Chronic Care Programme
Treatment guidelines
Systemic Lupus Erythematosus
Chronic condition
Consultations protocols
Preferred treating provider
Notes
 preferred as indicated by option
 referral protocols apply
Option/plan
Provider
GMHPP
Gold Options
G1000, G500
and G200.
Blue Options
B300 and B200.
GMISHPP
General Practitioner
Paediatrician
Cardiologist
Neurologist
Physician
Pulmonologist
Dermatologist
Mild
Maximum consultations per annum
 Initial consultation
 Follow-up consultation
Tariff codes
New Patient
Existing Patient
1
1
1
1
0183; 0142; 0187; 0108
Severe
New & Existing patient
1
1
Investigations protocols
Type
Provider
Tariff
code
Urine dipstick (per stick,
irrespective of the number of
tests on stick)
Blood glucose: quantitative
Blood glucose: strip test with
photometric reading
ECG without effort
Flow volume test:
inspiration/expiration
ESR
CRP
ANF (Auto-antibodies by
labelled anti-bodies)
Anti-DNA
Anti-phospholipids
antibodies
Haemoglobin estimation
Leucocytes: total count
Platelets
AST
ALT
GGT
Alkaline phosphatase
Serum albumin
Serum potassium
GP; Specialist;
Pathologist
Maximum investigations per annum
New patient
Existing patient
New & Existing
patient
4188
6
4
6
GP; Specialist;
Pathologist
GP; Specialist;
Pathologist
GP or Specialist
(see list)
GP or specialist
(see list)
GP; Specialist;
Pathologist
Pathologist
Pathologist
4057
1
1
1
4050
1
1
1
1232
1
0
1
1168
1
0
1
3743
4
2
4
3947
3934
1
1
1
1
1
2
Pathologist
Pathologist
4182
3934
1
1
1
1
2
2
GP; Specialist;
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
3762
4
4
6
3785
3797
4130
4131
4134
4001
3999
4113
4
4
0
0
0
0
0
1
4
4
0
0
0
0
0
1
6
6
6
6
1
6
1
4
Serum sodium
Serum urea
Serum creatinine
Creatinine clearance
Urine protein (quantitative)
Pathologist
Pathologist
Pathologist
Pathologist
Pathologist
ICD 10 coding
4114
4151
4032
4223
4213
1
2
2
1
1
1
2
2
1
1
4
4
4
2
2
M32. L93.
General
Systemic lupus erythematosus (SLE or lupus) is a chronic autoimmune disease that can be
fatal, though with recent medical advances, fatalities are becoming increasingly rare. As with
other autoimmune diseases, the immune system attacks the body’s cells and tissue, resulting in
inflammation and tissue damage. SLE can affect any part of the body, but most often harms the
heart, joints, skin, lungs, blood vessels, liver, kidneys and nervous system. The course of the
disease is unpredictable, with periods of illness (called flares) alternating with remission. Lupus
can occur at any age, and is most common in women, particularly of non-European descent.[1]
Lupus is treatable symptomatically, mainly with corticosteroids and immunosuppressants, though
there is currently no cure. Survival in patients with SLE in the United States, Canada and Europe
is approximately 95% at 5 years, 90% at 10 years, and 78% at 20 years.[2]
Classification
Lupus is a chronic autoimmune disease. Clinically, it can affect multiple organ systems including
the heart, skin, joints, kidneys and nervous system. There are several types of lupus; generally
when the word 'lupus' alone is used, it refers to the systemic lupus erythematosus or SLE as
discussed in this article. Other types include:

Drug-induced lupus erythematosus, a drug-induced form of SLE; this type of lupus can
occur equally for either gender

Lupus nephritis, an inflammation of the kidneys caused by SLE

Discoid lupus erythematosus, a skin disorder which causes a red, raised rash on the
face,and scalp. Discoid Lupus occasionally (1-5%) develops into SLE[3]

Subacute cutaneous lupus erythematosus, which causes non-scarring skin lesions on
patches of skin exposed to sunlight[4]

