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Rheumatoid Arthritis
Diagnosis and Current Management


     Dr. Ankur Nandan Varshney
         Institute of Medical Sciences
           Banaras Hindu University
Introduction
   Commonest inflammatory joint disease seen in clinical
    practice affecting approx 1% of population.
   Chronic multisystem disease of unknown cause.
   Characterized by persistent inflammatory synovitis
    leading to cartilage damage, bone erosions, joint
    deformity and disability.
Onset
    Although Rheumatoid arthritis may present at any age, patients most
     commonly are first affected in the third to sixth decades.
    Female: male 3:1
    Initial pattern of joint involvement could be:-
1)   Polyarticular : most common
2)   Oligoarticular
3)   Monoarticular
    Morning joint stiffness > 1 hour and easing with physical activity is
     characteristic.
    Small joints of hand and feet are typically involved.
Clinical Manifestations


   Articular

   Extra-articular
Articular manifestation

   Pain in affected
    joint aggravated by
    movemnt is the
    most common
    symptom.

   Morning stiffness
    ≥1 hr
   Joints involved -
Relative incidence of joint
             involvement in RA
   MCP and PIP joints of hands & MTP of feet   90%
   Knees, ankles & wrists-                     80%
   Shoulders-                                  60%
    Elbows-                                     50%
   TM, Acromio - clavicular & SC joints-        30%
Joints involved in RA
   Don’t forget the cervical spine!!
      Instability at cervical spine can lead to
    impingement of the spinal cord.

   Thoracolumbar, sacroiliac, and distal
    interphalangeal joints (DIP)of the hand are
    NOT involved.
PIP Swelling
Ulnar Deviation, MCP Swelling,
     Left Wrist Swelling
Extra-articular
            manifestations
    Present in 30-40%
   May occur prior to arthritis
   Patients that are more likely to get are:
       High titres of RF/ anti-CCP
       HLA DR4+
       Male
       Early onset disability
       History of smoking
Extraarticular Involvement
   Constitutional symptoms ( most common)
   Rheumatoid nodules(30%)
   Hematological-
       normocytic normochromic anemia
       leucocytosis /leucopenia
       thrombocytosis
   Felty’s syndrome-
      Chronic nodular Rheumatoid Arthritis
     Spleenomegaly

     Neutropenia
   Respiratory- pleural effusion, pneumonitis ,
    pleuro-pulmonary nodules, ILD
   CVS-asymptomatic pericarditis , pericardial
    effusion, cardiomyopathy
   Rheumatoid vasculitis- mononeuritis multiplex,
    cutaneous ulceration, digital gangrene, visceral
    infarction
   CNS- peripheral neuropathy, cord-compression
    from atlantoaxial/midcervical spine subluxation,
    entrapment neuropathies
   EYE- kerato cunjunctivitis sicca, episcleritis,
    scleritis
Rheumatoid nodule
Laboratory investigations in RA
   CBC- TLC, DLC, Hb, ESR & GBP

   Acute phase reactants

   Rheumatoid Factor (RF)

   Anti- CCP antibodies
Rheumatoid Factor (RF)
   Antibodies that recognize Fc portion of IgG
   Can be IgM , IgG , IgA
   85% of patients with RA over the first 2 years become RF+

