Inflammatory markers in endometriosis: reduced peritoneal neutrophil response in minimal endometriosis
Christopher Finne Riley1, Mette Haase Moen, Vibeke Videm
1Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Background:
Inflammation is considered to play a role in the pathogenesis of endometriosis. Inflammatory activation in endometriosis was tested based on the hypothesis that pain and endometriosis stage are related to the degree of local and systemic inflammation.
Methods:
Eighteen patients with endometriosis and 14 controls without endometriosis were studied. Cancer antigen 125 and C-reactive protein were analyzed in blood, and in aspirated peritoneal fluid, lactoferrin, myeloperoxidase (neutrophil granulocyte activation marker), sC5b-9 (terminal complement complex), soluble intercellular adhesion molecule 1 (marker for extent of endometriotic tissue), neopterin, and tumor necrosis factor alpha (monocyte/macrophage activation) were evaluated and related to pain, endometriosis stage, and clinical data.
Results:
None of the measured markers were different between control and endometriosis patients, or in women with or without menstrual pain, dyspareunia, or other types of pelvic pain. Lactoferrin and myeloperoxidase concentrations were significantly lower in patients with endometriosis stage I compared to control patients and endometriosis patients with stage III/IV disease. As expected, cancer antigen 125 concentrations were increased in endometriosis patients of stage III/IV.
Conclusions:
Neutrophil granulocytes in endometriosis patients may have a lowered ability to respond to weak activation signals, while in more extensive endometriosis stronger neutrophil activation may be related to a proinflammatory effect of endometriotic tissue.