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RHEUMATOID ARTHRITIS
Version 2 Final
EBM – Rheumatoid Arthritis
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1. Introduction
Rheumatoid arthritis is a chronic autoimmune disease, producing joint
damage mediated by cytokines, chemokines, and metalloproteases. It is
speculated that rheumatoid arthritis is a relatively new disease because
there is a surprising lack of historical evidence for its existence.
Description
It is a common systemic disease characterised by a chronic inflammatory
synovitis which typically affects the peripheral joints but which may affect
any synovial joint in the body and periarticular synovial structures (bursae
and tendon sheaths). It can manifest as a single episode of painful, stiff
joints lasting a few months or as an aggressive, destructive arthritis that
progresses rapidly to severe physical disability. Most frequently the
patient follows a relapsing and remitting course over many years. [1]
Rheumatoid arthritis is typically a distal, symmetrical, small joint
polyarthritis involving the proximal interphalangeal and metacarpo- and
metatarsophalangeal joints of the hands and feet, knees and cervical
spine. The shoulders, elbows and hips are less frequently involved but
can cause considerable morbidity. [2]
The disease is regarded as an autoimmune disease and can have extra-
articular manifestations that may involve cardiovascular, respiratory,
nervous and lymphatic/haematological systems and the skin, connective
tissues, eyes, and mouth.
Equally important to affected individuals is the potential loss of social and
financial independence. [3]
The disease also exerts a considerable burden on society in terms of
direct (i.e. medical care) and indirect (ability to work) costs. [4]
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2. Aetiology
Aetiology
Although rheumatoid arthritis is regarded as an autoimmune disease,
details of its pathogenesis remain unclear. It is probably a multifactorial
disease which occurs when several risk factors occur simultaneously.
There is considerable evidence for an important genetic component and
a substantial portion of this risk seems to lie in the HLA region (HLA-
DR4).
Predominant non-genetic factors include a theoretical ubiquitous infective
cause or trigger and environmental influences. [5] The onset of
rheumatoid arthritis occurs more commonly in winter [2]. Cigarette
smoking is also thought to play a role. [6]
Hormonal influences may be significant because use of the oral
contraceptive pill postpones or modifies the presentation. Clinical signs
and symptoms vary in intensity with the menstrual cycle, often abate
during pregnancy and flare in the post partum period.
Interestingly, in middle aged men nonarticular features (fever, weight
loss, anaemia, pleural effusions and vasculitic lesions) may dominate the
clinical picture. [2]
The main pathology in rheumatoid arthritis is an auto-immune mediated
thickening and inflammation of the synovial membrane, which becomes
infiltrated with inflammatory cells. The synovial lining layer becomes
continuous with vascular tissue, termed pannus, which grows over
cartilage and causes erosion of articular cartilage and underlying bone
due to its high content of macrophages and osteoclasts.
With time this results in degeneration of the cartilage and the joint.
Plasma cells in the subsynovium synthesise large quantities of
immunoglobulin much of which is IgG and IgM rheumatoid factor (i.e.
immunoglobulin with reactivity to self Ig-G). These autoantibodies form
immune complexes that activate complement and this can cause or
maintain local inflammation.
Several observations suggest that the inflammation in rheumatoid arthritis
is a T-Cell mediated phenomenon.
Rheumatoid nodules develop in about 30% of patients with RA. They are
granulomas consisting of a central necrotic area surrounded by palisaded
histiocytic macrophages, all enveloped by lymphocytes, plasma cells, and
fibroblasts. Nodules and vasculitis can also develop in many visceral
organs. [7] Other granuloma formation may be seen on the surface of
the pleura, pericardium and endocardial valves.
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Prevalence
Rheumatoid arthritis affects about 1% of the American and Western
European population with much lower rates in oriental and black
populations. Although virtually non-existant in Nigeria, prevalence among
US blacks is around 1%. There is a ratio of 3:1 females to males. It may
occur at any age, onset is rare under 20 and over 80 (1) and peaks in the
fourth and fifth decade.
The sex difference is most pronounced in those with early onset disease,
6:1 females to males, but is almost equal by age 65 years.
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3. Characteristics signs and symptoms in
articular rheumatoid arthritis
The common symptoms and signs are joint swelling, stiffness and
deformity, nodules, vasculitis and malaise.
Onset may be acute with simultaneous inflammation in multiple joints but
is more often insidious with progressive joint involvement. Affected joints
are tender, swollen and warm and both active and passive movements
are limited. This is due to joint effusion and florid synovitis.
