Background Thrombocytopenia was sometimes shown in clinical medical treatment in patients with rheumatoid arthritis (RA). The causes of thrombocytopenia in patients with RA are various. Drug induced thrombocytopenia and idiopathic thrombocytopenia are ones of these causes. The diagnosis of thrombocytopenia is important because the method of treatment depends on it.
Objectives Increased levels of platelet associated IgG (PAIgG) found in patients with idiopathic thrombocytopenia. We investigated in the relationship between platelet and PAIgG to evaluate the clinical significance in patients with RA.
Methods Total 266 patients (60 males: 206 females) with RA were enrolled in this study. The serum level of PAIgG were examined. We evaluated age at onset of RA, age of PAIgG test, disease duration of RA, platelet number, platelet bindable IgG (PBIgG), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), anti-cyclic citrullinated peptide antibody (ACPA), matrix metalloproteinase-3 (MMP-3), Disease activity score including a 28-joint count (DAS28)-CRP, DAS28-ESR, simplified disease activity index (SDAI), clinical disease activity index (CDAI), and methotrexate (MTX) dose between PAIgG(+) and (−) groups.
Results PAIgG were positive in 60.9% (162/266). There were no significant differences in age at onset of RA, age of PAIgG test, disease duration of RA, PBIgG, CRP, ESR, ACPA, MMP-3, DAS28-CRP, DAS28-ESR, SDAI, CDAI, and MTX dose between PAIgG(+) and (−) groups. There were significant differences only in RF and platelet number between PAIgG(+) and (−) groups. RF were higher in PAIgG(+) than those in (−) significantly (126.4 IU/mL vs. 84.4 IU/mL, p=0.03). RF(+) rate were also higher in PAIgG(+) than those in (−) significantly (75.3%: 122/162 vs. 61.5% 64/104, p=0.02). Platelet number were lower in PAIgG(+) than those in (−) significantly (207,000/μL vs. 218,000/μL, p=0.03). However, the PAIgG(+) patients whose platelet number were under normal limit were only 11.1% (18/162). There was no significant difference compared with PAIgG(−) patients whose platelet number were under normal limit (8.7%: 9/104).
Conclusions PAIgG shows high value in immune thrombocytopenia, systemic lupus erythematosus, etc. However, we found high PAIgG(+) rate in RA which usually shows thrombocytosis. Although platelet number in PAIgG(+) were lower significantly, the mean value was within normal limit. The rates under normal limit between 2 groups were not different significantly. Although PAIgG had small effect on platelet number in RA, RF were higher in PAIgG(+) significantly. Further investigation is needed to evaluate the clinical significance of PAIgG in patients with RA.
Disclosure of Interest None declared