In the five years since the last edition of the Manual, the clinical and investigative tectonic plates of rheumatology have shifted in a profound manner, all to the good of our patients. Through a combination of explosions in our knowledge about the basic mechanisms of disease, advances in our appreciation of the clinical “personalities” of autoimmune and musculoskeletal disorders, and the rapidity with which basic scientific wisdom is catapulted into therapeutic advances at the bedside, our patients are living longer and better lives. Nowhere is this sea change better seen than in the development of world-wide use of biologic drugs such as tumor necrosis factor (TNF) alpha blockers. The three commercially-available anti-TNF drugs have significantly and safely improved the lives of hundreds of thousands of patients with rheumatoid arthritis (RA), psoriatic arthritis, spondyloarthropathies, inflammatory bowel disease, and other systemic inflammatory disorders. Despite these advances, we are still treating the pathogenesis of diseases (such as RA) and not their etiology; although we can now block a centrally important pro-inflammatory cytokine, we are still unable to identify and destroy the etiologic agents that initiate the process of RA. However, just as systemic diseases such as rheumatic fever, polio, syphilis, and tuberculosis fell to the development of antibiotics in the last century, similar paradigm shifts will likely occur in the field of rheumatology.

We have moved from a “wait and see” attitude with regard to so many disorders to a “get tough and take no prisoners” approach, stimulated by the fact that we know that illnesses such RA, if not countered early and aggressively, are intrinsically joint damaging, life shortening, and work ending. Rheumatologists have adopted therapeutic approaches employed by our colleagues in the field of endocrinology and oncology. We now employ induction and maintenance treatment regimens in many diseases in order to optimally balance optimal disease control with drug-related side effects and we do so to achieve a “no evidence of disease” (NED) status. Just as endocrinologists aim for “tight control” of diabetes by decreasing glycosylated hemoglobin levels so as to avoid the development of neuropathy, nephropathy, and retinopathy, so do rheumatologists “aim” at decreasing signs and symptoms of RA inflammation using sensitive and responsive clinical research tools such as the Health Assessment Questionnaire and the Disease Activity Score. Given the amazing effectiveness of anti-TNF medications, we have even resurrected the term "disease remission" and aim for it day by day in our care of our patients.

We have learned a great deal about both the diseases we treat and the medications that we use to treat them. The former is possible through data obtained from randomized, controlled trials, observational studies, and advances in clinical epidemiology and health services research. The latter has arisen from drug trials, post-marketing surveillance, and robust registries. In view of our newfound ability to really make a difference in the lives of our patients, Early Arthritis Centers have arisen, first in Europe and more recently in the US, in an attempt to treat RA and other inflammatory disorders as close to their onset as possible. Studies have recently shown that with self-limited, one year courses of anti-TNF drugs, sustained remissions can be achieved.

Systemic inflammatory disorders such as RA and systemic lupus erythematosus (SLE) not only affect joints and kidneys, respectively, but they are associated with significant collateral damage in the form of premature atherosclerosis and osteoporosis. Life span is shortened in RA by approximately 10 years due primarily to ischemic heart disease. Thus, these disorders demand a global approach, one that not only focuses on the characteristic disease manifestations themselves but also those tissues affected by the “spill over” effect of systemic inflammation. We now treat RA and SLE like we would diabetes, with low-dose aspirin, aggressive lipid lowering, and smoking avoidance.

We have changed the look of our Manual to make it more user-friendly, added new chapters in order to keep the manual up-to-date in this rapidly changing field, and always kept in mind the need to deliver information in its most edible and rapidly digested form. We have carefully integrated the new science into each line of the Manual in an attempt to easily bring our increasing knowledge of the basic science to your patient. It is only with early disease recognition and the institution of the proper therapeutic approach that we can prolong our patients' lives and keep our patients disease- and damage-free, functional, and productive.

Stephen A. Paget, MD
Allan Gibofsky, MD, JD
John F. Beary, III, MD
Thomas P. Sculco, MD

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