Rheumatoid Arthritis 

  • Author: Katherine Temprano, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Dec 29, 2011
 

Background

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. The hallmark feature of this condition is persistent symmetric polyarthritis (synovitis) that affects the hands and feet, although any joint lined by a synovial membrane may be involved. Extra-articular involvement of organs such as the skin, heart, lungs, and eyes can be significant. (See Clinical Presentation.)

No test results are pathognomonic for rheumatoid arthritis, but the presence of both anti-CCP antibodies and rheumatoid factor is highly specific for rheumatoid arthritis (RA). (See Workup.)

Early therapy with disease-modifying antirheumatic drugs (DMARDs) has become the standard of care, as it not only can more efficiently retard disease progression than later treatment but also may induce more remissions. (See Treatment Strategies and Management.) Many of the newer DMARD therapies, however, are immunosuppressive in nature, leading to a higher risk for partially masked serious bacterial, and sometimes fungal, infections. (See Complications.)

Macrophage activation syndrome is a life-threatening complication of rheumatoid arthritis (RA) that requires immediate treatment with high-dose steroids and cyclosporin A. (See Complications.)

Cervical spine involvement usually affects C1-C2 and may potentially cause serious neurologic consequences. Patients who are to undergo intubation or procedures that may involve manipulation of the neck should undergo careful evaluation of the cervical spine. (See Physical Examination.)

Optimal care of patients with RA requires an integrated approach of pharmacologic and nonpharmacologic therapies, such as DMARDs, biologics, NSAIDs, analgesics, glucocorticoids, and immunomodulators. (See Medication.)

Next

Anatomy

Joint involvement is the characteristic feature of rheumatoid arthritis (RA). In general, the small joints of the hands and feet are affected in a relatively symmetric distribution. The most commonly affected joints, in order of decreasing frequency, include the metacarpophalangeal (MCP), wrist, proximal interphalangeal (PIP), knee, metatarsophalangeal (MTP), shoulder, ankle, cervical spine, hip, elbow, and temporomandibular joints. (See Physical Examination.)

Previous
Next

Pathophysiology

The pathogenesis of RA is not completely understood. An external trigger (eg, infection, trauma) that triggers an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals. Synovial cell hyperplasia and endothelial cell activation are early events in the pathologic process that progresses to uncontrolled inflammation and consequent cartilage and bone destruction. Genetic factors and immune system abnormalities contribute to disease propagation.

CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils play major cellular roles in the pathophysiology of rheumatoid arthritis (RA), whereas B lymphocytes produce autoantibodies (ie, rheumatoid factors [RFs]). Abnormal production of numerous cytokines, chemokines, and other inflammatory mediators (eg, tumor necrosis factor alpha [TNF-alpha], interleukin [IL]–1, IL-6, transforming growth factor beta [TGF-beta], IL-8, fibroblast growth factor [FGF], platelet-derived growth factor [PDGF]) has been demonstrated in patients with RA. Ultimately, inflammation and exuberant proliferation of synovium (ie, pannus) leads to destruction of various tissues, including cartilage, bone, tendons, ligaments, and blood vessels. Although the articular structures are the primary sites involved by RA, other tissues are also affected.

Previous
Next

Etiology

The cause of RA is unknown. Genetic, environmental, hormonal, immunologic, and infectious factors may play significant roles. Socioeconomic, psychologic, and lifestyle factors (eg, tobacco use; main environmental risk[1] ) may influence disease outcome. There may be an association between smoking, earlier disease onset and the shared epitope in patients with early RA.[2]

Genetics

Genetic factors account for 50% of the risk for developing RA.[3] Approximately 60% of US patients with rheumatoid arthritis carry a shared epitope of the HLA-DR4 cluster, which constitutes one of the peptide-binding sites of certain HLA-DR molecules associated with RA (eg, HLA-DR beta *0401, 0404, or 0405); in addition, HLA-DR1 (HLA-DR beta *0101) also carries this shared epitope and confers risk, particularly in certain southern European areas. Other HLA-DR4 molecules (eg, HLA-DR beta *0402) do not share the same epitope and do not confer risk.

Genes other than those of the major histocompatibility complex (MHC) are also involved, and results from sequencing genes of families with RA suggest the presence of several susceptibility genes and several resistance genes. Juvenile idiopathic arthritis is a genetically complex trait in which multiple genes are important for disease onset and manifestations. The IL2RA/CD25 gene has recently been implicated as a juvenile idiopathic arthritis susceptibility locus, as has the VTCN1 gene.[4]

Infectious agents

For many decades, numerous infectious agents have been suggested to induce RA. Among these are Mycoplasma organisms, Epstein-Barr and rubella viruses, and others. This supposition is further supported indirectly by the following:

  • Occasional reports of flulike disorders preceding the start of arthritis
  • The inducibility of arthritis in experimental animals with different bacteria or bacterial products (eg, streptococcal cell walls)
  • The presence of bacterial products, including bacterial RNA, in patients' joints
  • The activity of several agents that have antimicrobial effects as disease-modifying drugs (eg, gold salts, antimalarials, minocycline)

Hormones

Sex hormones may play a role in RA, as evidenced by the disproportionate number of females with this disease, its amelioration during pregnancy, its recurrence in the early postpartum period, and its reduced incidence in women using oral contraceptives. Hyperprolactinemia may be a risk factor for RA.[5]

Immunologic factors

All of the major immunologic elements play fundamental roles in the initiation, propagation, and maintenance of the autoimmune process of RA. The exact orchestration of the cellular and cytokine events that lead to pathologic consequences, such as synovial proliferation and subsequent joint destruction, is complex. It involves T and B lymphocytes, antigen-presenting cells (APCs) (eg, B cells, macrophages, dendritic cells), and numerous cytokines. Aberrant production and regulation of both proinflammatory and anti-inflammatory cytokines and cytokine pathways are found in RA.

T cells are assumed to play a pivotal role in the initiation of RA, and the key player in this respect is assumed to be the T helper 1 (Th1) CD4 cells. (Th1 cells produce IL-2 and interferon [IFN] gamma.) These cells may subsequently activate macrophages and other cell populations, including synovial fibroblasts. Macrophages and synovial fibroblasts are the main producers of the proinflammatory cytokines TNF-alpha and IL-1. Experimental models suggest that synovial macrophages and fibroblasts may become autonomous and thus lose responsiveness to T-cell activities in the course of the disease.

B cells are important in the pathologic process and may serve as antigen-presenting cells. B cells also produce numerous autoantibodies (eg, RF,to citrullinated proteins) and secrete cytokines.

