Hospitalization of the suicidal patient.

The safety needs of the suicidal patient are of the utmost importance. Decisions concerning the admission of such patients into the hospital are often difficult, and clinicians usually are anxious and ambivalent during this process. In this era of decreased resources, when clinicians are increasingly aware of suicidal danger and of safety requirements, it is even more critical that the inpatient psychiatric unit be used judiciously. There are risks and benefits involved in the use of a psychiatric inpatient program, and there are risks and benefits to not using such a facility. Development of safe treatment plans for suicidal patients is reviewed in the context of the psychodynamic formulation and therapeutic alliance.

Does treatment with antidepressant medication increase suicidal behavior?

Suicidal ideation and behavior are commonly associated with psychiatric conditions, in particular the affective disorders. Patients diagnosed with Major Depression carry an estimated lifetime risk of suicide ranging from 15-30%. In recent years increasing attention has been paid to the psychobiology of suicide. Serotonin, an indolamine neurotransmitter, has been implicated as playing a role in suicidal behavior, especially in depressed patients. Treatment of depressive episodes with antidepressant medication has greatly improved the prognosis for survival through the suicidal period and recovery from the depressive episode. However, there has been considerable debate about the significance of reports that antidepressants may, on occasion, adversely affect depressed patients. Recently this has received much attention in the United States of America, particularly involving the antidepressant fluoxetine. In this paper we briefly outline previous studies on the role of serotonin in suicidal behavior in depression; and review the debate about antidepressants adversely affecting suicidal behavior. Possible mechanisms involving effects on the serotonergic system that could account for some of these adverse reactions are discussed, and a contextual framework is developed for interpreting clinical data on this important phenomenon.

Lack of erythrocyte superoxide dismutase change during human senescence.

Superoxide dismutase (SOD), widely distributed in aerobic organisms, catalyzes dismutation of the superoxide free radical, O2-, to oxygen and hydrogen peroxide and apparently protects against oxygen toxicity. In human erythrocytes, O2- arises from autoxidation of oxyhemoglobin and SOD activity is copper-dependent. Since human erythrocyte copper content has been reported to decline in the fifth decade of life, we investigated the age dependence of human erythrocyte SOD activity. The mean SOD activity, assayed by inhibition of epinephrine autoxidation, was 415 +/- 66 units/g cells or 50 +/- 11 units/mg non-Hb protein. No significant difference was observed between young and old adults, and no correlations were detected with sex, state of health of the donor, or with blood hemoglobin content. The lack of general decline of SOD activity with age narrows the possible mechanisms for an involvement of O2- in senescence. SOD may yet decline in other longer-lived tissues or, as suggested by Fridovich, a constant low level of damage may be caused by imperfect scavenging of O2- by SOD. If such a mechanism is operative, it appears not to affect synthesis of SOD in erythrocyte precursor cells into the eighth decade of human life.