Neonatal lupus, a rare disease affecting babies born to women with SLE, Sjögren's
syndrome or sometimes no autoimmune disorder. It is theorized that maternal antibodies
attack the fetus, causing skin rash, liver problems, low blood counts (which gradually
fade) and heart block leading to bradycardia.[4]
Signs and symptoms
SLE is one of several diseases known as "the great imitators" [5] because its symptoms vary so
widely it often mimics or is mistaken for other illnesses, and because the symptoms come and go
unpredictably. Diagnosis can be elusive, with patients sometimes suffering unexplained
symptoms and untreated SLE for years. Common initial and chronic complaints are fever,
malaise, joint pains, myalgias and fatigue. Because they are so often seen with other diseases,
these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in
conjunction with other signs and symptoms (below), however, they are considered suggestive.
Common symptoms explained
Dermatological manifestations
As many as 30% of patients present with some dermatological symptoms (and 65% suffer such
symptoms at some point), with 30% to 50% suffering from the classic malar rash (or butterfly
rash) associated with the disease. Patients may present with discoid lupus (thick, red scaly
patches on the skin). Alopecia, mouth, nasal, and vaginal ulcers, and lesions on the skin are also
possible manifestations.
Musculoskeletal manifestations
Patients most often seek medical attention for joint pain, with small joints of the hand and wrist
usually affected, although any joint is at risk. The Lupus Foundation of America "estimates more
than 90 percent will experience joint and/or muscle pain at some time during the course of their
illness".[6] Unlike rheumatoid arthritis, lupus arthritis is less disabling and it usually does not
cause severe destruction of the joints. Fewer than 10 percent of people with lupus arthritis will
develop deformities of the hands and feet.[6]
Hematological manifestations
Anemia and iron deficiency may develop in as many as half of patients. Low platelet and white
blood cell counts may be due to the disease or a side-effect of pharmacological treatment. Patients
may have an association with antiphospholipid antibody syndrome (a thrombotic disorder) where
autoantibodies to phospholipids are present in the patient's serum. Abnormalities associated with
antiphospholipid antibody syndrome include a paradoxical prolonged PTT (which usually occurs
in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of
such findings have earned the term "lupus anticoagulant positive". Another autoantibody finding
in lupus is the anticardiolipin antibody which can cause a false positive test for syphilis.
Cardiac manifestations
Patients may present with inflammation of various parts of the heart, such as pericarditis,
myocarditis, and endocarditis. The endocarditis of SLE is characteristically non-infective
(Libman-Sacks endocarditis) and involves either the mitral valve or the tricuspid valve.
Atherosclerosis also tends to occur more often and advance more rapidly in SLE patients than in
the general population.[7][8][9]
Pulmonary manifestations
Lung and pleura inflammation can cause pleuritis, pleural effusion, lupus pneumonitis, chronic
diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, pulmonary
hemorrhage.
Hepatic involvement
See autoimmune hepatitis
Renal involvement
Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or
chronic renal impairment may develop with lupus nephritis, leading to acute or end stage renal
failure. Because of early recognition and management of SLE, end stage renal failure occurs in
less than 5% of patients.
Histologically, a hallmark of SLE is membranous glomerulonephritis with "wire loop"
abnormalities.[10] This finding is due to immune complex deposition along the glomerular
basement membrane leading to a typical granular appearance in immunofluorescence testing.
Neurological manifestations
About 10% of patients may present with seizures or psychosis. A third may test positive for
abnormalities in the cerebrospinal fluid.
T-cell abnormalities
Abnormalities in T cell signaling are associated with SLE, including deficiency in CD45
phosphatase and increased expression of CD40 ligand.
Other rarer manifestations
lupus gastroenteritis, lupus pancreatitis, lupus cystitis, autoimmune inner ear disease,
parasympathetic dysfunction, retinal vasculitis, and systemic vasculitis.
Other abnormalities include:

Increased expression of FcεRIγ, which replaces the sometimes deficient TCR ζ chain

