Immune Activation In Treatment Resistant Depression

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Nearly 30% of depressed patients fail to display an adequate response to psy-chopharmacological treatment and at least 60% fail to achieve complete remission (Fawcett, 1994; Hornig-Rohan and Amsterdam, 1994). Despite advances in psy-chopharmacological treatment the mortality and morbidity of this disorder render depression a major public health hazard in most countries.

The biological basis of treatment resistance in depression still remains unclear. Several lines of research have suggested that a variety of biological markers may be abnormal in treatment resistant depression (TRD). The study of these indices may enhance our understanding of why some patients do not respond to conventional treatment, and may help identify which therapies might be successful for particular patients or groups of patients.

There are findings that suggest the involvement of HPA axis hyperactivity in the pathogenesis of TRD. Christiansen et al. (1989) found poor response to antidepressant treatment in major depressed patients with high spontaneous Cortisol levels. Others (Mc Leod, 1972; Amsterdam et al., 1983, 1994) observed a poor response to tricyclic antidepressants in patients displaying pathological responses on the dexametha-sone suppression test (DST). Moreover, the findings of Murphy et al. (1991) and of

Amsterdam et al. (1994) suggested that steroid suppressive treatment may be of some efficacy in TRD patients with persistent abnormality of HPA axis.

There are a few existing studies which suggest that TRD is accompanied by a very pronounced apr (e.g. Sluzewska et al., 1995b, 1996a, 1997a; Van Hunsel et al., 1996).

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