eMedicine Specialties > Rheumatology > Rheumatoid Arthritis
Felty Syndrome
Updated: Dec 3, 2008
Introduction
Background
Felty syndrome (FS), which was first described in 1924, is a potentially serious condition that is associated with seropositive (rheumatoid factor [RF]–positive) rheumatoid arthritis (RA).1 Felty syndrome is characterized by the triad of RA, splenomegaly, and granulocytopenia. Although many patients with Felty syndrome are asymptomatic, some develop serious and life-threatening infections secondary to granulocytopenia.
For additional information on rheumatoid arthritis, see Medscape’s Rheumatoid Arthritis Resource Center.
Pathophysiology
Although the pathophysiology of Felty syndrome is not fully understood, evidence points to splenic sequestration and subsequent granulocyte destruction. Studies performed almost 50 years ago demonstrated lower granulocyte counts in the splenic vein compared with those in the splenic artery. Researchers have shown immune complexes coating granulocytes, diminished granulocyte growth factor levels, and numerous circulating autoantibodies, including those against granulocyte surface antigens. T-cell large granular lymphocyte leukemia (TLGL) and Felty syndrome share overlapping pathophysiologic features.2
In 2002, a study in Germany examined 15 patients with neutropenia due to Felty syndrome and matched them to a control group of 16 patients with normocytic RA. In addition, 16 patients with neutropenia and systemic lupus erythematosus (SLE) were matched to a control group of 16 patients with SLE. Antibodies against granulocyte colony-stimulating factor (G-CSF) were measured. Eleven patients with Felty syndrome demonstrated anti–G-CSF immunoglobulin G (IgG); none of the patients in the RA control group demonstrated anti–G-CSF IgG. Six patients with both neutropenia and SLE and 6 patients in the SLE control group also had anti–G-CSF antibodies. These antibodies appeared to have a neutralizing effect on G-CSF.3
Frequency
United States
Felty syndrome affects approximately 1-3% of all patients diagnosed with RA, and RA occurs in about 1% of the general population. The true prevalence of Felty syndrome is difficult to ascertain because many affected patients are asymptomatic. Felty syndrome is rare in children. The prevalence of Felty syndrome may be decreasing with the advent of more potent antirheumatic agents. It seems to be quite rare in the African American population.
International
Few data suggest that the international frequency of Felty syndrome differs from that of the United States.
Mortality/Morbidity
Although many individuals with Felty syndrome are asymptomatic, others progress and develop life-threatening infections. Pulmonary and skin infections are common. The level of debilitation due to the underlying RA, along with the extent of immunosuppression used in treating both RA and Felty syndrome, heavily influence mortality and morbidity. One study from southwest England observed 32 patients with Felty syndrome; 5 patients died of overwhelming bronchopneumonia during a mean follow-up period of 5.2 years. Curiously, in the past 20 years in the United States, the frequency of hospitalization for rheumatoid vasculitis and ultimate splenectomy in patients with Felty syndrome has dropped, possibly because of earlier and more aggressive treatment of RA, controlling the disease before the manifestations of Felty syndrome appear.
Race
Felty syndrome is most common in whites and is uncommon in blacks. The human leukocyte antigen DR4 (HLA-DR4) genotype, which is a marker for more aggressive RA and more frequent extra-articular manifestations in whites, is strongly associated with Felty syndrome.
Sex
Felty syndrome is more common in females, with an approximate female-to-male ratio of 3:1. Underreporting and asymptomatic cases cause difficulty in determining the true sex ratio.
Age
Felty syndrome is most common during the fifth through the seventh decades of life. The condition is usually associated with more than 10 years of preceding RA activity. Men are affected with Felty syndrome earlier in the course of RA than women are.
Clinical
History
- Many years of aggressive destructive rheumatoid arthritis (RA) precede the onset of Felty syndrome. On occasion, RA and Felty syndrome simultaneously develop. The extra-articular manifestations of RA (eg, rheumatoid nodules, pleuropericarditis, vasculitis, peripheral neuropathy, episcleritis, other forms of eye involvement, Sjögren syndrome, adenopathy, skin ulcers) are more common in patients who develop Felty syndrome.
