drugs used in joint diseases dr sanjeewani fonseka department of pharmacology
TRANSCRIPT
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Drugs used in joint diseases
Dr Sanjeewani Fonseka
Department of Pharmacology
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OBJECTIVES
• List the classes of drugs that are used in the treatment of RA
• Describe the mechanism of action, pharmacokinetics and adverse effects of the above drugs
• Explain the basis of disease modifying drugs
• Explain the basis of drug treatment of OA and gout
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Rheumatoid arthritis
• Chronic synovial inflammation
• Autoimmune
• Cytokine networks are responsible for inflammation & joint destruction– Tumor Necrosis Factor-α (TNF-α)– Interleukins - 1,6,17
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Disability in Early RA
• Inflammation– Swollen– Stiff– Sore– Warm
• Fatigue
• Potentially Reversible
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Periarticular OsteopeniaJoint Space Narrowing
ErosionsMal-Alignment
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Disability in RA
• Most of the disability in RA is a result of the INITIAL burden of disease
• People get disabled because of:– Inadequate control– Lack of response– Compliance
• GOAL: control the disease early on!
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Drugs for RA• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs (DMARDs)– Synthetic– Biologic
• Glucocorticoids
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NSAIDs
• Cyclo-oxygenase inhibitors
• Do not slow the progression of the disease
• Provide partial relief of pain and stiffness
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NSAIDs
• Non-selective COX inhibitors– Ibuprofen– Diclofenac sodium
• COX–2 inhibitors– celecoxib
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COX-2 Inhibitors
• COX-2 inhibitors appear to be as effective NSAIDs
• Associated with less GI toxicity
• However increased risk of CV events
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Read
Side effects of
• non selective NSAID
• COX – II inhibitors
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Drugs for RA• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs (DMARDs)– Synthetic– Biologic
• Glucocorticoids
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90% of the joints involved in RA are affected within the first year
SO TREAT IT EARLY
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Disability in Late RA (Too Late)
• Damage– Bones– Cartilage– Ligaments and
other structures
• Fatigue
• Not Reversible
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DMARDs
Disease Modifying Anti-Rheumatic Drugs
• Reduce swelling & inflammation
• Improve pain
• Improve function
• Have been shown to reduce radiographic progression (erosions)
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DMARDs
• Synthetic
• Biologic
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Synthetic DMARDs
• Methotrexate
• Sulphasalazine
• Chloroquine
• Hydroxychloroquine
• Leflunomide
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Synthetic DMARDs
• Methotrexate
• Sulphasalazine
• Chloroquine
• Hydroxychloroquine
• Leflunomide
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Methotrexate (MTX)• Dihydrofolate reductase inhibitor
• ↓ thymidine & purine nucleotide synthesis
• “Gold standard” for DMARD therapy
• 7.5 – 30 mg weekly
• Absorption variable• Elimination mainly renal
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MTX adverse effects
• Hepatotoxicity• Bone marrow suppression• Dyspepsia, oral ulcers• Pneumonitis
• Teratogenicity
• Folic acid reduces GI & BM effects
• Monitoring– FBC, ALT, Creatinine
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Synthetic DMARDs
• Methotrexate
• Sulphasalazine
• Chloroquine
• Hydroxychloroquine
• Leflunomide
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Sulphasalazine
• Sulphapyridine + 5-aminosalicylic acid
• Remove toxic free radicals
• Remission in 3-6 month
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• Elimination hepatic
• Dyspepsia, rashes, BM suppression
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Synthetic DMARDs
• Methotrexate
• Sulphasalazine
• Chloroquine /Hydroxychloroquine
• Leflunomide
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Chloroquine, Hydroxychloroquine
• Mechanism unknown– Interference with antigen processing ?– Anti- inflammatory and immunomodulatory
• For mild disease
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Chloroquine cont
• Take a month to see the effect
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Chloroquine cont
Side effects
• Irreversible Retinal toxicity, corneal deposits
• Ophthalmologic evaluation every 6 months
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Synthetic DMARDs
• Methotrexate
• Sulphasalazine
• Chloroquine
• Hydroxychloroquine
• Leflunomide
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Leflunomide
• Competitive inhibitor of dihydroorotate dehydrogenase (rate-limiting enzyme in de novo synthesis of pyrimidines)
• Reduce lymphocyte proliferation
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Leflunomide cont
• Oral
• T ½ - 4 – 28 days due to EHC
• Elimination hepatic
• Action in one month
• Avoid pregnancy for 2 years
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Side effects of leflunomide
• Hepatotoxicity
• BM suppression
• Diarrhoea
• rashes
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Combination therapy (using 2 to 3) DMARDs at a time works better than
using a single DMARD
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Common DMARD Combinations
• Triple Therapy– Methotrexate, Sulfasalazine, Hydroxychloroquine
• Double Therapy– Methotrexate & Leflunomide– Methotrexate & Sulfasalazine– Methotrexate & Hydroxychloroquine
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DMARDs
• Synthetic
• Biologic
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BIOLOGIC THERAPY
• Complex protein molecules
• Created using molecular biology methods
• Produced in prokaryotic or eukaryotic cell cultures
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Biologics
• Monoclonal Antibodies to TNF– Infliximab – Adalimumab
• Soluble Receptor Decoy for TNF– Etanercept
• Receptor Antagonist to IL-1– Anakinra
• Monoclonal Antibody to CD-20– Rituximab
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Tumour Necrosis Factor (TNF)
• TNF is a potent inflammatory cytokine
• TNF is produced mainly by macrophages and monocytes
• TNF is a major contributor to the inflammatory and destructive changes that occur in RA
• Blockade of TNF results in a reduction in a number of other pro-inflammatory cytokines (IL-1, IL-6, & IL-8)
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Macrophage
Any Cell
Trans-Membrane Bound TNF
TNF Receptor
Soluble TNF
How Does TNF Exert Its Effect?
