A chronic systemic inflammatory autoimmune disease of unknown
cause, involving synovial joints, resulting in joint deformities
and functional limitations if not adequately controlled. The
disease can also produce systemic inflammation and involve
extra-articular structures and organs (e.g. skin, lungs, heart and
eyes).
The precise cause is unknown. Various factors can contribute and
include:
- Environmental: Smoking induces formation of
citrullinated peptides in susceptible individuals leading to
formation of antibodies to Cyclic Citrullinated Peptides (anti-CCP)
and Rheumatoid Factors (RF) triggering auto-immunity which
underlies Rheumatoid Arthritis (RA)
- Infection: Various pathogens (e.g. viruses and
mycoplasma) induce inflammation and triggers autoimmunity in a
susceptible host leading to RA. None of the potential pathogens
appear to be RA specific, and no specific pathogen is definitely
linked to RA
- Hormonal: Female predominance, ~3 fold
>males. Estrogen may play a role in RA development by
facilitating immune system activation
- Genes: Play role in susceptibility
- May account for ~50% risk of developing RA
- May impact disease severity
- Class II MHC genes (containing a specific 5-amino acid sequence
in the hyper variable region of HLA-DR4, called the SHARED
EPITOPE), have been implicated
- Immunologic Factors:
- Complex process involving T and B lymphocytes, antigen
presenting cells (macrophages and dendritic cells) and cytokines.
The latter may have pleiotropic actions and multiple targets and
may exhibit both pro-inflammatory and anti-inflammatory actions.
Controlling the balance between competing cytokines is considered
as an important therapeutic goal. Key pro-inflammatory cytokines
are TNF, IL-1, and IL-6
- T cells activates macrophages/synovial fibroblasts which
produces proinflammatory cytokines leading to initiation of RA
- B cells produce autoantibodies/cytokines eventually
contributing to pathological injury
- The synovial membrane is ultimately
transformed into pannus tissue with activated synovial cells and
osteoclasts eroding cartilage and bone
Pathogenesis is not completely understood, but may include:
- Autoimmune reaction triggered by infection/trauma → synovial
hypertrophy → joint inflammation (synovitis)
- Subsequent uncontrolled inflammation → cartilage and bone
destruction
- Increased immune activity in genetically susceptible
individuals, facilitate the disease
- Immune activity involves:
- T cells, phagocytes, fibroblasts, osteoclasts, and
neutrophils
- B cells produce characteristic autoantibodies (i.e. rheumatoid
factors [RFs] and anti-CCP)
- Aberrant production of numerous cytokines, inflammatory
mediators (e.g. TNF & IL-1), and growth factors ensues
- Inflammation, excessive proliferation of synovium, formation of
granulation tissue (i.e. pannus) promotes tissue destruction
- Some experience a gradual onset, with slow progression of signs
and symptoms, however many patients may present with progressive
joint pain and stiffness, functional limitation and radiographic
damage
- RA is also associated with significant morbidity and increased
mortality, primarily related to cardiovascular disease and
infections
- RA has been redefined as of 2010 by ACR/EULAR,
based on the following criteria
Signs and symptoms include:
- Gradual onset, slowly progressive joint pain
- Morning stiffness ( may last 45 minutes or longer)
- Functional limitation
- Constitutional symptoms
- Fatigue/malaise
- Anorexia
- Generalized weakness
- Low grade fever
- Boutonniere deformity: PIP joint is flexed and DIP joint
hyperextended
- Swan-neck deformity: DIP joint is flexed and the PIP joint is
hyperextended
- Baker's cyst: The synovial sac of knee joint produces a bulge
into the popliteal space and forms a cystic swelling, which can
rupture and cause pain
Extra-articular manifestations:
- Less common with better therapy
- Subcutaneous rheumatoid nodules at sites of pressure and
chronic irritation
- Damage to the ligaments and tendons
- Vasculitis causing leg ulcers
- Lymphadenopathy
- Felty's syndrome (splenomegaly and leukopenia)
- Sjögren's syndrome (dry eyes, mouth, skin etc.)
