rheumatology
DESCRIPTION
RheumatologyTRANSCRIPT
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ARTHRITIS Inflammation of the
Joint(over 100 specific diseases)
Rheumatoid Arthritis
Gout
Degenerative Joint Diseases
Ankylosing spondylitis
JRA
Psoriatic Arthritis
Bacterial Arthritis
Systemic Lupus Erythematosus
Scleroderma
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ARTHRITIS: Inflammation of the Joint
Pain
Swelling
Redness
Warmth
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IL-8 IL-6
GM-CSF
IL-1 TNF-
FGF
Fibroblast/ type B synovial
cells
Metalloproteinases Prostaglandins
Complement
IL-6
IL-1 IL-6
IL-8 GM-CSF M-CSF
Macrophage/ type A synovial cells
IL-1 TNF-
Adhesion molecule
expression on blood vessels
HLA-DR Complement
metalloptoteinases
CYTOKINE NETWORKS IN SYNOVITIS
+ FEEDBACK
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IL-8 IL-6
GM-CSF
IL-10
IL-1 TNF-
FGF
Fibroblast/ type B synovial
cells
Metalloproteinases Prostaglandins
Complement
IL-6
TGF-IL-4
IL-1 IL-6
IL-8 GM-CSF M-CSF
Macrophage/ type A synovial cells
IL-1 TNF-
Adhesion molecule
expression on blood vessels
HLA-DR Complement
metalloptoteinases
CYTOKINE NETWORKS IN SYNOVITIS
+ FEEDBACK
- FEEDBACK
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Points to Remember
Cells involved in Inflammation:
- macrophage, fibroblast, T-cells
Pro inflammatory cytokines:
- IL-1, TNF alpha, IL-6
- IL-8, FGF, GM-CSF
Anti inflammatory cytokine:
- IL-10, TGF-B, IL-4
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Degenerative Joint Disease / Osteoarthritis
A group of disorder in which the balance between degeneration and synthesis within the cartilage and subchondral bone is disturbed resulting to cartilage and subchondral bone destruction
Dippe, Paul
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Osteoarthritis
Most common form of arthritis 10% of the worlds population 50% of people over the age of 60 years At age 75, more than 80% of people have
symptoms of the disease More common in women than in men
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Risk Factors for Osteoarthritis
Age Female sex Race Genetic factors Repetitive stress Obesity Congenital / Developmental defects Prior inflammatory joint dse. Metabolic / Endocrine disorders
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Clinical Features Deep ache, localized pain Aggravated by activity, relieved by rest Transient joint stiffness Bony swelling, crepitus Progressive cartilage loss
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Biochemical markers in Osteoarthritis
Major tissue of origin
Biochemical markers
Synovium Hyaluran, type 2 collagen propeptide, proteases
Subchondral bone Type 1 collagen crosslinks, osteocalcin, alk. phosphatase, Cart. oligomeric protein (COMP)
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Management of Degenerative Joint Disease
Non-pharmacologic Pharmacologic Surgery
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Changes in lifestyle for patients with Osteoarthritis
General measures - Maintain optimal weight
- Encourage activity and regular general exercise
- Maintain positive approach
Specific measures - Strengthening of local muscles
- Use of appropriate footwear and walking aids
- Pay attention to specific problems caused by disability (such as shopping, housework, and job)
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Pharmacologic Agents
1. Analgesics Simple Analgesics (acetaminophen) Other Analgesics (opioids, tramadol)
or combination
Acetaminophen is the first line agent for OA ACR recommendation
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Pharmacologic Agents
1. Analgesics
2. NSAIDs Anti inflammatory effects Safety concern
- renal, GI, platelet function
- CV risk
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PhospholipidsPhospholipase A
Arachidonic Acid
( PG, thromboxanes, prostacyclins)
LipooxygenaseCyclooxygenase
(-) NSAID’s
(leukotrienes, bradykinin)
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Mechanism of Action of NSAIDs – New hypothesisArachidonic Acid
Prostaglandins Prostaglandins
Protection of gastric mucosa
Homeostasis
Mediates painInflammation and fever
Conventional NSAIDs
COX-1 COX-2
Coxibs
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COX-1 COX-2
- produces PG from AA - produces PG from AA
- constitutively expressed - inducible - governs PG production - governs PG production that mediate hemostatic that mediate inflammation function - essentially important in: gastric, bowel mucosa kidney, platelets
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Risks factors for UGI adverse events
Age >65 y.o. Co-morbid clinical conditions Oral glucocorticoids History of PUD; UGIB Anticoagulants
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Pharmacologic Agents
Few joint involvement NSAIDs, capsaicin
1. Analgesics
2. NSAIDs
3.Topical Agents
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Pharmacologic Agents
(+) effusion Relief lasts for a few weeks
1. Analgesics
2. NSAIDs
3.Topical Agents
4. Intraarticular
Steroid Injection
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Pharmacologic Agents
1. Analgesics
2. NSAIDs
3.Topical Agents
4. Intraarticular Steroid
Injection
5. DMOAD’s Modify morphologic changes in
the joints
- glucosamine / chondroitin
- viscosupplementation
- doxycycline
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Pharmacologic Agents1. Analgesics
2. NSAIDs
3.Topical Agents
4. Intraarticular Steroid
Injection
5. DMOAD’s
6. Other Agents Antidepressants Mild tranquilizers
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Surgical Treatment for Osteoarthritis
History of joint locking
- arthroscopy for removal of loose body Persistent synovitis
- arthroscopic washout or radioisotope synovectomy
Joint replacement is highly effective for hip & knee
- consider early referral for opinion
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Points to Remember - Osteoarthritis
Most common form of arthritis Identify risk factors
- age is the most powerful risk factor• Deep ache localized pain related to activity• Hand lesions
- heberdens, bouchards nodes• Progressive cartilage loss• Paracetamol – 1st line agent
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Rheumatoid Arthritis
Chronic, inflammatory Articular, extra-articular Oligo, polyarticular Young, female/male ratio (4:1) Remission and relapse Unknown etiology
- genetic predisposition (HLA-DR4)
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Rheumatoid Arthritis Etiology is unknown
- Genetics
- HLA DR4
- Infection
- mycoplasma, EBV, CMG, parvo, rubella virus
- “Superantigens”
- staph, strep, M. arthritidis
- Environmental
- cigarette smoking
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Extra-articular manifestation of RA rheumatoid nodules vasculitis pulmonary
- pleural effusion, fibrosing alveolitis, nodules cardiac
- pericarditis, mitral valve disease, conduction defects skin
- palmar erythema, cutaneous vasculitis Feltys syndrome
- sero (+) RA, splenomegaly, neutropenia
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Extraarticular Manifestations of RA
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Immune Abnormalities Rheumatoid Factor - anti - immunoglobulins - anti IgG/IgM - immunologic hallmark - Rose-Waaler assay - (+) 80% of RA pts. - high titer associated - extra-articular sx - progressive disease
- poor prognosis ANA
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Other causes of (+) RF test:
- other CTD - leishmaniasis
- viral infections - TB
- leprosy - liver diseases
- SBE - sarcoidosis
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Revised criteria for RA diagnosis- symmetrical joint involvement*- joint stiffness of at least1 hour duration*- Involvement of at least 3/14 joints of the body*- Hand joint involvement*- (+) subcutaneous nodules- (+) RA test- radiographic findings
- Juxtaarticular osteoporosis, cystic lesions, evosions
• * At least 6 weeks duration• 4/7 criteria
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Treatment of RA
Experimental
agents
Cyclophosphamide,MTX, Azathioprine
Gold salts, antimalarials, Penicillamine
Salicylates, NSAIDS, analgesics
Education, rest, exercise, social service
IntraarticularSteroid injection
Mechanical devices
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DMARDs
Non-analgesic Slow onset of action – 10-20 weeks More toxic than NSAIDs Mechanism of action:
– Decrease leukotriene B4 synthesis in neutrophils– Decreases IL-1 concentration in SF
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Disease Modifying Drugs (DMARD’s)
Gold salts Antimalarials Sulfasalazine D- Penicillamine Methotrexate Cyclosporin-A
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Biologic Agents
Anti TNF
- Etanercept
- Infliximab
- Adalimumab• T cell inhibitor