Increased and sustained calcium levels in T cells

Moderate increase of inositol triphosphate

Reduction in PKC phosphorylation

Reduction in Ras-MAP kinase signaling
 Deficiencies in protein kinase A I activity
Diagnosis
Microphotograph of a histological section of human skin prepared for direct immunofluorescence
using an anti-IgG antibody. The skin is from a patient with systemic lupus erythematosus and
shows IgG deposit at two different places : the first is a band-like deposit along the epidermal
basement membrane ("lupus band test" is positive), the second is within the nuclei of the
epidermal cells (anti-nuclear antibodies are present).
Some physicians make a diagnosis on the basis of the ACR classification criteria (see below). The
criteria, however, were established mainly for use in scientific research (i.e. inclusion in
randomized controlled trials), and patients may have lupus but never meet the full criteria.
Anti-nuclear antibody testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay
of serologic testing for lupus. Antiphospholipid antibodies occur more often in SLE, and can
predispose for thrombosis. More specific are the anti-smith and anti-dsDNA antibodies. Other
tests routinely performed in suspected SLE are complement system levels (low levels suggest
consumption by the immune system), electrolytes and renal function (disturbed if the kidney is
involved), liver enzymes and a complete blood count.
Formerly, the lupus erythematosus (LE) cell test was not commonly used for diagnosis because
those LE cells are only found in 50-75% of SLE patients, and are also found in some patients with
rheumatoid arthritis, scleroderma, and drug sensitivities. Because of this, the LE cell test is now
performed only rarely and is mostly of historical significance.[16]
Diagnostic criteria
The American College of Rheumatology (ACR) has established eleven criteria in 1982,[17] which
were revised in 1997[18] as a classificatory instrument to operationalise the definition of SLE in
clinical trials. They were not intended to be used to diagnose individual patients and do not do
well in that capacity. For inclusion in clinical trials, patients must meet the following three criteria
to be classified as having SLE: (i) patient must present with four of the below eleven symptoms
(ii) either simultaneously or serially (iii) during a given period of observation.
1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis
(inflammation of the membrane around the heart)sensitivity = 56%; specificity = 86%
(pleural is more sensitive; cardiac is more specific)[19]
2. Oral ulcers: include oral or nasopharyngeal ulcers
3. [[Arthritis]]: nonerosive arthritis of two or more peripheral joints, with tenderness,
swelling or effusionsensitivity = 86%; specificity = 37%[19]
4. [[Photodermatitis|Photosensitivity]] (exposure to ultraviolet light causes rash). sensitivity
= 43%; specificity = 96%[19]
5. Blood: Hematologic disorder: Hemolytic anemia (low red blood cell count) or leukopenia
(white blood cell count<4000/ul), lymphopenia ( <1500/ul ) or thrombocytopenia
(<100000/uL) in the absence of offending drug.sensitivity = 59%; specificity = 89%[19]
Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune
complex-induced inflammation, or to congenitally complement deficiency, which may
predispose to SLE.
6. Renal disorder: More than 0.5 g per day protein in urine, or cellular casts seen in urine
under a microscope.sensitivity = 51%; specificity = 94%[19]
7. [[Anti-nuclear antibody]] test positive. sensitivity = 99%; specificity = 49%[19]
8. Immunologic disorder: Positive anti-Sm, anti-ds DNA, anti-phospholipid antibody and/or
false positive serological test for syphilis. sensitivity = 85%; specificity = 93%[19].
Presence of anti-ss DNA in 70% of patients (though also positive in patients with
rheumatic disease and healthy persons[20])
9. Neurologic disorder: Seizures or psychosis. sensitivity = 20%; specificity = 98%[19]
10. [[Malar rash]] (rash on cheeks). sensitivity = 57%; specificity = 96%[19]
11. Discoid lupus (red, scaly patches on skin which cause scarring) sensitivity = 18%;
specificity = 99%[19]
A useful mnemonic for these 11 criteria is SOAP BRAIN MD: Serositis (8), Oral ulcers (4),
Arthritis (5), Photosensitivity (3), Blood Changes (9), Renal involvement (proteinuria or casts)
(6), ANA (10), Immunological changes (11), Neurological signs (seizures, frank psychosis) (7),
Malar Rash (1), Discoid Rash (2).
Some patients, especially those with antiphospholipid syndrome, may have SLE without four
criteria and SLE is associated with manifestations other than those listed in the criteria.[21][22][23]
[edit] Alternative criteria
Recursive partitioning has been used to identify more parsimonious criteria.[19] This analysis
presented two diagnostic classification trees:
1. Simplest classification tree: LSE is diagnosed if the patient has an immunologic disorder (antiDNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash.

