8 1998 Martin Dunitz Ltd
International Journal of Psychiatry in Clinical Practice 1998 Volume 2 Pages 147- 148
147
Cyproterone acetate and striae
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of North Carolina on 11/06/14 For personal use only.
DAMIAN MOHAN’, RICHARD TAYLOR~AND JAMES A MACKEITH3 ’Lecturer in Forensic Psychiatry, Broadmoor Hospital and University of Southampton; ’Senior Renslrar and 3Consultant Forensic Psychiatrist, Denis Hill Unit, Maudsley Hospital, London
I
Correspondence Address Dr Damian Mohan, Professonal Unit, Richard Dadd Centre, Broadmoor Hospital, Crowthorne, Berks, RG45 7EG, UK E-mail: [email protected]
Received 19 November 1997; accepted for publication 22 December 1997
I
CASE REPORT
DISCUSSION
We report the development of multiple disfiguring striae in a 22-year-old man with a diagnosis of Asperger’s syndrome, who was given the antilibidinal drug cyproterone acetate. He was detained in hospital on a restriction order, having been convicted of indecent assault of two children. There was poor compliance with a behavioural programme and psychological therapies over a period of 19 months, and there was little evidence to suggest that these interventions were of benefit. So, after giving his informed consent in the presence of a solicitor, the patient was commenced on cyproterone acetate 50 mg twice a day. A response was noted, in that he reported no sexual arousal whatsoever. Four months after treatment commenced, there was a marked decrease in his arousal as measured by penile plethysmography. Six months after treatment commenced, pink striae were observed over his abdomen, on the back of his shoulders and on his thighs. (See Figures 1 and 2.) He had no previous history of dermatological problems. In addition to the development of striae, he was also found to have some gynaecomastia. One of his liver enzymes, alanine aminotransferase,rose to 54 IUA (normal range 7 - 40). The cyproterone was discontinued, since when he reported a slight increase in his level of sexual arousal. An endocrine opinion was sought. Cushing’s syndrome was excluded by a dexamethasone test. LH, FSH, testosterone and sex-hormone-binding globulin were all found to be within normal limits. A consultant from the endocrine clinic was at a loss to explain the abdominal striae.
Striae or ‘stretch marks’ have the appearance of atrophic skin which is initially pinkish in colour, passing through a phase of angry red or purple and generally fading to white. These are common benign clinical phenomena of uncertain aetiology. They are typically seen during pregnancy; in adolescence; in Cushing’s disease; following rapid weight gain; following debilitating infection; and following prolonged adrenal corticosteroid therapy. It is thought that elevated steroid hormone levels may have an effect on skin elasticity, giving rise to a predisposition to striae formation in the presence of other mechanical factors such as rapid weight gain. Young adults are thought to be more susceptible, due to differences in collagen.’ In a study of striae thought to occur secondary to neuroleptic treatment: it was found that younger patients who were overweight before treatment and who then gained weight during neuroleptic treatment were especially prone to striae formation. Our patient’s weight had increased from 76 kg to 101 kg over a period of approximately one year while he was in hospital, following an increase in consumption of high-calorie foods while he was detained on a medium secure unit. It was noted that he was gaining weight before treatment started. The pharmaceutical manufacturers were contacted. They knew of no reports of the occurrence of striae in patients who were prescribed cyproterone acetate, either in their own internal database of adverse events or the on-line databases of Medline and Excerpta Medica.
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of North Carolina on 11/06/14 For personal use only.
148
D Mohan et a1
CONCLUSION In this patient, the development of striae occurred shortly after the commencement of cyproterone acetate. The other factor that may have been assbciated with the development of the striae is the patient’s weight gain. From this case study it is not possible to distinguish which of the above factors was of greater aetiological significance, or indeed, if these factors are collectively of aetiological significance,but we consider that these associations warrant reporting. Striae are unsightly, and their development in this case necessitated stopping the cyproterone acetate. The patient found the disfiguration distressing. Given that this
1. Schuster S (1979) The cause of striae distensae. Acta Derm Venereol 59: 161-9.
medication appeared to be the only method of treatment that was lowering his libido, its discontinuation has had an adverse effect on his progress.