Tenderness of affected joints is a very sensitive sign and synovial
thickening, eventually of all affected joints, is a most specific sign.
Symmetrical involvement of hands (PIP and MCP), feet (MTP), wrists,
elbows and ankles is typical but any joint may be affected
Generally patients complain of feeling unwell in themselves and present
with loss of function and pronounced stiffness more than pain. Morning
stiffness of more than 60 minutes is almost pathognomonic of active
rheumatoid arthritis. Stiffness of more than 60 minutes duration may also
occur after prolonged inactivity and at night. [7]
Inflammatory tenosynovitis can erode through tendons causing rupture
and compression of nerves by synovitis and this can commonly lead to in
carpal tunnel syndrome. [8]
Individual joints may be affected as follows:
Cervical spine
Frequently involved. Atlanto-axial subluxation gives rise to neck pain,
neck stiffness, paraesthesiae and sensory changes. Abnormal gait and
urinary retention or incontinence occurs if there is spinal cord
involvement.
A "Cock robin" posture is due to erosion of vertebral body(ies) in cervical
and upper thoracic areas.
Hands and wrists
Fixed deformities, particularly flexion contractures, may develop rapidly;
ulnar deviation of the fingers with an ulnar slippage of the extensor
tendons off the metacarpophalangeal joints is typical, as are swan-neck
and boutonnière deformities. Over time the metacarpophalangeal joints
sublux. Range of movement and strength may be dramatically reduced.
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Carpal tunnel syndrome can result from wrist synovitis pressing on the
median nerve.
Ulnar deviation Boutonniere deformity
Feet and ankles
In decreasing frequency there can be involvement of metatarsal
phalangeal joints, talonavicular, subtalar, and ankle joints. Lateral
deviation of the toes causes hallux valgus. Dorsal subluxation of the
metatarsophalangeal joints uncovers the heads of the metatarsals and
may cause metatarsalgia, a painful sensation of “walking on marbles”.
Both medial and lateral arches may collapse, resulting in pes planus and
heel valgus, accelerated by rupture of the tendon of tibialis posterior, a
frequent association. Metatarsophalangeal joint” [2] involvement can also
cause hammer toes.
Shoulders
Effusions with inflamed rotator cuff tendons give rise to painful abduction
arcs and loss of shoulder movements. Rupture of the rotator cuff can
occur.
Elbows
75% of patients with rheumatoid arthritis complain of elbow pain, 20%
severely. Joint effusions, progressing to bony destruction may occur.
Range of movement and strength decreases, especially in pronation and
supination.
Hips
Subtle reduction of internal rotation.
In established rheumatoid arthritis, secondary degenerative changes can
result in rest pain.
After a variable period of time, rheumatoid arthritis may become inactive
and may then be described as " burnt out". At this stage there may be no
swelling or redness, but deformed joints, surgical scars and muscle
wasting may all be evident.
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The degree of nonarticular involvement varies and may precede articular
disease.
Appendix 1 outlines the common extra articular manifestations.
Revised criteria for classification of rheumatoid arthritis (1987):
Any four criteria must be present to diagnose rheumatoid arthritis. Criteria
1- 4 must have been present for at least six weeks.
1.
morning stiffness for an hour or more
2.
arthritis of three or more joint areas
3.
arthritis of hand joints (wrist, metacarpophalangeal or proximal
interphalangeal)
4.
symmetrical arthritis
5.
rheumatoid nodules
6.
serum rheumatoid factor by a method positive in less than 5% of
normal control subjects
7.
radiographic changes (hand x-ray changes typical of rheumatoid
arthritis
that
must
include
erosions
or
unequivocal
bony
decalcification). [9]
Patterns of Onset
There are several distinct patterns of onset.
Insidious onset
In 70% of cases, increasing joint involvement develops over weeks or
months. This has a relatively poor prognosis. Usually peripheral small
joint involvement is followed by proximal joint (knees and hips)
involvement.
Palindromic
In about 20% of patients, persistent joint disease is preceded by self
limiting attacks of a few days of synovitis in various joints. About 50% of
patient who have these self limiting attacks eventually develop chronic
rheumatoid arthritis.
Explosive onset
10% of cases show precipitate onset with severe symmetrical
polyarticular involvement occurring over 24 to 48 hours. Paradoxically
they seem to do better in the longer term. [10], [11]
Systemic onset
Fever, myalgia, weight loss, anaemia, pleural effusions and vasculitic
lesions may be severe sometimes in the absence of marked joint
pathology. It is particularly common in middle aged men.
