title: The expression and concentration of CD40 ligand in normal pregnancy, preeclampsia, and hemolytic anemia, elevated liver enzymes and low platelet count (HELLP) syndrome.
abstract: Preeclampsia has been associated with increased platelet activation detected before disease onset. Inappropriate activation of platelets may be involved in pathogenesis in preeclampsia by promoting coagulation and thrombosis and also as a mediator of inflammation. The exaggerated platelet activation and inflammation leading to endothelial damage in preeclampsia can be explained by the CD40-CD40 ligand (CD40L) system. Expression of CD40L on platelets was determined by whole-blood flow cytometry, and serum levels of soluble CD40L (sCD40L) were measured by enzyme-linked immunosorbent assay in 11 women with mild preeclampsia, 11 women with severe preeclampsia, and six women with hemolytic anemia, elevated liver enzymes and low platelet count (HELLP) syndrome compared with 13 normotensive pregnant women as a control group. The platelet surface expression of CD40L was significantly higher in women with mild and severe preeclampsia and HELLP compared with normal pregnancy group (P = 0.001; P ≤ 0.001; P = 0.003, respectively), with no significant difference being found between women with mild preeclampsia compared with HELLP and severe preeclampsia compared with HELLP (P = 0.2; P = 0.8, respectively). The serum concentration of sCD40L was significantly higher in women with mild and severe preeclampsia and HELLP compared with the normal pregnancy group (P = 0.001; P ≤ 0.001; P = 0.022, respectively), with no significant difference being found between women with mild compared with severe preeclampsia or HELLP and severe preeclampsia compared with HELLP (P = 0.7; P = 0.6; P = 0.6, respectively). In conclusion, the higher expression and concentration of CD40L in women with preeclampsia and HELLP syndrome compared with normal pregnant women may indicate an exaggerated activation of platelets and endothelial cells in the disorder.
authors.affiliation: Department of Clinical Pathology, Mansoura University, Mansoura, Egypt. hanan.azzam@yahoo.com
authors.forename: Hanan A G
authors.initials: HA
authors.lastname: Azzam
authors.forename: Nashwa K
authors.initials: NK
authors.lastname: Abousamra
authors.forename: Hossam
authors.initials: H
authors.lastname: Goda
authors.forename: Reda
authors.initials: R
authors.lastname: El-Shouky
authors.forename: Abdel-Hady
authors.initials: AH
authors.lastname: El-Gilany
mesh_terms: D000328:Adult; D001792:Blood Platelets / Q000378:metabolism*; D023201:CD40 Ligand / Q000096:biosynthesis / Q000097:blood / Q000235:genetics / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression; D017359:HELLP Syndrome / Q000097:blood*; D006801:Humans; D007249:Inflammation; D015539:Platelet Activation; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy / Q000097:blood*; D011250:Pregnancy Complications, Hematologic / Q000097:blood / Q000209:etiology; D011446:Prospective Studies; D012709:Serum Albumin / Q000032:analysis; D012995:Solubility; D019851:Thrombophilia / Q000097:blood / Q000209:etiology; D055815:Young Adult
chemical_list: D012709:Serum Albumin; D023201:CD40 Ligand