Title:Can Cytokines be used as an Activation Marker in Rheumatoid Arthritis?
Volume: 21
Issue: 8
Author(s): Fatih Öner Kaya, Yeşim Ceylan, Belkız Öngen İpek, Zeynep Güneş Özünal, Gülbüz Sezgin and Selim Nalbant*
Affiliation:
- Department of Internal Medicine, Faculty of Medicine Research and Education Hospital, Maltepe University, Istanbul,Turkey
Keywords:
CRP, erythrocyte sedimentation rate, TNF- α, soluble TNF- α receptor, IL-1B, IL-10, DAS-28.
Abstract:
Aims: The etiopathogenesis of Rheumatoid Arthritis (RA) is not clearly understood.
However, the role of the cytokines play an important part in this mechanism. We aimed to bring a
new approach to the concept of 'remission' in patients with RA.
Background: RA is a chronic, autoimmune, inflammatory disease that involves small joints in the
form of symmetrical polyarthritis and progresses with exacerbations and remissions. Pain,
swelling, tenderness and morning stiffness are typical of the joints involved. Although it is approached
as primary joint disease, a wide variety of extra-articular involvements may also occur. It
is an interesting pathophysiological process, the exact cause of which is still unknown, with many
environmental, genetic and potentially undiscovered possible factors in a chaotic manner.
Objective: In this cross-sectional study, sedimentation rate (ESR), C- Reactive protein (CRP), Tumor
necrosis factor (TNF)-α, soluble-TNF-α receptor (TNF-R), Interleukin (IL)-1B and IL-10
were measured in three groups which were healthy volunteers, patients with RA in the active period,
and patients with RA in remission. Disease activity score-28 (DAS-28) was calculated in active
RA and RA in remission.
Methods: This study included 20 healthy volunteers, 20 remission patients with RA and 20 active
RA patients. Venous blood samples were collected from patients in both healthy and RA groups.
Results: RA group consisted 43 (71.6%) female and 17 (28.4%) male. Control group consisted 11
(55%) female and 9 (45%) male. TNF-R was significantly high only in the active group according
to the healthy group (p=0.002). IL-10 was significantly high in active RA, according to RA in remission
(p=0.03). DAS-28 was significantly high in active RA, according to RA in remission
(p=0.001).
In the active RA group, ESR and TNF-R had a positive correlation (r:0.442; p=0.048). In the active
RA group, there was also a positive correlation between TNF-R and CRP (r:0.621; p=0,003). Both
healthy and active RA group had significant positive correlation between ESR and CRP (r: 0.481;
p=0.032 and r: 0,697; p=0,001 respectively).
Conclusion: TNF-R can be the main pathophysiological factor and a marker showing activation.
TNF-R can be very important in revealing the effect of TNF on the disease and the value of this effect
in the treatment and ensuring the follow-up of the disease with CRP instead of ESR in activation.