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Search Results: 1 - 10 of 219951 matches for " Eric L. Matteson "
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Erdheim-Chester Disease with Right Atrial Tumor and “Temporal Arteritis”  [PDF]
Joseph Skalski, William D. Edwards, Eric L. Matteson
Open Journal of Rheumatology and Autoimmune Diseases (OJRA) , 2012, DOI: 10.4236/ojra.2012.23008
Abstract: Erdheim-Chester disease is an unusual syndrome characterized by non-Langerhans cell histiocytosis which can mimic rheumatologic diseases. We report a case of Erdheim-Chester masquerading as giant cell arteritis, which was success-fully managed with anakinra as anti IL-1 therapy.
Open-Label, Pilot Study of the Safety and Clinical Effects of Rituximab in Patients with Rheumatoid Arthritis-Associated Interstitial Pneumonia  [PDF]
Eric L. Matteson, Tim Bongartz, Jay H. Ryu, Cynthia S. Crowson, Thomas E. Hartman, Paul F. Dellaripa
Open Journal of Rheumatology and Autoimmune Diseases (OJRA) , 2012, DOI: 10.4236/ojra.2012.23011
Abstract: Objective: To investigate the clinical effect of rituximab (RTX) in the management of progressive rheumatoid arthritis related interstitial lung disease (RA-ILD). Methods: A total of 10 patients with progressive RA-ILD were enrolled into this 48-week, open-label treatment study. Treatment was with RTX at 1000 mg at day 1, day 15, and again at weeks 24 and 26, with concomitant methotrexate therapy. Results: The study included 4 men and 6 women. Of 7 evaluable patients at week 48, the diffusing capacity to carbon monoxide had worsened by at least 15% in 1 patient, was stable in 4 patients, and increased by >15% of baseline value in 2 patients. The forced vital capacity declined by at least 10% in 1 patient, was stable in 4 patients, and increased by at least 10% in 2 patients. High resolution computed tomo-graphy of the chest showed improvement in 1 patient, and was unchanged in 5. Three patients were withdrawn, one who had an infusion reaction at week 0, one at week 5 who was hospitalized for congestive heart failure at week 5 and who later died at week 32 of complications following a traumatic hip fracture, and one died at week 6 of possible pneumonia. Conclusions: In this pilot study of 10 patients with RA-ILD treated with RTX, measures of lung disease remained stable in the majority of study completers. Further research is needed to clarify whether this treatment has a role in management of RA-ILD.
Response to commentary by Dixon and Silman on the systematic review and meta-analysis by Bongartz et al.
Eric L Matteson, Tim Bongartz, Alex J Sutton, Iain Buchan
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar2033
Abstract: Meta-analyses of valid randomized trials of like agents ensure that, in the absence of a treatment effect, patients with rheumatoid arthritis in the intervention and placebo groups should share the same risk for developing serious infections or malignancy. Etanercept, although it needs study, was not included in our analysis because it is dissimilar from the anti-TNF agents.A particular advantage of such trials is that there is almost complete follow up of each treatment arm, with patients maintained in the assigned groups for intent-to-treat analysis at least for the randomized portion of the trial, even if drug exposure is discontinued for whatever reason. The appropriate statistical analysis of such comparator groups in the trial context of equivalent follow up in each arm is an odds ratio rather than incidence rate ratio. Dixon and Silman raise the possibility of bias in our analysis because of the greater dropout rate in the placebo arm, potentially leading to a lower detection threshold for malignancies in the placebo compared with the treatment arm. We found no evidence for a difference in detection thresholds in the placebo follow-up period, which was equivalent to the treatment arm in duration for the controlled phase of the studies on which we performed the analysis. Dixon and Silman also note a classification or detection bias for serious infections because of the greater likelihood of placebo patients being hospitalized. In this case our analysis would underestimate the true risk for serious infection in treated compared with control patients.In practice, lack of efficacy with the standard dose of 3 mg/kg of infliximab results in many patients using higher doses; as many as 61% of patients with rheumatoid arthritis after 1 year of use receive, on average, 4.9 mg/kg of infliximab [3]. The manufacturer's product label for infliximab allows doses up to 10 mg/kg of infliximab for partial responders [4]. Thus, not only are our findings applicable to clinical