sensitivity = 92%

specificity = 92%
2. Full classification tree: Uses 6 criteria.

sensitivity = 97%

specificity = 95%
Other alternative criteria have been suggested.[24]
Common misdiagnoses
Porphyria
Porphyrias are complex genetic disorders that share many symptoms with lupus, but impact the
enzymes responsible for building heme, a component needed in heme proteins. Porphyrias are
ecogenic disorders requiring both environmental and genetic backgrounds to manifest with a
variety of symptoms and medical complications. They are noted for photosensitivity and have
been associated with transient and permanent production of autoantibodies. The five major forms
of dominantly inherited porphyrias (acute intermittent porphyria, porphyria cutanea tarda,
hereditary coproporphyria, variegate porphyria and erythropoietic protoporphyria) have been
detected in systemic lupus erythematosus and discoid lupus patients over the past 50 years.
Physicians should have a high degree of suspicion of porphyrias in all lupus cases and act
accordingly when patients are in a medical crisis that may be due to an underlying acute hepatic
porphyria. Drug-induced lupus and photosensitivity warrant an investigation for an underlying
porphyria since multiple drug reactions are a hallmark complication of porphyrias. Patients with
both lupus and porphyrias should avoid porphyrinogenic drugs and hormone preparations.
Patients with acute hepatic porphyrias (acute intermittent porphyria, hereditary coproporphyria,
variegate porphyria) have been detected in lupus patients with severe life-threatening "lupus"
complications known as neurolupus. Symptoms are identical to acute hepatic porphyria attacks
and include seizures, psychosis, peripheral neuropathy and syndrome of inappropriate antidiuretic
hormone (SIADH) associated with dangerously low sodium levels (hyponatremia). Porphyria
attacks require intervention with intravenous glucose, heme preparations and the discontinuation
of dangerous porphyrinogenic drugs including antiseizure drugs. Several other lupus
complications have been associated with porphyrias including pancreatitis and pericarditis.
Porphyrin testing should be performed on urine, stool/bile and blood to detect all types of
porphyrias, and repeat testing should be performed in suspicious cases. Appropriate enzyme tests
or DNA testing should also be pursued to obtain a complete diagnosis which could include a dual
porphyria.
Common dual diagnoses
SLE is sometimes diagnosed in conjunction with other conditions, including Rheumatoid
Arthritis, Scurvy and Fibromyalgia.
Treatment
As lupus erythematosus is a chronic disease with no known cure, treatment is restricted to dealing
with the symptoms; essentially this involves preventing flares and reducing their severity and
duration when they occur. There are several means of preventing and dealing with flares,
including drugs, alternative medicine and lifestyle changes.
Drug therapy
Due to the variety of symptoms and organ system involvement with Lupus patients, the severity
of the SLE in a particular patient must be assessed in order to successfully treat SLE. Mild or
remittent disease can sometimes be safely left untreated. If required, non-steroidal antiinflammatory drug and anti-malarials may be used.
Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce incidence of
flares, the process of the disease, and lower the need for steroid use; when flares occur, they are
treated with corticosteroids. DMARDs commonly in use are anti-malarials and
immunosuppressants (e.g. methotrexate and azathioprine). Hydroxychloroquine (trade name
Plaquenil) is an FDA approved anti-malarial used for constitutional, cutaneous, and articular
manifestations, while Cyclophosphamide (trade names Cytoxan and Neosar) is used for severe
glomerulonephritis or other organ-damaging complications, and in 2005, mycophenolic acid
(trade name CellCept) became accepted for treatment of lupus nephritis.
In more severe cases, medications that modulate the immune system (primarily corticosteroids
and Immunosuppresive drug immunosuppressants) are used to control the disease and prevent