- Abatacept• B cell inhibitor
- Rituximab• Interleukin 1 receptor antagonist
- Anakinra
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Adverse effects of Biologic Agents
Opportunistic infection CHF Demyelinating disease Systemic lupus erythematosus Injection site reaction Neutropenia
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Factors Associated with Poorer Prognosis
Insidious polyarticular onset Male patients Extraarticular manifestations Functional disability at one year after start of disease Substantially raised concentration of RF Presence of HLA-DR4 X-ray evidence of erosion within three years of start
of disease
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Points to Remember
Polyarticular, symmetrical Joints stiffness more than 1 hour Cartilage destruction, bone erosions Asso. with deformities, extra articular features ACR revised criteria for diagnosis Disease modifying, biologic agents
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Gouty Arthritis King of diseases; disease of Kings inflammatory arthritis due to urates acute, episodic monoarthritis polyarticular Hyperuricemia
- biochemical hallmark
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Classification of Hyperuricemia and Gout Primary- Enzymatic Defect
HGPRT deficiency PRPP overactivity
Secondary- Endogenous
Family history Body build Kidney function, HPN Inc. cell breakdown
- Exogenous diet, drugs alcohol, stress starvation
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Renal Handlingof Urates
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Gouty Arthritis
Statements - Hyperuricemia is not gout
- Gout is a result from hyperuricemia
- Extremely painful episodes of arthritis
- Tendency to abuse NSAIDS, steroids
- Treatable / Preventable
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The most important differential diagnosis for acute gouty attack is
infection
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“ The most feared complication of Gouty Arthritis is kidney involvement “
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Risk Factors for the Development of Gout Alcohol Association of alcohol consumption and the risk of incident gout
- 12 year cohort study
- Biennial questionnaires
- 47,150 male health professionals with no gout at baseline Alcohol intake strongly associated with an increased risk of gout
- Highest risk with beer consumption
- Moderate risk with liquor consumption
- Lower risk with wine consumption
Choi et al. Lancet, 2004;363:1277-1281
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Risk Factors for the Development of Gout Diet
High meat consumption
High seafood consumption
High dairy consumption
High consumption of purine-rich vegetable
risk gout
risk gout
risk of gout
no association
Choi et al. NEJM, 2004;350(11):1093-1103
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Risk Factors for the Development of GoutDrugs
- low dose steroids- aspirin- anti TB drugs - pyrazinamide- diuretics
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Treatment
Acute Attack - NSAIDS, Colchicine - Analgesics - IV/IM corticosteroids - Non pharmacologic measures
Hyperuricemia - Allopurinol - Uricosuric drugs
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PROPHYLACTIC COLCHICINE DOSES
CClr > 60
CClr 40-60
CClr 30-40
CClr < 30
0.6 mg BID
0.6 mg QD
0.6 mg Q2 Days
0.6 mg Q3 Days
- COLCHICINE NOT EXTRACTED BY DIALYSIS
- DO NOT USE IN DIALYSIS PATIENTS
- REDUCE COLCHICINE BY 50% FOR AGE >= 70
- CAUTION WITH DRUG INTERACTIONS: e.g., CSA, Statins, Macrolides, Gemfibrozil
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Points to Remember
Acute, episodic; mono/oligoArthritis Hyperuricemia – biochemical hallmark (+) uric acid crystal on SF, tophi – definitive Dx Young male, post menopausal women Provocative factors:
- inc. purine foods
- trauma, surgery
- alcohol ingestion
- ACTH, glucocorticoid withdrawal
- hypouricemic therapy
- medical illness – stroke, MI
- drugs – diuretics, PZA, low dose aspirin
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Spondyloarthropathies Ankylosing spondylitis Psoriatic arthritis Reiters disease / Reactive arthritis Enteropathic arthritis (IBD)
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General Features Familial aggregation – HLA-B27 ( - ) rheumatoid factor test Asymmetric peripheral oligoarthritis Axial skeleton involvement Sacroiliitis – low back pain Enthesopathic
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Ankylosing Spondylitis Marie Strumpell disease, Bechterews disease 2nd – 3rd decade of life Male preponderance – 3:1 ratio Syndesmophyte formation ( bamboo spine ) Enthesitis, sacroiliitis
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Clinical Features Dull pain, insidious onset Low back morning stiffness
- relieved by activity, aggravated by rest• Peripheral asymmetric oligoarthritis• Acute anterior uveitis
- most common extra articular Mx• Aortic insufficiency• ( + ) Schobers test
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Radiographic Findings
Syndesmophyte formation
- ossification of annulus fibrosus Vertebral body disk margin erosion “Squaring” of vertebral bodies Sclerosis of SI joint, sacroiliitis
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Diagnosis Modified NY criteria (1984)
- Hx of inflammatory back pain
- LOM sagittal, frontal planes of LS
- limited chest expansion
- definite radiographic sacroiliitis
Definite AS:
- evidence of sacroiliitis + any of the other 3 criteria
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AS vs other causes of LBP
Age of onset before 40 Insidious onset Duration of sx > than 3 months before medical attention is
sought Prolonged morning stiffness Improvement with exercise
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Treatment
No definitive treatment
- appropriate exercise program
- NSAID’s
- sulfasalazine
- methotrexate
- intralesional cortisone injection
- biologic agents
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Reactive Arthritis / Reiters Disease
Asymmetric oligoarthritis Urethritis Conjunctivitis Mucocutaneous lesion
- balanitis
- keratoderma blenorrhagica
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Clinical Forms Post enteric infection
- shigella (flexneri), salmonella,
yersinia, campylobacter
Post genital infection
- chlamydia trachomatis
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Psoriatic Arthritis
5 - 42 % of patients with psoriasis Unknown cause Indirect evidence:
- infection
- trauma
- inc. humoral / cellular immunity
- cytokine driven
- abn. fibroblast, dendritic cell, PMN function
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Major Types of Psoriatic Arthritis Asmmetric oligoA
- most common Symmetric polyA
- RA like features DIP involvement
- nail lesion Arthritis mutilans
- deformities, young patients Psoriatic spondylitis
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Treatment Patient education Physical / occupational therapy NSAID’s Methotrexate + folic acid Sulfasalazine Gold salts Antimalarials
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Enteropathic Arthritis ( IBD )
Ulcerative colitis / Crohn’s disease Intestinal bypass surgery Whipples disease (intestinal lipodystrophy)
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Features
oligoA, asymmetric Spondylitis, sacroiliitis Clubbing of fingers Development of amyloid – crohn’s Osteoporosis – inactivity malabsorption, steroids
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Points to Remember HLA - B27 association (-) RA factor exam Clinical features - Musculoskeletal - peripheral oligoA - enthesitis - sacroiliitis, spondylitis - Systemic - psoriasis - IBD - conjunctivitis, iritis - genito urinary inflammation - carditis
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Systemic Lupus Erythematosus
chronic, inflammatory multiorgan, multisystemic unknown etiology
– autoantibodies– immune complexes
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Theories Immunologic
– autoantibodies, immune complexes activity of polyclonal T;B cells
Genetics concordance in monozygotic than dizygotic twins (24 – 58%: 0 – 6%)– complement deficiencies – C1q, C2, C3, C4
Genetics– HLA-DR2 – DR3 tissue types– Defective C4AQO allele
marker for ethnic groups Environment
– UV-B, UV-A rays– alfalfa, chemicals (hydrazine)– virus, type-C oncorna
Hormonal– woman, reproductive life– NZ mice
estrogen activates disease androgens protective
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Clinical Manifestations
Musculoskeletal
- arthritispolyarticular, rheumatoid likejoint deformitiesnon-erosive
- myopathyactive diseasedrug-induced (hypoK, steroids, antimalarials)
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Clinical Manifestations
Malar rash– photosensitive, flat
or raised– non-scarring
Cutaneous
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Clinical Manifestations
Discoid rash– 20 %– circular, raised borders– central, atrophic,
hypopigmented area– scarring– photosensitive
Cutaneous
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Clinical Manifestations
Oral ulcers– painless, shallow– buccal mucosa– disease activity
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Lupus band test- deposition of IgG at
dermal-epidermal junction
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Renal - pyuria, hematuria, proteinuria, casts (UA)
- subendothelial, subepithelial mesangial deposits (E/M)
- renal biopsy best guide to nephritis severity
- focal, mesangial, membranous, diffuse proliferative
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Clinical Manifestations
Nervous system- overdiagnosed- CNS, PNS- cognitive dysfunction most frequent- seizures, psychosis- neuropathy, autonomic dysfunction- MRI (contrast) acute, chronic- lumbar tap active disease, infection
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Clinical Manifestations
Hematologic- anemia NN, hemolytic
- leukopenia, lymphopenia
- thrombocytopenia
- arterial, venous thrombosis
- lupus anticoagulant, anticardiolipin prolong PTT (APS)
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Clinical Manifestations
Cardiopulmonary– carditis
pericarditis most common myocarditis arrhythmias endocarditis valvular insufficiency transesophageal
echocardiogram
– Libmann-Sacks
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Laboratories ANA
- best screening test (WIL-2 or Hep-2 cells)
- (+) test nonspecific; supports diagnosis
- other conditions:Elderly chronic inflammatory conditionsother CTDs viral infections
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Laboratories Autoantibodies in SLE
- anti-dsDNAnephritis, activityrelatively disease specific
- anti-Smcutaneous, musculoskeletal
- anti-Ro (SS-A)neonatal, elderly lupusANA negative lupusmay cause nephritis
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- anti-La (SS-B) always associated with Ro Sjogrens syndrome, low risk for nephritis
- anti-histones drug-induced
- anti-phospholipids 3 types – LA, aCL, false VDRL test LA, aCL clotting abnormalities, fetal loss, platelet
antibodies for B2 glycoprotein
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- antierythrocyte hemolysis
- antineuronal diffuse CNS lupus
- antiribosomal CNS lupus – Psychosis
- antiRNP MCTD
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Revised Criteria for SLE
Malar rash Discoid rash Photosensitivity Oral ulcers Arthritis, non-erosive, polyarticular Serositis carditis, pleuritis, effusion
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Revised Criteria for SLE Renal– +++ protein (U/A), >500mg/24hrs
Hematologic– blood “-penias”
Neurologic– seizures, psychosis
Immunologic– dsDNA, Sm, antiphospholipid
(+) ANA
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Revised Criteria for SLE 4/11 criteria 97 % sensitivity; 98 % specificity SOAP, BRAIN, MD
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Treatment
no cure, rare complete sustained remission non-pharmacologic
- doctor-patient relationship
- education
- support group
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Pharmacologic Therapy NSAIDs, analgesics
– MS Sx
antimalarials – cutaneous vasculitis– opthalmologic consult
Steroids– major organ– monitor side effects– oral / pulse therapy
Immunosuppressives– azathioprine, cyclophosphamide, chlorambucil, MTX– oral / pulse therapy
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Others– plasmapheresis – cyclosporins– immunoablation
high dose CYP– antibodies to CD4
suppress T/B cell– IVIG– stem cell transplant
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Prognosis
Factors assoc’d w/ poor prognosis
- creatinine levels
- hypertension
- nephrotic syndrome
- anemia, albumin, low C3/C4 at diagnosis
- low socioeconomic status
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Cause of Death
1st decade
- infection, active disease 2nd decade
- thromboembolic events
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Osteoporosis
Silent disease Systemic skeletal disease1
– Low bone mineral density (BMD)BMD 2.5 standard deviations below the
mean BMD of young adults– Microarchitectural deterioration of bone tissue– Bone fragility– Increased risk for fracture
1Consensus Development Conference. Am J Med. 1991.
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Wasnich RD: Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 4th edition, 1999, p 257
Incidence Rates for Vertebral, Wrist and Hip Fractures in Women After Age 50
40
30
20
10
50 60 7080
Vertebrae
Hip
Wrist
Age (Years)
Ann
ual i
ncid
ence
pe
r 10
00 w
omen
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Non-Modifiable
• Age• Female sex• Maternal family history of
hip fracture• Low birth weight• Disease predisposing to
osteoporosis
Risk factors taken from Jordan & Cooper Best Practice and Res Clin Rheumatol, 2002Categorized by Eli Lilly & Co.
Potentially Modifiable
• History of falls• Body mass index• Drug therapy (e.g.
corticosteroid use, use of anti-convulsants)
• Primary or secondary amenorrhea
• Early menopause• Smoking• Excessive alcohol
consumption• Dietary calcium and vitamin D
deficiency
Risk Factors for Osteoporosis and Fracture
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IndirectIndirecteffectseffects
Unitary model for postmenopausal bone loss: role of oestrogen deficiency
Directly increases Directly increases osteoclast number osteoclast number
and longevityand longevity
DietaryDietarycalciumcalcium
(decreased (decreased absorption)absorption)
SecondarySecondaryhyperparathyroidismhyperparathyroidism
Increased boneIncreased boneresorptionresorption
BoneBonelossloss
Decreased Decreased bonebone
formationformation
RemodellingRemodellingimbalanceimbalance
??
Adapted from: Riggs BL, et al. J Bone Miner Res 1998;13:763–73Adapted from: Riggs BL, et al. J Bone Miner Res 1998;13:763–73
OestrogenOestrogendeficiencydeficiency
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Glucocorticoid dose Dependent Effect on Fracture Risk
0.99
1.77
5.18
1.55
2.59
2.27
0
1
2
3
4
5
6
Hip Vertebral
Type of Fracture
Relative Risk of Fracture
<2.5 mg
2.5 mg-7.5 mg
>7.5 mg
Dose*
Van Staa TP, et al. J Bone Miner Res. 2000.*Prednisolone equivalent
N = 488 470
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Most rapid bone loss occurs in the first 6-12 Most rapid bone loss occurs in the first 6-12 months of Steroid therapymonths of Steroid therapy
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WHO definition of osteoporosis
The T-score– the number of SDs from the mean (average) value of BMD at
peak bone massPatient category T-score
Normal Above –1
Osteopenia Between –1 and –2.5
Osteoporosis <–2.5
Established osteoporosis <–2.5 with non-traumatic fracture
Patient category T-score
Normal Above –1
Osteopenia Between –1 and –2.5
Osteoporosis <–2.5
Established osteoporosis <–2.5 with non-traumatic fracture
WHO Study Group. WHO Technical Report Series 843, Geneva WHO Study Group. WHO Technical Report Series 843, Geneva Switzerland: WHO;1994:1–129Switzerland: WHO;1994:1–129
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How should patients be evaluated to determine if they have osteoporosis? AACE recommend that evaluation include– a comprehensive medical examination– X-rays in patients with suspected vertebral fractures– BMD measurements– assessment of risk factors for fractures
NOF guidelines are generally similar, but with greater emphasis on BMD testing
Neither guidelines take into account bone markers for diagnosing osteoporosis
AACE Osteoporosis Task Force. Endocr Pract 2003;9:545–64 AACE Osteoporosis Task Force. Endocr Pract 2003;9:545–64 http://www.nof.org/professionals/clinical.htmhttp://www.nof.org/professionals/clinical.htm
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Diagnosis and assessment
X-rays
BMD
Ultrasound
Bone markers
Bone biopsy and histomorphometry
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Indications for Bone Density MeasurementsIndications for Bone Density Measurements
• estrogen deficient women estrogen deficient women
-- perimenopauseperimenopause
