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MJA Logo Managing Arthritis

The role of the rheumatologist in managing arthritis

Laurence E Clemens

MJA 2001; 175: S97-S101
 

Summary - Osteoarthritis - Inflammatory arthritis - Planning an optimal management program - Assessing response to treatment - Providing expert opinion, advice and education - Conclusion - References - Register to be notified of new articles by e-mail - Current contents list - More articles on Rheumatology


Summary
When and why should a patient with arthritis see a rheumatologist?
  • To establish or confirm the diagnosis:
    — aim for diagnosis within six weeks of onset.
  • To plan an optimal management program:
    — early, aggressive treatment is essential to achieve the best outcome in patients with inflammatory arthritis.
  • To assess the response to treatment:
    — failure to respond to treatment requires a change in drug regimen
    — objective measures of disease activity should be used.

Arthritis is a ubiquitous condition affecting both sexes of every age, race and culture. The Australian Burden of Disease study revealed osteoarthritis to be the fourth most common cause of years lost due to disability.1 The recognised forms of arthritis range from the most common, osteoarthritis, present radiologically in more than 70% of those over 65, to rare conditions such as Lyme disease and haemophilia. Each year 8.5 million Australians attend their general practitioner (GP) because of arthritis.2 Most of these patients will have their problems dealt with expertly by their GP. The rheumatologist has specific roles in diagnosis and investigation, planning a coordinated management plan, assessing response to treatment, and providing expert opinion, advice and education.

The successful management of arthritis requires close cooperation between the patient, the GP, and the rheumatologist, and may involve other health professionals, such as a physiotherapist, podiatrist, occupational therapist, social worker or plastic or orthopaedic surgeon.


Osteoarthritis
When to refer

Diagnostic uncertainty

If there is uncertainty about the diagnosis of osteoarthritis, an opinion from a rheumatologist is appropriate. Neck and back pain, with or without radicular referral, may be due to spondylosis, but other conditions need to be considered, including osteoporosis and metastatic malignancy. Knee pain may be due to spontaneous osteonecrosis, and hip region pain may stem from trochanteric bursitis. Plain x-ray films are generally sufficient to demonstrate the changes of osteoarthritis, but additional imaging, including magnetic resonance imaging (MRI), may occasionally be needed (eg, in suspected osteonecrosis or possible cervical cord compression). New MRI techniques offer the opportunity to identify bone and cartilage changes earlier in the course of osteoarthritis than plain x-ray films.3 This allows accurate assessment of osteoarthritis treatments on the basis of observed structural changes.

Specific treatments

Corticosteroid injections can provide lasting relief from pain in osteoarthritic joints.4 Small joints in the hands, especially the first carpometacarpal joint, the knees and occasionally the hips can benefit. Joints should not be injected more often than three to four times annually because of the potential risk of cartilage damage. Intra-articular injections of hyaluronan extracts and glycosaminoglycans may ease symptoms, but more research is required to demonstrate effects on disease progression. A more detailed review of treatment measures is given by March and Stenmark and McColl.5,6

Referral for surgery or allied health care

Total joint replacement is the most cost-effective treatment for severe hip and knee disease. Timing for referral for surgery depends on pain, function, other health problems and social issues. Arthroscopy of osteoarthritic joints may provide diagnostic information and symptomatic relief as a result of debridement and lavage. Physiotherapists can provide joint protection advice and exercises to improve range of movement and strengthen muscle. Moulded orthotics can be helpful for patients with midtarsal and metatarsophalangeal osteoarthritis.


Inflammatory arthritis
Advances in our understanding of pathophysiology, an increased awareness of health outcomes and the recent development of new therapies have led to major changes in the management of inflammatory arthritis. The guiding principles are early diagnosis, and early intervention with a regimen that aims for remission.

