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Felty Syndrome HELP
Based on 48 articles published since 2010

These are the 48 published articles about Felty Syndrome that originated from Worldwide during 2010-2020.
+ Citations + Abstracts
Pages: 1 · 2
1 Review Inflammatory arthritis and crystal arthropathy: Current concepts of skin and systemic manifestations. 2018

Fazel, Mahdieh / Merola, Joseph F / Kurtzman, Drew J B. ·Division of Dermatology, The University of Arizona College of Medicine, Tucson, Arizona, USA. · Division of Rheumatology and Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. · Division of Dermatology, The University of Arizona College of Medicine, Tucson, Arizona, USA. Electronic address: kurtzman@email.arizona.edu. ·Clin Dermatol · Pubmed #30047436.

ABSTRACT: Systemic inflammatory disorders frequently involve the skin, and when cutaneous disease develops, such dermatologic manifestations may represent the initial sign of disease and may also provide valuable prognostic information about the underlying disorder. Familiarity with the various skin manifestations of systemic disease is therefore paramount and increases the likelihood of accurate diagnosis, which may facilitate the implementation of an appropriate treatment strategy. An improvement in quality of life and a reduction in the degree of morbidity may also be a realized benefit of accurate recognition of these skin signs. With this context in mind, this review highlights the salient clinical features and unique dermatologic manifestations of rheumatoid arthritis, adult-onset Still's disease, and the crystal arthropathy, gout.

2 Review Neutropaenia and splenomegaly without arthritis: think rheumatoid arthritis. 2018

Aslam, Fawad / Cheema, Rabia S / Feinstein, Michael / Chang-Miller, April. ·Department of Rheumatology, Mayo Clinic Arizona, Scottsdale, Arizona, USA. · Internal Medicine, St. Mary's Hospital, Waterbury, Connecticut, USA. · Department of Hematology and Oncology, Mayo Clinic Arizona, Scottsdale, Arizona, USA. ·BMJ Case Rep · Pubmed #30002215.

ABSTRACT: Felty syndrome(FS) is an uncommon, but severe, extra-articular manifestation of rheumatoid arthritis (RA). It occurs in patients with longstanding RA. It is extremely rare for RA to present as FS or develop after initially presenting as neutropaenia and splenomegaly. We describe a case of 47-year-old woman who was diagnosed simultaneously with FS and possible RA after testing positive for anticyclic citrullinated peptide antibody, but a negative rheumatoid factor. She had an excellent response to methotrexate. We review the existing literature of such cases and emphasise the importance of serological testing for RA in patients presenting with neutropaenia and splenomegaly, even in the absence of joint symptoms or prior diagnosis of RA.

3 Review Chronic neutropenia in LGL leukemia and rheumatoid arthritis. 2017

Gazitt, Tal / Loughran, Thomas P. ·University of Washington, Seattle, WA; and. · University of Virginia, Charlottesville, VA. ·Hematology Am Soc Hematol Educ Program · Pubmed #29222254.

ABSTRACT: This section reviews the diagnostic criteria and pathogenesis of large granular lymphocyte (LGL) leukemia. There is a particular focus on the overlap of LGL leukemia and rheumatoid arthritis (Felty's syndrome). Current understanding of the mechanisms of neutropenia in these disorders is discussed. Finally, treatment indications and therapeutic recommendations are outlined.

4 Review None 2017

Kneitz, C / Atta, J / Burkhardt, H. ·Klinik für Innere Medizin II (Rheumatologie und Klinische Immunologie, Geriatrie), Klinikum Südstadt Rostock, Am Südring 91, 18059, Rostock, Deutschland. christian.kneitz@kliniksued-rostock.de. · Tumortherapie-Center, Prof. Dr. Stehling Institut für bildgebende Diagnostik, Strahlenbergerstr. 110 - AlphaHaus, 63067, Offenbach am Main, Deutschland. atta@tumortherapie-center.de. · Abteilung Rheumatologie, Medizinische Klinik II, Universitätsklinikum Frankfurt, Goethe Universität Frankfurt am Main, Theodor-Stern Kai 7, 60590, Frankfurt am Main, Deutschland. harald.burkhardt@kgu.de. ·Z Rheumatol · Pubmed #28971213.