- Scleromalacia
- Episcleritis
- Involvement of the cervical spine can cause atlantoaxial
subluxation and spinal cord compression
- Cardiac: Pericarditis, valvular disease,
pericardial effusion (usually asymptomatic)
- Lung: Pleural effusion with very low glucose
level, pulmonary nodules, infiltrates and fibrosis
- Blood: Anemia with normal MCV
- Nerve: Mononeuritis multiplex
- Skin: Nodules at pressure points
History:
Detailed history should include:
- History of joint pain
- Duration
- Number of joints involved
- Frequency
- History of stiffness/swelling over the joints
- History of constitutional symptoms e.g. fatigue, malaise,
weakness
- Inquiries about quality of life
- Inquiries if disease interferes with daily activities
- Family history of RA
Physical Examination:
Is
required for assessment of joint inflammation and structural
deformity, by the clients care giver and should include:
- Assessment of symmetric joint swelling is characteristic of
RA
- Palpation of joint can distinguishes swelling from bony
enlargement
- Pain occurring with both active and passive movement is a
hallmark of joint inflammation should be reported
- Persistent inflammation of tendons and muscles of the
joints
Laboratory Tests:
The
presence of prognostic features should be assessed at baseline and
considered when making treatment decisions; they are also used to
monitor the disease activity and medication effects:
Pretreatment or baseline
investigations include:
- CBC, LFTs, urea, creatinine
- ESR-usually elevated as is CRP paralleling the disease
activity
- CRP (C reactive protein)
- RF (rheumatoid factor); an immunoglobulin antibody
- Present in ~75% of patients
- Reflects disease activity to some extent, but not usually
measured serially
- ANTI-CCP (anti-cyclic citrullinated peptide antibodies) highly
specific in early disease
Screening before starting
biologic therapy:
- Hepatitis B and C (and HIV in high-risk patients)
- Screening for latent tuberculosis is recommended prior to
anti-TNF, abatacept, and tocilizumab
- Baseline antinuclear antibody (ANA) may be considered
Imaging:
X-rays:
- First choice for screening of affected joints
MRI:
- Expensive but may provide more detail of erosions, synovitis
and bone edema
Ultrasound:
- May help in visualizing effusions, erosions and synovitis by
Grey scale and power Doppler assessments
- Helpful in assessing some joints (e.g. hip joints) in obese
patients
Bone scan:
- Radionuclide scans distinguish between inflammatory and
non-inflammatory processes
- Bone densitometry (DEXA) provides info regarding
osteoporosis
Diagnostic procedures:
- Arthrocentesis: To diagnose superimposed septic arthritis
Diagnostic criteria:
- Early intervention improves disease outcome and decreases joint
damage
- The criteria are aimed at assessing those with clinical
synovitis or with synovitis not explained by any other cause. The
number and types of joints (large and/or small) involved, serology
for (rheumatoid factor) RF and/or (anti-citrullinated protein
antibody) ACPA, acute phase reactants (CRP and ESR) and duration of
symptoms are all taken into account when making the diagnosis of
RA. Patients presenting with new symptoms as well as those with
existing erosive disease should be reassessed to determine if they
fulfill the 2010 criteria for RA
- RA has been redefined as of 2010 by ACR/EULAR,
based on the following criteria
- Pharmacological Interventions
- Non-pharmacological Interventions
- Surgical Interventions
PHARMACOLOGICAL INTERVENTIONS:
- Patients are symptomatically treated as they present to the
clinic. Previously undiagnosed patients with possible RA diagnosis
should be given an urgent referral to the rheumatologist for
definitive diagnosis and treatment
- Treatment approach has undergone major changes over the years:
- NSAIDs are beneficial only for relief of symptoms
- NSAIDs have no effect on disease retardation
- Irreversible joint damage may occur in early disease
1. NSAIDs:
- Recommended for the relief of symptomatic pain and inflammation
(if present)
- No longer used as the sole first-line agent for RA
2. Disease modifying antirheumatic drugs
(DMARDs):
Start DMARDs immediately if patient
has active disease.