- Patients with Felty syndrome often report current symptoms of mild inflammatory joint disease caused by synovitis. The patient's history, however, usually reveals a long preceding period of active and aggressive joint disease, which can be confirmed by physical examination and plain radiography. Some patients present with quiescent or so-called "burned-out" joint disease. A lack of synovitis or active joint disease should not dissuade the clinician from considering the diagnosis of Felty syndrome.
- Patients with Felty syndrome commonly present with bacterial infections of the skin and respiratory tract. An aggressive level of immunosuppression directed at the underlying RA may contribute to the susceptibility to infection.
- Patients may present with left upper quadrant pain, initiated by splenic infarcts or capsular distension.
Physical
- Splenomegaly, possibly nonpalpable
- Hepatomegaly, usually mild
- Lymphadenopathy
- Weight loss
- Rheumatoid nodules
- Sjögren syndrome
- Articular findings of long-standing RA
- Joint deformities typical of RA
- Synovitis (joint swelling and tenderness), may be mild at presentation
- Small-vessel inflammation (vasculitis)
- Lower-extremity ulcers
- Palpable purpura and brownish pigmentary changes of the lower extremities
- Periungual infarcts
- Signs of systemic vasculitis
- Mononeuritis multiplex
- Extremity ischemia
- Others findings, including pleuritis, peripheral neuropathy, episcleritis, and signs of portal hypertension
Causes
- Risk factors for Felty syndrome include the following:
- RF positivity in high titers
- Long-standing disease
- Aggressive and erosive synovitis: Patients with Felty syndrome may present with mild RA, but Felty syndrome is clearly associated with severe disease and extra-articular manifestations.
- HLA-DR4 positivity and DR4 homozygosity: This may be due to the presence of HLA-DR4 in patients who have severe disease.
- Extra-articular RA manifestations
Differential Diagnoses
| Cirrhosis | Systemic Lupus Erythematosus |
| Lymphoma, Non-Hodgkin | Tuberculosis |
| Myeloproliferative Disease | |
| Sarcoidosis | |
| Sjogren Syndrome |
Other Problems to Be Considered
Chronic infection
Drug reactions
Other rheumatologic diseases
Infiltrative diseases
HIV infection
Neutropenia with large granular lymphocytosis (LGL), also known as pseudo-Felty syndrome
Workup
Laboratory Studies
- CBC count with differential is as follows:
- Obtain a white blood cell (WBC) count and differential, which are crucial when determining the degree of granulocytopenia. Studies show that the greatest risk for infection is a granulocyte count less than 1000/µL. Bear in mind, however, that the level of neutropenia varies over time without medical intervention. Granulocyte dysfunction and an absolute decrease in the number of granulocytes may predispose to infection.
- Anemia and thrombocytopenia may result from hypersplenism.
- Anemia of chronic disease may result from the underlying inflammatory disease.
- Mild elevations of alkaline phosphatase and transaminase levels may occur.
- Almost all patients with Felty syndrome (98%) have high titers of RF. This is because extra-articular manifestations of rheumatoid arthritis (RA) are strongly associated with RF.
- Antinuclear antibodies (ANAs), found in 67% of cases; antihistone antibodies; and even antineutrophil cytoplasmic antibodies (perinuclear pattern; p-ANCA), found in 77% of cases, commonly occur in patients with Felty syndrome. The significance of autoantibodies in Felty syndrome is unknown, and their contribution, if any, to the disease itself is uncertain.
- Erythrocyte sedimentation rate (ESR) and serum immunoglobulin levels are invariably elevated in patients with Felty syndrome.
- Cryoglobulins may be present.
Imaging Studies
- Radionuclide studies, ultrasonography, or computed tomography (CT) scanning may define the presence and extent of splenomegaly. The same modalities can also be used to assess patient response to therapy.
Procedures
- Bone marrow aspiration and biopsy are especially important to rule out LGL syndrome. The bone marrow of patients with Felty syndrome shows adequate megakaryocytes and myeloid hyperplasia with arrested development at the level of immature cell forms.
Histologic Findings
An unusual type of liver involvement known as nodular regenerative hyperplasia is associated with Felty syndrome. It is characterized by mild portal fibrosis or lymphocyte and plasma cell infiltration but is not typical of cirrhosis. It may be complicated by portal venule occlusion and regenerative nodule formation.
