Rheumatoid Arthritis: Teng GG

Danila MI, Patkar NM, Curtis JR, Saag KG, Teng GG. · Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Curr Opin Rheumatol. · Pubmed #18388526 No free full text.

Abstract: PURPOSE OF REVIEW: To summarize the recent literature concerning the role of TNF-alpha in heart failure, epidemiology of heart failure in rheumatoid arthritis and risk of heart failure associated with biologic disease-modifying antirheumatic drugs in rheumatoid arthritis. RECENT FINDINGS: TNF-alpha has been implicated in the pathogenesis of heart failure. It has direct deleterious effects on the myocardium in the setting of acute injury or chronic heart failure. In animal models, TNF-alpha is important in cardiac remodeling, leading to cardiac dysfunction following acute injury. Both incident and worsening heart failure have been reported in patients with rheumatoid arthritis who are treated with anti-TNF-alpha therapy. Recent cohort studies, however, have shown no increased risk and, in some, a protective effect on the risk of heart failure. Certain traditional cardiovascular risk factors have a relatively lesser contribution to cardiovascular morbidity and mortality in patients with rheumatoid arthritis, suggesting that disease-related perturbations of the cytokine network may contribute to the excess risk of heart failure in these patients. SUMMARY: Overall mortality in rheumatoid arthritis has remained stagnant despite advances in rheumatoid arthritis and heart failure management and improved cardiovascular mortality in the general population. Heart failure prevalence is increased in patients with rheumatoid arthritis and leads to greater mortality. Despite current expert consensus contraindicating the use of anti-TNF-alpha agents in patients with moderate to severe heart failure, epidemiological studies in rheumatoid arthritis have not consistently substantiated this association.

Patkar NM, Teng GG, Curtis JR, Saag KG. · Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama 35294-3408, USA. · Curr Opin Rheumatol. · Pubmed #18388525 No free full text.

Abstract: PURPOSE OF REVIEW: Rheumatoid arthritis patients have higher risk for infections due to comorbidities, underlying immunosuppression and use of glucocorticoids and disease modifying antirheumatic drugs. The association between treatment with antitumor necrosis factor alpha agents and serious infections, including opportunistic infections such as tuberculosis, in rheumatoid arthritis patients remains controversial. We present recent literature on this topic with a focus on clinical applications of this new data. RECENT FINDINGS: Prospective cohort studies and population-based registries have described the incidence and risk of serious infections in large rheumatoid arthritis patient populations of antitumor necrosis factor alpha users. Although some studies have suggested a one and one-half to two-fold increased risk, especially immediately after initiating the treatment, not all have shown an elevated risk for serious bacterial infections or tuberculosis. SUMMARY: Although antitumor necrosis factor alpha agents may be independent risk factors for infections there is an absolute low rate of infection in those treated with these agents (approximately 5 per 100 patient-years). Screening for latent tuberculosis with tuberculin skin testing is effective, and compliance with the recommendations for preventing this disease in recipients of antitumor necrosis factor alpha agents has partially decreased the risk of infections. Clinical suspicion toward developing infection in those being treated with antitumor necrosis factor alpha agents, particularly earlier in the treatment course, is important for effective management of patients.

Patkar NM, Curtis JR, Teng GG, Allison JJ, Saag M, Martin C, Saag KG. · Center for Education and Research on Therapeutics of Musculoskeletal Disorders, University of Alabama at Birmingham, Birmingham, AL 35294-3408, USA. · J Clin Epidemiol. · Pubmed #18834713 No free full text.

Abstract: OBJECTIVE: To evaluate diagnostic properties of International Classification of Diseases, Version 9 (ICD-9) diagnosis codes and infection criteria to identify bacterial infections among rheumatoid arthritis (RA) patients. STUDY DESIGN AND SETTING: We performed a cross-sectional study of RA patients with and without ICD-9 codes for bacterial infections. Sixteen bacterial infection criteria were developed. Diagnostic properties of comprehensive and restrictive sets of ICD-9 codes and the infection criteria were tested against an adjudicated review of medical records. RESULTS: Records on 162 RA patients with and 50 without purported bacterial infections were reviewed. Positive and negative predictive values of ICD-9 codes ranged from 54%-85% and 84%-100%, respectively. Positive predictive values of the medical records based criteria were 84% and 89% for "definite" and "definite or empirically treated" infections, respectively. Positive predictive value of infection criteria increased by 50% as disease prevalence increased using ICD-9 codes to enhance infection likelihood. CONCLUSION: ICD-9 codes alone may misclassify bacterial infections in hospitalized RA patients. Misclassification varies with the specificity of the codes used and strength of evidence required to confirm infections. Combining ICD-9 codes with infection criteria identified infections with greatest accuracy. Novel infection criteria may limit the requirement to review medical records.

Saag KG, Teng GG, Patkar NM, Anuntiyo J, Finney C, Curtis JR, Paulus HE, Mudano A, Pisu M, Elkins-Melton M, Outman R, Allison JJ, Suarez Almazor M, Bridges SL, Chatham WW, Hochberg M, MacLean C, Mikuls T, Moreland LW, O'Dell J, Turkiewicz AM, Furst DE, Anonymous00442. · University of Alabama, Birmingham, AL, USA. · Arthritis Rheum. · Pubmed #18512708 links to  free full text

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Teng GG, Turkiewicz AM, Moreland LW. · Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama, 1717 6th Ave South, Birmingham, AL 35294-7201, USA. · Expert Opin Biol Ther. · Pubmed #16120053 No free full text.

Abstract: T cell costimulation is believed to be crucial in orchestrating immune responses that lead to inflammation and destruction in rheumatoid arthritis (RA). Abatacept is a novel recombinant CTLA4Ig fusion protein that selectively modulates costimulation via interrupting the CD28:CD80/86 pathway, resulting in downregulation of T cell activation and multiple ensuing effector mechanisms. Abatacept has been shown to be efficacious, either when given alone or in combination with methotrexate, in patients with active RA, including anti-TNF failures. Improvements in clinical signs and symptoms, slowing of radiological progression, and enhancement in patient function and pain have been reported in clinical trials. Infusions were well-tolerated with a favourable safety profile similar to placebo and no appreciable immunogenicity. Abatacept is the first in a new class of biological response modifiers called costimulatory blockers.