Article Text

FRI0156 Do changes in adipocytokines correlate with changes to disease activity in rheumatoid arthritis? findings from the tomorrow study
  1. M Tada1,
  2. K Inui2,
  3. Y Sugioka3,
  4. T Okano2,
  5. K Mamoto2,
  6. T Koike3,
  7. H Nakamura2
  1. 1Orthopaedic Surgery, Osaka City General Hospital
  2. 2Orthopaedic Surgery
  3. 3Center of Senile Degenerative Disorders, Osaka City University Graduate School of Medicine, Osaka, Japan


Background Cytokines released from mast cells evoke inflammation and correlate with arteriosclerotic lesions and autoimmune disease1. The relationship between disease activity and lipid metabolism is a notable in research surrounding rheumatoid arthritis (RA). RA patients without disease control reportedly show high titers of leptin or adiponectin as adipocytokines2.

Objectives We analyzed the interaction between changes in disease activity and adipocytokines using data from the TOMORROW (TOtal Management Of Risk factors in Rheumatoid arthritis patients to lOWer morbidity and mortality clinical trial) study, a 10-year prospective study (registration number, UMIN000003876).

Methods We analyzed data collected from the cohort of the TOMORROW study including 193 patients with RA and age- and sex-matched 194 healthy individuals (controls). We compared changes in leptin and adiponectin (Δleptin and Δadiponectin) in both groups between baseline and after 3 years. Correlations with the change in disease activity (ΔDAS28ESR) during 3 years and changes in Δleptin and Δadiponectin in RA were investigated by univariate analysis.

Results Leptin levels increased in both groups. No significant differences in Δleptin were seen between RA (0.21 ng/ml) and controls (0.18 ng/ml; p=0.37). On the other hand, adiponectin was significantly decreased in controls (-3.3 μg/ml) compared to RA (-1.8 μg/ml; p=0.01). Negative correlations between Δleptin and Δadiponectin were detected in the RA group (r=-0.29, p<0.01). The correlation between adiponectin and DAS28ESR was positive both at baseline (r=0.22, p=0.01) and after 3 years (r=0.18, p=0.01). However, no such tendencies were seen for leptin. Table 1 shows details of the correlations with changes in adipocytokine. In terms of the relationship with ΔDAS28ESR, no correlation was seen with Δleptin (r=0.07, p=0.31) or Δadiponectin (r=-0.01, p=0.91). Changes in lipid metabolic markers and fat percentages were detected as predictive factors for Δadipocytokines.

Table 1.

Correlations with changes in adipocytokine by univariate analysis

Conclusions Leptin increased and adiponectin decreased over the course of 3 years. Correlations between Δadipocytokines and ΔDAS28ESR were not detected. RA patients with high disease activity show higher adiponectin titers.


  1. Benoist C., Mathis D. Mast cell in autoimmune disease. Nature. 2002; 420: 875–8.

  2. Cho H., Lin J., Chen W., et al. Baseline adiponectin and leptin levels in predicting an increased risk of disease activity in rheumatoid arthritis: a meta-analysis and systematic review. Autoimmunity. 2016; 49: 547–53.


Disclosure of Interest None declared

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