[Adrenal gland cysts. Our experience]. / Le cisti del surrene. Nostra esperienza.

Adrenal cysts are an uncommon finding, in most cases unexpectedly discovered in the evaluation of nonspecific abdominal pain or at autopsy. Cystic adrenal masses can be classified into neoplastic and non-neoplastic aetiologies. The distinction between malignant and benign adrenal cysts can still be difficult. Cysts of neoplastic aetiology occur as a result of necrosis and cystic degeneration within both benign and malignant tumours. Non-neoplastic cysts have been conventionally divided into four categories: endothelial (45%), haemorrhagic or pseudocystic (39%), epithelial (9%) and parasitic (7%). Small adrenal cysts are clinically silent, while cysts of large size can cause displacement and compression of adjacent organs. The radiological aim is to detect the adrenal mass and CT is regarded as the best method available for this detection, although a differentiation between benign and malignant tumours can be difficult. Here we report our experience in nine patients with adrenal cysts. Abdominal pain was the dominant sign, two patients were hypertensive, one presented a palpable mass at abdominal examination and another presented oligomenorrhea with hypertrichosis, in five patients the adrenal mass was discovered unexpectedly during radiologic examination. All cysts in our patients were unilateral. All patients were examined by ultrasound and CT, one by RM, three by 75Se-Seleniumcholesterol cortical scintigraphy and two by 131I-MIBG medullary scintigraphy. In three patients a percutaneous aspiration of the cyst was performed via a posterior approach with CT or US guidance. This approach has been used for diagnostic and therapeutic purposes. Examination of aspirated cyst fluid for steroid hormones showed markedly elevated cortisol levels compared with normal plasma cortisol levels in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium antagonists and hormone release. VII. Effects of gallopamil infusion on insulin and C peptide release in normal subjects.

It is known that insulin release is calcium-dependent and that calcium-antagonists, blocking calcium transport across cell membranes, inhibit it, especially interfering with the second phase of insulin secretion. Gallopamil (GAL) is a new calcium-antagonist that, although structurally similar to verapamil, has more potency. It blocks slow calcium channels and fast sodium channels. Even if it has been demonstrated in vitro, there is no evidence that GAL is able to impair the glucose-induced insulin release in humans. We have submitted five normal subjects (24-36 yr old) to oral glucose tolerance test (OGTT, 75 g of glucose p.o.) and OGTT plus GAL infusion test (1 mg i.v. as a bolus, followed by a 2 mg/hr infusion for 2.5 hr, starting 30 min before glucose load), in two different days, to determine the effects of GAL on insulin and C peptide release after oral glucose load. In opposite with verapamil effects, we found that GAL did not reduce the peak levels of insulin and C peptide, but the peak response was delayed and the incremental areas tended to increase during GAL infusion, so that an impairment of glucose tolerance was equally obtained. This study indicates that different calcium-antagonist drugs exert differential effects on insulin release and their action on glucose homeostasis should be kept in mind because of the large use of these drugs in cardiac patients.