ABSTRACT: Hematological alterations can often be observed during rheumatic diseases. The effects can be clinically severe, ranging from anemia of different grades of severity, through increased risk of hemorrhage due to thrombocytopenia up to severe infections as a result of high-grade leukocytopenia. The clinical sequelae for patients are predominantly determined by the extent of cytopenia. The underlying disease itself can initially be considered as the cause. Examples are anemia as a result of chronic inflammation, antibody-mediated thrombocytopenia as in systemic lupus erythematosus (SLE) or granulocytopenia within the framework of Felty's syndrome. Immunosuppressive treatment also often leads to alterations in the blood constituents. Although some substances, such as cyclophosphamide can suppress all three cell types, there are also selective effects, such as isolated thrombocytopenia under treatment with tocilizumab and JAK inhibitors. The differential diagnostic clarification of cytopenia can be difficult and necessitates a systematic work-up of the course of the disease and the subsequent treatment. The reviews of anemia, leukocytopenia and thrombocytopenia presented here summarize the most important components of the differentiation of hematological alterations in patients with rheumatic diseases.

5 Review Management of neutropenia in patients with rheumatoid arthritis. 2015

Lazaro, Estibaliz / Morel, Jacques. ·Service de médecine interne, hôpital du Haut-Lévêque, université de Bordeaux, 33604 Pessac, France. Electronic address: estibaliz.lazaro@chu-bordeaux.fr. · Service de médecine interne, hôpital du Haut-Lévêque, université de Bordeaux, 33604 Pessac, France; Département de rhumatologie, hôpital Lapeyronie, université de Montpellier 1, 34295 Montpellier cedex 5, France. ·Joint Bone Spine · Pubmed #25819216.

ABSTRACT: Neutropenia is defined as a neutrophil count lower than 1.5g/L, with categorization as mild, moderate, or severe when the count is 1.5-1g/L, 1-0.5g/L, or<0.5g/L, respectively. The main complication is infection, whose risk increases with the depth and duration of the neutropenia. Comprehensive etiological investigations are mandatory to determine the best treatment strategy. Constitutional neutropenia is rarely seen in everyday rheumatology practice. It predominantly affects patients of African descent and is usually moderate and well tolerated. Congenital neutropenia due to genetic abnormalities is severe and chiefly seen in the pediatric population. Most cases of neutropenia in patients with rheumatoid arthritis (RA) are acquired. Medications are the most common causes, making detailed history-taking crucial. Many medications used to treat RA can induce neutropenia. Folic acid deficiency should be sought routinely in patients taking methotrexate. A less common cause of neutropenia is an RA-related autoimmune reaction. Splenomegaly suggests Felty's syndrome, which is accompanied with large granular lymphocytic (LGL) leukemia in 40% of cases. The treatment depends on the depth of the neutropenia and findings from the etiological workup. A neutrophil count below 0.5g/L, a fever, and the presence of clinical signs indicate a life-threatening condition requiring emergent treatment. In other patients, the first step is immediate discontinuation of any possibly involved drugs, simultaneously with the etiological workup.

6 Review Treatment of pseudo Felty's syndrome: Is there a place for rituximab? 2015

Verhoeven, Frank / Guillot, Xavier / Prati, Clément / Wendling, Daniel. ·Department of rheumatology, CHRU de Besançon, 2, Boulevard Fleming, 25030 Besançon, France. · Department of rheumatology, CHRU de Besançon, 2, Boulevard Fleming, 25030 Besançon, France. Electronic address: dwendling@chu-besancon.fr. ·Joint Bone Spine · Pubmed #25623522.

