Arthritis

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Description of arthritis in comprehensive manner

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  • Destructive effects of TNF
    TNF triggers multiple destructive effects in RA. In part, it stimulates osteoclasts to resorb bone, ultimately resulting in bone erosions visible on x-ray.1 TNF also induces the proliferation of synoviocytes, which in turn produces inflammation due to the release of inflammatory mediators.2,3 As depicted here, inflammation not only causes pain and swelling but also has been shown to precede joint damage.2,4 Chondrocytes are a third target of TNF activation, producing collegenase that degrades cartilage and eventually causes joint space narrowing.1,5
    In addition to these effects, TNF plays an early role in the inflammatory process by stimulating activation of T cells by foreign antigens.2,3 TNF also induces expression of adhesion molecules, thereby promoting the migration of macrophages and lymphocytes into the synovium.5
     
    References: 1. Goronzy JJ, Weyand CM. Rheumatoid arthritis: epidemiology, pathology, and pathogenesis. In: Klippel JH, ed. Primer on the Rheumatic Diseases. 11th ed. Atlanta, Ga: Arthritis Foundation; 1997:155-174. 2. Carpenter AB. Immunology and inflammation. In: Wegener ST, ed. Clinical Care in the Rheumatic Diseases. Atlanta, Ga: American College of Rheumatology; 1996:9-14. 3. Albani S, Carson DA. Etiology and pathogenesis of rheumatoid arthritis. In: Koopman WJ, ed. Arthritis and Allied Conditions: A Textbook of Rheumatology. Vol 1. 13th ed. Baltimore, Md: Williams & Wilkins; 1997:979-992. 4. McGonagle D, Conaghan PG, O'Connor P, et al. The relationship between synovitis and bone changes in early untreated rheumatoid arthritis: a controlled magnetic resonance imaging study. Arthritis Rheum. 1999;42:1706-1711. 5. Rosenberg AE. Skeletal system and soft tissue tumors. In: Cotran RS, ed. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, Pa: W.B. Saunders Company; 1994:1213-1271.
  • Characteristics of JIA
    To be considered JIA, onset must occur before 16 years of age.
    JIA is heterogeneous: the presentation of the disease and its natural history vary among individuals and over time.
    The disease is typically classified into categories based on the symptoms displayed and their severity:
    - Systemic arthritis
    - Oligoarthritis
    - Rheumatoid-factor positive (RF+) polyarthritis
    - Rheumatoid-factor negative (RF-) polyarthritis
    - Enthesitis-related arthritis (inflammation of tendons and ligaments at the site of connection to bone)
    - Psoriatic arthritis
    - Undifferentiated
    References:
    Goldmuntz EA, White PH. Juvenile idiopathic arthritis: a review for the pediatrician. Pediatr Rev 2005;27(4):e24-25. PMID: 16581950.
    http://www.ncbi.nlm.nih.gov/pubmed?term=16581950
    Kemper A, Coeytaux R, Sanders G, et al. Disease-Modifying Antirheumatic Drugs (DMARDs) in Children With Juvenile Idiopathic Arthritis (JIA). Comparative Effectiveness Review No. 28 (Prepared by the Duke Evidence-based Practice Center under Contract No. HHSA 290-2007-10066-I). Rockville, MD: Agency for Healthcare Research and Quality; September 2011. AHRQ Publication No. 11-EHC039-EF. Available at www.effectivehealthcare.ahrq.gov/dmardsjia.cfm.
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  • ANIMATED SLIDE (CLICK FOR EACH BULLET POINT)
    Perceptions about AS are still wrong today. Physicians diagnose AS late, because they think it is rare, not a serious disease and that patients don’t die as a result of the disease. Patients often seek care late for the same reasons.
  • Pictures are from the CRI website (http://www.cri-net.com/) and are free for use
    IRM des sacro-iliaques – Rehaussement du signal après injection de gadolinium témoignant de l’existence d’une sacro-iliite droite (spondylarthrite ankylosante débutante)
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  • 2 first Pictures come from following website: http://www.rheumatologie-berlin.de/probability/early.php?m_id=9&s_id=91, the third one from the CRI website (http://www.cri-net.com/)
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  • Dactylitis=painfull swelling of the whole digit caused by inflammation
  • Pictures from the CRI website (http://www.cri-net.com/)
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  • Currently, there is a long delay, from 5 to 10 years, between the first occurrence of AS symptoms and a diagnosis of AS. Two major reasons can be named for such a delay:
    There is certainly a low awareness of AS among nonrheumatologists and it can be seen as a major challenge for any physician in primary care to think of and to identify patients with inflammatory spine disease among the large group of patients with chronic back pain, most often of another origin.
    (b) Radiographic sacroiliitis grade 2 bilaterally or grade 3 or 4 unilaterally is usually a requirement for making the diagnosis of AS according to the modified New York criteria.
    However, radiographic changes indicate chronic changes and damage of the bone and are the consequence of inflammation and not active inflammation itself. Since AS is a slowly progressing disease as far as radiographic changes are concerned, definite sacroiliitis on plain radiographs appears relatively late, frequently taking several years of continuous or relapsing inflammation
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  • Sensitivity 82.9%, specificity 84.4%; n=649 patients with chronic back pain and age at onset <45 yrs.
    Imaging arm (sacroiliitis) alone has a sensitivity of 66.2% and a specificity of 97.3%. ** Note: Elevated CRP is considered
    a SpA feature in the context of chronic back pain
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  • Since the BASDAI and BASFI alone do not give a complete disease measurement assessment of the AS patient, the ASAS response criteria was developed. In essence, this combines aspects of the BASDAI and BASFI into one criteria.
    ABSTRACT from A&R article follows:
    Objective. To develop criteria for symptomatic improvement in patients with ankylosing spondylitis (AS), using outcome domain data from placebo controlled clinical trials of nonsteroidal anti-inflammatory drugs (NSAIDs).
    Methods. Patient data from 5 short-term, randomized, controlled trials were used to assess equivalence, reliability, and responsiveness of multiple items in the 5 outcome domains for AS treatment: physical function, pain, spinal mobility, patient global assessment, and inflammation. At least one measure per domain was responsive (standardized response mean of >0.5), except for the spinal mobility domain, which was omitted from the criteria. We developed and tested candidate improvement criteria in a random two-thirds subset from the 3 largest trials and used the remaining one-third for validation. These 3 largest trials included 923 patients (631 receiving NSAIDs, 292 in placebo groups). We selected the multiple domain definition that best distinguished NSAID treatment from placebo by chi-square test and that had a placebo response rate of <25%. Results. Candidate definitions were changes in single domains and in multiple measure indices, as well as combinations of improvements in multiple domains. Worsening in a domain was defined as a change for the worse of >20% and a net change for the worse of >10 units on a scale of 0–100. Partial remission (for comparison purposes) was defined as an end-of-trial value of <20/100 in each of the 4 domains. Among 20 candidate criteria, change of >20% and >10 units in each of 3 domains and absence of worsening in the fourth discriminated best in the development subset (51% of patients improved with NSAIDs, 25% with placebo; x2 5 36.4, P < 0.001). Results were confirmed in the validation subset. Almost all patients satisfying the definition of partial disease remission at the end of the trial had also improved by this criterion. Among all 923 patients, improvement rates using this criterion were 49% for NSAID-treated patients and 24% for placebo-treated patients. Conclusion. Although further validation using data from new trials is still needed, we conclude that we have developed a clinically valid, easy-to-use measure of short-term improvement in AS.
  • PsA is one of a group of disorders known as the spondyloarthropathies. PsA is a chronic, progressive inflammatory disorder affecting the joints and skin characterized by osteolysis and bony proliferation. C
    PsA can range from mild and non-destructive in nature to a severely rapid and destructive arthropathy. Radiographic damage can be noted in up to 47% of patients at a median interval of two years despite clinical improvement on standard DMARD therapy.
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  • Signs and symptoms of PsA in include morning stiffness lasting >30 minutes in 50% of patients, nail involvement in up to 90% of patients (as compared to 40% of psoriasis patients). Patients may present with joint deformity and less pain than is usually seen in RA. Dactylitis may be noted in >40% of patients, eye inflammation in 7-33% of cases. Finally, distal extremity swelling with pitting edema has been reported in 20% of patients as the first isolated manifestation of PsA.
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    ########## Presentation updated on Monday, 16 March, 2009 by KAB3 ##########
    ########### Presentation updated on Wednesday, 4 August, 2010 ###########
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    ########### Presentation 'PsA Optimize_core_18SEP08_WIRE.ppt' created on Thursday, 18 September, 2008 ###########
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    Medical Review: No Slide: 5/68
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    ########### Presentation updated on Wednesday, 4 August, 2010 ###########
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  • Two important features of PsA that cause significant problems for PsA patetients. Data to be shared later will show significant benefit of anti-tnf therapy in this regard.