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Mono and Pauci articular onset
Patients with limited joint involvement, usually young women, who are
persistently seronegative for rheumatoid factor; usually pursues a benign
course. [2]
Polymyalgic onset
Limb girdle muscle symptoms may precede overt arthropathy particularly
in the elderly. It may be difficult to differentiate from polymyalgia
rheumatica initially. There is an impressive response to steroids initially
but less so with progression of synovitis.
Examination
Soft boggy swelling of synovitis and knee effusions are common.
Crepitus is found in early disease of degenerative joints.
Joint counts - tenderness and swelling are measured separately. Swollen
joint count is a better measure of inflammation than tender joint count
because tenderness may be due to other causes whereas swelling is
usually not.
Investigations: A detailed table of investigations and prognostic factors
generally undertaken in Rheumatoid Arthritis is given in Appendix 2.
Differential Diagnosis
Most exclusions are relative since two diseases causing arthritis can
coexist.
Polymyalgia rheumatica
In the elderly, onset of proximal manifestations may be confused with
polymyalgia rheumatica
Osteoarthritis
Typically, the OA patient stiffens whilst sitting down to lunch whereas a
rheumatoid arthritis patient is usually enjoying the best part of their day.
Crystal Arthropathies (gout, pseudogout)
Crystal deposition in joints may mimic the swelling and redness of
rheumatoid arthritis.
SLE
Rheumatoid arthritis shares many features with other collagen vascular
diseases, particularly SLE. [7]
Acute rheumatic fever
Here there is a typical migratory joint involvement pattern.
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Sarcoidosis
Granulomatous reticulosis affecting almost any organ, including the small
bones of the hands and feet.
Amyloidosis
Amyloid accumulation can be found in various organs.
Whipples disease
Malabsorption syndrome of which arthritis can be one of the
manifestations.
Inflammatory bowel disease
Crohn’s disease and ulcerative colitis are both frequently associated with
inflammatory joint manifestations.
Investigations
Until recently, Rheumatoid Factor (RF) was the test of choice. Recently,
an assay of anti-CCP (antibody to cyclic citrullinated peptide) has
become available and is showing promise of increased sensitivity and
specificity (67% and 95% respectively, versus 69 and 85% for RF). Its
exact role is yet unclear. [12]
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4. Treatment
The goals of treatment are to control synovitis, relieve pain, maintain
function, improve quality of life and minimise drug side effects while being
cost effective. [13]
Deterioration in joint function and x-ray changes occur most rapidly early
in the disease because cartilage had limited capacity for regeneration.
Therefore all patients with rheumatoid arthritis should be referred early for
specialist opinion.
Management by a multidisciplinary team via hospital is considered best
practice today. [14] Treatment plans have to take account of co-
morbidities, age, expectations and lifestyle. [8]
Evidence is now accumulating that early, more aggressive intervention
can improve longer term disease outcome. [15]
Drugs
Two main drug classes are considered in the treatment of rheumatoid
arthritis.
Non-steroidal anti-inflammatory drugs (NSAIDS) and Disease modifying
antirheumatic drugs (DMARDS).
NSAIDs – reduce joint pain and swelling but may take up to two weeks to
start having an effect. There may be gastrointestinal and renal side
effects and they are more toxic than previously appreciated. They do not
reduce disability over the long term.
(They are fully discussed in the sections on osteo-arthritis)
DMARDS – are used to relieve pain and swelling, and to improve
function. In addition, it is considered that they may reduce disease
progression.
The use of these drugs is indicated in all patients who continue to
have active disease (stiffness, joint pains and elevated ESR) after
three months of NSAID treatment.
A major review of clinical trials of their use was undertaken by Clinical
Evidence (June 2005) [13] who reported on their effectiveness
(beneficial, likely to be beneficial and inconclusive) in conjunction with
first or second line treatment options.
The DMARD methotrexate is widely used as first-line treatment in people
with rheumatoid arthritis because of consensus about its effectiveness in
practice.
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Sulfasalazine and combined treatment with methotrexate and
sulfasalazine are as effective as methotrexate in improving pain, joint
swelling, and function in people with early rheumatoid arthritis who have
not previously received DMARDs.
Antimalarials may improve symptoms and function in DMARD-naïve
people, and are reasonably well tolerated, but radiological evidence of
erosion is more marked with antimalarials than with sulfasalazine.
There is a variety of DMARDs available for second-line treatment of
rheumatoid arthritis. However there is no clear evidence that any one is
superior to another.
Methotrexate , sulfasalazine , penicillamine , and leflunomide cause
similar improvements in symptoms and function when given to people as
second-line DMARD treatment, although methotrexate causes fewer
adverse effects.