Small vessel vasculitis History, classification, etiology, histopathology, clinic, diagnosis and treatment
Iglesias Gamarra,Antonio; Matteson,Eric L; Restrepo,José Félix;
Revista Colombiana de Reumatología , 2007,
Abstract: small-vessel vasculitis is a convenient descriptor for a wide range of diseases characterized by vascular inflammation of the venules, capillaries, and/or arterioles with pleomorphic clinical manifestations. the classical clinical phenotype is leukocytoclastic vasculitis with palpable purpura, but manifestations vary widely depending upon the organs involved. histopathologic examination in leukocytoclastic vasculitis reveals angiocentric segmental inflammation, fibrinoid necrosis, and a neutrophilic infiltrate around the blood vessel walls with erythrocyte extravasation. the etiology of small-vessel vasculitis is unknown in many cases, but in others, drugs, post viral syndromes, malignancy, primary vasculitis such as microscopic polyarteritis, and connective tissue disorders are associated. the diagnosis of small-vessel vasculitis relies on a thorough history and physical examination, as well as relevant antibody testing including antinuclear antibody and antineutrophil cytoplasmic antibody, hepatitis b and c serologies, assessment of complement, immunoglobulins, blood count, serum creatinine, liver function tests, urinalysis, radiographic imaging, and biopsy. the treatment is based primarily on corticosteroid and immunosuppressive agents.
Small vessel vasculitis History, classification, etiology, histopathology, clinic, diagnosis and treatment Vasculitis de peque os vasos Historia, clasificación, etiología, histopatología, clínica, diagnóstico y tratamiento
Antonio Iglesias Gamarra,Eric L Matteson,José Félix Restrepo
Revista Colombiana de Reumatología , 2007,
Abstract: Small-vessel vasculitis is a convenient descriptor for a wide range of diseases characterized by vascular inflammation of the venules, capillaries, and/or arterioles with pleomorphic clinical manifestations. The classical clinical phenotype is leukocytoclastic vasculitis with palpable purpura, but manifestations vary widely depending upon the organs involved. Histopathologic examination in leukocytoclastic vasculitis reveals angiocentric segmental inflammation, fibrinoid necrosis, and a neutrophilic infiltrate around the blood vessel walls with erythrocyte extravasation. The etiology of small-vessel vasculitis is unknown in many cases, but in others, drugs, post viral syndromes, malignancy, primary vasculitis such as microscopic polyarteritis, and connective tissue disorders are associated. The diagnosis of small-vessel vasculitis relies on a thorough history and physical examination, as well as relevant antibody testing including antinuclear antibody and antineutrophil cytoplasmic antibody, hepatitis B and C serologies, assessment of complement, immunoglobulins, blood count, serum creatinine, liver function tests, urinalysis, radiographic imaging, and biopsy. The treatment is based primarily on corticosteroid and immunosuppressive agents. El término vasculitis de peque os vasos describe a un grupo de enfermedades caracterizadas por inflamación de vénulas, capilares y/o arteriolas con manifestaciones clínicas pleomórficas. El fenotipo clínico clásico es la vasculitis leucocitoclástica con púrpura palpable, pero con manifestaciones que varían ampliamente dependiendo del órgano comprometido. La histología en la vasculitis leucocitoclástica revela una inflamación segmentaria angiocéntrica, necrosis fibrinoide e infiltrado neutrofílico alrededor de los vasos sanguíneos, con extravasación de eritrocitos. La etiología de las vasculitis de peque os vasos es desconocida, en muchos casos, pero en otros se ha asociado con drogas, síndromes post virales, neoplasias, vasculitis primarias como la poliarteritis microscópica, y enfermedades del tejido conjuntivo. El diagnóstico de las vasculitis de peque os vasos se basa en la historia clínica y el examen físico, así como con estudio de anticuerpos como los anticuerpos antinucleares y los anticuerpos contra el citoplasma de los neutrófilos, serología de hepatitis B y C, determinación de inmunoglobulinas, complemento, creatinina sérica, función renal, urianálisis, estudios de imágenes y biopsia. El tratamiento se basa primariamente en el uso de corticosteroides e inmunosupresores.
