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Eric L Matteson

Publications and source records attributed to Eric L Matteson.

At least 19 recordsLinked to original sources
PubMed2007

CD56-expressing T cells that have features of senescence are expanded in rheumatoid arthritis.

OBJECTIVE: T cells deficient in CD28 expression have been implicated in the pathogenesis of rheumatoid arthritis (RA). Given that CD28-null T cells are functionally heterogeneous, we undertook this study to screen for novel receptors on these cells. METHODS: Seventy-two patients with RA (ages 35-84 years) and 53 healthy persons (32 young controls ages 19-34 years, 21 older controls ages 39-86 years) were recruited. Phenotypes and proliferative capacity of T cells from fresh leukocytes and of long-term cultures were monitored by flow cytometry. Lung biopsy specimens from patients with RA-associated interstitial pneumonitis (IP) were examined by immunohistochemistry. Receptor functionality was assessed by crosslinking bioassays. RESULTS: Chronic stimulation of CD28(+) T cells in vitro yielded progenies that lacked CD28 but that gained CD56. Ex vivo analysis of leukocytes from patients with extraarticular RA showed a higher frequency of CD56(+),CD28-null T cells than in patients with disease confined to the joints or in healthy controls. CD56(+),CD28-null T cells had nil capacity for proliferation, consistent with cellular senescence. CD56(+) T cells had skewed T cell receptor (TCR) alpha/beta-chain usage and restricted TCR third complementarity-determining region spectra. Histologic studies showed that CD56(+) T cells were components of cellular infiltrates in RA-associated IP. CD56 crosslinking on T cells sufficiently induced cytokine production, although CD56/TCR coligation induced higher production levels. CONCLUSION: Chronic activation of T cells induces counterregulation of CD28 and CD56 expression. The loss of CD28 is accompanied by the gain of CD56 that confers TCR-independent and TCR-dependent activation pathways. We propose that accumulation of CD56(+) T cells in RA contributes to maladaptive immune responses and that CD56(+) T cells are potential targets for therapy.

Adult↗
PubMed2006

Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: systematic review and meta-analysis of rare harmful effects in randomized controlled trials.

CONTEXT: Tumor necrosis factor (TNF) plays an important role in host defense and tumor growth control. Therefore, anti-TNF antibody therapies may increase the risk of serious infections and malignancies. OBJECTIVE: To assess the extent to which anti-TNF antibody therapies may increase the risk of serious infections and malignancies in patients with rheumatoid arthritis by performing a meta-analysis to derive estimates of sparse harmful events occurring in randomized trials of anti-TNF therapy. DATA SOURCES: A systematic literature search of EMBASE, MEDLINE, Cochrane Library, and electronic abstract databases of the annual scientific meetings of both the European League Against Rheumatism and the American College of Rheumatology was conducted through December 2005. This search was complemented with interviews of the manufacturers of the 2 licensed anti-TNF antibodies. STUDY SELECTION: We included randomized, placebo-controlled trials of the 2 licensed anti-TNF antibodies (infliximab and adalimumab) used for 12 weeks or more in patients with rheumatoid arthritis. Nine trials met our inclusion criteria, including 3493 patients who received anti-TNF antibody treatment and 1512 patients who received placebo. DATA EXTRACTION: Data on study characteristics to assess study quality and intention-to-treat data for serious infections and malignancies were abstracted. Published information from the trials was supplemented by direct contact between principal investigators and industry sponsors. DATA SYNTHESIS: We calculated a pooled odds ratio (Mantel-Haenszel methods with a continuity correction designed for sparse data) for malignancies and serious infections (infection that requires antimicrobial therapy and/or hospitalization) in anti-TNF-treated patients vs placebo patients. We estimated effects for high and low doses separately. The pooled odds ratio for malignancy was 3.3 (95% confidence interval [CI], 1.2-9.1) and for serious infection was 2.0 (95% CI, 1.3-3.1). Malignancies were significantly more common in patients treated with higher doses compared with patients who received lower doses of anti-TNF antibodies. For patients treated with anti-TNF antibodies in the included trials, the number needed to harm was 154 (95% CI, 91-500) for 1 additional malignancy within a treatment period of 6 to 12 months. For serious infections, the number needed to harm was 59 (95% CI, 39-125) within a treatment period of 3 to 12 months. CONCLUSIONS: There is evidence of an increased risk of serious infections and a dose-dependent increased risk of malignancies in patients with rheumatoid arthritis treated with anti-TNF antibody therapy. The formal meta-analysis with pooled sparse adverse events data from randomized controlled trials serves as a tool to assess harmful drug effects.