Methotrexate leads to improvement within six to eight weeks. Other
DMARDs take three to six months to produce a beneficial effect. Relapse
occurs if the drug is discontinued (11). Some are less toxic than
previously thought and are more effective analgesics than NSAIDs over
long periods.
A recent introduction has been the class of drug known both as tumour
necrosis factor antagonists (TNFAs) and cytokine inhibitors.
Etanercept and Infliximab are the two examples currently in use and it is
considered that in second line therapy adding either to methotrexate is
more effective than using methotrexate alone.[16]
Infliximab allows rapid disease control and reduces rheumatoid arthritis
disease activity. It appears to have an acceptable safety profile in trials to
date.
Etanercept appears to reduce radiological progression.
Currently both etanercept and infliximab have to be administered by
injection. For maintenance, etanercept 25mg. twice weekly and infliximab
200mg (3mg./Kg.) eight weekly. However etanercept appears to be
associated with fewer side effects.
Oral gold was less effective than both methotrexate and sulfasalazine in
improving measures of disease activity in people with rheumatoid
arthritis, although it had less toxicity. Reviews found that oral gold and
antimalarial drugs caused comparable improvements in measures of
disease activity, but that oral gold was less effective than penicillamine.
Parenteral gold caused similar improvements in measures of disease
activity compared with methotrexate, but caused more adverse effects.
Parenteral gold is associated with higher levels of toxicity than most of
the other commonly used disease-modifying antirheumatic drugs. It also
had higher total drop out rates than the other drugs.
Corticosteroid use is controversial. Although corticosteroids reduce the
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rate of progression of the disease they are generally avoided because of
long term effects. They are indicated for life threatening complications of
RA such as vasculitis or pericarditis. Intra-articular steroid injections are
used for one or two affected joints. Their current effectiveness as either
first or second line therapy is classed as “unknown”.
Occupational Therapy
In everyday practice, the substantial impact of skilled occupational
therapy (OT) intervention on quality of life for patients with RA is clear.
The OT approach is multifaceted and includes:
Activities of daily living, particularly washing, toileting, dressing, cooking,
eating and working. Sometimes the provision of equipment and
adaptations is fundamental to the management of RA. [17]
Joint protection including adapting movement patterns, assistive devices,
rest regimens, energy conservation techniques, exercise and splinting.
Studies in patients with longer disease duration have shown encouraging
results. [18]
Physiotherapy
Thorough physical therapy evaluation should be performed initially,
including functional assessment (transfer status, gait analysis, activities
of daily living etc.), range of movement of all joints, strength, posture and
respiratory status. This gives a baseline for future reference and an
accurate and objective basis for treatment goals. [19]
Exercise and physiotherapy are used to maintain or to improve muscle
tone in order to prevent or correct deformities and to maintain or increase
joint mobility and function.
The aim is to achieve the right balance between exercise and rest. Strong
muscles protect joints, but inflamed joints should be rested initially and
then gradually worked through a full range of non weight-bearing
exercises.
A variety of treatment modalities including heat therapies, cold therapies,
electrotherapy (e.g.TENS), mobilisation and massage are used in
physical therapy.
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Splinting
Is used:
To rest actively inflamed joints at night and during flare ups.
For stabilisation in optimum position for use
To prevent deformity and contractures
Support splints may preserve adequate function
and improve pain but may restrict dexterity.
One study showed splinting produced no change
in grip strength and there was no difference in
grip strength between various pain levels. [20]
Surgery
Pain is the primary indication for surgery. The most common procedures
involve hip, knee, shoulder, elbow and hand joint replacements. Other
procedures include synovectomies, wrist stabilisation, forefopot
arthroplasties and excision of the head of the radius.
Strong willed, strong boned, strong
muscled and well informed patients
are the best candidates for surgery
but post operative restoration of
function is difficult to predict and a
multidisciplinary approach is
needed. Unfortunately most
patients do not fit this profile, and a
frailer patient with osteoporosis, either due to the disease mechanism,
disuse osteopenia or therapeutic steroid use, is the norm, making surgery
technically more difficult and complications more common.
Different types of surgical intervention are appropriate to different stages
of the disease process:
Early synovitis : non-operative/splinting
Persistent synovitis : synovectomy of joints, which continue to have active
synovitis despite local steroid injections, may prevent erosions
Specific deformation : reconstructive
Severe crippling : salvage
The most successful procedures for rheumatoid arthritis are carpal tunnel
release, resection of metatarsal heads, total knee arthroplasty (after
which synovitis disappears) and total hip arthroplasty.