ABSTRACT: OBJECTIVE: Pseudo Felty's syndrome (PFS) is an uncommon syndrome occurring in Rheumatoid Arthritis and characterized by a monoclonal expansion of lymphocytes with neutropenia. Methotrexate is the first line recommended treatment. In case of incomplete response, cyclophosphamide may be used for hematological features but does not share the same efficacy on arthritis. We investigate the effect of rituximab in PFS as second line treatment. METHODS: This is a retrospective study about six cases of PFS treated with methotrexate and/or rituximab. RESULTS: Five women and 1 man (mean age: 66 years) were included. All patients were positive for rheumatoid factor and five were anti CCP positive. All patients presented bone erosions, three had splenomegaly. The disease duration was between 0 and 19 years at large granular lymphocyte (LGL) leukemia diagnosis. Methotrexate was effective and well tolerated for two patients with a follow up of 7 and 4 years. For a third patient, the hematological symptoms were predominant and he received after methotrexate, several infusions of cyclophosphamide. Three patients (2 T-cell and 1 NK-cell LGLL) were treated with rituximab (two 1000 mg infusions) with a decreased DAS28 and an increased neutrophil count, with subsequent courses of rituximab one to three years later with the same efficacy. This treatment was well tolerated without infectious events after a follow up of one and three years. CONCLUSION: Methotrexate is effective in near half of cases of PFS. In second line, rituximab may be a therapeutic option with good efficacy and tolerance.

7 Review Acquired inhibitors to factor VIII and fibrinogen in the setting of T-cell large granular lymphocyte leukemia: a case report and review of the literature. 2015

Murphy, Peter W / Brett, L Kyle / Verla-Tebit, Emaculate / Macik, B Gail / Loughran, Thomas P. ·aDepartment of Internal Medicine bDivision of Hematology and Oncology, University of Virginia School of Medicine, Charlottesville, Virginia, USA. ·Blood Coagul Fibrinolysis · Pubmed #25396761.

ABSTRACT: Large granular lymphocyte (LGL) leukemia is an indolent lymphoproliferative malignancy which dysregulates humoral immunity and underlies the myriad autoimmune phenomena. We describe a 62-year-old woman with Felty's syndrome who developed a severe bleeding diathesis. Laboratory evaluation demonstrated acquired inhibitors to both factor VIII (FVIII) and fibrinogen, likely secondary to T-cell LGL leukemia. After a complicated course, the patient's inhibitors were extinguished with rituximab and high-dose corticosteroids. Bleeding was controlled with alternating FEIBA (factor eight inhibitor bypassing activity) and recombinant activated FVII. This report reviews the literature comparing the efficacy of various treatment modalities for both disorders. To our knowledge, this is the first reported case of a patient with LGL leukemia acquiring an inhibitor to FVIII or fibrinogen.

8 Review Syndromes affecting skin and mucosa. 2014

Koutlas, Ioannis G. ·Division of Oral and Maxillofacial Pathology, School of Dentistry, University of Minnesota, 515 Delaware Street SE #16-116B, Minneapolis, MN 55455, USA. Electronic address: koutl001@umn.edu. ·Atlas Oral Maxillofac Surg Clin North Am · Pubmed #25171995.

ABSTRACT: -- No abstract --

9 Review Felty's syndrome with hyperthyroidism: a case report and literature review. 2014

Huang, Tianlun / Liu, Mengyuan / Xu, Gaosi. ·Department of Rheumatology, Second Affiliated Hospital, Nanchang, China. ·Int J Rheum Dis · Pubmed #24472276.

ABSTRACT: -- No abstract --

10 Review Citrullination of autoantigens implicates NETosis in the induction of autoimmunity. 2014

Dwivedi, Nishant / Radic, Marko. ·Program in Cellular and Molecular Medicine, Boston Children's Hospital and Harvard Medical School, , Boston, Massachusetts, USA. ·Ann Rheum Dis · Pubmed #24291655.

