INFO - Assessment of systemic lupus erythematosus (SLE); laboratory findings

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Clin Exp Rheumatol 2005; 23 (Suppl. 39): S120-S132

" Assessment of systemic lupus erythematosus "

Excerpt:

While the hallmark of SLE is the presence

of antinuclear antibodies, a number

of laboratory abnormalities characterize

lupus.

Serologically, the production of various

autoantibodies is the immunopathologic

basis of disease. A positive ANA is

perhaps the most important finding to

establish initially, as this implicates

autoimmunity. However, a positive

ANA is non-specific and can be found

in 5-20% of the normal population (21,

22). Anti-Sm antibodies are also diagnostic

of SLE, seen with a frequency of

30-40%. Conversely, ANA-negative

lupus, while extremely rare, may exist.

Antibodies to double-stranded DNA

(dsDNA) are found in 40-60% of SLE

patients. They are associated with renal

involvement but do not correlate well

with disease activity. In fact, in a prospective

study, anti-dsDNA levels fell

on the day of a flare, possibly owing to

deposition of antibodies in the tissues

at the peak of clinical disease (23).

Therefore, while patients with elevated

levels of anti-dsDNA over many years

of disease have a poorer prognosis

compared to those who do not, acute

changes in the titers of anti-dsDNA do

not predict disease flare at the next

clinic visit.

Antiphospholipid antibodies may also

be found in lupus (50%) and can cause

venous and arterial thromboses, as well

as recurrent fetal loss. Assessment is by

the detection of antibodies to cardiolipin

or to beta-2 glycoprotein 1, or by

the presence of a lupus anticoagulant,

which is marked by prolonged clotting

times that are not corrected by mixing

studies in vitro. Anti-SSA/Ro and anti-

SSB/La are associated with secondary

Sjögren's syndrome, subacute cutaneous

lupus erythematosus, neonatal

lupus, and photosensitivity.

Autoantibodies lead to the formation of

immune complexes, which activate and

consume complement. Hence, measuring

levels of C3, C4, or total hemolytic

complement CH50 may be helpful in

the diagnosis of lupus (24), as well as

in the routine monitoring of SLE patients.

However, hypocomplementemia

is not specific to SLE and can be found

in any disease in which there is a large

antigen-antibody load. Prospective studies

have not found changes in C3 or

C4 to predict overall disease activity,

but they were reduced with hematologic

and renal flares on the same day the

flare occurred (25).

Hematologic abnormalities are common

findings in SLE. Anemia may

reflect chronic inflammation, renal disease,

iron deficiency or gastrointestinal

loss. In addition, an autoimmune, hemolytic

anemia caused by autoantibodies

against red blood cell antigens (Coombs

positivity) can occur (26). An appropriate

reticulocytosis excludes marrow

suppression as the underlying etiology

of the anemia.

Leukopenias and thrombocytopenias

are common in SLE patients. They are

thought to be secondary to antibodies

directed against cell surface antigens.

As with the other cytopenias, infection,

malignancy, and adverse drug effects

need to be ruled out.

http://www.clinexprheumatol.org/pdf/vol23/s39/s39_pdf/19lam.pdf

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