•   A negative RF may be repeated 4-6 monthly for the first two year of
    disease, since some patients may take 18-24 months to become
    seropositive.
•   PROGNISTIC VALUE- Patients with high titres of RF, in general,
    tend to have POOR PROGNOSIS, MORE EXTRA ARTICULAR
    MANIFESTATION.
Causes of positive test for RF
   Rheumatoid arthritis
   Sjogrens syndrome
   Vasculitis such as polyarteritis nodosa
   Sarcoidosis
   Systemic lupus erythematosus
   Cryoglobulinemia
   Chronic liver disease
   Infections- tuberculosis , bacterial endocarditis, infectious
    mononucleosis, leprosy, syphilis, leishmaniasis.
   Malignancies
   Old age(5% women aged above 60)
Anti-CCP
   IgG against synovial membrane peptides
    damaged via inflammation
   Sensitivity (65%) & Specificity (95%)
   Both diagnostic & prognostic value
   Predictive of Erosive Disease
     Disease severity
     Radiologic progression
     Poor functional outcomes
Acute Phase Reactants
Positive acute phase reactants (↑)   Negative acute phase reactants (↓)
Mild elevations                      – Albumin
   – Ceruloplasmin                   – Transferrin
   – Complement C3 & C4
Moderate elevations
   – Haptoglobulin
   – Fibrinogen (ESR)
   – α 1 – acid glycoprotein
   – α 1 – proteinase inhibitor
Marked elevations
   – C-reactive protein (CRP)
   – Serum amyloid A protein
 Elevated APRs( ESR, CRP )
 Thrombocytosis
 Leukocytosis
 ANA
     30-40%
 Inflammatory synovial fluid
 Hypoalbuminemia
Radiographic Features
   Peri-articular osteopenia
   Uniform symmetric joint space narrowing
   Marginal subchondral erosions
    Joint Subluxations
   Joint destruction
   Collapse

   Ultrasound detects early soft tissue lesions.
   MRI has greatest sensitivity to detect
    synovitis and marrow changes.
Diagnostic Criterias
ACR Criteria (1987)
   1.Morning Stiffness ≥1 hour
   2.Arthritis of ≥ 3 joints observed by physician      simulteneously-
    Rt/Lt-PIP, MCP,wrist, elbow,            knee, ankle, MTP
   3.Arthritis of hand joints-PIP,MCP,wrist
   4. Symmetric arthritis
   5. Rheumatoid nodules
   6. Positive Rheumatoid Factor
   7. Radiographic Erosions or periarticular osteopenia in hand or wrist
    joints

   Criteria 1-4 must be present for ≥6 wks
   Must have ≥4 criteria to meet diagnosis of RA
2010 ACR/EULAR Classification Criteria
   a score of ≥6/10 is needed for classification of a patient as having definite RA
   A. Joint involvement
    SCORE
   1 large joint
    0
   2−10 large joints
    1                                                                              1−3 small
    joints (with or without involvement of large joints)                             2
   4−10 small joints (with or without involvement of large joints)                            3
   >10 joints (at least 1 small joint)††
    5

   B. Serology (at least 1 test result is needed for classification)
   Negative RF and negative ACPA                                                              0
   Low-positive RF or low-positive ACPA                                                       2
   High-positive RF or high-positive ACP
    3

   C. Acute-phase reactants (at least 1 test result is needed for classification)
   Normal CRP and normal ESR                                                                  0
   Abnormal CRP or normal ESR                                                                 1
Management
Goals of management
   Focused on relieving pain
   Preventing damage/disability
   Patient education about the disease
   Physical Therapy for stretching and range of motion
    exercises
   Occupational Therapy for splints and adaptive
    devices
   Treatment should be started early and should be
    individualised .
   EARLY AGGRESSIVE TREATEMNT
Treatment modalities for RA
   NSAIDS
   Steroids
   DMARDs
   Immunosuppressive therapy
   Biological therapies
   Surgery
NSAIDS
Non-Steroidal anti-inflammatories
 (NSAIDS) / Coxibs for symptom control

1)   Reduce pain and swelling by inhibiting COX

2)   Do not alter course of the disease.

3)   Chronic use should be minimised.

