Elevated soluble Fas ligand levels may suggest a role for apoptosis in women with endometriosis.
OBJECTIVE
To evaluate soluble Fas ligand concentrations in serum and peritoneal fluid from women with endometriosis and from fertile controls without endometriosis, and to study levels of soluble Fas ligand in conditioned media of cultured endometrial stromal cells.


METHODS
Prospective, experimental trial.


METHODS
Two academic IVF centers.


METHODS
Twenty-nine fertile women without endometriosis and 57 infertile women with endometriosis (32 with stage I or II disease and 25 with stage III or IV disease).


METHODS
Enzyme-linked immunosorbent assay was used to measure soluble Fas ligand concentrations in paired samples of serum and peritoneal fluid from women with and without endometriosis. Concentrations were also measured in conditioned media of cultured endometrial stromal cells at basal conditions and after stimulation with interleukin-8 (0.001-10 ng/mL) and tumor necrosis factor-alpha (1-10 ng/mL).


RESULTS
Compared with fertile controls and women with early-stage of endometriosis, women with moderate to severe endometriosis had elevated serum (87.2 +/- 6.4, 88.2 +/- 6.9, and 162.3 +/- 7.8 pg/mL, respectively) and peritoneal fluid (81.0 +/- 6.0, 80.5 +/- 6.8, and 166.2 +/- 10.3 pg/mL, respectively) concentrations of soluble Fas ligand. Serum levels of soluble Fas ligand positively correlated with levels in peritoneal fluid. Comparison of patients in the same menstrual cycle in each group revealed that increased levels of soluble Fas ligand in patients with advanced endometriosis were not attributable to the difference in cycle phases. Soluble Fas ligand was not detected in conditioned media of endometrial stromal cells under baseline conditions or after stimulation.


CONCLUSIONS
Serum and peritoneal fluid of women with moderate to severe endometriosis contain elevated concentrations of soluble Fas ligand compared to women with minimal or mild endometriosis and women without endometriosis. These findings suggest a role for apoptotic dysregulation in the pathophysiology of endometriosis.
Garcia-Velasco
Juan A
JA
IVI-Madrid, Madrid, Spain. jgvelasco@ivi.es
Mulayim
Naciye
N
Kayisli
Umit A
UA
Arici
Aydin
A
D017209:Apoptosis; D001202:Ascitic Fluid / Q000737:chemistry*; D002478:Cells, Cultured; D017077:Culture Media, Conditioned; D004715:Endometriosis / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000378:metabolism / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D007247:Infertility, Female / Q000209:etiology / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000032:analysis* / Q000097:blood*; D008597:Menstrual Cycle; D012995:Solubility; D017154:Stromal Cells / Q000378:metabolism
D017077:Culture Media, Conditioned; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins