Oral Presentation Annual Meetings of the Endocrine Society of Australia and Society for Reproductive Biology and Australia and New Zealand Bone and Mineral Society 2016

Dopa-testotoxicosis: a novel drug toxicity of dopamine agonists in male prolactinoma patients (#128)

Sunita MC De Sousa 1 2 3 , Ian M Chapman 2 4 , Henrik Falhammar 5 6 7 , David J Torpy 2 4
  1. Hormones and Cancer Group, Cancer Division, Garvan Institute of Medical Research, Sydney, NSW, Australia
  2. Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA, Australia
  3. SA Adult Genetics Unit, Royal Adelaide Hospital, Adelaide, SA, Australia
  4. School of Medicine, University of Adelaide, Adelaide, SA, Australia
  5. Menzies School of Health Research, Royal Darwin Hospital, Darwin, NT, Australia
  6. Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
  7. Department of Endocrinology, Metabolism and Diabetes, , Karolinska University Hospital, Stockholm, Sweden

Background: Impulse control disorders (ICD) including gambling, hypersexuality, compulsive shopping and binge eating have recently been recognised as side effects of dopamine agonists (DAs). The vast majority has been described in the treatment of Parkinson’s disease and restless legs syndrome where pathological gambling is the predominant DA-associated ICD (1). Little is known about the nature of ICDs in the prolactinoma setting where endocrine factors, specifically testosterone fluctuations, may influence behaviour (2). Methods: We performed a multicenter retrospective cohort study of eight men who developed hypersexuality following initiation of DA therapy for prolactinomas. Results: The men had no prior history of psychiatric disease, but each developed disruptive hypersexuality with manifold consequences, including relationship discord, financial loss, reduced work performance, and illicit activity. Two men also developed pathological gambling. Cabergoline, bromocriptine and quinagolide were all implicated. The onset of hypersexuality ranged from days to years after DA commencement. Some men notably had normal pre-treatment testosterone levels, however these values were in the lower half of the reference range and rose into the upper half with DA initiation suggesting they had relative hypogonadism at baseline. Six men received no androgen replacement and increases in testosterone were solely attributable to DA therapy. Prolactin and testosterone consistently improved to be close or within the reference range by the time of symptom onset. Symptoms were reversible with DA cessation. Conclusions: We hypothesise that this phenomenon is due to synergy between mesolimbic reward pathway stimulation by DAs, together with rapid restoration of the eugonadal state after prolonged hypogonadism. We refer to this unique drug toxicity as ‘dopa-testotoxicosis’. The condition is likely under-reported due to the highly personal nature of the symptoms and we suggest a simple written questionnaire to screen for it. Treatment will generally include cessation of DAs in affected men, and often pituitary surgery for prolactinoma resection.

  1. Moore TJ, Glenmullen J, Mattison DR. Reports of pathological gambling, hypersexuality, and compulsive shopping associated with dopamine receptor agonist drugs. JAMA Intern Med. 2014;174(12):1930-3.
  2. Andela CD, Scharloo M, Pereira AM, et al. Quality of life (QoL) impairments in patients with a pituitary adenoma: a systematic review of QoL studies. Pituitary. 2015;18(5):752-76.