Adalimumab↗
PubMed2006

Lack of detection of human retrovirus-5 proviral DNA in synovial tissue and blood specimens from individuals with rheumatoid arthritis or osteoarthritis.

OBJECTIVE: Prior studies have suggested an association of human retrovirus 5 with rheumatoid arthritis. The purpose of this study was to determine if human retrovirus-5 proviral DNA is present in synovial tissue and blood specimens from patients with rheumatoid arthritis or osteoarthritis, or those without joint disease. METHODS: Synovial tissue and whole blood from 75 patients with rheumatoid arthritis, 75 patients with osteoarthritis, and 50 patients without a primary arthritis diagnosis were assayed by real-time quantitative polymerase chain reaction (PCR) using primers that amplify a 186-bp fragment of human retrovirus-5 proviral DNA. RESULTS: A total of 200 tissue specimens, 200 mononuclear cells, and 196 of 200 granulocyte specimens tested negative for human retrovirus-5 proviral DNA. No association between human retrovirus 5 and rheumatoid arthritis or osteoarthritis (P = 0.516) was identified. Granulocyte specimens from 4 patients, 2 with rheumatoid arthritis and 2 with osteoarthritis, yielded a low positive human retrovirus-5 proviral DNA signal (83-1,365 copies of human retrovirus-5 proviral DNA/ml blood). CONCLUSION: Contrary to prior reports, we did not find an association between human retrovirus 5 and rheumatoid arthritis or osteoarthritis using a real-time PCR assay. Our findings are consistent with the recent finding that human retrovirus 5 is actually rabbit endogenous retrovirus H.

Adolescent↗
PubMed2006

Incidence of noncardiac vascular disease in rheumatoid arthritis and relationship to extraarticular disease manifestations.

OBJECTIVE: To investigate the incidence of noncardiac vascular disease in patients with rheumatoid arthritis (RA) and its relationship to systemic extraarticular disease in a community-based cohort. METHODS: A retrospective medical record review of 609 patients with incident RA diagnosed during 1955-1994 was carried out in Olmsted County, Minnesota. Patients were followed up from 1955 to 2000 (median followup 11.8 years). Incident noncardiac vascular disease and severe extraarticular RA manifestations (including pericarditis, pleuritis, and vasculitis) were recorded according to predefined criteria, and incidence rates were estimated. Using Cox proportional hazards models, the risk (hazard ratio [HR]) of developing vascular events was assessed in patients with and without severe extraarticular RA. RESULTS: Cerebrovascular and peripheral arterial events occurred in 139 patients (22.8%). The 30-year cumulative incidence rates of peripheral arterial events, cerebrovascular events, and venous thromboembolic events were estimated to be 19.6%, 21.6%, and 7.2%, respectively. The presence of severe extraarticular RA manifestations was found to be associated with all subgroups of noncardiac vascular disease except cerebrovascular disease alone (HR 2.3, 95% confidence interval [95% CI] 1.2-4.3 for peripheral arterial events; HR 3.7, 95% CI 1.3-10.3 for venous thromboembolic events; HR 1.5, 95% CI 0.7-3.2 for cerebrovascular events) after adjusting for age, sex, body mass index, smoking, and rheumatoid factor status. CONCLUSION: This is the first study to assess the incidence of noncardiac vascular disease in RA. Severe extraarticular RA was associated with all forms of noncardiac vascular disease except cerebrovascular disease alone. Similar to cardiac disease, the excess risk of noncardiac vascular disease in RA is likely to be related, in part, to the systemic inflammation associated with the extraarticular manifestations of RA.

Arthritis, Rheumatoid↗
PubMed2006

Morphologic and quantitative assessment of CD20+ B cell infiltrates in rheumatoid arthritis-associated nonspecific interstitial pneumonia and usual interstitial pneumonia.

