XXXX and mortality.

@entity1 @entity308 @entity4697 @entity734 @entity65
Evidence so far indicates two sources for excess mortality in @entity4697 --suicide and @entity65 . The risk for eventual suicide may rival that for primary @entity308 , but the predictors and the necessary antecedents probably differ. The lapse between diagnosis and suicide may be larger for @entity4697 , and complications such as secondary @entity308 and @entity734 may be necessary. There are few well-established predictors for primary @entity308 despite many relevant studies. The risk for suicide in @entity4697 is barely recognized, and established predictors are accordingly remote. One study has demonstrated excess @entity65 among males with @entity4697 , and another from the same center has provided weak support. Only one additional study has provided the necessary detail as to sex and cause, and those findings were quite supportive, although the subjects may have been mixed diagnostically. There are numerous feasible explanations for excess @entity65 in @entity4697 and even some reason to believe that successful treatment might lessen it. To so advise @entity1 would be not only premature at this point but unnecessary and countertherapeutic--unnecessary because these @entity1 are motivated by discomfort to seek treatment and countertherapeutic because @entity65 is what many of these @entity1 pathologically fear. Rather, the findings suggest focus for future study. The initial findings of excess @entity65 in males badly need replication, as do the more recent findings of Kahn et al. Likewise, animal models may reveal some of the pathophysiologic mechanisms at work. It is hoped that these efforts will converge in the not-too-distant future.
