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Diagnosis and management sle
1. DIAGNOSIS AND MANAGEMENT
OF
SYSTEMIC LUPUS ERYTHEMATOSUS
A PRESENTATION BY DR. ASHVINI K. LOMROD
UNDER THE GUIDANCE OF DR. C.K. MEENA SIR
JLN MEDICAL COLLEGE, AJMER
2. Systemic+ Lupus+ Erythematosus
Systemic - The disease can affect organs and tissues throughout the
body.
Lupus [ Latin for wolf ] It refers to the rash that was thought to
resemble a wolf bite.
Erythematosus [ Greek word for red ] â It refers to the color of the
rash.
3. DEFINITION
â˘A systemic autoimmune disease with relapsing
and remitting course that can affect almost any
organ system in which organs and cells undergo
damage mediated by tissue binding
autoantibodies and immune complexes.
5. ⢠Gender â 90% women(women to men ratio 9:1) in child bearing age. Flares
also become some what less common after menopause in women have chronic
SLE.
Female sex is permissive for SLE because:
- Hormone effects
- Genes on X-chromosome
-Epigenetic differences between genders
Estradiol binds to receptors on T & B lymphocytes increasing activation &
survival of these cells, thus favouring prolonged immune response.
So women are exposed to estrogen containing OCP and hormone replacement
therapy have an increased risk of developing SLE.
People with more X-chromosomes(XXX karyotypes,Klinefelterâs syndrome)
have a significant increased risk for SLE.
6. ⢠Age â 15-44 yrs are commonly affected.
â˘Race & Ethnicity â More common in urben than rural areas.
Highest prevalence is in black women and lowest
is in white men.
⢠Family History - A brother or sister of a patient with the disorder
has 20 times the risk as someone without an
immediate family member with SLE.
7. â˘Environmental Triggers â Sunlight, cold, fatigue, stress, chemicals and
certain drugs.
*Sunlight : Ultraviolet rays (UVB or UVA) Shorter UVB wavelengths cause
the most harm.
*Viruses : EBV ( The cause of mononucleosis)
*Smoking : May increase the risk for skin and kidney problems in women
who have the disease.
*Tobacco
*Chemicals: Occupational exposure to crystalline silica as a possible trigger.
Some prescription medications are associated with a temporary
lupus syndromes (drug-induced lupus),which resolves after these
drugs are stopped.
❠Drinking alcohol(2 glasses of wine a week or ½ of an alcoholic drink daily)
reduces the risk of SLE.
8. * Hormone Replacement Therapy : increases the risk for blood clots and
heart problems as well as breast cancer.
Guidelines recommend HRT the lowest possible dose for the shortest
possible time. Women with SLE who have active disease, antiphospholipid
Antibodies or a history of blood clots or heart disease should not use HRT.
* Oral Contraceptives : Caution against taking OCPs( Estrogen could
trigger lupus flare-ups).However, recent evidence indicate that OCs are
safe, at least for women with inactive or stable lupus. Lupus can cause
complications in its early stages. The estrogen in OCs increase the risk for
blood clots.(Risk particularly for women with antiphospholipid syndrome)
10. ⢠SLE - The most common type and is the type of lupus that
can lead to serious systemic complications.
⢠Cutaneous lupus erythematosus - Confined to the skin
and does not affect other parts of the body. About 10% of
people with this type of lupus go on to develop SLE.
⢠Discoid lupus erythematosus - A type of cutaneous lupus
that produces a potentially scarring disc shaped rash on the
face, scalp or ears.
11. ⢠Drug-induced lupus - Temporary and mild form of lupus
due to some drugs like Hydralazine, ACE inhibitors, and
calcium channel blockers, hydrochlorothiazide. Symptoms
resolve once the medication is stopped.
⢠Neonatal lupus - A rare condition that sometimes affects
infants born to mothers who have SLE. Babies with
neonatal lupus are born with skin rash, liver problems, and
low blood counts and may develop heart problems.
13. Role of Genetics and Environment
â˘Environment
⢠Cell damage by environmental triggers causes apoptosis that leads to release of
apoptotic bodies+parts of nucleus [ now exposed to other parts of body ]
⢠Genetics â Susceptibility genes and their effect on immune system.
