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Objective: Influenza epidemics can have consequences in terms of morbidity and mortality for the patients. This work assesses influenza outbreaks in order to validate and optimize alert and control measures in a psychiatric hospital., Method: The prospective monitoring of influenza episodes was conducted for 8 years in 19 units of a mental health hospital. Rapid influenza diagnostic tests were used. The study of the episodes with confirmed influenza cases was carried out., Results: Influenza monitoring and alert were essential with information and laboratory-confirmed cases. Influenza was common with a total of 20 episodes for the studied period. A maximum of 25% (5/20) of the units were affected in 2008-2009. Rapid influenza diagnostic tests allowed a quick identification with an average time of 1.5 days. Mainly, control measures limited the spread of the influenza virus in units with patient not at high risk of complications. On the other hand, antiviral curative treatment and chemoprophylaxis are essential in units with patients at high risk of complications., Conclusion: In a psychiatric hospital, influenza management has to take into account the exposed patient's risks for influenza complications and to adapt the strategy according to the risks identified., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Tropisetron and ondansetron, which are potent and selective 5-hydroxytryptamine (5-HT3) receptor antagonists, were both metabolized by human liver microsomes to several metabolites. These metabolites include the major metabolites found in humans, which are the 5-, 6-, and 7-hydroxy tropisetron and the 7- and 8-hydroxy ondansetron. The cytochrome P-450 (CYP) 2D6 inhibitor quinidine (1 microM) reduced the hydroxylation of tropisetron (67%) and ondansetron (18%). Confirmation of CYP2D6 involvement in the hydroxylation of tropisetron and ondansetron was obtained by the formation of these metabolites in recombinant V79 cells expressing human CYP2D6. The CYP3A substrate/inhibitor, cyclosporine A (CsA) had little effect on tropisetron hydroxylation (< 10%), whereas CsA and triacetyloleandomycin reduced ondansetron 7- and 8-hydroxylation up to 27%. Substrates for CYP1A (phenacetin and acetanilide), CYP2C (mephenytoin), and CYP2E (chlorzoxazone) had negligible inhibitory effects on the hydroxylation of either tropisetron or ondansetron. For the CYP2D6-dependent O-demethylation of dextromethorphan, tropisetron and ondansetron were competitive inhibitors with Ki values of 14 and 29 microM, respectively. The CYP3A specific metabolism of CsA was also competitively inhibited by tropisetron (Ki = 2.1 mM) and ondansetron (Ki = 31 microM). Other metabolites, which are only minor in vivo were also inhibited by CsA, 47-60% for tropisetron metabolism and 43% for ondansetron metabolism. To summarize, this study has identified the involvement of CYP2D6 in the formation of the hydroxylated metabolites of tropisetron and ondansetron and in addition of CYP3A in ondansetron hydroxylation. Because these are the major pathways in vivo, coadministration of drugs competing for CYP2D6 and possibly CYP3A4 could influence the human kinetics of tropisetron and ondansetron.