Treatment
Medical Care
The best treatment for Felty syndrome is to control the underlying rheumatoid arthritis (RA). Immunosuppressive therapy for RA often improves granulocytopenia and splenomegaly; this finding reflects the fact that Felty syndrome is an immune-mediated disease. Most of the traditional medications used to treat RA have been used in the treatment of Felty syndrome. No well-conducted, randomized, controlled trials support the use of any single agent. Most reports on treatment regimens involve small numbers of patients.
- Historically, most patients were once treated with gold salts, reflective of their long history of use in RA prior to the advent of methotrexate; however, the response of the condition is slow. Older studies report a response rate of 60-80%. Intramuscular aurothioglucose (Solganal) was the agent most commonly used, but it is now used very infrequently.
- Methotrexate acts faster than gold and now is the preferred agent of rheumatologists for treating RA. As experience using methotrexate in Felty syndrome increases, this drug is likely to become the agent of choice for therapy. If urgent correction of neutropenia is unnecessary, most practicing rheumatologists use this drug first when treating Felty syndrome. It is usually combined with folic acid to minimize adverse effects. Note that the beneficial effects of methotrexate may not be evident for 4-8 weeks.
- The potential for leukopenia limits the use of cyclophosphamide, although it may have a role in some cases. A recent report described 2 patients with refractory Felty syndrome who responded to high-dose cyclophosphamide; however, physicians have had far more experience using cyclophosphamide for rheumatoid vasculitis and other serious RA extra-articular manifestations than for Felty syndrome. For this reason, it is not an initial choice of therapy.
- Penicillamine is being used less frequently for RA because of its adverse effect profile. Penicillamine is never a first-choice therapy for patients with Felty syndrome.
- Etanercept, adalimumab, and infliximab are all newer agents prescribed for RA. These agents act by blocking the effects of tumor necrosis factor-a (TNF-a). These drugs are very effective in the treatment and control of RA, although the experience of using them for Felty syndrome is limited.4
- Intravenous immunoglobulin (IVIG) does not show reproducibly demonstrable success.
- Recombinant granulopoietic growth factors, such as G-CSF and granulocyte-monocyte colony-stimulating factor (GM-CSF), effectively and quickly raise the granulocyte count, which is important in patients with life-threatening infections. Initial treatment of patients with Felty syndrome and life-threatening infections should include the administration of a growth factor. Long-term use of G-CSF appears to be well tolerated, although hypersensitivity vasculitis and flare-ups of the underlying RA in these patients have been reported.
- At high doses, corticosteroids can increase the granulocyte count, partly through demargination. This effect does not persist when tapering the patient to a typical low dose (<10 mg/d) used for RA articular disease. Empiric administration of high-dose intravenous methylprednisolone is often prescribed for Felty syndrome, but the effect is time limited. Long-term use of high-dose corticosteroids further increases the risk for infection. Corticosteroids should probably be viewed as a second-line treatment modality.
- Case reports in the past few years have noted a lack of efficacy with rituximab (Rituxan),5 a response to leflunomide (Arava),6,7 and a response to salazosulfapyridine.8 These were all single-patient reports.
Surgical Care
Splenectomy is recommended only in patients with severe intractable disease who exhibit no improvement with medical therapy and experience recurrent or serious infection. Less commonly, extrinsic hemolysis or recurrent cutaneous ulcers may indicate a need for splenectomy. Granulocytopenia recurs in approximately 25% of patients who have undergone splenectomy.
Consultations
- Rheumatologist
- Hematologist
- Infectious diseases specialist
Activity
Dictate patient activity according to infection risk and spleen size. Recommend that the patient avoid any activity that could result in blunt trauma to the left upper quadrant.
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Gold compounds
These agents inhibit immune reactions.
Aurothioglucose (Solganal)
Disease-modifying antirheumatic drug (DMARD). Less experience with the PO preparation (Auranofin) for Felty syndrome.