4)   Most common side effect related to GI tract.
Corticosteroids in RA
   Corticosteroids , both systemic and intra-articular are
    important adjuncts in management of RA.
   Indications for systemic steroids are:-
    1.   For treatment of rheumatoid flares.
    2.   For extra-articular RA like rheumatoid vasculitis and
         interstitial lung disease.
    3.   As bridge therapy for 6-8 weeks before the action of
         DMARDs begin.
    4.   Maintainence dose of 10mg or less of predinisolone daily
         in patients with active RA.
    5.   Sometimes in pregnancy when other DMARDs cannot be
         used.
Disease Modifying Anti-rheumatic Agents
   Drugs that actually alter the disease course .
   Should be used as soon as diagnosis is made.
   Appearance of benefit delayed for weeks to
    months.
   NSAIDS must be continued with them until true
    remission is achieved .
   Induction of true remission is unusual .
DMARDs
Commonly used        Less commonly used
Methotrexate         Chloroquine

Hydroxychloroquine   Gold(parenteral &oral)

Sulphasalazine       CyclosporineA

Leflunomide          D-penicillamine/bucillamine

                     Minocycline/Doxycycline
                     Levamisole
                     Azathioprine,cyclophosphamide,
                     chlorambucil
Clinical information about DMARDs
NAME              DOSE                 SIDE EFFECTS MONITORING ONSET OF
                                                               ACTION

1) Hydroxycloro   200mg twice daily    Skin pigmentation Fundoscopy&          2-4 months
   quine          x 3 months, then     , retinopahy        perimetry yearly
                  once daily           ,nausea, psychosis,
                                       myopathy




2) Methotrexate   7.5-25 mg once a     GI upset,           Blood counts,LFT 1-2 months
                  week orally,s/c or   hepatotoxicity,     6-8 weekly,Chest
                  i/m                  Bone marrow         x-ray annually,
                                       suppression,        urea/creatinine 3
                                        pulmonary          monthly;
                                       fibrosis            Liver biopsy
Clinical information about DMARDs contnd..
NAME            DOSE              SIDE EFFECTS MONITORING ONSET OF
                                                          ACTION

3)Sulphasala-   2gm daily p.o     Rash,             Blood counts       1-2 months
                                  myelosuppression, ,LFT 6-8 weekly
  zine
                                  may reduce sperm
                                  count




4)Leflunomide   Loading 100 mg    Nausea,diarrhoea,   LFT 6-8 weekly   1-2 months
                daily x 3 days,   alopecia,
                then 10-20 mg     hepatotoxicity
                daily p.o
When to start DMARDs?

   DMARDs are indicated in all patients with RA who
    continue to have active disease even after 3 months
    of NSAIDS use.
   The period of 3 months is arbitary & has been
    chosen since a small percentage of patients may go in
    spontaneous remission.
   The vast majority , however , need DMARDs and
    many rheumatologists start DMARDs from Day 1.
How to select DMARDs?
   There are no strict guidelines about which DMARDs
    to start first in an individual.
   Methotrexate has rapid onset of action than other
    DMARD.
   Taking in account patient tolerance, cost
    considerations and ease of once weekly oral
    administration METHOTREXATE is the DMARD
    of choice, most widely prescribed in the world.
Should DMARDs be used singly or
            in combination?
   Since single DMARD therapy (in conjunction with
    NSAIDS) is often only modestly effective , combination
    therapy has an inherent appeal.

   DMARD combination is specially effective if they include
    methotrexate as an anchor drug.

   Combination of methotrexate with leflunamide are
    synergestic since there mode of action is different.
Limitations of conventional DMARDs
1)   The onset of action takes several months.
2)   The remission induced in many cases is partial.
3)   There may be substantial toxicity which
     requires careful monitoring.
4)   DMARDs have a tendency to lose effectiveness
     with time-(slip out).
    These drawbacks have made researchers look
     for alternative treatment strategies for RA- The
     Biologic Response Modifiers.
Immunosuppresive therapy
Agent               Usual dose/route        Side effects

Azathioprine        50-150 mg orally        GI side effects ,
                                            myelosuppression, infection,
                    .
Cyclosporin A       3-5 mg/kg/day       .   Nephrotoxic , hypertension ,
                                            hyperkalemia

