Biomedical subjects
Publications and source records attributed to A Rocco.
A patient with a completely calcified chromophobe adenoma is reported. Endocrine evaluation revealed very high prolactin levels. Such extensive calcifications in prolactin-secreting adenomas are extremely rare. The possible pathogenetic mechanisms of this association are discussed.
Bovine brain phospholipid liposomes (BC-PL) reduce plasma prolactin (PRL) levels in humans after acute administration and counteract the metoclopramide- and sulpiride-induced hyperprolactinaemia. However, BC-PL, like nomifensine, a dopamine (DA) reuptake inhibitor and therefore an indirect dopaminergic compound, does not influence TRH-induced hyperprolactinaemia. Moreover, BC-PL and nomifensine reduce plasma PRL levels in hyperprolactinaemic PCO syndromes but not in PRL secreting pituitary adenomas. The results obtained indicate that BC-PL antagonizes the DA blockade-induced hyperprolactinaemia and that the main site of action of BC-PL seems to be at the hypothalamic level; however a concomitant pituitary effect cannot be ruled out.
Plasma prolactin (PRL) levels modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. The data gathered indicate that benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. It is not possible to exclude, however, that benserazide could exert its biological activity through the production of active metabolites in vivo.
The effect of sauvagine (SAU), a frog skin peptide, on prolactin (PRL) levels was studied in vivo and in vitro. Subcutaneous administration of SAU (20 micrograms/kg) reduced plasma PRL levels in normal adult male rats and suppressed the suckling-induced rise of PRL in lactating rats even at doses of 1 and 5 micrograms/kg. Perfusion of isolated and dispersed rat pituitary cells in vitro with increasing doses of SAU (from 5 x 10(-10) to 1.7 x 10(-8)M) induced a significant dose-related decrease of PRL secretion in the eluate. These results indicate that SAU is a potent PRL inhibiting factor and that its action is exerted at the pituitary level. If SAU or a SAU-related peptide is present in the mammalian brain, it can be tentatively hypothesized that this peptide plays an important role in the control of PRL secretion.
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Circadian rhythms of prolactin have been evaluated in thirteen untreated parkinsonian patients before and after 15 days of treatment with L-Dopa + carbidopa. The 24th secretory pattern was not significatively different from that observed in controls. The L-Dopa + carbidopa therapy does not change the basal circadian prolactin (PRL) rhythm. These results suggest that the tubero-infundibular dopaminergic system (TIDA) and the PRL secretion are conserved in untreated parkinsonian patients (PP). During chronic L-Dopa + carbidopa therapy, the basal PRL levels, evaluated in 21 PP, showed a correlation with the severity of clinical features. The effects of single doses of apomorphine, bromocriptine, lisuride and haloperidol, were studied on serum levels of PRL in 21 PP divided in two groups of "responders" and "non-responders". Haloperidol induced an enhancement of serum PRL; the dopaminergic drugs, apomorphine, bromocriptine and lisuride inhibited basal PRL secretion. It seems that the TIDA system, in Parkinson disease is not significatively altered, even though presenting a remarkable slower response in "non-responders" to L-Dopa therapy. We also evaluated the effect of L-Dopa, L-Dopa + carbidopa, bromocriptine, lisuride, nomifensine and deprenyl on growth hormone secretion in six PP. The endocrine effects of dopaminergic drugs show a mild rise in comparison with controls suggesting an important alteration in the dopamine (DA) control of growth hormone (GH).
Ten normoprolactinemic and 10 hyperprolactinemic patients, all with polycystic ovary syndrome (PCO), were subjected to prolactin (PRL) stimulatory tests with thyrotropin-releasing hormone (TRH), 200 microgram intravenously, and haloperidol (a dopamine-blocking agent), 1 mg intramuscularly. The results were compared with those of 8 women with idiopathic hyperprolactinemia and 10 normal female volunteers. Distinctive features of PCO were elevated plasma concentrations of luteinizing hormone, estrone, and testosterone in the presence of normal estradiol, whereas in idiopathic hyperprolactinemia estradiol was reduced. Both groups of patients with PCO exhibited responses to TRH and haloperidol significantly higher than the controls (P less than .001), whereas only the hyperprolactinemic PCO patients reacted with an excessive PRL discharge (P less than .001). As expected, the response to both secretagogue agents was blunted in patients with idiopathic hyperprolactinemia. The present report discusses the possible implication of estrogen and the dopaminergic system in the mechanisms leading to hyperprolactinemia and enhanced PRL release in PCO.