OBJECTIVE: B lymphocytes are emerging as important elements in the events leading to joint destruction in rheumatoid arthritis (RA). However, B lymphocytes have not been studied in rheumatoid arthritis (RA)-associated lung disease. We performed a morphologic and quantitative analysis of B lymphocytes and plasma cells in RA-associated interstitial pneumonia (IP) in comparison with idiopathic IP and normal lungs. METHODS: Open-lung biopsy specimens from patients with RA-associated IP (n = 18), patients with idiopathic IP (n = 21), and control subjects (n = 11) were stained with antibodies to CD20 and CD138. Morphologic patterns of stained specimens were characterized and staining was quantified using computer-assisted image analysis. RESULTS: In RA-associated IP, marked follicular B cell hyperplasia was detected, which was limited almost entirely to peribronchiolar lymphoid aggregates. Plasma cells were also present in large numbers, but showed a more diffuse tissue infiltration. Quantification of B cells demonstrated higher cellularity in RA-associated IP (median 2.0%, interquartile range [IQR] 1.0-5.7) as compared with idiopathic IP (0.9%, IQR 0.5-2.1). Control specimens showed a significantly smaller number of B cells compared with both diseases (0.4%, IQR 0.1-1.3). In RA patients who were smokers and in those who were male, the proportion of CD20+ tissue areas further increased to 4.3% (IQR 1.0-5.8) and 3.9% (IQR 0.7-6.9), respectively. CONCLUSION: We demonstrated a significant follicular B cell hyperplasia in RA-associated IP. The differences between RA-associated IP and idiopathic IP imply a differential emphasis of B cell-mediated mechanisms in the 2 diseases despite radiologic and histologic similarities and provide a rationale for studying functional aspects of B cell involvement in the pathogenesis of RA-associated IP.

Adult↗
PubMed2006

Lyme myositis.

Myositis has been reported as a rare manifestation of Lyme disease, and Lyme myositis can be an important consideration in the differential diagnosis of unusual cases, especially in patients who live in or travel to endemic areas. We report the case of a 43-year-old man who presented with focal myositis of the proximal lower extremity and was subsequently diagnosed as having Lyme myositis. The patient had previously experienced a febrile illness and rash, but had no ongoing symptoms of Lyme disease. Myositis was confirmed by magnetic resonance imaging and muscle biopsy; Borrelia burgdorferi infection was confirmed by Lyme serology and polymerase chain reaction testing of synovial fluid and biopsy material. The current case is reviewed in the context of findings from previous case descriptions.

Adult↗
PubMed2006

Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis.

OBJECTIVE: To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. METHODS: Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. RESULTS: The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF positivity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. CONCLUSION: Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.

Adult↗
PubMed2006

Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial.

OBJECTIVE: Glucocorticoid (GC) therapy for giant cell arteritis (GCA) is effective but requires prolonged administration, resulting in adverse side effects. The goal of the current study was to test the hypothesis that induction treatment with high-dose pulse intravenous (IV) methylprednisolone permits a shorter course of therapy. METHODS: Twenty-seven patients with biopsy-proven GCA were enrolled in a randomized, double-blind, placebo-controlled study to receive IV methylprednisolone (15 mg/kg of ideal body weight/day) or IV saline for 3 consecutive days. All patients were started on 40 mg/day prednisone and followed the same tapering schedule as long as disease activity was controlled. The numbers of patients with disease in remission after 36, 52, and 78 weeks of treatment and taking <or=5 mg/day prednisone were compared. Cumulative prednisone dose, number of relapses, and development of adverse GC effects were assessed. RESULTS: Ten of the 14 IV GC-treated patients, but only 2 of 13 control patients, were taking <or=5 mg/day prednisone at 36 weeks (P = 0.003). This difference was maintained; there was a higher number of sustained remissions after discontinuation of treatment in the IV GC-treated group and a lower median daily dose of prednisone at 78 weeks (P = 0.0004). The median cumulative dose of oral prednisone, excluding the IV GC dose, was 5,636 mg in the IV GC-treated group compared with 7,860 mg in the IV saline-treated group (P = 0.001). CONCLUSION: Initial treatment of GCA with IV GC pulses allowed for more rapid tapering of oral GCs and had long-term benefits, with a higher frequency of patients experiencing sustained remission of their disease after discontinuation of treatment.

Administration, Oral↗
PubMed2006

Large-vessel involvement in giant cell arteritis.

