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INVESTIGATIONS OF SYSTEMIC
LUPUS ERYTHEMATOSUS
Assessed by:
Prof Dr Abdel Aal ElKamshoushi
1. NURAMALINA BINTI YAHAYA (10-5257)
2. NOOR HAKIMAH HIDAYAH BT MOHD
RAHIM (10-5-258)
3. NURHAKIM BIN IBRAHIM (10-5-259)
4. MEDHAT AHMED ELSAYED YOUSSEF
(1037)
INVESTIGATIONS OF SYSTEMIC
LUPUS ERYTHEMATOSUS
Introduction
Systemic lupus erythematosus (SLE) is a chronic inflammatory
autoimmune disease. It can affect nearly every organ system in the body
which the symptoms may vary widely between individuals.
The classic presentation of a triad of fever, joint pain and rash in a woman
of childbearing age should prompt investigation into the diagnosis of SLE
Laboratory Findings
(By Nuramalina Binti Yahaya 10-5-257)
There is no definitive test for diagnosing SLE but some laboratory test can
be very helpful in supporting the diagnosis of SLE.
There are several standard laboratory studies of SLE:
1. Complete blood count, CBC
It is very essential test because all cellular elements of blood can be
affected.
It helps screen for leucopenia, lymphopenia, anaemia,
thrombocytopenia and prolonged activated partial thromboplastin
time (aPTT).
2. Serum creatinine may be used in the diagnosis of kidney affection
in SLE
3. Urinalysis
The result will be low serum albumin with persistent proteinuria and
membranous GN.
Also with microscopic analysis, red and white blood cells casts in
urinary sediment may be present in proliferative GN.
Other laboratory tests that may be used are:
1. Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
It is nonspecific finding of SLE as it indicates systemic inflammation.
However, it can be used in order to monitor the patient because
when both markers are markedly elevated, suspect of increase
activity of infectious process are occurred.
2. Complement levels.
4.1 If SLE-like symptoms are present and the ANA test is positive,
other tests for SLE will be administered.
4.2 If SLE-like symptoms are not present and the test is positive,
either look for other causes, or the results will be ignored if the
patient is feeling healthy.
ANA Subtypes.
5. Anti-double stranded DNA (Anti-ds DNA) is more likely to be found
only in patients with SLE. It may play an important role in injury to
blood vessels found in SLE, and high levels often indicate kidney
involvement. Anti-ds DNA levels tend to fluctuate over time and
may even disappear.
6. Anti-Sm antibodies are also usually found only with SLE. Levels
are more constant and are more likely to be detected in AfricanAmerican patients. Although many lupus patients may not have this
antibody, its presence almost always indicates SLE.
7. When the ANA is negative but the diagnosis is still strongly
suspected, a test for anti-Ro (also called anti-SSA) and anti-La (also
called anti-SSB) antibodies may identify patients with a rare
condition called ANA negative, Ro lupus. These autoantibodies may
be involved in the sun-sensitive rashes experienced by patients with
SLE and are also found in association with neonatal lupus syndrome,
in which a pregnant mother's antibodies cross the placenta and
cause inflammation in the developing child's skin or heart.
8. Antiphospholipid antibodies. Around half of patients with SLE
have antiphospholipid antibodies, which increase the risk for blood
clots, strokes, and pregnancy complications. If suspects SLE blood
abnormalities, tests may be able to detect the presence of the two
major antiphospholipid antibodies: lupus coagulant antibody and
anticardioplin antibody.
9. As with the ANA, these antibodies have a tendency to appear and
disappear. Patients who have these autoantibodies as well as blood
clotting problems or frequent miscarriages are diagnosed with
antiphospholipid syndrome (APS), which often occurs in SLE but can
also develop independently. [2]
And when the x ray is done in the hip joint, there is probability to find the
avascular necrosis due to prolonged used of steroid as a treatment.
This chest x-ray is taken from a patient with lupus demonstrates a rightsided pleural effusion (yellow arrow) and atelectasis with scarring in the
left lung base (blue arrow). In severe complications, a fibrothorax may
develop.