Diagnosis and investigation
Most patients with arthritis will be accurately diagnosed by their GP, but difficulties arise with recent onset, undifferentiated inflammatory arthritis, inflammatory arthritis in the elderly and uncommon and rare forms of arthritis.

Recent onset inflammatory arthritis
The essential question with recent onset inflammatory arthritis is "Does this patient have rheumatoid arthritis?".

Irreversible bony damage occurs very early in patients with rheumatoid disease. Seventy per cent of patients whose bones erode will suffer erosion within two years of onset of symptoms.7 MRI studies reveal bony changes within four months of onset in many patients (Box 1).8 It is this bony damage that eventually destroys joints and disables function. Preventing this process is the primary goal of treatment.

Rheumatoid arthritis is a clinical diagnosis. The presence of joint pain, swelling and stiffness in a symmetrical pattern, with involvement of metacarpophalangeal and metatarsophalangeal joints, is typical, but there is a broad differential diagnosis for patients presenting with this picture (Box 2).

To fulfil criteria for rheumatoid arthritis, symptoms must be present for at least six weeks. Elevated erythrocyte sedimentation rate (ESR) or raised levels of C reactive protein (CRP) are suggestive of, but not specific for, rheumatoid arthritis. A positive rheumatoid factor strengthens the diagnosis, but is only present at onset in 30%-40% of patients.

Alternative diagnoses

A detailed history and examination may reveal associated symptoms or signs indicating a diagnosis. Examples include alopecia and rash in systemic lupus erythematosus (SLE); occult or overt psoriasis raising the possibility of psoriatic arthropathy; Raynaud's phenomenon; sicca symptoms; early sclerodactyly or muscle pain and tenderness suggesting other connective tissue diseases; or a history of travel and exposure to mosquitoes, raising the possibility of arbovirus infection. Patients with fibromyalgia syndrome can pose a particular diagnostic problem, as their presenting symptoms of stiffness, arthralgia, myalgia and fatigue often mimic early inflammatory disease.10

What investigations should be performed?

Screening tests for a patient with inflammatory polyarthritis are:

  • full blood examination

  • ESR or serum CRP level

  • rheumatoid factor test

  • antinuclear antibody screening.

X-rays of affected joints are unlikely to provide diagnostic clues but are helpful as a baseline.

A wide range of additional tests may be undertaken, depending on the diagnosis suspected. In general, these would be performed by the rheumatologist after a full clinical assessment.

Prediction of severity

Once a diagnosis of persisting inflammatory arthritis, most likely rheumatoid disease, has been established, the next question is: can the severity of this condition be predicted?

Factors predicting a poor outcome, and thus warranting aggressive early disease modifying antirheumatic drug (DMARD) treatment, are:

  • female sex

  • positive rheumatoid factor

  • elevated acute-phase markers (ESR/CRP)

  • functional impairment

  • HLA DR4 genotype.

The decision in favour of aggressive treatment is best made by the rheumatologist, who will attempt to select the most appropriate treatment regimen for the individual patient.

Long term outcomes

Long-term outcomes of patients with rheumatoid arthritis have been shown to be disappointing. These outcomes include radiographic progression, functional disability, joint replacement surgery, accelerating healthcare costs, extra-articular disease, and premature mortality.9

Inflammatory arthritis in the elderly
The progressive ageing of the Australian population is leading to increasing numbers of patients over the age of 65 presenting with significant inflammatory arthritis. Most of these patients will also have evidence of degenerative musculoskeletal disease including osteoarthritis, cervical and lumbar spondylosis, and rotator cuff damage. Accurately identifying inflammatory arthritis in the setting of degenerative joint disease can be difficult, leading to either over- or under-treatment.

Older patients can develop arthritis due to any cause. Common forms of inflammatory arthritis in the elderly are:

  • late onset rheumatoid arthritis

  • myalgic onset rheumatoid arthritis

  • chronic calcium pyrophosphate dihydrate crystal deposition arthritis

  • secondary gout associated with diuretic therapy and renal impairment

  • inflammatory osteoarthritis

  • paraneoplastic arthritis.