  • Dactylitis is characterized by swelling of a digit and may be acute with painful inflammatory changes, or chronic changes where the digit remains swollen despite the disappearance of acute inflammation. Digits with dactylitis are referred to as sausage digits. Dactylitis is recognized as one of the cardinal features of PsA, occurring in up to 40% of patients. Feet are most commonly affected. Dactylitis-involved digits show more radiographic damage.
    Shown here is psoriasis involving the first, third and fourth toes accompanied by PsA of the interphalangeal joints of the third and fourth toes and dactylitis. The “sausage shape” of these toes is caused by soft-tissue swelling.
  • Entheses are the regions at which a tendon, ligament, or joint capsule attaches to bone. The entheses act to dissipate biomechanical stress and are subjected to repeated microtraumas. Inflammation at the entheses is called enthesitis and is a hallmark feature of PsA. The pathogenesis of enthesitis has yet to be fully elucidated. Isolated peripheral enthesitis may be the only rheumatologic sign of PsA in a subset of patients.
  • Psoriatic arthritis is an inflammatory disease, the manifestations of which may include:
    Inflammatory arthritis which over time typically progresses to involve greater numbers of joints and can result in joint damage in over 40% of patients
    Psoriasis
    Diffuse swelling of the fingers and toes known as dactylitis
    Enthesitis, which is the inflammation of the point of insertion of tendons, ligaments or joint capsules into bone. Shown here is swelling in the ankle region resulting from the inflammation of the Achilles tendon at the point of insertion into the heel. This is a common site of enthesopathy.
  • 1Moll JMH, Wright V. Psoriatic arthritis. Semin Arthritis Rheum 1973;3:55-78
    2Gladman DD et al. Q J Med. 1987;62(238):127-41
    3Torre Alonso JC et al. Br J Rheumatol. 1991;30(4):245-50
    4Helliwell PS & Taylor WJ, Ann Rheum Dis 2005;64:3-8
    5 Gladman et al. Derm therapy 2009;22:40-55
    It is important to note that since the original Moll and Wright publication of 1973, the proportion of each subgroup has been changed. The symmetric polyarthritis in the original publication was only 15% and now was shown to be the predominant group. The last 3 bullet points are as in Moll&Wright’s ref.
    Helliwell & Taylor, ARD, 2005: Fig.1 shows different distributions of Sym. PolyA and Asym. OligoA according to different references.
    For a recent review on SUBTYPES of PsA, PsA classification and a suggestion for a NEW classification, check out Coates & Helliwell, Clinical Rheumatology, July 2008.
    Ref1973 Moll1987 Gladman1991 Torre
    -----------------------------------------------------------------------------------------------------------------------------
    DIP<5%DIP involvement
    found in all groups-----------------------------------------------------------------------------------------------------------------------------
    Arth. Mutilans5%4%
    -----------------------------------------------------------------------------------------------------------------------------
    Symmetric Arth.15% (= PolyA?)30.5% sym PolyA*37% OligoA
    + 36% PolyA
    No differentiation
    ------------------------------------------------------------------------------------------------between symA and
    Asymmetric Arth.>70% OligoA28% Asym. OligoAasymA.
    + MonoA+ 30.5% asym PolyA*
    -----------------------------------------------------------------------------------------------------------------------------
    Ankyl.Arth.5%23% SpondA
    -----------------------------------------------------------------------------------------------------------------------------
    HLA-B27Not mentionedNot mentioned
    ########## Presentation updated on Wednesday, 4 August, 2010 by GIB1 ##########
    ########## Presentation updated on Thursday, 18 September, 2008 by ANDO ##########
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    associated with SpondA
    -----------------------------------------------------------------------------------------------------------------------------
    *Torre, 1991, talks about 61% PolyA, with equal repartition of sym.A and asymA.
     
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  • Juxtaarticular: The prefix "juxta-" comes from the Latin preposition meaning near, nearby, close.
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    ########### Presentation updated on Wednesday, 4 August, 2010 ###########
    Author: GIB1 Purpose: Optimize slide decks QA: 04-Aug-10 Review By: 04-Feb-11
    Review Type: Scientific, Reference Check, Compliance Review and HCC Office Slide: 18/108 Golimumab-Specific Deck: Yes
    ########### Presentation 'PsA Optimize_core_18SEP08_WIRE.ppt' created on Thursday, 18 September, 2008 ###########
    Author: ANDO QC&C: 18-Sep-08 Review By: 18-Mar-09
    Medical Review: No Slide: 7/68
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  • Triad = Reiter’s syndrome
    KB = hyperkeratotic lesions on the palms of hands and soles of feet
  • NSAIDS first for mild disease
    DMARDS for >5 jt involvement – start w/ MTX, then add LEF, then add TNF a inh.
  • ACR response slide included in RA presentation
  • Arthritis

    1. 1. Sushil Paudel, MS Orthopaedics (AIIMS) TUTH
    2. 2. Types of arthritis Symptoms of arthritis Signs of arthritis Treatment of arthritis
    3. 3. Rheumatoid arthritis (RA) Osteoarthritis (OA) Sero-negative arthritis  Ankylosing spondylitis  Psoriatic arthritis  Reactive arthritis  Enteropathic arthritis Crystal arthropathies
    4. 4. stands for :  A: ALIGNMENT  B: BONY MINERALIZATION  C: CARTILAGE SPACE  D: DISTRIBUTION  S: SOFT TISSUE
    5. 5. Normal joint structure
    6. 6. NORMAL SUBCHONDRAL BONE DESTRUCTION
    7. 7.  A chronic joint disorder in which there is progressive softening and disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes) and capsular fibrosis
    8. 8. Primary or idiopathic Secondary  Infection  Dysplasia  Perthes  SCFE  Trauma  AVN
    9. 9. Genetic Metabolic Hormonal Mechanical Ageing
    10. 10. Disparity between:- stress applied to articular cartilage and strength of articular cartilage
    11. 11. Increased stress (F/A) Increased load eg BW or activity Decreased area eg varus knee or dysplastic hip
    12. 12. Weak cartilage age stiff eg ochronosis soft eg inflammation abnormal bony support eg AVN
    13. 13. Joint space narrowing Osteophytosis Subchondral cysts Subchondral sclerosis
    14. 14.  Femoral neck buttressing  Tilt deformity ( flattening of head surface with osteophyte at anteroinferior aspect)  Superior >medial migration  Secondary OA due to previous trauma or inflammatory arthritis
    15. 15.  Erect weight-bearing AP film  Unicompartmental  Sharpening of tibial prominence  Loose bodies  Varus deformity  Patellar tooth sign – irregular anterior patellar surface
    16. 16. OA Affecting Foot
    17. 17.  Vacuum Phenomenon  Accumulation of Nitrogen  Degenarative etiology  Better seen in Extension  Excludes infective etiology  In peripheral joints physiological
    18. 18. SPGR T1W
    19. 19. SPGR T2 FATSAT
    20. 20. pain swelling stiffness deformity instability loss of function
    21. 21. Analgesia Oral viscosupplements Intrarticular steroids Intrarticular viscosupplements Altered activity Walking aids Physiotherapy
    22. 22. arthroscopy osteotomy arthrodesis excision arthroplasty replacement arthroplasty
    23. 23.  Bilateral symmetry  Periarticular soft tissue swelling  Uniform joint space loss  Marginal erosions  Juxta-articular osteoporosis  Joint deformity
    24. 24.  Inflammation ◦ Swollen ◦ Stiff ◦ Sore ◦ Warm  Fatigue  Potentially Reversible
    25. 25. RA
    26. 26.  Boutonniere deformity : flexion deformity at PIP jt & hyperextension at DIP • Swan neck deformity : combination of flexion at DIP and extension at PIP
    27. 27. B/L KNEE ANKYLOSIS RA
    28. 28. RA-foot deformity
    29. 29.  Atlantodental interspace > 3.0mm  Odontoid erosions  Subluxation  Pseudo basilar invagination  Reduced disc space  Apophyseal joint: erosion, sclerosis, ankylosis  Sharpened pencil spinous process
    30. 30. ADI > 3.0mm
    31. 31. Soft tissue swelling Rotator cuff rupture Head erosions Tapered distal clavicle due to erosions Irregular coracoid process
    32. 32.  Enlarged Olecranon bursa  Fat pad sign  Supinator notch sign: erosion at proximal ulna
    33. 33. RA-ELBOW
    34. 34. Uniform bicompartmental joint space loss Patellofemoral joint also involved Soft tissue swelling Baker’s cyst Subchondral cysts
    35. 35. T1W T1GRE
    36. 36. ◦ Rheumatoid arthritis is a synovial disease -Osteoarthritis is a disease of the cartilage. -Volar subluxation never in osteoarthritis Normal joint
    37. 37. Unicompartmental Bicompartmental
    38. 38.  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!