The hyperactive and hyperplastic synovial membrane is ultimately transformed into pannus tissue and invades cartilage and bone, the latter being degraded by activated osteoclasts. The major difference between RA and other forms of inflammatory arthritis, such as psoriatic arthritis, does not lie in their cytokine patterns but rather in the highly destructive potential of the RA synovial membrane and in the local and systemic autoimmunity. Whether these 2 events are linked is unclear; however, the autoimmune response conceivably leads to the formation of immune complexes that activate the inflammatory process to a much higher degree than normal. This theory is supported by the much worse prognosis of RA among patients with positive RF results.

Previous
Next

Epidemiology

Worldwide, the annual incidence of rheumatoid arthritis is approximately 3 cases per 10,000 population, and the prevalence rate is approximately 1%, increasing with age and peaking at age 35-50 years. Rheumatoid arthritis affects all populations, although the disease is much more prevalent in some groups (eg, 5-6% in some Native American groups) and much less prevalent in others (eg, black persons from the Caribbean region). First-degree relatives of individuals with RA are at an increased risk (2- to 3-fold) of the disease. Disease concordance in monozygotic twins is approximately 15-20%, suggesting that nongenetic factors play an important role. Because the worldwide frequency of RA is relatively constant, a ubiquitous infectious agent has been postulated to play an etiologic role.

Women are affected by RA approximately 3 times more often than men,[6, 7] but sex differences diminish in older age groups.[6] In investigating whether the higher rate of RA among women could be linked to certain reproductive risk factors, a study from Denmark found that the rate of RA was higher in women who had given birth to just 1 child than it was in women who had delivered 2 or 3 offspring.[8] However, no increased rate was found in women who were nulliparous or who had a history of lost pregnancies. Time elapsed since pregnancy also is significant; in 1- to 5-year postpartum period a decreased risk for RA has been recognized, even in those with higher-risk HLA markers.[9]

The Denmark study also found a higher rheumatoid arthritis risk among women with a history of preeclampsia, hyperemesis during pregnancy, or gestational hypertension.[8] The authors suggested that this portion of the data indicated that a reduced immune adaptability to pregnancy may exist in women who have a predisposition to the development of RA or that there may be a link between fetal microchimerism (in which fetal cells are present in the maternal circulation) and RA.

Previous
Next

Prognosis

Outcome is compromised when the diagnosis and treatment are delayed. The clinical course of rheumatoid arthritis is generally one of exacerbations and remissions. Approximately 40% of patients with this disease become disabled after 10 years, but outcomes are highly variable.[10] Some patients experience a relatively self-limited disease, and others have a chronic progressive illness.

Improvements in the detection of early joint injury have provided a previously unappreciated view of the ubiquity and importance of early joint damage. Nonetheless, predicting the course of an individual case of rheumatoid arthritis at the outset remains difficult, although the HLA-DRB1*04/04 genotype, a high serum titer of autoantibodies (eg RF, anti-cyclic citrullinated peptide [CCP]), extra-articular manifestations, a large number of involved joints, age younger than 30 years, female sex, and systemic symptoms all correlate with an unfavorable prognosis in terms of joint damage and disability. Insidious onset is also an unfavorable sign.

A retrospective study used logistic regression to analyze clinical and laboratory assessments in patients with RA taking only methotrexate.[11] The authors found that measures of C-reactive protein (CRP) and swollen joint count after 12 weeks of methotrexate administration were most associated with radiographic progression at week 52.

There is generally a much worse prognosis of RA among patients with positive RF results, but the absence of RF does not necessarily portend a good prognosis. Other laboratory markers of a poor prognosis include early radiologic evidence of bony injury, persistent anemia of chronic disease, elevated levels of the C1q component of complement, and the presence of anti-CCP antibodies (See Workup).

Rheumatoid arthritis that remains persistently active for longer than 1 year is likely to lead to joint deformities and disability.[12] Periods of activity lasting only weeks or a few months followed by spontaneous remission portend a better prognosis.

Cardiovascular morbidity and mortality are increased in patients with RA. Nontraditional risk factors appear to play an important role. Myocardial infarction, myocardial dysfunction, and asymptomatic pericardial effusions are common; symptomatic pericarditis and constrictive pericarditis are rare. Myocarditis, coronary vasculitis, valvular disease, and conduction defects are occasionally observed. RA also is associated with cardiovascular risk factors, both traditional and nontraditional.

The overall mortality rate in patients with RA is reportedly 2.5 times that of the general population. In those with severe articular and extra-articular disease, the mortality rate approaches that of patients with 3-vessel coronary disease or stage IV Hodgkin disease. Much of the excess mortality derives from infection, vasculitis, and poor nutrition. With the exception of lymphoma, mortality from cancer is unchanged.

Previous
Next

TNF and Mortality

The leading cause of excess mortality in RA is cardiovascular disease, followed by infection, respiratory disease, and malignancies. The effects of concurrent therapy, which is often immunosuppressive, may contribute to mortality in RA. However, studies suggest that control of inflammation may improve mortality.

A large national prospective cohort study over a mean of 4 years demonstrated that anti-TNF therapy was not associated with a significant increase or decrease in mortality and did not increase any additional risk or benefit on overall mortality risk when compared with standard nonbiologic DMARD therapy.[13] The results from another study confirmed that the risk of serious infection and malignancy is not increased in patients receiving anti-TNF therapy when the patients have early RA and have not been previously treated with DMARDS and/or methotrexate (MTX).[14]

A systematic review and meta-analysis reported on the risk of malignancy in patients with rheumatoid arthritis treated with TNF inhibitors. The data reviewed showed that the risk of malignancy, particularly lymphoma, was not increased with TNF inhibitor treatment. However, they did appear to increase the risk of skin cancer, including melanoma.[15]

Most data on disability rates derive from specialty units caring for referred patients with severe disease. Little information is available on patients cared for in primary care community settings. Estimates suggest that more than 50% of these patients remain fully employed, even after 10-15 years of disease, with one third having only intermittent low-grade disease and another one third experiencing spontaneous remission.

Patients taking anti-TNF agents must avoid live-virus vaccines.

Previous
Next

Patient Education

Patient education and counseling are well worth the time invested, because they help to reduce pain, disability, and frequency of physician visits. These represent the most cost-effective intervention for rheumatoid arthritis.

Informing the patient of the diagnosis

With a potentially disabling disease such as rheumatoid arthritis, the act of informing the patient of the diagnosis takes on major importance. The goal is to satisfy the patient's informational needs regarding the diagnosis, prognosis, and treatment in appropriate detail. Careful questioning and empathic listening are required to understand the patient's perspective, requests, and fears.

