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Arthritis Clinical Trials, Diagnosis, and Treatment
Thank you for your interest in clinical trials for Arthritis.

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Arthritis

Arthritis (from Greek arthro-, joint + -itis, inflammation; plural: arthritides) is a group of conditions where there is damage caused to the joints of the body. Arthritis is the leading cause of disability in people over the age of 55.

There are many forms of arthritis, each of which has a different cause. Rheumatoid arthritis and psoriatic arthritis are autoimmune diseases in which the body is attacking itself. Septic arthritis is caused by joint infection. Gouty arthritis is caused by deposition of uric acid crystals in the joint that results in subsequent inflammation. Additionally, there is a less common form of gout that is caused by the formation of needle shaped crystals of calcium pyrophosphate. This form of gout is known as pseudogout. The most common form of arthritis, osteoarthritis is also known as degenerative joint disease and occurs following trauma to the joint, following an infection of the joint or simply as a result of aging. There is emerging evidence that abnormal anatomy may contribute to early development of osteoarthritis.

Current Research

For current research articles click - here

History and Physical Examination

All arthritides feature pain. Patterns of pain differ among the arthritides and the location. Osteoarthritis is classically worse at night or following rest. Rheumatoid arthritis is generally worse in the morning; in the early stages, patients often do not have symptoms following their morning shower. In elderly people and children, pain may not be the main feature, and the patient simply moves less (elderly) or refuses to use the affected limb (children).

Elements of the history of the pain (onset, number of joints and which involved, duration, aggravating and relieving factors) all guide diagnosis. Physical examination typically confirms diagnosis. Radiographs are often used to follow progression or assess severity in a more quantitative manner.

Blood tests and X-rays of the affected joints often are performed to make the diagnosis.

Screening blood tests may be indicated if certain arthritides are suspected. This may include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen and specific antibodies.

Many people associate cracking joints with arthritis; however, there is no evidence to support such an association. A joint is an area where two or more bones meet. This area is surrounded by joint fluid to protect the bones from rubbing against each other. When a joint is cracking, the fluid is pushed out and the "cracking" sound is the result of a high pressure of fluid. Rheumatoid arthritis is what happens when there is a loss of fluid in the joints causing damage to the lining of the joint itself. There is no evidence that cracking your knuckles causes such damage.

Types of Arthritis

Primary forms of arthritis:
  • Osteoarthritis
  • Rheumatoid arthritis
  • Septic arthritis
  • Gout and pseudogout
  • Juvenile arthritis
  • Still's disease
  • Ankylosing spondylitis
Secondary to other diseases:
  • Systemic lupus erythematosus (SLE)
  • Henoch-Schönlein purpura
  • Psoriatic arthritis
  • Reactive arthritis (Reiter's syndrome)
  • Hemochromatosis
  • Hepatitis
  • Wegener's granulomatosis (and many other vasculitis syndromes)
  • Familial Mediterranean fever (FMF), HIDS (hyperimmunoglobulinemia D and periodic fever syndrome) and TRAPS (TNF-alpha receptor associated periodic fever syndrome).
  • Inflammatory Bowel Disease (Including Crohn's Disease and Ulcerative Colitis)
Diseases that can mimic arthritis include:
  • Pierre Marie-Bamberger syndrome (hypertrophic pulmonary osteoarthropathy, a paraneoplastic phenomenon of lung cancer)
  • Multiple myeloma
  • Osteoporosis


Treatment

Treatment options vary depending on the type of arthritis and include physical and occupational therapy, and medications (symptomatic or targeted at the disease process causing the arthritis). Arthroplasty (joint replacement surgery) may be required in eroding forms of arthritis.