    39. 39. NSAIDS Steroids Oral Intra-articular DMARDS Synthetic Methotrexate Hydroxychloroquine Leflunomide Sulfasalazine
    40. 40.  Monoclonal Antibodies to TNF ◦ Infliximab ◦ Adalimumab  Soluble Receptor Decoy for TNF ◦ Etanercept  Receptor Antagonist to IL-1 ◦ Anakinra  Monoclonal Antibody to CD-20 ◦ Rituximab
    41. 41.  Cyclo-oxygenase inhibitors  Do not slow the progression of the disease  Provide partial relief of pain and stiffness
    42. 42. Disease Modifying Anti-Rheumatic Drugs  Reduce swelling & inflammation  Improve pain  Improve function  Have been shown to reduce radiographic progression (erosions)
    43. 43.  Dihydrofolate reductase inhibitor  ↓ thymidine & purine nucleotide synthesis  “Gold standard” for DMARD therapy  7.5 – 30 mg weekly  Absorption variable  Elimination mainly renal
    44. 44.  Hepatotoxicity  Bone marrow suppression  Dyspepsia, oral ulcers  Pneumonitis  Teratogenicity  Folic acid reduces GI & BM effects  Monitoring ◦ FBC, ALT, Creatinine
    45. 45.  Sulphapyridine + 5-aminosalicylic acid  Remove toxic free radicals  Remission in 3-6 month
    46. 46.  Elimination hepatic  Dyspepsia, rashes, BM suppression
    47. 47.  Mechanism unknown ◦ Interference with antigen processing ? ◦ Anti- inflammatory and immunomodulatory • For mild disease
    48. 48. Side effects  Irreversible Retinal toxicity, corneal deposits  Ophthalmologic evaluation every 6 months
    49. 49.  Competitive inhibitor of dihydroorotate dehydrogenase (rate-limiting enzyme in de novo synthesis of pyrimidines)  Reduce lymphocyte proliferation
    50. 50.  Oral  T ½ - 4 – 28 days due to EHC  Elimination hepatic  Action in one month  Avoid pregnancy for 2 years
    51. 51.  Hepatotoxicity  BM suppression  Diarrhoea  rashes
    52. 52.  Triple Therapy ◦ Methotrexate, Sulfasalazine, Hydroxychloroquine  Double Therapy ◦ Methotrexate & Leflunomide ◦ Methotrexate & Sulfasalazine ◦ Methotrexate & Hydroxychloroquine
    53. 53. • Complex protein molecules • Created using molecular biology methods • Produced in prokaryotic or eukaryotic cell cultures
    54. 54.  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)
    55. 55. Trans-Membrane Bound TNF Soluble TNF Strategies for Reducing Effects of TNF Macrophage Monoclonal Antibody (Infliximab & Adalimumab)
    56. 56.  Infection ◦Common (Bacterial) ◦Opportunistic (Tb)  Demyelinating Disorders  Malignancy  Worsening CHF
    57. 57.  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)
    58. 58.  Most common childhood chronic disease causing disability.  About 7/100,00 newly diagnosed children with JIA per year.  Prevalence about 1/1,000 children = 1,000 children in BC with JIA.  7 subtypes.  Disease begins at any time during childhood or adolescence.
    59. 59.  To be considered JIA, onset must occur before 16 years of age.  JIA is heterogeneous: the presentation of the disease and its natural history vary among individuals and over time.  The disease is typically classified into categories based on the symptoms displayed and their severity.  Systemic arthritis  Oligoarthritis  Rheumatoid-factor positive (RF+) polyarthritis  Rheumatoid-factor negative (RF-) polyarthritis  Enthesitis-related arthritis  Psoriatic arthritis  Undifferentiated G.ahrq.gov/dmardsjia.cfm.
    60. 60.  Child under 16 years old  At least one joint with objective signs of arthritis: › Swelling, or two of the following: pain with movement, warmth of the joint, restricted movement, or tenderness  Duration of more than 6 weeks  Other causes have been excluded (ex. Infections, Lupus and other connective tissue diseases, malignancies)
    61. 61.  All kids with JIA have fevers.  All kids with JIA have rashes.  A child with joint pain (but no arthritis) must have JIA.  All arthritis is painful.  If a child has a positive rheumatoid factor, they must have arthritis.  If x-rays are normal, there is no arthritis.
    62. 62.  Heterogeneous group of diseases characterized by chronic inflammatory processes involving the synovial membrane, cartilage, and bone  The classification of JIA subgroups based on clinical and laboratory characteristics including the number of affected joints and the presence of autoimmune markers  Th1 cell-mediated disorder, driven by a population of T cells producing inflammatory cytokines and chemokines
    63. 63.  Joint pain, stiffness, and swelling: These are the most common symptoms of JRA, but many children do not recognize, or do not report, pain. Stiffness and swelling are likely to be more severe in the morning.  Loss of joint function: Pain, swelling, and stiffness may impair joint function and reduce range of motion. Some children are able to compensate in other ways and display little, if any, disability. Severe limitations
    64. 64.  Limp: A limp may indicate a particularly severe case of JRA, although it also may be due to other problems that have nothing to do with arthritis, such as an injury. In JRA, a limp often signals knee involvement.
    65. 65.  Eye irritation, pain, and redness: These symptoms are signs of eye inflammation. The eyes may be sensitive to light. In many cases, however, eye inflammation has no symptoms. If the inflammation is very severe and not reversed, it can cause loss of vision. The most common types of eye
    66. 66.  Recurrent fevers: Fever is high and comes and goes with no apparent cause. Fever may “spike” (go high) as often as several times in one day.  Rash: A light rash may come and go without explanation.
    67. 67.  Myalgia (muscle aches): This is similar to that achy feeling that comes with the flu. It usually affects muscles throughout the whole body, not just one part.
    68. 68.  Lymph node swelling. Swollen lymph nodes are noticed most often in the neck and under the jaw, above the clavicle, in the armpits, or in the inguinal region.  Weight loss. This is common in children with JRA. It may be due to the child’s simply not feeling like eating.
    69. 69.  Growth problems: Children with JRA often grow more slowly than average. Growth may be unusually fast or slow in an affected joint, causing one arm or leg to be longer than the other. General growth abnormalities may be related to having a chronic inflammatory condition such as JRA or to the treatment, especially glucocorticoids
    70. 70.  ANA (antinuclear antibody)  RF (Rheumatoid factor )  CRP (C-reactive protein)  ESR (erythrocyte sedimentation rate)  CCP (Cyclic Citrullinated Peptide Antibody) test
    71. 71.  The goals: eliminate active disease, normalize joint function, preserve normal growth, prevent long-term joint damage, and prevent patient disability  The American College of Rheumatology Pediatric 30 criteria (ACR Pedi 30) defines improvement as involving at least 3 of 6 core set variables, with no more than 1 of the remaining variables worsening by > 30%.
    72. 72.  The 6 core set includes ◦ Physician global assessment ◦ active joint count ◦ number of joints with limited range of motion ◦ Inflammatory markers ◦ patient or parent assessments
    73. 73. Medication s Doses (mg/kg) Side effects Aspirin 50-120 Stomack pain, vomiting, gastrointestinal bleedings, headache, blood in the urine, fluid retention, thinning and scarring of the skin (especially with naproxen), stomach ulcer (aspirin). Ibuprofen 10-30 Tolmentin 10-15 Naproxen 5-20
    74. 74. Medications Doses (mg/kg) Side effects Hydroxychlo- roquine (Plaquenil) 5-7 Upset stomach, skin rash and a eye damage. A child who takes this drug should have his/her eyes examined at least every six months by an ophthalmologist Sulfasalazine (Azulfadine)
    75. 75. Medication s Doses(weekly, depending from body weight ) Side effects Auranofin, Ridaura, Myochrysine Solganol 20 kg – 10 mg 30 kg – 20 mg 40 kg – 30 mg 50 kg – 40 mg > 50 kg – 50 mg Skin rash, mouth sores, kidney problems, a low blood count or anemia
    76. 76. Medication s Doses Side effects Methotrexate (Rbeumatrex) Azathioprine (Imuran) Cyclophospha mide (Cytoxan) Typically 7.5 to 25 mg a week Loss of appetite, nausea or vomiting, skin rash, unusual bleeding or bruising, tiredness or weakness, sterility.
    77. 77.  Biologic Agents, which blocks the protein TNF Etanercept (Enbrel) Infliximab (Remicade)  Glucocorticoid Drugs (Dexamethasone, Methylprednisolone, Cortef, Prednisolone and Prednisone)  Analgesics (acetaminophen [Tylenol, Panadol], tramadol [Ultram])
    78. 78.  Therapeutic exercises  Sports and Recreational Activities  Splints
    79. 79.  Morning Stiffness Relief  Diet  Eye Care  Dental Care  Surgery
    80. 80. .
