Management of Rheumatoid Arthritis

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Transcript Management of Rheumatoid Arthritis

Management of Rheumatoid
Arthritis
Raad Makadsi
NICE guidelines on the management
of Rheumatoid Arthritis Feb 2009
• Key priorities for implementation
• Referral for specialist treatment
Investigations
• Rheumatoid factor
• Anti-cyclic citrullinated peptide (CCP)
antibodies if: they are negative for
rheumatoid factor, and
• X-ray the hands and feet
• Once the diagnosis is made
• there is a need to inform decision-making
about starting combination therapy
Communication and education
• Explain the risks and benefits of Treatment
• Offer verbal and written information
• Education
• Offer the opportunity to take part in
existing educational activities, including
self-management programmes
The multidisciplinary team
• Specialist nurse - who is responsible for
coordinating the care
• Physiotherapy
• Occupational therapy
• Psychological interventions (for example,
relaxation, stress management and
cognitive coping skills])
• Podiatrist (Functional insoles and
therapeutic footwear)
DMARDs
• Offer a combination of DMARDs
• Ideally within 3 months
• Corticosteroids oral, intramuscular or intraarticular
DMARDs
• When sustained and satisfactory levels of
disease control have been achieved,
cautiously try to reduce drug doses
• If combination DMARD therapy is not
appropriate, start DMARD mono-therapy
• Patients in whom disease-modifying or
biological drug doses are being decreased
or stopped, arrangements should be in
place for prompt review
Glucocorticoids
• Short-term - recent-onset or established
disease to rapidly decrease inflammation
• Long - term - In established RA continue
glucocorticoids when:
- the long-term complications of
glucocorticoid
therapy have been fully
discussed
- all other treatment options (including
biological drugs) have been offered
Biological drugs
• Offer anti-TNF if patient failed two
DMARDs including Methotrexate
• Do not offer the combination of tumour
necrosis factor-α (TNF-α) inhibitor therapy
and anakinra for RA
Symptom control
• Paracetamol, codeine or compound
analgesics)
• Oral NSAIDs/COX-2 inhibitors should be
used at the lowest effective dose for the
shortest possible period of time
• If RA patient needs to take low-dose
aspirin consider other analgesics before
substituting or adding an NSAID or COX-2
inhibitor (with a PPI)
Monitoring rheumatoid arthritis
• Measure CRP and DAS28 regularly
• In early active RA, measure CRP and
DAS28 monthly until treatment has
controlled the disease to a level previously
agreed with the person with RA
Monitoring rheumatoid arthritis
• In satisfactorily controlled established RA
Offer patients review appointments at a
frequency and location suitable to their
needs
• Make sure they:
- have access to additional visits for
disease flares
- know when and how to get rapid access
to specialist care
- Have an on going drug monitoring
RA annual review
• Assess disease activity and damage
• Functional ability (HAQ)
• Comorbidities, such as hypertension, IHD,
osteoporosis and depression
• Look for complications, such as vasculitis
and cervical spine, lung or eyes
involvement
RA annual review
• Organise appropriate cross referral within
the multidisciplinary team
• Need for referral for surgery
• The effect the disease is having on a
person's life
Vit D role
• Calcium homeostasis
• Bone metabolism
• Regulates many other cellular functions
including immunmodulations
SOURCES
• Sunlight and ultraviolet light photoisomerize provitamin D to vitamin D3
(cholecalciferol) in the skin
• Diet fortified milk, fatty fish, cod-liver oil,
and, to a lesser extent, eggs
ABSORPTION AND METABOLISM
• Dietary vitamin D micelles, -absorbed by
enterocytes, -packaged into chylomicrons.
• Chylomicrons - liver - Vit D hydroxylation
to form 25-hydroxyvitamin D (25OHD)
• Kidney- hydroxylation to 1,25dihydroxyvitamin D (1,25OHD)
• 1,25OHD active form of vitamin D
ABSORPTION AND METABOLISM
• More than 25 metabolites identified, each
with different biologic activities
• The synthesis of vitamin D is closely
coupled to calcium homeostasis, and is
modulated by parathyroid hormone, serum
calcium, and phosphorus levels
DEFICIENCY AND RESISTANCE
caused by one of four mechanisms :
• Inadequate dietary vitamin D, fat malabsorptive
disorders, and/or lack of photoisomerization
• Impaired hydroxylation by the liver to produce
25-hydroxyvitamin D
• Impaired hydroxylation by the kidneys to
produce 1,25-dihydroxyvitamin D
• End organ insensitivity to vitamin D metabolites
(hereditary vitamin D resistant rickets)
• In early stage Vitamin D deficiency,
hypophosphatemia is more marked than
hypocalcemia
• Persistent deficiency, hypocalcemia occurs and
causes secondary hyperparathyroidism,
• This leads to phosphaturia, demineralization of
bones
• More prolonged, lead to osteomalacia in adults
and rickets in children.
• Glucocorticoids inhibit intestinal vitamin Ddependent calcium absorption and therefore can
cause osteomalacia
• Vitamin D stores decline with age, especially in
the winter
• Vit D and calcium supplementation can reduce the
risk of falls and fractures in the elderly
• The Recommended Dietary Allowance for
vitamin D is 600 International Units for
adults Age 70 years and for children 1 to
18 years of age
• For adults 71 years and older, 800 units
(20 micrograms) daily is recommended
• Excessive doses of vit D in adults can
result in intoxication
• Symptoms of acute intoxication are due to
hypercalcemia and include confusion,
polyuria, polydipsia, anorexia, vomiting,
and muscle weakness
• Long-term intoxication can cause bone
demineralization and pain. In children, the
hypercalcemia can cause brain injury
CLINICAL MANIFESTATIONS
• Osteomalacia may be asymptomatic and
present radiologically as osteopenia.
• Diffuse bone pain
• polyarthralgias,
• muscle weakness, and difficulty walking Waddling gate
• Fracture
• Muscle spasms, cramps
Investigations
•
•
•
•
Alkaline phosphatase elevated
Serum calcium and phosphorus reduced
25-hydroxyvitamin D (calcidiol) <15 ng/mL
PTH elevated
Radiographic findings
• Changes in vertebral bodies —
• softening leads to a concavity of the vertebral
bodies called codfish vertebrae. The vertebral
disks appear large and biconvex.
• There may be spinal compression fractures,
but these are more common in osteoporosis.
• Looser zones — Looser pseudofractures,
• Stress fractures
• Vitamin D3 (cholecalciferol) is available in 400,
800, 1000, 2000, 5000, 10,000, and 50,000
unit capsules
IM injection can be extremely painful
• Vitamin D2 (ergocalciferol) is available for oral
use in 400 and 50,000 unit capsules
A previously available IM preparation is now
difficult to obtain