Prolactin response to d-fenfluramine in obsessive-compulsive patients, and outcome of fluvoxamine treatment

1997 ◽  
Vol 170 (6) ◽  
pp. 554-557 ◽  
Author(s):  
Palmiero Monteleone ◽  
Francesco Catapano ◽  
Stefania Dl Martino ◽  
Ciro Ferraro ◽  
Mario Maj
Keyword(s):  
Depressive Symptomatology ◽  
Plasma Prolactin ◽  
Healthy Controls ◽  
Obsessive Compulsive ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Compulsive Disorder ◽  
Before And After ◽  
Prolactin Response ◽  
Drug Free

BackgroundAlthough several studies have directly explored serotonin (5-HT) transmission in patients with obsessive compulsive disorder (OCD), their results have been inconsistent and their clinical relevance is doubtfulMethodAccording to a double-blind placebo-controlled design, plasma prolactin (PRL) response to a specific serotonergic probe, d-fenfluramine, was measured in 20 drug-free obsessive compulsive patients and in 20 matched healthy controls. After the neuroendocrine test, 5 patients completed a lO-week treatment with fluvoxamine. Psychopathological assessment was performed before and after therapy.ResultsPRL response in OCD patients was blunted under the drug-free condition; correlated inversely with pretreatment ratings of obsessive-compulsive and depressive symptomatology; and correlated inversely with the improvement in obsessive-compulsivescore observed after fluvoxamine treatment.ConclusionsThese results support the idea of a dysfunction of 5-HT transmission in OCD, and suggest that the greater this impairment, the better the response to drugs which selectively block the reuptake of 5-HT.

Brain 5-HT function in obsessive-compulsive disorder

1997 ◽  
Vol 171 (3) ◽  
pp. 280-282 ◽  
Author(s):  
N. A. Fineberg ◽  
A. Roberts ◽  
S. A. Montgomery ◽  
P. J. Cowen
Keyword(s):  
Obsessive Compulsive Disorder ◽  
Healthy Controls ◽  
Obsessive Compulsive ◽  
Age And Gender ◽  
Compulsive Disorder ◽  
Therapeutic Advantage ◽  
Neuroendocrine Function ◽  
Prolactin Response ◽  
And Gender ◽  
Drug Free

BackgroundDrugs that potentiate brain serotonin (5-HT) neurotransmission are effective in the treatment of obsessive–compulsive disorder (OCD), but it is unclear whether disturbances in brain 5-HT function play a role in the pathophysiology of OCD.MethodWe studied the prolactin response to the selective 5-HT releasing agent d-fenfluramine in 14 non-depressed, drug-free OCD patients, and 14 healthy controls matched for age and gender.ResultsThe prolactin response to d-fenfluramine was significantly increased in OCD patients compared with controls.ConclusionsThe disparate results of studies of 5-HT neuroendocrine function in OCD make it unlikely that disturbances of brain 5-HT function play a central role in the pathophysiology of OCD. Increased brain 5-HT neurotransmission in non-depressed OCD subjects may represent an adaptive neurobehavioural mechanism which can be amplified to therapeutic advantage by treatment with 5-HT potentiating drugs.

5-HT neuroendocrine function in major depression: prolactin and cortisol responses to D-fenfluramine

1996 ◽  
Vol 26 (6) ◽  
pp. 1191-1196 ◽  
Author(s):  
S. B. G. Park ◽  
D. J. Williamson ◽  
P. J. Cowen
Keyword(s):  
Healthy Controls ◽  
Endocrine Response ◽  
Melancholic Depression ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Neuroendocrine Function ◽  
Depressed Patients ◽  
Cortisol Responses ◽  
Prolactin Response ◽  
Drug Free

SynopsisWe studied the prolactin and cortisol responses to the 5-HT releasing agent, D-fenfluramine in 31 drug-free depressed patients and 29 healthy controls, using a double-blind, placebo-controlled design. There was no difference in either endocrine response between depressives and controls. Examining the sexes separately, or restricting comparisons to patients with melancholic depression, did not lead to any differences between the groups. Our findings suggest that in contrast to other 5-HT neuroendocrine probes such as L-tryptophan and clomipramine, the prolactin response to fenfluramine are not consistently blunted in depressed patients.

Plasma prolactin response to d-fenfluramine is blunted in bulimic patients with frequent binge episodes

1998 ◽  
Vol 28 (4) ◽  
pp. 975-983 ◽  
Author(s):  
P. MONTELEONE ◽  
F. BRAMBILLA ◽  
F. BORTOLOTTI ◽  
C. FERRARO ◽  
M. MAJ
Keyword(s):  
Plasma Levels ◽  
Rating Scales ◽  
Low Frequency ◽  
Significant Negative Correlation ◽  
Plasma Prolactin ◽  
Healthy Controls ◽  
Obsessive Compulsive ◽  
Double Blind ◽  
Obsessive Compulsive Symptoms ◽  
Plasma Prl

Background. Abnormalities of brain serotonin (5-HT) transmission have been implicated in the pathophysiology of bulimia nervosa (BN), but no conclusive data have yet been provided. The purpose of this study was to assess 5-HT transmission via the measurement of the prolactin (PRL) response to the specific 5-HT releasing agent d-fenfluramine (d-FEN) in both patients with BN and comparison subjects.Methods. According to a double-blind placebo-controlled design, plasma PRL response to d-FEN was measured in 14 drug-free bulimics and 14 matched healthy controls. In both patients and controls, eating-related psychopathology, depressive and obsessive–compulsive symptoms, and aggressiveness were measured by rating scales.Results. Baseline plasma levels of PRL and 17β-oestradiol were significantly reduced in bulimic patients, whereas basal plasma levels of cortisol did not significantly differ from healthy controls. PRL response to d-FEN was not different between patients and controls as groups, but it was significantly blunted in bulimics with high frequency bingeing ([ges ]2 binge episodes per day; N=7) as compared to both those with low frequency bingeing ([les ]1 binge episode per day; N=7) and matched controls. A significant negative correlation emerged between the frequency of binge episodes and the hormone response to d-FEN. Moreover, although patients scored higher than healthy subjects on rating scales assessing depressive and obsessive–compulsive symptoms and aggressiveness, no significant correlation was found between these measures and the PRL response to d-FEN.Conclusions. These results support the idea that serotonin transmission is impaired in bulimic patients with frequent binge episodes.

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