Telling patients more than they are intellectually or psychologically prepared to handle (a common practice) risks making the experience so intense as to trigger withdrawal. Conversely, failing to address issues of importance to the patient compromises the development of trust. The patient needs to know that the primary physician understands the situation and is available for support, advice, and therapy as the need arises. Encouraging the patient to ask questions helps to communicate interest and caring.

Discussing prognosis and treatment

Patients and families do best when they know what to expect and can view the illness realistically. Many patients fear crippling consequences and dependency.

The most common disease manifestations should be described. Without building false hopes, the physician can point out that spontaneous remissions can occur and that more than two thirds of patients live independently without major disability. In addition, emphasize that much can be done to minimize discomfort and to preserve function. A review of available therapies and their efficacy helps patients to overcome feelings of depression stemming from an erroneous expectation of inevitable disability (See Treatment Strategies and Management). Even in those with severe disease, guarded optimism is now appropriate, given the host of effective and well-tolerated disease-modifying treatments that are emerging.

Abandonment is a major fear. Patients are relieved to know that they will be closely observed by the primary physician and healthcare team, working in conjunction with a consulting rheumatologist and physical/occupational therapist, all of whom are committed to maximizing the patient's comfort and independence and to preserving joint function.

Dealing with misconceptions

Several common misconceptions regarding rheumatoid arthritis deserve attention. A substantial proportion of patients and their families feel that they have done something to cause the illness. Explaining that no known controllable precipitants exist helps to eliminate much unnecessary guilt and self-recrimination. Dealing in an informative, evidence-based fashion with a patient who expresses interest in alternative and complementary forms of therapy can help limit expenditures on ineffective treatments.

Another misconception is that a medication must be expensive to be helpful. Generic nonsteroid anti-inflammatory drugs (NSAIDs), low-dose prednisone,[10] and the first-line disease-modifying agents are quite inexpensive, yet they are remarkably effective for relieving symptoms, a point that bears emphasizing. The sense that one must be treated with the latest TNF inhibitor can be addressed by a careful review of the overall treatment program and the proper role of such agents in the patient's plan of care.

The active participation of the patient and family in the design and implementation of the therapeutic program helps to boost morale and to ensure compliance, as does explaining the rationale for the therapies used. The family also plays an important part in striking the proper balance between dependence and independence. Household members should avoid overprotecting the patient (eg, refraining from intercourse out of fear of hurting the patient) and should work to sustain the patient's pride and ability to contribute to the family. Allowing the patient with RA to struggle with a task is sometimes constructive.

Supporting the patient with debilitating disease

Persons with long-standing severe disease who have already sustained much irreversible joint destruction benefit from an emphasis on comfort measures, supportive counseling, and attention to minimizing further debility. Such patients need help in grieving for their disfigurement and loss of function.

An accepting, unhurried, empathic manner allows the patient to express feelings. The seemingly insignificant act of touching does much to restore a sense of self-acceptance. Attending to pain with increased social support, medication, and a refocusing of attention to function is useful. A trusting and strong patient-doctor relationship can do much to sustain a patient through times of discomfort and disability.

For patient education resources, see the Arthritis Center and Muscle Disorders Center, as well as Rheumatoid Arthritis, Juvenile Rheumatoid Arthritis, Understanding Rheumatoid Arthritis Medications, Chronic Fatigue Syndrome, and Chronic Pain.

Previous
Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Katherine Temprano, MD  Assistant Professor of Internal Medicine, Division of Rheumatology, St Louis University School of Medicine

Katherine Temprano, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American College of Rheumatology

Disclosure: Nothing to disclose.

Coauthor(s)

Howard R Smith, MD  Adjunct Professor of Medicine, Case Western Reserve University School of Medicine; Chief of Rheumatology, Director of The Herbert Bell Pain Management Center, Director of Research, Cleveland Clinic, Huron Hospital

Howard R Smith, MD is a member of the following medical societies: American College of Rheumatology and Ohio State Medical Association

Disclosure: Pfizer Honoraria Speaking and teaching; Roche Consulting fee Consulting

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Edward Bessman, MD Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Sarjoo M Bhagia, MD Consulting Staff, OrthoCarolina; Voluntary Teaching Faculty, Carolinas Rehabilitation

Sarjoo M Bhagia, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Heather Lyn Carone, MD Attending Physician, Department of Emergency Medicine, St Vincent Mercy Medical Center

Heather Lyn Carone, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gino A Farina, MD, FACEP, FAAEM Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Kavita Gupta, DO, MEng Department of Orthopedics, Center of Physical Medicine and Rehabilitation, University of Dentistry and Medicine of New Jersey

Kavita Gupta, DO, MEng is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, Association of Academic Physiatrists, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

John A Kare, MD Assistant Professor of Emergency Medicine, Charles R Drew University of Medicine and Science/UCLA, Director of Research, Department of Emergency Medicine, Martin Luther King Jr/Charles R Drew Medical Center

John A Kare, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Student Association/Foundation, and Emergency Medicine Residents Association

Disclosure: Nothing to disclose.

Randall W King, MD, FACEP Assistant Clinical Professor of Emergency Medicine, The University of Toledo College of Medicine; Director, Emergency Medicine Residency Program, Associate Chair, Department of Emergency Medicine, St Vincent Mercy Medical Center

Randall W King, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Ohio State Medical Association, and Society for Academic Emergency Medicine

Disclosure: Challenger corporation None Physician Advisory Board; Ohio ACEP Consulting fee Editor Rivers review text Emergency Medicine

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Robert J Nowinski, DO Clinical Assistant Professor of Orthopaedic Surgery, Ohio State University College of Medicine and Public Health, Ohio University College of Osteopathic Medicine; Private Practice, Orthopedic and Neurological Consultants, Inc, Columbus, Ohio

Robert J Nowinski, DO is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Osteopathic Surgeons, American Medical Association, American Osteopathic Association, Ohio Osteopathic Association, and Ohio State Medical Association

Disclosure: Tornier Grant/research funds Other; Tornier Honoraria Speaking and teaching

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Elizabeth Salt, ARPN, PhD Assistant Professor, Division of Rheumatology, University of Kentucky College of Nursing; Rheumatology Nurse Practitioner, University of Kentucky Chandler Medical Center

Elizabeth Scarbrough, MSN is a member of the following medical societies: American College of Rheumatology, Council for the Advancement of Nursing Science, and Sigma Theta Tau International

Disclosure: Nothing to disclose.