Joint replacement surgery has revolutionised the outlook for RA patients
because it relieves pain and improves function.
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Cemented hip implants have 90% success rate. There is a higher failure
rate in rheumatoid arthritis than in osteoarthritis and revision outcome is
much poorer. Excision arthroplasty (Girdlestone) as a salvage procedure
is still performed in failed primary and revision arthroplasty.
Tendon transfers across the wrist may redirect line of muscle action
where a joint deformity is exacerbated by the “bowstringing” effect of
tendons crossing that joint, which have come to lie eccentrically due to
the initial deformity.
Podiatry and Dietetics
Appropriate footwear and orthoses are effective with regards to comfort
level, and stride speed and length. [21]
Both weight management particularly when weight bearing joints are
involved, and interventions to address cachexia where patients do less
well and have poorer functional status can be effective. [22]
Analysis of clinical trials of fish oil supplementation in RA concluded that
while there was reduction in the number of tender joints and in duration of
morning stiffness, no effect was seen on disease activity or progression
of RA. [23]
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5. Prognosis
All studies of RA over ten years or more show severe morbidity [24] and
patients with rheumatoid factor appear to have a more severe course.
Spontaneous remission in RA usually occurs within the first two years.
However 50 - 90% of those affected have progressive disease [24] and
even after five years of antirheumatic drug therapy, complete remission is
rare. [25]
Almost 50% of patients show joint space narrowing and/or erosion in the
first two years, therefore permanent articular damage is often present
which is progressive in almost all patients.
About 50% of maximum scores for joints space narrowing and
radiographic erosion is seen by five years of disease.
Decline in functional status is seen in most patients with RA over periods
longer than a decade. Many patients, however, show an improvement in
morning stiffness over this time suggesting “burn out” but this stil leaves
significant losses in functional capacity.
Clinical markers derived from joint counts, and functional status
measures including patient self-report questionnaires, demographic
measures and co-morbidity studies appear to be the most effective
currently available data to predict mortality in rheumatoid arthritis.
Formal education level is highly predictive of morbidity and mortality in
RA, a more formal education correlating with less morbidity and mortality.
A hypothesis has been proposed that low formal education is a variable
that identifies behavioural risk factors predisposing to the aetiology and
poor outcomes of most chronic diseases and is probably related to
efficiency in using medical services, problem solving capacity, sense of
personal responsibility, capacity to cope with stress, life stress, social
isolation, health focus of control and learned helplessness [24].
Many patients with mild disease are not referred and do well. Functional
outcome of RA after about six years of disease is fairly good and while
functional impairment of different joints had progressed, most patients
were still classed as mildly disabled. [26]
In a ten-year follow up study of hospital admissions:
25% were considered fit for most activities
40% had moderate functional impairment
25% were severely disabled
10% were wheelchair bound [2]
In the United States, among men 18 – 65 years with arthritis only 56%
were working compared with 89% of men with no arthritis. Amongst
women with arthritis 31% were working compared with 62% of women
with no arthritis [24].
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Work disability is seen within ten years of disease onset in at least 50%
of patients younger than 65 years who were working at the time of
disease onset.
Work disability has been primarily studied for patients under care referral
centres and may not represent all patients with rheumatoid arthritis [24].
Poor outcomes in terms of functional disability correlates with female sex
and seropositivity.
Life Expectancy
Rheumatoid arthritis significantly shortens life expectancy. Higher
mortality rates are found among patients with persistent joint
inflammation, seropositivity, functional loss, and lower levels of
education. Overall the disease decreases life expectancy by three to ten
years in both men and women. They die of expected causes, e.g.
cardiovascular, cerebrovascular or malignant disease, but at a younger
age [8].
The most important determinants of prognosis are the severity and
persistence of disease activity.
Disease that remains confined to the hands and feet has a good
prognosis.
Some features have shown association with a poor outcome and are
given in Appendix 3.
Measures indicating functional disability, as well as age and co-
morbidities, predict five-year mortality more effectively than laboratory
data. Measures of inflammatory activity may underestimate long tem
outcomes in rheumatoid arthritis.
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6. Main Disabling Effects
An important feature of the musculoskeletal system is that any
impairment alters the biomechanics of contralateral joint structures or
those continuous in the kinetic chain. This usually also increases baseline
energy expenditure for activity.
Pain, deformity, muscle wasting and flexion contracture may all contribute
towards functional impairment.
Extra-articular manifestations may further contribute towards the overall
level of functional impairment.
