Systemic lupus erythematosus (SLE)
PM&R News • December 2020
A 16-year-old black female presents to her primary care physician with symptoms of fatigue, musculoskeletal pain, and a facial rash. On examination she is noted to be thin with malar skin changes. No other abnormality is found.
Description
- Autoimmune disorder – systemic autoantibodies
- Multiple phenotypic presentations
- Remitting and relapsing course is common
Anatomy: Dependent on phenotypes expressed: any organ system can be involved
Pathophysiology
- Increased predisposition → cell damage (2/2 environment or infections) secondary to self-antigens → immune activation of T & B cells → immunity mediator release (cytokines, complement system, autoantibody activation) and ultimately tissue damage
Epidemiology
- U.S.: 20-150/100,000
- Females: 164 (Caucasians) – 406 (African Americans)/100,000
- Risk factors
- Female (10x > males): estrogen and prolactin encourage autoimmunity
- Child-bearing age: 16-55 (65%)
- (Androgens are protective)
- Genetics potentially have a role
- Klinefelter: 14x greater risk
- Drugs: > 100 triggers
- Ethnicity: African Americans > Asians & Hispanics > Caucasians
- Female (10x > males): estrogen and prolactin encourage autoimmunity
Differential Diagnoses:Rheumatoid Arthritis, Mixed connective tissue disease (SLE + systemic sclerosis + polymyositis), Undifferentiated connective tissue disease, Systemic sclerosis, Sjögren’s, Vasculitis, Behçet syndrome, Dermatomyositis and polymyositis , Adult Still’s disease, Kikuchi disease, Serum sickness, Fibromyalgia, Multiple sclerosis, Infections, Malignancies, and Thrombotic thrombocytopenic purpura.
Presentation/ Clinical Manifestations
- Symptoms
- Constitutional (90%): commonly initial presentation (fatigue, fever, weight loss)
- Photosensitivity* (90%): abnormal skin reaction that lasts weeks-months
- MC: malar rash or discoid lesion
- Brittle, broken hair
- MSK Issues (80-90%): polyarthritis/arthralgias (typically small joints and symmetrical)
- This is an early symptom
- Neuro Issues: MC → Intractable Headaches (50%)
- Also: delirium, psychosis, seizures, cognitive dysfunction
- Pleuritis (MC pulm manifestation)
- Raynaud Phenomenon*
- Joint pain/swelling*
- Pericarditis/serositis symptoms*
- Inquiry of drug reactions* (see table at end for a comprehensive list)
- Physical Exam findings
- Mucocutaneous lesions (80%): Acute/Subacute/Chronic cutaneous lupus erythematosus (A/S/CCLE) malar (butterfly) rash/photosensitive, widespread rash/ MC form: Discoid lupus erythematosus (DLE) ; respectively
- Malar: cheeks/bridge of nose: erythematous, raised, and pruritic
- Oral/Nasal ulcers*: typically painless
- Rheumatoid nodules
- Anemia: 50%
- CV: Pericarditis + exudative effusions(MC cardio manifestation)
- Also affects valves, pericardium/myocardium, conductive system, coronary arteries
- GI issues (dysmotility → ascites → pancreatitis)
- Ocular issues (keratoconjunctivitis sicca (dry eye syndrome) → optic neuritis)
- Renal involvement (50%)
- Hair loss*: “patchy or frontal/peripheral”
- Mucocutaneous lesions (80%): Acute/Subacute/Chronic cutaneous lupus erythematosus (A/S/CCLE) malar (butterfly) rash/photosensitive, widespread rash/ MC form: Discoid lupus erythematosus (DLE) ; respectively
*Up to date notes most commonly observed findings when suspecting SLE
Diagnosis
- Labs:
- CBC with diff
- Serum, creatinine
- UA
- ESR/CRP levels
- urine protein:creatinine ratio
- Antinuclear antibodies (ANA): diagnostic hallmark; (+) in 97%; seen in other disorders
- Gold standard: Immunofluorescence assay
- If Positive, proceed with the below testing:
- Anti-Ds-DNA antibodies (95% Sp): 60-70%
- Gold standard: Farr radioimmunoassay test
- Anti-Smith antibodies (99% Sp): <30%
- Antiphospholipid antibodies
- Complements C3 and C4: ↓; indicative of depletion and potential estimates of severity
- Imaging and biopsy: dependent on involved organs and clinical presentation
-
Definitive Diagnosis: “…no single clinical feature or lab abnormality can confirm a diagnosis of SLE. SLE is diagnosed based on the constellation of signs, symptoms and appropriate laboratory workup.”