Roberto Sandoval, MD Consulting Staff, Department of Emergency Medicine, Anaheim Memorial Medical Center, La Palma Intercommunity Hospital

Roberto Sandoval, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association

Disclosure: Nothing to disclose.

Joseph E Sheppard, MD Professor of Clinical Orthopedic Surgery, Chief of Hand and Upper Extremity Service, Department of Orthopedic Surgery, University of Arizona Health Sciences Center, University Physicians Healthcare

Joseph E Sheppard, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Society for Surgery of the Hand, and Orthopaedics Overseas

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Roman V Voytsekhovskiy, MD Fellow in Hand Surgery, Department of Orthopedic Surgery, Rush University Medical Center

Disclosure: Nothing to disclose.

Eleby R Washington III, MD, FACS Associate Professor, Department of Surgery, Division of Orthopedics, Charles R Drew University of Medicine and Science

Eleby R Washington III, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Medical Association, International College of Surgeons, and National Medical Association

Disclosure: Nothing to disclose.

Richard Worthington MD, Department of Emergency Medicine, Wood County Hospital

Richard Worthington is a member of the following medical societies: American College of Emergency Physicians, Ohio State Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References

  1. Carlens C, Hergens MP, Grunewald J, Ekbom A, Eklund A, Hoglund CO, et al. Smoking, use of moist snuff, and risk of chronic inflammatory diseases. Am J Respir Crit Care Med. Jun 1 2010;181(11):1217-22. [Medline].

  2. Ruiz-Esquide V, Gómez-Puerta JA, Cañete JD, Graell E, Vazquez I, Ercilla MG, et al. Effects of smoking on disease activity and radiographic progression in early rheumatoid arthritis. J Rheumatol. Dec 2011;38(12):2536-9. [Medline].

  3. Barton A, Worthington J. Genetic susceptibility to rheumatoid arthritis: an emerging picture. Arthritis Rheum. Oct 15 2009;61(10):1441-6. [Medline].

  4. Hinks A, Ke X, Barton A, Eyre S, Bowes J, Worthington J. Association of the IL2RA/CD25 gene with juvenile idiopathic arthritis. Arthritis Rheum. Jan 2009;60(1):251-7. [Medline].

  5. Barrett JH, Brennan P, Fiddler M, Silman AJ. Does rheumatoid arthritis remit during pregnancy and relapse postpartum? Results from a nationwide study in the United Kingdom performed prospectively from late pregnancy. Arthritis Rheum. Jun 1999;42(6):1219-27. [Medline].

  6. Ahlmén M, Svensson B, Albertsson K, Forslind K, Hafström I. Influence of gender on assessments of disease activity and function in early rheumatoid arthritis in relation to radiographic joint damage. Ann Rheum Dis. Jan 2010;69(1):230-3. [Medline].

  7. Areskoug-Josefsson K, Oberg U. A literature review of the sexual health of women with rheumatoid arthritis. Musculoskeletal Care. Dec 2009;7(4):219-26. [Medline].

  8. Jørgensen KT, Pedersen BV, Jacobsen S, Biggar RJ, Frisch M. National cohort study of reproductive risk factors for rheumatoid arthritis in Denmark: a role for hyperemesis, gestational hypertension and pre-eclampsia?. Ann Rheum Dis. Feb 2010;69(2):358-63. [Medline].

  9. Guthrie KA, Dugowson CE, Voigt LF, Koepsell TD, Nelson JL. Does pregnancy provide vaccine-like protection against rheumatoid arthritis?. Arthritis Rheum. Jul 2010;62(7):1842-8. [Medline]. [Full Text].

  10. Lipsky PE. Harrison's Principles of Internal Medicine. In: Isselbacher KJ, Braunwald E, Fauci AS, et al. Rheumatoid arthritis. 17th ed. New York, NY: McGraw-Hill; 1994:1648-55.

  11. Weinblatt ME, Keystone EC, Cohen MD, Freundlich B, Li J, Chon Y, et al. Factors associated with radiographic progression in patients with rheumatoid arthritis who were treated with methotrexate. J Rheumatol. Feb 2011;38(2):242-6. [Medline].

  12. Sokka T, Kautiainen H, Möttönen T, Hannonen P. Work disability in rheumatoid arthritis 10 years after the diagnosis. J Rheumatol. Aug 1999;26(8):1681-5. [Medline].

  13. Lunt M, Watson KD, Dixon WG, Symmons DP, Hyrich KL. No evidence of association between anti-tumor necrosis factor treatment and mortality in patients with rheumatoid arthritis: results from the British Society for Rheumatology Biologics Register. Arthritis Rheum. Nov 2010;62(11):3145-53. [Medline].

  14. Thompson AE, Rieder SW, Pope JE. Tumor necrosis factor therapy and the risk of serious infection and malignancy in patients with early rheumatoid arthritis: A meta-analysis of randomized controlled trials. Arthritis Rheum. Jun 2011;63(6):1479-85. [Medline].

  15. Mariette X, Matucci-Cerinic M, Pavelka K, et al. Malignancies associated with tumour necrosis factor inhibitors in registries and prospective observational studies: a systematic review and meta-analysis. Ann Rheum Dis. Nov 2011;70(11):1895-904. [Medline].

  16. Komano Y, Harigai M, Koike R, Sugiyama H, Ogawa J, Saito K. Pneumocystis jiroveci pneumonia in patients with rheumatoid arthritis treated with infliximab: a retrospective review and case-control study of 21 patients. Arthritis Rheum. Mar 15 2009;61(3):305-12. [Medline].

  17. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. Sep 2010;69(9):1580-8. [Medline].

  18. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. Sep 2010;62(9):2569-81. [Medline].

  19. Varache S, Cornec D, Morvan J, et al. Diagnostic Accuracy of ACR/EULAR 2010 Criteria for Rheumatoid Arthritis in a 2-Year Cohort. J Rheumatol. Jul 2011;38(7):1250-7. [Medline].

  20. Britsemmer K, Ursum J, Gerritsen M, van Tuyl L, van Schaardenburg D. Validation of the 2010 ACR/EULAR classification criteria for rheumatoid arthritis: slight improvement over the 1987 ACR criteria. Ann Rheum Dis. Aug 2011;70(8):1468-70. [Medline].

  21. Katchamart W, Johnson S, Lin HJ, Phumethum V, Salliot C, Bombardier C. Predictors for remission in rheumatoid arthritis patients: A systematic review. Arthritis Care Res (Hoboken). Aug 2010;62(8):1128-43. [Medline].

