Just who is at risk for organ damage? What factors contribute to it? How does it impact patients and their lives? And, most importantly, what treatment strategies can slow its progress? 


Patients at Risk

How many of your patients with SLE could be at risk for developing permanent organ damage?

Organ damage begins to accrue early, with as many as 50% of patients showing evidence of irreversible damage* within 5 years of SLE diagnosis7-9

* Based on Systemic Lupus International Collaborating Clinics /American College of Rheumatology Damage Index (SDI) measurements

Percentage of patients with permanent organ damage7,8

Chart showing the percentage of patients with permanent organ damage (by SDI) at 1 Year and 5 Years

Damage is defined as an irreversible tissue injury occurring after SLE diagnosis and lasting at least 6 months.9 SDI is the internationally agreed and validated measure of organ damageA limitation of the SDI is that it may also capture damage that may not be related to SLE specifically.

Patient Burden

How can permanent organ damage affect your patients?

Icon: Organ Damage leads to the risk of additional damage and icreased mortality

leads to the risk of additional damage and increased mortality8,11,12

Long-Term Considerations

Patients with SLE now live longer, with survival rates improving significantly over the last 50 years.10 This improved longevity has created a situation where SLE patients accrue more organ damage over time. Evidence also indicates that clinicians should be particularly vigilant during the early course of SLE.

Once organ damage occurs, the risk of additional damage and mortality are increased.8,11,12 Patients at risk for further damage should be monitored closely for adverse effects of medication and the development of co-morbidities and complications of SLE.8  

Even with low/moderate disease activity, patients still accrue organ damage. Multiple factors may contribute to damage accrual, including the chronic use of corticosteroids.4,7 In particular, the risk of cumulative steroid dose may be more important to consider than duration of exposure.13

Icon: No Clinical Symptoms

Hidden Damage

There is also a risk of organ damage accrual while the patient is completely unaware. For example, osteonecrosis may be asymptomatic in patients with SLE.14 Cardiovascular disease may also be subclinical in patients with SLE—prevalence of plaques in internal carotid arteries is 3 times higher and endothelial dysfunction, an early marker of atherosclerosis, is 2 times as common compared to the control group.15,16 

Which organs can be affected?

Several organ systems are commonly involved in SLE and should be carefully monitored for disease activity. Commonly-involved organ systems include the following: central nervous; renal; gastrointestinal; mucous membranes; cardiovascular; mucocutaneous; hematologic; musculoskeletal; and, pulmonary.4

Severity of the disease can vary from mild to potentially fatal, due to detrimental organ damage.17 

  • Skin

    Mucocutaneous involvement is almost universal in SLE. Manifestations include18:

    • rashes
    • photosensitivity
    • nasal and oral ulcers
    • alopecia
  • Brain

    Neuropsychiatric syndromes can affect many patients with SLE.19  They range from mild to severe. Common manifestations include:

    • cognitive dysfunction
    • headache
    • depression
    • anxiety
  • Eyes

    SLE may affect almost any part of the eye and the visual pathway. If a patient has ophthalmic issues, he or she should be referred to an ophthalmologist. The following symptoms may be a sign of potential complications.20

    • blurriness
    • dry eyes
    • loss of vision
    • pain
  • Heart

    Risks of coronary heart disease and stroke are significantly higher for patients with SLE compared to general population.21,22

    • Patients with SLE are at 2 to 10 times increased risk of CHD.
  • Kidneys

    Renal damage is one of the most serious complications of SLE.10 Usually manifesting during the early stage of SLE, renal disease has consistently been shown to be a major cause of mortality in patients with SLE.10

    • Urinalysis abnormalities or renal dysfunction exist in 35% of patients early in the course of the disease.23
    • Up to 60% of patients with SLE may develop clinically relevant nephritis over the course of their disease.24
  • Bones

    Patients with SLE are 5 times more likely to have a bone fracture than age-matched controls.25

    This is primarily due to the prolonged use of steroids in their treatment and age at SLE diagnosis.

    • The relative risk of osteoporotic fractures is increased 1.9-fold with a cumulative dose of 36.5 g of corticosteroids.26

Contributing Factors

What factors contribute to organ damage?

Persistent disease activity is linked to increased organ damage, which, in turn, is predictive of increased damage and mortality.

The changeable nature of SLE may make it difficult to predict when disease activity—in the form of flares—will occur.2

Complicating the picture, no consensus exists on how to assess patient outcomes and measure disease activity. Tools27-29, including SELENA-SLEDAI, BILAG and PGA, have been developed for use in clinical trials, but their use in real-world practice is limited. 

Drug-related side effects can also contribute to the accrual of organ damage.

  • Chronic corticosteroid use is associated with cataracts, diabetes mellitus, atherosclerotic heart disease, osteoporosis and osteonecrosis, and fluid retention17
  • Opportunistic infections and certain malignancies can develop, most often in patients receiving chronic immunosuppressive therapy30
  • Long-term use of NSAIDs is associated with GI bleeding and kidney damage17
  • There is evidence for multiple beneficial effects of hydroxychloroquine in SLE; however, patients should be monitored for potential retinal toxicities.31


Prevention and Management

How can organ damage be prevented or managed?

Minimize disease activity and flares

  • Persistent disease activity can result in ongoing organ damage4
    • Since damage predicts subsequent damage and death, prevention of the damage accrual should be a major therapeutic goal in SLE32
  • Prevention of flares (especially severe flares) is a realistic target in SLE and should be a therapeutic goal32

EULAR treatment recommendations highlight the importance of controlling disease activity and flares while also limiting steroid dose.27

EULAR=European League Against Rheumatism

Chart showing the irreversible damage accrual that may occur in SLE patients with long-term persistent disease activity

Graphical representation of a hypothetical disease course of a patient with SLE.

Reduce glucocorticoid use as much as possible

  • Glucocorticoids are invaluable in the treatment of SLE; however, their chronic use has consistently shown to increase irreversible damage in patients with lupus, a major predictor of morbidity and mortality33
    • In general, the risk of organ damage increases at 7.5 mg/day34
Graphic showing glucocorticoids usage greater than or equal to 7.5 mg/day leads to a 1.7 times greater risk of developing any new organ damage
Graphic showing glucocorticoids usage greater than or equal to 7.5 mg/day leads to a 1.7 times greater risk of developing any new organ damage
  • Dosage should be reduced to the minimum needed to control disease, or eliminated if possible.32,33,35 

Monitor for subclinical activity

  • Regular monitoring should be undertaken to detect "silent variables"36 
    • At 3-4-month intervals for patients with mild or inactive disease.

More Information


Can you do more to decrease disease activity and prevent flares with the lowest possible dose of glucocorticoids?3,27,32

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