Late onset rheumatoid arthritis

Rheumatoid arthritis can occur at any age but has a peak incidence in the fourth and fifth decades. There appears to be an increasing number of patients over 65 developing rheumatoid arthritis. This may be due solely to the ageing population, or may represent a true increase in incidence in the later decades of life. Late onset rheumatoid arthritis may be advanced at presentation and can be difficult to diagnose because of coexisting nodal osteoarthritis, and an overall increase in rheumatoid factor positivity in the elderly.

There is a misconception that late onset rheumatoid arthritis is a mild disease, but it can be very severe in older patients, with disability and suffering increased by coexisting diseases and the lack of physical and emotional reserves and social support. Aggressive disease, at any age, deserves aggressive treatment.

Myalgic onset rheumatoid arthritis

Polymyalgia rheumatica has a reported incidence of up to 400 in 100 000.11 Differentiating myalgic onset rheumatoid arthritis from polymyalgia rheumatica may be difficult. Some patients with late onset rheumatoid arthritis present with symptoms indistinguishable from those of polymyalgia rheumatica, with their major complaints being caused by shoulder joint involvement. Clues to the diagnosis of myalgic onset rheumatoid arthritis include a strongly positive rheumatoid factor, evidence of synovitis affecting joints distal to the knees and elbows, the presence of erosions on x-ray, and the finding of extra-articular features such as nodules or sicca symptoms. Treatment with modest levels of prednisolone initially controls the rheumatoid synovitis, but as the dose is tapered more typical manifestations of rheumatoid arthritis appear, with involvement of small joints in the hands and feet.

Chronic calcium pyrophosphate dihydrate crystal deposition disease

Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease can present as a chronic inflammatory arthritis, with the joint distribution mimicking rheumatoid arthritis or osteoarthritis.12 Morning stiffness, elevated ESR and raised CRP levels can occur. The diagnosis may be suggested by the pattern of joint involvement, with a mixture of findings typical of osteoarthritis and rheumatoid arthritis, but is confirmed by x-ray films showing chondrocalcinosis and joint fluid containing positively birefringent crystals of CPPD (Box 3). Chondrocalcinosis is much more common than acute or chronic CPPD arthritis, being present on x-ray in 10% of 60-year-olds, rising to 45% in those aged over 90.

Secondary gout associated with diuretic therapy

The widespread use of diuretic drugs for the control of hypertension and cardiac failure has been associated with the development of secondary tophaceous gout, particularly in women with a degree of renal impairment.13 These patients frequently have pre-existing nodal osteoarthritis, with a long history of symptoms of osteoarthritis with the more recent occurrence of episodic pain and swelling in the distal interphalangeal joints. Examination reveals tophaceous deposits. Differentiation from inflammatory arthritis may require aspiration and crystal identification (Box 4).

Uncommon and rare forms of arthritis
True septic arthritis caused by bacterial infection is an uncommon condition, but any suspicion that this may be present warrants immediate aspiration of affected joints and should prompt an urgent referral to a rheumatologist.

Crystal arthritis, caused by gout or pseudogout, can be indistinguishable from septic arthritis and, if there is uncertainty about the diagnosis, joint fluid must be obtained and sent for microscopic examination, including cell count, gram stain, crystal identification and culture.

Arthritis thought to be associated with an underlying connective tissue disease or one of the less common inflammatory arthropathies warrants referral for further investigation and development of a management plan.

Rheumatologists are very aware of the importance of early diagnosis and investigation in patients presenting with acute arthritis. A phone consultation with a rheumatologist is strongly recommended to ensure the patient is seen as soon as possible.


Planning an optimal management program
Once the diagnosis has been established, a management plan must be decided. This will involve both a drug regimen and non-pharmacological measures, both of which are described for osteoarthritis in other articles in this Supplement.5,6 A crucial element is recruiting the patient as part of the management team. The GP plays an essential role in supervising the program, including monitoring for drug side effects.