⢠loss of self tolerance [ immune system recognizes parts of nucleus as self antigens ]
⢠Self Ag presentation by DCs,
⢠Defective complement system,
⢠Impaired clearance of apoptotic cells
⢠Aberrant lymphocyte activity[unregulated T cell dependent B cell activation]
⢠Production of autoantibodies
14. ⢠Antigen-Antibody complexes / Immune Complexes deposition in various body tissues
[ basement membranes ] results
â Local inflammation
â Local complement activation
â Local apoptosis
â Positive feedback loop
⢠DNA is the main antigen for which antibodies are formed
⢠IgG is the most âpathogenicâ because it forms intermediate sized complexes that can get
to the small places and block them
⢠Injury is caused by
Mainly deposition of immune complexes and
Binding of antibodies to various cells and tissues.
⢠In most patients, autoantibodies are present for a few years before the first clinical
symptom appears
18. Constitutional
⢠Fatigue â Mild to extreme
⢠Malaise
⢠Fever â any pattern
⢠Anorexia
⢠Weight loss
⢠lymphadenopathy
⢠Arthralgia
19. Musculoskeletal
⢠Arthralgia , myalgia
⢠Polyarthritis [ 2 or more peripheral joint ] - Intermittent,mild to disabling,soft tissue swelling,
tenderness,Nonerosive,MC in hands,wrists and knees
⢠Joint deformities (hands and feet)-In 10% cases ,erosions can be identified on ultrasound
(rarely on x-rays)
⢠Myopathy /myositis
⢠Ischemic necrosis of bone
ârhupusâ-some patients of SLE have rheumatoid like arthritis with erosions and fulfill
criteria for both RA and SLE so may be coded having both diseases
21. Cutaneous
⢠Photosensitivity-skin rash on Sun exposed areas due to sunlight
⢠Malar rash âMC acute SLE rash-photosensitive,slightly raised erythema,occasionaly scally,
on the face(butterfly rash-malar eminences and nasal bridge)but sparing nasolabialfold,
ears,chin,neck and chest,upper backand extensor surfaces of the arms
⢠Discoid rash (DLE)-MC chronic dermatitis in lupus,lesions roughly circular with slightly
raised ,scaly hyperpigmented erythematous rims and depigmented,atrophic centers
(permanently damaged dermal appendages)
⢠Subacute cutaneous lupus
⢠Oral lesions-Erythema of palate,tongue and oral mucosa,papules,vesicles and petechiae.oral
or nasopharyngial ulceration usually painless
⢠Alopacia
⢠Others-urticaria,
⢠Vasculitis rash
⢠Raynodes phenomena
24. Photosensitive systemic lupus erythematosus (SLE) rashes typically occur on the face or extremities
which are sun exposed regions. Although the interphalangeal space are affected, the metacarpophalangeal
(MCP) and proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints are spared.
30. Renal
⢠50 % of lupus pts will have kidney involvement in their life ,of these 50 % will have
serious kidney disease
⢠Persistent proteinuria > 0.5 grams / 24 hrs (or greater than 3+), cellular casts ( may be
red cells ,hemoglobin,granular, tubular,mixed)
⢠Nephritis (Lupus nephritis) âthe most serious manifestation and also predict outcome
(prognosis)
⢠Renal Failure because of Glomerulonephritis is the leading cause of death among lupus
patients.
⢠Nephrotic syndrome
⢠ESRD
31. GIT
⢠Nonspecific â Nausea, vomitting, diarrhea
⢠Diffuse abdominal pain-autoimmune peritonitis and/or intestinal vasculitis
⢠Abnormal liver enzymes (more often due to therapy than to
SLE itself)
⢠Mesenteric Vasculitis
⢠Sepsis and bleeding
32. Thromboembolic events
Patients of Antiphospholipid syndrome due to hypercoagulable state
more prone to clots [ venous or arterial ] that can leads to
⢠Deep vein thrombosis
⢠Hepatic vein thrombosis
⢠Stroke
⢠Myocardial infarction
33. Ocular
⢠Common but less serious - Sicca syndrome
Conjunctivitis
Episcleritis
⢠Serious manifestations - Retinal vasculitis
Optic neuritis
⢠Fundoscopy shows sheathed, narrow retinal arterioles and white
hard exudate called âCytoid bodyâ
41. LN-Treatment
In general, class III and IV disease, as well as class V accompanied by III or IV
disease, should be treated with aggressive immunosuppression if possible,
because there is a high risk for end-stage renal disease (ESRD) if patients are
untreated or undertreated.