Cardiovascular co-morbidity in rheumatic diseases
Carl Turesson,Lennart TH Jacobsson,Eric L Matteson
Vascular Health and Risk Management , 2008,
Abstract: Carl Turesson1,2, Lennart TH Jacobsson1, Eric L Matteson21Department of Rheumatology, Malm University Hospital, Malm , Sweden; 2Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, USAAbstract: Patients with rheumatic disorders have an increased risk of cardiovascular disease (CVD). This excess co-morbidity is not fully explained by traditional risk factors. Disease severity is a major risk factor for CVD in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Shared disease mechanisms in atherosclerosis and rheumatic disorders include immune dysregulation and inflammatory pathways, which are potential targets for therapy. Lessons from RA and SLE may have implications for future research on the pathogenesis of atherosclerotic vascular disease in general. Recent data indicate that suppression of inflammation reduces the risk of CVD morbidity and mortality in patients with severe RA. The modest, but clinically relevant, efficacy of atorvastatin treatment in RA adds to the evidence for important anti-inflammatory properties for statins. There is increased recognition of the need for structured preventive strategies to reduce the risk of CVD in patients with rheumatic disease. Such strategies should be based on insights into the role of inflammation in CVD, as well as optimal management of life style related risk factors. In this review, the research agenda for understanding and preventing CVD co-morbidity in patients with rheumatic disorders is discussed.Keywords: rheumatoid arthritis, systemic lupus erythematosus, cardiovascular disease, inflammation
Magnetic Resonance Elastography for Liver Fibrosis in Methotrexate Treatment  [PDF]
Deana D. Hoganson, Jun Chen, Richard L. Ehman, Jayant A. Talwalkar, Clement J. Michet Jr., Meng Yin, Cynthia S. Crowson, Eric L. Matteson
Open Journal of Rheumatology and Autoimmune Diseases (OJRA) , 2012, DOI: 10.4236/ojra.2012.22003
Abstract: Introduction: Hepatic magnetic resonance elastography (MRE) allows for noninvasive assessment of liver fibrosis. The purpose of this study was to evaluate the usefulness of MRE in detecting and quantifying liver fibrosis in patients with rheumatoid arthritis (RA) who have received methotrexate (MTX). Methods: The association between mean liver stiffness value as determined by MRE and variables of interest was determined. The decision for a liver biopsy in participants with an abnormal liver stiffness was made based on clinical judgment. Results: Sixty-five RA patients were enrolled. Mean liver stiffness value by MRE was abnormal in 7 patients, suggestive of hepatic injury. As a result of findings from the MRE, biopsies were performed in 5 patients and all correlated with elevated liver stiffness values. Elevated mean liver stiffness values were associated with body mass index (BMI) (OR = 1.18 per 1 kg/m2; 95% CI: 1.03, 1.36; p = 0.017). Neither the total MTX dose nor the duration of MTX treatment was associated with mean liver stiffness value (p = 0.51 and P = 0.20, respectively). Conclusion: MRE provides a reliable, non-invasive assessment of liver fibrosis in patients with RA receiving MTX. Patients with RA receiving MTX who have an elevated BMI may be at increased risk for chronic hepatic injury, regardless of MTX cumulative dose or duration of treatment.