ABSTRACT: Tolerance blocks the expression of autoantibodies, whereas autoimmunity promotes it. How tolerance breaks and autoantibody production begins thus are crucial questions for understanding and treatment of autoimmune diseases. Evidence implicates cell death and autoantigen modifications in the initiation of autoimmune reactions. One form of neutrophil cell death called NETosis deserves attention because it requires the post-translational modification of histones and results in the extracellular release of chromatin. NETosis received its name from NET, the acronym given to Neutrophil Extracellular Trap. The extracellular chromatin incorporates histones in which arginines have been converted to citrullines by peptidylarginine deiminase IV (PAD4). The deiminated chromatin may function to capture or 'trap' bacterial pathogens, thus generating an extracellular complex of deiminated histones and bacterial cell adjuvants. The complex of bacterial antigens and deiminated chromatin may be internalised by host phagocytes during acute inflammatory conditions, as arise during bacterial infections or chronic autoinflammatory disorders. The uptake and processing of deiminated chromatin together with bacterial adjuvants by phagocytes may induce the presentation of modified histone epitopes and co-stimulation, thus yielding a powerful stimulus to break tolerance. Autoantibodies to deiminated histones are prevalent in Felty's syndrome patients and are present in systemic lupus erythematosus (SLE) and patients with rheumatoid arthritis (RA). These observations clearly implicate histone deimination as an epigenetic mark that can act as an autoantibody stimulant.

11 Review [Large granular lymphocyte leukemia: clinical and pathogenic aspects]. 2013

Lazaro, E / Duffau, P / Chaigne Delalande, S / Greib, C / Pellegrin, J-L / Viallard, J-F. ·Service de médecine interne, hôpital du Haut Lévêque, avenue Magellan, 33604 Pessac, France. estibaliz.lazaro@chu-bordeaux.fr ·Rev Med Interne · Pubmed #23928096.

ABSTRACT: Large granular lymphocyte leukemia (LGL) is a hematologic disorder characterized by a monoclonal expansion of large lymphocytes containing azurophilic granules with a T CD3(+)CD57(+) or Natural Killer (NK) CD3(-)CD56(+) phenotype. The World Health Organization (WHO) classification identifies three entities: the T LGL, the chronic lymphoproliferative disorder of NK-cells, and the aggressive NK-cell leukemia. T LGL and chronic lymphoproliferative disorder of NK-cells are indolent diseases frequently associated with cytopenias and a wide spectrum of auto-immune manifestations. Neutropenia can lead to recurrent bacterial infections, which represent an indication of initiating a treatment in most of the cases. Immunosuppressive therapies are usually used in this context. In contrast, aggressive NK-cell leukemia follows a fulminant course with a poor prognosis because patients are refractory to most of the treatments. There is now a considerable interest in the pathophysiology of the disease with the perspective of new therapeutic options.

12 Review Felty's syndrome without rheumatoid arthritis? 2013

Rozin, Ap / Hoffman, R / Hayek, T / Balbir-Gurman, A. ·B. Shine Department of Rheumatology, Rambam Health Care Campus and Technion, POB 9602, Haifa 31096, Israel. a_rozin@rambam.health.gov.il ·Clin Rheumatol · Pubmed #23292482.

ABSTRACT: Felty's syndrome (FS) is characterized by neutropenia and splenomegaly in patients with seropositive (RF+, anti-CCP+) rheumatoid arthritis (RA). As a result of neutropenia, affected persons are increasingly susceptible to infections. In the majority of patients, FS appears in the course of long-standing and well-established RA. Manifestations of FS without clinical but only with laboratory features of RA are extremely rare. We present a case of severe neutropenia and mild splenomegaly in a patient with high titers of RF and anti-CCP. For 4 years, patient's neutropenia remained asymptomatic. The neutropenia reduction to agranulocytosis was followed by successful methotrexate-corticosteroid therapy. Efficacy of the standard anti-RA therapy confirmed autoimmune mechanism of the Felty's neutropenia. The most important lesion from our case is to recognize this condition in the range of autoimmune rheumatic diseases without delay. We reviewed literature with non-articular FS.

