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Emerging Concepts In Treating Psoriatic Arthritis (PSA)-Baseball
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Emerging Concepts In Treating Psoriatic Arthritis

- By Linda Davis, MHS, PA-C

Psoriatic arthritis presents an array of challenges to patients and clinicians. With this in mind, this author discusses the prevalence and potential etiologies of the disease, provides an overview of current diagnostic criteria, and offers perspectives on appropriate treatment.



How challenging is it to cope with psoriatic arthritis (PSA)? One study found that the physical and mental functioning of patients with PsA may be affected as much as those with cancer, arthritis, hypertension, heart disease, diabetes and depression. The chronic autoimmune disease also affects one’s social and economic well-being. A mail survey by the Psoriasis Foundation found that the jobs of those with PsA were affected due to missed work or discrimination. People with PsA may also have concerns with sexual activity and embarrassment at the appearance of the skin condition.

Psoriasis occurs in approximately two percent of the population of North America and Europe. According to two Mayo Clinic population-based studies that give varying figures, five to 30 percent of psoriatic legions are associated with inflammatory arthritis.1,2

Psoriatic arthritis occurs more often (one to three percent) in Caucasians. While the male-to-female ratio has been widely debated for the disease, data pooled from 10 different studies indicates a slightly higher incidence in females than in males (1.04:1). The onset of PsA generally occurs between the ages of 30 and 40.

While clinicians commonly diagnose rheumatic diseases based on pattern recognition, the diagnosis of psoriatic arthritis is somewhat difficult as it involves two diseases that are assessed and treated by two different sub-specialists.

Fortunately, specific criteria (involving clinical and X-ray features) are being developed for PsA. In recent years, there have also been considerable advances in understanding the pathophysiology of the immune system and these advances have led to the development of newer, advanced therapies that have been shown to be effective against both disease components.

Photo courtesy of Raymond Pertusi, MD Hand deformities in cases of PsA can include mild changes in the skin, moderate changes in the nails with erythema, swelling and flexion at the DIPs. In this case, the right hand is worse than the left.

Essential Keys To Diagnosing PsA
Psoriatic arthritis was first recognized in the 19th century. On the basis of epidemiological and clinical studies in the 1960s, various researchers found the arthritis component of PsA was seronegative.

In the 1970s, they included PsA in the broader category of the spondyloarthritides due to its similarity to reactive arthritis and ankylosing spondylitis (AS). In 1991, the American College of Rheumatology (ACR) developed criteria for the classification of spondyloarthropathy.

With these criteria as a guide, clinicians may diagnose PsA in patients with a history of psoriasis and asymmetric synovitis. There may be other criteria involved but these two are the cornerstone for PsA diagnosis.

For any patient assessment, the skin often provides valuable diagnostic clues that may lead to a specific diagnosis or at least limit the list of possibilities.


Photo courtesy of Raymond Pertusi, MD In this case, arthritic changes have already occurred including possible early telescoping. This may indicate the possible onset of arthritis mutilans.
Traditional psoriasis evaluation is dependent on the amount of skin involvement covered by lesions or the body surface affected (BSA). With this in mind, there are three categories of skin involvement.
• Mild. These patients have less than three percent coverage, mainly on extensor surfaces.
• Moderate. The patients have three to 10 percent coverage.
• Severe. These patients have greater than 10 percent coverage and it may involve the torso, for which the term guttate applies.

Approximately, 65 percent of patients with PsA have mild disease while 35 percent have moderate to severe disease.
Psoriatic arthritis may present in multiple forms, affect one or more joints and may have additional features of other spondyloarthritides. It is often associated with dactylitis or enthesitis.

There is no correlation between psoriatic lesions and the severity of arthritis. Skin lesions occur first in 60 to 70 percent of cases and joints may not be affected until eight to 10 years later. However, in 15 to 20 percent of cases, the two manifestations occur within one year of each other. The cause of this transition within the disease process is unknown but genetic and environmental components are suspected.

How To Recognize The Different Subtypes Of PsA
The original diagnostic criteria from Moll and Wright are simple and the most frequently used guidelines in current studies. The criteria are inflammatory arthritis, the presence of psoriasis and the absence of rheumatoid factor (RF). In 1973, Moll and Wright separated PsA into five subtypes based on a large case series of patients.3

Pattern one is arthritis of the distal interphalangeal joints (DIPs). This occurs in 15 percent of cases. Pattern two is asymmetric oligoarthritis, which occurs in 30 percent of cases. Pattern three is symmetrical polyarthritis, which occurs in 40 percent of cases and is very similar to rheumatoid arthritis (RA). The fourth pattern consists of axial involvement of the spine and sacroiliac joint, and occurs in five percent of cases. The last pattern, arthritis mutilans, also occurs in five percent of cases.

