systemic lupus erythematosus (sle) heidi roppelt, md assistant professor of medicine associate...
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Systemic Lupus Systemic Lupus Erythematosus (SLE)Erythematosus (SLE)
Heidi Roppelt, MDAssistant Professor of Medicine
Associate Program Director Division of RheumatologyDirector of the osteoporosis Center
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History of LupusHistory of Lupus
1200 AD: Term lupus is used for the first time to describe ulcerations on the face, literally means wolf.– Skin rash, like a wolf, seems to eat away
the skin and destroy it– Skin looked like it had been bitten away by
a wolf– Frightening appearance of lupus sufferers-
thought to look like werewolves.
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History of LupusHistory of Lupus 1828- First described by a British dermatologist:
– multiple cases of similar skin lesions on face 1890s- Sir William Osler noticed patients with
distinct skin lesions also had internal organ involvement
1948- LE cell seen as commonality of patients with lupus at the Mayo Clinic
1954- proteins against one’s own tissue (antibodies) were discovered specific for lupus– Steroids used for first time in these patients
1970s: Lupus Foundation Organized
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SLE: Chronic, inflammatory, SLE: Chronic, inflammatory, autoimmune disease affecting autoimmune disease affecting
multiple organsmultiple organs
LUPUS
LUNGS
HEART KIDNEY
BLOOD
SKIN
BRAIN
LIVER/ PANCREAS JOINTS
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Incidence of LupusIncidence of Lupus
Affects approx 1 million AmericansMore than 16,000 new cases each yearFirst degree relatives have a 3% chance
of developing the disease Identical Twins: second twin developing
disease is between 25-65%
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Incidence in PopulationsIncidence in PopulationsIn America:
– Incidence of lupus between 25-64 years of age is 1 in 700 Caucasian women
– In African American women, it is 1 in 265 womenDifferent Populations are affected differently:
– Caucasians- blood and skin involvement– Hispanics- kidney involvement– African Americans- generally more aggressive
disease involving all organs
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Criteria for Lupus (4 of 11)Criteria for Lupus (4 of 11)
Malar Rash Kidney Disease Discoid Rash Neurologic Disorder Positive ANA Hematologic disorder Photosensitivity Positive Antibodies Oral Ulcers Arthritis Serositis
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Malar rash–Fixed erythema, flat or raised, over the face- sparing the nasolabial folds
Discoid rash–Raised patches, adherent keratotic scaling,follicular plugging; frequently causes scarring
Photosensitivity–Skin rash induced by sunlight
Oral or nasopharyngeal ulcers–Usually painless
Arthritis–Nonerosive, inflammatory in two or more peripheral joints
Serositis–Pleuritis or pericarditis
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Renal disorder –Persistent proteinuria or cellular casts
Neurologic disorder–Seizures or psychosis
Hematologic–Hemolytic anemia, leukopenia (<4,000/mm3), lymphopenia (<1,500/mm3), or thrombocytopenia (<100,00/mm3)
Immunologic disorder–Antibodies to dsDNA or SM or positive antiphospholipid antibodies (IgG or IgM antibodies, lupus anticoagulant, or false-positive serologic test positive serologic test for syphilis)
Antinuclear antibody test–Positive
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Epidermal LesionsEpidermal Lesions
Malar (Butterfly Rash)– 50 % of patients with lupus develop this after UV
exposure– May proceed overt SLE by months or occur as
acute manifestation– May last for hours to days and often reoccurs– Biopsy: Immunoglobulins and complements at
dermal-epidermal junction: “Lupus-Band Test”– DDx: Rosacea, facial flushing, seborrheic, atopic,
contact dermatitis
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Malar Rash
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Systemic lupus Systemic lupus erythematosus: malar rash, erythematosus: malar rash,
faceface
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Epidermal LesionsEpidermal Lesions
Discoid Lupus– Seen in 25 % of patients with systemic lupus– Can occur independent of SLE
Low titer ANA and low titer Anti-Ro antibodies 10 % of these will progress to systemic lupus erythematosus
– Usually seen on face, neck, scalp, and upper torso– Discrete, erythematosus, infiltrated plaques extending
into hair follicles– Leave depressed scars, hyper/hypo pigmentation– DDx: Psoriasis, Eczema, Lichen Planus, and Actinic
Keratosis
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PhotosensitivityPhotosensitivity
Occurs in 60-100% of patients with SLEDevelopment of erythematous,
sometimes raised/ puritic rash approximately 24-48 hours after sun exposure– UV-B light most commonly responsible