-- early menopause early menopause
-- premenopausepremenopause• radiologic osteoporosisradiologic osteoporosis• previous low-trauma fractureprevious low-trauma fracture• corticosteroid therapycorticosteroid therapy
>7.5mg/day x 3 months>7.5mg/day x 3 months• diseases causing secondary osteoporosisdiseases causing secondary osteoporosis• monitor treatment responsemonitor treatment response
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Biochemical markersof bone turnover in osteoporosis
Formation (reflect osteoblast activity)
Resorption (reflect osteoclast activity)
Serum osteocalcin
Serum total and bone alkaline phosphatase
Serum type I collagen propeptide
Urinary pyridinolines and deoxypyridinoline
Urinary and serum CTX*
Urinary and serum N-telopeptide of the alpha chain of type I collagen (NTX)*
Formation (reflect osteoblast activity)
Resorption (reflect osteoclast activity)
Serum osteocalcin
Serum total and bone alkaline phosphatase
Serum type I collagen propeptide
Urinary pyridinolines and deoxypyridinoline
Urinary and serum CTX*
Urinary and serum N-telopeptide of the alpha chain of type I collagen (NTX)*
*CrossLaps*CrossLapsTMTM
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Candidates for therapy: the AACE guidelines The AACE guidelines indicate that the following women may benefit from pharmacologic therapy
– women with a prior vertebral or hip fracture
– women with BMD T-score –2.5 without risk factors
– women with borderline-low BMD if risk factors are present
– women in whom nonpharmacologic preventive measures are ineffective
AACE Osteoporosis Task Force. Endocr Pract 2003;9:545–64AACE Osteoporosis Task Force. Endocr Pract 2003;9:545–64
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Therapeutic options for osteoporosisStimulators of bone formation - Fluoride - Parathyroid hormone
Mixed mechanism of action - Vitamin D and metabolites - Strontium ranelate
Recommended for all women at risk for osteoporosis - Calcium and vitamin D
Inhibitors of bone resorption
Bisphosphonates- Alendronate- Etidronate- Risedronate
Calcitonin
Estrogen ± progestin
Selective estrogen receptor modulators (SERMs)- Raloxifene
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Osteoporosis preventionT-score >–2.5
Osteopenia
treatment with or without
previous fracture
Osteoporosis treatment with multiple fractures and at risk for hip fracture
50 55 60 65 70 75 80 85
Raloxifine
Age (years)
HRT
Therapeutic Management of Postmenopausal Osteoporosis
Teriparatide
Bisphosphonates
Adapted from Seeman & Eisman, MJA Vol 180 15 March 2004, p298-303
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Optimal Daily Calcium Requirements
1300 mg
1000 mg
1200 mg
Recommended CalciumIntake (Daily)
Age
1997 Recommended Dietary Intakes
9-18 years
19-50 years
51 years or older
National Academy Press. Available at: http://books.nap.edu/catalog/5776.html. 1999.
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Recommendations for Vitamin D Intake
Europe
The Scientific Committee for Food of the Commission of the EuropeanCommunities recommends 400 IU of vitamin D daily for the elderly (age 65)
United States
The Institute of Medicine has defined adequate daily intake of vitamin Daccording to age Adults up to age 50 200 IU Adults 51–70 400 IU Adults >70 600 IU
No toxic effects reported in 61 healthy adults given 4000 IU/day in a clinicalstudy to assess the efficacy and tolerability profile of high vitamin D intake
Adapted from European Commission. Report on osteoporosis in the European community: Action on prevention. Luxembourg: Office for Official Publications of the European Communities, 1998; Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: Institute of Medicine, National Academy Press, 1997; Vieth R et al Am J Clin Nutr 2001;73:288–294.