- Active RA patients: Require frequent monitoring (every
1-3months)
- Patients with well controlled disease: May be monitored less
frequently
- DMARD: Should be adjusted every 3-6 months, to achieve
treatment goals
REF: Bykerk V P et al. J Rheumatol 2011; 38:11
Types of DMARDs:
A. Nonbiologic DMARDs:
Includes and are usually chosen to initiate therapy, due to fast
onset of action and less toxicity
- Methotrexate (MTX): Most preferred of all the
DMARDs
- 7.5-25 mg per week PO, plus folic acid 5 mg PO daily to prevent
from toxicity
- Although unlabeled route; SC route may be more effective and
better tolerated, especially at doses greater than 15 mg/week. Dose
should be escalated quickly to at least 15-20 mg/week in most
patients
- Monitor CBC, renal, and liver function every 8-12 weeks
- Contraindicated in renal disease
- Most patients treated with MTX exhibit clinical and
radiological improvement, a change in therapy should be considered
in patients with radiographic progression despite adequate clinical
response
- Sulfasalazine: 500 mg/day; max: 2-3 g/day;
3-month trial. Monitor CBC, liver enzymes every 8-12 weeks. Screen
for G6PD deficiency
- Hydroxychloroquine: Dose is based on body
weight not to exceed 400 mg/day; or 6.5 mg/kg/day in general. Used
in milder forms or in combination with other DMARDs. Yearly
ophthalmologic exam. Adjust dose in renal insufficiency
- Minocycline /Cyclosporin/Azathioprine: Can be
considered as alternative options
- Leflunomide: 10-20 mg/day. Modifies T-cell
function to decrease autoimmune activity and reduce structural
damage. Side effects: GI disturbances, hair loss, hypertension,
liver and lung toxicity; also potentially teratogenic
- Intramuscular gold /D-penicillamine: Rarely
induce sustained remission. Have been largely replaced by more
effective agents
Note:
Glucocorticoids may be used for flare-ups while initiating or
waiting for DMARDs to take affect. Lowest possible effective dose
for short time period is suggested
- Prednisone: 5-10mg/day is commonly used in
patients to bridge the therapy in early RA. Once the disease is
controlled; it should be weaned to the lowest possible dose, and
then stopped to avoid adverse effects
- Combination therapy with DMARDs indicated if:
- Poor prognostic features
- Moderate to high disease activity in newly diagnosed
patients
- Poor response to monotherapy
- MTX is used as an
anchor agent
B. Biologic DMARDs:
- Switch to biological agents if:
- At least 2 nonbiologic DMARDs (including MTX), have failed to
control disease activity with mono or combination therapy after 3
months of targeted dose
- Agents include:
- Tumor necrosis factor inhibitors
- Infliximab
- Adalimumab
- Etanercept
- Golimumab
- Certolizumab pegol
- T cell costimulatory inhibitors
- B lymphocyte depleting agent
- Interleukin 6 (IL-6) antagonist
- IL-1receptor antagonist
No evidence to suggest that one is superior to the other, though
anakinra appears to be least effective agent, except for Adult
Still's disease variant of RA. Combination with MTX appears to be
the most effective regimen for most biologics.
If a patient achieves sustained remission after discontinuation of
NSAID and glucocorticoids, a reduction in traditional and biologic
DMARD can be attempted.
NON-PHARMACOLOGICAL INTERVENTIONS:
Supportive measures
- Nutrition
- Rest
- Physical measures
- Joint splinting
- Orthopedic or athletic shoes
- Exercises
- Heat and cold therapy
- Paraffin baths
- Massage
Surgical
Interventions:
- Tendon reconstruction, joint fusion, and joint replacement are
potential treatment modalities to prevent disability in advanced
RA
Follow-up
Recommendations
- Monitor patient regularly
- Address risk factors and evaluate for osteoporosis, a major
comorbidity that can result from the disease itself or
corticosteroid use
- Cardiovascular disease is the number one cause of death.
