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MRCP PACES Consultations (History, Miscellaneous) > Systemic Lupus Erythematosus > Flashcards

Systemic Lupus Erythematosus Flashcards

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1
Q

SLE is an autoimmune disease caused by __ and __ manifestation on __, __ and __

A

Autoantibodies and complement deposition
Manifestation on skin, joint, multiorgan dysfunction

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2
Q

Epidemiology of SLE

A
  1. Female > male (10-15 times)
  2. Age 15-45 years old
  3. 3-4 times higher in non-Caucasian (African-American, Asian, Hispanic)
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3
Q

Laboratory hallmark of SLE

A
  1. Elevated ANA (very sensitive but not specific)
    - Most specific: Peripheral or rim pattern
    - Commonest but least specific: speckled pattern
    - Nucleolar pattern -> scleroderma
  2. dsDNA - highly specific, correlates with lupus nephritis activity
  3. Histones (H1, H2A, H2B, H3, H4)
  4. anti-Sm - highly specific, no activity correlation
  5. Ribosomal P proteins - highly specific
  6. Low C3 and low C4

Others:
1. U1-RNP - MCTD
2. Ro/SSA - scleroderma, neonatal lupus
3. La/SSB - scleroderma, neonatal lupus
4. Antiphospholipids

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4
Q

Memorising characteristic manifestations of SLE (ACR 1997 Criteria for SLE)
(SOAP-BRAIN-MD)

A

S: serositis - pleuritis, pericarditis
O: oral or nasal ulcers
A: arthritis (non-erosive)
P: photosensitivity rashes

B: blood disorders - haemolytic anaemia, leukopenia, lymphopenia, thrombocytopenia
R: renal involvement: proteinuria, cellular casts
A: ANA
I: immunologic - dsDNA, anti-Sm, APLAs
N: neurologic - seizures, psychosis

M: malar rashes
D: discoid rashes

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5
Q

ACR/EULAR Classification of SLE (2017)

A

Highly sensitive (96%), specific (93%)
Mandatory ANA + at least 10 point criteria

Mandatory criteria:
1. ANA titre > 1:80

Points criteria (at least 10 points):
- Do not count if due to other cause than SLE
- at least 1 clinical criterion

Clinical
1. Renal involvement
- Class 3/4 nephritis - 10
- Class 2/5 nephritis - 8
- Proteinuria >0.5g/day - 4

  1. Arthritis - 6
  2. Serosal
    - Pericarditis - 6
    - Pleural or pericardial effusion - 5
  3. Mucocutaneous
    - Cutaneous lupus - 6
    - Subacute cutaneous or discoid lupus - 4
    - Oral ulcers - 2
    - Non-scarring alopecia - 2
  4. Neuropsychiatry
    - Seizure - 5
    - Psychosis - 3
    - Delirium - 2
  5. Haematologic
    - AIHA - 4
    - Thrombocytopenia - 4
    - Leukopenia - 3
  6. Constitutional - Fever - 2

Laboratory
1. SLE-specific antibodies
- anti-dsDNA or anti-Smith - 6

  1. Complement proteins
    - Low C3 and C4 - 4
    - Low C3 or C4 - 3
  2. Any APLAs - 2
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6
Q

Describe the different types of lupus

A

A. SLE
- Multiple organs can be involved
- ANA and SLE specific antibodies
- Variable prognosis

B. Subacute cutaneous SLE
- Skin only involvement
- ANA negative, SSA or SSB positive
- 5-10% eventual progress to SLE

C. Drug-induced lupus
- Systemic but without CNS or renal
- Anti-histone antibodies
- Improves when drug stopped

D. Discoid lupus
- Skin only involvement
- ANA negative
- Rarely progresses to SLE unless ANA turns positive

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7
Q

ANA-negative SLE

A

Rare

  1. Must have excluded less sensitive test
    (must run ANA using HEp-2 assay)
  2. Positive cytoplasmic antigens - antibodies to SSA/Ro-52kD (TRIM-21) or ribosomal P
  3. Severe proteinuria (loss of Igs and unable to bind to HEp-2)
    -> ANA turns positive with treatment
  4. Post-cytotoxic therapy in remission
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8
Q