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Trans-Membrane Bound TNF
Soluble TNF
Strategies for Reducing Effects of TNF
Macrophage
Monoclonal Antibody (Infliximab & Adalimumab)
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Side Effects
• Infection–Common (Bacterial)–Opportunistic (Tb)
• Demyelinating Disorders• Malignancy• Worsening CHF
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Drugs for RA• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs (DMARDs)– Synthetic– Biologic
• Glucocorticoids
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Glucocorticoids
• Potent anti-inflammatory drugs
• Serious adverse effects with long-term use
• To control the diaseas
• Indications– As a bridge to effective DMARD therapy
– Systemic complications (e.g. vasculitis)
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Route of steroid
• Oral
• Intra- articular
• IM - depot
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Osteoarthritis
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Osteoarthritis
• Most common joint disorder worldwide
• Diagnosed on clinical presentation and supported by radiography.
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Clinical Features
• Age of Onset > 40 years
• Commonly Affected Joints
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Goals of Treatment
• Control pain and swelling
• Minimize disability
• Improve the quality of life
• Prevent progression
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NSAIDs
• Tend to avoid for long-term use
• Indomethacin should be avoided for long-term use in patients with hip OA– associated with accelerated joint
destruction
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• Read – different classes of NSAID that can be used in OA
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Topical NSAIDs
• Effect was not apparent at three to four weeks
• Topical NSAIDs were generally inferior to oral NSAIDs
• Topical route was safer than oral use
• Topical Diflofenac (1% gel or patch)
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• Corticosteroid – intra- articular injections
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Glucosamine Sulfate
• Glycoprotein derived from marine exoskeletons or produced synthetically
• Found - tendons, ligaments, cartilage, synovial fluid
• ? disease modifying agent in osteoarthritis.
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• orally, intravenously, intramuscularly, and intra-articularly
• provide pain relief, reduce tenderness, and improve mobility in patients with OA
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Hyaluronic acids
– Injected into the joint capsule to reduce friction and improves articulation (act as synovial fluid)
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GOUT
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GOUT
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TREATMENT GOALS
• Rapidly end acute flares
• Protect against future flares
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Acute Flare
• NSAIDS
• Colchicine
• Corticosteroids
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Colchicine
Colchicine- reduces pain, swelling, and inflammation; pain subsides within 12 hrs and relief occurs after 48 hrs
Prevent migration of neutrophils to joints
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Side effects
• Nausea
• Vomiting
• Diarrhea
• Rahes
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TREATMENT GOALS
• Rapidly end acute flares
Protect against future flares
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URICOSURIC AGENTS
• Probenecid
• Increased secretion of urate into urine
• Reverses most common physiologic abnormality in gout ( 90% pt.s are underexcretors)
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• Hypoxanthine
• Xanthine
• Uric acid
XO
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• Hypoxanthine
• Xanthine
• Uric acid
XO ALLOPURINOL
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XANTHINE OXIDASE INHIBITOR
• Allopurinol
• Effective in overproducers
• May be effective in underexcretors
• Can work in pt.s with renal insufficiency
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Summary
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Drugs for RA• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs (DMARDs)– Synthetic– Biologic
• Glucocorticoids
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RA
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OA
• Pain relief
• Glucosamine Sulfate
• Hyaluronic acids injections
• Surgery
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TREATMENT OF GOUT
• Colchicine, NSAID, steroids – acute attack
• Allopurinol- decreases the production of uric acid
• Probenecid - prevent absorption of uric acid in the tubules of kidney
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OBJECTIVES
• List the classes of drugs that are used in the treatment of RA
• Describe the mechanism of action, pharmacokinetics and adverse effects of the above drugs
• Explain the basis of disease modifying drugs
• Explain the basis of drug treatment of OA and gout