13 Review Autoimmune manifestations in large granular lymphocyte leukemia. 2012

Bockorny, Bruno / Dasanu, Constantin A. ·Department of Medicine, University of Connecticut Medical Center, Farmington, CT 06030-1235, USA. bbockorny@resident.uchc.edu ·Clin Lymphoma Myeloma Leuk · Pubmed #22999943.

ABSTRACT: Large granular lymphocyte (LGL) leukemia features a group of indolent lymphoproliferative diseases that display a strong association with various autoimmune conditions. Notwithstanding, these autoimmune conditions have not been comprehensively characterized or systematized to date. As a result, their clinical implications remain largely unknown. The authors offer a comprehensive review of the existing literature on various autoimmune conditions documented in the course of T-cell LGL (T-LGL) leukemia. Though some of them are thought be secondary to the LGL leukemia, others could be primary and might even play a role in its pathogenesis. A considerable clinico-laboratory overlap between T-LGL leukemia associated with rheumatoid arthritis and Felty's syndrome suggests that they are just different eponyms for the same clinical entity.

14 Review Neutrophil activation and B-cell stimulation in the pathogenesis of Felty's syndrome. 2012

Dwivedi, Nishant / Radic, Marko. ·Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA. ·Pol Arch Med Wewn · Pubmed #22814518.

ABSTRACT: Felty's syndrome (FS) is a severe arthritic disorder that features chronic neutrophil activation and progresses to neutropenia and susceptibility to unabated infections. The life‑threatening manifestations of FS have focused the attention of clinical experimenters who have made persistent efforts to find new and effective therapies. This review highlights important milestones in the research on FS and draws attention to recent studies on the antigen specificity of antibodies present in patients' sera. Recent data have indicated that immunoglobulins G (IgGs) in patients with FS bind selectively and specifically to deiminated histones and neutrophil extracellular chromatin traps (NETs). Deimination is the conversion of certain arginine residues in proteins to citrullines by the enzyme peptidylarginine deiminase 4. Earlier observations had indicated that IgGs in FS patients avidly bind to citrullinated peptides. These observations suggest that NETosis, the type of cell death that is defined by the release of NETs, provides autoantigens that stimulate B cell responses in this patient group. This insight parallels recent observations in other autoimmune conditions and lends support to the paradigm that NETosis plays a leading role in the pathogenesis of antiself immune responses. 

15 Review One case of Felty's syndrome efficiently treated with rituximab. 2012

Tomi, Anne-Laurence / Lioté, Frédéric / Ea, Hang-Korng. ·Hôpital Lariboisière, Rheumatology Department, pôle appareil locomoteur, centre Viggo-Petersen, 2 rue Ambroise-Paré, Paris, France. ·Joint Bone Spine · Pubmed #22401785.

ABSTRACT: Felty's syndrome (FS) is a rare association of rheumatoid arthritis (RA), neutropenia and splenomegaly. Mechanisms of neutropenia in FS are unclear but involve both innate and humoral immunity, impaired granulopoiesis and decreased granulocyte half-life. Several treatments have been used without clear efficiency. We report a patient with FS efficiently treated with rituximab (RTX), the monoclonal anti-CD20 antibody. A literature review of FS treated with RTX was performed.

16 Review Biological agents in the management of Felty's syndrome: a systematic review. 2012

Narváez, Javier / Domingo-Domenech, Eva / Gómez-Vaquero, Carmen / López-Vives, Laura / Estrada, Paula / Aparicio, María / Martín-Esteve, Irene / Nolla, Joan Miquel. ·Department of Rheumatology, Hospital Universitario de Bellvitge-IDIBELL, Barcelona, Spain. fjnarvaez@bellvitgehospital.cat ·Semin Arthritis Rheum · Pubmed #22119104.