Risk factors for SLE

A
  1. Environmental
    - Smoking, viral (EBV, CMV), silica, UV light, pesticides, gut microbiome, demyelinating drugs
  2. Genetics
    - First degree relatives with SLE
    - Identical twins
    - MHC - HLA DR2, DR3
    - Complement deficiency
  3. Gender and hormone
    - Women of childbearing age
    - Klinefelter (14 fold risk)
    - Rare in Turner’s syndrome
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9
Q

Pathogenesis of CNS manifestation of SLE

A

Diffuse manifestation - transient, reversible with therapy
Focal manifestation - permanent, pathological lesions on autopsy

Possible endothelial dysfunction
- Complement activation during acute lupus
- Progoagulant factors (APLAs)
- Thrombosis and emboli
- Microvasculoparhy and disruption of BBB
- Influx of cells, autoantibodies and cytokines into CNS

Associated autoantibodies:
1. Antiphospholipids
2. Antineuronal
2. Ribosomal P
4. NMDA receptor
5. AQP4/NMO

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10
Q

What are the neuropsychiatric manifestations of SLE?
- Diffuse
- Focal

A

Diffuse
1. Acute confusional state and coma
2. Cognitive dysfunction and dementia
3. Psychosis, depression, anxiety
4. Intractable headache (pseudotumour cerebri)
5. Aseptic meningitis

Focal
1. Stroke syndromes
2. Seizures
3. Chorea, ataxia, hemiballismus
4. Demyelinating syndromes
5. Transverse myelitis

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11
Q

Approach to SLE patient presenting with neuropsychiatry changes

A

Differential diagnoses:
1. Neuropsychiatric SLE
2. Prednisolone incuded psychosis
3. Delirium - infection
4. Metabolic abnormalities
5. Primary mental illness not due any secondary causes

Evaluation:
1. Signs and symptoms for SLE, localise infections
2. Examination for focal neurological deficits
3. Labs and imaging to exclude infection
4. Check SLE labs: C3/C4, anti-dsDNA levels
5. Consider specific NPSLE serologies: anti-ribosomal P, anti-NMO
6. Lumbar puncture, OP, CSF testing
7. MRI brain +/- spinal cord +/- angiogram/venogram
8. EEG

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12
Q

Respiratory manifestation of SLE

A
  1. Pleuritis (commonest)
    - Bilateral involvement. Elevated CRP. Consider infection
  2. Acute lupus pneumonitis with/without pulmonary haemorhage
    - Ground glass changes. Associated with APLAs
    - Progressive to ILD
    - Broncoscopy: DAH +/- infection
  3. ILD/fibrosis
    - Rare in non-overlap SLE, common in MCTD or prior lupus pneumonitis
    - Medication effect (nitrofurantoin) or overlap with anti-synthetase antibody syndrome
  4. Pulmonary hypertension
  5. Shrinking lung syndrome - reduced lung volume
    - A/w phrenic neuropathy, myopathy, pleural fibrosis
  6. Crytogenic organisign pneumonia
    - Responsive to steroids
    - Overlap with anti-synthetase antibody syndrome
  7. Infections, especially atypicals
    - Tree in bud appearance
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13
Q

Cardiac manifestations in SLE

A
  1. Pericarditis +/- left pleural effusion
    - Treat with colchicine
  2. Myocarditis (rare)
    - Presents as heart failure, tachycardia. Elevated trops
    - Consider myocardial biopsy
  3. Coronary vasculitis (rare)
  4. Secondary atherosclerotic CAD and MI (commonest)
  5. Secondary hypertensive disease - kidney failure, chronic steroids use
  6. Medication induced cardiomyopathy - hydroxycholoquine
  7. Valvular disease in APS
  8. Libman-Sacks endocarditis/verrucae
    - Posterior leaflet of mitral valve or aortic valve
    - Leads to embolic stroke
    - high concomitant subacute bacterial endocarditis
    - TEE more sensitive than TTE
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14
Q

Gastrointestinal manifestations of SLE

A

Usually rare, and unlikely due to SLE
UNLESS patient has active SLE in other organs and abnormal serologies

  1. Oesophageal dysmotility
    - Upper 1/3 involvement, esp in SLE myositis, overlap syndromes
  2. Pancreatitis - usually non SLE related (gallstones, alcohol, hyperTG)
    - Medication (azathioprine)
    - Diffusely active if due to SLE
  3. Serositis
  4. Mesenteric vasculitis, bowel oedema, fat stranding
    - Associated with active SLE
  5. Hepatitis - from mediaction, or non-lupus
    - Must not have anti-smooth muscle and anti-LKM if due to SLE
  6. Intestinal pseudo-obstruction
  7. Protein losing enteropathy
    - Low albumin without proteinuria
    - Chronic diarrhoea, generalised oedema
    - Diagnosed with fecal alpha-1 antitrypsin or transferrin
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15
Q

What are the indications for renal biopsy in SLE patient?