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Widespread Prevalence of Vitamin D Inadequacy* Regardless of
Geographic Location
*Vitamin D inadequacy was defined as serum 25(OH)D <30 ng/ml; **Interim results of ongoing study
Study Design: Observational, cross-sectional study of 1285 community-dwelling women with osteoporosis from 18 countries to evaluate serum 25(OH)D distribution.
Adapted from Lim S-K et al. Poster presented at ISCD, February 16–19, 2005, New Orleans, Louisiana,USA; Heaney RP Osteoporos Int 2000;11:553–555.
Pre
vale
nce
(%
)
0
10
30
40
60
80
90
LatinAmerica
51%
63%
AsiaAll
59%
Australia
59%
Europe
52%
Regions
N=1285 81%
MiddleEast
50
70
20
In a cross-sectional observational international study in 1285 postmenopausal women with osteoporosis**
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Probable Reasons for High Prevalence of Vitamin D Inadequacy in
Postmenopausal Women
Lack of sunlight exposure Vitamin D is not common in the diet The ability to synthesize vitamin D in the skin
decreases with age Lack of compliance taking daily supplements
Adapted from Marcus R Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill Medical Publishing Division, 2001:1715–1743; Bringhurst FR Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill Medical Publishing, 2005:2238–2249; Matsuoka LY J Clin Endocrinol Metab 1987;64:1165–1168; Parfitt AM Am J Clin Nutr 1982;36:1014–1031; Lawson RM Clin Nutr 2000;19:171–175.
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Appropriateneuromuscular
function
Appropriateneuromuscular
function
Vitamin D Inadequacy* Has Important Consequences
*Vitamin D inadequacy is defined as serum 25(OH)D <30 ng/ml.
Adapted from Parfitt AM et al Am J Clin Nutr 1982;36:1014–1031; Allain TJ, Dhesi J Gerontology 2003;49:273–278; Holick MF Osteoporos Int 1998;8(suppl 2):S24–S29; DeLuca HF Metabolism 1990;39(suppl 1):3–9; Pfeifer M et al Trends Endocrinol Metab 1999;10:417–420; Lips P. In: Draper HH, ed. Advances in Nutritional Research. New York, Plenum Press, 1994:151–165.
Bone mineraldensity
Bone mineraldensity
Parathyroidhormone
Parathyroidhormone
Calcium absorptionCalcium
absorption
Risk of fractureRisk of fracture
Artistic rendition
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Bisphosphonate mechanismof action
Adapted from: Bone H, et al. Clin Ther 2000;22:15–25 Adapted from: Bone H, et al. Clin Ther 2000;22:15–25
RESTINGRESTING
RESORPTIONRESORPTION
OsteoclastOsteoclast
FORMATIONFORMATION
OsteoblastsOsteoblasts
BISPHOSPHONATES BISPHOSPHONATES INHIBIT OSTEOCLAST INHIBIT OSTEOCLAST
-MEDIATED BONE-MEDIATED BONERESORPTIONRESORPTION
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PTH - Mechanism of Action
PTH binds to cell surface G protein-coupled receptor
Stimulates differentiation of bone lining cells and
preosteoblasts to osteoblasts
Decreases apoptosis of osteoblasts
Net increase in number and action of bone forming
osteoblasts
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Osteoporosis has been thought of as a silentOsteoporosis has been thought of as a silent
epidemic….this is not true anymore. At present,epidemic….this is not true anymore. At present,
there is much noise in the field of research for there is much noise in the field of research for
its prevention, diagnosis and treatment.its prevention, diagnosis and treatment.
Ego Seeman ARCOS meeting, Feb 2002
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One of the Many Faces of Osteoporosis
“You could have floored me when they told me. It’s very frightening, very frightening…I don’t want to end up in a nursing home incapacitated.”
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Thank You !Please visit:
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