2. Hinson J, Sumway M, Yadalam K et a1 (1992) Cutaneous striae in neuroleptic treatment. Ann Clin Psychiatry 4: 221 - 5.
International Journal of Psychiatry in Clinical Practice 1998 Volume 2 Pages 147- 148
147
Cyproterone acetate and striae
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of North Carolina on 11/06/14 For personal use only.
DAMIAN MOHAN’, RICHARD TAYLOR~AND JAMES A MACKEITH3 ’Lecturer in Forensic Psychiatry, Broadmoor Hospital and University of Southampton; ’Senior Renslrar and 3Consultant Forensic Psychiatrist, Denis Hill Unit, Maudsley Hospital, London
I
Correspondence Address Dr Damian Mohan, Professonal Unit, Richard Dadd Centre, Broadmoor Hospital, Crowthorne, Berks, RG45 7EG, UK E-mail: [email protected]
Received 19 November 1997; accepted for publication 22 December 1997
I
CASE REPORT
DISCUSSION
We report the development of multiple disfiguring striae in a 22-year-old man with a diagnosis of Asperger’s syndrome, who was given the antilibidinal drug cyproterone acetate. He was detained in hospital on a restriction order, having been convicted of indecent assault of two children. There was poor compliance with a behavioural programme and psychological therapies over a period of 19 months, and there was little evidence to suggest that these interventions were of benefit. So, after giving his informed consent in the presence of a solicitor, the patient was commenced on cyproterone acetate 50 mg twice a day. A response was noted, in that he reported no sexual arousal whatsoever. Four months after treatment commenced, there was a marked decrease in his arousal as measured by penile plethysmography. Six months after treatment commenced, pink striae were observed over his abdomen, on the back of his shoulders and on his thighs. (See Figures 1 and 2.) He had no previous history of dermatological problems. In addition to the development of striae, he was also found to have some gynaecomastia. One of his liver enzymes, alanine aminotransferase,rose to 54 IUA (normal range 7 - 40). The cyproterone was discontinued, since when he reported a slight increase in his level of sexual arousal. An endocrine opinion was sought. Cushing’s syndrome was excluded by a dexamethasone test. LH, FSH, testosterone and sex-hormone-binding globulin were all found to be within normal limits. A consultant from the endocrine clinic was at a loss to explain the abdominal striae.
Striae or ‘stretch marks’ have the appearance of atrophic skin which is initially pinkish in colour, passing through a phase of angry red or purple and generally fading to white. These are common benign clinical phenomena of uncertain aetiology. They are typically seen during pregnancy; in adolescence; in Cushing’s disease; following rapid weight gain; following debilitating infection; and following prolonged adrenal corticosteroid therapy. It is thought that elevated steroid hormone levels may have an effect on skin elasticity, giving rise to a predisposition to striae formation in the presence of other mechanical factors such as rapid weight gain. Young adults are thought to be more susceptible, due to differences in collagen.’ In a study of striae thought to occur secondary to neuroleptic treatment: it was found that younger patients who were overweight before treatment and who then gained weight during neuroleptic treatment were especially prone to striae formation. Our patient’s weight had increased from 76 kg to 101 kg over a period of approximately one year while he was in hospital, following an increase in consumption of high-calorie foods while he was detained on a medium secure unit. It was noted that he was gaining weight before treatment started. The pharmaceutical manufacturers were contacted. They knew of no reports of the occurrence of striae in patients who were prescribed cyproterone acetate, either in their own internal database of adverse events or the on-line databases of Medline and Excerpta Medica.
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of North Carolina on 11/06/14 For personal use only.
148
D Mohan et a1
CONCLUSION In this patient, the development of striae occurred shortly after the commencement of cyproterone acetate. The other factor that may have been assbciated with the development of the striae is the patient’s weight gain. From this case study it is not possible to distinguish which of the above factors was of greater aetiological significance, or indeed, if these factors are collectively of aetiological significance,but we consider that these associations warrant reporting. Striae are unsightly, and their development in this case necessitated stopping the cyproterone acetate. The patient found the disfiguration distressing. Given that this
1. Schuster S (1979) The cause of striae distensae. Acta Derm Venereol 59: 161-9.
medication appeared to be the only method of treatment that was lowering his libido, its discontinuation has had an adverse effect on his progress.
2. Hinson J, Sumway M, Yadalam K et a1 (1992) Cutaneous striae in neuroleptic treatment. Ann Clin Psychiatry 4: 221 - 5.