    81. 81.  Identify diagnostic criteria for gout  Identify 3 treatment goals for gout  Name the agents used to treat the acute flares of gout and the chronic disease of gout
    82. 82.  Prevalence increasing  May be signal for unrecognized comorbidities : ( Not to point of searching) Obesity (Duh!) Metabolic syndrome DM HTN CV disease Renal disease
    83. 83.  ORGAN MEATS  WILD GAME  SEAFOOD  LENTILS  PEAS  ASPARAGUS  YEAST  BEER Rich foods have a higher concentration of protein. This could cause major problems for a person afflicted with gout.
    84. 84.  Urate: end product of purine metabolism  Hyperuricemia: serum urate > urate solubility (> 6.8 mg/dl)  Gout: deposition of monosodium urate crystals in tissues
    85. 85.  Hyperuricemia caused by Overproduction Underexcretion  No Gout w/o crystal deposition
    86. 86.  Urate  Oevrproduction Underexcretion  Hyperuricemia  ________________________________________  Silent Gout Renal Associated  Tissue manifestations CV events &  Deposition mortality
    87. 87.  Purines are not properly processed in our body  Excreted through kidneys and urine  Hyperuricemia- build-up of uric acid in body and joint fluid
    88. 88.  Asymptomatic hyperuricemia  Acute Flares of crystallization  Intervals between flares  Advanced Gout & Complications
    89. 89.  Abrupt onset of severe joint inflammation, often nocturnal; Warmth, swelling, erythema, & pain; Possibly fever  Untreated? Resolves in 3-10 days  90% 1st attacks are monoarticular  50% are podagra
    90. 90.  90% of gout patients eventually have podagra : 1st MTP joint
    91. 91.  Can occur in other joints, bursa & tendons
    92. 92.  Asymptomatic  If untreated, may advance  Intervals may shorten  Crystals in asx joints  Body urate stores increase
    93. 93.  Chronic Arthritis  X-ray Changes  Tophi Develop  Acute Flares continue
    94. 94.  Chronic Arthritis  Polyarticular acute flares with upper extremities more involved
    95. 95.  Solid urate deposits in tissues
    96. 96.  Irregular & destructive
    97. 97.  Long duration of hyperuricemia  Higher serum urate  Long periods of active, untreated gout
    98. 98.  Hx & P.E.  Synovial fluid analysis  Not Serum Urate
    99. 99.  Not reliable  May be normal with flares  May be high with joint Sx from other causes
    100. 100.  Male  Postmenopausal female  Older  Hypertension  Pharmaceuticals: Diuretics, ASA, cyclosporine
    101. 101.  Transplant  Alcohol intake Highest with beer Not increased with wine  High BMI (obesity)  Diet high in meat & seafood
    102. 102.  The Gold standard  Crystals intracellular during attacks  Needle & rod shapes  Strong negative birefringence
    103. 103.  Acute Gout: septic arthritis, pseudogout, Reactive arthritis, acute rheumatic fever and other crystalline arthropathies.  Chronic tophaceus gout: Rheumatoid Arthritis, Pseudogout, seronegative spondyloarthropathies and erosive osteoarthritis.
    104. 104.  Similar Acute attacks  Different crystals under Micro; Rhomboid, irregular in CPPD
    105. 105.  Both have polyarticular, symmetric arthritis  Tophi can be mistaken for RA nodules
    106. 106.  Diet is usually impractical, ineffective and rarely adhered to in clinical practice.  Indications for pharmacological therapy includes: inability to reverse secondary causes, tophaceus gout, recurrent acute gout and nephrolithiasis.
    107. 107. 139 •Treat acute flare rapidly with anti- inflammatory agent •Initiate urate-lowering therapy to achieve sUA <6 •Use concomitant anti-inflammatory prophylaxis for up to 6 mo to prevent mobilization flares INITIATE (acute flare) RESOLVE (urate-lowering therapy) 139 •Continue urate lowering therapy to control flares and avoid crystal deposition •Prophylaxis use for at least 3-6 months until sUA normalizes MAINTAIN (treatment to control sUA)
    108. 108.  Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation  Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause
    109. 109.  Control inflammation & pain & resolve the flare  Not a cure  Crystals remain in joints  Don’t try to lower serum urate during a flare  Choice of med not as critical as alacrity & duration
    110. 110.  NSAIDS  Colchicine  Corticosteroids
    111. 111. Colchicine- reduces pain, swelling, and inflammation; pain subsides within 12 hrs and relief occurs after 48 hrs Prevent migration of neutrophils to joints
    112. 112. Side effects  Nausea  Vomiting  Diarrhea  Rahes
    113. 113.  Colchicine : Not as effective “late” in flare Drug interaction : Statins, Macrolides, Cyclosporine Contraindicated in dialysis pt.s Cautious use in : renal or liver dysfunction; active infection, age > 70
    114. 114.  The choice of pharmacologic agent depends on severity of the attack ◦ Monotherapy for mild/moderate attack ◦ Combination therapy for severe attack or those refractory to monotherapy  Acceptable combination therapy approaches include ◦ Colchicine and NSAIDS ◦ Oral steroids and colchicine ◦ Intra-articular steroids with all other modalities  Continue current therapy during flare  Patient education on signs of flare for self treatment 146Kanna D, et al. Arthritis Care Res (Hoboken). 2012 Oct;64(10):1447-61
    115. 115.  Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation  Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause
    116. 116.  Hyperuricemia ≠ Gout  Goal sUA < 6  Use prophylaxis for at least 3 months after initiating gout therapy  Do not stop gout medication unless patient is showing evidence of drug toxicity or adverse reaction  Ask your friendly rheumatologist for help! 148
    117. 117.  Colchicine : 0.5-1.0 mg/day  Low-dose NSAIDS  Both decrease freq & severity of flares  Prevent flares with start of urate-lowering RX Best with 6 mos of concommitant RX  Won’t stop destructive aspects of gout
    118. 118.  Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation  Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause
    119. 119.  Lower urate to < 6 mg/dl : Depletes Total body urate pool Deposited crystals  RX is lifelong & continuous  MED choices : Uricosuric agents Xanthine oxidase inhibitor
    120. 120.  Probenecid, (Losartan & fenofibrate for mild disease)  Increased secretion of urate into urine  Reverses most common physiologic abnormality in gout ( 90% pt.s are underexcretors)
    121. 121.  Patients taking uricosuric agents are at risk for urolithiasis. This can be decreased by ensuring high urinary output and by adding sodium bicarbonate 1 gram TID.  The available agents include: probenecid (1-2 g/day) and sulfinpyrazone (50-400 mg BID).  Dose should be increased to decrease uric acid < 6.0 mg/ml
    122. 122.  Allopurinol :  Blocks conversion of hypoxanthine to uric acid  Effective in overproducers  May be effective in underexcretors  Can work in pt.s with renal insufficiency
    123. 123. 158 hypoxanthine uratexanthine XO XO XO=xanthine oxidase Allopurinol and febuxostat inhibit xanthine oxidase and block uric acid formation Markel A. IMAJ, 2005. 158
    124. 124.  Oxypurinol, allopurinol metabolite, cleared by kidney and accumulates in patients with renal failure  Oxypurinol inhibits xanthine oxidase  Increased oxypurinol related to risk of allopurinol hypersensitivity syndrome allopurinol oxypurinol Xanthine Oxidase Stevens- Johnson Syndrome Allopurinol Hypersensitivity Syndrome Toxic Epidermal Necrolysis 159
    125. 125.  Allopurinol decreases uric acid in overproducers and underexcreters; it is also indicated in patients with a history of urolithiasis, tophaceus gout, renal insufficiency and in prophylaxis of tumor lysis syndrome.
    126. 126.  Allopurinol: usual dose is 300 mg/day. Maximal recommended dose is 800 mg/day.  In renal insufficiency dose should be decreased to 200 mg/day for creatinine clearance < 60ml/min and to 100 mg/day if clearance < 30 ml/min).
    127. 127.  Start with small doses of allopurinol to reduce the risk of precipitating an acute gout attack.  Most common side effects are rash (2% of patients) but rarely patients can develop exfoliative dermatitis that can be lethal.  Chronic use of colchicine (0.6-1.2 mg/day) is used as prophylaxis for acute attacks.
    128. 128.  2% of all allopurinol users develop cutaneous rash  Frequency of hypersensitivity 1 in 260  DRESS syndrome ◦ Drug Reaction, Eosinophilia, Systemic Symptoms  20% mortality rate  Life threatening toxicity: vasculitis, rash, eosinophilia, hepatitis, progressive renal failure  Treatment: early recognition, withdrawal of drug, supportive care ◦ Steroids, N-acetyl-cysteine, dialysis prn Markel A. IMAJ, 2005. Terkeltaub RA, in Primer on the Rheumatic Disease, 13th ed. 2008. 163
    129. 129.  Base choice on above considerations & whether pt is an overproducer or underexcretor : Need to get a 24-hr. urine for urate excretion: < 700 --- underexcretor (uricosuric) > 700 --- overproducer (allopurinol/ febuxostat)
    130. 130. Allopurinol Uricosuric Issue in renal disease X X Drug interactions X X Potentially fatal hypersen- sitivity syndrome X Risk of nephrolithiasis X Mutiple daily dosing X
    131. 131.  RX gaps :  Can’t always get urate < 6  Allergies  Drug interactions  Allopurinol intolerance  Worse Renal disease
    132. 132.  Non-purine selective inhibitor of xanthine oxidase  Lowers serum uric acid levels more potently than allopurinol while having minimal effects on other enzymes associated with purine and pyrimide metabolism  Frequent adverse events reported in clinical trials liver function abnormalities, nausea, arthralgias, and rash  Available as 40- and 80-mg tablets  Recommended starting dosage is 40 mg orally once daily. If serum uric acid concentrations are not less than 6 mg/dL after two weeks, the dosage can be increased to 80 mg orally once daily  Dosage adjustments are not needed in elderly patients or patients with mild or moderate renal or hepatic impairment. .