Common measurements of overall severity of disease include grip
strength, global severity, joint count, morning stiffness, HAQ-DI scale
[Appendix 4], ESR and haemoglobin level.
Signs of synovitis are most useful in the assessment of disease activity.
The reduction in the range of movement is a useful indicator of current or
potential functional problems. An indication of the activities of daily living
likely to be affected beyond certain reductions is given in [Appendix 5]
Most individuals with early rheumatoid arthritis can perform tasks of daily
living, although with discomfort or impaired efficiency. This is achieved
because people adapt and work within their pain and limited joint
movement. When contractures or joint deformity progresses beyond a
certain range for a joint the impairment will result in a functional deficit.
[27]
Functional disability progresses more rapidly in the first few years than in
the latter course of the disease and 50% of patients have considerable
difficulty performing their pre-morbid domestic, work and social functions
within six years of their first clinic visit.
Pain, which is unpredictable and varies in intensity and duration, is a key
feature of RA and night time pain often contributes to sleep disturbance.
[28]
Fatigue due to poor sleep and functional impairment may both adversely
affect social activity which in turn may adversely affect mood. This may
account for depressive symptoms occurring more commonly in those
suffering from RA than in the general population.
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7. References
[1] Walker, D J. Rheumatoid Arthritis. Arthritis & Rheumatism Council for Research
Collected reports on rheumatic diseases 1995
[2] Wordsworth, B P. Rheumatoid arthritis Section 18.4 Oxford Textbook of Medicine
Third Edition Oxford University Press 1996 CD-ROM
[3] Young A, Dixey J, Cox N, Davies P, Devlin J, Emery P, et al. How does functional
disability in early rheumatoid arthritis (RA) affect patients and their lives?
Results of 5 years of follow-up in 732 patients from the Early RA Study (ERAS).
Rheumatol 2000; 39: 603-11.
[4] Jantti J, Aho K, Kaarela K, Kautiainen H. Work disability in an inception cohort of
patients with seropositive rheumatoid arthritis: a 20 year study.
Rheumatology 1999; 38: 1138-41.
[5] Gestel van AM et al. Evaluation of rheumatoid arthritis disease activity and
outcome. Ballieres Clin Rheumatol 1997; 11 (1): 27-48
[6] Silman AJ. Rheumatoid arthritis. In: Silman AJ, Hochberg MC, eds. Epidemiology
of the rheumatic diseases, 2nd ed. Oxford, Oxford Press, 2004: chapter 2, 31-71.
[7] Merck Manual Professional. www.merck.com/mmpe/sec04/ch034/ch034b.html
(Last full review/revision November 2005 Content last modified April 2007)
[8] Ahern MJ. et al.
Rheumatoid arthritis. Med J Aust 1997; 166 (3): 156-161
[9] Arnett FC et al. The American Rheumatism Association 1987 revised criteria for
the classification of rheumatoid arthritis. Arthritis Rheumatism 1988; 31: 315-324
[10] Young A. Early Rheumatoid Arthritis Study (ERAS) Rheumatoid.org.uk
27/05/04
[11] Rheumatoid Arthritis Essentials Sock19.tripod.com
[12] Nishimura K, et alMeta-analysis: Diagnostic Accuracy of Anti–Cyclic Citrullinated
Peptide Antibody and Rheumatoid Factor for Rheumatoid Arthritis.
Ann Intern
Med. 2007;146:797-808.
[13] Walker-Bone, K., Fallow, S. Rheumatoid Arthritis
BMJ Clinical Evidence June 2005
[14] Vliet Vlieland TP, Breedveld FC, Hazes JM. The two-year follow-up of a
randomized comparison of in patient multidisciplinary team care and routine
out-patient care for active rheumatoid arthritis. Br J Rheumatol 1997; 36: 82-5.
[15] van Jaarsveld CH, Jacobs JW, van der Veen MJ, Blaauw AA, Kruize AA,
Hofman DM, et al. Aggressive treatment in early rheumatoid arthritis: a
randomised controlled trial. On behalf of the Rheumatic Research Foundation,
Utrecht, The Netherlands. Ann Rheum Dis 2000; 59: 468-77.
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[16] Dhillon S. Lyseng-Williamson KA. Scott LJ. Etanercept: a review of its use in the
management of rheumatoid arthritis. Drugs. 67(8):1211-41, 2007
[17] Helewa A, Goldsmith CH, Lee P, Bombardier C, Hanes B, Smythe HA et al.
Effects of occupational therapy home service on patients with rheumatoid
arthritis. Lancet 1991; 337: 1453-6.