Sunlight, fluorescent lights Glass inhibits its penetration
– UV-A (some patients)
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Systemic lupus erythematosus: photosensitive Systemic lupus erythematosus: photosensitive erythematosus rash, upper backerythematosus rash, upper back
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Epidermal LesionsEpidermal Lesions
Subacute Cutaneous Lupus– 10 % of systemic lupus patients will develop this
lesion– 50 % of patients with this lesion will develop
systemic lupus– Associated with more photosensitivity than
systemic lupus patients– Affected areas: shoulders, neck, forearms, and
upper torso– Face is generally spared– Scarring does not occur
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AlopeciaAlopecia Occurs in majority of SLE patients Scarring
– Discoid Lupus Non-scarring
– Lupus Hair Thinning and breakage of hair at times of increased
disease activity. Returns to normal once disease is quiescent
– Telogen Effluvium (Premature Hair Loss) 3 months after stressful event- hair loss Glucocorticoids, Emotional Stress, Pregnancy, etc. Will grow back to normal
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Raynaud’s PhenomenonRaynaud’s Phenomenon
Triphasic color change in fingers:– White Blue Red
Occurs upon exposure to cold or even to emotional stress
If begins later in life, can be a clue to underlying autoimmune disease which may develop in months- years
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Raynauds Picture
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Systemic lupus erythematosis: vasculitis, Systemic lupus erythematosis: vasculitis, handshands
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Musculoskeletal Musculoskeletal Manifestations and LupusManifestations and Lupus
ArthralgiasArthritisOsteonecrosisMyalgiaOsteoporosis
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Systemic lupus erythematosus: Jaccoud’s arthropathy
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Systemic lupus erythematosus: Systemic lupus erythematosus: interarticular dermatitis, handsinterarticular dermatitis, hands
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Hematologic Manifestations of Hematologic Manifestations of SLESLE
Anemia– Autoimmune
Leukopenia– WBC < 4,000
Autoimmune thrombocytopenia– Usually correlates with disease activity
Increased risk of clotting– Anticardiolpin antibodies– Lupus Anticoagulant
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Antiphospholipid antibody syndrome: Antiphospholipid antibody syndrome: clinical manifestationsclinical manifestations
Arterial thrombosis
Venous thrombosis
Valvular abnormalities
Pregnancy loss and infertility
Livedo reticularis
Neurologic complications– cerebrovascular
thrombosis– Chorea
Catastrophic APS syndrome
Thrombocytopenia
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Clinical criteria•Vascular thrombosis•Pregnancy morbidity(a) One or more unexplained deaths of a fetus at or beyond the 10th week of gestation, or(b) One or > premature births at or before the 34th week of gestation because of severe preeclampsia or eclampsia, or severe placental insufficiency, or(c) Three or > unexplained consecutive spontaneous abortions before the 10th week of gestation
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Laboratory criteria• Anticardiolipin antibody (IgG and/or IgM)
medium or high titer, on 2 or more occasions, at least 12 weeks apart
• Lupus anticoagulant present in plasma, on 2 or more occasions at least 12 weeks apart
• Anti-b2 glycoprotein-I antibody (IgG and/or IgM) present on two or more occasions, at least 12 weeks apart
Definite APS if at least 1 clinical criteria and 1 laboratory criteria are met
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Kidney Disease and SLEKidney Disease and SLEAbnormal urinalysis +/- proteinuria present
in 50% at diagnosis, eventually 70%Most renal disease occurs within the first
6-36 months6 Classes of renal disease:
Class I Minimal mesangial LNClass II Mesangial proliferative LNClass III Focal LN* (50% of glomeruli)III (A): active lesionsIII (A/C): active and chronic lesionsIII (C): chronic lesions
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Kidney Disease and SLEKidney Disease and SLE
6 Classes of renal disease cont:Class IV Diffuse LN
– Diffuse segmental (IV-S) or global (IV-G) LN
– IV (A): active lesions– IV (A/C): active and chronic lesions– IV (C): chronic lesions
Class V Membranous LNClass VI Advanced sclerosing LN
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Heart Disease and SLEHeart Disease and SLE
Increased incidence of Myocardial Infarctions– Higher cholesterol- need to monitor! Target
LDL<100 even <80– Can get direct involvement of blood
vesselsPericarditisValvular disease
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Lung Disease and SLELung Disease and SLE
Pleuritis– Pleuritic Chest Pain
Acute PneumonitisAcute Lung HemorrhageInterstitial lung disease
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Systemic lupus erythematosus: nervous Systemic lupus erythematosus: nervous
system manifestationssystem manifestations Seizures Headache Stroke syndromes Transverse myelitis (may be
associated with APS) Aseptic meningitis Peripheral neuropathy Cranial neuropathy Mononeuritis multiplex Ataxia Psychiatric disorders
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Gastrointestinal Gastrointestinal Manifestations of SLEManifestations of SLE
Abdominal Pain (30%)– Serositis/ Peritonitis– Mesenteric Ischemia
DyspepsiaPancreatitisAbnormal Liver Enzymes
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Menstrual Function, Menstrual Function, Menopause in SLEMenopause in SLE
Menstrual Function– Menorrhagia- heavy menstrual flow (15%)– Amennorhea- autoimmune activity against ovaries
or from immunosuppressive agents Menopause
– Symptoms of SLE seem to lessen– Higher risk of osteoporosis– Higher risk of heart disease
Oral Contraceptive Use– No increased risk of disease flares– Avoid in those with antiphospholipid positivity
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Pregnancy and SLEPregnancy and SLE
Pregnancy is NOT advised during active disease
Patient should be in remission for at least 6 months
Disease can become very aggressive during pregnancy– Renal involvement– Neurologic
Premature birth
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Neonatal LupusNeonatal Lupus
Rash that occurs in newbornsMothers are positive for specific
antibodies seen in lupus (and also in Sjogren’s syndrome)– Anti-Ro/ SSA and Anti-La/ SSB antibodies
Resolves in 6-8 monthsChild does NOT have lupus
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Subacute cutaneous lupus
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Autoantibody-disease associations: Autoantibody-disease associations: SLE and drug-induced lupusSLE and drug-induced lupus
Antigen SLE Drug-Induced LE
dsDNA 40% No
Histone 70% >95%
Sm antigen 30% No
RNP 30% No
SS-A/Ro 35% No
SS-B/La 15% No
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Drug-induced lupus: definite Drug-induced lupus: definite drug associationsdrug associations
Hydralazine Procainamide Minocycline Chlorpromazine Isoniazid Penicillamine Methyldopa Interferon-alpha
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Laboratory DataLaboratory Data
Non-specific Tests– ANA – Complement C3/ C4– ESR
Specific Tests (Antibodies)– Anti-double stranded DNA– Anti- Smith– Anti-ENA Ab (Anti-Ro/ Anti-La/ Anti-RNP)
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ANA (Anti-Nuclear antibody)ANA (Anti-Nuclear antibody) Studies have shown that 10-25% of normal, healthy people
have a positive ANA Other situations in which ANA is positive
– Autoimmune Diseases Rheumatoid Arthritis Scleroderma Thyroid Disease Autoimmune Hepatitis Sjogren’s syndrome
– Infections– Certain medications– Advanced age
Can I have SLE without a positive ANA?– Yes, but extremely rare
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TreatmentTreatment
General management–Fatigue–Support groups–Avoid sun exposure–Minimize risk factors for
cardiovascular disease–osteoporosis
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TreatmentTreatment
NSAIDS–May cause aseptic meningitis and
cognitive dysfunction–Monitor for renal, hepatic, GI side
effects–monitor CBC, LFT’s, BUN/CR,
urinalysis
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TreatmentTreatment
Corticosteroids– Relatively low doses for treatment of
Constitutional sx, arthritis, cutaneous manifestations, serositis
– High doses for treating nephritis, cerebritis, hematologic abnl, vasculitis
– Mainstay of therapy during pregnancy– Side effects: osteonecrosis, hyperglycemia,
HTN, hyperlipidemia, osteoporosis
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TreatmentTreatment
Hydroxychloroquine (plaquenil)– Prevent flares– Effective for rx of mild skin disease,
arthritis, mild serositis, constitutional sx– May have antithrombotic effects, lipid
lowering effects– Monitor for macular damage;
fundoscopic/ visual field checks q6months
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TreatmentTreatment
Azathioprine (Imuran)–Purine analogue inhibiting nucleic
acid synthesis; affects humoral and cellular immunity
–Steroid sparing agent for rx of non-renal manifestations of SLE, or nephritis
–Bone marrow and GI toxicity
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TreatmentTreatment
Cyclophosphamide– Most commonly used for treatment for
severe organ system disease, and nephritis
– Hemmorrhagic cystitis, bladder ca, gonadal toxicity
Use of GNRH agonists, Mesna to prevent
– Most commonly given monthly IV for six months
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TreatmentTreatment
Other:–Mycophenylate mofetil (Cellcept)–Methotrexate– IVIG