classic rheumatoid arthritis
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2014 ◽  
Vol 8 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Mohammad Bagher Owlia ◽  
Kam Newman ◽  
Mojtaba Akhtari

Felty’s syndrome (FS) is characterized by the triad of seropositive rheumatoid arthritis (RA) with destructive joint involvement, splenomegaly and neutropenia. Current data shows that 1-3 % of RA patients are complicated with FS with an estimated prevalence of 10 per 100,000 populations. The complete triad is not an absolute requirement, but persistent neutropenia with an absolute neutrophil count (ANC) generally less than 1500/mm3 is necessary for establishing the diagnosis. Felty’s syndrome may be asymptomatic but serious local or systemic infections may be the first clue to the diagnosis. FS is easily overlooked by parallel diagnoses of Sjӧgren syndrome or systemic lupus erythematosus or lymphohematopoietic malignancies. The role of genetic (HLA DR4) is more prominent in FS in comparison to classic rheumatoid arthritis. There is large body of evidence that in FS patients, both cellular and humoral immune systems participate in neutrophil activation, and apoptosis and its adherence to endothelial cells in the spleen. It has been demonstrated that proinflammatory cytokines may have inhibitory effects on bone marrow granulopoiesis. Binding of IgGs to neutrophil extracellular chromatin traps (NET) leading to neutrophil death plays a crucial role in its pathophysiology. In turn, "Netting" neutrophils may activate auto-reactive B cells leading to further antibody and immune complex formation. In this review we discuss on basic pathophysiology, epidemiology, genetics, clinical, laboratory and treatment updates of Felty’s syndrome.


1988 ◽  
Vol 31 (2) ◽  
pp. 267-271 ◽  
Author(s):  
W. Neal Roberts ◽  
Lawren H. Daltroy ◽  
Ronald J. Anderson

Rheumatology ◽  
1988 ◽  
Vol 27 (5) ◽  
pp. 418-420 ◽  
Author(s):  
R. H. WHITE ◽  
R. J. TEITSCHEID ◽  
D. L. ROBBINS

1979 ◽  
Vol 7 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Jerome A Hubsher ◽  
Ian M Ballard ◽  
Barry R Walker ◽  
Jerome A Gold

Preliminary clinical studies showed that oxaprozin (4,5 Diphenyl-2-oxazolepropionic acid) has anti-inflammatory and analgesic properties with a plasma half-life of about 40 hours. Consequently, a multicentre, double-blind parallel trial was conducted for 12 weeks at thirteen investigator sites, utilizing 212 patients with classic rheumatoid arthritis and comparing oxaprozin 600 mg/day, oxaprozin 1200 mg/day and aspirin 3900 mg/day. Both the oxaprozin and aspirin-treated patients had statistically significant improvement from baseline periods, in most key categories evaluated. Oxaprozin administered twice a day (b.i.d.) was as effective as aspirin administered four times a day (q.i.d.) and caused significantly less tinnitus (p < 0.001). Fewer patients receiving high dose oxaprozin (2%) dropped out of the study because of unsatisfactory response than did those receiving aspirin (10%). There were no clinically significant laboratory abnormalities in the gastro-intestinal, renal, hepatic or haematological parameters monitored. This study suggests that oxaprozin is effective and well tolerated in the treatment of rheumatoid arthritis.


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