  22. Varache S, Narbonne V, Jousse-Joulin S, et al. Is routine viral screening useful in patients with recent-onset polyarthritis of a duration of at least 6 weeks? Results from a nationwide longitudinal prospective cohort study. Arthritis Care Res (Hoboken). Nov 2011;63(11):1565-70. [Medline].

  23. O'Dell JR, Haire CE, Erikson N, Drymalski W, Palmer W, Eckhoff PJ, et al. Treatment of rheumatoid arthritis with methotrexate alone, sulfasalazine and hydroxychloroquine, or a combination of all three medications. N Engl J Med. May 16 1996;334(20):1287-91. [Medline].

  24. Mjaavatten MD, van der Heijde DM, Uhlig T, et al. Should Anti-citrullinated Protein Antibody and Rheumatoid Factor Status Be Reassessed During the First Year of Followup in Recent-Onset Arthritis? A Longitudinal Study. J Rheumatol. Nov 2011;38(11):2336-41. [Medline].

  25. Suter LG, Fraenkel L, Braithwaite RS. Role of magnetic resonance imaging in the diagnosis and prognosis of rheumatoid arthritis. Arthritis Care Res (Hoboken). May 2011;63(5):675-88. [Medline].

  26. Gandjbakhch F, Foltz V, Mallet A, Bourgeois P, Fautrel B. Bone marrow oedema predicts structural progression in a 1-year follow-up of 85 patients with RA in remission or with low disease activity with low-field MRI. Ann Rheum Dis. Dec 2011;70(12):2159-62. [Medline].

  27. Zayat AS, Conaghan PG, Sharif M, et al. Do non-steroidal anti-inflammatory drugs have a significant effect on detection and grading of ultrasound-detected synovitis in patients with rheumatoid arthritis? Results from a randomised study. Ann Rheum Dis. Oct 2011;70(10):1746-51. [Medline].

  28. Kelleher MO, McEvoy L, Yang JP, Kamel MH, Bolger C. Lateral mass screw fixation of complex spine cases: a prospective clinical study. Br J Neurosurg. Oct 2008;22(5):663-8. [Medline].

  29. Cakir B, Käfer W, Reichel H, Schmidt R. [Surgery of the cervical spine in rheumatoid arthritis. Diagnostics and indication]. Orthopade. Nov 2008;37(11):1127-40; quiz 1141. [Medline].

  30. Narváez JA, Narváez J, Serrallonga M, De Lama E, de Albert M, Mast R, et al. Cervical spine involvement in rheumatoid arthritis: correlation between neurological manifestations and magnetic resonance imaging findings. Rheumatology (Oxford). Dec 2008;47(12):1814-9. [Medline].

  31. Bongartz T, Sutton AJ, Sweeting MJ, Buchan I, Matteson EL, Montori V. 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. JAMA. May 17 2006;295(19):2275-85. [Medline].

  32. Sohl S, Renner R, Winter U, Bodendorf M, Paasch U, Simon JC, et al. [Drug-induced lupus erythematosus tumidus during treatment with adalimumab]. Hautarzt. Oct 2009;60(10):826-9. [Medline].

  33. Ramos-Casals M, Brito-Zerón P, Soto MJ, Cuadrado MJ, Khamashta MA. Autoimmune diseases induced by TNF-targeted therapies. Best Pract Res Clin Rheumatol. Oct 2008;22(5):847-61. [Medline].

  34. Branch DW. Pregnancy in patients with rheumatic diseases: obstetric management and monitoring. Lupus. 2004;13(9):696-8. [Medline].

  35. [Guideline] Saag KG, Teng GG, Patkar NM, Anuntiyo J, Finney C, Curtis JR. American College of Rheumatology 2008 recommendations for the use of nonbiologic and biologic disease-modifying antirheumatic drugs in rheumatoid arthritis. Arthritis Rheum. Jun 15 2008;59(6):762-84. [Medline].

  36. Bili A, Sartorius JA, Kirchner HL, Morris SJ, Ledwich LJ, Antohe JL, et al. Hydroxychloroquine use and decreased risk of diabetes in rheumatoid arthritis patients. J Clin Rheumatol. Apr 2011;17(3):115-20. [Medline].

  37. Solomon DH, Massarotti E, Garg R, et al. Association between disease-modifying antirheumatic drugs and diabetes risk in patients with rheumatoid arthritis and psoriasis. JAMA. Jun 22 2011;305(24):2525-31. [Medline].

  38. Lipsky PE, van der Heijde DM, St Clair EW, Furst DE, Breedveld FC, Kalden JR, et al. Infliximab and methotrexate in the treatment of rheumatoid arthritis. Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group. N Engl J Med. Nov 30 2000;343(22):1594-602. [Medline].

  39. Rigby W, Ferraccioli G, Greenwald M, et al. Effect of rituximab on physical function and quality of life in patients with rheumatoid arthritis previously untreated with methotrexate. Arthritis Care Res (Hoboken). May 2011;63(5):711-20. [Medline].

  40. Tosh JC, Wailoo AJ, Scott DL, Deighton CM. Cost-effectiveness of combination nonbiologic disease-modifying antirheumatic drug strategies in patients with early rheumatoid arthritis. J Rheumatol. Aug 2011;38(8):1593-600. [Medline].

  41. Furst DE, Breedveld FC, Kalden JR, Smolen JS, Burmester GR, Sieper J, et al. Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2007. Ann Rheum Dis. Nov 2007;66 Suppl 3:iii2-22. [Medline].

  42. Matsudaira R, Tamura N, Sekiya F, Ogasawara M, Yamanaka K, Takasaki Y. Anti-Ro/SSA Antibodies Are an Independent Factor Associated with an Insufficient Response to Tumor Necrosis Factor Inhibitors in Patients with Rheumatoid Arthritis. J Rheumatol. Nov 2011;38(11):2346-54. [Medline].

  43. Galloway JB, Hyrich KL, Mercer LK, et al. Risk of septic arthritis in patients with rheumatoid arthritis and the effect of anti-TNF therapy: results from the British Society for Rheumatology Biologics Register. Ann Rheum Dis. Oct 2011;70(10):1810-1814. [Medline]. [Full Text].

  44. Lan JL, Chen YM, Hsieh TY, et al. Kinetics of viral loads and risk of hepatitis B virus reactivation in hepatitis B core antibody-positive rheumatoid arthritis patients undergoing anti-tumour necrosis factor alpha therapy. Ann Rheum Dis. Oct 2011;70(10):1719-25. [Medline].