Evaluate and manage CV risk factors; low dose aspirin may be used
as prophylactic therapy
Prognosis
- Poor prognostic findings:
- Persistent moderate to severe disease
- Positive anti-CCP antibody
- Inheritance of shared epitope
- Early or advanced age at disease onset
- 50% cannot function in primary job within 10 years of
onset
MEDICATIONS:
NSAIDs-Analgesic
TYPES
- Salicylates
- Acetic acid derivatives
- Diclofenac
- Etodolac
- Indomethacin
- Sulindac
- Enolic acid (Oxicam) derivatives
- Meloxicam
- Piroxicam
- Tenoxicam
- Napthylkanone derivatives
- Propionic acid derivatives (profens)
- Fenoprofen
- Flurbiprofen
- Ibuprofen
- Ketoprofen
- Naproxen
- Oxaprozin
- COX-2 inhibitors
NSAIDs
Mechanism(s):
- Prostaglandins are common locally produced chemicals mediating
pain, fever, and inflammation
- These drugs reversibly inhibit cyclooxygenase-1 and 2 (COX-1
and 2) enzymes
- This results in decreased formation of prostaglandin
precursors
Acetylsalicylic acid: (additional MODE OF
ACTION)
- Irreversibly interferes with the production of thromboxane
A2 within the platelet, thus inhibiting platelet
aggregation
NSAIDs Doses:
Salicylates: (rarely used for RA therapy at
present)
Aspirin
- 325-650 mg PO daily, every 4-6 hrs; Max. 4 g/day
Diflunisal
- 500-1000 mg/day PO in 2 divided doses
Renal impairment:
- ClCr<50 mL/minute: Decrease by 50% of normal
dose
Acetic
Acid Derivatives:
Diclofenac
- Immediate-release: 50 mg PO BID or TID; Max.
150 mg/day
- Slow-release: 75-100 mg PO
once a day; Max. 150 mg/day
- Rectal suppository: 50-100 mg/day; Max. 100
mg/day or combined dose(rectal+oral) is 150 mg/day
Diclofenac/Misoprostol
- 50 mg/200 mcg and 75 mg/200 mcg tablets; Max. 150 mg
Diclofenac/day
Etodolac
- Immediate-release: 200-300 mg PO BID or TID;
Max. 1000 mg/day
Indomethacin
- 25-50 mg PO BID or TID; Max. 200 mg/day
- Extended-release: 75 mg PO BID or TID; Max.
150 mg/day
Sulindac
- 150-200 mg PO BID; Max.400 mg/day
Enolic
Acid (Oxicam) Derivatives:
Meloxicam
- 7.5 mg PO once daily; may increase to 15 mg daily; Max. 15
mg/day
Piroxicam
- 10-20 mg PO once daily; Max. 20 mg/day
Tenoxicam
- 10-20 mg PO once daily; usual dose 20 mg PO once daily
Napthylkanone Derivative:
Nabumetone
- 1000 mg PO once daily; may increase upto 2000 mg/day in 2
divided doses
Renal impairment:
- ClCr 30-49 mL/minute: 750 mg/day may increase upto 1500
mg/day
Propionic
Acid Derivatives (profens):
Fenoprofen
- 300-600 mg PO TID or QID; Max. 3.2 g/day
Flurbiprofen
- 200-300 mg PO daily in 2,3 or 4 divided doses
Note: Do not administer more than 100 mg per
single dose; Max 300 mg/day
Ibuprofen
- 200-800 mg PO TID or QID; Max. 3.2 g/day
Ketoprofen
- Regular release: 150-200 mg PO TID or QID; Max. 300 mg/day
- Extended release: 200 mg PO daily
- Renal
impairment:
- Mild: 150 mg/day
- Severe (Clcr <25mL/min): 100 mg/day
Naproxen
- Regular release: 250-500 mg PO BID; may increase to 1.5
g/day
- Extended release: 750-1000 mg PO BID or once daily
- EC-Naproxen + IR-Esomeprazole: 375/20 mg or 500/20 mg PO
BID
Oxaprozin
- 600-1200 mg PO daily; Max. 1800 mg or 26 mg/kg, whichever is
less
COX-2
inhibitors:
Celecoxib
- Initial 100 mg PO BID may increase to 200 mg/day PO BID; Max.
200 mg/day
Analgesic, Non-NSAID
Mechanism:
- Analgesic action: Inhibits the synthesis of prostaglandins in
the central nervous system
- Antipyretic action: Inhibits the hypothalamic heat-regulating
center
Dose:
Acetaminophen
- 325-650 mg PO every 4-6 hrs or 1000 mg PO TID or BID; Max. of 4
g/day and 1 gm/dose
Corticosteroid
- Betamethasone
- Methylprednisolone acetate (most commonly used)
- Triamcinolone acetonide
- Triamcinolone hexacetonide
Mechanism:
- Decreases inflammation and the normal immune response through
multiple mechanisms, also suppresses adrenal function at high dose,
also has mineralocorticoid activity.