Correction: Effects of cyclophosphamide on pulmonary function in patients with scleroderma and interstitial lung disease: a systematic review and meta-analysis of randomized controlled trials and observational prospective cohort studies
Carlotta Nannini, Colin P West, Patricia J Erwin, Eric L Matteson
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2679
Abstract:
Effects of cyclophosphamide on pulmonary function in patients with scleroderma and interstitial lung disease: a systematic review and meta-analysis of randomized controlled trials and observational prospective cohort studies
Carlotta Nannini, Colin P West, Patricia J Erwin, Eric L Matteson
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2534
Abstract: The primary outcomes were the mean change in forced vital capacity and in diffusing capacity for carbon monoxide after 12 months of therapy in patients treated with cyclophosphamide.Three randomized clinical trials and six prospective observational studies were included for analysis. In the pooled analysis, the forced vital capacity and the diffusing capacity for carbon monoxide predicted values after 12 months of therapy were essentially unchanged, with mean changes of 2.83% (95% confidence interval = 0.35 to 5.31) and 4.56% (95% confidence interval = -0.21 to 9.33), respectively.Cyclophosphamide treatment in patients with systemic sclerosis-related interstitial lung disease does not result in clinically significant improvement of pulmonary function.Scleroderma (systemic sclerosis (SSc)) is an autoimmune connective tissue disorder characterized by microvascular injury, excessive fibrosis of the skin and distinctive visceral changes that can involve the lungs, heart, kidneys and gastrointestinal tract [1]. Interstitial lung disease (ILD) occurs in patients who have CREST (Calcinosis, Raynaud, ESophagitis, Telangiectases), limited cutaneous systemic sclerosis-lcSSc and diffuse cutaneous scleroderma (dcSSc), but it is somewhat more common in patients who have diffuse disease [2,3]. The ILD that occurs in scleroderma patients includes a number of entities, as summarized in Table 1[4]. The prevalence of ILD in scleroderma varies from 25% to 90% depending on the ethnic background of the patients studied and on the method used to detect the ILD [5].Pulmonary function tests with evaluation of the forced vital capacity (FVC), the total lung capacity and the diffusing lung capacity of carbon monoxide (DLCO), chest radiography and high-resolution computed tomography are common clinical tests used to evaluate lung disease in scleroderma. Imaging reveals fibrotic changes of lung parenchyma. Previous research has found pulmonary function tests to reveal a restrictive pattern in
Histoplasmosis infection in patients with rheumatoid arthritis, 1998-2009
Timothy C Olson, Tim Bongartz, Cynthia S Crowson, Glenn D Roberts, Robert Orenstein, Eric L Matteson
BMC Infectious Diseases , 2011, DOI: 10.1186/1471-2334-11-145
Abstract: Medical record review of all patients with a diagnosis of RA who developed new histoplasmosis infection in an endemic region between Jan 1, 1998 and Jan 30, 2009 and who were seen at Mayo Clinic in Rochester, Minnesota was performed.Histoplasmosis was diagnosed in 26 patients. Most patients were on combination therapies; 15 were on anti-tumor necrosis factor (anti-TNF) agents, 15 on corticosteroids and 16 on methotrexate. Most received more than 6 months of itraconazole and/or amphotericin treatment. Two patients died of causes unrelated to histoplasmosis. Anti-TNF treatment was restarted in 4/15 patients, with recurrence of histoplasmosis in one.In this largest single center series of patients with RA and histoplasmosis in the era of immunomodulatory therapy, we found that most patients had longstanding disease and were on multiple immunomodulatory agents. Most cases were pulmonary; typical signs and symptoms of disease were frequently lacking.Histoplasma capsulatum is a dimorphic fungus widely distributed in nature and is limited to the Midwest and Southeastern United States. After inhalation, the fungus transforms into a pathogenic yeast form. Optimal host defense against Histoplasma capsulatum requires interaction between macrophages and T-cells. Patients with rheumatic diseases receiving immunomodulatory and immunosuppressive therapies may be at increased risk for histoplasmosis, although reports of this infectious complication in this population primarily derived from case reports.The most recent epidemiologic information for histoplasmosis was described in large urban outbreaks in Indianapolis that occurred between 1978 and 1993. The rate of dissemination of histoplasmosis from these studies has been cited at 0.46 per 1000 infected persons [1]. However immunosuppression has been a clearly identified risk factor in disseminated disease, and extrapulmonary disease occurs especially in immunocompromised patients [2]. Known immunosuppressive conditions noted to i
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