Module 3.2.2 (Management of SLE) Flashcards

1
Q

What are the risk factors for SLE?

A
  • Females have 9 fold higher risk
  • Genetics (44% factor)
  • Infection
  • Smoking
  • Chemicals
  • Medications
  • Exposure to UV light
  • Diet
  • Stress
  • Pregnancy
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2
Q

How to do the diagnosis of SLE? Describe in further detail.

A

Diagnosis based on clinical S and S, lab tests and neuroimaging (CT and MRI)

Presenting symptoms:

  • Musculoskeletal symptoms, fatigue, rash
  • Organs are often affected sequentially rather than concurrently
  • Can co-exist with other autoimmune diseases

Diagnosis based on 4 or more than 4 of these symptoms

  • Serositis –> inflammation of the lining around the lungs and the heart
  • Oral ulcers
  • Arthritis –> joint pain and swelling of more than or equal to 2 joints
  • Photosensitivity
  • Blood dyscrasias (anaemia, leucopenia, lymphopenia, thrombocytopenia)
  • Renal involvement (proteinuria or cellular casts in urine(
  • Antinuclear-antibodies (ANA)
  • Imunnologic phenomena –> antibodies to double stranded DNA or anti-SM antibodies or antiphospholid antibody
  • Neurologic disorders –> seizures or psychosis
  • Malar rash –> rash on cheeks and nose, often in the shape of a butterfly
  • Discoid rash –> red, raised, round patches. Commonly on scalp and face.
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3
Q

Describe what a mild,moderate and severe flare is in SLE.

A

Mild flare

  • New onset low-grade fevers, malar rash, arthralgias, increasing fatigue, mild leucopaenia

Moderate flare

  • Pleuritic chest pain, swelling of the wrists, elevated APRs (CRP, ESR)

Severe flare

  • New-onset renal insufficiency and significant proteinuria (lupus nephritis)
  • Low C3, C4 elevated dSDNA antibodies and APRs
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4
Q

What medications to exclude when making a diagnosis of SLE? Symptoms resolve when these medications are ceased.

A
  • Procainamide
  • Disopyramide
  • Hydralazine
  • Propylthiouracil
  • Chlorpromazine
  • Lithium
  • Carbamazepine
  • Phenytoin
  • Sulfasalazine
  • Hydrochlorothiazide
  • Simvastatin
  • Interferons
  • TNF-a inhibitors
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5
Q

Aims of treatment for SLE

A
  • Prevent organ damage
  • Minimise drug toxicity
  • Improve QOL
  • Ensure long-term survival
  • Engage patients in disease management
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6
Q

What are some non pharmacological treatment options for SLE?

A

Sun protection

  • Avoid exposure to UV light; SPF 50+ sunscreens

Diet and nutrition

  • Healthy balanced diet
  • Monitor vitamin D levels
  • Fish oil at least 2.7g daily (omega 3)
  • Sodium restriction in hypertension and/or nephritis

Exercise

  • To address loss of muscle mass, bone demineralisation, loss of stamina

Smoking cessation

  • Smoking is associated with more active disease, increases CV risk, and may decrease the efficacy of hydroxychloroquine

Immunisations

Treat comorbid conditions

  • Atherosclerosis, pulmonary hypertension, antiphospholipid syndrome, osteopaenia or osteoporosis
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7
Q

What is first-line pharmacological treatment for SLE? What does this medication do?

A

Hydroxychloroquine 200-400mg daily 1st line unless C/I

  • Relieves constitutional (fatigue), musculoskeletal and mucocutaneous symptoms.
  • May reduce flare rates, thrombotic events, organ damage, mortality.
  • Reduces lipid levels.
  • Ocular toxicity is a AE –> regular ophthalmology review every 6-12 months
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8
Q

MILD SLE (skin joint and mucous involvement). What drugs are used to cure it?

A
  • Hydroxychloroquine (delayed onset of action)
  • Use NSAIDs in the meantime
  • and/or short-term low dose corticosteroid (< 7.5mg prednisolone daily)
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9
Q

MODERATE SLE (significant but non-organ threatening disease). What drugs are used to cure it?

A
  • Hydroxychloroquine
    • short term prednisolone 5-15 mg daily (tapered once hydroxychloroquine has taken effect)
  • steroid-sparing immunosuppressant (e.g. azathioprine 1.5-2.5 mg/kg daily or methotrexate 10-25 mg PO/subcut once weekly) often required
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10
Q

SEVERER OR LIFE-THREATENING SLE (major organ involvement e.g. renal, CNS). What drugs are used to cure it?

A

Intensive immunosuppressive therapy to control disease and stop tissue injury.

  • IV methylprednisolone 0.5-1g daily for 3 days
  • Alone or in combination with other immunosuppressants

> mycophenolate mofetil or sodium

> azathioprine

> cyclophosphamide orally or IV

> rituximab

then less intensive and less toxic to help remission and prevent flares –> including down tritration of corticosteroid

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11
Q

What are some other pharmacological treatments for SLE?

A

Biological DMARDs

  • role in SLE unclear

Rituximab –> two doses of 1g IV, given 2 weeks apart

  • No benefit in heterogenous SLE populations
  • Potential role in certain patient subgroups (e.g. refractory lupus nephritis)

Belimumab –> 10mg/kg IV on days 0, 14 and 28, then every 4 weeks

  • Add on therapy in SLE
  • No data in severe SLE with CNS involvement or nephritis
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12
Q

For reproductive health in women with SLE;

A) COC can induce SLE flare in some women, what needs to be monitored

B) Pregnancy can induce SLE flare, what to do before and during pregnancy.

C) Can HRT be used for post-menopause

A

A)

  • Monitored clinically after 3 months. Monitor ESR, CRP, and DNA antibody levels
  • If significant flare –> consider alternative contraceptive (progesterone only or condoms)

B)

  • Ensure good control before conception
  • Recommended to continue hydroxychloroquine throughout pregnancy

C)

  • Yes, it is not associated with an increase in flares.
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13
Q

How is monitoring done for SLE?

A
  • Clinical monitoring –> S and S

Laboratory markers

  • APRs (acute phase reactants such as ESR and CRP), anti-dsDNA antibodies, C3/C4 (reduces in disease flare)
  • CLCr, urinalysis, spot urine protein to creatinine ratio (monitor for the onset of lupus nephritis)
  • FBP because of SLE but also immunosuppressants cause blood dyscrasias

Drug side effects may be confused with SLE

  • e.g. hypomania with high-dose corticosteroids, abnormal LFTs with methotrexate

Infection due to immunosuppression

  • May also be hard to distinguish from a disease flare
  • CRP may be more elevated than ESR in infection
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