The symptoms of depression during the postpartum are not distinct from depressions occurring at other periods of life, and

the MEK inhibitor drugs temporal association of symptoms with the postpartum period is the critical diagnostic feature, similar to perimenopausal depression. PPDs are not associated with an abnormality of reproductive function143; nonetheless, women with a history of PPD display an abnormal mood Inhibitors,research,lifescience,medical response to changes in reproductive hormones simulating endocrine events occurring at delivery.144 Despite the absence of endocrine abnormalities in this condition, there has been interest in whether supplementing reproductive endocrine function during the immediate postpartum could prevent or diminish depression. Open studies of progesterone for the treatment of PPD were conducted by Dalton,145 who reported a reduced recurrence rate of postnatal depression in women using prophylactic progesterone compared with untreated women.146 Nonetheless, as with studies of progesterone in PMS, the absence of controlled trials examining the efficacy of progesterone Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical in PPD limited the utility of Dalton’s observations. In fact, one double-blind, placebocontrolled study of 180 postpartum women, treated

with either norethisterone enanthate or placebo, showed an increased risk of developing depressive symptoms following treatment with norethisterone.147 Thus, as with PMS, current evidence does not support a role for progesterone in the treatment of PPD. Similar to earlier reports of progesterone’s Inhibitors,research,lifescience,medical efficacy, an open trial in women at risk for puerperal psychosis demonstrated that high-dose

estrogen treatment resulted in a lower than expected 1-year relapse rate (9% compared with an expected 35%-60% without prophylaxis).148 Varying doses of estrogen (Premarin® ranging in dose from 0.625 Inhibitors,research,lifescience,medical to 10 mg per day or IV estradiol 25 mg every 8 hours) were administered immediately postpartum and then tapered over 4 weeks. It was suggested that estrogen administration could attenuate the rapid puerperal drop in estradiol levels, thereby reducing the negative impact of the postpartum “estrogen withdrawal state” on mood. In a follow-up study, Grégoire et al149 tested the suggestion that estradiol withdrawal caused PPD in a double-blind, placebo-controlled study of estradiol in 61 women who developed major Dichloromethane dehalogenase depression within 3 months of delivery. Eighty percent of the patients receiving estrogen patch experienced a significant reduction in depression severity after 3 months of treatment, compared with 31 % of the placebo-treated group. Reductions in mood symptoms on estrogen therapy were observed in women regardless of concurrent antidepressant use, and estrogen’s antidepressant effects were rapid and observed after 2 to 3 weeks of treatment. A similar rapid response to estradiol was also recently reported in an open-label trial of sublingual estradiol,150 similar to the timing of the response to estradiol in perimenopausal depression.