Primary early onset dysthymia, biochemical correlates of the therapeutic response to fluoxetine: I. Platelet monoamine oxidase and the dexamethasone suppression test.

A subgroup of primary dysthymic patients have been reported to respond to traditional antidepressants and, more recently, to the newer serotonergic agents. Two putative biological markers of affective illness, platelet monoamine oxidase (MAO) activity and plasma cortisol levels following dexamethasone administration, were explored for their diagnostic and predictive potential in dysthymia. Compared to controls, patients had significantly lower platelet MAO activity. Among patients, those that responded to treatment with the serotonergic agent, fluoxetine, had lower pretreatment MAO activity than nonresponders. Higher pretreatment plasma cortisol levels following dexamethasone were also associated with a positive treatment response to this medication. These findings support the view that there is a biological substrate for some subgroups of dysthymics. This biological component may involve the hypothalamic pituitary adrenal axis and serotonergic system(s).