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Egyptian Rheumatology and Rehabilitation. 2007; 34 (1-2): 67-81
in English | IMEMR | ID: emr-82469

ABSTRACT

Despite being a physiological process, pregnancy has been noted by clinicians to have various impacts on different diseases in general and on immune-modulated diseases in particular. Concerning rheumatoid arthritis [RA], several studies reported a favorable outcome of the disease during pregnancy. Several researches looked at this pregnancy-induced improvement as a result of a change in the T helper 1/T helper 2 [Th1/Th2] function with predominance of Th2 function. To assess the status of serum levels of soluble tumor necrosis factor receptor [sTNF-R], interleukin-1 receptor antagonist [IL-1Ra] and soluble CD30 [sCD30] -during the three trimesters of pregnancy- in pregnant ladies and evaluate their relations to disease activity in RA patients. The study was performed on 21 pregnant RA patients, of whom only 17 completed the study. They were subjected to clinical assessment of their disease activity and had their sera tested for the level of the three aforementioned indirect Th2 cell function markers. This clinical examination and serum tests were performed once in each pregnancy trimester. These results were compared to those of thirty other controls: ten non-pregnant RA patients, ten pregnant healthy subjects and ten non-pregnant healthy subjects. The study showed definite and significant higher levels of sTNF-R and IL-1Ra in pregnant RA patients and pregnant healthy subjects when compared with non-pregnant controls. These rises of markers levels were negatively correlated with the disease activity. There were no corresponding differences in levels of sCD30 in the two groups. We conclude that during pregnancy there is a differential predominance of Th2 cell function involving an increase in some anti-inflammatory cytokines that could explain the clinical improvement of RA during pregnancy


Subject(s)
Humans , Female , Pregnancy/physiology , Receptors, Interleukin-1 , Tumor Necrosis Factors , Ki-1 Antigen , Disease Progression , T-Lymphocytes, Helper-Inducer
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