Cyclophosphamide    50 -150 mg orally       Myelosuppression , gonadal
                                            toxicity ,hemorrhagic cystitis ,
                                            bladder cancer
BIOLOGICS IN RA
    Cytokines such as TNF-α ,IL-1,IL-10 etc. are key
     mediators of immune function in RA and have
     been major targets of therapeutic manipulations in
     RA.
    Of the various cytokines,TNF-α has attaracted
     maximum attention.
    Various biologicals approved in RA are:-
1)   Anti TNF agents : Infliximab Etanercept Adalimumab
2)   IL-1 receptor antagonist : Anakinra
3)     IL-6 receptor antagonist : Tocilizumab
4)   Anti CD20 antibody : Rituximab
5)   T cell costimulatory inhibitor : Abatacept
Agent        Usual dose/route          Side effects              Contraindications

Infliximab   3 mg/kg i.v infusion at   Infusion reactions,       Active
(Anti-TNF)   wks 0,2 and 6 followed    increased risk of         infections,uncontrolled
             by maintainence dosing    infection, reactivation   DM,surgery(with hold for 2
             every 8 wks               of TB ,etc                wks post op)
             Has to be combined
             with MTX.


Etanercept   25 mg s/c twice a wk      Injection site            Active
                                       .
                                       reaction,URTI ,
(Anti-TNF)   May be given with MTX                               infections,uncontrolled
             or as monotherapy.        reactivation of           DM,surgery(with hold for 2
                                       TB,development of         wks post op)
                                       ANA,exacerbation
                                       of demyelenating
                                       disease.



Adalimumab   40 mg s/c every 2     Same as that of               Active infections
(Anti-TNF)   wks(fornightly)       infliximab
             May be given with MTX
             or as monotherapy
Agent           Usual                Side effects             Contraindications
                  dose/route

  Anakinra        100 mg s/c once       Injection site            Active infections
   (Anti-IL-1)    daily                 pain,infections,
                  May be given with     neutropenia
                  MTX or as
                  monotherapy.

Abatacept         . mg/ kg body wt.
                  10                   Infections, infusion     Active infection
(CTLA-4-IgG1      At 0, 2 , 4 wks &    reactions                TB
Fusion protien)   then 4wkly                                    Concomittant with other
Co-stimulation                                                  anti-TNF-α
inhibitor


Rituximab         1000 mg iv at        Infusion reactions       Same as above
(Anti CD20)       0, 2, 24 wks         Infections


Tocilizumab       4-8 mg/kg            Infections, infusion     Active infections
( Anti IL-6)      8 mg/kg iv monthly   reactions,dyslipidemia
2012 ACR Update
How to monitor Tt in RA?
   Disease activity is assesed by several parameters…
    duration of morning stiffness,tender joint count,swollen
    joint count,observer global assessment,patient global
    assessment,visual analogue scale for pain,health
    assessment questionnaire,ESR,NSAID pill count,DAS
    score etc..
•   Patient on MTX,SSZ or leflunamide show clinical
    improvement in 6-8 wks.
•   Patient should be observed for 6 months before
    declaring a DMARD ineffective.
How long should Tt. be continued?
   Once remission is achieved , maintenance dose for
    long period is recommended.
   Relapse occurs in 3-5 months (1-2 months in case of
    MTX) if drug is discontinued in most instances.
   DMARDs are discontinued by patients because of
    toxicity or secondary failure(common after 1-2 yrs)
    and such patients might have to shift over different
    DMARDs over 5-10 yrs.
   Disease flare may require escalation of DMARD dose
    with short course of steroids.
Surgical Approaches
   Synovectomy is ordinarily not recommended for patients with
    rheumatoid arthritis, primarily because relief is only transient.
   However, an exception is synovectomy of the wrist, which is
    recommended if intense synovitis is persistent despite medical
    treatment over 6 to 12 months. Persistent synovitis involving
    the dorsal compartments of the wrist can lead to extensor
    tendon sheath rupture resulting in severe disability of hand
    function.
   Total joint arthroplasties , particularly of the knee, hip, wrist,
    and elbow, are highly successful.
    Other operations include release of nerve entrapments (e.g.,
    carpal tunnel syndrome), arthroscopic procedures, and,
    occasionally, removal of a symptomatic rheumatoid nodule.
Thank you.