Dosing
Adult
10 mg IM first wk (test dose), 25 mg IM second wk, then 50 mg IM qwk; if improved, 25-50 mg IM q2-4wk
Pediatric
0.25 mg/kg IM first wk, increases of 0.25 mg/kg can be made qwk until maintenance dose of 0.75-1 mg/kg IM qwk is reached; not to exceed 25 mg/dose
Doses are administered qwk for 20 doses, then continued at 2- to 4-wk intervals
Interactions
Increased toxicity with penicillamine, hydroxychloroquine, and cytotoxic agents
Contraindications
Documented hypersensitivity; renal disease; history of blood dyscrasias; hepatic disease; thrombocytopenia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Check CBC and UA every 1-2 doses, obtain baseline renal tests and LFTs; toxicities include rash, oral ulcers, proteinuria, cytopenia, enterocolitis, and corneal and lens chrysiasis
Immunosuppressive agents
These agents inhibit key factors in the immune system responsible for immune reactions.
Methotrexate (Rheumatrex)
Antineoplastic agent that is immunosuppressive at lower doses. Very effective in treating RA. Antirheumatic effects may take several weeks to become apparent. Unknown mechanism of action in treatment of inflammatory disorders; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Succinct guidelines for use and monitoring are available from the American College of Rheumatology.
Dosing
Adult
7.5-25 mg PO single dose qwk, may be divided but total dose must be administered over 24 h; higher doses may be administered IM/SC; highly recommended that concomitant folic acid (1 mg/d) be administered with methotrexate to ameliorate potential adverse effects
Pediatric
5-15 mg/m2/wk PO/SC single dose or 3 divided doses administered 12 h apart
Interactions
PO aminoglycosides may decrease absorption and blood levels of concurrent PO methotrexate (MTX); charcoal lowers MTX levels; coadministration with etretinate may increase hepatotoxicity of MTX; indomethacin and phenylbutazone can increase MTX plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity of MTX; may increase plasma levels of thiopurines
Contraindications
Documented hypersensitivity; alcoholism; hepatic disease; immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia)
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Monitor CBC monthly and monitor liver and renal function q1-3mo during therapy (may need to monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); MTX has toxic effects on hematologic, GI, pulmonary, and neurologic systems; skin rash and oral ulcers may occur; discontinue if significant drop in blood counts occurs; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly with MTX (possibility of increased toxicity with NSAIDs including salicylates has not been tested)
Cyclophosphamide (Cytoxan)
Antineoplastic alkylating agent and immunosuppressive agent. Reduces the number of B and T cells. Increases risk for infection.
Dosing
Adult
1-2 mg/kg/d PO; alternatively, 750-1000 mg/m2 IV qmo (begin with 500 mg/m2 if CrCl <30 mL/min)
Pediatric
Not established
Interactions
Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects of cyclophosphamide; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life of cyclophosphamide while decreasing metabolite concentrations; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity of cyclophosphamide; inhibits cholinesterase activity for up to 10 d after an IV dose, which can potentiate the effect of succinylcholine chloride
Contraindications
Documented hypersensitivity; severely depressed bone marrow function; pregnancy; breastfeeding; acute or chronic infection; history of malignancy
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
High toxicity profile (eg, oncogenic, alopecia, infertility, emetogenic); regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis
Colony-stimulating factors
These agents stimulate production, maturation, and activation of neutrophils and increase migration and cytotoxicity of neutrophils.
Filgrastim (Neupogen)
A solid record of success is emerging with the use of these agents in patients with Felty syndrome and infections that are not responding to antibiotics alone. Most experience has been with the use of G-CSF.
Dosing
Adult
Both G-CSF and GM-CSF may be administered SC or IV; G-CSF doses are 5 mcg/kg/d; dose can be increased by 5 mcg/kg/d if no response is apparent after 1-2 wk; a baseline CBC and a recheck twice weekly should guide therapy duration; once the ANC is >1000/µL for 3 d, the agent can be discontinued
Pediatric
G-CSF 5 mcg/kg/d SC/IV
Interactions
Do not use 12-24 h before or 24 h after administering cytotoxic chemotherapy because these drugs increase sensitivity of rapidly dividing myeloid cells to cytotoxic chemotherapy
Contraindications
Documented hypersensitivity to this drug or class of drugs; hypersensitivity to E coli proteins
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause bone pain, musculoskeletal pain, nausea, vomiting, and rash; cutaneous vasculitis, exacerbation of the underlying RA, Sweet syndrome (acute neutrophilic dermatosis), myelodysplastic syndrome, acute myeloid leukemia, leukocytosis, or possible tumor growth may occur
Sargramostim (Leukine)
GM-CSF stimulates division and maturation of earlier myeloid and macrophage precursor cells. Reportedly increases granulocytes in 48-91% of patients.