What is the importance of biopsy?

A

Indications
1. Increasing creatinine without alternative cause
2. Proteinuria > 1g/day
3. Proteinuria >0.5g/day wtih haematuria or cellular casts

Importance of biopsy
1. Histologic changes of chronicity - scarring, fibrosis indicates less likely responsive to therapy
2. Evaluate for microthrombotic disease in APS
3. Calculated scoring on disease activity (mixed predictive value, no longer universally use)

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16
Q

SLE Glomerulonephritis Classification Sytem (2004)

A

Class I - minimal mesangial
- No clinical manifestation
- Histology: mesangial immune deposits on IF / EM

Class II - mesangial proliferative
- Microscopic haematuria, proteinruia, rare HTN
- Histology: mesangial hypercellularity or matrix expansion, few subepithelial/subendothelial deposit

Class III - focal (A: active; C: chronic)
- Haematuria, proteinuria, HTN
- Reduced GFR or nephrotic syndrome
- Histology: < 50% glomeruli affected; almost uniformly involved. EM - immune deposits, some mesangial and some subedothelial space

Class IV - diffuse (S: segmental; G: global; A and C)
- Haematuria, nephrotic range proteinuria
- Cellular casts, reduced GFR, HTN
- Hypocomplementaemia, elevated dsDNA
- Histology: > 50% glomeruli involvement; generalised hypercellularity of mesangial and endothelial cells; extensive deposition. EM immune complxes in both subendothelial and subepithelial

Class V - membranous
- Extensive proteinuria, minimal haematuria
- Minimal renal function abnormalities
- Histology: granular global or segmental subepithelial immune deposits

Class VI - advanced sclerosing
- CKD
- Histology > 90% global glomerulosclerosis without residual activity

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17
Q

Serologic tests for lupus nephritis follow up

A
  1. dsDNA - elevates with disease flare
  2. Complement levels - decrease with active disease
    (Some patients have chronic partial C4 deficiency, thus C3 might be more useful for follow up)
  3. ANCA - perinuclear (PR3)
    (MPO not useful)

Caveats:
Some patients can develop GN even with normal complements and no dsDNA

18
Q

What are risk factors for SLE nephritis progression to ESRF?

A
  1. African american, Hispanics, especially males
  2. Low SES
  3. Poor medication compliance
  4. Pooly controlled comorbids: DM, HTN
  5. persistent elevatec creatinine or failure to normalise on therapy
  6. Persistent proteinuria > 6 months of treatment
  7. Renal biopsy - crescent (high disease activity) or interstitial fibrosis (chronic)
19
Q

Pathologic scoring of lupus nephritis

A

Based on chronicity and activity

Chronicity
1. Glomerular sclerosis
2. Fibrous crescent
3. Fibrous adhesions
4. Interstitial fibrosis

Activity
1. Cellular proliferation
2. Fibrinoid necrosis
3. Cellular crescents
4. Hyaline thrombi

20
Q

Treatment for severe lupus nephritis
- To note: different for SLE without severe nephritis
- Class III/IV treatment differs from class V

A

Class III and IV lupus nephritis - induction and maintenance

Induction therapy
1. IV methylprednisolone 500mg-1g OM for 3 days
2. Followed by prednisolone 1mg/kg/day (crescent) or 0.5mg/kg/day (no crescent)
- Taper after a few weeks to lowest effective dose
3. Immunosuppressives: choice of
A. MMF 2-3g/day for 6 months (better in Hispanics, African)
B. IV cyclophosphamide
(NIH high dose regime: 500-1000 mg/m2 monthly x6)
(Eurolupus low dose regime: 500mg every 2 weeks x6)