recurrence of symptoms (known as flares). Patients who require steroids frequently may develop
obesity, diabetes mellitus, diabetes and osteoporosis. Depending on the dosage, corticosteroids
can cause other side effects such as a puffy face, an unusually large appetite and difficulty
sleeping. Those side effects can subside if and when the large initial dosage is reduced, but long
term use of even low doses can cause elevated blood pressure and cataracts. Due to these side
effects, steroids are avoided if possible.
Since a large percentage of Lupus patients suffer from varying amounts of chronic pain, stronger
prescription analgesics may be used if over-the-counter drugs, mainly non-steroidal antiinflammatory drug do not provide effective relief. Moderate pain in Lupus patients if typically
treated with mild prescription opiates such as Dextropropoxyphene (trade name Darvocet), and
Co-codamol (trade name Tylenol #3). Moderate to severe chronic pain is treated with stronger
opioids such as Hydrocodone (trade names Lorcet, Lortab, Norco, Vicodin, Vicoprofen) or
longer-acting continuous release opioids such as Oxycodone (trade names OxyContin), MS
Contin, or Methadone. The Fentanyl Duragesic Transdermal patch is also a widely-used treatment
option for chronic pain due to Lupus complications because of its long-acting timed release and
easy usage. When opioids are used for prolonged periods drug tolerance, chemical dependency
and (rarely) addiction may occur. Opiate addiction is not typically a concern for Lupus patients,
since the condition is not likely to ever completely disappear. Thus, lifelong treatment with
opioids is fairly common in Lupus patients that exhibit chronic pain symptoms; accompanied by
periodic titration that is typical of any long-term opioid regimen.
UVA1 phototherapy
In 1987, Tina Lomardi, MD first reported that long-wave ultraviolet radiation (UVA1) had a
favorable effect on disease activity in SLE model mice.[citation needed] In 1987, McGrath, Bak and
Michalski reported in Arthritis and Rheumatism, Vol.30, No. 5, May, that long-wave ultraviolet
radiation (UVA1) had a favorable effect on disease activity in SLE model mice ( "Ultraviolet-A
Light Prolongs Survival and Improves Immune Function in Hybrid Mice") Both McGrath and
independent Dutch searchers have repeatedly reproduced these findings in SLE patients. [25]
Devices for administering therapeutic doses of UVA1 are available in Europe but not in the U.S.
The U.S. Food and Drug Administration Office of Science and Technology conducted UVA1
phototherapy studies in an SLE mouse model in 1997 "to prepare for future reviews of UVAemitting tanning devices for such clinical applications".[26] Some patients, however, have taken
matters into their own hands. Chicago-based reporter and lupus patient Anthony DeBartolo built
his own 8-lamp UVA1 home tanning device which delivers the same 6 to 8 joule therapeutic dose
of McGrath's 24-lamp clinical research equipment. DeBartolo's experiences were published in the
2004 book, "Lupus Underground." [27].
Lifestyle changes
Other measures such as avoiding sunlight or covering up with sun protective clothing can also be
effective in preventing problems due to photosensitivity. Weight loss is also recommended in
overweight and obese patients to alleviate some of the effects of the disease, especially where
joint involvement is significant.
Treatment research
Other immunosuppressants (drugs that lower the body's normal immune response) and bone
marrow transplant autologous stem cell transplants are under investigation as a possible cure.
Recently, treatments that are more specific in modifying the particular subset of the immune cells
(e.g. B- or T- cells) or cytokine proteins they secrete have been gaining attention. Research into
new treatments has recently been accelerated by genetic discoveries, especially mapping of the
human genome. According to a June 2006 market analysis report by Datamonitor, treatment for
SLE could be on the verge of a breakthrough as there are numerous late-Phase trials currently