    133. 133.  Therapeutic goal of urate-lowering therapy is sUA <6.0 mg/dL  Urate lowering therapy indications: ◦ Recurrent gout attacks ◦ Tophi and/or radiographic changes on initial presentation  Address associated risk factors and comorbidities – tailor to the individual 168 Zhang W, et al. Ann Rheum Dis. 2006; 65: 1312-1324. 168
    134. 134.  Lifestyle Modification for all patients with gout  Xanthine Oxidase Inhibitor (XOI) first-line urate-lowering pharmacologic therapy  Target sUA <6 at minimum, sUA <5 better  Starting dose of allopurinol should be 100mg, less in CKD with titration above 300mg prn if needed (even in CKD)  Continue prophylaxis for 3 (no tophi) – 6 months (tophi) after achieving target sUA 169Khanna D, et al. Arthritis Care Res . 2012 Oct;64(10):1431-46
    135. 135.  Gout is chronic with 4 stages  Uncontrolled gout can lead to severe disease  Separate RX for flares & preventing advancement  Many meds for flares  Treating the disease requires lowering urate  Get a 24-hr urine for urate excretion
    136. 136.  Calcium pyrophosphate Crystal Deposition Disease (CPPD) is the syndrome secondary to the calcium pyrophosphate in articular tissues.  This includes: Chondrocalcinosis, Chronic CPPD and Pseudogout.
    137. 137.  Etiology: It is unknown, but can be secondary to changes in the cartilage matrix or secondary to elevated levels of calcium or inorganic pyrophosphate.  Pathology: CPPD crystals are found in the joint capsule and fibrocartilaginous structures. There is neutrophil infiltration and erosions.
    138. 138.  Demographics: It is predominantly a disease of the elderly, peak age 65 to 75 years old. It has female predominance (F:M, 2-7:1).  Prevalence of chondrocalcinosis is 5 to 8% in the general population.
    139. 139.  Disease Associations: hyperthyroidsm, hypocalciuria, hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidsm, gout, neuropathic joints, amyloidosis, trauma and OA.
    140. 140.  Clinical Manifestations  Pseudogout: Usually presents with acute self- limited attacks resembling acute gout. The knee is involved in 50% of the cases, followed by the wrist, shoulder, ankle, and elbow.
    141. 141.  In 5% of patients gout can coexist with pseudogout.  The diagnosis is confirmed with the synovial fluid analysis and/or the presence of chondrocalcinosis in the radiographs.  Acute Pseudogout primarily affects men.
    142. 142.  Chondrocalcinosis: Generally is an incidental finding in XRays.  Diagnostic Tests: Inflammatory cell count in the synovial fluid. Rhomboidal or rodlike intracellular crystals. Imaging studies reveal chondrocalcinosis usually in the knee, but can be seen in the radial joint, symphisis pubis and intervertebral discs.
    143. 143.  Chronic CPPD: predominately affects women; it is a progressive, often symmetric, polyarthritis.  Usually affects the knees, wrists, 2nd and 3rd MCP’s, hips, spine, shoulders, elbows and ankles.  Chronic CPPD differs from pseudogout in its chronicity, involvement of the spine and MCP’s.
    144. 144.  Differential Diagnosis: Includes septic arthritis, gout, inflammatory OA, Rheumatoid Arthritis, neuropathic arthritis and Hypertrofic Osteoarthropathy.
    145. 145.  Therapy: It is similar to gout and includes intrarticular corticosteroids. Colchicine can be used in acute attacks and also in prophylaxis. There is no specific treatment for chronic CPPD. It is important to treat secondary causes and colchicine could be helpful.
    146. 146.  HLA B-27  Enthesitis  Synovitis  Osteitis
    147. 147. Spondyloarthropathies Axial and Peripheral AMOR criteria (1990) ESSG criteria (1991) Axial Spondyloarthritis ASAS classification 2009 Ankylosing spondylitis Prototype of axial spondylitidis Modified New York criteria 1984 Peripheral Spondyloarthritis ASAS classification 2010 Psoriatic arthritis From Moll & Wright 1973 to CASPAR criteria 2006 Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44 Taylor et al. Arthritis & Rheum 2006;54:2665-73 Van der Heijde et al. Ann Rheum Dis 2011;70:905-8 ESSG: European Spondyloarthropathy Study Group ASAS: Assessment of Spondyloarthritis International Society CASPAR: Classification criteria for psoriatic arthritis Infliximab (IFX) and Golimumab (GLM) indications
    148. 148.  AS is a chronic, progressive immune-mediated inflammatory disorder that results in ankylosis of the vertebral column and sacroiliac joints1  The spine and sacroiliac joints are the common affected sites1 ◦ Chronic spinal inflammation (spondylitis) can lead to fusion of vertebrae (ankylosis)1 1 Taurog JD. et al. Harrison‘s Principles of Internal Medicine, 13 th Ed. 1994: 1664-67.
    149. 149. Normal interspace 2-5mm B/L symmetric Lower two third Rosary bead appearance Reactive sclerosis Bony ankylosis osteoporosis SACROILITIS
    150. 150.  Romanus lesion(erosion)  Squaring, Osteoporosis  Shiny corner sign  Marginal Syndesmophytes  Bamboo spine  Trolley-track sign  Dagger sign SPINE
    151. 151. • Mortality figures parallel RAMortality figures parallel RA6,7,86,7,8  ““Rare”Rare”  ““Not” a serious disease, functional limitation isNot” a serious disease, functional limitation is mildmild  ““Rarely shortens life”Rarely shortens life” • Burden of disease significant in pain, sick leave, early retirementBurden of disease significant in pain, sick leave, early retirement3,4,53,4,5 • 0.1-0.9%0.1-0.9%1,21,2 11 Sieper J et al.Sieper J et al. Ann Rheum Dis.Ann Rheum Dis. 2002; 61 (suppl 3);iii8-18.2002; 61 (suppl 3);iii8-18. 22 Lawrence RC., Arthritis Rheum 1998; 41:778-99.Lawrence RC., Arthritis Rheum 1998; 41:778-99. 33 Zink A., et al.,Zink A., et al., J RheumatolJ Rheumatol 2000; 27:613-22.2000; 27:613-22. 44 Boonen A.Boonen A. Clin Exp RheumatolClin Exp Rheumatol. 2002;20(suppl 28):S23-S26.. 2002;20(suppl 28):S23-S26. 55 Gran JT, et al.Gran JT, et al. Br J RheumatolBr J Rheumatol. 1997;36:766-771.. 1997;36:766-771. 66 Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94.Wolfe F., et al. Arthritis Rheum. 1994 Apr;37(4):481-94. 77 Myllykangas-Luosujarvi R, et al.Myllykangas-Luosujarvi R, et al. Br J Rheumatol.Br J Rheumatol. 1998;37:688-690.1998;37:688-690. 88 Khan MA, et al.Khan MA, et al. J Rheumatol.J Rheumatol. 1981;8:86-90.1981;8:86-90. 99 Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22.Braun J., Pincus T., Clin Exp Rheumatol. 2002; 20(6 Suppl 28):S16-22.
    152. 152.  The incidence of AS may be underestimated due to unreported cases1  HLA-B27 gene is associated with AS6  Age of onset typically between 15 and 35 years1,2,3  2-3 times more frequent in men than in women6 1 The Spondylitis Association of America. Available at: www.spondylitis.org. Accessed December 2,2004. 61(suppl 3);iii8–18. 6 Khan MA. Ann Intern Med. 2002;136:896–907.