  45. Agency for Healthcare Research and Quality. Choosing Medications for Rheumatoid Arthritis. Available at http://effectivehealthcare.ahrq.gov/ehc/products/14/85/RheumArthritisClinicianGuide.pdf. Accessed April 19, 2010.

  46. Finzel S, Rech J, Schmidt S, et al. Repair of bone erosions in rheumatoid arthritis treated with tumour necrosis factor inhibitors is based on bone apposition at the base of the erosion. Ann Rheum Dis. Sep 2011;70(9):1587-93. [Medline].

  47. [Best Evidence] van Vollenhoven RF, Ernestam S, Geborek P, Petersson IF, Cöster L, Waltbrand E. Addition of infliximab compared with addition of sulfasalazine and hydroxychloroquine to methotrexate in patients with early rheumatoid arthritis (Swefot trial): 1-year results of a randomised trial. Lancet. Aug 8 2009;374(9688):459-66. [Medline].

  48. [Best Evidence] Visser K, van der Heijde D. Optimal dosage and route of administration of methotrexate in rheumatoid arthritis: a systematic review of the literature. Ann Rheum Dis. Jul 2009;68(7):1094-9. [Medline]. [Full Text].

  49. [Best Evidence] Fleischmann R, Vencovsky J, van Vollenhoven RF, Borenstein D, Box J, Coteur G. Efficacy and safety of certolizumab pegol monotherapy every 4 weeks in patients with rheumatoid arthritis failing previous disease-modifying antirheumatic therapy: the FAST4WARD study. Ann Rheum Dis. Jun 2009;68(6):805-11. [Medline].

  50. Smolen J, Landewé RB, Mease P, Brzezicki J, Mason D, Luijtens K. Efficacy and safety of certolizumab pegol plus methotrexate in active rheumatoid arthritis: the RAPID 2 study. A randomised controlled trial. Ann Rheum Dis. Jun 2009;68(6):797-804. [Medline].

  51. [Best Evidence] Emery P, Fleischmann RM, Moreland LW, Hsia EC, Strusberg I, Durez P. Golimumab, a human anti-tumor necrosis factor alpha monoclonal antibody, injected subcutaneously every four weeks in methotrexate-naive patients with active rheumatoid arthritis: twenty-four-week results of a phase III, multicenter, randomized, double-blind, placebo-controlled study of golimumab before methotrexate as first-line therapy for early-onset rheumatoid arthritis. Arthritis Rheum. Aug 2009;60(8):2272-83. [Medline].

  52. Edwards JC, Szczepanski L, Szechinski J, Filipowicz-Sosnowska A, Emery P, Close DR. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med. Jun 17 2004;350(25):2572-81. [Medline].

  53. Eisenberg R. Update on rituximab. Ann Rheum Dis. Nov 2005;64 Suppl 4:iv55-7. [Medline].

  54. Smolen JS, Aletaha D, Koeller M, Weisman MH, Emery P. New therapies for treatment of rheumatoid arthritis. Lancet. Dec 1 2007;370(9602):1861-74. [Medline].

  55. [Best Evidence] Bingham CO 3rd, Looney RJ, Deodhar A, Halsey N, Greenwald M, Codding C. Immunization responses in rheumatoid arthritis patients treated with rituximab: results from a controlled clinical trial. Arthritis Rheum. Jan 2010;62(1):64-74. [Medline].

  56. [Best Evidence] Askling J, van Vollenhoven RF, Granath F, Raaschou P, Fored CM, Baecklund E, et al. Cancer risk in patients with rheumatoid arthritis treated with anti-tumor necrosis factor alpha therapies: does the risk change with the time since start of treatment?. Arthritis Rheum. Nov 2009;60(11):3180-9. [Medline].

  57. Orencia (abatacept) [package insert]. Princeton, NJ: Bristol-Myers Squibb; 2011. [Full Text].

  58. Myasoedova E, Crowson CS, Nicola PJ, et al. The influence of rheumatoid arthritis disease characteristics on heart failure. J Rheumatol. Aug 2011;38(8):1601-6. [Medline].

  59. Colebatch AN, Marks JL, Edwards CJ. Safety of non-steroidal anti-inflammatory drugs, including aspirin and paracetamol (acetaminophen) in people receiving methotrexate for inflammatory arthritis (rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, other spondyloarthritis). Cochrane Database Syst Rev. Nov 9 2011;11:CD008872. [Medline].

  60. Luqmani R, Hennell S, Estrach C, Basher D, Birrell F, Bosworth A, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of rheumatoid arthritis (after the first 2 years). Rheumatology (Oxford). Apr 2009;48(4):436-9. [Medline].

  61. Göksel Karatepe A, Günaydin R, Türkmen G, Kaya T. Effects of home-based exercise program on the functional status and the quality of life in patients with rheumatoid arthritis: 1-year follow-up study. Rheumatol Int. Nov 5 2009;[Medline].

  62. Kamioka H, Tsutani K, Okuizumi H, Mutoh Y, Ohta M, Handa S. Effectiveness of aquatic exercise and balneotherapy: a summary of systematic reviews based on randomized controlled trials of water immersion therapies. J Epidemiol. 2010;20(1):2-12. [Medline].

  63. Lemmey AB, Marcora SM, Chester K, Wilson S, Casanova F, Maddison PJ. Effects of high-intensity resistance training in patients with rheumatoid arthritis: a randomized controlled trial. Arthritis Rheum. Dec 15 2009;61(12):1726-34. [Medline].

  64. Macedo AM, Oakley SP, Panayi GS, Kirkham BW. Functional and work outcomes improve in patients with rheumatoid arthritis who receive targeted, comprehensive occupational therapy. Arthritis Rheum. Nov 15 2009;61(11):1522-30. [Medline].

  65. Williams SB, Brand CA, Hill KD, Hunt SB, Moran H. Feasibility and outcomes of a home-based exercise program on improving balance and gait stability in women with lower-limb osteoarthritis or rheumatoid arthritis: a pilot study. Arch Phys Med Rehabil. Jan 2010;91(1):106-14. [Medline].

  66. O'Brien ET. Surgical principles and planning for the rheumatoid hand and wrist. Clin Plast Surg. Jul 1996;23(3):407-20. [Medline].

  67. Brent RL. Teratogen update: reproductive risks of leflunomide (Arava); a pyrimidine synthesis inhibitor: counseling women taking leflunomide before or during pregnancy and men taking leflunomide who are contemplating fathering a child. Teratology. Feb 2001;63(2):106-12. [Medline].

  68. Temprano KK, Bandlamudi R, Moore TL. Antirheumatic drugs in pregnancy and lactation. Semin Arthritis Rheum. Oct 2005;35(2):112-21. [Medline].