  1. Consider switching if fail to improve on MMF -> Cyc and vice versa. And if fail, consider rituximab or CNI

Class V lupus nephritis
1. Oral prednisolone 0.5mg/kg/day for 6 months
2. MMF 2-3g/day for 6 months
3. Add on CNI (tacrolimus, cyclosporin) if needed
4. IV cyclosporin if treatment fails

Maintenance post-induction - adjucts
1. Hydroxycloroquine, azathioprine
2. ACEi or ARBs if proteinuria > 0.5g/day, control BP < 130/80
3. Statin
4. Stop smoking
5. Counsel against pregnancy while in active nephritis or teratotoxic drugs
6. Rituximab

21
Q

Considerations for high dose vs low dose cyclophosphamide (NIH high dose vs Eurolupus low dose)

A

Low dose
Pros: fewer serious infections, lesser infertility (premature ovarian failure), lesser bladder toxicity
Cons: higher rate of fail to respond

Premature ovrian failure and bladder cancer correlates with cumulative dose (>10-15g total) and age (>30 years)

Emerging studies:
CALIBRATE study - rituximab 1g + cyc 500-750mg + belimumab (not promising)

22
Q

Cyclophosphamide infusion protocol

A

A. Pre-medications
1. +/- Dexamethasone or hydrocortisone
2. Anti-emetics: metoclopramide or ondansetron

B. Adjuncts
1. Mesna - pre-dose as IV, post-dose as oral x2
- Reduces risk of haemorrhagic cystitis
2. Premature gonadal failure prevention
- IM Gonadotropin-releasing hormon (Lupron) 3.75mg, 10 days prior to CYC … or
- IM testosterone 200mg 2 weekly

23
Q
  1. Progression of lupus nephritis to ESRF
  2. Survivability of ESRF lupus nephritis on dialysis
  3. Lupus nephritis recurence post-transplantation
A

25% lupus nephritis progress to ESRF over 10 years
(1-2% of all ESRF cases)

Clinical course and survival on dialysis favourable (80-90% 5 year survival)

Excellent candidate for transplantation
- Living donor better than cadaveric

Recurrence: 2-11%
- And recurrence unlikely lead to allograft loss
- Retroanaluysis - similar incidence of graft survival rates as non-lupus patient, except in APS (thrombosis)

24
Q

Haematologic manifestations of SLE

A
  1. AIHA
  2. Leukopenia (lymphopenia, neutropenia)
  3. Thrombocytopenia
  4. APS
  5. Anaemia of chronic disease
  6. Thrombotic thrombocytopenia purpura (TTP)
  7. Macrophage activation syndrome (MAS)
25
Q

What is macrophage activation syndrome (MAS)

A

Can be triggered by EBV or CMV infection

Fatal condition - inability of liver to synthesise proteins such as fibrinogen, high TG, high ferritin, high IL-2 receptor (CD25)

Resulting in fever, cytopenias, organ dysfunction, splenomegaly, low ESR

Criteria:
1. High ferritin
2. Thrombocytopenia <181
3. AST >48
4. Hypertriglyceridaemia
5. Low fibrinogen

26
Q

Haemolytic anaemia workup

A
  1. FBC
  2. PBF - spherocytes vs schistocytes
  3. LDH - raised
  4. Haptoglobin - low
  5. Bilirubin - total and direct
  6. Reticulocytes
  7. Direct Coombs test
27
Q

When and how would you treat thrombocytopenia in SLE

A

Treat if platelet < 30 or with significant bleeding

  1. Steroids, consider pulse if severe
  2. IVIG: 2g/kg (0.4g/kg/day for 5 days)
  3. Anti-D in Rh-positive non splenectomised pt
  4. IV rituximab - response > 1 year 18-35%
  5. Splenectomy

Second line agents
- AZA, MMF, CNIs, Danazol, Cyclophosphamide, fostamatinib, dapsone, vincristine

Novel agents
- Thrombopoietin receptor agonist
(romiplostim, elterombopag, avatrombopag)
> Very expensive (85k per year)
> Tends to recur when drug is stopped

28
Q

TTP in SLE
- Manifestations
- Important lab findings
- Treatment

A

Manifestations
1. Fever
2. Altered mental status
3. Worsening renal function
4. Haemolytic anaemia
5. Thrombocytopenia

