Effect of naloxone on TRH-induced PRL and TSH response in normal man.

The effect of naloxone on PRL and TSH response to TRH was studied in 8 normal men. PRL response to TRH was unaffected by the administration of naloxone. TSH response to TRH was significantly decreased by naloxone, considering the maximum absolute increment (p less than 0.01) and the areas under curves (p less than 0.05). In conclusion, the PRL response to TRH may be unaffected by endogenous opioids or naloxone and we were unable to reveal a possible opioid effect in our experimental conditions. TSH response to TRH seems to be affected by endogenous opioids, possibly due to an indirect or direct action on TRH and/or on the pituitary.

[Determination of prolactin secretion in idiopathic galactorrhea]. / Valutazione della secrezione di prolattina nella galattorrea idiopatica.

We have studied 15 women with idiopathic galactorrhoea and normal serum PRL basal values, regularly menstruating, with normal x-ray of the sella turcica and mammography. The patients were not suffering from other endocrine diseases nor taking medications known to cause galactorrhoea. These subjects and 5 normal women were submitted to an evaluation of the serum PRL circadian rhythm, to TRH test for PRL and TSH, metoclopramide test for PRL, and basal determination of TT3 and TT4. The results did not show any significant difference between the two groups and did not reveal any abnormality of PRL secretion in the patients. These data, resulting from a homogeneous series of patients, support the hypothesis of an increased sensitivity of breast receptors to PRL, or of the secretion of heterogeneous forms of PRL, biologically active on mammary tissue, but not detected by current RIA methods for PRL.

[Changes in hormonal and biochemical parameters in gastric adenocarcinoma]. / Modificazioni di parametri ormonali e biochimici nell'adenocarcinoma gastrico.

In 51 patients with gastric adenocarcinoma the fasting blood concentrations of hCG, beta hCG, alpha subunits, ADH, calcitonin, enteroglucagon, gastrin, GH, melatonin, somatostatin, estradiol, CEA and pepsinogen I in the peripheral vein were estimated by radioimmunoassay at the time of diagnosis and, in those who underwent surgery, 7 days after the operation, to determine the incidence of the modifications of the above mentioned substances' blood levels and the existence of possible markers. In presence of increases of the examined parameters greater than 50%, considering M +/- 2 SD of 10 control subjects as normal range, the tumours were examined immunohistochemically. In patients with gastric adenocarcinoma, in comparison with normal subjects, we found significant higher blood levels of hCG alpha subunits, gastrin and CEA and lower of melatonin, pepsinogen I and GH. The immunohistological results demonstrated CEA in both examined cases, alpha subunits in 2 of 6 (respectively in dysplasic areas and in surrounding non neoplastic mucosa) and enteroglucagon in 1 of 3 (dysplasic areas). Our results indicate that none of the parameters we examined, because of their non-specificity or of the low incidence of their modifications, can be considered a marker of gastric adenocarcinoma.

Effect of metergoline on serum prolactin stimulated by TRH.

The PRL response to TRH was evaluated before and after acute administration of metergoline, an antiserotonin drug, in healthy subjects. The drug was given to two groups of 6 subjects each, at the dose of 4 and 8 mg respectively, either po or by im route. Metergoline significantly inhibited the PRL response to TRH; no significant difference was found between the two doses and the administration routes. Although these findings suggest that the drug may directly inhibit lactotropic cells, an action of metergoline on central nervous system to stimulate PIF or to inhibit PRF release cannot be ruled out, and might as well explain the inhibition of the PRL response to TRH.

Differences in cortisol, aldosterone and testosterone responses to ACTH 1-17 administered at two different times of day.

The effects of 100 micrograms, i.m. of the analog ACTH 1-17 administered at 0800 and 1800 on the secretion of cortisol, aldosterone and testosterone have been studied in normal subjects: 8 male and 8 female. The group as a whole and the males had significantly greater absolute and percent increments in plasma cortisol after administration at 1800. In the females, there was only a greater percent increment in cortisol after the evening administration. The heptadecapeptide always significantly stimulated serum aldosterone, with no difference between the two times of administration. In the females, ACTH 1-17 significantly stimulated testosterone, with a more protracted secretion after the evening administration. In the males, there was always a significant testosterone decrease after the administration of the drug, with no difference between morning and evening. In conclusion, 100 micrograms i.m. of the analog ACTH 1-17 stimulates cortisol secretion more when given during the circadian nadir of plasma cortisol, but only in men. ACTH 1-17 increases testosterone in women and decreases it in men, whereas it seems to increase aldosterone secretion in both sexes.

Nomifensine, TRH and insulin-induced hypoglycemia tests in the diagnosis of prolactinomas.

Nomifensine, TRH and insulin-induced hypoglycemia tests were carried out in 37 cases of hyperprolactinemia: 25 were due to PRL-secreting pituitary tumors, 6 cases to GH and PRL-secreting pituitary tumors and 6 to pituitary and suprasellar non secreting tumors. Nomifensine failed to suppress the serum PRL in all subjects and PRL responses to TRH and insulin-induced hypoglycemia were impaired in all patients, irrespective of the origin of hyperprolactinemia. The uniform pattern of PRL response to the above tests in patients with hyperprolactinemia of variable etiology suggests that none of them is specific for prolactinomas.