Elevated Th1/Th2 Cell Ratios in a Pregnant Woman with a History of RSA, Secondary Sjögren’s Syndrome and Rheumatoid Arthritis Complicated with One Fetal Demise of Twin Pregnancy
Article first published online: 27 JUL 2007
DOI: 10.1111/j.1600-0897.2007.00506.x
Additional Information
How to Cite
Kwak-Kim, J., Lee, S.-K. and Gilman-Sachs, A. (2007), Elevated Th1/Th2 Cell Ratios in a Pregnant Woman with a History of RSA, Secondary Sjögren’s Syndrome and Rheumatoid Arthritis Complicated with One Fetal Demise of Twin Pregnancy. American Journal of Reproductive Immunology, 58: 325–329. doi: 10.1111/j.1600-0897.2007.00506.x
Publication History
- Issue published online: 27 JUL 2007
- Article first published online: 27 JUL 2007
- Submitted February 14, 2007; accepted May 24, 2007.
- Abstract
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Keywords:
- Multiple pregnancies;
- recurrent abortion;
- rheumatoid arthritis;
- Sjögren’s syndrome;
- Th1/Th2 response
Problem
Elevated Th1/Th2 cytokine producing CD3+/CD4+ cell ratios were reported in women with a history of recurrent spontaneous abortion (RSA) and multiple implantation failures. We report, significantly elevated Th1/Th2 cell ratios were noticed in a pregnant woman with twin pregnancies complicated with one fetal demise, who had a history of RSA, secondary Sjögren’s syndrome (SS), and rheumatoid arthritis.
Method of study
Case report.
Results
Peripheral blood Th1/Th2 cell ratios were significantly elevated 3 weeks prior to a fetal demise of twin pregnancies at 20 week gestation. Two weeks after fetal demise, the ratio of intracellular tumor necrosis factor-α/interleukin-10 producing CD3+/CD4+ cells in peripheral blood was further increased to three times higher than prior ratio. Elevated Th1/Th2 ratio was down regulated after increasing dose of IVIg treatment. The patient gave birth to a male baby weighing 2650 g at 36 weeks gestation. No serious complications were found in the patient or the baby.
Conclusion
Systemic inflammatory immune response pre-exists prior to a fetal demise and the degree of inflammatory immune response got worse with a presence of fetal demise in utero. We infer that the placenta is not an immunological barrier to maternal Th1/Th2 immune responses.

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