James F. Fries

Bio: James F. Fries is an academic researcher from Stanford University. The author has contributed to research in topics: Rheumatoid arthritis & Arthritis. The author has an hindex of 100, co-authored 369 publications receiving 83589 citations. Previous affiliations of James F. Fries include University of Saskatchewan & National Institutes of Health.

Abstract 31: Cardiovascular Health at Young and Middle Ages and Dementia in Older Age - The Chicago Heart Association Detection Project in Industry Study

Abstract: Background: Data are sparse regarding the association of cardiovascular health (CVH) in younger/middle age with the diagnosis of dementia later in life. Methods: We used linked data from the Chicag...

Patient based method of assessing adverse events in clinical trials in rheumatology: the revised Stanford Toxicity Index.

Abstract: We describe the progress towards developing a patient rated toxicity index that meets all of the patient-important attributes defined by the OMERACT Drug Safety Working Party. These attributes are frequency, severity, importance to patient, importance to the clinician, impact on economics, impact on activities, and integration of adverse effects with benefits. The Stanford Toxicity Index (STI) has been revised to collect all attributes with the exception of impact on activities. However, since the STI is a part of the Health Assessment Questionnaire (HAQ), impact on activities is collected by the HAQ. In particular, a new question asks patients to rate overall satisfaction, taking into consideration both benefits and adverse effects. The next step in the development of this tool is to ensure that the STI meets the OMERACT filter of truth, discrimination, and feasibility. Although truth and feasibility have been confirmed by comparisons within the ARAMIS database, discrimination needs to be assessed in clinical trials.

Rheumatoid arthritis: radiographic progression is getting milder.

Abstract: Dr. Sokka and colleagues1 have made an important contribution to the growing evidence that outcomes in rheumatoid arthritis (RA) have been improving over time. We believe, however, that Sokka, et al are too evenhanded in their discussion of the 3 explanations for their data: (1) selfselection, (2) milder disease, and (3) improvement in treatment. While these potential explanations are not mutually exclusive, we believe that the overwhelmingly dominant cause must be the great increase in use of disease modifying antirheumatic drugs (DMARD) proven to retard functional decline and radiographic progression. Self-selection of milder patients is effectively precluded by the entry criteria Sokka, et al have used. They present compelling graphic evidence of individual patient trends across cohorts showing nearly identical baseline values but a profound reduction in the number of patients with high radiographic progression slopes; this reduction is even more striking in the seropositive patients. The differences over time are due to an almost complete absence of rapid radiographic deterioration in the later cohorts, consistent with more aggressive tratment. To address the question whether RA is becoming a milder disease, one needs to examine data from successive incidence cohorts where baseline health status measurements have been performed consistently over the years. We analyzed baseline functional disability in a large (n = 3035) prospective muticenter study, and found no substantial changes over a 20 year period in baseline values of early RA cases. On the other hand, we found a 2% annual decline in functional disability in our cohorts over the past 2 decades2,3. Sokka, et al report the same thing with radiographic endpoints; no difference in median Larsen scores at baseline over time, but large differences after 5 years. In contrast to the stability of baseline severity over time, there have been dramatic changes toward DMARD based treatment strategies4, with reduction in duration of disease at first DMARD, and increases in the number of DMARD per patient, relative effectiveness of available DMARD, numbers of patients taking DMARD and DMARD combinations, and percentage of courses on DMARD over time2,5. For a strongly positive effect from these well documented trends not to have occurred would have to mean that all of our clinical trials and observational studies have been wrong. We now have better treatments and better treatment strategies and better functional outcomes and better radiographic outcomes. We should not be afraid to connect the dots.

The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis.

Abstract: The revised criteria for the classification of rheumatoid arthritis (RA) were formulated from a computerized analysis of 262 contemporary, consecutively studied patients with RA and 262 control subjects with rheumatic diseases other than RA (non-RA). The new criteria are as follows: 1) morning stiffness in and around joints lasting at least 1 hour before maximal improvement; 2) soft tissue swelling (arthritis) of 3 or more joint areas observed by a physician; 3) swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints; 4) symmetric swelling (arthritis); 5) rheumatoid nodules; 6) the presence of rheumatoid factor; and 7) radiographic erosions and/or periarticular osteopenia in hand and/or wrist joints. Criteria 1 through 4 must have been present for at least 6 weeks. Rheumatoid arthritis is defined by the presence of 4 or more criteria, and no further qualifications (classic, definite, or probable) or list of exclusions are required. In addition, a "classification tree" schema is presented which performs equally as well as the traditional (4 of 7) format. The new criteria demonstrated 91-94% sensitivity and 89% specificity for RA when compared with non-RA rheumatic disease control subjects.

The 1982 revised criteria for the classification of systemic lupus erythematosus

Abstract: The 1971 preliminary criteria for the classification of systemic lupus erythematosus (SLE) were revised and updated to incorporate new immunologic knowledge and improve disease classification. The 1982 revised criteria include fluorescence antinuclear antibody and antibody to native DNA and Sm antigen. Some criteria involving the same organ systems were aggregated into single criteria. Raynaud's phenomenon and alopecia were not included in the 1982 revised criteria because of low sensitivity and specificity. The new criteria were 96% sensitive and 96% specific when tested with SLE and control patient data gathered from 18 participating clinics. When compared with the 1971 criteria, the 1982 revised criteria showed gains in sensitivity and specificity.

Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus.

Abstract: In 1982, the Diagnostic and Therapeutic Criteria Committee of the American College of Rheumatology (ACR)published revised criteria for the classification of systemiclupus erythematosus (SLE) (1). During the ensuing decade several investigators, including Drs. Graham Hughes and Donato Alarcon-Segovia, among others, have described the presence and clinical associations or antiphospholipid antibodies in patients with SLE, as well as the occurrence of theprimary antiphospholipid syndrome (2-5). In 1992, Piette and colleagues suggested that the ACR revised criteria be reevaluated in light of the above discoveries (6).

The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee.

Abstract: To develop criteria for the classification of fibromyalgia, we studied 558 consecutive patients: 293 patients with fibromyalgia and 265 control patients. Interviews and examinations were performed by trained, blinded assessors. Control patients for the group with primary fibromyalgia were matched for age and sex, and limited to patients with disorders that could be confused with primary fibromyalgia. Control patients for the group with secondary-concomitant fibromyalgia were matched for age, sex, and concomitant rheumatic disorders. Widespread pain (axial plus upper and lower segment plus left- and right-sided pain) was found in 97.6% of all patients with fibromyalgia and in 69.1% of all control patients. The combination of widespread pain and mild or greater tenderness in greater than or equal to 11 of 18 tender point sites yielded a sensitivity of 88.4% and a specificity of 81.1%. Primary fibromyalgia patients and secondary-concomitant fibromyalgia patients did not differ statistically in any major study variable, and the criteria performed equally well in patients with and those without concomitant rheumatic conditions. The newly proposed criteria for the classification of fibromyalgia are 1) widespread pain in combination with 2) tenderness at 11 or more of the 18 specific tender point sites. No exclusions are made for the presence of concomitant radiographic or laboratory abnormalities. At the diagnostic or classification level, the distinction between primary fibromyalgia and secondary-concomitant fibromyalgia (as defined in the text) is abandoned.