Our findings demonstrate that molecular analysis of cytological specimens is feasible and that its results in combination with cytology improves the diagnostic performance of traditional cytology.

The second rhTSH-Tg was informative in patients who had first stimulated Tg detectable but not in those who had undetectable Tg at the first test, in which the only patient with recurrence was diagnosed by neck US. Thus, rhTSH-Tg should be repeated only in patients who have had a positive first rhTSH-Tg and negative imaging.

Autoimmune gastritis is an additional factor affecting l-T(4) requirement in patients with autoimmune thyroiditis. Serum PCA measurement should be considered in patients with an unexplained high requirement of l-T(4).

In conclusion, our study demonstrates a high, age-dependent prevalence of PCA in an unselected large population of patients with AIT.

Our study demonstrates that ghrelin secretion is negatively affected by autoimmune gastritis, and its serum level represents the most sensitive and specific noninvasive marker for selecting patients at high risk for ABG.

We evaluated the outcome of radioiodine (RAI) therapy in 100 consecutive patients treated in the period 2000-2001 for hyperthyroidism due to Graves' disease (GD), toxic adenoma (TA) and toxic multinodular goiter (TMG). Thyroid function was measured before and after therapy every 3-6 months up to 3 yr. Three years after therapy, 75% of TA patients were euthyroid, 18.7% were hypothyroid and 6.3% hyperthyroid. Of the TMG patients, 62.2% were euthyroid, 18.9% were hypothyroid and 18.9% hyperthyroid. In GD patients euthyroidism was achieved in 12.9% of the patients, hypothyroidism in 74.2% and hyperthyroidism persisted in 12.9%. Definitive hypothyroidism was significantly higher in GD (p<0.0001) than in TA and TMG patients. Overall, positive effect of RAI (definitive hypothyroidism or euthyroidism) was very high: 93.7% in TA, 81.1% in TMG and 87.1% in GD patients. Thyroid volume reduction was observed in all patients, but was higher in GD patients (mean reduction of 76%) and in TA patients (mean nodule reduction of 69%). In TMG, mean reduction was of 32%. The median activity of RAI received by the 86 cured patients was 555 MBq (15 mCi) compared to 407 Mbq (11 mCi) received by the 14 patients who remained hyperthyroid. No influence was found between outcome and clinical parameters at the moment of 131-I therapy. In conclusion, our results indicate that RAI therapy is highly effective and safe for the control of hyperthyroidism.

In order to evaluate the effects of gonadotropin-releasing hormone (GnRH) analogs on calcium metabolism, we studied 12 girls with central precocious puberty (CPP) who were treated with the GnRH agonist D-Trp6-GnRH every 28 days. The patients' mean age +/- SD was 5.9 +/- 2.1 years. The patients were studied before commencement and after 6 and 12 months of treatment. We also studied 12 age-matched healthy girls who served as controls. Bone mineral content was measured by dual-photon densitometry with 125I, in the distal third of the left radius. We evaluated the serum levels of calcium, phosphate, magnesium, parathyroid hormone, calcitonin, 25-hydroxy-vitamin D and the 24-h urinary excretion of calcium, phosphate and magnesium. All of these parameters were found to be normal before and during the treatment in both groups. At the beginning of the study, the patients with CPP had significantly higher bone mineral content than controls (0.51 +/- 0.12 g/cm2 vs. 0.39 +/- 0.09, p < 0.001); after 6 months contents were 0.42 +/- 0.11 vs. 0.41 +/- 0.05, p < 0.01; and after 12 months 0.44 +/- 0.11 vs. 0.44 +/- 0.05, NS, for treatment and control groups, respectively. This difference remained after 6 months of treatment, while after 12 months no significant difference between patients and controls was found. Our study shows that girls with CPP have an increased bone mineral content and that GnRH analogs modify bone density with a consequent reduction, it seems, that is not related to any of the calcium parameters studied.

Our results show that ghrelin secretion is not modulated by acute GH increase observed in GHS subjects during GHRH plus arginine infusion. The similar decrease of serum ghrelin after GHRH plus arginine stimulation in both GHS and GHD subjects demonstrated that there is no negative feedback of GH on ghrelin secretion.