Photo courtesy of Raymond Pertusi, MD Here one can see dystrophic hyperkeratosis. There are six different nail changes which occur in 90 percent of patients with PsA.

Arthritis mutilans is the most devastating type of pattern. It results in widespread shortening of the digits (telescoping) and can even lead to anklyosing and contractures in other digits. Radiography is helpful in all of these cases.

Other Pertinent Clues To The Clinical Presentation
Six different patterns of nail changes occur in 90 percent of PsA patients. These nail changes may include pitting, horizontal ridging, onycholysis, yellowish discoloration of the nail margins, dystrophic hyperkeratosis and/or a combination of these findings. Other extraarticular manifestations include ocular inflammation, conjunctivitis or uveitis. These manifestations reportedly affect seven to 33 percent PsA patients. Joint pain symptoms of PsA are usually less severe but may resemble RA.

Since there are no specific laboratory tests for PsA, it may take three to 11 years before one can obtain a correct diagnosis. If you pursue lab tests, the RF and antinuclear antibodies (ANA) are negative. Analysis of synovial fluid shows a predominance of leukocytes, primarily neutrophils. Radiographs may show changes characteristic of PsA. When warranted, ultrasound and magnetic resonance imaging (MRI) can show enthesitis and tendon sheath effusions that may be difficult to assess on physical examination.

The course of the disease varies depending upon clinical presentation. Widely varying estimates of clinical outcomes have been reported with PsA. The disease can range from mild to the most severe variety with the crippling arthritis mutilans. Overall, erosive disease develops with deformity and disability, and leads increased morbidity and mortality.

Clinicians may see PsA in conjunction with HIV in more severe cases. Treatment with antiretroviral agents tends to put the disease into remission whereas biologics and disease modifying antirheumatic drugs (DMARDs) are contraindicated in these cases.

Photo courtesy of Raymond Pertusi, MD Here is an example of moderate PsA. Arthritic changes have occurred in the patient’s feet with erythema, swelling and the crossing of toes as well as nail changes.

Case Study: When A Patient With Longstanding Plaque Psoriasis Develops Inflammatory Arthritis
Adam is a 49-year old mechanic who presents to your clinic with a 10-year history of plaque psoriasis. He has a recent history of inflammatory arthritis and his skin disease has grown worse. Adam’s dermatologist referred him because he is also complaining of musculoskeletal pain. While the dermatologist has utilized ultraviolet B therapy and vitamin D ointment, Adam still has plaques covering several extensor surfaces.

While playing baseball two weeks before the onset of his joint pain, Adam remembers sliding into home base and hitting his right side against the catcher. Afterward, Adam notices additional plaques with a red and silver discoloration at the injured areas of skin. His joint symptoms include pain in both hands as well as his right knee, left ankle and the balls of both feet.

Adam reports one hour of morning stiffness and not feeling like himself due to the pain and inability to perform certain job functions. He has started taking an over-the-counter antiinflammatory but says it has not helped much. His sleep has been disrupted and nonrestorative due to the pain, and his wife is worried he is getting more difficult to get along with and staying home from work.

Adam is unable to walk without limping and his shoes hurt his feet. He cannot get his wedding ring off due to the swelling in his right finger.

The patient assessment shows 16 swollen joints and 18 tender joints, with swelling of the right fourth digit and significant nail changes with pitting and yellowish discoloration. There is tenderness of his left Achilles tendon insertion and plaques involve 20 percent of body surface.

Photo courtesy of Raymond Pertusi, MD Mild PsA includes less than three percent body coverage. Skin changes, as shown above, occur mainly on extensor surfaces.

The clinician decides labs are not indicated and instead orders X-rays of the hands and feet. The X-rays show areas of joint space narrowing and erosion. The clinician notes a classic “pencil-in-cup” deformity on the fourth digit of the right hand.

Exploring The Range Of Treatment Options
It is of the utmost importance to educate the patient on how to cope with PsA. The Arthritis Foundation Web site (http://www.arthritis.org) is a great tool to use. It provides patient education on the disease and its various treatments.
The ideal therapy should attack the skin and joints affected by PsA. Non-pharmacological treatments may include physical therapy with water aerobics. Tai chi and massage therapy may help to improve flexibility.