    153. 153. Axial manifestations: • Chronic low back pain • With or without buttock pain • Inflammatory characteristics: – Occurs at night (second part) – Sleep disturbance – Morning stiffness • Limited lumbar motion • Onset before age of 40 years Sengupta R & Stone MA. Inflammatory back pain (IBP) = Characteristic symptom MRI sacro-iliac joint
    154. 154. AS: Characteristic Pathologic FeaturesAS: Characteristic Pathologic Features Sieper J. Arthritis Res Ther 2009;11:208 Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035 • Chronic inflammation in: – Axial structures (sacroiliac joint, spine, anterior chest wall, shoulder and hip) – Possibly large peripheral joints, mainly at the lower limbs (oligoarthritis) – Entheses (enthesitis) • Bone formation particularly in the axial joints
    155. 155. Most striking feature of AS = New bone formation in the spine with: Spinal syndesmophytes Ankylosis Both can be seen on conventional radiography Bamboo spine and bilateral sacroiliitis X-ray showing syndesmophytes Even in patients with longer- standing disease, syndesmophytes are present in ~ 50% patients and a smaller percentage will develop ankylosis Sieper J. Arthritis Res Ther 2009;11:208
    156. 156. Marginal erosions and new bone formation
    157. 157. Unilateral sacroiliitis
    158. 158. Peripheral manifestations Enthesitis Peripheral arthritis Dactylitis 1 Cruyssen BV et al. Ann Rheum Dis 2007;66:1072-1077 2 Sidiropoulos PI et al. Rheumatology 2008;47:355-361 2
    159. 159. The first abnormality to appear in swollen joints associated with spondyloarthropathies is an enthesitis2 Likelihood of erosions is higher for digits with dactylitis than those without1 1 Brockbank. Ann Rheum Dis 2005;62:188-90; 2 McGonagle et al. The Lancet 1998;352.
    160. 160. EAM Prevalence in AS Patients (%) Anterior uveitis 30-50 IBD 5-10 Subclinical inflammation of the gut 25-49 Cardiac abnormalities Conduction disturbances Aortic insufficiency 1-33 1-10 Psoriasis 10-20 Renal abnormalities 10-35 Lung abnormalities Airways disease Interstitial abnormalities Emphysema 40-88 82 47-65 9-35 Bone abnormalities Osteoporosis Osteopenia 11-18 39-59 Elewaut D & Matucci MC. Rheumatology 2009;48:1029-1035 Terminal ileitis Anterior uveitis Cardiac abnormalities
    161. 161. Bad QoL1 ◦ Pain ◦ Sleep problems ◦ Fatigue ◦ Loss of mobility and dependency ◦ Loss of social life Effect employability1 Higher rate of mortality2 High socio-economic consequences AS=23.7 years 90.2 83.1 62.4 54.1 0 20 40 60 80 100 Stiffness Pain Fatigue Poor SleepN=175 AS mean duration: 23.7 yr PercentageofPatients(%) 1
    162. 162. Adapted from Feldtkeller E et al. Rheumatol Int 2003;23:61–66 Sengupta R & Stone MA. Nat Clin Pract Rheumatol 2007;3:496-503 First symptoms First diagnosis Age in years Males (n=920) Females (n=476) 0 0 10 20 30 40 50 60 70 20 40 80 60 100 PercentageofPatients(%) Average delay in diagnosis: 8.8 years B27(+) 8.5 vs B27(-) 11.4 Delay  Worse clinical outcomes contributing to both physical and work-related disability
    163. 163.  Modified New York Criteria for AS1 ◦ Low back pain > 3 months (improved by exercise and not relieved by rest) ◦ Limitation of lumbar spinal motion in sagittal and frontal planes ◦ Chest expansion decreased relative to normal ◦ Bilateral sacroilitis grade 2-4 or unilateral sacroilitis grade 3 or 4  Detection of sacroilitis via X-ray or MRI1 ◦ MRI can be used for earlier detection of inflammation (enthesitis) at other sites.  There is no specific laboratory test for AS1 ◦ ESR and CRP can indicate inflammation  50-70% of active AS patients will have increased ESR and CRP2 ◦ Rheumatoid factor is not associated with AS ◦ HLA-B27 1 Khan M, Ankylosing Spondylitis-the facts; 2002:Oxford University Press:94-98. 2 Sieper J, et al. Ann Rheum Dis. 2002;61(Suppl 8).
    164. 164. Diagnostic Standard for AS: Modified NYDiagnostic Standard for AS: Modified NY Classification Criteria (1984)Classification Criteria (1984)11 • Clinical components: – Low back pain and stiffness for more than 3 months which improves with exercise, but is not relieved by rest – Limitation of motion of the lumbar spine in both the sagittal and frontal planes – Limitation of chest expansion relative to normal values correlated for age and sex • Radiological component: – Sacroiliitis Grade >2 bilaterally or Grade 3-4 unilaterally Definite AS if the radiological criterion is associated with at least one clinical criterion2 Probable AS if three clinical criteria present or radiologic criteria present without clinical criteria2 1 Linden VD et al. Arthritis Rheum 1984;27:361-368 2 Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008 • Old criteria • Defined before TNF blockers • Sacroiliitis detectable by X-ray occurs lately • No magnetic resonance imaging (MRI) • Used for clinical trial
    165. 165. Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008 Brandt HC et al. Ann Rheum Dis 2007;66:1479-84 Time (years) Back Pain Syndesmophytes Radiographic stage (Ankylosing Spondylitis) Back Pain Radiographic sacroiliitis Modified NY criteria (1984) Diagnostic Standard for AS: Modified NYDiagnostic Standard for AS: Modified NY Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d) The greatest problem in the management of AS was the lack of effective treatments. In recent years, NSAIDs and TNF-blockers have been shown to have good efficacy in the treatment of AS.
    166. 166. Adapted from Rudwaleit M et al. Arthritis Rheum 2005;52:1000-1008 Time (years) Back Pain IBP MRI active sacroiliitis Back Pain Syndesmophytes Radiographic stage (Ankylosing Spondylitis) Pre-radiographic stage (Axial undifferentiated SpA) Back Pain Radiographic sacroiliitis Modified NY criteria (1984) Diagnostic Standard for AS: Modified NYDiagnostic Standard for AS: Modified NY Classification Criteria (1984) (Cont’d)Classification Criteria (1984) (Cont’d) • Recent application of MRI techniques has demonstrated (and confirmed) that ongoing active (“acute”) inflammation in fact does occur in the sacroiliac joints and/or spine prior to the appearance of changes detectable radiographically • The presence and absence of radiographic sacroiliitis in patients with SpA represent different stages of a single disease continuum
    167. 167. In patients with back pain ≥3 months and age at onset <45 years Sacroiliitis* on imaging plus ≥1SpA feature** HLA-B27 plus ≥2 other SpA features** **SpA features: •Inflammatory back pain •Arthritis •Enthesitis (heel) •Uveitis •Dactylitis •Psoriasis •Crohn’s disease/ulcerative colitis •Good response to NSAIDs •Family history for SpA •HLA-B27 •Elevated CRP *Sacroiliitis on imaging: •Active (acute) inflammation on MRI highly suggestive of sacroiliitis associated with SpA or •Definite radiographic sacroiliitis according to modified New York criteria Rudwaleit M et al. Ann Rheum Dis 2009;68(6):770-6 OR
    168. 168.  Patients will be categorized as an ASAS 20 responder if the patient achieves the following: ◦ >20% improvement from baseline and absolute baseline improvement of >10 (on a 0-100mm scale) in at least 3 of the following 4 domains:  Patient global assessment  Spinal pain  Function (BASFI)  Inflammation  Average of the last 2 BASDAI questions concerning level and duration of morning stiffness ◦ No deterioration from baseline (>20% and absolute change of at least 10 on a 0-100 mm scale) in the potential remaining domain Anderson JJ, et al. Arthritis Rheum. 2001;44(8):1876–1886.
    169. 169.  Chronic progressive, inflammatory disorder of the joints and skin1 ◦ Characterized by osteolysis and bony proliferation1 ◦ Clinical manifestations include dactylitis, enthesitis, osteoperiostitis, large joint oligoarthritis, arthritis mutilans, sacroiliitis, spondylitis, and distal interphalangeal arthritis1  PsA is one of a group of disorders known as the spondyloarthropathies2  Males and females are equally affected3  PsA can range from mild nondestructive disease to a severely rapid and destructive arthropathy3 ◦ Usually Rheumatoid Factor negative3  Radiographic damage can be noted in up to 47% of patients at a median interval of two years despite clinical improvement with standard DMARD therapy4 1 Taylor WJ. Curr Opin Rheumatol. 2002;14:98–103. 2 Mease P. Curr Opin Rheumatol. 2004;16:366–370. 3 Brockbank J, et al. Exp Opin Invest Drugs. 2000;9:1511–1522. 4 Kane D, et al. Rheumatology. 2003;42:1460–1468.