Doses:
Betamethasone (Intra-articular):
- Hip: 1-2 ml
- Knee, ankle, shoulder: 1 ml
- Elbow, wrist: 0.5-1 ml
- Metacarpophalangeal, sternoclavicular: 0.25-0.5 ml
Methylprednisolone (Intra-articular):
- Ankle, shoulder: 40 mg dose
- Hip: 80-160 mg
- Knee: 40-80 mg
- Elbow, wrist: 20-40 mg
- Small joint like MCP, PIP, DIP, SC joint: 10 mg
Triamcinolone acetonide (Intra-articular):
- Large joints: 5-40 mg
- Small joints: 2.5-10 mg
Triamcinolone hexacetonide (Intra-articular):
- Large joints: 10-20 mg
- Small joints: 2-6 mg
NONBIOLOGIC DMARDs
Antimetabolite/Antirheumatic
Agent
Mechanism:
- It is a folate antagonist that inhibits DNA synthesis and cell
reproduction
- Inhibits purine and thymidylic acid synthesis
- It also has immune modulator and anti-inflammatory actions
Dose:
Methotrexate
- Oral: Initiate at 7.5-15 mg/week PO given as a
single dose or divided in 3 equal doses at 12 hour intervals for 3
doses along with folic acid; Max. 25 mg/week
- Subcutaneous: 7.5-25 mg once weekly
Anti-inflammatory (5-Aminosalicylic Acid
Derivative)
Mechanism:
- Actual mechanism not determined
- Interferes with secretion by prostaglandin synthesis
inhibition
Dose:
Sulfasalazine
Slow release formulation prescribed as
follows:
- Week 1 = 500 g/day PO at bed time daily
- Week 2 = 500 g/day PO BID
- Week 3 = 500 g/day PO in the morning and 1000 g PO at
bedtime
- Week 4 and onwards: 1000 g/day PO BID
- Note: May increase
to maximum 3 g/day, if response to 2 g/day is inadequate after 2
months of use
Antirheumatic Agent, Gold
Compound
- Sodium Aurothiomalate (rarely used in current management of
RA)
Mechanism:
- Unknown, may decrease prostaglandin synthesis or may alter
cellular mechanisms by inhibiting sulfhydryl systems
- It exhibits anti-inflammatory, antiarthritic and
immunomodulating effects
Dose:
Sodium Aurothiomalate
- Intramuscular Injections: 1st week: 10 mg IM,
2nd week: 25 mg IM, then 25 to 50 mg IM weekly for the
next 20 weeks or until toxicity occur
- Maintenance: 50 mg IM tapered progressively to
every 2 to 4 weeks according to clinical response and tolerance,
and maintained indefinitely
Antirheumatic-Immunomodulator
Agent
Mechanism:
- Inhibits pyrimidine synthesis via dihydroorotate dehydrogenase,
resulting in antiproliferative and anti-inflammatory effects
Dose:
Leflunomide
- 20 mg PO daily; may decrease dose to 10 mg PO daily if 20 mg PO
is not tolerated well
Anti-inflammatory-Antimalarial
Mechanism:
- Exact mode of action in controlling these diseases is
unknown
- Antirheumatic/immunosuppressive effects:
Inhibits rheumatoid factor, acute phase reactants, and many
enzymes
Dose:
Hydroxychloroquine (rarely used now)
- Start 200-400 mg/day PO; do not exceed 6.5 mg/kg dose
- Note: Eye checkups
for retinal toxicity required on an annual basis
Immunosuppressant Agent
Mechanism:
- Complete mechanism of immunosuppression is not fully known
- It antagonizes purine metabolism and may inhibit synthesis of
DNA, RNA, and proteins
- May also interfere with cellular metabolism and inhibit
mitosis
Dose:
Azathioprine
- Start 1 mg/kg/day PO daily or in 2 divided doses for 6-8 weeks;
may increase by 0.5 mg/kg every 4 weeks, up to 2.5 mg/kg/day; for
minimum of 12 weeks
- Maintenance dose: Reduce dose by 0.5 mg/kg
(~25 mg daily) every 4 weeks until lowest effective dose is
reached
BIOLOGIC DMARDs
Tumor necrosis factor (TNF)
Inhibitors
- Infliximab
- Adalimumab
- Etanercept
- Certolizumab pegol