Echocardiography
Echocardiography is used to assess for pericardial effusion, pulmonary
hypertension, or verrucous Libman-Sacks endocarditis
Cardiac MRI
There are some investigators have suggested that cardiac MRI (CMR)
provides an excellent alternative to clinical assessment,
electrocardiography, and echocardiography for diagnosing SLE
myocarditis. They reported that patients who were positive for infectious
myocarditis on CMR were more symptomatic than those with active SLE
disease and that more than 50% of patients with CMR-positive myocarditis
had a concurrent positive endomyocardial biopsy. [3]
Cardiovascular System
Pericarditis and valve nodules were among the first clinical manifestations
described in SLE. It is only recently that the extent of premature
atherosclerotic disease has been well documented. Pericarditis (Chapter
77) is the most common cardiac manifestation, but it is sometimes
recognized only on imaging studies or at autopsy. It is a component of the
generalized serositis that is often a feature of SLE and is associated with
local autoantibodies and immune complexes. Pericarditis is usually
manifested as substernal chest pain that is improved by bending forward
and can be exacerbated by inspiration or coughing. The symptoms and
effusions associated with pericarditis are quite responsive to moderatedose (20 to 30 mg/day of prednisone) corticosteroid
treatment. Structural valve abnormalities in SLE range from sterile
nodules originally described by Libman and Sacks to nonspecific valve
thickening. The nodules are immobile and usually located on the atrial
side of the mitral valve and sometimes on the arterial side of the aortic
valve. Right-sided lesions are rare.
These structural changes may in some cases result in valvular
regurgitation. Although valve nodules are detected in most patients with
SLE at autopsy, clinically significant valvular heart disease is much less
common (1 to 18%). The verrucous valvular lesions of Libman and Sacks
are most likely inflammatory in nature and may be associated with the
presence of antiphospholipid antibodies. Premature and accelerated
atherosclerosis is increasingly recognized as being prevalent in lupus
patients, and preclinical atherosclerotic carotid plaque has been
documented in 37% of SLE patients as opposed to 15% of age- and sexmatched controls. Traditional cardiovascular risk factors apply, but the
diagnosis of SLE is itself a significant risk factor for premature
atherosclerosis. Although the lupus-specific mechanisms that confer
additional risk for atherosclerosis have not been defined, it is likely that
chronic inflammation associated with immune system activation
contributes to the accumulation of vascular damage. Mortality from
atherosclerosis may be up to 10 times greater in patients with SLE than in
age- and sex-matched controls. Although not specific to SLE, Raynauds
phenomenon (Chapter 80), characterized by episodic vasospasm and
occlusion of the digital arteries in response to cold and emotional stress, is
a feature in up to 60% of SLE patients and contributes to pain and
sometimes necrosis of the distal ends of extremities. The character of the
digits classically changes from pallor to cyanosis and then to rubor as
vascular perfusion becomes impaired. In addition, small arteries,
arterioles, and capillaries can be affected by vasculitis and fibrinoid
necrosis with clinical manifestations that include periungual
telangiectases,
abdominal pain, and neuropsychiatric symptoms.
Pulmonary System
REFERENCES
[1] http://www.webmd.com/lupus/guide/laboratory-tests-useddiagnose-evaluate-sle?page=2
http://emedicine.medscape.com/article/332244-overview
[2] http://umm.edu/health/medical/reports/articles/systemic-lupuserythematosus
http://www.docstoc.com/docs/445715/Systemic-Lupus-ErythematosusDefinition
http://en.wikipedia.org/wiki/Systemic_lupus_erythematosus#Laboratory_te
sts
[3] http://emedicine.medscape.com/article/332244-overview
http://emedicine.medscape.com/article/332244-clinical
http://radiopaedia.org/articles/musculoskeletal-manifestations-of-systemiclupus-erythematosus
[4] Goldmans Cecil Medicine 24th Edition