ABSTRACT: OBJECTIVE: To review and summarize the information available on the effectiveness and safety of biological therapies in refractory Felty's syndrome (FS). METHODS: We describe a case of FS with severe neutropenia and recurrent bacterial infections unresponsive to disease-modifying antirheumatic drug treatment and long-term administration with granulocyte colony-stimulating factor, in which treatment with rituximab (RTX) was useful and resulted in a sustained neutrophil response. Current evidence on the use of biological therapies in FS is also analyzed through a systematic review of the English-language literature, based on a PubMed search. RESULTS: Available data on the use of biological therapies in refractory FS are based only on several case reports and are limited to the use of RTX and some anti-tumor necrosis factor α agents (etanercept, infliximab, and adalimumab). Including the case described here, data are available on 8 patients treated with RTX. A sustained increase in the absolute neutrophil count (>1500/mm(3)) was observed in 62.5% (5/8) of these patients after 1 cycle of treatment. In most of them, the hematological response was accompanied by a parallel improvement in biological markers of inflammation and other clinical manifestations of FS (arthritis, recurrent infections, systemic symptoms, etc). After a median follow-up of 9 months (range, 6-14), only 1 of these patients relapsed and neutropenia reappeared; in this patient, retreatment was rapidly effective. No significant adverse events related to RTX therapy were reported. Experience with anti-tumor necrosis factor agents is limited to 6 patients, none of whom presented any sustained increase in neutrophil count. CONCLUSIONS: Although it is not yet possible to make definite recommendations, the global analysis of all cases reported to date only supports the use of RTX as a second-line therapy in patients with refractory FS.

17 Review The spectrum of large granular lymphocyte leukemia and Felty's syndrome. 2011

Liu, Xin / Loughran, Thomas P. ·Department of Medicine, Penn State Hershey Cancer Institute, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033-0850, USA. Xliu2@hmc.psu.edu ·Curr Opin Hematol · Pubmed #21546829.

ABSTRACT: PURPOSE OF REVIEW: Patients with chronic large granular lymphocyte (LGL) leukemia often have rheumatoid arthritis (RA), neutropenia and splenomegaly, thereby resembling the manifestations observed in patients with Felty's syndrome, which is a rare complication of RA characterized by neutropenia and splenomegaly. Both entities have similar clinical and laboratory presentation, as well as a common genetic determinant, HLA-DR4, indicating they may be part of the same disease spectrum. This review paper seeks to discuss the underlying pathogenesis and therapeutic algorithm of RA, neutropenia and splenomegaly in the spectrum of LGL leukemia and Felty's syndrome. RECENT FINDINGS: We hypothesize that there may be a common pathogenic mechanism between LGL leukemia and typical Felty's syndrome. Phenotypic and functional data have strongly suggested that CD3 LGL leukemia is antigen-activated. Aberrations in the T-cell repertoire with the emergence of oligoclonal/clonal lymphoid populations have been found to play a pivotal role in pathogenesis of RA. The biologic properties of the pivotal T cell involved in RA pathogenesis are remarkably similar to those in leukemic LGL. SUMMARY: RA-associated T-cell LGL leukemia and articular manifestations of typical Felty's syndrome are not distinguishable. A common pathogenetic link between LGL leukemia and RA is proposed.

18 Review Management of autoimmune neutropenia in Felty's syndrome and systemic lupus erythematosus. 2011

Newman, Kam A / Akhtari, Mojtaba. ·Department of Internal Medicine, Jamaica Hospital Medical Center, NY 11418, United States. ·Autoimmun Rev · Pubmed #21255689.