[18] Hammond A, Lincoln N, Sutcliffe L. A crossover trial evaluating an educational-
behavioural joint protection programme for people with rheumatoid arthritis.
Patient Education Council 1999; 37: 19-32.
[19] Ganz SB et al. General overview of rehabilitation in the rheumatoid patient
Rheumatic Dis. clinics of N America
[20] Anderson K et al. Immediate effect of working splints on grip strength of arthritic
patients. Aust Occup Ther Journal 1987; 34(1): 26-31
[21] MacSween A, Brydson G, Hamilton J. The effect of custom moulded ethyl vinyl
acetate foot orthoses on the gait of patients with rheumatoid arthritis.
Foot 1999; 9:128-3.
[22] Helliwell M, Coombes EJ, Moody BJ, Batstone GF, Robertson JC.
Nutritional status in patients with Rheumatoid Arthritis.
Ann Rheum Dis 1984; 43: 386-90.
[23] Fortin P, Lew RA, Liang MH, Wright EA, Beckett LA, Chalmers TC et al.
Validation of a meta-analysis: The effects of fish oil in Rheumatoid Arthritis.
J Clin Epidemiol 1995; 48: 1379-90.
[24] Pincus T et al. The side effects of rheumatoid arthritis: joint destruction,
disability and early mortality. Br J Rheumatol 1993; 32(1): 28-37
[25] Wolde S., et al. Randomised placebo controlled study of stopping second line
in rheumatoid arthritis. Lancet 1996; 347: 347 – 352
[26] Eberhardt, K.B. Functional disability and impairment in early rheumatoid
arthritis – development over five years. J Rheumatol 1994; 21(6); 1051 – 55
[27] Dalgas M. et al. Disability issues in rheumatoid arthritis. Physical Med and
Rehab Clinics of North America 1994; 5(4): 859 – 865
[28] Ferguson SJ. Et al. Broken sleep, pain, social activity and depressive
symptoms in rheumatoid arthritis. Aust. J Psychol. 1996; 48(1): 9 – 14
[29] Kirwan JR, Reeback JS., Stanford Health Assessment Questionnaire modified
to assess disability in British patients with rheumatoid arthritis.
Br. J. Rheumatol.1986 May;25(2):206-9
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Appendix 1
Common extra-articular manifestations of Rheumatoid Arthritis
Skin
Subcutaneous
nodules.
Vasculitis.
Thinning
and
ulceration.
Eyes
Episcleritis (<1%). Keratoconjunctivitis sicca (15-25%).
Cardiac
Pericarditis
and
pericardial
effusions
– 50% of
asymptomatic patients undergoing echocardiography have
evidence of pericarditis [12]
Constrictive pericarditis. Aortitis
Conduction defects
Coronary arthritis
Myocarditis
Respiratory
Crico-arytenoid joint inflammation. Interstitial lung disease
(frequently found at autopsy). Visceral nodules. Pleural
effusions. Bronchiolitis obliterans. Pulmonary arteritis.
Neurological
Atlanto-occipital subluxation and spinal cord compression.
Carpal tunnel syndrome and entrapment neuropathy.
Mononeuritis multiplex. Muscle wasting. Peripheral
neuropathy.
Haematological Anaemia of chronic disease. Thrombocytosis
General
Rheumatoid nodules are characteristic and are found in
25-50%. They form subcutaneously in bursae and along
tendon sheaths, over pressure points e.g. olecranon, ulna
border of forearm. Achilles tendon and ischial spines.
Splenomegaly and lymphadenopathy. Sjögrens syndrome.
Sicca symptoms – dry mouth. Low grade fever.
Amyloidosis in internal organs.
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Appendix 2
Investigations and prognostic factors in Rheumatoid arthritis
Prognostic Indicators
Elevated ESR in 90%, plasma viscosity, C-reactive
protein (acute phase indicators – persistently
elevated associated with worse prognosis). C-
reactive protein is better indicator than ESR or
viscosity [27].
FBC
Hb 8-10 in 80% normochromic normocytic anaemia
Thrombocytosis may be present Neutropenia and
splenomegaly = Felty’s syndrome (2%)
Rheumatoid factors
Antibodies to altered gamma globulin are present in
about 70%. Various tests – different sensitivity and
specificity. High titres broadly correlate with more
severe disease. False positive results occur more
frequently with ages.
Synovial Fluid
Cloudy, sterile, reduced viscosity, 3000 – 50,000
WBCs per microlitre Synovial fluid complement is
often less than 30% serum level.