In the first few months of treatment, the patient may attend a rheumatologist every two or four weeks to allow assessment of response and adjustment of therapy. Once the condition has been stabilised, attendance may be reduced to three- to six-monthly.

Adjustment of DMARD therapy is usually left in the hands of the rheumatologist, particularly when combination therapy is being given.


Assessing response to treatment
The recognition of the need for aggressive early treatment of inflammatory arthritis and the availability of more effective treatments, including biological agents targeted at specific cytokines (such as the tumour necrosis factor Alpha image-blockers etanercept and infliximab), has led to more patients receiving treatment with expensive drugs. Combination DMARD treatment with one, two or three agents is now commonplace.

Rational use of traditional and new therapies requires accurate assessment of response to treatment.

What should we measure, and when?
An increasingly important role of the rheumatologist is to decide when current therapy is inadequate and should be stopped or augmented with an additional agent. The Pharmaceutical Benefits Scheme already sets criteria for the prescribing of certain DMARDs (leflunomide, cyclosporin). If the new biological agents (tumour necrosis factor Alpha image-blockers) become available on the Pharmaceutical Benefits Scheme, it is almost certain that there will be not only starting criteria but also minimum response criteria to be met before continuation of therapy will be allowed.

The most widely used criteria for measuring disease response in rheumatoid arthritis clinical trials are the American College of Rheumatology (ACR) core set (ESR, patient global assessment, health assessment questionnaire, tender joint count, swollen joint count). This can be measured as an ACR score of 20, 50 or 70, corresponding to a 20%, 50% or 70% improvement over baseline levels.14 At present the use of the ACR core set is uncommon, with most clinicians relying on acute phase markers, patient's report of efficacy and a limited active joint count. The use of the full core set, particularly the health assessment questionnaire, to assess treatment response should lead to a more evidence-based use of available DMARDs.


Providing expert opinion, advice and education
Most patients with arthritis attend a rheumatologist to obtain an expert opinion regarding diagnosis and prognosis, and for advice on management. Often their GP has already correctly diagnosed their condition and has initiated appropriate baseline treatment.

Information on arthritis, both reliable and misleading, abounds. There are excellent sources such as the Arthritis Foundation of Australia <www.arthritisfoundation.com.au> and its affiliates, but others including the Internet, television, magazines, and the increasingly sophisticated marketing programs of over-the-counter products leave much to be desired, and corrected.

The rheumatologist has a role in providing informed comment on new treatments and "breakthroughs". Providing detailed, reader-friendly, up-to-date printed information for patients and GPs is an important responsibility.

On the broader front, rheumatologists should also act as patient advocates and, if necessary, be politically active in their support of national and international initiatives, such as Arthritis Week and the Bone and Joint Decade.


Conclusion
In 1901 Osler wrote on arthritis deformans of the "inconvenience and crippling necessarily associated with the disease", suggesting that this was an inevitable prospect for patients.15 A hundred years on we are in the position to contemplate the successful suppression of inflammatory arthritis and talk of cure is not frivolous. To achieve the best outcome for our patients we must be prepared to embrace new therapies and collaborate closely.