Dosing
Adult
60-500 mcg/m2 IV over 2 h to 5-12 mcg/m2/d SC
Pediatric
Not established
Interactions
Lithium and corticosteroids may potentiate myeloproliferative effects
Contraindications
Documented hypersensitivity; excessive myeloid blasts (>10%) in bone marrow or peripheral blood
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Diffuse bone ache or pain may result from stimulation of bone marrow cells; caution in malignancies with myeloid characteristics
Follow-up
Further Inpatient Care
- Admission is mandatory for patients with serious life-threatening infections. Patients need cultures and parenteral antibiotics.
- Acknowledge the possibility of infection with encapsulated organisms because splenomegaly may be a marker for a dysfunctional reticuloendothelial system incapable of clearing these organisms. Staphylococcus aureus, streptococcal species, and gram-negative rods are potential infecting organisms.
Further Outpatient Care
- Schedule patients with Felty syndrome for regular follow-up with a rheumatologist to monitor therapy and to assess progress.
- No firm guidelines address immunization practice in patients with Felty syndrome, but ensuring vaccination against encapsulated organisms seems prudent.
Complications
- Splenic rupture
- Life-threatening infection
- Toxicity due to immunosuppressive regimens
- Portal hypertension and gastrointestinal bleeding due to nodular regenerative hyperplasia of the liver
Prognosis
- Granulocytopenia is defined as an absolute neutrophil count (ANC) of less than 2000/µL, and the infection risk increases as the ANC drops. Infection incidence increases significantly when the polymorphonuclear leukocyte (PMN) count is less than 1000/µL.
- Lymphoproliferative malignancies were more prevalent in a retrospective study of male patients with Felty syndrome treated at the Department of Veterans Affairs. In particular, the patients had an increased prevalence of non-Hodgkin lymphoma.9
Patient Education
- Educate patients with Felty syndrome about the warning signs of infection and ensure that they have ready access to medical care.
- Some practitioners supply patients with Felty syndrome with a broad-spectrum oral antibiotic to take at the first signs of a bacterial infection. Instruct patients that this is an individualized decision and advise them to contact their physician immediately if such a situation develops.
Miscellaneous
Medicolegal Pitfalls
- Failure to acknowledge that many of the regimens used to treat rheumatoid arthritis (RA) can cause bone marrow suppression and neutropenia
- Failure to diagnose Felty syndrome, thereby attributing the granulocytopenia to the RA treatment regimen
- Failure to realize that active infection can transiently elevate the WBC count and mask the underlying condition
- Failure to perform repeated examination of the abdomen in patients with RA, which is necessary to find early splenomegaly
Special Concerns
- Neutropenia with LGL
- This condition, often referred to as pseudo-Felty syndrome, is a chronic leukemia characterized by a clonal expansion of cytotoxic T cells bearing the CD16 and CD57 markers. The large granular lymphocytes may occur in both the periphery and the bone marrow.
- LGL is an unusual entity that occurs in less than 1% of patients with RA. LGL usually develops at the onset of RA, while Felty syndrome occurs later in the disease course.
- The sex incidence is equal, and the severity of the underlying RA is less marked.
- Neutropenia may occur in conjunction with a normal or increased total WBC count.
- Thrombocytopenia, anemia, and splenomegaly may occur. In some situations, differentiation from Felty syndrome may require immunophenotype analysis.
- Therapy for LGL is rarely necessary.
References
Felty AR. Chronic arthritis in the adult associated with splenomegaly and leukopenia. Bull Johns Hopkins Hosp. 1924;35:16.
Burks EJ, Loughran TP Jr. Pathogenesis of neutropenia in large granular lymphocyte leukemia and Felty syndrome. Blood Rev. Sep 2006;20(5):245-66. [Medline].