In contrast, treatment for lupus nephritis is not recommended in patients with
class I or II disease or with extensive irreversible changes.
43. LABORATORY TESTS
⢠Antinuclear antibodies [ANA]-Sensitive but not specific
⢠Anti -ds DNA-[ More specific ], targets double-stranded DNA, seen during active disease
⢠4 RNA associated antibodies -
Anti-Sm [Smith] â[ More specific ]Targets ribonucleoproteins
Anti Ro /SSA- antibody
Anti La/SSB- antibody
Anti âRNP
⢠Antiphopholipid antibody- [Less specific to Lupus] Targets protein bound to phospholipid
Lupus anticoagulent [ Lupus antibody ]
Anti-B2 glycoprotein 1 AB
Anti-cardiolipin
44. ⢠Coombs test- Hemolytic anemia
.
⢠Complete blood count-Hemolytic anemia with reticulocytosis
Leukopenia-less than 4,000 / cu mm on 2 or more occasions
Lymphopenia-less than 1,500 / cu mm on 2 or more occasions
Thrombocytopenia-less than 100,000 /cu mm , in the absence of offending drugs
⢠Erythrocyte sedimentation rate
⢠RFT,LFT ,Lipid profile
⢠C-reactive protein
⢠Urine routine and microscopy and 24 hrs protein and creatinine estimation
45. ⢠Complement levels [ C3 and C4 ] - Decreased (C3 level < 5.5 mg/dl)
⢠Chest radiography and chest CT scanning-
ILD, pneumonitis, pulmonary emboli, alveolar haemorrhages
⢠Joint radiograpy-periarticular osteopenia and soft tissue swelling without
erosions
⢠Echocardiography-pericardial effusion
⢠â ESR, â anti ds-DNA and âC3 may indicate disease âflareâ
46. Skin Biopsy
LUPUS BAND TEST (60%)
Deposition of Ig at the dermoepidermal junction (DEJ), injury
to basal keratinocytes, and inflammation dominated by T
lymphocytes in the DEJ and around blood vessels and dermal
appendages. Clinically unaffected skin may also show Ig deposition
at the DEJ
47. Renal biopsy
⢠In the recent Systemic Lupus International Collaborating Clinic (SLICC)
criteria for classification of SLE, a diagnosis can be established on the
basis of renal histology alone without meeting additional criteria .
⢠The pattern and severity of injury are important in diagnosis and in
selecting the best therapy.
⢠Recommended for every SLE patient with any clinical evidence of
nephritis
⢠Not recommended as a screening test
48. Histologic abnormalities in blood vessels
⢠Leukocytoclastic vasculitis is most common.
⢠Not specific for SLE but may indicate active disease
Lymph node biopsies
⢠Nonspecific diffuse chronic inflammation.
⢠Usually performed to rule out infection or malignancies.
49.
50. MANAGEMENT
⢠There is no cure for SLE and complete sustained remissions are
rare so management aims to induce remissions of acute flares ,
maintenance therapy and thereby preventing organ damage
⢠Many patients with SLE have âflaresâ, in which symptoms
suddenly worsen and then settle down for long periods of time.
51.
