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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

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nice guidelines on the management of rheumatoid arthritis feb 2009
NICE guidelines on the management of Rheumatoid Arthritis Feb 2009
  • Key priorities for implementation
  • Referral for specialist treatment
investigations
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
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
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
DMARDs
  • Offer a combination of DMARDs
  • Ideally within 3 months
  • Corticosteroids oral, intramuscular or intra-articular
dmards1
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
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
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
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
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 arthritis1
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
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 review1
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
Vit D role
  • Calcium homeostasis
  • Bone metabolism
  • Regulates many other cellular functions including immunmodulations
sources
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
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 1,25-dihydroxyvitamin D (1,25OHD)
  • 1,25OHD active form of vitamin D
absorption and metabolism1
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
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)
slide22

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 D-dependent 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
slide23

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
slide24

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
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
investigations1
Investigations
  • Alkaline phosphatase elevated
  • Serum calcium and phosphorus reduced
  • 25-hydroxyvitamin D (calcidiol) <15 ng/mL
  • PTH elevated
radiographic findings
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
slide29

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