History

While evidence of primary ankle (kaki) osteoarthritis has been discovered in dinosaurs, the first known traces of human arthritis date back as far as 4500 BC. It was noted in skeletal remains of Native Americans found in Tennessee and parts of what is now Olathe, Kansas. Evidence of arthritis has been found throughout history, from Ötzi, a mummy (circa 3000 BC) found along the border of modern Italy and Austria, to the Egyptian mummies circa 2590 BC. Around 500 BC willow bark gained popularity when it was discovered to help relieve some of the aches and pains of arthritis. It wasn't until more than 2,000 years later, in the early 1820s, that European scientists began to scientifically study the chemical compound in willow bark that alleviated the arthritis symptoms. They discovered the compound was salicin. When they isolated salicin, however, they found it was very noxious to the stomach. Almost 80 years later, in 1897, an employee of Bayer Company -- then a dye production company -- named Felix Hoffman discovered how to isolate the compound and make it less irritating to the stomach. Hoffman was attempting to make the drug in order to help his father, who was suffering from arthritis. In 1899, Bayer Company trademarked Hoffman's discovery under the name "Aspirin." Today it is believed that over a trillion tablets of aspirin have been sold worldwide.


(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Arthritis)





Findings From Current Research

Arthritis Burden and Impact are Greater Among U.S. Women than Men: Intervention Opportunities

Authors: Theis KA, Helmick CG, Hootman JM

Arthritis Program, Centers for Disease Control and Prevention, Atlanta, Georgia.

Objectives: To summarize arthritis burden and impact among women compared with men, using updated surveillance and impact measures; to describe public health approaches to arthritis; and to review effective, evidence-based arthritis self-management interventions. Results: Arthritis continues to burden the U.S. population as the leading cause of physical disability and affects women disproportionately: women with arthritis report greater prevalence of activity and work limitations, psychological distress, and severe joint pain than their male counterparts. Three main public health interventions can reduce arthritis impact: self-management education, physical activity, and weight management. Self-management education programs are proven to reduce pain and depression, delay disability, improve self-efficacy, physical function, and quality of life, and reduce healthcare costs. Appropriate physical activity decreases pain, improves function, and delays disability. The American College of Rheumatology recommends maintaining a healthy weight to benefit patients with hip or knee osteoarthritis. Women appear more receptive to certain information delivery methods (i.e., physician counseling) than men, suggesting gender-specific targeting of interventions may be of use. Conclusions: Effective interventions remain underused. The Centers for Disease Control and Prevention Arthritis Program and its partners, including state arthritis programs, continue their efforts to build the arthritis public health science base, monitor burden and impact, evaluate and disseminate evidence-based interventions, and work to decrease and delay disability, and increase quality of life among those with arthritis. As new approaches are developed, women and other disproportionately impacted groups merit particular consideration in tailoring and delivering programs to reduce arthritis burden.

Journal: J Womens Health (Larchmt). 2007 May;16(4):441-453
Adapted from PubMed; click here to access full journal article.




Etanercept: A Review of its Use in the Management of Rheumatoid Arthritis

Authors: Dhillon S, Lyseng-Williamson KA, Scott LJ.

Wolters Kluwer Health | Adis, Auckland, New Zealand, an editorial office of Wolters Kluwer Health, Conshohocken, Pennsylvania, USA

Etanercept (Enbrel((R))), a soluble fusion protein that binds specifically to the cytokine human tumour necrosis factor (TNF), is approved for subcutaneous use in the treatment of patients with moderate to severe active rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing arthritis and plaque psoriasis in the US, Italy, the rest of the EU and other countries worldwide. Subcutaneous etanercept was efficacious and generally well tolerated in several large, well designed, clinical trials and in the clinical-practice setting in adult patients with rheumatoid arthritis, including methotrexate-naive patients with early disease and those with long-standing, treatment-resistant active disease. Etanercept plus methotrexate combination therapy was generally superior to either monotherapy in reducing disease activity and structural joint damage, as well as improving health-related quality of life (HR-QOL). Furthermore, etanercept monotherapy was superior to placebo and at least as effective as methotrexate therapy in reducing disease activity and improving HR-QOL in patients with early or refractory disease. The beneficial effects of etanercept monotherapy or combination therapy were sustained in the long term (</=9 years). Some pharmacoeconomic analyses suggest that etanercept is a cost-effective option in the treatment of patients with rheumatoid arthritis. Direct head-to-head comparisons with other biological agents would help to definitively position etanercept with respect to these agents. Nevertheless, extensive clinical experience indicates that etanercept is a valuable treatment option in adult patients with long-standing moderate to severe active rheumatoid arthritis and an emerging option in those with early disease.

Journal: Drugs. 2007;67(8):1211-1241
Adapted from PubMed; click here to access full journal article.




