[Diet and nutrition in nephrolitiasis]. / Dieta e nutrizione nella calcolosi renale.

Nephrolitiasis is a frequent metabolic disease, with a high rate of recurrences. Epidemiological studies reveal that about 80% of all kidney stones are composed of calcium salts (75% calcium oxalate), while about 5% are pure uric acid. Urolithiasis is a multifactorial disease with several underlying disorders of metabolism: that is why diet is an important treatment, especially in the prevention of recurrences. Nutritional intervention is based on a high water intake, physiological calcium intake, modest sodium and animal protein restriction and vitamin C intake <2 gr daily. In case of diagnosed disorders of specific metabolic pathways, a low oxalate, low purine-diet should be advisable.

[Diet and chronic corticosteroid therapy]. / La dieta in corso di terapia corticosteroidea cronica.

Corticosteroid therapy is widely used in the acute and chronic treatment of different diseases, with consequent possible onset of typical side effects on multiple systems of the organism, including also energy metabolism and metabolism of water and minerals (sodium, potassium, calcium and phosphorus). Clinical signs, related to the type and dosage of the steroidal drug, may lead to secondary illnesses with variable degrees of severity, depending on proneness of the individual patient and on the underlying disease that motivated the treatment. The role of dietetic intervention in the management of a patient chronically receiving corticosteroid therapy is not ancillary, although often underestimated, its aim being the reduction of some long-term therapy related side effects, and the correction of major metabolic derangements. In particular, the diet shall be moderately rich in protein (1.5 g/Kg/day of proteins) and low in fat (< 30% of calories, obtained mostly from unsaturated fatty acids), based mainly on complex carbohydrates (80%), providing 50% of the caloric intake. Diet has to be specifically characterized by food containing little sodium and yielding high amounts of water, calcium, magnesium and potassium. Minor directions concern the reduced intake of ethanol and purines. The efficacy of supplementation with antioxidant vitamins (vitamin C and E) and selenium is currently under investigation.

Giant prolactinomas in men: efficacy of cabergoline treatment.

OBJECTIVE: The term 'giant prolactinoma' can be used for tumours larger than 4 cm in diameter and/or with massive extrasellar extension. Cabergoline (CAB), a long-lasting dopamine agonist (DA), safe and well tolerated, is effective in normalizing PRL levels and inducing tumour shrinkage in micro- and macroprolactinomas. The purpose of this prospective study was to evaluate the efficacy and safety of CAB also for giant prolactinomas. PATIENTS AND METHODS: Ten men with giant prolactinomas with a median age of 44.8 years were treated with CAB. Before CAB, four patients had previously undergone transsphenoidal surgery without modifying the parasellar extension of the tumour or their visual defects. Pretreatment serum prolactin (PRL) levels ranged between 1230 and 22 916 micro g/l (mean +/- SEM: 5794 +/- 1996) and tumour volume was between 21.8 and 105.5 cm3 (mean +/- SEM: 50.7 +/- 8.8). CAB was administered at an initial low dose of 0.5 mg three times a week and, in five patients who did not achieve serum PRL normalization, the dose was progressively increased up to 10.5 mg/week. The duration of treatment was 13-68 months (mean 38.9). PRL levels and pituitary target organ hormones were assayed before, after 30 days and then every 3 months after the beginning of CAB treatment. Magnetic resonance imaging (MRI) was carried out before, after 1-3 months, after 6 months and then every 10-12 months to evaluate tumour shrinkage. RESULTS: In every patient, a significant PRL decrease (P = 0.0086) of at least 96% of the pretreatment values occurred (from 5794 +/- 1996 to 77 +/- 38, mean +/- SEM); a persistent normalization of PRL levels was achieved in five out of 10 patients (50%) beginning from the first 3-6 months of CAB treatment (only one patient needed 12 months of therapy). A significant tumour shrinkage (P = 0.0003) was achieved after 12 months of therapy in nine out of 10 patients (90%), with a volume reduction greater than 95% in three, of 50% in four and 25% in two patients. Tumour volume decreased from 50.7 +/- 8.8 to 28.6 +/- 9.4 and then to 22.3 +/- 8.8 cm3 (mean +/- SEM) after 6 and 12 months of CAB treatment, respectively. An improvement of visual field defects (VFD) was obtained in six of the seven patients presenting visual impairment before CAB treatment. Among the eight patients presenting libido and potency (L-P) failure, five normalized their PRL levels. In two of these a complete restoration of libido and potency was observed. Three patients with secondary hypoadrenalism and a patient with secondary hypothyroidism were treated with substitutive therapy during all the study time. The drug was well tolerated by all patients and no one discontinued the therapy. CONCLUSIONS: These data suggest that, in giant, aggressive prolactinomas, CAB represents a first-line therapy effective in reducing PRL levels and determining tumour shrinkage.

