Borderline personality disorder and polycystic ovary syndrome

In their letter to the editor, Trisno et al., (2016) have presented a highly informative case history in which borderline personality disorder (BPD) was associated with polycystic ovary syndrome (PCOS). The PCOS was diagnosed when the patient was found to have raised serum testosterone, lowered sex hormone binding globulin, low oestradiol levels and a raised fasting glucose level. Oestrogen and progesterone supplements, along with metformin, produced substantial improvement in the patient’s mental state, after a poor response to appropriate treatment with medications and Dialectical Behaviour Therapy. It is significant that she reported exacerbation of her affective symptoms and drive to self-harm premenstrually, when oestrogen and progesterone levels were falling.

The authors noted reports of an association of PCOS with personality disorders (including BPD) and emotional/behavioural difficulties. Apart from the significance of disruption of gonadal hormones in BPD mentioned by the authors, other hormones such as oxytocin, liothyronine, cortisol and prolactin have been implicated in BPD. The role of oestrogen and progesterone in this disorder remains uncertain, but the female preponderance in BPD strengthens this association. The addition of an oral contraceptive may aggravate elements of the clinical state and fluctuations in oestrogen levels appear more significant than the absolute levels (DeSoto et al., 2003).

Clinically, families and other observers of patients with BPD report that signs of emotional dysregulation, relationship difficulties and negative self-perception appear to begin after puberty and then develop into the personality disorder diagnosable after the age of 18 years. The major changes in gonadal hormones during puberty again suggest that they may carry a significant role in the nature of BPD, particularly because the levels are changing. Perhaps the childhood abuse so common in BPD might also contribute to dysregulation of gonadal hormone release, reminiscent of the alterations in hypothalamic–pituitary–adrenal (HPA) axis function (Zimmerman and Choi-Kain, 2009).

BPD is also known to have a significant association with bipolar disorders (Bassett, 2012), and disruptions of gonadal hormone regulation (including oestrogen) have also been identified in bipolar disorders (Kenna et al., 2009; Meinhard et al., 2014).

In the case reported by Trisno et al., we do not know whether the addition of oestradiol, progesterone and metformin would have been effective without the previous treatments, nor do we have the benefit of subsequent observations to assess the persistence of improvement over time. However, their observations of this patient are of considerable interest for understanding the pathophysiology of BPD and for options in treatment. BPD is a very serious disorder, and our current management options are of limited value. Further clinical observation and research into the role of gonadal hormones in BPD could be very productive.

See Letter by Trisno et al., 50(4): 385.