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Although prednisone is often described as the main corticosteroid involved, other members of the steroid family can also cause psychosis, which has been described at low doses (1 mg/kg body weight) (19), and as high doses (≥7 mg/kg body weight, 20). Other agents used to treat depression, including moclobemide, gabapentin, and risperidone, cause a similar increase in serum corticosteroids (21), which explains the high rate of psychosis in these patients. Treatment with anastrozole and fluoxetine also decreases the level of cortisol and the levels of 5-hydroxytryptamine (5-HT) receptors, as well as increases the levels of the tryptophan, melatonin, thymol and tryptophan hydroxylase enzymes (22,23). The clinical effect of these drugs on the serotonin system is relatively unclear (24), but is thought to be mediated mainly through 5-HT3 receptor antagonizing agents (25). In addition, they increase the levels of tryptophan hydroxylase, which may explain the apparent shift in the time of fluoxetine treatment (24) and other possible symptoms related to 5-HT3 receptor antagonists (26). The pathogenesis of depressive illness remains largely unknown. Early studies found that chronic fluoxetine treatment was associated with a higher risk of depression in women and children (27). Several studies were conducted since then to investigate whether fluoxetine is causally associated with the emergence of symptoms during depressive illness. These studies have led to a number of hypotheses. One of the first was the idea that depression may be a consequence of oxidative stress and/or lipid peroxidation leading to mitochondrial malfunction. Although this could have some support, and there is now convincing evidence for the metabolic defects in animal models of depression associated with oxidative stress, a significant effect of fluoxetine on the rate of progression could not be established if this effect was indeed causal. However, other studies that used antidepressant with a high molecular weight formulation have failed to confirm that fluoxetine causes depressive symptoms (28), even when compared with a placebo (29). The effect of fluoxetine on the rate of progression of depressive symptoms is further complicated by the fact that other agents that cause both depressive symptoms and an increase in 5-HT levels have been found to decrease the rate of depression (30–32). Thus, it may be that other members of the serotonin syndrome, such as clomipramine, fluphenazine, and tryptophan hydrox Similar articles:

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