Diagnostic approach, genetic screening and prognostic factors of medullary thyroid carcinoma.

Medullary thyroid carcinoma is the least frequent thyroid neoplasm; it originates in thyroid parafollicular cells (calcitonin secreting C cells). In 80% of cases it is sporadic, in the remaining 20% it is familial, associated or not to other endocrinopathies as pheochromocytoma and hyperparathyroidism (MEN 2A, MEN 2B, and isolated familial medullary thyroid carcinoma). Preclinical diagnosis in relatives of affected subjects (preferably at pediatric age) is essential for successful therapy and is performed with genetic and biochemical screening tests. The genetic screening is based on DNA analysis (RET proto-oncogene mutations) of the patient, and if positive of all first degree relatives, to separate sporadic (somatic mutations) from familial (germline mutations) forms. The biochemical screening is based on calcitonin determination and its increase after pentagastrin stimulation, (a peculiar characteristic of medullary thyroid carcinoma, the first biochemical disorder in a subject at risk) and is mainly used in genetically silent familial medullary thyroid carcinoma. The principal negative prognostic factors of medullar thyroid carcinoma and the debate concerning the use of calcitonin determination in the diagnosis of the "cold" thyroid nodule have been analyzed.

Medical therapy of benign thyroid diseases.

Main guide-lines of medical therapy of benign thyroid diseases are reviewed. The most common drug therapy of the various forms of hyperthyroidism is represented by thionamide drugs (methimazole and propylthiouracil). Therapeutic protocols are diversified according to the disease. In Graves'disease medical therapy may present the definitive treatment, leading to remission in little less than 50% of cases while in hyperfunctioning nodular thyroid diseases, medical therapy is merely in preparation for ablation therapy. Other drugs used in hyperthyroidism are also mentioned (inorganic iodine, potassium perchlorate, beta-blockers). Thyroxine replacement therapy in the various forms of hypothyroidism is then analyzed, discussing in particular the therapeutic protocols and follow-up of the various forms of hypothyroidism. Finally, the controversy about the indications and efficacy of TSH-suppressive thyroxine therapy is considered.

Effect of acute and chronic administration of tamoxifen on GH response to GHRH and on IGF-I serum levels in women with breast cancer.

Tamoxifen, an estrogen antagonist, is usually employed in the treatment of breast cancer. Its mechanism of action is not well known because an antiproliferative effect of the drug has been shown also in estrogen receptor negative tumors, most likely mediated by the inhibition of local growth factors and particularly IGF-I. However, the action of tamoxifen on the GH-IGF-I axis is still open to investigation. We have investigated the influence of acute and chronic treatment with tamoxifen on GH response to GHRH and IGF-I serum levels in six postmenopausal women with metastatic breast cancer. A GHRH test (50 microg i.v. at time 0, GH determinations at 0, 15, 30, 60, 90 and 120 min) was performed (a) basally, (b) 3 h after 40 mg oral administration of tamoxifen and (c) after 8 weeks of 20 mg twice a day oral tamoxifen treatment. IGF-I was measured basally and after chronic tamoxifen therapy. No significant modifications in GH response to GHRH were observed after acute or chronic treatment with tamoxifen vs the basal test. On the contrary, chronic tamoxifen treatment induced a significant decrease in serum IGF-I levels. Basal pretreatment levels of 123+/-18 microg/l were suppressed to 65+/-11 microg/l (mean suppression 47%, P < 0.001). These preliminary data confirm the inhibitory effect of tamoxifen on IGF-I production but seem to exclude the possibility that this effect may be due to an inhibition of GH secretion.