[Predicting length of stay in Italian Psychiatric Forensic Hospitals: a survival analysis]. / I fattori predittivi della durata di degenza in Ospedale Psichiatrico Giudiziario: un'analisi di sopravvivenza.

UNLABELLED: Admission to an Italian Forensic Hospital (OPG) results in formal exit from psychiatric care provided by NHS community based psychiatric services. The length of stay in such facilities is often perceived as a factor negatively affecting the opportunity for reintegration in the community. METHOD: Factors predicting length of stay in OPG were investigated by means of a survival analysis carried out on a cohort of 118 inmates of three OPGs (Castiglione delle Stiviere, Reggio Emilia and Montelupo Fiorentino), who represent the whole forensic population from 3 different geographical areas at 30.06.97; all discharges occurred in the following 18 months were examined. RESULTS: In survival analyses conducted on individual predictors, five variables predicted a longer stay: type of offenses (homicide: 706.6 weeks vs. 307.1 for minor offenses and 194.7 for grievous bodily harm, log-rank = 31.8, p < 0.001), type of admission (RR = 0.98, CI 95% 0.97-0.99, p < 0.001), the diagnosis of schizophrenia (621.9 weeks vs. 398.9 weeks or less for other diagnoses; log rank = 9.08, df = 3, p = 0.028), BPRS thought disturbance score (RR = 0.89, CI 98% 0.81-0.98, p < 0.01), hospital of stay (314.6 weeks in Montelupo Fiorentino vs. 706.6 for Reggio Emilia and 621.9 for Castiglione delle Stiviere; log-rank = 9.64, df = 2, p < 0.001). In a Cox linear regression model three significant factors were selected: type of offenses stype of admission, diagnosis of schizophrenia. CONCLUSIONS: Judicial factors are relevant in determining the length of stay in OPG. The diagnosis of schizophrenia seems to play an independent role in predicting a longer stay.

Inhibition by azelastine of the effects of platelet-activating factor in lungs from actively sensitised guinea-pigs.

The effect of azelastine on platelet-activating factor (PAF)-induced bronchoconstriction and mediator release in isolated lungs from actively sensitised guinea-pigs was investigated. Guinea-pigs were actively sensitised with two s.c. injections of 10 micrograms ovalbumin in 1 mg Al (OH)3 at a 2-week interval. One week after the second injection, the lungs were removed and challenged intra-arterially with PAF or arachidonic acid. In some experiments lungs from non-immunised guinea-pigs were injected with PAF or histamine. Bronchoconstriction, the release of thromboxane (TX)B2 or leukotriene (LT)-like material and the histamine content of the effluent were evaluated. Azelastine was given s.c. at 10 or 100 micrograms/kg, 4 h before lung removal. Azelastine (100 micrograms/kg) did not inhibit PAF-induced bronchoconstriction and mediator release from lungs from non-immunised guinea-pigs. In contrast, the hyperresponsiveness to 1 ng PAF observed in lungs from actively sensitised animals was dose dependently inhibited by azelastine. Azelastine did not reduce the histamine-induced bronchoconstriction and consequent TXB2 release from lungs from immunised guinea-pigs, indicating that the protective effect exerted against hyperresponsiveness to PAF was not due to histamine antagonism. Azelastine also reduced arachidonic acid-induced bronchoconstriction and LT-like material release from sensitised lungs, regardless of the presence of indomethacin. These results suggest that inhibition of lung hyperresponsiveness to PAF by azelastine may result from an interference with leukotriene synthesis.