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Rheumatoid arthritis current diagnosis and treatment

  • 1. Rheumatoid Arthritis Diagnosis and Current Management Dr. Ankur Nandan Varshney Institute of Medical Sciences Banaras Hindu University
  • 2. Introduction  Commonest inflammatory joint disease seen in clinical practice affecting approx 1% of population.  Chronic multisystem disease of unknown cause.  Characterized by persistent inflammatory synovitis leading to cartilage damage, bone erosions, joint deformity and disability.
  • 3. Onset  Although Rheumatoid arthritis may present at any age, patients most commonly are first affected in the third to sixth decades.  Female: male 3:1  Initial pattern of joint involvement could be:- 1) Polyarticular : most common 2) Oligoarticular 3) Monoarticular  Morning joint stiffness > 1 hour and easing with physical activity is characteristic.  Small joints of hand and feet are typically involved.
  • 4. Clinical Manifestations  Articular  Extra-articular
  • 5. Articular manifestation  Pain in affected joint aggravated by movemnt is the most common symptom.  Morning stiffness ≥1 hr  Joints involved -
  • 6. Relative incidence of joint involvement in RA  MCP and PIP joints of hands & MTP of feet 90%  Knees, ankles & wrists- 80%  Shoulders- 60%  Elbows- 50%  TM, Acromio - clavicular & SC joints- 30%
  • 7. Joints involved in RA  Don’t forget the cervical spine!! Instability at cervical spine can lead to impingement of the spinal cord.  Thoracolumbar, sacroiliac, and distal interphalangeal joints (DIP)of the hand are NOT involved.
  • 9. Ulnar Deviation, MCP Swelling, Left Wrist Swelling
  • 10.
  • 11.
  • 12. Extra-articular  manifestations Present in 30-40%  May occur prior to arthritis  Patients that are more likely to get are:  High titres of RF/ anti-CCP  HLA DR4+  Male  Early onset disability  History of smoking
  • 13. Extraarticular Involvement  Constitutional symptoms ( most common)  Rheumatoid nodules(30%)  Hematological-  normocytic normochromic anemia  leucocytosis /leucopenia  thrombocytosis  Felty’s syndrome-  Chronic nodular Rheumatoid Arthritis  Spleenomegaly  Neutropenia
  • 14. Respiratory- pleural effusion, pneumonitis , pleuro-pulmonary nodules, ILD  CVS-asymptomatic pericarditis , pericardial effusion, cardiomyopathy  Rheumatoid vasculitis- mononeuritis multiplex, cutaneous ulceration, digital gangrene, visceral infarction  CNS- peripheral neuropathy, cord-compression from atlantoaxial/midcervical spine subluxation, entrapment neuropathies  EYE- kerato cunjunctivitis sicca, episcleritis, scleritis
  • 16. Laboratory investigations in RA  CBC- TLC, DLC, Hb, ESR & GBP  Acute phase reactants  Rheumatoid Factor (RF)  Anti- CCP antibodies
  • 17. Rheumatoid Factor (RF)  Antibodies that recognize Fc portion of IgG  Can be IgM , IgG , IgA  85% of patients with RA over the first 2 years become RF+ • A negative RF may be repeated 4-6 monthly for the first two year of disease, since some patients may take 18-24 months to become seropositive. • PROGNISTIC VALUE- Patients with high titres of RF, in general, tend to have POOR PROGNOSIS, MORE EXTRA ARTICULAR MANIFESTATION.
  • 18. Causes of positive test for RF  Rheumatoid arthritis  Sjogrens syndrome  Vasculitis such as polyarteritis nodosa  Sarcoidosis  Systemic lupus erythematosus  Cryoglobulinemia  Chronic liver disease  Infections- tuberculosis , bacterial endocarditis, infectious mononucleosis, leprosy, syphilis, leishmaniasis.  Malignancies  Old age(5% women aged above 60)