Pharmacologic therapy follows the step-up plan. Nonsteroidal antiinflammatory drugs (NSAIDs) are usually the first line of treatment for pain, provided the patient does not have any gastrointestinal (GI) issues. Also keep in mind that a proton pump inhibitor can be helpful to prevent occurrences of abdominal symptoms.

Generally, it is best to avoid steroids in PsA treatment as skin lesions tend to exacerbate with attempted tapering of steroids. However, if enthesitis or a specific joint is problematic, an intraarticular or local steroid injection may be helpful.

Oral DMARDs are indicated as the next line of therapy. Disease modifying antirheumatic drugs such as methotrexate, sulfasalazine and leflunomide show modest improvement in mild to moderate PsA.

Tumor necrosis factor (TNF) inhibitors help with both joint pain and skin legions. Effective TNF inhibition results in rapid and dramatic improvement in the clinical disease and may allow the patient to return to previous levels of job function. Some studies also support the use of anti-TNF agents in inhibiting radiographic disease progression.

Photo courtesy of Raymond Pertusi, MD In the most common presentation of PsA (60 to 70 percent of cases), skin lesions present first and joints are not affected until eight to 10 years later. However, it is important to note than in 15 to 20 percent of cases, these manifestations may appear within one year of each other.

Other biologic drugs currently in development for PsA may attack the disease closer to the point of origin at which the skin changes its nature.

Research is underway to determine the immunologic etiology of this disease and to develop other immunologic therapies directed at resolving skin issues.

Photo courtesy of Raymond Pertusi, MD One should examine behind the ears and scalp for patches of psoriasis.

Prior to initiating any DMARD agents or TNF inhibitors, it is prudent to screen for tuberculosis with a tuberculin skin test as well as a chest X-ray. If a patient does have tuberculosis, onecan pursue appropriate treatment for that condition and then begin biologic therapy.

One should also evaluate complete blood counts (CBC), renal and liver function before beginning therapy and every two to three months after with subsequent clinic visits.

Contraindications to this type of therapy would be cancer (specifically lymphoma), demyelinating diseases (multiple sclerosis), lupus, tuberculosis, congestive heart failure and immunosuppressive diseases.

Considering Biologic Medications: What You Should Tell Patients About Potential Risks
Warn your patient that one aspect of taking immunosuppressants such as biologics is the reduced ability of one’s immune system to fight off common infections on biologic therapy.

Educate your patient on how to reduce the risk of common bacterial or viral disease. This includes encouraging an annual influenza vaccine and the pneumonia vaccine every five years.

With biologics, there is a one to three percent increased risk of lymphoma. For the two self-injected biologics (adalimumab, etanercept) and infliximab, which clinicians provide via infusion, there is a possibility of an administration site reaction. However, this is generally self limiting.

Other Important Considerations In Treatment
Other peripheral issues in regard to PsA include poor sleep due to pain, fatigue and psychological issues. Some patients may need counseling to help deal with depression due to PsA and self-esteem associated with concerns due to extensive plaques. Encourage smoking cessation as well as patients with PsA who smoke generally have more severe illness with an increased risk for pulmonary infections.

Photo courtesy of Raymond Pertusi, MD In these X-rays of PsA, note the classic pencil-in-cup deformities, erosions and sclerotic margins. Note the proximal interphalangeal joints (PIPs) of the left second digit and the PIPs of the right third and fourth digits.

Clinicians should emphasize continuous monitoring and follow-up even if the patient’s disease is stable and improved. Determine the interval of these visits according to the severity of his or her disease and individual therapy. Symptom evaluation includes gauging the duration of morning stiffness, severity of pain and level of fatigue.

Your physical exam should include an evaluation of skin findings, tender and/or swollen joints and range of motion.
At the first visit, one should complete a health assessment questionnaire (HAQ) consisting of eight questions that address activities of daily living. One may also use an overall state of disease questionnaire such as a Short Form (SF) Health Survey with seven questions to determine the impact of this disease on a particular individual. The Beck Depression Inventory asks seven questions relating to state of mind and is helpful in determining if depression exists and at what level to help decide if treatment is necessary.

One may also opt for a physician global assessment and patient global assessment. Clinicians may use some or all of these to help facilitate treatment goals for the patient.