- Up to date recommends referral to experienced rheumatologist:
- Exclude other diagnoses + fulfills the 1997 American College of Rheumatology (ACR) criteria OR
- the 2012 Systemic Lupus International Collaborating Clinics (SLICC) criteria
- Probable dx: 2-3 ACR or SLICC criteria + 1 of the following:
- Optic neuritis, aseptic meningitis
- Glomerular hematuria
- Pneumonitis, pulmonary hemorrhage, or pulmonary hypertension, interstitial lung disease
- Myocarditis, verrucous endocarditis (Libman-Sacks endocarditis)
- Abdominal vasculitis
- Raynaud phenomenon
- Elevated acute phase reactants (eg, ESR and CRP)
- Up to date recommends referral to experienced rheumatologist:
Treatment
- Goals: Improve morbidity, decrease mortality, reduce the risk of organ damage, ↑ QOL, patient education
- Individualized and dependent on manifestations
- Pharmacologic: hydroxychloroquine or chloroquine
- Mild: +/- NSAIDs ; +/- short-term glucocorticoids (low dose; ie: prednisone <5mg qd)
- Mod (constitutional, cutaneous, MSK, or hematologic): + short-term prednisone (5-15 mg)
- Severe: immunosuppressive therapy → systemic glucocorticoids (high-doses): 1-2 mg/kg/day of prednisone +/- other immunosuppressive agents
- Monitoring: CBC, ESR, CRP, spot urine protein and creatinine, serum creatinine, eGFR, anti-double-stranded deoxyribonucleic acid (dsDNA), and C3 & C4.
Complications
- Increased risk for: seizures, strokes, fibromyalgia (20%), aseptic meningitis, demyelinating syndrome, movement disorders, cranial/peripheral neuropathies, depression/anxiety/psychosis, lupus nephritis (proteinuria Sx’s: HTN, hematuria, proteinuria, LE edema, ↑Creatinine), CAD (2/2 coronary vasculitis or atherosclerosis), spontaneous abortions (more so with AP antibodies), and non-Hodgkin lymphoma
Prognosis
- Poor if any of the following present: renal disease, HTN, male sex, extremes of age at presentation, low SES, black race, and/or Antiphospholipid antibodies.
- 2-5x higher mortality
Patient Education
- Triggers for flare-ups: Estrogen (OCPs and hormone replacement therapy), UV light, sulfa-based drugs, smoking (dose-dependent), silica exposure, viral infections, vitamin D deficiency, alfalfa sprouts, and canavanine containing foods.
- Sun protection
- Diet and exercise
- Smoking cessation
- Immunizations (see chart at end)
- Avoiding certain meds
- Pregnancy/contraception counseling
References:
- https://emedicine.medscape.com/article/332244-overview
- https://www.ncbi.nlm.nih.gov/books/NBK535405/
- https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-systemic-lupus-erythematosus-in-adults
- https://www.uptodate.com/contents/overview-of-the-management-and-prognosis-of-systemic-lupus-erythematosus-in-adults?topicRef=4668&source=see_link
- https://www.uptodate.com/contents/epidemiology-and-pathogenesis-of-systemic-lupus-erythematosus?topicRef=4668&source=see_link
- Vignette
Photo by Mustafa Omar on Unsplash
Review Question
What foods should be avoided in those with SLE?Answer
Foods to avoid include: garlic, alfalfa sprouts, and echinacea.