PURPOSE OF REVIEW: Large-vessel involvement in giant cell arteritis occurs in over a quarter of patients with this disease. Stenosis of the primary and secondary branches of the aorta may cause claudication and tissue gangrene, whereas aortitis may lead to aneurysm formation and dissection, often many years after the initial diagnosis. RECENT FINDINGS: Subsets of giant cell arteritis are probably caused by variations in the pathobiology of the disease. Radiographic imaging with some form of angiography is essential to reach a proper diagnosis. Although survival in giant cell arteritis is generally good, subsets of patients with aneurysm formation have a markedly diminished life expectancy. Glucocorticosteroids continue to be the mainstay of treatment for giant cell arteritis and its complications. SUMMARY: Advances in diagnostic techniques including proteomic and genomic approaches should improve our understanding of the pathogenesis as well as the assessment of disease activity and extent. We provide a suggested algorithm for the evaluation of patients with large-vessel disease in giant cell arteritis.

Algorithms↗
PubMed2006

Hearing loss in rheumatoid arthritis.

OBJECTIVE: The objective of this study was to evaluate whether patients with rheumatoid arthritis (RA) are more likely to have subclinical hearing loss compared with persons without RA. METHODS: This is a case-control cross-sectional study of 29 patients with RA with disease duration greater than 5 years. Five males and five females were recruited into each decade category (age 40-49, 50-59, and 60-69). These cases were matched in a 1:1 ratio by sex and age to 30 control subjects. A comprehensive set of audiometric and disease severity assessments were performed. RESULTS: Seventeen (59%) of 29 patients with RA had abnormal hearing for at least one frequency (four in one ear, 13 in two ears) by audiometry as did 14 (47%) of 30 control subjects (five in one ear, nine in two ears). The percentage of patients with hearing loss (% RA vs. % control subjects) was: 45% versus 40% sensorineural, 10% versus 7% conductive, and 3% versus 0% mixed hearing loss. In RA versus control subjects, acoustic reflex threshold was abnormal in 17% versus 7%; speech reception threshold was abnormal in 10% versus 3%. Tympanometry and otoacoustic emission findings were similar in both groups. Word recognition did not differ between patients with RA and control subjects. In patients with RA/control subjects, hearing handicap, dizziness, and health assessment questionnaires were abnormal in 28%/7%, 14%/3%, and 72%/7%, respectively. CONCLUSION: There was no difference found in objective audiometric measurements in patients with RA compared with non-RA control subjects. Subjectively patients with RA were more likely to perceive themselves as having hearing disturbances, which may be related to overall disease related functional impairment.

Acoustic Impedance Tests↗
PubMed2006

Interstitial lung disease in primary Sjögren syndrome.

BACKGROUND: Primary Sjögren syndrome (pSS) has been associated with various histologic patterns of interstitial lung disease (ILD). METHODS: We retrospectively identified 18 patients with pSS and suspected ILD who underwent lung biopsies (14 surgical biopsies and 9 bronchoscopic biopsies) at our institution during a 13-year period from 1992 through 2004. Histopathologic findings were analyzed and correlated with radiologic features and outcome. RESULTS: Median age was 62 years (range, 34 to 78 years), and 15 patients (83%) were women. Most patients presented with dyspnea and cough. Chest radiographs demonstrated bilateral infiltrates, and high-resolution CT revealed abnormalities of various types including ground-glass, consolidation, reticular, and nodular opacities. The major histopathologic patterns included nonspecific interstitial pneumonia (NSIP) [five patients], organizing pneumonia (OP) [four patients], usual interstitial pneumonia (UIP) [three patients], lymphocytic interstitial pneumonia (three patients), primary pulmonary lymphoma (two patients), and diffuse interstitial amyloidosis (one patient). In four patients (three with OP and one with amyloidosis), the diagnosis was established on transbronchial biopsy results. Treatment commonly included prednisone with or without another immunosuppressive agent. During the follow-up period (median, 38 months), most patients improved or remained stable except three patients with UIP, one patient with NSIP, and one patient with amyloidosis. Seven patients (39%) died, including three deaths from acute exacerbation of interstitial pneumonia. CONCLUSIONS: A variety of histologic patterns can be seen in patients with pSS-associated ILD. Those with UIP tended to have progression of lung disease. Death from acute exacerbation of interstitial pneumonia may occur in patients with pSS-associated ILD.

Adrenal Cortex Hormones↗