ABSTRACT: Autoimmune neutropenia, caused by neutrophil-specific autoantibodies is a common phenomenon in autoimmune disorders such as Felty's syndrome and systemic lupus erythematosus. Felty's syndrome is associated with neutropenia and splenomegaly in seropositive rheumatoid arthritis which can be severe and with recurrent bacterial infections. Neutropenia is also common in systemic lupus erythematosus and it is included in the current systemic lupus classification criteria. The pathobiology of the autoimmune neutropenia in Felty's syndrome and systemic lupus erythematosus is complex, and it could be a major cause of morbidity and mortality due to increased risk of sepsis. Treatment should be individualized on the basis of patient's clinical situation, and prevention or treatment of the infection. Recombinant human granulocyte colony-stimulating factor is a safe and effective therapeutic modality in management of autoimmune neutropenia associated with Felty's syndrome and systemic lupus erythematosus, which stimulates neutrophil production. There is a slight increased risk of exacerbation of the underlying autoimmune disorder, and recombinant human granulocyte colony-stimulating factor dose and frequency should be adjusted at the lowest effective dose.

19 Review Gastrointestinal and hepatic manifestations of rheumatoid arthritis. 2011

Ebert, Ellen C / Hagspiel, Klaus D. ·Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. jeydels@yahoo.com ·Dig Dis Sci · Pubmed #21203902.

ABSTRACT: Rheumatoid arthritis (RA), characterized by inflammation of the synovium and surrounding structures, has a prevalence of 0.5-1%. Rheumatoid vasculitis (RV) is an inflammatory condition of the small- and medium-sized vessels that affects up to 5% of patients with RA with intestinal involvement in 10-38% of these cases. Clinically apparent RV of the gastrointestinal (GI) tract, while rare, is often catastrophic, resulting in ischemic ulcers and bowel infarction. Vasculitis of the colon may present as pancolitis clinically similar to ulcerative colitis. Rectal biopsies that include submucosal vessels are positive for vasculitis in up to 40% of cases. Abnormal esophageal motility in RA may result in heartburn and dysphagia. Chronic atrophic gastritis may be associated with hypergastrinemia and hypo- or achlorhydria, promoting small bowel bacterial overgrowth. RA is the most common cause of secondary amyloidosis with GI symptoms in 22% of affected patients. Although amyloid is usually found in the liver, it is rarely evident clinically. Felty's syndrome occurs in less than 1% of patients with RA and is characterized by neutropenia and splenomegaly. The liver may be involved with portal fibrosis or nodular regenerative hyperplasia. Liver histology is abnormal in 92% of RA patients at autopsy, although the changes are usually mild without associated hepatomegaly. Drug-induced liver disease may occur with aspirin, sulfasalazine, and methotrexate. Significant liver damage is rare if the drug is discontinued or the patient is properly monitored. RA can affect both the GI tract and the liver; changes are usually mild except with RV.

20 Review High avidity cytokine autoantibodies in health and disease: pathogenesis and mechanisms. 2010

Watanabe, Masato / Uchida, Kanji / Nakagaki, Kazuhide / Trapnell, Bruce C / Nakata, Koh. ·Department of Respiratory Medicine, Kyorin University School of Medicine, Tokyo 181-8611, Japan. ·Cytokine Growth Factor Rev · Pubmed #20417147.

ABSTRACT: Numerous reports have documented the presence of autoantibodies working against naturally occurring cytokines in humans in health and disease. In most instances, their physiological and pathophysiological significance remains unknown. However, recent advances in the methodologies for detecting cytokine autoantibodies and their application in research focused on specific disorders have shown that some cytokine autoantibodies play an important role in the pathogenesis of disease. Additionally, levels of cytokine autoantibodies may also correlate with disease severity and progression in certain infectious and autoimmune diseases but not in others. This suggests that cytokine-specific pathogenic differences exist. While multiple lines of evidence support the notion that high avidity cytokine autoantibodies are present and likely to be ubiquitous in healthy individuals, their potential physiological role, if any, is less clear. It is believed that they may function by scavenging pro-inflammatory cytokines and thereby inhibiting deleterious 'endocrine' effects, or by serving as carrier proteins, providing a 'reservoir' of inactive cytokines and thus modulating cytokine bioactivity. A central hypothesis is that sustained or repeated high-level exposure to cytokines triggers defects in T-cell tolerance, resulting in the expansion of existing cytokine autoantibody-producing B cells.

