What is systemic lupus erythematosus?

SLE (lupus) is a chronic autoimmune disease where the immune system attacks the body's own tissues — causing inflammation and damage in any organ. It is characterised by autoantibody production (particularly ANA and anti-dsDNA), complement activation and immune complex deposition. SLE affects approximately 5 million people globally, with a 9:1 female predominance and onset typically in women aged 15-40 — making it one of the most impactful conditions for women's health and reproductive years.

What are the symptoms of SLE?

SLE is the "great imitator" with diverse manifestations: constitutional (fatigue — present in >90%; fever; weight loss); musculoskeletal (arthralgia and arthritis — most common symptom, 90%); skin (malar rash, photosensitivity, discoid rash, oral ulcers, hair loss); kidneys (lupus nephritis — haematuria, proteinuria); neuropsychiatric (seizures, psychosis, stroke — neuropsychiatric SLE, NPSLE); blood (haemolytic anaemia, thrombocytopenia, leucopenia); cardiopulmonary (pleuritis, pericarditis, myocarditis, pulmonary hypertension); and thrombosis (antiphospholipid syndrome in approximately 30-40%).

Why does SLE affect women so much more than men?

The pronounced female predominance of SLE reflects sex hormone effects on immune function: oestrogens promote B-cell survival and autoantibody production; testosterone has immunosuppressive effects. SLE onset coincides with reproductive years (oestrogen peak) and may improve after menopause. Pregnancy flares are common. X-chromosome genes related to immune function may also contribute — XX females have "overdoses" of some immune genes. Despite lower incidence, men with SLE may have more severe organ involvement.

What is lupus nephritis?

Lupus nephritis (LN) — kidney inflammation from immune complex deposition — develops in 30-50% of SLE patients and is the main determinant of long-term outcome. It presents with proteinuria (the first sign), haematuria, hypertension and renal impairment. Kidney biopsy diagnoses and classifies LN by ISN/RPS classification (Class I-VI — from minimal to advanced sclerosing). Standard treatment: corticosteroids + mycophenolate mofetil (or cyclophosphamide for severe proliferative LN) + belimumab and/or voclosporin (new standard of care).

What is the role of hydroxychloroquine?

Hydroxychloroquine (HCQ) — an antimalarial — is taken by virtually all SLE patients throughout their lives unless contraindicated. Its benefits: reduces flare frequency by approximately 50%; prevents lupus nephritis; reduces thrombosis risk; lowers mortality; has antilipidaemic effects; is safe in pregnancy. The importance of HCQ was dramatically highlighted during COVID-19 — when SLE patients needed to continue HCQ despite global shortages from unproven COVID-19 use.

What are the new treatments for SLE?

Beyond hydroxychloroquine and corticosteroids: Belimumab (BLyS inhibitor — reduces B-cell survival): approved for SLE and LN; Voclosporin (calcineurin inhibitor): approved for LN in combination with mycophenolate — dramatically improves renal response rates; Obinutuzumab (anti-CD20): Phase 3 trials showing significant benefit in LN. JAK inhibitors (baricitinib) and anifrolumab (type I interferon receptor antibody) — approved for active SLE.

How does SLE affect pregnancy?

SLE significantly complicates pregnancy: spontaneous miscarriage rate is 2-3 times higher; preeclampsia occurs in 15-30%; preterm birth in 25%; and fetal growth restriction is common. Anti-Ro/SSA antibodies cause neonatal lupus (skin rash, heart block in approximately 2-3% of exposed fetuses — potentially requiring pacemaker). Mycophenolate is teratogenic and must be stopped 3+ months before conception. Hydroxychloroquine is safe and protective. Pregnancies should be planned during sustained quiescence.

Why does SLE take so long to diagnose?

SLE mimics many other conditions — particularly in early stages: arthralgia mimics rheumatoid arthritis; rash mimics eczema or rosacea; fatigue mimics depression or anaemia; neurological symptoms suggest many causes. The ANA screening test has low specificity (10-15% of healthy people are ANA-positive). SLE classification requires meeting ≥10 points across domains in the 2019 ACR/EULAR criteria — not always met early. Average diagnostic delay of 6 years causes significant morbidity from untreated disease.

What ethnic groups are most affected?

SLE is more common and more severe in women of African, African-Caribbean, Asian and Hispanic ancestry than in white European-ancestry women. Black women have 3-4 times higher prevalence, more lupus nephritis, more severe disease, and higher mortality than white women. This disparity reflects genetic factors (APOL1 variants increase lupus nephritis risk in African ancestry), socioeconomic factors reducing healthcare access, and potentially environmental exposures.

How does GMJ News cover SLE?