Radiology
Early disease –soft tissue swelling only later –
periarticular osteoporosis, joint space narrowing
(articular cartilage) and marginal erosions, then joint
degeneration
and
deformity.
The
rate
of
deterioration clinically and radiologically is highly
variable. X-rays are used to monitor progression.
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Appendix 3
Features associated with poor outcome in RA
Persistently high acute phase response
High titre of rheumatoid factor
Erosion during the first year
Family history of rheumatoid arthritis
HLA-DR4
Extra-articular disease
Insidious onset
Female sex
Low educational attainment
High level of functional disability
Low socio-economic status
Early age of onset (10)
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Appendix 4
Health Assessment Questionnaire (Modified for British
rheumatoid arthritis patients ) [29]
Patient Label
Date
We are interested in learning how your illness affects your ability to function in daily life.
Please feel free to add any comments at the end of this form.
PLEASE TICK ONE RESPONSE WHICH BEST DESCRIBES YOUR USUAL ABILITIES
OVER THE PAST WEEK:
Without ANY
With SOME With MUCH
Unable to do
difficulty
difficulty
difficulty
Score = 0
Score = 1
Score = 2
Score= 3
1. DRESSING AND
GROOMING
- Are you able to
Dress yourself, including
tying shoelaces and doing
buttons?
Shampoo your hair?
2. RISING - Are you able
to
Stand up from an armless
straight chair?
Get in and out of bed?
3. EATING - Are you
able to
Cut your meat?
Lift a full cup or glass to
your mouth?
Open a new carton of milk
(or soap powder)?
4. WALKING - Are you
able to
Walk outdoors on flat
ground?
Climb up five steps?
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PLEASE TICK AIDS OR DEVICES THAT YOU USUALLY USE FOR ANY OF THESE
ACTIVITIES:
Walking stick
Crutches
Devices for dressing e.g.
Special or built-up chair
buttonhook, zipper pull,
Wheelchair
long handled shoe horn
Walking frame
Other (please specify)
Built-up or special utensils
PLEASE TICK ANY CATEGORIES FOR WHICH YOU USUALLY NEED HELP FROM
ANOTHER PERSON:
Dressing and grooming
Rising
Eating
Walking
Without
With SOME
With MUCH
ANY
Unable to do
difficulty
difficulty
difficulty
Score = 0
Score = 1
Score = 2
Score= 3
5. HYGIENE - Are you
able to
Wash and dry your entire
body?
Take a bath?
Get on and off the toilet?
6. REACH - Are you able
to
Reach and get down a 5lb
object (e.g. a bag of
potatoes) from above your
head?
Bend down to pick up
clothing from the floor?
7. GRIP - Are you able to
Open car doors?
Open jars which have been
previously opened?
Turn taps on and off?
8. ACTIVITIES - Are you
able to
Run errands and shop?
Get in and out of a car?
Do chores such as
vacuuming, housework or
light gardening?
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PLEASE TICK AIDS OR DEVICES THAT YOU USUALLY USE FOR ANY OF THESE
ACTIVITIES:
Jar opener (for jars
Long handled appliances for
Raised toilet seat
previously opened)
reach
Bath seat
Bath rail
Other (please specify)
PLEASE TICK ANY CATEGORIES FOR WHICH YOU USUALLY NEED HELP FROM
ANOTHER PERSON:
Errands and
Hygiene
Reach Gripping and opening things
housework
SCORING OF HAQ
Add the maximum score for each of the 8 sections and divide by 8 to give a score
between 0-3.
If aid/device or help is needed the score for that activity automatically = 2 (
unless 3 has
already been ticked.)
Normal function = 0
Most affected function = 3
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Appendix 5
Joint
Reduction to
Effect on
Temporo-mandibular
< 2.5 cms of opening
Biting, eating
Temporo-mandibular
Fusion
Chewing
Shoulder
< 90° Abduction
Washing , dressing
Elbow
< 140° Flexion
Dressing (top buttons)
Elbow
< 80° Flexion
Carrying a shopping bag
Elbow
< 40° supination
Use pen or pencil
Elbow
< 60° pronation
Operating yale type lock
Hip
< 110° flexion
To rise unaided
Hip
< 90° flexion
To sit comfortably
Knee
< 90° flexion
To rise unaided
Knee
< 45° flexion
Walk or use stairs
Knee
< Full extension
Walking steadily
Knee
> 20° fixed flexion deformity
Fatigue on walking
Ankle
< 20° plantar flexion
Difficulty walking
< 10° dorsiflexion
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