  • 19. Anti-CCP  IgG against synovial membrane peptides damaged via inflammation  Sensitivity (65%) & Specificity (95%)  Both diagnostic & prognostic value  Predictive of Erosive Disease  Disease severity  Radiologic progression  Poor functional outcomes
  • 20. Acute Phase Reactants Positive acute phase reactants (↑) Negative acute phase reactants (↓) Mild elevations – Albumin – Ceruloplasmin – Transferrin – Complement C3 & C4 Moderate elevations – Haptoglobulin – Fibrinogen (ESR) – α 1 – acid glycoprotein – α 1 – proteinase inhibitor Marked elevations – C-reactive protein (CRP) – Serum amyloid A protein
  • 21.  Elevated APRs( ESR, CRP )  Thrombocytosis  Leukocytosis  ANA  30-40%  Inflammatory synovial fluid  Hypoalbuminemia
  • 22. Radiographic Features  Peri-articular osteopenia  Uniform symmetric joint space narrowing  Marginal subchondral erosions  Joint Subluxations  Joint destruction  Collapse  Ultrasound detects early soft tissue lesions.  MRI has greatest sensitivity to detect synovitis and marrow changes.
  • 23.
  • 24.
  • 25.
  • 27. ACR Criteria (1987)  1.Morning Stiffness ≥1 hour  2.Arthritis of ≥ 3 joints observed by physician simulteneously- Rt/Lt-PIP, MCP,wrist, elbow, knee, ankle, MTP  3.Arthritis of hand joints-PIP,MCP,wrist  4. Symmetric arthritis  5. Rheumatoid nodules  6. Positive Rheumatoid Factor  7. Radiographic Erosions or periarticular osteopenia in hand or wrist joints  Criteria 1-4 must be present for ≥6 wks  Must have ≥4 criteria to meet diagnosis of RA
  • 28. 2010 ACR/EULAR Classification Criteria  a score of ≥6/10 is needed for classification of a patient as having definite RA  A. Joint involvement SCORE  1 large joint 0  2−10 large joints 1 1−3 small joints (with or without involvement of large joints) 2  4−10 small joints (with or without involvement of large joints) 3  >10 joints (at least 1 small joint)†† 5  B. Serology (at least 1 test result is needed for classification)  Negative RF and negative ACPA 0  Low-positive RF or low-positive ACPA 2  High-positive RF or high-positive ACP 3  C. Acute-phase reactants (at least 1 test result is needed for classification)  Normal CRP and normal ESR 0  Abnormal CRP or normal ESR 1
  • 30. Goals of management  Focused on relieving pain  Preventing damage/disability  Patient education about the disease  Physical Therapy for stretching and range of motion exercises  Occupational Therapy for splints and adaptive devices  Treatment should be started early and should be individualised .  EARLY AGGRESSIVE TREATEMNT
  • 31. Treatment modalities for RA  NSAIDS  Steroids  DMARDs  Immunosuppressive therapy  Biological therapies  Surgery
  • 32. NSAIDS Non-Steroidal anti-inflammatories (NSAIDS) / Coxibs for symptom control 1) Reduce pain and swelling by inhibiting COX 2) Do not alter course of the disease. 3) Chronic use should be minimised. 4) Most common side effect related to GI tract.
  • 33. Corticosteroids in RA  Corticosteroids , both systemic and intra-articular are important adjuncts in management of RA.  Indications for systemic steroids are:- 1. For treatment of rheumatoid flares. 2. For extra-articular RA like rheumatoid vasculitis and interstitial lung disease. 3. As bridge therapy for 6-8 weeks before the action of DMARDs begin. 4. Maintainence dose of 10mg or less of predinisolone daily in patients with active RA. 5. Sometimes in pregnancy when other DMARDs cannot be used.
  • 34. Disease Modifying Anti-rheumatic Agents  Drugs that actually alter the disease course .  Should be used as soon as diagnosis is made.  Appearance of benefit delayed for weeks to months.  NSAIDS must be continued with them until true remission is achieved .  Induction of true remission is unusual .