The Health Status of Retired American Football Players: Super Bowl III Revisited

Authors: Nicholas SJ, Nicholas JA, Nicholas C, Diecchio JR, McHugh MP

Nicholas Institute of Sports Medicine and Athletic Trauma, Lenox Hill Hospital, New York, New York

BACKGROUND: Despite a perception that retired professional football players have poor health, there are little supporting data. HYPOTHESIS: Retired football players have poor health compared with age-matched population norms. STUDY DESIGN: Cross-sectional study; Level of evidence, 4. METHODS: Thirty-six of 41 members of the 1969 Super Bowl winning team were contacted 35 years after that event (3 were deceased, and no contact information was available for 2). Players completed an SF-36 health survey and a medical history and football-specific questionnaire. Each player's football-related injury history before 1969 was documented from medical records. It was estimated that there was 80% power to detect a 10% difference in physical and mental health scores between the retired football players (age, 62 +/-3 y) and population norms (n = 741) at an alpha level of 0.05. RESULTS: SF-36 scores for physical and mental health were not different from age-matched norms (physical health P =.69; mental health P =.49). The most prevalent medical conditions were arthritis (24 of 36 players), hypertension (13 of 36 players), and chronic low back pain (13 of 36 players). SF-36 physical health scores were 21% lower in players with arthritis (P <.01) and back pain (P <.05) compared with the other players. Physical health scores were 19% above normal for players without arthritis (P <.01) and not different from normal for players with arthritis (6% lower; P =.6). Four of 8 players who had major ligamentous injuries to the knee before 1969 had total knee arthroplasty in the intervening years, compared with 3 of the remaining 28 players (P <.05). The men played professional football for 8.3 +/-3.8 years, and 33 players (94%) reported having had "very fulfilling" (n = 24) or "somewhat fulfilling" (n =9) careers. CONCLUSION: These professional football players had long and fulfilling careers with no apparent long-term detrimental effects on physical or mental health scores despite a high prevalence of arthritis.

Journal: Am J Sports Med. 2007 May 21
Adapted from PubMed; click here to access full journal article.




A Pilot Study of Tumor Necrosis Factor Inhibition in Erosive/Inflammatory Osteoarthritis of the Hands

Authors: Magnano MD, Chakravarty EF, Broudy C, Chung L, Kelman A, Hillygus J, Genovese MC

From the Division of Immunology and Rheumatology, Stanford University, Palo Alto, California, USA.

OBJECTIVE: To determine if anti-tumor necrosis factor (TNF) therapy (adalimumab) can safely improve symptoms of erosive/inflammatory osteosteoarthritis oarthritis (EOA). METHODS: This was an open-label pilot trial in 12 patients with EOA. Patients > 45 years old with EOA of the hands defined by >/= 2 tender and >/= 2 swollen joints (distal interphalangeal, proximal interphalangeal, first carpometacarpal) despite nonsteroidal antiinflammatory drug therapy were eligible. Patients were excluded for autoimmune arthritis, recent disease modifying antirheumatic drug use, prior use of anti-TNF therapy, infection, malignancy, or poorly controlled medical conditions. All patients received adalimumab 40 mg every other week for 12 weeks. Safety was assessed 4 weeks after the final dose. Primary endpoints included safety and American College of Rheumatology (ACR) response. RESULTS: Patients were predominantly female with a mean age of 60 years and 12 years of arthritis. All patients completed the study and safety followup. Adverse events were mild without necessitating discontinuation of study drug. After 12 weeks, there was a statistically significant improvement in the number of swollen joints compared to baseline (p < 0.01). One patient achieved an ACR20 response and 42% achieved an OMERACT-OARSI response. Although we detected no statistically significant improvement in the number of tender joints, grip strength, disability, pain, or global disease assessments, trends suggested modest improvement in all efficacy measures. CONCLUSION: This small open-label study of patients with EOA demonstrated that adalimumab was well tolerated. Treatment with adalimumab for 3 months did not significantly improve the signs and symptoms of EOA and most patients did not achieve an ACR20. Trends suggested improvement and individual patients had some benefit. Factors limiting interpretation of this study include the lack of a control group, outcomes chosen, number of patients treated, and the duration of treatment.