  69. Chambers CD, Johnson DL, Robinson LK, Braddock SR, Xu R, Lopez-Jimenez J. Birth outcomes in women who have taken leflunomide during pregnancy. Arthritis Rheum. May 2010;62(5):1494-503. [Medline].

  70. Parke A, West B. Hydroxychloroquine in pregnant patients with systemic lupus erythematosus. J Rheumatol. Oct 1996;23(10):1715-8. [Medline].

  71. Østensen M, Förger F, Nelson JL, Schuhmacher A, Hebisch G, Villiger PM. Pregnancy in patients with rheumatic disease: anti-inflammatory cytokines increase in pregnancy and decrease post partum. Ann Rheum Dis. Jun 2005;64(6):839-44. [Medline].

  72. Ahlmén M, Svensson B, Albertsson K, Forslind K, Hafström I,. Influence of gender on assessments of disease activity and function in early rheumatoid arthritis in relation to radiographic joint damage. Ann Rheum Dis. Jan 2010;69(1):230-3. [Medline].

  73. Amgen. (2008). Kineret®. Personal communication with Kijung Sung-Thay, PharmD.

  74. Bristol-Myers Squibb. Use of Orencia during pregnancy and effects on fertility. Personal communication with Kelly S. Park, PharmD, MBA, representative of Bristol-Myers.

  75. Bruno MA, Wakefield RJ. Arthritis in Color: Advanced Imaging of Arthritis. In: Chapter 5: Ultrasound of rheumatoid arthritis. In: Bruno MA, Mosher TJ, Gold GE, eds. Philadelphia, PA: Saunders-Elsevier; 2009:96-122.

  76. Cheung PP, Dougados M, Gossec L. Reliability of ultrasonography to detect synovitis in rheumatoid arthritis: a systematic literature review of 35 studies (1,415 patients). Arthritis Care Res (Hoboken). Mar 2010;62(3):323-34. [Medline].

  77. Cyteval C. Doppler ultrasonography and dynamic magnetic resonance imaging for assessment of synovitis in the hand and wrist of patients with rheumatoid arthritis. Semin Musculoskelet Radiol. Mar 2009;13(1):66-73. [Medline].

  78. Decker M, Rothermundt C, Holländer G, Tichelli A, Rochlitz C. Rituximab plus CHOP for treatment of diffuse large B-cell lymphoma during second trimester of pregnancy. Lancet Oncol. Aug 2006;7(8):693-4. [Medline].

  79. Fiocco U, Ferro F, Vezzù M, Cozzi L, Checchetto C, Sfriso P, et al. Rheumatoid and psoriatic knee synovitis: clinical, grey scale, and power Doppler ultrasound assessment of the response to etanercept. Ann Rheum Dis. Jun 2005;64(6):899-905. [Medline]. [Full Text].

  80. Friedrichs B, Tiemann M, Salwender H, Verpoort K, Wenger MK, Schmitz N. The effects of rituximab treatment during pregnancy on a neonate. Haematologica. Oct 2006;91(10):1426-7. [Medline].

  81. Fukae J, Kon Y, Henmi M, Sakamoto F, Narita A, Shimizu M. Change of synovial vascularity in a single finger joint assessed by power doppler sonography correlated with radiographic change in rheumatoid arthritis: comparative study of a novel quantitative score with a semiquantitative score. Arthritis Care Res (Hoboken). May 2010;62(5):657-63. [Medline].

  82. Johnson DL, et al. Pregnancy outcomes in women exposed to adalimumab: an update on the OTIS Autoimmune Diseases in Pregnancy project. Available at http://www.otispregnancy.org/readResource.php?r=108643. Accessed May 24, 2010.

  83. Kane S, Ford J, Cohen R, Wagner C. Absence of infliximab in infants and breast milk from nursing mothers receiving therapy for Crohn's disease before and after delivery. J Clin Gastroenterol. Aug 2009;43(7):613-6. [Medline].

  84. Keystone EC, Kavanaugh A, Weinblatt ME, Patra K, Pangan AL. Clinical consequences of delayed addition of adalimumab to methotrexate therapy over 5 years in patients with rheumatoid arthritis. J Rheumatol. May 2011;38(5):855-62. [Medline].

  85. Kimby E, Sverrisdottir A, Elinder G. Safety of rituximab therapy during the first trimester of pregnancy: a case history. Eur J Haematol. Apr 2004;72(4):292-5. [Medline].

  86. Klink DT, van Elburg RM, Schreurs MW, van Well GT. Rituximab administration in third trimester of pregnancy suppresses neonatal B-cell development. Clin Dev Immunol. 2008;2008:271363. [Medline].

  87. Moskovitz DN, Bodian C, Chapman ML, Marion JF, Rubin PH, Scherl E. The effect on the fetus of medications used to treat pregnant inflammatory bowel-disease patients. Am J Gastroenterol. Apr 2004;99(4):656-61. [Medline].

  88. Murashima A, Watanabe N, Ozawa N, Saito H, Yamaguchi K. Etanercept during pregnancy and lactation in a patient with rheumatoid arthritis: drug levels in maternal serum, cord blood, breast milk and the infant's serum. Ann Rheum Dis. Nov 2009;68(11):1793-4. [Medline].

  89. Möller B, Bonel H, Rotzetter M, Villiger PM, Ziswiler HR. Measuring finger joint cartilage by ultrasound as a promising alternative to conventional radiograph imaging. Arthritis Rheum. Apr 15 2009;61(4):435-41. [Medline].

  90. Naraghi AM, White LM, Patel C, Tomlinson G, Keystone EC. Comparison of 1.0-T extremity MR and 1.5-T conventional high-field-Strength MR in patients with rheumatoid arthritis. Radiology. Jun 2009;251(3):829-37. [Medline].

  91. Naredo E, Bonilla G, Gamero F, Uson J, Carmona L, Laffon A. Assessment of inflammatory activity in rheumatoid arthritis: a comparative study of clinical evaluation with grey scale and power Doppler ultrasonography. Ann Rheum Dis. Mar 2005;64(3):375-81. [Medline]. [Full Text].

  92. Olech E, Crues JV 3rd, Yocum DE, Merrill JT. Bone marrow edema is the most specific finding for rheumatoid arthritis (RA) on noncontrast magnetic resonance imaging of the hands and wrists: a comparison of patients with RA and healthy controls. J Rheumatol. Feb 2010;37(2):265-74. [Medline].