References
  1. Mathers C, Vos T, Stevenson C, et al. The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors. Med J Aust 2000; 172: 52-596.
  2. Access Economics. The prevalence,cost and disease burden of arthritis in Australia-2001. Melbourne: Arthritis Foundation of Australia, 2001.
  3. Broderick LS, Turner DA, Renfrew DL, et al. Severity of articular cartilage abnormality in patients with osteoarthritis: evaluation with fast spin-echo MR vs arthroscopy. Am J Roentgenol 1994; 162: 99-103.
  4. Hochberg MD, Altman RD, Brandt KD, et al. Guidelines for the medical management of osteoarthritis: Part II. Osteoarthritis of the knee. Arthritis Rheum 1995; 38: 1541-1546.
  5. March LM, Stenmark J. Non-pharmacological approaches to managing arthritis. Med J Aust 2001; 175 Suppl 3: S102-S107.
  6. McColl GJ. Pharmacological therapies for the treatment of osteoarthritis. Med J Aust 2001; 175 Suppl 3: S108-S111.
  7. Brook A, Corbett M. Radiographic changes in early rheumatoid disease. Ann Rheum Dis 1977; 36: 71-73.
  8. McQueen FM, Stewart N, Crabbe J, et al. Magnetic resonance imaging of the wrist in early rheumatoid arthritis reveals high prevalence of erosions at four months after symptom onset. Ann Rheum Dis 1998; 57: 350-356.
  9. Pincus T, Breedveld FC, Emery P. Does partial control of joint inflammation prevent long term joint damage? Clinical rationale for combination therapy with antirheumatic drugs. Clin Exp Rheum 1999; 17 Suppl 18: S2-S7.
  10. Leech M, Littlejohn GO. Fibromyalgia. Current Therapeutics 2000; 41:0 14-21.
  11. Zilko PJ. Polymyalgia rheumatica and giant cell arteritis. In: Brooks PM, editor. MJA practice essentials rheumatology. Sydney: AMPCo, 1997.
  12. Klippel JH. Primer of rheumatic diseases. 11th ed. Atlanta: Arthritis Foundation, 1997: 226.
  13. Puig JG, Michan AD, Jimenez ML, et al. Female gout: clinical spectrum and uric acid metabolism. Arch Intern Med 1991; 151: 726-732.
  14. Felson DT, Anderson JJ, Boers M, et al. The American Rheumatology Association preliminary definition of improvement in rheumatoid arthritis. Arthritis Rheum 1995; 38: 727-735.
  15. Osler W. The principles and practice of medicine. 4th ed. Edinburgh: Young and Pentland, 1901.


Authors' Details
Department of Rheumatology, St Vincent's Hospital, Fitzroy, VIC.
Laurence E Clemens, MB BS, FRACP, Director.

Reprints will not be available from the author. Correspondence:
Dr L E Clemens, 2 Erin Street, Richmond, VIC 3121.
lclemensATnetspace.net.au

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1: Diagnostic imaging — rheumatoid arthritis

Plain x-ray (a) and MRI (b) of the wrist in a patient with six-month history of rheumatoid arthritis, showing bone damage in the carpus before the appearance of definite erosions on plain films.

Image A
Image a
Image B
Image b
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2: Differential diagnosis of polyarthritis
 
Inflammatory
 
 Viral arthritis
 Rheumatoid arthritis
 Polymyalgia rheumatica
 Psoriatic arthritis
 Polyarticular crystal arthritis
 Reactive arthritis
 Enteropathic arthritis
 Ankylosing spondylitis
 
Connective tissue diseases
 
 Systemic lupus erythematosus
 Mixed connective tissue disease
 Primary Sjögren's syndrome
 Polyarteritis nodosa
 Scleroderma
 Polymyositis
 
Other
 
 Generalised osteoarthritis
 Septic arthritis
 Paraneoplastic syndrome
 Subacute bacterial endocarditis
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3: Diagnostic imaging — crystal deposition disease

Chronic calcium pyrophosphate dihydrate (CPPD) crystal deposition arthropathy involving wrist, thumb carpometacarpal joint and matacarpophalangeal joints of the thumb and index finger. X-ray shows severe osteoarthritic change at the first carpometacarpal joint, cystic change in the carpus and chondrocalcinosis of the triangular ligament.

Image 1 Image 1a
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4: Diagnostic imaging — gout

Tophaceous gout in an elderly woman with pre-existing nodal ostesarthritis. Diuretic therapy and underlying mild renal impairment contributed to the condition.

image
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