Important lab findings
1. PBF: schistocytes, microangiopathic HA (MAHA)
2. LDH very high
3. Possible Coombs positive AIHA and spherocytes
4. ADAMTS13 activity/inhibitor profile - low (Ab against it)

Treatment
1. Plasma exchange with FFP replacement (plasmapheresis) - removes autoAb and vWF multimers
2. Second line - antiplatelets, steroids, IST
3. Maintenance with steroids and ISTs
4. Eculizumab (C5 monoclonal antibody) in refractory cases

29
Q

Joint manifestations of SLE

A

Pain and tenderness more severe than degree of swelling, but rarely destruction of bones

  1. Tenosynovitis
  2. Jaccoud arthritis (non-erosive) in 10-35%
    - MCPJ subluxation, ulnar deviation, swan neck from lax joint capsules, tendons, ligaments
  3. Reversible deformities early, fixed at late stage
  4. Erosive, symmetric polyarthritis (Rhupus)
    - RA resembling fixed deformity with radiographic erosions and possible positive RF / CCP
30
Q

Treatment of SLE with arthritis without end organ involvement

A
  1. NSAIDs and COX2i
    - Beware of APLAs and APS
    - Avoid ibuprofen - risk of aseptic meningitis
  2. Celecoxib may cause rashes (sulphur based)
  3. Meloxicam, etodolac
  4. Antimalarial drugs
  5. Others: MTX, leflunomide, AZA, MMF
31
Q

Mucocutaneous lesions in SLE

A

Common rashes
1. Malar rash
2. Oral ulcers
3. Discoid rash and scarring alopecia
4. Subacute rash

Uncommon rashes
1. Bullous lesions
2. Palpable purpura - small vessel vasculitis
3. Urticaria - anti-C1q Ab
4. Panniculitis and subcutaneous nodules (lupus profundus)
5. Livedo reticularis - in APLAs
6. Perniosis (distal vasculopathy

Pathology
1. Interface dermatitis or dermatomyositis
2. Immunoglobulin deposition at dermal epidermal junction (lupus band test on IF)
3. Drug induced in > 50 years old with SCLE

Treatment
1. Avoid sunlight - apply sunblock
2. Control SLE activity
3. Hydroxychloroquine
4. Dapsone - vesicular lupus skin lesions
5. Thalidomine - mouth ulcer (must avoid pregnancy)
6. Belimumab - recalcitrant discoid or subacute rashes
7. Others: MTX, MMF, AZA, rituximab

32
Q

Differentiating SLE hand rash vs dermatomyositis

A

SLE - erythematous over dorsum of hands and fingers, affecting skin between joints

Dermatomyositis - lesion over MCPJ and PIPJ (Gottron’s papules)

— Insert picture for comparison

33
Q

How may a patient with SLE present with alopecia?

A
  1. Active disease - diffuse stress alopecia (telogen effluvium)
    - 2-4 months after severe flare, massive hair shedding
    - Reversible once disease is controlled
  2. Discoid lupus - patchy hair loss
    - Permanent -> hair follicle inflammation and damage
  3. Drug induced (cyclophosphamide) - diffuse hair loss
    - Reversible after therapy discontinued
  4. Vasculitis or Ab against hair follicles - focal alopecia areata-like with patchy hair loss
34
Q

Topical steroids and alternatives for skin lesions in SLE

A

Facial - low to medium potency non-fluorinated
(hydrocortisone, desonide)

Trunk/arm - medium potency, fluorinated
(betamethasone valerate, triamcinolone acetonide)

Hypertrophic - high potency, fluorinated
(betamethasone diproprionate, clobetasol)

Alternatives
Topical tacrolimus BD for 3 weeks

35
Q

Management of resistant SCLE

A
  1. Stop smoking - affects HCQ effect
  2. Hydroxychloroquine: LE > SCLE > DLE
  3. Steroids < 30mg/day
  4. Belimumab
  5. Bullous: dapsone
  6. SCLE: MMF, metinoids, cyclosporine, dapsone
  7. DLE: HCQ +/- quinacrine, thalidomide, cyclosporin
  8. Lupus profundus: dapsone
  9. > 50% chronic lesions: tacrolimus, MMF, belimumab
  10. Vasculitis: systemic ISTs
  11. Hyperkeratotic: oral retinoids
  12. Trial drugs: apremilast, ustekinumab, JAK inhibitors
36
Q