    170. 170. Spondyloarthritis (SpA)  The prevalence of SpA is comparable to that of RA (0.5–1.9%)1,2 Psoriasis (Pso)  Psoriasis affects 2% of population  7% to 42% of patients with Pso will develop arthritis3 Psoriatic Arthritis  A chronic and inflammatory arthritis in association with skin psoriasis4  Usually rheumatoid factor (RF) negative and ACPA negative5 ◦ Distinct from RA  Psoriatic Arthritis is classified as one of the subtypes of spondyloarthropathies ◦ Characterized by synovitis, enthesitis, dactylitis, spondylitis, skin and nail psoriasis4 1 Rudwaleit M et al. Ann Rheum Dis 2004;63:535-543; 2 Braun J et al. Scand J Rheumatol 2005;34:178-90; 3 Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009; 4 Mease et al. Ann Rheum Dis 2011;70(Suppl 1):i77–i84. doi:10.1136/ard.2010.140582; 5 Pasquetti et al. Rheumatology 2009;48:315–325 Juvenile SpA Reactive arthritis Arthritis associated with IBD PsA Undifferentiated SpA (uSpA) Ankylosing spondylitis (AS) RA: Rheumatoid arthritis
    171. 171.  Affects men & women equally  Occurs in 4-6% up to 30% of patients with known psoriasis ◦ 60 – 70%: Skin psoriasis first ◦ 15%: Psoriatic arthritis first ◦ 15%: Skin and arthritis diagnosed at same time
    172. 172.  Prevalence of psoriasis in the general population: 0.1-2.8%.  Prevalence of psoriasis in arthritis patients: 2.6-7.0%.  Prevalence of arthritis in the general population: 2-3%.  Prevalence of arthritis in psoriatic patients: 6- 42%. Epidemiological Evidence
    173. 173.  Morning stiffness lasting >30 min in 50% of patients1  Ridging, pitting of nails, onycholysis – up 90% of patients vs nail changes in only 40% of psoriasis cases2,3  Patients may present with less joint tenderness than is usually seen in RA1  Dactylitis may be noted in >40% of patients2,4  Eye inflammation (conjunctivitis, iritis, or uveitis) — 7–33% of cases; uveitis shows a greater tendency to be bilateral and chronic when compared to AS2  Distal extremity swelling with pitting edema has been reported in 20% of patients as the first isolated manifestation of PsA5 1 Gladman DD. In: Up To Date. Available at: www.uptodate.com. Accessed December 3, 2004. 2 Taurog JD. In: Harrison's Online McGrawHill. Available at: http://www3.accessmedicine.com/popup.aspx? aID=94996&print=yes. Accessed January 2,2005. 3 Gladman DD. Rheum Dis Clin N Amer. 1998;24:829–844. 4 Veale D, et al. Br J Rheumatol. 1994;33:133–38. 5 Cantini F, et al. Clin Exp Rheumatol. 2001;19:291–296.
    174. 174. Helliwell PS & Taylor WJ. Ann Rheum Dis 2005;64(2:ii)3-8 Fitzgerald “Psoriatic Arthritis” in Kelley’s Textbook of Rheumatology, 2009 *Low levels of RF and ACPA can be found in 5-16% of patients; **To a lesser degree than in RA ***Spinal disease occurs in 40-70% of PsA patients
    175. 175. 1 Gladman D et al. Arth & Rheum 2007;56:840; 2 Kane. D et al. Rheum 2003;42:1460-1468 3 Gladman D et al. Ann Rheum Dis 2005;64:188–190; 4 Lawry M. Dermatol Ther 2007;20:60- 67 Enthesopathy (38%)2 Dactyilitis (48%)3 DIP involvement (39%)2 Back involvement (50%)1 Nail psoriasis (80%)4, 5 SkinInvolvement In nearly 70% of patients, cutaneous lesions precede the onset of joint pain, in 20% arthropathy starts before skin manifestations, and in 10% both are concurrent. 6 DIP: Distal interphalangeal
    176. 176. Pso patients6-8 • Psychosocial burden • Reactive depression • Higher suicidal ideation • Alcoholism  Metabolic Syndrome3-5 • Hyperlipidemia • Hypertension • Insulin resistent • Diabetes • Obesity ⇒ Higher risk of Cardiovascular disease (CVD) Ocular inflammation1 (Iritis/Uveitis/ Episcleritis) IBD2 1 Qieiro et al. Semin Arth Rheum 2002;31:264; 2 Scarpa et al. J Rheum 2000;27:1241; 3 Mallbris et al. Curr Rheum Rep 2006;8:355; 4 Neimann et al. J Am Acad Derm 2006;55:829; 5 Tam et al. 2008;47:718; 6 Kimball et al. Am J Clin Dermatol 2005;6:383-392; 7 Naldi et al. Br J Dermatol 1992;127:212-217; 8 Mrowietz U et al. Arch Dermatol Res 2006;298(7):309-319
    177. 177. D a c t y lit is E n t h e s it is P s o r ia t ic A r t h r it is Ritchlin C. J Rheumatol. 2006;33:1435–1438. Helliwell PS. J Rheumatol. 2006;33:1439–1441.
    178. 178. ACR Slide Collection on the Rheumatic Diseases; 3rd edition. 1994. 1 Brockbank J, et al. Ann Rheum Dis. 2005;64:188–190. 2 Veale D, et al. Br J Rheumatol. 1994;33:133–38. • Diffuse swelling of a digit may be acute, with painful inflammatory changes, or chronic wherein the digit remains swollen despite the disappearance of acute inflammation1 • Also referred to as “sausage digit”1 • Recognized as one of the cardinal features of PsA, occurring in up to 40% of patients1,2 • Feet most commonly affected1 • Dactylitis involved digits show more radiographic damage1
    179. 179.  Entheses are the regions at which a tendon, ligament, or joint capsule attaches to bone1  Inflammation at the entheses is called enthesitis and is a hallmark feature of PsA1,2  Pathogenesis of enthesitis has yet to be fully elucidated2  Isolated peripheral enthesitis may be the only rheumatologic sign of PsA in a subset of patients3 1 McGonagle D. Ann Rheum Dis. 2005;64(Suppl II):ii58–ii60. 2 Anandarajah AP, et al. Curr Opin Rheumatol. 2004;16:338–343. 3 Salvarani C. J Rheumatol. 1997;24:1106–1140.
    180. 180. Achilles Tendon Insertion Erosion Plantar Spur Achilles Tendon Spur
    181. 181. ACR Slide Collection on the Rheumatic Diseases; 3rd edition. 1994. Data on file, Centocor, Inc.
    182. 182. Oligoarthritis Distal Arthritis  
    183. 183. Polyarticular Pattern
    184. 184. Arthritis Mutilans
    185. 185. Tuft resorption Periostitis
    186. 186.  Distal asymmetric distribution  Ray pattern  Soft tissue swelling( sausage/spindle)  Preserved bone density  Marginal erosions  Fluffy periosteitis
    187. 187.  Pencil in cup deformity  Mouse ear sign  Arthritis mutilans  Nonmarginal syndesmophytes  Bilateral asymmetric involvenent of SI joint
    188. 188.  Including 5 clinical patterns: ◦ Asymmetric mono-/oligoarthritis (~30% [range 12-70%])1-4 ◦ Symmetric polyarthritis (~45% [range 15-65%])1-4 ◦ Distal interphalangeal (DIP) joint involvement (~5%)1 ◦ Axial (spondylitis and Sacroiliitis) (HLA-B27) (~5%)1,3 ◦ Arthritis Mutilans (<5%)1,3 References see notes • However patterns may change over time and are therefore not useful for classification 5 HLA: Human leucocytes antigen
    189. 189. McHugh et al. Rheum 2003;42:778-783 Clinical subgroups at baseline and follow-up: Monoarthritis Monoarthritis Oligoarthritis Oligoarthritis DIP DIP Polyarthritis Polyarthritis Spondyloarthritis Spondyloarthritis Mutilans Mutilans No clinical evidence of joint disease
    190. 190.  Inflammatory articular disease (joint, spine, or entheseal)  With ≥3 points from following categories: − Psoriasis: current (2), history (1), family history (1) − Nail dystrophy (1) − Negative rheumatoid factor (1) − Dactylitis: current (1), history (1) recorded by a rheumatologist − Radiographs: (hand/foot) evidence of juxta-articular new bone formation  Specificity 98.7%, Sensitivity 91.4% Taylor et al. Arthritis & Rheum 2006;54: 2665-73
    191. 191. Spondyloarthropathies Axial and Peripheral AMOR criteria (1990) ESSG criteria (1991) Axial Spondyloarthritis ASAS classification 2009 Ankylosing spondylitis Prototype of axial spondylitidis Modified New York criteria 1984 Peripheral Spondyloarthritis ASAS classification 2010 Psoriatic arthritis From Moll & Wright 1973 to CASPAR criteria 2006 Sieper et al. Ann Rheum Dis 2009;68:ii1-ii44 Taylor et al. Arthritis & Rheum 2006;54:2665-73 Van der Heijde et al. Ann Rheum Dis 2011;70:905-8 ESSG: European Spondyloarthropathy Study Group ASAS: Assessment of Spondyloarthritis International Society CASPAR: Classification criteria for psoriatic arthritis Infliximab (IFX) and Golimumab (GLM) indications