  • 35. DMARDs Commonly used Less commonly used Methotrexate Chloroquine Hydroxychloroquine Gold(parenteral &oral) Sulphasalazine CyclosporineA Leflunomide D-penicillamine/bucillamine Minocycline/Doxycycline Levamisole Azathioprine,cyclophosphamide, chlorambucil
  • 36. Clinical information about DMARDs NAME DOSE SIDE EFFECTS MONITORING ONSET OF ACTION 1) Hydroxycloro 200mg twice daily Skin pigmentation Fundoscopy& 2-4 months quine x 3 months, then , retinopahy perimetry yearly once daily ,nausea, psychosis, myopathy 2) Methotrexate 7.5-25 mg once a GI upset, Blood counts,LFT 1-2 months week orally,s/c or hepatotoxicity, 6-8 weekly,Chest i/m Bone marrow x-ray annually, suppression, urea/creatinine 3 pulmonary monthly; fibrosis Liver biopsy
  • 37. Clinical information about DMARDs contnd.. NAME DOSE SIDE EFFECTS MONITORING ONSET OF ACTION 3)Sulphasala- 2gm daily p.o Rash, Blood counts 1-2 months myelosuppression, ,LFT 6-8 weekly zine may reduce sperm count 4)Leflunomide Loading 100 mg Nausea,diarrhoea, LFT 6-8 weekly 1-2 months daily x 3 days, alopecia, then 10-20 mg hepatotoxicity daily p.o
  • 38. When to start DMARDs?  DMARDs are indicated in all patients with RA who continue to have active disease even after 3 months of NSAIDS use.  The period of 3 months is arbitary & has been chosen since a small percentage of patients may go in spontaneous remission.  The vast majority , however , need DMARDs and many rheumatologists start DMARDs from Day 1.
  • 39. How to select DMARDs?  There are no strict guidelines about which DMARDs to start first in an individual.  Methotrexate has rapid onset of action than other DMARD.  Taking in account patient tolerance, cost considerations and ease of once weekly oral administration METHOTREXATE is the DMARD of choice, most widely prescribed in the world.
  • 40. Should DMARDs be used singly or in combination?  Since single DMARD therapy (in conjunction with NSAIDS) is often only modestly effective , combination therapy has an inherent appeal.  DMARD combination is specially effective if they include methotrexate as an anchor drug.  Combination of methotrexate with leflunamide are synergestic since there mode of action is different.
  • 41. Limitations of conventional DMARDs 1) The onset of action takes several months. 2) The remission induced in many cases is partial. 3) There may be substantial toxicity which requires careful monitoring. 4) DMARDs have a tendency to lose effectiveness with time-(slip out).  These drawbacks have made researchers look for alternative treatment strategies for RA- The Biologic Response Modifiers.
  • 42. Immunosuppresive therapy Agent Usual dose/route Side effects Azathioprine 50-150 mg orally GI side effects , myelosuppression, infection, . Cyclosporin A 3-5 mg/kg/day . Nephrotoxic , hypertension , hyperkalemia Cyclophosphamide 50 -150 mg orally Myelosuppression , gonadal toxicity ,hemorrhagic cystitis , bladder cancer
  • 43. BIOLOGICS IN RA  Cytokines such as TNF-α ,IL-1,IL-10 etc. are key mediators of immune function in RA and have been major targets of therapeutic manipulations in RA.  Of the various cytokines,TNF-α has attaracted maximum attention.  Various biologicals approved in RA are:- 1) Anti TNF agents : Infliximab Etanercept Adalimumab 2) IL-1 receptor antagonist : Anakinra 3) IL-6 receptor antagonist : Tocilizumab 4) Anti CD20 antibody : Rituximab 5) T cell costimulatory inhibitor : Abatacept