- Golimumab
Mechanism:
- Neutralizes the biological activity of TNFα by
- Binding with high affinity to the soluble and transmembrane
forms of TNFα
- Inhibits binding of TNFα with its receptors
- Leads to an overall reduction in inflammation
Note: Etanercept also neutralize TNFβ (lymphotoxin
α)
Dose:
Infliximab
- In combination with methotrexate: 3 mg/kg IV
at 0, 2, and 6 weeks, then 3 mg/kg IV every 8 weeks thereafter; may
increase dose to 10 mg/kg or decrease dosing interval to as often
as every 4 weeks if needed
Adalimumab
- 40 g SC every other week; may increase dose to 40 mg SC every
week
Etanercept
- 50 mg SC once weekly; may be given as 25 mg SC twice weekly
(individual doses should be at 3 or 4 days apart)
Certolizumab pegol
- 400 mg SC at 0, 2 and 4 weeks; then 200 mg every other week;
may consider maintenance dose of 400 mg every 4 weeks
Golimumab
- In combination with methotrexate: 50 mg SC
once per month
Antirheumatic, Disease Modifying; Interleukin-1
Receptor Antagonist
- Anakinra (used only for adult Still's disease variant of
RA)
Mechanism:
- Antagonist of the interleukin-1 (IL-1) receptor
- Endogenous IL-1 is induced by inflammatory stimuli and mediates
a variety of immunological responses, including degradation of
cartilage (loss of proteoglycans) and stimulation of bone
resorption
Dose:
Anakinra
- 100 mg SC once daily. Administer at approximately the same time
each day
Renal impairment
- ClCr <30 mL/min or End Stage Renal Disease: 100 mg SC every
other day
Antirheumatic, Disease Modifying; Interleukin-6
Receptor Antagonist
Mechanism:
- Antagonist of the interleukin-6 (IL-6) receptor
- Endogenous IL-6 is induced by inflammatory stimuli and mediates
a variety of immunological responses
- Inhibition of IL-6 leads to a reduction in cytokine and acute
phase reactant production
Dose:
Tocilizumab
- 4 mg/kg IV infusion over 1 hour every 4 weeks; may be increased
to 8 mg/kg based on clinical response. Maximum 800 mg/infusion
Antirheumatic, Disease Modifying; Selective
T-Cell Costimulation Blocker
Mechanism:
- Selective costimulation modulator
- Inhibits T-cell (T-lymphocyte) activation by binding to CD80
and CD86 on antigen presenting cells (APC), thus blocking the
required CD28 interaction between APCs and T cells
Dose:
Abatacept
Note: Administered as a 30-minute intravenous
infusion utilizing weight based dosing and following the initial IV
infusion, repeat IV dose (using the same weight-based dosing) at 2
weeks and 4 weeks after the initial infusion, and every 4 weeks
thereafter.
- Weight
- <60 kg: 500 mg
- 60-100 kg: 750 mg
- >100 kg: 1000 mg
Biologic-Selective B cell
Depleter
Mechanism:
- Binds specifically to the antigen CD20 (human
B-lymphocyte-restricted differentiation antigen, Bp35) on the cell
surface
- Activate complement-dependent B-cell cytotoxicity; and to human
Fc receptors, mediating cell killing through an antibody-dependent
cellular toxicity
Dose:
Rituximab (IV infusion)
- Initial 1000 mg followed two weeks later by the second 1000
dose; subsequent courses may be administered every 24 weeks (based
on clinical evaluation), if necessary may be repeated no sooner
than 16 weeks following the previous course
Note: Infusions should be administered in a
setting where full resuscitation facilities are available, and
under the close supervision. Also administer 100 mg IV
methylprednisolone 30 minutes prior to both Rituximab infusions.
