Abstract
Fifty-one rheumatoid arthritis (RA) patients were enrolled to assess the gene expression of tumor necrosis factor-alpha (TNF-α) by reverse transcription quantitative polymerase chain reaction (qRT-PCR) in etanercept-treated RA patients, with some emphasis on clinical and biological markers of disease. The results revealed that the ΔCt mean range in total, male and female RA patients and controls was 1.286 ± 1.226 - 4.023 ± 0.856 and the differences were not. Laboratory and clinical findings in subgroups of patients also showed no significant variations in the distribution of 2-ΔΔCt means, with the exception of anti-cyclic citrullinated peptide (ACCP) antibodies. The lowest expression was observed in moderate positive patients (1.566 ± 1.104) compared to low and high positive patients (4.061 ± 1.366 and 9.668 ± 3.518, respectively) for ACCP antibodies, and the difference was significant (p = 0.043). Inspecting the 2-ΔΔCt means in duration of disease and gender revealed that male patients recorded a lower mean than female patients (0.827 ± 0.550 vs. 4.143 ± 1.317) at 10 years duration of disease, female patients showed a lower mean than male patients (1.242 ± 0.372 vs. 5.607 ± 3.334). However, both differences were not significant. It is concluded that etanercept was effective in normalizing the TNF gene expression, but variations that were related to gender, duration of disease and some biological markers of disease, were observed.
Highlights
Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease of the connective tissues
The results revealed that the ∆Ct mean range in total, male and female rheumatoid arthritis (RA) patients and controls was 1.286 ± 1.226 - 4.023 ± 0.856 and the differences were not
Inspecting the 2−∆∆Ct means in duration of disease and gender revealed that male patients recorded a lower mean than female patients (0.827 ± 0.550 vs. 4.143 ± 1.317) at 10 years duration of disease, female patients showed a lower mean than male patients (1.242 ± 0.372 vs. 5.607 ± 3.334)
Summary
Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease of the connective tissues. Genetic and environmental factors are involved in RA initiation, as well as the severity of disease course [1]. It is characterized by a synovial inflammation of small joints (hands and feet) and large joints (shoulder and knees). Localized inflammation of joints is progressed (i.e. synovitis) and results in cartilage and bone destruction. Both innate and adaptive immune responses are involved in the inflammatory process, in which cytokines play important role in the inflammation and advancing the disease [5]
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