  • 44. Agent Usual dose/route Side effects Contraindications Infliximab 3 mg/kg i.v infusion at Infusion reactions, Active (Anti-TNF) wks 0,2 and 6 followed increased risk of infections,uncontrolled by maintainence dosing infection, reactivation DM,surgery(with hold for 2 every 8 wks of TB ,etc wks post op) Has to be combined with MTX. Etanercept 25 mg s/c twice a wk Injection site Active . reaction,URTI , (Anti-TNF) May be given with MTX infections,uncontrolled or as monotherapy. reactivation of DM,surgery(with hold for 2 TB,development of wks post op) ANA,exacerbation of demyelenating disease. Adalimumab 40 mg s/c every 2 Same as that of Active infections (Anti-TNF) wks(fornightly) infliximab May be given with MTX or as monotherapy
  • 45. Agent Usual Side effects Contraindications dose/route Anakinra 100 mg s/c once Injection site Active infections (Anti-IL-1) daily pain,infections, May be given with neutropenia MTX or as monotherapy. Abatacept . mg/ kg body wt. 10 Infections, infusion Active infection (CTLA-4-IgG1 At 0, 2 , 4 wks & reactions TB Fusion protien) then 4wkly Concomittant with other Co-stimulation anti-TNF-α inhibitor Rituximab 1000 mg iv at Infusion reactions Same as above (Anti CD20) 0, 2, 24 wks Infections Tocilizumab 4-8 mg/kg Infections, infusion Active infections ( Anti IL-6) 8 mg/kg iv monthly reactions,dyslipidemia
  • 47.
  • 48. How to monitor Tt in RA?  Disease activity is assesed by several parameters… duration of morning stiffness,tender joint count,swollen joint count,observer global assessment,patient global assessment,visual analogue scale for pain,health assessment questionnaire,ESR,NSAID pill count,DAS score etc.. • Patient on MTX,SSZ or leflunamide show clinical improvement in 6-8 wks. • Patient should be observed for 6 months before declaring a DMARD ineffective.
  • 49. How long should Tt. be continued?  Once remission is achieved , maintenance dose for long period is recommended.  Relapse occurs in 3-5 months (1-2 months in case of MTX) if drug is discontinued in most instances.  DMARDs are discontinued by patients because of toxicity or secondary failure(common after 1-2 yrs) and such patients might have to shift over different DMARDs over 5-10 yrs.  Disease flare may require escalation of DMARD dose with short course of steroids.
  • 50. Surgical Approaches  Synovectomy is ordinarily not recommended for patients with rheumatoid arthritis, primarily because relief is only transient.  However, an exception is synovectomy of the wrist, which is recommended if intense synovitis is persistent despite medical treatment over 6 to 12 months. Persistent synovitis involving the dorsal compartments of the wrist can lead to extensor tendon sheath rupture resulting in severe disability of hand function.  Total joint arthroplasties , particularly of the knee, hip, wrist, and elbow, are highly successful.  Other operations include release of nerve entrapments (e.g., carpal tunnel syndrome), arthroscopic procedures, and, occasionally, removal of a symptomatic rheumatoid nodule.

Editor's Notes

  1. Figure 68.7 Boutonnière and swan-neck deformities. The boutonnière deformity - PIP flexion and DIP hyperextension - results from relaxation of the central slip, with 'buttonholing' of the PIP joint between the lateral bands. The swan-neck deformity - MCP flexion, PIP hyperextension and DIP flexion - may be mobile, snapping or fixed. Its pathogenesis may be related primarily to PIP or MCP involvement. Combinations of MCP and PIP involvement are less frequent. (Adapted with permission from Hastings DE and Welsh RP. Surgical reconstruction of the rheumatoid hand. Toronto: Orthopaedic Medical Management Corporation; 1979.)