being carried out.[28] There have been promising advances in the area of stem cell research
implicating a treatment with adult stem cells being harvested from the patients themselves.[29] [30]
Medicine formularies
Plan or option
GMHPP
Gold Options
Link to appropriate Mediscor formulary
G1000, G500 and
G200
Blue Options
B300 and B200
GMISHPP
Blue Option B100
[Core]
n/a
Epidemiology
Previously believed to be a rare disease, Lupus has seen an increase in awareness and education
since the 1960s. This has helped many more patients get an accurate diagnosis making it possible
to estimate the number of people with lupus. In the United States alone, it is estimated that
between 270,000 and 1.5 million people have lupus, making it more common than cystic fibrosis
or cerebral palsy. The disease affects both females and males, though young women are
diagnosed nine times more often than men. SLE occurs with much greater severity among
African-American women, who suffer more severe symptoms as well as a higher mortality
rate.[32] Worldwide, a conservative estimate states that over 5 million people have lupus.
Although SLE can occur in anyone at any age, it is most common in women of childbearing age.
It affects 1 in 4000 people in the United States, with women becoming afflicted far more often
than men. The disease appears to be more prevalent in women of African, Asian, Hispanic and
Native American origin but this may be due to socioeconomic factors. People with relatives who
suffer from SLE, rheumatoid arthritis or thrombotic thrombocytopenic purpura are at a slightly
higher risk than the general population.
Prognosis
Prognosis
In the 1950s, most patients diagnosed with SLE lived fewer than five years. Advances in
diagnosis and treatment have improved survival to the point where over 90% of patients now
survive for more than ten years and many can live relatively asymptomatically. The most
common cause of death is infection due to immunosuppression as a result of medications used to
manage the disease. Prognosis is normally worse for men and children than for women.
Fortunately, if symptoms are present after age 60, the disease tends to run a more benign course.
The ANA is the most sensitive screening test while Anti-Sm (Anti Smith) is the most specific.
The ds-DNA (double-stranded DNA) antibody is also fairly specific and often fluctuates with
disease activity. The ds-DNA titer is therefore sometimes useful to diagnose or monitor acute
flares or response to treatment.[31]
Epidemiology
Prevention
Lupus is not understood well enough to be prevented, but when the disease develops, quality of
life can be improved through flare prevention. The warning signs of an impending flare include
increased fatigue, pain, rash, fever, abdominal discomfort, headache and dizziness. Early
recognition of warning signs and good communication with a doctor can help individuals with
lupus remain active, experience less pain and reduce medical visits.[4]Prevention of complications
during pregnancy
Prevention of complications during pregnancy
While most infants born to mothers with lupus are healthy, pregnant mothers with SLE should
remain under a doctor's care until delivery. Neonatal lupus is rare, but identification of mothers at
highest risk for complications allows for prompt treatment before or after birth. In addition, SLE
can flare during pregnancy and proper treatment can maintain the health of the mother for longer.
Women pregnant and known to have the antibodies for anti-Ro (SSA) or anti-La (SSB) should
have echocardiograms during the 16th and 30th weeks of pregnancy to monitor the health of the
heart and surrounding vasculature.[4]
References
1. LUPUS FOUNDATION OF AMERICA. Retrieved on 2007-07-04.
2. [http://www.accessmedicine.com/content.aspx?aID=2859070 Harrison's Internal
Medicine, 17th ed. Chapter 313. Systemic Lupus Erythematosus.
3. Discoid Lupus Erythematosus
4.
abcd
Handout on Health: Systemic Lupus Erythematosus. The National Institute of
Arthritis and Musculoskeletal and Skin Diseases. National Institutes of Health (August