52. Conservative management
⢠NSAIDs, salicylates (Ecotrin a and St. Josephâs aspirin approved by FDA for use in SLE )
for arthritis / arthralgia- Doses toward upper limit of recommended range usually required
⢠Antimalarials(HCQ,CQ,quinacrine)-for dermatitis, arthritis, fatigue
⢠Systemic glucocorticosteroids( low dose)
⢠Belimumab
⢠lupus dermatitis-topical sunscreens [ SPF 15 at least ; 30+ preferred],antimalarials, topical
glucocorticoids and/or tacrolimus and systemic glucocorticoids with or without
mycophenolate for severe or unresponsive cases
54. Systemic glucocorticoids
⢠MPS and Prednisolone
MPS 500-1000 mg IV over 1 hour OD for 3 days
followed by
0.5 - 1 mg/kg per day prednisolone PO
Currently
0.5 - 1 mg/kg per day prednisolone PO for 4-6 weeks therefore tappered as soon as
condition improves usually to a dose 5-10 mg daily
0.07â0.3 mg/kg prednisolone per day or qod for milder disease
55. Cytotoxic/immunosuppressive therapy
⢠Methotrexate
[for dermatitis, arthritis]
10â25 mg once a week, PO or SC, with folic acid; decrease dose if CrCl<60 mL/min
⢠Cyclophosphamide
⢠IV
Low dose : 500 mg every 2 weeks for 6 doses maintenance with MMF or
AZA. High dose: 7â25 mg/kg q month Ă 6; consider mesna administration
with dose
⢠Oral
1.5â3 mg/kg per day; decrease dose for CrCl <25 mL/min
56. ⢠Mycophenolate
MMF: 2â3 g/d PO for induction therapy,
1â2 g/d for maintenance therapy; max 1 g bid if CrCl <25 mL/min
MPA: 360â1080 mg bid; caution if CrCl<25 mL/min
⢠Azathioprine
2â3 mg/kg per day PO for induction; 1â2 mg/kg per day for maintenance; decrease frequency
of dose if CrCl <50 mL/min
⢠Belimumab
10 mg/kg IV wks 0, 2, and 4, then monthly
⢠Rituximab
[ for patients resistant to above therapies ]
375 mg/m2 q wk Ă 4 or 1 g q 2 wks Ă 2
57. SERIOUS OR COMMON ADVERSE EFFECTS OF
DRUGS USED IN SLE
⢠NSAIDS-aseptic meningitis,elevated liver enzymes,decreased renal functions,vasculitis of
skin,MI,ototoxicity,tinitus,allergic reactions,dermatitis,gi events,ARF,edema,HTN
⢠Topical GC-skin atrophy,contact dermatitis,,folliculitis,hypopigmentation,infection
⢠Topical sunscreens-contact dermatitis
⢠HCQ-retinal damage,cornial opacity myopathy ,neuropathy
⢠MTX-megaloblastic anemia at low doses and bone marrow suppression at high doses
⢠GC-infections,HTN,hyperglycemia,hypokalemia,allergic reactions,cushingoid
changesCHF,fragile skin,menstrual abnormalities,osteoporosis
59. Lifestyle changes to help cope with SLE.
⢠Get plenty of rest (fatigue is another common SLE symptom)
⢠Salt restriction [ if HTN ] , avoid fat [ for hyperlipidaemia ] , calcium supplements with
steroid therapy
⢠Engage in regular light-to-moderate exercise to help fight fatigue and heart disease, and to keep
joints flexible
⢠Avoid excessive sunlight exposure, and wear sunscreen (ultraviolet light is the one of the main
triggers of flares)
⢠Don't smoke and avoid exposure to second-hand tobacco smoke
60. PREVENTIVE THERAPIES
Prevention of complications of SLE and its therapy
⢠Suppressing recurrent urinary tract infections.
⢠Providing appropriate vaccinations [ the administration of influenza and pneumococcal ]. [
Vaccination with attenuated live viruses is generally discouraged in patients who are
immunosuppressed ].
⢠Prevention of osteoporosis .
[ Postmenopausal women can be protected from steroid-induced osteoporosis
with either bisphosphonates or denosumab. Safety of long-term use of these
strategies in women is not well established ].
⢠Control of hypertension
⢠Prevention strategies for atherosclerosis
monitoring and treatment of dyslipidemias
management of hyperglycemia and obesity.
61. DIFFERENTIAL DIAGNOSIS
⢠Chronic fatigue syndrome
⢠Undifferentiated connective tissue disease
⢠Primary Sjogren`s syndrome
⢠Primary antiphospholipid syndrome
⢠Fibromyalgia with positive ANA
⢠Idiopathic thrombocytopenic purpura
⢠Drug-induced lupus
⢠Early RA
⢠Systemic vasculitis
62. SLE & PREGNANCY
⢠Increases the risk of spontaneous abortion, IUD, preeclampsia,IUGR and
preterm birth
⢠Prognosis best for both mother and child when SLE is quiescent for at least 6
months before the pregnancy and mothers renal function stable and normal
or near normal
⢠Lupus nephritis can get worse during pregnancy
⢠In general pregnancy does not cause flares of SLE
⢠When flares do develop ,they often occur during the first or second trimester
or during first few months after delivery
63. SPECIAL CONDITIONS IN SLE THAT MAY REQUIRE ADDITIONAL
OR DIFFEENT THERAPY
Crescentic Lupus Nephritis
The presence of cellular or fibrotic crescents in glomeruli with
proliferative glomerulonephritis indicates a worse prognosis Most
authorities currently recommend that high-dose cyclophosphamide is
the induction therapy of choice, in addition to high-dose
glucocorticoids.
