Antinuclear Antibody (cont.)
Can medications cause ANAs to be produced?
Many medications can sometimes stimulate the production of ANAs, including
procainamide (Procan SR), hydralazine, and dilantin. ANAs that are stimulated by medication are
referred to as drug-induced ANAs. This does not necessary mean that
any disease is present when these ANAs are "induced." Sometimes
diseases are associated with these ANAs, and they are referred to as
drug-induced diseases.
ANAs are defined in certain patterns. What does this mean?
ANAs present different "patterns" depending on the
staining of the cell nucleus in the laboratory: homogeneous or diffuse; speckled;
nucleolar; and peripheral or rim. While these
patterns are not specific for any one illness, certain illnesses can
more frequently be associated with one pattern or another. The patterns then can sometimes give the doctor further clues as to types of illnesses to look for in evaluating a patient. For
example, the nucleolar pattern is more commonly seen in the disease
scleroderma. The speckled pattern is seen in many conditions and in
people who do not have any autoimmune disease.
Are ANAs always associated with illness?
No. ANAs can be found in approximately 5% of the normal
population, usually in low titers (low levels). These people usually have no
disease. Titers of lower than 1:80 are less likely to be significant. (ANA
titers of less than or equal to 1:40 are considered negative.) Even higher
titers are often insignificant in patients over 60 years of age. Ultimately, the
ANA result must be interpreted in the specific context of an individual
patient's symptoms and other test results. It may or may not be significant in a
given individual.
REFERENCES: Clinical Primer of Rheumatology, Lippincott Williams & Wilkens, edited by William Koopman, et al., 2003.
Kelley's Textbook of Rheumatology, W B Saunders Co, edited by Shaun Ruddy, et al., 2000.
Shiel, WC, et al. The Diagnostic Associations of Patients With Antinuclear Antibodies Referred to a Community Rheumatologist, J Rheumatology 1989;16:782-5.
Last Editorial Review: 4/23/2008
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