Dopa-testotoxicosis: disruptive hypersexuality in hypogonadal men with prolactinomas treated with dopamine agonists.
Dopamine agonists are the first line of therapy for prolactinomas, with high rates of biochemical control and tumour shrinkage. Toxicity is considered to be low and manageable by switching of agents and dose reduction. Dopamine agonist-induced impulse control disorders are well described in the neurology setting, but further data are required regarding this toxicity in prolactinoma patients. We performed a multicenter retrospective cohort study of eight men with prolactinomas and associated central hypogonadism. The eight men had no prior history of psychiatric disease, but each developed disruptive hypersexuality whilst on dopamine agonist therapy at various doses. Cabergoline, bromocriptine and quinagolide were all implicated. Hypersexuality had manifold consequences, including relationship discord, financial loss, reduced work performance, and illicit activity. We hypothesise that this phenomenon is due to synergy between reward pathway stimulation by dopamine agonists, together with rapid restoration of the eugonadal state after prolonged hypogonadism. We refer here to this distinct drug toxicity as 'dopa-testotoxicosis'. Given the profound impact in these patients and their families, cessation of dopamine agonists should be considered in men who develop hypersexuality, and pituitary surgery may be required to facilitate this. Awareness of this distinct impulse control disorder should enable further research into the prevalence, natural history and management of 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 hypersexuality and other behavioural symptoms within the first six months of dopamine agonist treatment.
Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia. Sunita.DeSousa@sa.gov.au.|SA Clinical Genetics Service, Women's and Children's Hospital, Adelaide, Australia. Sunita.DeSousa@sa.gov.au.|Hormones and Cancer Group, Garvan Institute of Medical Research, Sydney, Australia. Sunita.DeSousa@sa.gov.au.
Sunita M C
SM
De Sousa
Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia.|School of Medicine, University of Adelaide, Adelaide, SA, Australia.
Ian M
IM
Chapman
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.|Menzies School of Health Research, Royal Darwin Hospital, Darwin, Australia.|Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden.
Henrik
H
Falhammar
School of Medicine, University of Adelaide, Adelaide, SA, Australia.
David J
DJ
Torpy
D000328:Adult; D000368:Aged; D000634:Aminoquinolines / Q000009:adverse effects* / Q000627:therapeutic use; D001971:Bromocriptine / Q000009:adverse effects* / Q000627:therapeutic use; D000077465:Cabergoline; D018491:Dopamine Agonists / Q000627:therapeutic use*; D004873:Ergolines / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007006:Hypogonadism / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D010911:Pituitary Neoplasms / Q000188:drug therapy*; D015175:Prolactinoma / Q000188:drug therapy*; D012189:Retrospective Studies; D012735:Sexual Dysfunction, Physiological / Q000139:chemically induced*
D000634:Aminoquinolines; D018491:Dopamine Agonists; D004873:Ergolines; D001971:Bromocriptine; C046650:quinagolide; D000077465:Cabergoline
Dopamine agonists; Hypersexuality; Impulse control disorders; Prolactinoma