64. Membranous Lupus Nephritis
Immunosuppression is not recommended unless proteinuria is in the
nephrotic range (although treatment with ACE inhibitors or angiotensin II
receptor blockers is recommended).
In those patients, recent prospective controlled trials suggest that alternate-
day glucocorticoids plus cyclophosphamide or mycophenolate mofetil or
cyclosporine are all effective in the majority of patients in reducing
proteinuria.
65. Pregnancy and Lupus
⢠Fertility rates for men and women with SLE are probably normal.
⢠Rate of fetal loss is increased (approximately two- to threefold) in women with SLE.
⢠Fetal demise is higher in mothers with high disease activity, antiphospholipid antibodies,
and/or active nephritis.
⢠Suppression of disease activity can be achieved by administration of systemic
glucocorticoids.
⢠Glucocorticoids [ Pregnancy category A (no evidence of teratogenicity in human studies)]
⢠Cyclosporine, tacrolimus, and rituximab [category C (may be teratogenic in animals but no
good evidence in humans) ];
⢠Azathioprine, hydroxychloroquine, mycophenolate mofetil, and cyclophosphamide
[category D (there is evidence of teratogenicity in humans, but benefits might outweigh
risks in certain situations) ];
⢠Methotrexate [ category X (risks outweigh benefits)].
66. ⢠Therefore, active SLE in pregnant women should be controlled with hydroxychloroquine and,
if necessary, prednisone/prednisolone at the lowest effective doses for the shortest time required.
⢠Azathioprine may be added if these treatments do not suppress disease activity.
The cardiac manifestations can be life-threatening.
Recent evidence shows that hydroxychloroquine treatment of an anti-Ro-positive mother whose
infant develops congenital heart block significantly reduces the chance that subsequent fetuses
will develop heart block ,also with dexamethasone
A small proportion develops severe flares requiring aggressive glucocorticoid therapy or early
delivery.
Poor maternal outcomes are highest in women with active nephritis or irreversible organ
damage in kidneys, brain, or heart.
67.
68. Lupus and Antiphospholipid Syndrome (APS)
⢠Patients with SLE who have venous or arterial clotting and/or repeated fetal losses and at
least two positive tests for antiphospholipid antibodies have APS
⢠Should be managed with long-term anticoagulation .
⢠A target international normalized ratio (INR) of 2.0â2.5 is recommended for patients with
one episode of venous clotting.
⢠An INR of 3.0â3.5 is recommended for patients with recurring clots or arterial clotting,
particularly in the CNS.
⢠Recommendations are based on both retrospective and prospective studies of post treatment
clotting events and adverse effects from anticoagulation.
69. Microvascular Thrombotic Crisis
(Thrombotic Thrombocytopenic Purpura, Hemolytic-Uremic Syndrome)
⢠This syndrome of hemolysis, thrombo cytopenia, and microvascular thrombosis in
kidneys, brain, and other tissues carries a high mortality rate and occurs most commonly in
young individuals with lupus nephritis.
⢠The most useful laboratory tests are identification of schistocytes on peripheral blood
smears, elevated serum levels of lactate dehydrogenase, and antibodies to ADAMS13
⢠Plasma exchange or extensive plasmapheresis is usually life-saving; most authorities
recommend concomitant glucocorticoid therapy; there is no evidence that cytotoxic drugs are
effective.
70. Lupus Dermatitis
⢠Minimize exposure to ultraviolet light [ appropriate clothing and sunscreens ] .
⢠Topical glucocorticoids and antimalarials (such as hydroxychloroquine) reduces lesion
severity in most patients and are relatively safe.
⢠Systemic treatment with retinoic acid is a useful strategy in patients with inadequate
improvement on topical glucocorticoids and antimalarials; adverse effects are potentially
severe (particularly fetal abnormalities),
⢠Extensive, pruritic, bullous, or ulcerating dermatitis usually improve promptly after
institution of systemic glucocorticoids; tapering may be accompanied by flare of lesions, thus
necessitating use of a second medication such as hydroxychloroquine, retinoids, or cytotoxic
medications such as methotrexate, azathioprine, or mycophenolate mofetil.
