Biomedical subjects

F Baronti

Publications and source records attributed to F Baronti.

21 records · Page 2Linked to original sources

PubMed1986

The role of MAO-b inhibitors in the treatment of Parkinson's disease.

The classical treatment of Parkinson's disease (PD) using L-dopa plus a peripheral decarboxylase inhibitor (DI) often leads after 3-5 years to the onset of the so-called long-term L-dopa syndrome (LTS). LTS could depend on the chronic overload of L-dopa + ID and could be due to a consequent "receptor disease" and derangement of the neuronal functionality mainly in regard to the enzymatic chains, storage mechanisms and hyperactivity of the monoamine oxidase type B (MAO B). Deprenyl is a selective MAO-B inhibitor thought to be able to slow down the catabolism of dopamine and therefore to allow a decrease of the therapeutic regimen of L-dopa while in the meantime to obtain a more stable plasma and tissue levels and a constant therapeutic response. 76 parkinsonian patients were studied. Their L-dopa regimen was halved and 10 days after (-)deprenyl was added. After the decrease of L-dopa therapy a worsening of symptomatology was observed as expected. The association with (-)deprenyl was able to reverse this trend and when the inhibition of MAOB was really effective patients showed an improvement of symptoms even when compared to baseline values. No relevant side effects were observed and no patients dropped out.

Adult↗

PubMedDate not supplied

Growth hormone secretion in Alzheimer's disease: 24-hour profile of basal levels and response to stimulation and suppression studies.

The 24-h growth hormone secretory pattern and GH response to growth hormone releasing hormone, the alpha 2-adrenoceptor agonist clonidine and the somatostatin-analogue SMS 201-995 were evaluated in 9 patients with Alzheimer's disease and 9 age- and body body-matched control subjects. The secretory profile did not differentiate between patients and controls. Both secreted the largest amount of GH during the early nighthours between 22.00-02.00, whereas the majority of daytime GH levels were below the assay's detection limit (0.4 ng/ml). No difference was found in GH response to GHRH between patients and controls. All subjects showed significantly enhanced GH secretion after GHRH. Dividing the patients into two groups according to age-of-onset (less than 60 years greater than), there was a trend toward larger GH responses to GHRH for the early-onset group. No other parameter differentiated the groups. GH levels after clonidine were blunted in all subjects but one AD patient, probably due to an age-dependent attenuation frequently observed in subjects over 45 years of age. Finally, the administration of the somatostatin-analogue did not render conclusive results, since spontaneous decline of GH concentration was already beginning 2 hours before the drug was given and continued steadily throughout the observation period. In conclusion, patients with only mild to moderate degree of Alzheimer's disease have no prominent changes in GH regulation.

Aged↗

PubMedDate not supplied

[Changes in the nigrostriatal dopamine receptor compartment after continuous dopaminergic infusions in Parkinson disease].

Motor fluctuations often complicate chronic levodopa treatment of Parkinson's disease. Pharmacologically, these phenomena are characterized by a progressive shortening of the duration of action of levodopa and a gradual narrowing of the range of "optimally effective" doses, able to improve parkinsonian akinesia without inducing abnormal involuntary movements. The effects of a continuous intravenous infusion of levodopa lasting 9 +/- 0.3 days on these clinical-pharmacological indices have been studied in 12 parkinsonian patients. Continuous infusion therapy gradually ameliorated motor fluctuations by more than 40%, and this improvement lasted for at least 6 days after resuming standard oral therapy. Moreover, levodopa duration of action was prolonged by about 30%, and the range of "optimally effective" dose was widened by about 50%. The above data suggest the possibility of plastic modifications of the pathogenetic mechanisms underlying motor fluctuations in Parkinson's disease, and a potential deleterious effect of intermittent oral therapy. Consequently, continuous dopaminergic stimulation, when used in the early stages of the disease, might theoretically have a prophylactic role on the development or worsening of motor fluctuations.

Aged↗