Journal: J Rheumatol. 2007 May 15
Adapted from PubMed; click here to access full journal article.




Can Exercise Influence Low Bone Mineral Density in Children with Juvenile Rheumatoid Arthritis?

Authors: Gannotti ME, Nahorniak M, Gorton GE 3rd, Sciascia K, Sueltenfuss M, Synder M, Zaniewski A

University of Hartford (M.E.G., K.S., M.S., M.S, A.Z.), Hartford, Connecticut and Shriners Hospital for Children (M.N., G.E.G.), Springfield, Massachusetts.

PURPOSE:: Low bone mineral density (BMD) is a common secondary condition associated with juvenile idiopathic arthritis (JIA). The purpose of this review was evaluate the literature pertinent to designing an effective, safe weight-bearing exercise program to reduce the risk of low BMD in children with JIA. SUMMARY OF KEY POINTS:: Thirty-seven articles on the risk of low BMD and children with JIA, weight-bearing interventions to improve BMD in healthy children, or safety and efficacy of exercise interventions with children with JIA were critiqued on the basis of their design. Three highly rated studies confirmed the multifactorial nature of low BMD in children with JIA, two highly rated studies support the efficacy of weight-bearing interventions for increasing BMD in children who are healthy, and one moderately rated study demonstrated the safety of low impact exercise by children with JIA. STATEMENT OF CONCLUSIONS AND RECOMMENDATIONS FOR CLINICAL PRACTICE:: Weight-bearing activities should be included in exercise programs for individuals with JIA, although more research is needed to determine the amount, duration, and frequency of weight-bearing activity needed to reduce the risk for low BMD.

Journal: Pediatr Phys Ther. 2007 Summer;19(2):128-39.
Adapted from PubMed; click here to access full journal article.




Sleep and the Affective Response to Stress and Pain

Authors: Hamilton NA, Catley D, Karlson C

Department of PsychologyUniversity of Kansas, Lawrence, KS, US. nancyh@ku.edu

Objective: The current study examined sleep disturbance (i.e., sleep duration, sleep quality) as a correlate of stress reactivity and pain reactivity. Design and Outcome Measures: An ecological momentary assessment design was used to evaluate the psychosocial functioning of men and women with fibromyalgia or rheumatoid arthritis (N = 49). Participants recorded numeric ratings of pain, the occurrence of a stressful event, as well as positive and negative affect 7 times throughout the day for 2 consecutive days. In addition, participants reported on their sleep duration and sleep quality each morning. Results: Sleep disruption was not found to be an independent predictor of affect. However, sleep was found to buffer the relationship between stress and negative affect and the relationship between pain and both positive and negative affect. Conclusion: These results are consistent with a model in which good-quality sleep acts as a biobehavioral resource that minimizes allostatic load. ((c) 2007 APA, all rights reserved).

Journal: Health Psychol. 2007 May;26(3):288-95
Adapted from PubMed; click here to access full journal article.




Synovial Mast Cells: Role in Acute and Chronic Arthritis

Authors: Nigrovic PA, Lee DM

Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, and Division of Immunology, Children's Hospital Boston, Boston, MA, USA.

Mast cells reside in the normal synovium and increase strikingly in number in rheumatoid arthritis and other joint diseases. Given the broad spectrum of activity of this lineage, it has for decades been considered probable that mast cells are involved in the pathophysiology of synovitis. Recent work in murine arthritis has substantiated this suspicion, showing that mast cells can contribute importantly to the initiation of inflammatory arthritis. However, the role of the greatly expanded population of synovial mast cells in established arthritis remains unknown. Here we review the current understanding of mast cell function in acute arthritis and consider the potentially important influence of this cell on key processes within the chronically inflamed synovium, including leukocyte recruitment and activation, fibroblast proliferation, angiogenesis, matrix remodeling, and injury to collagen and bone. We also consider recent evidence supporting an immunomodulatory or anti-inflammatory role for mast cells as well as pharmacologic approaches to the mast cell as a therapeutic target in inflammatory arthritis.

Journal: Immunol Rev. 2007 Jun;217(1):19-37
Adapted from PubMed; click here to access full journal article.






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