Hellmich B, Csernok E, Schatz H, et al. Autoantibodies against granulocyte colony-stimulating factor in Felty's syndrome and neutropenic systemic lupus erythematosus. Arthritis Rheum. Sep 2002;46(9):2384-91. [Medline].
Ghavami A, Genevay S, Fulpius T, et al. Etanercept in treatment of Felty's syndrome. Ann Rheum Dis. Jul 2005;64(7):1090-1. [Medline].
Sordet C, Gottenberg JE, Hellmich B, et al. Lack of efficacy of rituximab in Felty's syndrome. Ann Rheum Dis. Feb 2005;64(2):332-3. [Medline].
Talip F, Walker N, Khan W, et al. Treatment of Felty's syndrome with leflunomide. J Rheumatol. Apr 2001;28(4):868-70. [Medline].
Talip F, Walker N, Khan W, et al. Treatment of Felty's syndrome with leflunomide. J Rheumatol. Apr 2001;28(4):868-70. [Medline].
Ishikawa K, Tsukada Y, Tamura S, et al. Salazosulfapyridine-induced remission of Felty's syndrome along with significant reduction in neutrophil-bound immunoglobulin G. J Rheumatol. Feb 2003;30(2):404-6. [Medline].
Gridley G, Klippel JH, Hoover RN, et al. Incidence of cancer among men with the Felty syndrome. Ann Intern Med. Jan 1 1994;120(1):35-9. [Medline].
Balint GP, Balint PV. Felty's syndrome. Best Pract Res Clin Rheumatol. Oct 2004;18(5):631-45. [Medline]. [Full Text].
Barton JC, Prasthofer EF, Egan ML, et al. Rheumatoid arthritis associated with expanded populations of granular lymphocytes. Ann Intern Med. Mar 1986;104(3):314-23. [Medline].
Breedveld FC, Fibbe WE, Hermans J, et al. Factors influencing the incidence of infections in Felty's syndrome. Arch Intern Med. May 1987;147(5):915-20. [Medline].
Campion G, Maddison PJ, Goulding N, et al. The Felty syndrome: a case-matched study of clinical manifestations and outcome, serologic features, and immunogenetic associations. Medicine (Baltimore). Mar 1990;69(2):69-80. [Medline].
Ellman MH. Leukocyte colony-stimulating factors for rheumatologists. J Clin Rheumatol. 1997;3(4):217-223.
Rashba EJ, Rowe JM, Packman CH. Treatment of the neutropenia of Felty syndrome. Blood Rev. Sep 1996;10(3):177-84. [Medline].
Rosenstein ED, Kramer N. Felty's and pseudo-Felty's syndromes. Semin Arthritis Rheum. Dec 1991;21(3):129-42. [Medline].
Starkebaum G. Use of colony-stimulating factors in the treatment of neutropenia associated with collagen vascular disease. Curr Opin Hematol. May 1997;4(3):196-9. [Medline].
Ward MM. Decreases in rates of hospitalizations for manifestations of severe rheumatoid arthritis, 1983-2001. Arthritis Rheum. Apr 2004;50(4):1122-31. [Medline].
Keywords
Felty syndrome, FS, Felty's syndrome, pseudo-Felty syndrome, pseudo-Felty's syndrome, rheumatoid arthritis, RA, splenomegaly, granulocytopenia, rheumatoid factor, RF, large granular lymphocytosis syndrome, LGL
Contributor Information and Disclosures
Author
Richard M Keating, MD, FACR, FACP, Professor of Medicine, Co-Director, The University of Chicago Arthritis Center, Department of Medicine, Section of Rheumatology, The University of Chicago
Richard M Keating, MD, FACR, FACP is a member of the following medical societies: American College of Physicians and American College of Rheumatology
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
Lawrence H Brent, MD, Associate Professor of Medicine, Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center
Lawrence H Brent, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, and American College of Rheumatology
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Grant/research funds Other; Amgen Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Immunology Honoraria Speaking and teaching
CME Editor
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Chief Editor
Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; Merck, Amgen, Biogen, Zimmer, Wyeth, Johnson&Johnson, Stryker, Medtronic, Zimmer.Abbott, Ownership interest Other; West Penn Allegheny Health System Consulting fee Consulting; Alpharma Honoraria Consulting; Proctor&Gamble Grant/research funds Independent contractor