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Five clinically normal male volunteers were given metoclopramide, 10 mg t.d.s. for 6 weeks. During treatment prolactin concentrations were elevated (over 50 ng/ml) in all. LH, FSH, testosterone and cortisol concentrations were not altered. No change was observed in LH or FSH responses to LHRH testing 4 weeks after the beginning of therapy, compared with pre-treatment values. A reduction in seminal volume and total sperm count were observed in each subject. Four noticed a decrease in libido and three lost spontaneous erections. While the metoclopramide-induced hyperprolactinaemia could be the cause of the observed changes in semen and erectile activity, it is possible that this dopamine receptor blocking drug might directly affect central or peripheral mechanism of erection, the testes or accessory organs.
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Nowadays in the western countries, the Work Musculoscheletal Disorders (WMSDs) are the most relevant work-related diseases either for the large number of at-risk workers and for the high prevalence of cases among them. Among WMSDs, the Carpal Tunnel Syndrome (CTS) is considered a sentinel event in occupational medicine and epidemiological surveillance systems were set up to study its temporal occurrence and spatial spread. Surprisingly enough, in our country the epidemiology of the WMSDs is still unknown; although observations of important clusters of cases are increasing, these pathologies are still largely underreported by medical doctors. In the high industrialised province of Brescia, Northwestern Italy, only 1% of the 25.000 occupational disease, collected by the occupational medicine and prevention service of the National Health Service (SPSAL) since 1989 to 1997, were coded as WMSDs. Even if the notification of these work-related disorders is compulsory by low since 1973, up-to-now very few cases were reported to SPSALs, and consequently active prevention programs were very few too. For that reason, a project of active surveillance of WMSDs diagnosed on the general population was carried out to improve their identification and to evaluate the work-related etiological fraction as well as to address primary prevention projects. During 1997-1999 618 upper limb musculoskeletal disorders were collected from 2 orthopaedic hospital divisions where cases underwent surgical treatment. 369 of them were interviewed by telephone (253 female, 116 man) and 128 cases (34%) were classified as probable professionally exposed to some known hazard. Female were prevalent (71%), involved particularly in textile, garments, plastic, food production and domestic services. Among men, construction, metallurgic and mechanic were the more frequent jobs. 116 WMSDs were reported to the National Insurance Institute (INAIL). The collection of these WMSDs was the basis for specific communications to the firm manager(s) and to the factory's medical doctor(s) with the aim to make it easy: i) a good health surveillance to exposed workers; ii) a specific risk assessment; iii) carrying out prevention programs and adopting personal protection equipments. Some problems are focused concerning the underreporting of cases, the anamnesis information, the fate of interventions to face the problem in the workplaces. A possible implementation of this project is also discussed to avoid a WMSds surveillance unlinked prevention programs of occupational risks.
Cerebral toxoplasmosis is the most common cause of focal CNS disease complicating AIDS and its incidence ranges from 3% to 40% of such patients. This opportunistic infection is generally due to reactivation of chronic toxoplasmosis as a consequence of severe immune deficiency. We present the clinical, neuroradiological and immunological findings of 15 AIDS patients with cerebral toxoplasmosis. All patients had focal neurological signs. CT-scan (13 cases) and NMR (2 cases) showed single or multiple mass lesions and edema. Serum IgG anti-Toxoplasma antibodies were positive in 14 patients; CSF specific IgG were positive in 5 out of 7 studied patients, while serum and CSF specific IgM were negative in all subjects. The intrathecal synthesis of anti-Toxoplasma antibodies were high in all 7 patients. A presumptive diagnosis of cerebral toxoplasmosis is based on the focal cerebral signs and neuroradiological findings. It is more frequently confirmed by the improvement of the clinical and neuroradiological picture during the treatment with pyrimethamine-sulphadiazine or clindamycin.