One may quantitatively measure PsA outcomes to determine the impact of the disease and course of treatment. Clinicians may use the disease activity scale (DAS 28) to assess disease activity and severity before and during treatment. The treating clinician should also obtain either the erythrocyte sedimentation rate (ESR) or C-reactive protein. One can subsequently use a specific calculation to obtain a final score, which corresponds to a given level of disease: mild, moderate or severe.

What About The Etiology Of PsA?
The other lab value is the plaque activity and severity index (PASI). This composite score weighs the fraction of body surface affected, and the nature and severity of the psoriatic changes within affected regions (induration, erythema and scaling). One can use these measurements to monitor progression or deterioration of the disease.

Your treatment goals include decreasing plaque height and scale to less than five percent, and lessening faint red coloration of erythema.

Final Notes
There is great interest in determining the best method to classify this disease and finding the most appropriate treatment for PsA.
The Classification of Psoriatic Arthritis (CASPAR) study group has been collecting prospective clinical and radiological data on clinic patients since 2002. The group is an international group of investigators, all of whom have a record of research in PsA. They sought 600 patients with PsA and 600 patients with a non-psoriatic arthropathy for the study. This project will reportedly test the diagnostic accuracy of existing classification rules for PsA but the results have not yet been published.

A National Psoriasis Foundation consensus paper published in the February 2007 issue of Archives of Dermatology offers a new way to consider psoriasis severity. This method eliminates the need for current classification terminology (mild, moderate, severe) and focuses on individual treatment rather than disease severity. It also emphasizes treatment of the emotional and physical aspects of PsA.4

Morbidity from PsA is substantial and comparable to patients with RA. Due to a newer understanding of the immune system and the discovery of TNF inhibitors, patients with PsA are now able to improve their quality of life. With the advent of the new biologic therapies designed to attack the immune system, hope is now being offered to those who have suffered from this disease.


References
1. Leonard DG, O'Duffy JD, Rogers RS. Prospective analysis of psoriatic arthritis in patients hospitalized for psoriasis. Mayo Clin Proc. 53: 511-518, 1978.
2. Shbeeb M, et al. The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991. J Rheumatol (27) May: 1247-1250, 2000.
3. Moll JM, Wright V. Familial occurrence of psoriatic arthritis. Ann Rheum Dis 1973;32:181–201.
4. Pariser DM, Bagel J, Gelfand JM, et al. National Psoriasis Foundation Clinical Consensus On Disease Severity. Arch Dermatol 2007;143:239-242.
5. NPF Benchmark Survey for Psoriatic Arthritis Recap of Results, National Psoriasis Foundation, 2002 http://www.psoriasis.org//files/pdfs/press/papresskit.pdf
6. Boulware, DW et al. Seronegative Spondyloarthropathy. In Koopman WJ, et al. (eds.): Clinical Primer of Rheumatology, Lippincott Williams and Wilkins, 2003, 127-163.
7. Elyan, M, Khan, MA. Spondyloarthropathies. In: Clinical Care in the Rheumatic Diseases, American College of Rheumatology, 2006, 117-185.
8. Helliwell, PS, Taylor, WJ. Classification and Diagnostic Criteria for Psoriatic Arthritis. Annals of the Rheumatic Diseases. (64): ii3-ii8, 2005.
9. Helliwell, PS, Wright, V. Clinical Features of Psoriatic Arthritis. In: Practical Rheumatology 1995, 235-244.
10. Mease, PJ Recent Advance in the Management of Psoriatic Arthritis. Curr Opin Rheumatol 16(4): 366-370, 2004.
11. Mease, PJ, Menter, A. Psoriatic Arthritis: Understanding Its Pathophysiology and Improving Its Diagnosis and Management. CME audioconference, 2005.
12. Mease, PJ, et al. New Horizons in TNF Inhibition – Targeting Psoriatic Arthritis. CME audioconference, 2004.
13. Paget, SA Treatment Strategies in Rheumatoid Arthritis. In: Rheumatoid Arthritis Disease Management Guide 2006, 101-130.
14. Taurog, JD. The Spondyloarthritides. In: Harrison’s Rheumatology 2006, 139-156.
15. Cush, JJ et al. Rheumatology: Diagnosis and Therapy 2005. 2nd ed. Lippincott, Williams, and Wilkins. 306-310.
16. Feldman, SR et al. The Psoriasis and Psoriatic Arthritis Pocket Guide: Treatment Algorithms and Management Options 2005. 2nd ed. National Psoariasis Foundation.
17. Klippel, JH et al. Primer on the Rheumatic Diseases 2001. 12th ed. ed. Arthritis Foundation. 239-258.

