Cortisol and prolactin responses to d-fenfluramine were measured in 10 drug-free normothymic patients with obsessive-compulsive disorder (OCD). The results were compared with these responses in 10 healthy controls and in 10 major depressives. The endocrine responses in OCD were significantly attenuated when compared to the healthy controls; however, the results were not specific to OCD as the depressives' responses were similarly blunted.

We report OCD and paraphilia in two male members of triplets (the two males being monozygotic twins), and discuss the possible aetiological factors for this previously unreported occurrence. We suggest that patients presenting with paraphilia should be examined for OCD and that a detailed sexual history should be obtained in all patients with OCD.

Service providers' views were congruent with each other, NICE guidelines and quality standards as proposed by the Royal College. Although clinicians feel that their service fulfils many practice guidelines, there remains areas in which adherence is felt to be lacking.

The growth hormone response to the acetylcholinesterase inhibitor pyridostigmine was measured in nine normothymic outpatients who met DSM-III-R criteria for obsessive-compulsive disorder. The responses were significantly elevated when compared to those found in a healthy comparison group (N = 9). The data suggest that cholinergic supersensitivity is present in obsessive-compulsive disorder.

The prolactin and thyroid‐stimulating hormone (TSH) responses to protirelin and the prolactin and cortisol responses to d‐fenfluramine were measured in 8 outpatients with DSM‐III‐R obsessive‐compulsive disorder (OCD). The results were compared to those in 8 age‐ and sex‐matched healthy controls. The responses to d‐fenfluramine were significantly attenuated in the OCD patients, but there was no significant difference between the responses to protirelin in OCD patients and healthy controls. The data suggest that, in OCD, blunting of prolactin responses to the serotonin‐releasing agent d‐fenfluramine is due to a central abnormality and not due to a pituitary deficit.