    192. 192.  Rheumatoid Arthritis ◦ Symmetric ◦ PIP, MCP, not distal ◦ Ulnar deviation, swan neck deformities ◦ Rheumatoid nodules  Ankylosing Spondylitis ◦ Strong HLA B27 association ◦ Male predominance ◦ Axial skeletal involvement – sacroilitis ◦ Bamboo spine ◦ Schober test demonstrating limited flexion Uptodate.com
    193. 193.  Reactive Arthritis ◦ LE arthritis ◦ 1-4 weeks after an infection ◦ Infectious agents:  Shigella  Salmonella  Yersinia  Campylobacter  Chlamydia ◦ Triad: urethritis, conjunctivitis, arthritis ◦ Keratoderma Blennorhagicum  Inflammatory Bowel Disease Associated ◦ Crohn’s ◦ LE distribution AAFP
    194. 194.  Bare area erosions  Terminal tuft erosions  Ray pattern  Irregular periosteal bone apposition  Feet more severely affected than hands’  Severe bone destruction without regional osteoporosis  Subluxations
    195. 195.  1 – NSAIDS  2 – DMARDS ◦ MTX ◦ Leflunomide ◦ Sulfasalazine ◦ Cyclosporine ◦ TNF α inhibitor  Coordinate b/w Rheumatology and Dermatology
    196. 196. Psoriatic Arthritis Response Criteria (PsARC)Psoriatic Arthritis Response Criteria (PsARC) Clegg D.O. et al. Arthritis Rheum 1996;39:2013.  Clinical assessment of joint improvement, no skin assessment  Improvement in at least 2 of 4 criteria, one of which must be tender or swollen-joint score ◦ Physician global assessment (> 1 unit) ◦ Patient global assessment (> 1 unit) ◦ Tender-joint score (> 30%) ◦ Swollen-joint score (> 30%)  No worsening in any criterion
    197. 197.  Urethritis, conjunctivitis, arthritis  Lower extremity  Osteoporosis/soft tissue swelling  Uniform joint space loss  Marginal erosion/periosteitis  Asymmetric broad based nonmarginal syndesmophytes  Bilateral asymmetric involvenent of SI joint
    198. 198. Reiter’s Disease
    199. 199.  Wave like hyperostosis  Flowing ossification  >4 contiguous vertebras  Thoracic spine  ossified anterior longitudinal ligament  Normal SI joint  Normal disc space
    200. 200.  Calcification of cartilage, synovium, capsule, tendon or ligaments  More than one joint exclusive of the intervertebral disks.  Crystals aspirated from joints showing absent or weakly positive birefringence  Joint-space narrowing, sclerosis, cyst formation  Bony fragmentation, and osteophytosis
    201. 201. Cartilage calcification  Degenarative  Gout, Pseudogout  Hemochromatosis  Wilson disease  ochronosis
    202. 202.  Hypertrophic- weight bearing joints  Disorganization  Bone destruction  Dislocation  Debris  Preserved bone density  Atrophic- non weight bearing joints  Amputated/lick candy stick
    203. 203.  Syringomyelia  Syphilis  Diabetes  Leprosy  Alcoholism  Multiple sclerosis  Trauma Neuropathic joint
    204. 204. Neuropathic
    205. 205.  Disc calcification  Vaccum phenomenon  Osteophytes  Ankylosis  Osteoporosis  Key is disc changes with advanced degenarative changes in unexpected locations
    206. 206.  Childbearing female  Hands affected predominantly  Bilateral symmetry  Osteoporosis  Normal joint spaces  calcification  Ulnar drifting/deformities  Hitch-hiker’s deformity  Soft tissue atrophy
    207. 207. SLE
    208. 208.  Recurrent attacks of rheumatic fever  Deforning nonerosive peripheral arthropathy  Normal joint space  Juxta articular osteoporosis  Soft tissue swelling  Ulnar drifting  Flexion at MCP
    209. 209.  Joint pain, swelling, and limitation of motion  3-5 th decade male  Knee> hip  Multiple intraarticular calcified nodules, uniform in size  Laminated to stippled appearance  Promote early degenarative disease  Chondrosarcoma in 5%
    210. 210. Synovial Osteochondromatosis
    211. 211. PD
    212. 212. PD
    213. 213.  Benign proliferative disorder of the synovium  May affect the joints, bursae, or tendon sheaths  Preserved joint space  No osteoporosis
    214. 214. PVNS
    215. 215. Haemophilic Arthropathy
    216. 216.  Resorption of distal tuft  Retraction of fingertips <20%  Soft tissue calcification  Disuse osteoporosis  Joints may be normal or erosive arthropathy
    217. 217. SCLERODERMA
    218. 218.  Usually monoarticular  Cartilage destruction  Subchondral bone erosion  Osteoporosis  Effusion  More aggressive course & bone destruction in pyogenic  Bony ankylosis
    219. 219.  Monoarticular involvement  Soft-tissue swelling  Joint effusions  Periarticular osteopenia  Marginal erosions.  Joint space narrowing is unusual
    220. 220. TIW T2W POSTGAD
    221. 221.  Bone erosion  Marrow signal abnormalities  Extra-articular extension  Soft tissue abscess
    222. 222. Postgad
    223. 223.  Chronic hemodialysis  Plasma cell dyscrasia  Bilateral  Juxtaarticular soft-tissue masses  Periarticular osteopenia  Subchondral cysts  Joint effusions, erosions  Preserved joint spaces
    224. 224.  Synovitis  Acne  Pustulosis  Hyperostosis  Osteitis  Sternoclavicular joint>Flat bones  Recurent osteomyelitis  Hot on bone scan
    225. 225.  Gout  Neuropathic  CPPD  PVNS  Synovial Chondronatosis  Postel’s arthritis
    226. 226.  JRA  Psoriatic  Reiter’s  Hemophilia  HPA
    227. 227.  Osteoarthritis  Gout  CPPD  Psoriatic  Anktlosing Spondylitis  Neuropathic  Reiter-chronic case
    228. 228.  Rheumatoid arthritis  JRA  Infective  Haemophilia  Scleroderma  SLE
    229. 229.  CPPD  GOUT  Alkaptonuria  Haemochromatosis  Wilson  Acromegaly
    230. 230. Acromegaly Increased joint spaceIncreased joint space
    231. 231.  DEGENRATIVE  RA  CPPD  AVN
    232. 232.  Ankylosing Spondylitis  Psoriasis  Inflammatory Bowel Disease
    233. 233.  Primary OA  Rheumatoid arthritis
    234. 234. DISTAL : Psoriasis Reiter’s syndrome Osteoarthritis PROXIMAL : RA CPPD
    235. 235.  OA  RA  CPPD  Ankylosing spondylitis  Pigmented villonodular synovotis  Synovial osteochondromatosis
    236. 236.  AS  IBD  PSORIASIS  REITER’S SYNDROME  OA  INFECTION
    237. 237. Certain questions to be answered  1). It is a monoarticular / pauci/ polyarticular involvement  2). It is synovial or chondropathic  3).if polyarticular, specific distribution and pattern  4). Sacroiliac and CVJ etc.  5). Clinical presentation (history)
    238. 238.  Any monoarticular synovial jt. Involvement is assumed to be infective unless proved otherwise.  Any monoarticular chondropathic jt. is considered as degenerative.  Polyarticular jt. Involvement s/o inflammatory noninfective etiology.
    239. 239. Synovial arthropathy:  1). Periarticular osteopenia  2). Jt. Space effusion (soft tissue)  3). Erosions  4). Loss of jt. space (late feature)
    240. 240. D/D of synovial arthritis  Infection- >3month---tuberculous acute onset— pyogenic  RA  Seronegative spondyloarthritis  GOUT
    241. 241. CHONDROPATHIC ARTHROPATHY:  Loss of jt. Space  Sclerosis  Osteophytes  Subchondral cyst.
    242. 242. D/D of chondropathic arthritis  OA  GOUT  CPPD  HEMOCHROMATOSIS.
    243. 243. If Polyarticular  Distribution  Ass. Findings  Chondrocalcinosis.
    244. 244. PSO RIASIS REITER'S RA; SLE NEURO PATHIC ALIG NM ENT O A CPPD G O UT PRESERVED SUBCHO NDRAL Pyogenic G ENERALIZED CT disorders JUXTAARTICULAR RA LO ST BO NY M INERALISATIO N O A CPPD HEM O CHRO . CARTILAG E SPACE LO SS PIP RA CPPD DIP O A ; REITER'S PSO RIASIS DISTRIBUTIO N INCREASED PSO RIASIS REITER'S DECREASED SCLERO DERM A DERM ATO M YO G ENERALISED LO CALISED RA G O UT SO FT TISSUE ARTHRITIS RA JRA NFECTIVE HEMOPHILIA SLE RA JRA HEMOPHILIA INFECTIVE SLE
    245. 245. ARTHRITS Erosive Erosive+ Productive NO Erosion/ Productive Productive RA Psoriasis OA SLE Gout Reiter, AS DISH Dermatomyositis Erosive OA JRA, Neuropathic

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