drugs used in joint diseases
DESCRIPTION
Drugs used in joint diseases. Dr Sanjeewani Fonseka Department of Pharmacology. 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 - PowerPoint PPT PresentationTRANSCRIPT
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Drugs used in joint diseases
Dr Sanjeewani FonsekaDepartment 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