2003). Retrieved on 2007-11-23.
5. Lupus: The Great Imitator
6.
ab
Joint and Muscle Pain Lupus Foundation of America
7. Yu Asanuma, M.D., Ph.D., Annette Oeser, B.S., Ayumi K. Shintani, Ph.D., M.P.H.,
Elizabeth Turner, M.D., Nancy Olsen, M.D., Sergio Fazio, M.D., Ph.D., MacRae F.
Linton, M.D., Paolo Raggi, M.D., and C. Michael Stein, M.D. (2003). "Premature
coronary-artery atherosclerosis in systemic lupus erythematosus". New England Journal
of Medicine 349 (Dec. 18): 2407-2414. doi:10.1056/NEJMoa035611. PMID 14681506
Abstract (full text requires registration).
8. Bevra Hannahs Hahn, M.D. (2003). "Systemic lupus erythematosus and accelerated
atherosclerosis". New England Journal of Medicine 349 (Dec. 18): 2379-2380. PMID
14681501 Extract (full text requires registration).
9. Mary J. Roman, M.D., Beth-Ann Shanker, A.B., Adrienne Davis, A.B., Michael D.
Lockshin, M.D., Lisa Sammaritano, M.D., Ronit Simantov, M.D., Mary K. Crow, M.D.,
Joseph E. Schwartz, Ph.D., Stephen A. Paget, M.D., Richard B. Devereux, M.D., and
Jane E. Salmon, M.D. (2003). "Prevalence and correlates of accelerated atherosclerosis in
systemic lupus erythematosus". New England Journal of Medicine 349 (Dec. 18): 23992406. doi:10.1056/NEJMoa035471. PMID 14681505 Abstract (full text requires
registration).
10. General Pathology Images for Immunopathology. Retrieved on 2007-07-24.
11. Anisur Rahman and David A. Isenberg (2008). "Review Article: Systemic Lupus
Erythematosus". N Engl J Med 358 (9): 929-939. PMID 18305268.
12. Mary K. Crow (2008). "Collaboration, Genetic Associations, and Lupus Erythematosus".
N Engl J Med 358 (9): 956-961. PMID 18204099.
13. Geoffrey Hom, Robert R. Graham, Barmak Modrek, et al. (2008). "Association of
Systemic Lupus Erythematosus with C8orf13–BLK and ITGAM–ITGAX". N Engl J Med
358 (9): 900-909. PMID 18204098.
14. University of South Carolina School of Medicine ledcture notes, Immunology,
Hypersensitivity reactions. General discussion of hypersensitivity, not specific to SLE.
15. Gaipl, U S; Kuhn, A; Sheriff, A; Munoz, L E; Franz, S; Voll, R E; Kalden, J R;
Herrmann, M (2006). "Clearance of apoptotic cells in human SLE.". Current directions in
autoimmunity 9: 173-87. PMID: 1639466 Abstract (full text requires registration).
16. NIM encyclopedic article on the LE cell test
17. Rheumatology.org article on the classification of rheumatic diseases
18. Revision of Rheumatology.org's diagnostic criteria
19. a b c d e f g h i j k Edworthy SM, Zatarain E, McShane DJ, Bloch DA (1988). "Analysis of
the 1982 ARA lupus criteria data set by recursive partitioning methodology: new insights
into the relative merit of individual criteria". J. Rheumatol. 15 (10): 1493-8. PMID
3060613.
20. UpToDate Patient information article on DNA antibodies
21. Asherson RA, Cervera R, de Groot PG, et al (2003). "Catastrophic antiphospholipid
syndrome: international consensus statement on classification criteria and treatment
guidelines". Lupus 12 (7): 530-4. doi:10.1191/0961203303lu394oa. PMID 12892393.
22. Sangle S, D'Cruz DP, Hughes GR (2005). "Livedo reticularis and pregnancy morbidity in
patients negative for antiphospholipid antibodies". Ann. Rheum. Dis. 64 (1): 147-8.
doi:10.1136/ard.2004.020743. PMID 15608315.
23. Hughes GR, Khamashta MA (2003). "Seronegative antiphospholipid syndrome". Ann.
Rheum. Dis. 62 (12): 1127. doi:10.1136/ard.2003.006163. PMID 14644846.
24. Hughes GR (1998). "Is it lupus? The St. Thomas' Hospital "alternative" criteria". Clin.
Exp. Rheumatol. 16 (3): 250-2. PMID 9631744.
25. Light therapy (with UVA-1) for SLE patients: is it a good or bad idea? -- Pavel 45 (6):
653 -- Rheumatology. Retrieved on 2007-07-04.
26. Ultraviolet-A1 (UVA1) Phototherapy of Systemic Lupus Erythematosus Food and Drug
Administration (FDA)
27. "Lupus Underground" by Anthony DeBartolo; Hyde Park Media, 2004[1]
28. Lead Discovery article on treatment of Lupus
29. Medical News Today article
30. Northwestern Memorial Hospital Press Release
31. [EARLY STEROIDS MAY PREVENT RELAPSES IN LUPUS, P Jarman (Published in
Journal Watch (General) July 18, 1995)
32. Lupus and African-American women