/day for a third week. There was a progressive increase in the serum T4 level. Serum T3 also increased, although this was significant only after the first week. Serum TSH was undetectable throughout the entire period of the study. This metabolic pattern is different from the response seen in cases of nontoxic endemic goitre, where small iodine supplements induce an increase in serum T4 but a decrease in serum T3. Furthermore, the present results may explain the phenomenon of iodine-induced or iodine-precipitated hyperthyroidism (Jod-Basedow) when patients with autonomous thyroid are presented with a high iodine intake. In contrast to the results obtained with small iodide doses, two other cases treated with large pharmacological doses of iodide showed a decrease in both serum T4 and serum T3. It is concluded that the physician should be aware of the possibility of precipitating or aggravating thyrotoxicosis in patients with an autonomous hot nodule by increasing their intake of iodine.