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Are there differential symptom profiles that improve in response to different pharmacological treatments of premenstrual syndrome/premenstrual dysphoric disorder?

Journal article
Authors Uriel Halbreich
P M Shaughn O'Brien
Elias Eriksson
Torbjörn Bäckström
Kimberly A Yonkers
Ellen W Freeman
Published in CNS drugs
Volume 20
Issue 7
Pages 523-47
ISSN 1172-7047
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 523-47
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Central Nervous System, drug effects, physiopathology, Drug Therapy, Combination, Estrogen Antagonists, therapeutic use, Female, Gonadotropin-Releasing Hormone, agonists, Humans, MEDLINE, statistics & numerical data, Meta-Analysis, Ovariectomy, methods, Premenstrual Syndrome, classification, drug therapy, physiopathology, surgery, Randomized Controlled Trials, Serotonin Uptake Inhibitors, therapeutic use
Subject categories Physiology

Abstract

Current evidence suggests that the accepted treatments for premenstrual syndrome (PMS)/premenstrual dysphoric disorder (PMDD) have similar overall efficacy. While these treatments are more effective than placebo, response rates associated with them are far from satisfactory (<60%), such that, irrespective of treatment modality, there remain a significant number of women who are unresponsive to current conventional pharmacological therapy. The available data on response rates of specific types of premenstrual symptoms to, or symptom profiles that are most amenable to, each treatment modality are limited and not well defined because most studies were not designed to assess specific symptom profiles. Those studies that have attempted to evaluate which symptom profiles respond to specific therapies have revealed variations within the individual modalities, as well as between the different modalities. It appears that suppression of ovulation ameliorates a broad range of behavioural as well as physical premenstrual symptoms. SSRIs are most effective for irritability and anxiety symptoms, with lesser efficacy for 'atypical' premenstrual symptoms. GABAergic compounds are most efficacious for anxiety and anxious/depressive symptoms, while dopamine agonists, particularly bromocriptine, are perhaps most efficacious for mastalgia. Overall treatment response rates may improve if treatments are targeted at well-defined subgroups of patients. Re-analysis of available datasets from randomised clinical trials may shed more light on the notion that targeting women with specific premenstrual symptom profiles for specific treatment modalities would improve response rates beyond the current ceiling of approximately 60%. Such information would also improve understanding of the putative pathophysiological mechanisms underlying PMS and PMDD, and may point to a more specific diagnosis of these conditions.

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