Article ; Online: Absence of Distinct Immunohistochemical Distribution of Annexin A5, C3b, C4d, and C5b-9 in Placentas From Patients With Antiphospholipid Antibodies, Preeclampsia, and Systemic Lupus Erythematosus.
2019 Volume 22, Issue 5, Page(s) 431–439
Abstract: Introduction: In pregnancy, the presence of preeclampsia (PEC), systemic lupus erythematosus (SLE), and/or antiphospholipid antibody syndrome (APLS) is characterized by poor obstetric outcomes, with potential adverse effects for both mother and fetus. ... ...
Abstract | Introduction: In pregnancy, the presence of preeclampsia (PEC), systemic lupus erythematosus (SLE), and/or antiphospholipid antibody syndrome (APLS) is characterized by poor obstetric outcomes, with potential adverse effects for both mother and fetus. Although the histopathologic changes observed in these entities have been well established, the pathogenic mediators associated with tissue injury are poorly understood. Methods: Forty placentas were evaluated, including 10 patients with preeclampsia, 9 with SLE, 11 with APLS, and 10 disease-free controls. Each case was subjected to a panel of immunohistochemical markers including C3b, C4d, Annexin A5, and C5b-9. Staining was graded on intensity and distribution. Results: C4d staining was distinctly different among disease groups and controls. Moreover, 6/10 PEC cases, 3/9 SLE cases, and 4/11 APLS cases showed at least focal staining for C4d. All controls were negative. Annexin A5 (AnxA5) staining showed intrinsic variability in all disease groups, while 10/10 controls showed diffuse, strong staining (2+ or 3+). C3b staining was heterogeneous among groups. Discussion: Previously, antiphospholipid antibody (aPLA)-associated pregnancy complications have been thought to be a consequence of a unique aPLA-mediated pathogenic mechanism. However, the immunohistochemical similarity (increased complement and decreased AnxA5 staining) observed in placentas from patients with APLS, PEC, and SLE suggests that aPLA-associated pregnancy complications may reflect a more general autoimmune mechanism. |
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MeSH term(s) | Annexin A5/analysis ; Annexin A5/biosynthesis ; Antiphospholipid Syndrome ; Complement C3b/analysis ; Complement C3b/biosynthesis ; Complement C4b/analysis ; Complement C4b/biosynthesis ; Complement Membrane Attack Complex/analysis ; Complement Membrane Attack Complex/biosynthesis ; Female ; Humans ; Immunohistochemistry ; Lupus Erythematosus, Systemic ; Peptide Fragments/analysis ; Peptide Fragments/biosynthesis ; Placenta/pathology ; Pre-Eclampsia ; Pregnancy ; Pregnancy Complications/immunology ; Retrospective Studies |
Chemical Substances | ANXA5 protein, human ; Annexin A5 ; Complement Membrane Attack Complex ; Peptide Fragments ; Complement C3b (80295-43-8) ; Complement C4b (80295-50-7) ; complement C4d (80295-52-9) |
Language | English |
Publishing date | 2019-03-28 |
Publishing country | United States |
Document type | Journal Article |
ZDB-ID | 1463498-3 |
ISSN | 1615-5742 ; 1093-5266 |
ISSN (online) | 1615-5742 |
ISSN | 1093-5266 |
DOI | 10.1177/1093526619836025 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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