FNAB under US guidance is a useful diagnostic modality in the evaluation of thyroid nodules in selected patients with MNG. Because the risk of thyroid malignancy in these nodules is comparable to that which exists in solitary thyroid nodules, the possibility of thyroid malignancy should be considered in all patients with MNG.

In studies of rat bone metabolism, trabecular bone density should be measured. Three established methods of measuring trabecular bone include trabecular bone volume by histomorphometry (BV/TV%), trabecular bone density by peripheral quantitative computerized tomography (pQCT), and areal bone density of trabecular-rich regions by dual x-ray absorptiometry (DXA). We compared the ability of these three methods to discriminate between orchiectomized (orchidectomized) rats and controls. Sixteen male Sprague-Dawley rats (400-425 g) were orchiectomized, and 16 others were controls. In vivo spine bone mineral density (BMD) was measured at the beginning of the study and again after 11 weeks. Rats were sacrificed, and ex vivo BMDs of the right femur and tibia were measured by DXA, followed by trabecular bone density of the right proximal tibia by pQCT. BT/TV% of the left proximal tibia was measured by histomorphometry. Differences between groups were detected by all three methods, but both the magnitude of the difference between groups and the variance of the measurements was much greater for histomorphometry and pQCT than for DXA. Consequently, the statistical significance for the difference between groups was comparable for all three methods. Of the sites measured with DXA, the proximal tibia had the greatest statistical significance for the difference between groups. In summary, all three methods can demonstrate the effect of orchiectomy on trabecular bone. The large differences between groups seen by histomorphometry are also seen by pQCT but not by DXA. We conclude that trabecular bone density by pQCT may be a reasonable surrogate for measurements by histomorphometry.

Risperidone is a novel antipsychotic agent that blocks both dopaminergic and serotonergic receptors. In several reports, clinically significant hyperprolactinemia has been reported in patients on this agent. However, the optimal management of risperidone-induced hyperprolactinemia has not been clarified. We reviewed the records of 5 patients with psychotic disorders who were evaluated for risperidone-induced hyperprolactinemia. There were 4 females and 1 male patient, aged 30-45 yr. All patients had significant hyperprolactinemia, with prolactin (PRL) levels ranging from 65.5 to 209 microg/l. All but 1 of these patients had manifestations of hypogonadism. In these 4 patients, risperidone therapy was continued and the dopamine agonists bromocriptine or cabergoline were added. In 3 out of 4 patients, such additional therapy reduced the PRL level and alleviated hypogonadism. None of the patients treated with these agents had a worsening of psychosis. We conclude that risperidone can cause clinically significant hyperprolactinemia in patients treated with this drug. If risperidone therapy must be continued in such patients, addition of the dopamine agonists bromocriptine or cabergoline may successfully alleviate hyperprolactinemia and the associated manifestations without worsening psychotic symptoms.