Acetaminophen and diphenhydramine may also be given prior to
rituximab.
a) Tips for patient care
Encourage
- Participation in activities of daily living
- Emphasize appropriate exercise, reduction of joint stress and
strengthening of muscles supporting the joint
- Weight lose to decrease stress on weight-bearing joints and
frequent rest periods between activities
- Use of appropriate adaptive devices for the performance of
activities of daily living
- Use appropriate footwear and any assistive devices, if
required
- Teach self-management and provide resources
- Consider consultation for occupational therapy
Drugs
- Evaluate risks and benefits of pharmacological therapy
- DMARDs are recommended as soon as possible in patients with
active disease
- Consider concurrent comorbidities while choosing the therapy/in
therapeutic decision
- Advise to take one NSAID at a time (with the exception of
low-dose ASA for cardiac and stroke prophylaxis)
- Misoprostol or proton pump inhibitors are recommended in
patients who are taking NSAIDs and are at increased risk for upper
gastrointestinal adverse events
- Evaluate cost, affordability and insurance coverage for
patients
Unlabeled/Alternate
uses
Include but not limited to:
- Acetylsalicylic acid
- Pre-eclampsia
- Antiphospholipid syndrome
- Methotrexate
- Ectopic pregnancy
- Systemic lupus erythematosus
- Minocycline
Counseling
- Patients with RA are prone to fatigue and muscle weakness,
advise rest when tired
- Avoid exercising tender, injured or severely inflamed
joints
- Educate about the importance of regular rheumatologist visits
for monitoring the course of the disease and medication side
effects
- Gentle exercise can help strengthen the muscles around
joints
- Emphasize adapting correct posture and body mechanics
- Inform patients that NSAIDs can cause GI bleeds that can occur
with or without warning
- Counsel women of child bearing age regarding potential
teratogenicity of DMARDs
Alerts
- Septic arthritis should be suspected for a single joint
flare-up in patient with established diagnosis of RA
- Long-term use of corticosteroids increase the risk of
osteoporosis
- Women of child bearing age taking DMARDs should use effective
contraception
- Discontinue NSAIDs (except ASA) in patients presenting with
acute coronary syndromes
- If required, an opioid analgesic (e.g. morphine) may be used as
an alternative for pain control in this setting
- NSAIDs may cause GI ulceration/bleeding, exacerbation of CHF,
as well as renal dysfunction and HTN
- COX-2 inhibitors may have a reduced risk of GI problems
Tips
- Early referral to a rheumatologist is recommended
- Combination DMARDs may be more effective than individual
drugs
- Evaluate joint and extra-articular involvement
- Pregnancy is associated with clinical improvement in at least
50% of patients
- May be related to elevated blood levels of free cortisol or to
enhanced phagocytosis of immune complexes
- Early aggressive treatment for RA can delay joint
destruction
- Joint protection techniques, heat and cold treatments, and
splints or orthotic devices to support and align joints may be very
helpful
- Avoid cold treatments if patient has poor circulation or
numbness
- Periodic evaluation for disease activity or disease progression
is recommended
- RA is associated with many complications such as:
- Pleuritis, Pericarditis, Eye inflammation, Osteoporosis, Heart
disease
- Occasionally surgery is needed to correct severely damaged
joints. Surgery may include:
- Synovectomy (Removal of the joint lining)
- Arthroplasty (joint replacement)
Expected
outcome
- There is no cure for rheumatoid arthritis
- Prognosis depends on the severity of symptoms
- Individuals who develop RA at young age usually get worse
quickly
- Early treatment of patients with the medications reduces joint
pain and damage
b) Scales and Tables
Core Resources:
- Aletaha D, Neogi T, Silman AJ et al.2010 Rheumatoid arthritis
classification criteria: an American College of
Rheumatology/European League Against Rheumatism collaborative
initiative. Arthritis & Rheumatism 2010, 69; 1580-1588
- Bykerk V P, Akhavan P, Hazelwood GS, et al. Canadian
Rheumatology Association Recommendations for Pharmacological
Management of Rheumatoid Arthritis with Traditional and Biologic
Disease-modifying Antirheumatic Drugs. J Rheumatol 2011; 38:11;
doi:10.3899/jrheum.110207
- Compendium of Pharmaceuticals and Specialties (CPS). Canadian
Pharmacist association. Toronto: Webcom Inc. 2012
- Day RA, Paul P, Williams B, et al (eds). Brunner &
Suddarth's Textbook of Canadian Medical-Surgical Nursing.
2nd ed. Philadelphia: Lippincott Williams and Wilkins;
2010
- Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington
Manual of Medical Therapeutics. 33rd ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2010
- Gray J, ed. Therapeutic Choices. Canadian Pharmacists
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