  93. Organization of Teratology Information Services (OTIS) Autoimmune Diseases in Pregnancy Project. Available at http://clinicaltrials.gov/ct2/show/NCT00116272. Accessed April 19, 2010.

  94. Ostensen M, Eigenmann GO. Etanercept in breast milk. J Rheumatol. May 2004;31(5):1017-8. [Medline].

  95. Pearman L, Last J, Fitzgerald O, Veale D, Joyce M, Rainford L. Rheumatoid arthritis: a novel radiographic projection for hand assessment. Br J Radiol. Jul 2009;82(979):554-60. [Medline].

  96. Rey J, Coso D, Roger V, Bouayed N, Belmecheri N, Ivanov V. Rituximab combined with chemotherapy for lymphoma during pregnancy. Leuk Res. Mar 2009;33(3):e8-9. [Medline].

  97. Roux CH, Brocq O, Breuil V, Albert C, Euller-Ziegler L. Pregnancy in rheumatology patients exposed to anti-tumour necrosis factor (TNF)-alpha therapy. Rheumatology (Oxford). Apr 2007;46(4):695-8. [Medline].

  98. Salaffi F, Carotti M, Manganelli P, Filippucci E, Giuseppetti GM, Grassi W. Contrast-enhanced power Doppler sonography of knee synovitis in rheumatoid arthritis: assessment of therapeutic response. Clin Rheumatol. Aug 2004;23(4):285-90. [Medline].

  99. Schwenzer NF, Kötter I, Henes JC, Schraml C, Fritz J, Claussen CD. The role of dynamic contrast-enhanced MRI in the differential diagnosis of psoriatic and rheumatoid arthritis. AJR Am J Roentgenol. Mar 2010;194(3):715-20. [Medline].

  100. Sinha A, Patient C. Rheumatoid arthritis in pregnancy: successful outcome with anti-TNF agent (Etanercept). J Obstet Gynaecol. Oct 2006;26(7):689-91. [Medline].

  101. Skomsvoll JF, Wallenius M, Koksvik HS, Rødevand E, Salvesen KA, Spigset O. Drug insight: Anti-tumor necrosis factor therapy for inflammatory arthropathies during reproduction, pregnancy and lactation. Nat Clin Pract Rheumatol. Mar 2007;3(3):156-64. [Medline].

  102. Strunk J, Heinemann E, Neeck G, Schmidt KL, Lange U. A new approach to studying angiogenesis in rheumatoid arthritis by means of power Doppler ultrasonography and measurement of serum vascular endothelial growth factor. Rheumatology (Oxford). Dec 2004;43(12):1480-3. [Medline].

  103. Suzuki T, Ito S, Handa S, Kose K, Okamoto Y, Minami M, et al. A new low-field extremity magnetic resonance imaging and proposed compact MRI score: evaluation of anti-tumor necrosis factor biologics on rheumatoid arthritis. Mod Rheumatol. 2009;19(4):358-65. [Medline]. [Full Text].

 
Previous
Next
 
Ankylosis in the cervical spine at several levels due to long-standing juvenile rheumatoid arthritis (also known as juvenile idiopathic arthritis).
Widespread osteopenia, carpal crowding (due to cartilage loss), and several erosions affecting the carpal bones and metacarpal heads in particular in a child with advanced juvenile rheumatoid arthritis (also known as juvenile idiopathic arthritis).
Rheumatoid changes in the hand. Photograph by David Effron MD, FACEP.
Rheumatoid nodules at the elbow. Photograph by David Effron MD, FACEP.
Soft-tissue swelling and early erosions in the proximal interphalangeal joints in a patient with rheumatoid arthritis of the hands.
Subluxation in the metacarpophalangeal joints, with ulnar deviation, in a patient with rheumatoid arthritis of the hands.
Coronal, T1-weighted magnetic resonance imaging scan shows characteristic pannus and erosive changes in the wrist in a patient with active rheumatoid arthritis. Courtesy of J. Tehranzadeh, MD, University of California at Irvine.
Lateral view of the cervical spine in a patient with rheumatoid arthritis shows erosion of the odontoid process.
Boutonniere deformity.
Anteroposterior radiograph of the knee shows uniform joint-space loss in the medial and lateral knee compartments without osteophytosis. A Baker cyst is seen medially (arrowhead).
Ultrasonography-guided synovial biopsy of the second metacarpophalangeal joint of the right hand in a patient with rheumatoid arthritis of the hands. The biopsy needle is seen as a straight echogenic line on the left side of the image in an oblique orientation.
Plain lateral radiograph of the normal cervical spine taken in extension shows measurement of anterior atlantodental interval (yellow line) and posterior atlantodental interval (red line).
Lateral flexion view of the cervical spine shows atlantoaxial subluxation.
Lateral view of the cervical spine in a patient with rheumatoid arthritis shows erosion of the odontoid process.
T1-weighted sagittal magnetic resonance image of the cervical spine shows basilar invagination with cranial migration of an eroded odontoid peg. There is minimal pannus. The tip of the peg indents the medulla, and there is narrowing of the foramen magnum due to the presence of the peg. Inflammatory fusion of several cervical vertebral bodies is shown.
Sagittal T2-weighted magnetic resonance image of the cervical spine in the same case as in Image above. The compromised foramen magnum is easily appreciated, and there is increased signal intensity within the upper cord; this is consistent with compressive myelomalacia. Further narrowing of the canal is seen at multiple levels.
Lateral radiograph of the same patient as in Images 4-5. Midcervical vertebral-body fusions are shown. The eroded peg is difficult to visualize, but inferior subluxation of the anterior arch of C1 is shown.
Lateral radiograph of a normal cervical spine shows the McGregor line. The odontoid tip should not protrude more than 4.5 mm above the line, which is drawn from the posterior edge of the hard palate to the most caudal point of the occiput.
Normal lateral magnified radiograph of the cervical spine shows the Ranawat method of detection of cranial settling. This method is used to measure the distance from the center of the pedicles (sclerotic ring) of C2 to a line drawn connecting the midpoints of the anterior and posterior arches of C1. (Normal values are 15 mm or greater for males and 13 mm or greater for females.)
Lateral radiograph of the cervical spine shows how the cervical height index (CHI) is calculated. The distance from the center of the sclerotic ring of C2 to the tip of the spinous process of C2 (dotted line) is measured. This is then divided into the distance from the center of the sclerotic ring of C2 to the midpoint of the inferior border of the body of C7. A CHI of less than 2 mm is a sensitive predictor of neurologic deficit.
total hip replacement, prosthesis, osteoarthritis, X-ray.
Assistive devices
Assistive Devices to Improve Independence
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.