GMJ News covers WHO SLE data, belimumab and voclosporin approvals, lupus nephritis outcomes, antiphospholipid syndrome, pregnancy in SLE, and ethnic disparities. SLE is directly relevant to PHIG's women's health priorities and the Georgian Medical Journal's rheumatology and nephrology coverage.

Home › Topics › Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus (SLE)

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Systemic lupus erythematosus (SLE) — the most common form of lupus — is a chronic autoimmune disease causing widespread inflammation that can damage any organ system: joints, skin, kidneys, brain, heart and lungs: it affects approximately 5 million people globally, with a striking 9:1 female predominance and peak onset in women of reproductive age 15-40 (WHO). Lupus nephritis — kidney involvement in approximately 30-50% of SLE patients — is the primary cause of organ failure and death in SLE. New targeted therapies (belimumab, voclosporin, obinutuzumab) are transforming lupus nephritis outcomes.

Key messages

5 million people — 9:1 female predominance

Systemic lupus erythematosus (SLE) affects approximately 5 million people globally with a striking 9:1 female predominance — and typically presents in women of reproductive age 15-40. It is the archetypal autoimmune disease (WHO).

Can affect any organ

SLE is a multisystem autoimmune disease — causing inflammation in joints, skin, kidneys, brain, lungs, heart, blood cells and blood vessels. Clinical manifestations are protean and vary widely between patients, making SLE one of medicine's great clinical challenges.

Lupus nephritis most serious

Lupus nephritis — kidney involvement in 30-50% of SLE patients — is the primary determinant of long-term prognosis. If untreated, it leads to end-stage kidney disease. Voclosporin and belimumab have transformed lupus nephritis outcomes.

Diagnostic delay

SLE takes an average of 6 years to diagnose from first symptoms — because it mimics many other conditions. The ACR/EULAR 2019 classification criteria standardise diagnosis. Antinuclear antibody (ANA) screening is the first-line diagnostic test.

Chronic condition requiring lifelong management

SLE is a relapsing-remitting disease requiring lifelong care. Hydroxychloroquine is taken by virtually all SLE patients — it reduces flare risk by 50%, prevents organ damage and reduces mortality.

Pregnancy and SLE

SLE significantly complicates pregnancy — increasing risk of miscarriage, preeclampsia, preterm birth and fetal growth restriction. Medications must be carefully managed (hydroxychloroquine is safe; mycophenolate is teratogenic). Pregnancies should be planned during disease quiescence.

Key statistics

people with SLE globally

WHO

9:1

female to male ratio

WHO/EULAR

15-40yr

typical age of onset

WHO

30-50%

of SLE patients develop lupus nephritis

WHO/EULAR

6yr

average diagnostic delay

Lupus Foundation/research

50%

flare rate reduction with hydroxychloroquine

Cochrane/EULAR

SLE prevalence (per 100,000 population) by ethnicity/region — published studies

Source: SLE disproportionately affects women of African, Asian and Hispanic ancestry.

Glossary of key terms

Antinuclear antibody (ANA)
WHO/ACR/EULARAutoantibodies targeting components of the cell nucleus — the cornerstone of SLE diagnosis. ANA is positive in >95% of SLE patients but is non-specific (positive in 10-15% of healthy individuals). A positive ANA should prompt testing for specific antibodies (anti-dsDNA, anti-Sm, anti-SSA/SSB).

Anti-dsDNA antibody
ACR/EULARAntibodies against double-stranded DNA — highly specific for SLE (90-95%). Titres correlate with disease activity — rising titres predict flares; declining titres indicate response to treatment. Pathogenic in lupus nephritis.

Hydroxychloroquine (HCQ)
WHO EML/ACR/EULARAn antimalarial drug used in virtually all SLE patients — the backbone of SLE therapy. Reduces flare risk by 50%, prevents organ damage, reduces mortality, is safe in pregnancy, and has cardiovascular protective effects. WHO Essential Medicine.

Belimumab (Benlysta)
FDA/EMAThe first biologic therapy specifically approved for SLE — a monoclonal antibody targeting BLyS (B-lymphocyte stimulator), reducing B-cell survival. Reduces flare rates, steroid requirements and lupus nephritis progression. Available IV and SC.

Lupus nephritis (LN)
WHO/ERA-EDTAKidney involvement in SLE — from immune complex deposition (IgG + anti-dsDNA + complement). Manifests as proteinuria, haematuria, hypertension, renal impairment. ISN/RPS classification grades severity (I-VI). Treated with glucocorticoids + mycophenolate or cyclophosphamide.

Malar (butterfly) rash
ACR/WHOAn erythematous ("blush") rash over the cheeks and nose bridge — one of the classic manifestations of SLE, occurring in approximately 50% of patients. Triggered or worsened by sun exposure. Spares the nasolabial folds (distinguishing from rosacea).