What are the lupus conditions that warrant high dose corticosteroids (>1mg/kg/day)

A
  1. Severe lupus nephritis
  2. CNS lupus, transverse myelitis
  3. Autoimmune thrombocytopenia with Plt < 30
  4. AIHA
  5. Acute pneumonitis
  6. Diffuse alveolar haemorrhage (DAH)
  7. Severe vasculitis with visceral organ involvement
  8. Pleuritis, pericarditis, peritonitis
  9. MAS
37
Q

Osteonecrosis and avascular necrosis risk in SLE

A

In patient with SLE presenting with progressive hip pain in the groin

Higher Risks
1. High dose prednisolone > 20mg/day over 1 month
2. Other end organ damage from steroid use
3. Antiphospholipid antibodies
4. Raynaud’s phenomenon

Considerations and Management
1. Consider septic arthritis as differential
2. MRI of bilateral hip (50% involvement of contralateral side)
3. Core decompression if >25% femoral head involved, and without bony collapse

38
Q

How does ESR, CRP , WBC count, complements help in identifying disease activity or infection in SLE?

A
  1. ESR - might remain elevated even when disease is controlled (persistent polyclonal gammopathy)
  2. CRP < 6 times ULN during disease flare
    - > 6 times suggestive of infection, systemic vasculitis, significant serositis
    - Fever + raised CRP - must rule out infection
  3. WBC
    - Leukopenia in SLE flare, or due to infection
    - Deceiving normal SLE in low WBC SLE in acute infection
    - Left shifting - infection
  4. Procalcitonin and lactate - bacterial infection
  5. Complements
    - Drop in SLE flare
    - Rise in infection
39
Q

Serology test for SLE disease activity and prediction of disease flare

A
  1. Low C3 (C4 may be chronically low)
  2. High dsDNA

Patients usually are serologically active and flare, but certain caveats:
1. Serologically active, never flare
2. Flare with no change to serology

Important to establish serology patterns of each patient

To adjust immunosuppression only in those who demonstrates serologically activity correlating with flare

40
Q

Overall review in management of SLE

A
  1. Explore other causes than SLE - infection, thrombosis, drug side effect, hypothyroidism, fibromyalgia, sleep apnoea

Mild disease - fatigue, arthritis, rash, serositis
1. NSAIDs - watch renal function, photosensitivity, aseptic meningitis
2. Hydroxychloroquine
3. Low dose prednisolone, taper to lowest effective dose
4. Methorexate or leflunomide

Moderate disease - unresponsive severe minor symptoms
1. MMF or AZA
2. Belimumab
3. Prednisolone 20-40mg/day
4. Calcineurin inhibitors (CyA or tacrolimus)

Severe disease - nephritis, CNS, pneumonitis, vasculitis, severe cytopenias
1. High dose prednisolone or pulse methylpred
2. Cytotoxic induction: CYC
(or biologics: rituximab - limited data)
3. Manitenance with AZA, MMF, CNI
4. Additional therapies might be needed
- Plasma exchange
- IVIg
- Stem cell transplant

41
Q

Emerging biologics and small molecule therapies in SLE

A
  1. Belimumab
  2. Rituximab

TNF-inhibitors - mixed or negative results
1. Abatacept
2. Epratuzumab
3. Tabalumab
4. Ocrelizumab
5. Tocilizumab

Oral JAK inhibitors - atacicept
Low dose IL-2 apremilast
Ustekinumab

42
Q

Commonest morbidities and mortalities in SLE

A

Morbidities
1. Renal failure
2. AVN
3. Neuropsychiatric deficits
4. Cardiovascular disease
5. Disfiguring skin lesion
6. Osteoporosis

Mortalities
1. Infection - each increase of pred by 10mg/day incrases risk 11 fold
2. Active SLE - lupus nephritis, CNS lupus, vasculitis, pneumonitis
3. Cardiovascular disease
4. Malignancy

Overall 5-year survival rate improved to 95%, 10-year 90% from early diagnosis and aggressive treatment

MRCP PACES Consultations (History, Miscellaneous) (23 decks)

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