21 Article 47-Year-Old Man With Pancytopenia and Fever. 2019

Hoversten, Katherine P / Higgins, Alexandra S / Ashrani, Aneel A. ·Resident in Internal Medicine, Mayo Clinic School of Graduate Medical Education, Rochester, MN. · Advisor to residents and Consultant in Hematology, Mayo Clinic, Rochester, MN. Electronic address: ashrani.aneel@mayo.edu. ·Mayo Clin Proc · Pubmed #31171117.

ABSTRACT: -- No abstract --

22 Article None 2018

Enselmann, Kai / Frasnelli, Andreas. ·1 Spitalzentrum Oberwallis, Spital Visp. ·Praxis (Bern 1994) · Pubmed #29642792.

ABSTRACT: -- No abstract --

23 Article A Case Report of Chikungunya Fever, Rheumatoid Arthritis, and Felty's Syndrome. 2018

Amaral, José Kennedy / Schoen, Robert T. ·Faculty of Medicine Estacio of Juazeiro de Norte, Juazeiro de Norte, Brazil. · Section of Rheumatology, Yale University School of Medicine, New Haven, CT, USA. robert.schoen@yale.edu. ·Rheumatol Ther · Pubmed #29536378.

ABSTRACT: INTRODUCTION: Chronic chikungunya (CHIK) arthritis, an inflammatory arthritis, often follows acute CHIK fever (CHIKF), a viral infection. The pathogenesis of chronic CHIK arthritis is poorly characterized, but may resemble other forms of inflammatory arthritis. Clinically, chronic CHIK arthritis sometimes mimics rheumatoid arthritis (RA). CASE REPORT: We report a patient with well-characterized CHIKF followed 2 months later by chronic CHIK arthritis not only resembling RA clinically, but also associated with RA biomarkers and extra-articular features, including Felty's syndrome (FS). CONCLUSIONS: We describe this patient's excellent response to methotrexate and discuss the implications her case provides in understanding this important emerging rheumatic disease.

24 Article Somatic 2018

Savola, Paula / Brück, Oscar / Olson, Thomas / Kelkka, Tiina / Kauppi, Markku J / Kovanen, Panu E / Kytölä, Soili / Sokka-Isler, Tuulikki / Loughran, Thomas P / Leirisalo-Repo, Marjatta / Mustjoki, Satu. ·Hematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Finland. · Department of Clinical Chemistry and Hematology, University of Helsinki, Finland. · University of Virginia Cancer Center; University of Virginia, Charlottesville, VA, USA. · Päijät-Häme Central Hospital, Lahti, Finland. · Faculty of Medicine, Tampere University, Finland. · Department of Pathology, University of Helsinki and HUSLAB, Helsinki University Hospital, Finland. · Laboratory of Genetics, HUSLAB, Helsinki University Hospital, Finland. · Rheumatology/Medicine, Jyväskylä Central Hospital, Finland. · Rheumatology, University of Helsinki and Helsinki University Hospital, Finland. · Hematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Center, Finland satu.mustjoki@helsinki.fi. ·Haematologica · Pubmed #29217783.

ABSTRACT: Felty syndrome is a rare disease defined by neutropenia, splenomegaly, and rheumatoid arthritis. Sometimes the differential diagnosis between Felty syndrome and large granular lymphocyte leukemia is problematic. Recently, somatic

25 Article Felty's Syndrome: A Qualitative Case Study. 2017

Woolston, Wendy / Connelly, Lynne M. · ·Medsurg Nurs · Pubmed #30304590.

ABSTRACT: Felty's syndrome is a triad of rheumatoid arthritis, splenomegaly, and neutropenia. This rare disorder is difficult to diagnose and produces many complications. The purpose of this descriptive qualitative case study was to provide a comprehensive, context-bound understanding of one patient's struggle with the condition.