Disease relevance of Felty's Syndrome

• The Felty syndrome and G-CSF-associated thrombocytopenia and severe anemia [1].
• We evaluated the clinical and hematologic response to methotrexate (MTX) in 4 women with Felty's syndrome (FS) who had had neutropenia for 1-3 years [2].
• In RA complicated by extraarticular manifestations, anti-GPI antibodies were observed in 18% of patients with rheumatoid nodules, 45% of patients with rheumatoid vasculitis, and 92% of patients with Felty's syndrome [3].
• Efficacy of lithium in rheumatoid arthritis with granulocytopenia (felty's syndrome). A preliminary report [4].
• Auranofin appears to be an effective treatment for Felty's syndrome, and to have a lower degree of toxicity than parenteral gold [5].

High impact information on Felty's Syndrome

• Cyclosporine in Felty's syndrome [6].
• Improvement of rheumatoid arthritis following splenectomy for Felty syndrome [7].
• Three patients with Felty syndrome were treated with gold sodium thiomalate [8].
• The ability of antigranulocyte antibody to fix the third component of complement (C3) to the granulocyte surface was investigated by an assay that quantitates the binding of monoclonal anti-C3 antibody to paraformaldehyde-fixed cells preincubated with Felty's syndrome serum in the presence of human complement [9].
• Letter: Lithium in Felty's syndrome [10].

Chemical compound and disease context of Felty's Syndrome

• Treatment of Felty's syndrome with low-dose oral methotrexate [11].
• Treatment of Felty's syndrome with auranofin and methylprednisolone [12].
• Conditions often associated with rheumatoid arthritis and also thought to have an immunologic basis, such as Sjögren's syndrome, Felty's syndrome, and rheumatoid vasculitis, and reactions to medications, such as gold and penicillamine, reveal an interesting spectrum of immunogenetic relationships [13].
• Cutaneous Kaposi's sarcoma developed eight months after initiation of prednisone treatment in a 58-year-old man with systemic rheumatoid disease (rheumatoid arthritis, Felty's syndrome, rheumatoid vasculitis, and myositis) [14].
• Molecular characterisation of C4 null alleles found in Felty's syndrome [15].

Biological context of Felty's Syndrome

• Phagocytosis and intracellular killing by polymorphonuclear cells from patients with rheumatoid arthritis and Felty's syndrome [16].
• DQw7 and the C4B null allele are in linkage disequilibrium and the B44-Bf *S-C4A*3-C4B*Q0-DR4-DQw7 haplotype accounts for five of 24 DR4 positive haplotypes assigned in subjects with Felty's syndrome [17].
• Tests for polymorphonuclear cell (PMN) chemotaxis, adherence, and electrophoretic mobility (EPM) were carried out on blood PMN isolated from 27 normal subjects, 16 patients with uncomplicated rheumatoid arthritis (RA), and 9 patients with Felty's syndrome [18].
• DQ A and DX A RFLPs were studied in DR4-positive rheumatoid arthritis, Felty's syndrome, and in DR4-positive control subjects, and in the light of the previously documented association between Felty's syndrome and the DQ B 3.1 allele (3b RFLP) [19].

Anatomical context of Felty's Syndrome

• In contrast to Felty's syndrome, granular lymphocyte expansions in rheumatoid arthritis usually occur in older patients, may appear simultaneously with arthritis, and are usually associated with normal or elevated blood leukocyte counts [20].
• The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated [21].
• OBJECTIVE: Patients with chronic clonal proliferation of large granular lymphocytes (LGL leukemia) often have splenomegaly, neutropenia, and rheumatoid arthritis (RA), thereby resembling the manifestations observed in patients with Felty's syndrome [22].
• Twenty patients with LGL proliferative disease were examined, including five T cell clones and a variety of polyclonal proliferations, some secondary to rheumatoid arthritis and Felty's syndrome; 17/20 showed high number of CD3+, CD8+, and CD57+ lymphocytes and 9/20 also had high numbers of CD16+ or CD 56+ positive lymphocytes [23].
• We have studied the CFU-GM and BFU-E in vitro growth in a neutropenic and anemic patient with Felty's syndrome, either before or one and three months after steroid therapy when neutrophils and erythrocytes returned to normal [24].

Gene context of Felty's Syndrome

• Complement C4B-null alleles in Felty's syndrome [25].
• The Caucasian patients had relatively severe disease and comprised 75 patients with RA vasculitis, 22 with Felty's syndrome and 89 who had undergone a joint replacement (hip or knee) within 15 years of the onset of disease [26].
• Whereas susceptibility to RA is strongly associated with a conserved HLA-DR beta epitope associated with several DRB1 alleles, it is primarily the Dw4 allele which is associated with progression to Felty's syndrome [27].
• The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome [28].
• TAP2 transporter gene polymorphisms have been ascertained in patients with rheumatoid arthritis (RA) and Felty's syndrome (FS) to determine whether particular alleles of this gene are disease associated [29].

Analytical, diagnostic and therapeutic context of Felty's Syndrome

• Cytotoxic chemotherapy for cancer in Felty's syndrome: role of lithium carbonate [30].
• Sera of 22 patients with Felty's syndrome and 14 patients with rheumatoid arthritis were tested in assays routinely used for the detection of neutrophil antibodies (i.e. immunofluorescence, agglutination and cytotoxicity tests) as well as in the antibody-dependent lymphocyte-mediated granulocytotoxicity test [31].
• Anti-IgG antibodies (anti-IgG) of the IgE class were studied in sera from patients with juvenile rheumatoid arthritis (JRA), rheumatoid arthritis (RA) and patients with Felty's syndrome (FS) by use of an indirect immunofluorescence technique [32].
• Twenty-one sera from 19 patients with Felty's syndrome were fractionated by gel filtration on Sephadex G-200 [33].

References