Arthritis Practitioner - ISSN: 1 - Volume 3 - Issue 5 - September 2007 - Pages: 30 - 35



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August 28, 2008

Emerging Concepts In Treating Rheumatoid Arthritis

A complimentary CME Webcast Event

To register for this Web Archive program, click on Complimentary CME Webcast Event


This activity is for nurse practitioners, physician assistants, rheumatologists and internal medicine physicians who treat patients with rheumatoid arthritis (RA).


Panelists/Lectures

"What You Should Know About Treating Early RA"
Nathan Wei, MD
Clinical Director
Arthritis and Osteoporosis Center
Frederick, Md.

"A Closer Look At The Efficacy And Safety Of Combination Therapy With Anti-TNF Agents"
Philip Mease, MD
Clinical Professor
University of Washington
School of Medicine
Chief, Rheumatology Clinical Research
Swedish Hospital Medical Center
Seattle

"What The Studies Reveal About Emerging Therapies For RA"
Salahuddin Kazi, MD
Chief of Rheumatology
Presbyterian Hospital
Dallas,Tx.

This activity is supported by an educational grant from Genentech and Biogen Idec. The activity is sponsored by the North American Center for Continuing Medical Education (NACCME).


Current Insights On Combination Therapy For Rheumatoid Arthritis

A complimentary CME Webcast Event
ON DEMAND
(Q&A with panelists to follow lectures)

To register for this Webcast program, click on Complimentary CME Webcast


This activity is geared to physicians, rheumatologists, nurses, physician assistants and nurse practitioners who treat rheumatoid arthritis.

Agenda And Faculty

“Treating RA: The Shift To A More Aggressive Therapeutic Approach”
Linda Davis, MHS, PA-C
Assistant Professor
University Of North Texas Health Science Center

“What The Literature Reveals About Combination Therapy”
Kevin M. Latinis, MD, PhD
Division of Allergy, Clinical Immunology and Rheumatology
University of Kansas Medical Center

“New Biologic DMARDs: Can They Have An Impact?”
Salahuddin Kazi, MD
Chief of Rheumatology
Presbyterian Hospital
Dallas, Texas

This activity is supported by an educational grant from Bristol-Myers Squibb. The activity is sponsored by the North American Center for Continuing Medical Education (NACCME).


A Guide To Viscosupplementation For Osteoarthritis Knee Pain

A complimentary CME Web Archive Event

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This activity is geared to physicians, nurses, physician assistants and nurse practitioners who treat osteoarthritis.

Agenda And Faculty

“A Closer Look At The Role Of Intraarticular Injections”
Frank Caruso, PA-C
Physician Assistant
Wake Forest University Baptist Medical Center
Winston-Salem, NC

“What The Literature Reveals About Viscosupplementation”
Nathan Wei, MD
Clinical Director
Arthritis and Osteoporosis Center
Frederick, MD

“Mastering The Technique Of Intraarticular Injections”
Mike Rudzinski, PA-C
Physician Assistant
Buffalo Veterans Affairs Medical Center
Buffalo, NY

This activity is supported by an educational grant from Genzyme.
The activity is sponsored by the North American Center for Continuing Medical Education (NACCME).



A Complimentary CME Webcast Event

A Guide To Infusion Therapy For Patients With Rheumatoid Arthritis

A Complimentary, On-Demand CME Webcast

To register for this Webcast program, click on Complimentary CME Webcast Event


This activity is geared to physicians, nurses, physician assistants and nurse practitioners who treat rheumatoid arthritis.

AGENDA and FACULTY

"Reviewing The Role of DMARDs In Treating RA"
Don Flinn, PA-C
Physician Assistant, McBride Clinic, Oklahoma City, Ok.
Vice-President, Society Of Physician Assistants In Rheumatology

"Assessing The Potential of Biologic Therapies"
Mark Genovese, MD
Associate Professor of Medicine
Division of Immunology And Rheumatology
Stanford University School Of Medicine

"What You Should Know About Infusion Therapy"
Nathan Wei, MD
Clinical Director
Arthritis and Osteoporosis Center
Frederick, Md.

This activity is supported by an educational grant from Bristol-Myers Squibb.

The activity is sponsored by the North American Center for Continuing Medical Education (NACCME).