[The principles of the treatment of pancreatic diabetes]. / A pancreas diabetes kezelési elvei.

In pancreatic diabetes the whole of the Langerhans islets are damaged, which means that both the beta-cells and the alpha-cells are damaged. Unpredictable oscillations of blood glucose level are common due to malabsorption and maldigestion and one may count with explicit proneness to hypoglycaemia. The defence against hypoglycaemia also diminishes due to the damage of glucagon secretion, which is often aggravated by alcohol consumption. If normoglycaemia in pancreas diabetes cannot be achieved with appropriate diet, insulin treatment is necessary. Oral antidiabetic agents are not expedient. The best metabolic state can be achieved at the expense of the least amount of hypoglycaemia by giving the necessary minimum portions of insulin in an intensive, conservative insulin therapy. There is not enough experience with insulin analogs in pancreatic diabetes, but it seems expedient to use long-acting insulin analogs. The treatment of pancreas diabetes is a teamwork in which everybody has a decisive role, the gastroenterologist, the diabetologist, the dietitian and the diabetes nurse as well.

Treatment of pituitary tumors: dopamine agonists.

The neurotransmitter/neuromodulator dopamine plays an important role in both the central nervous system and the periphery. In the hypothalamopituitary system its function is a dominant and tonic inhibitory regulation of pituitary hormone secretion including prolactin- and proopiomelanocortin-derived hormones. It is well known that dopamine agonists, such as bromocriptine, pergolide, quinagolide, cabergoline, and lisuride, can inhibit PRL secretion by binding to the D(2) dopamine receptors located on normal as well as tumorous pituitary cells. Moreover, they can effectively decrease excessive PRL secretion as well as the size of the tumor in patients having prolactinoma. Furthermore, dopamine agonists can also be used in other pituitary tumors. The major requirement for its use is that the tumor cells should express D(2) receptors. Therefore, in addition to prolactinomas, targets of dopamine agonist therapy are somatotroph tumors, nonfunctioning pituitary tumors, corticotroph pituitary tumors, Nelson's syndrome, gonadotropinomas, and thyrotropin-secreting pituitary tumors. It is also an option for the treatment of pituitary disease during pregnancy. Differences between the effectiveness and the resistance of different dopaminergic agents as well as the future perspectives of them in the therapy of pituitary tumors are discussed.

Dexamethasone and adrenocorticotropin suppress prolactin secretion in humans.

It has been demonstrated that the regulatory pathways mediating basal and/or stimulus-induced prolactin (PRL) release in mammals are highly sensitive to adrenal corticoid inhibitory influence. We have investigated the effect of four different doses of dexamethasone (DEX) and the effect of adrenocorticotropin on PRL secretion in 197 patients (169 female, 28 male; age: 18-66 yr) with suspected hypercortisolemia--but only those with a normal glucocorticoid suppression test were involved in the study--and in 66 female patients (age: 18-39 yr) with suspected adrenocorticotropin-dependent hyperandrogenism. Overnight (1 mg), low-dose (0.5 mg every 6 h for 2 d), high-dose (2 mg every 6 h for 2 d), and long-lasting administration of DEX (0.5 mg every 6 h for 5 d) resulted in a significant decrease in PRL levels compared to the baseline. Similarly, a reduction in PRL levels could be detected following injection of adrenocorticotropin (250 microg). In hyperprolactinemic patients, the DEX-induced increase in PRL (APRL, expressed in percentage of baseline) was significantly larger compared with normoprolactinemic subjects in all groups except those who received high-dose DEX) or adrenocorticotropin. These data clearly indicate that the secretory function of PRL cells in humans is sensitive to changes in the activity of the hypothalamo-pituitary-adrenal axis in a dose-dependent manner.