Study register · detail
Implications of dysregulated endogenous cannabinoid family members in the pathophysiology of endometriosis
Unclear
17 citations
SampleSonstige Evidenz
ControlHealthy fertile controls or sham controls
EndpointEndocannabinoid levels
Blindingn.a.
DesignSonstiges
Key finding
Study shows dysregulation of endocannabinoids in endometriosis (increased palmitoylethanolamide levels in lesions, reduced cannabinoid-2-receptor expression), without testing therapeutic intervention or clinical outcomes.
Summary
Review on the role of dysregulated endocannabinoid system members (e.g. anandamide, 2-AG) in endometriosis pathophysiology; mechanistic hypotheses, no clinical intervention data.
P
PopulationPatients with endometriosis and healthy fertile controls (sample size not specified), additionally a mouse model for endometriosis
I
InterventionNo intervention; mass spectrometry, mRNA and immunohistochemical analysis of plasma and tissue samples
C
ControlHealthy fertile controls or sham controls (mouse model)
O
OutcomePalmitoylethanolamide (PEA) significantly increased in endometriosis lesions vs. endometrium; cannabinoid-2-receptor expression significantly decreased in lesions; no significant changes in circulating endocannabinoids in plasma
Quality profile
Sample size
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Blinding
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Effect size
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Citations / year
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Abstract
Objective: To determine the involvement of the endocannabinoid (EC) family member in the pathophysiology of endometriosis (EMS).
Design: Mass spectrometry analysis of plasma and tissue samples from patients with EMS, controls, and a mouse model of EMS and messenger RNA and immunohistochemistry analysis of the samples from patients with EMS and controls.
Setting: Academic teaching hospital and university.
Patient(S): Patients with EMS and healthy fertile control subjects.
Intervention(S): None.
Main Outcome Measure(S): Endocannabinoid analysis in patient plasma, EMS lesions, and healthy endometrial samples.
Result(S): Circulating ECs were detected in the plasma samples, whereas no significant changes were observed in patients with EMS compared with healthy fertile controls. However, the palmitoylethanolamide levels were significantly higher in the EMS lesions than in the endometrium from patients with EMS. Similarly, genes involved in the EC signaling pathways were differentially expressed in the EMS lesions. Analysis of cannabinoid 1 and 2 receptors in the EMS lesions revealed a significantly lower cannabinoid 2 receptor expression, whereas no significant changes were observed in cannabinoid 1 receptor expression compared with those in the endometrium from both patients with EMS and healthy fertile controls. The palmitoylethanolamide levels were significantly elevated in plasma from EMS mice compared with that from sham controls and in EMS lesions compared with uterine samples.
Conclusion(S): Together, we provide evidence toward dysregulation of members of the ECs in both patients with EMS and the mouse model of EMS. These findings will advance the knowledge of the role of ECs in EMS and their potential implications as therapeutic targets. Elsevier Inc. All rights reserved.
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