⢠Topical tacrolimus - In therapy-resistant lupus dermatitis [possible increased risk for
malignancies ] dapsone or thalidomide [ the extreme danger of fetal deformities ]
71. EXPERIMENTAL THERAPIES
⢠Highly targeted experimental therapies targeting
⢠(1) activated B lymphocytes with anti-CD22 or TACI-Ig,
⢠(2) inhibition of IFN-ι,
⢠(3) inhibition of B/T cell second signal coactivation with CTLA-Ig,
⢠(4) inhibition of innate immune activation via TLR7 or TLR7 and 9,
⢠(5) induction of regulatory T cells with peptides from immunoglobulins or autoantigens;
⢠(6) suppression of T cells, B cells, and monocyte/macrophages with laquinimod; and
⢠(7) inhibition of lymphocyte activation by blockade of Jak/Stat. A few studies have used
vigorous untargeted immunosuppression with high dose cyclophosphamide plus anti-T
cell strategies, with rescue by transplantation of autologous hematopoietic stem cells for
the treatment of severe and refractory SLE. One U.S. report showed an estimated
mortality rate over 5 years of 15% and sustained remission in 50%.
72. DRUG-INDUCED LUPUS
⢠A syndrome of positive ANA associated with symptoms such as fever, malaise, arthritis or
intense arthralgias/myalgias, serositis, and/or rash, during therapy with certain medications
and biologic agents.
⢠Predominant in whites, has less female predilection than SLE.
⢠Rarely involves kidneys or brain.
⢠Rarely associated with anti-dsDNA.
⢠Commonly associated with antibodies to histones.
⢠Usually resolves over several weeks after discontinuation of the offending medication.
73. The most frequent drugs â
⢠Antiarrhythmics procainamide, disopyramide, and propafenone;
⢠Antihypertensive hydralazine;
⢠Angiotensin-converting enzyme inhibitors and beta blockers;
⢠Antithyroid propylthiouracil;
⢠Antipsychotics chlorpromazine and lithium;
⢠Anticonvulsants carbamazepine and phenytoin;
⢠Antibiotics isoniazid, minocycline, and nitrofurantoin (Macrodantin);
⢠Antirheumatic sulfasalazine;
⢠Diuretic hydrochlorothiazide;
⢠Antihyperlipidemics lovastatin and simvastatin;
⢠IFNs and TNF inhibitors
⢠ANA usually appears before symptoms; however, many of the medications mentioned above induce ANA in
patients who never develop symptoms of drug induced lupus. It is appropriate to test for ANA at the first hint of
relevant symptoms and to use test results to help decide whether to withdraw the suspect agent.
74. PATIENT OUTCOMES, PROGNOSIS AND SURVIVAL
⢠Survival in patients with SLE in the United States, Canada, Europe, and China is
approximately
⢠95% at 5 years,
⢠90% at 10 years,
⢠78% at 20 years.
⢠In the United States, African Americans and Hispanic Americans with a
mestizo heritage have a worse prognosis than whites, whereas Africans in Africa
and Hispanic Americans with a Puerto Rican origin do not.
75. Poor prognosis (~50% mortality in 10 years) in most series is associated with (at the
time of diagnosis)-
⢠High serum creatinine levels (>124 Οmol/L [>1.4 mg/dL]),
⢠Hypertension,
⢠Nephrotic syndrome (24-h urine protein excretion >2.6 g),
⢠Anemia (hemoglobin <124 g/L [<12.4 g/dL]),
⢠Hypoalbuminemia,
⢠Hypocomplementemia,
⢠Antiphospholipid antibodies,
⢠Male sex,
⢠Ethnicity (African American, Hispanic with mestizo heritage) and low socioeconomic
status.
Overall patient survival in SLE patients with renal transplants rejection compared to patients
with other causes of ESRD, is comparable (85% at 2 years).
Lupus nephritis occurs in approximately 10% of transplanted kidneys.
76. Morbidity-
⢠Disease associated[ primarily to chronic fatigue, arthritis, and
pain, as well as renal disease ]
⢠Corticosteroid associated
Mortality-
⢠Early[in first decade]-Active disease,renal failure and infection
⢠Late- Atherosclerosis [ thromboembolic events ]
![Systemic+ Lupus+ Erythematosus
Systemic - The disease can affect organs and tissues throughout the
body.
Lupus [ Latin for wolf ] It refers to the rash that was thought to
resemble a wolf bite.
Erythematosus [ Greek word for red ] â It refers to the color of the
rash.](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)