ANA Screen (Антитела к ядерным антигенам)

ANA Profile 12 (RDL)—also known as an antinuclear antibody (ANA) profile or fluorescent antinuclear antibody (FANA) panel—assesses autoantibodies directed against nuclear antigens using HEp‑2 indirect immunofluorescence, with reporting of ANA titer and pattern. The test supports screening for systemic autoimmune disorders, establishing and monitoring systemic lupus erythematosus (SLE), and evaluating suspected drug‑induced lupus, recognizing that a positive ANA is sensitive but not disease‑specific. When ANA is positive, the profile reflexes to disease‑associated autoantibodies and immune markers—anti‑dsDNA by Farr, anti‑Sm, anti‑Ro/SS‑A, anti‑La/SS‑B, anti‑U1 RNP, anti‑Scl‑70, anti‑centromere, anticardiolipin (IgG, IgA, IgM), anti‑TPO—and complement components C3 and C4 to aid differentiation among SLE, Sjögren syndrome, mixed connective tissue disease, limited/diffuse scleroderma, antiphospholipid antibody–associated conditions, and autoimmune thyroid disease. If ANA by IFA is negative, anti‑Ro/SS‑A is still performed to capture rare ANA‑negative cases.

Antinuclear antibodies represent a heterogeneous group of autoantibodies targeting nuclear constituents and occur across a range of autoimmune diseases, including systemic connective tissue disorders, autoimmune pancreatitis, and primary biliary cholangitis, as well as in some malignancies. In patients with clinical features suggestive of autoimmunity—such as fever of unknown origin, inflammatory joint symptoms, rash, or constitutional weakness—ANA serves as a screening assay; a positive result typically prompts disease‑specific follow‑up testing (eg, anti‑Scl‑70 for suspected systemic sclerosis or antimitochondrial antibodies for suspected primary biliary cholangitis). A negative ANA does not exclude autoimmune disease. ANA exhibits high sensitivity for systemic lupus erythematosus, being detectable in approximately 98% of cases. Repeatedly negative ANA results make SLE less likely, although early ANA‑negative SLE can occur and a small subset (about 2%) remains ANA‑negative throughout the disease course. In patients with clinical findings suggestive of SLE but negative ANA, testing for more specific markers—particularly anti‑dsDNA—is recommended; identification of anti‑dsDNA in a compatible clinical context supports the diagnosis even when ANA is absent. SLE typically evolves over time. An initial preclinical phase reflects genetic susceptibility (eg, HLA associations) without laboratory abnormalities. This is followed by a serologic phase in which autoantibodies appear before symptoms; ANA, anti‑Ro/SS‑A, anti‑La/SS‑B, and antiphospholipid antibodies are common at this stage. ANA positivity is associated with an approximately 40‑fold increased risk of SLE, and the mean interval from ANA emergence to symptom onset is about 3.3 years. Individuals with positive ANA warrant periodic rheumatologic follow‑up and laboratory reassessment. As clinical disease develops, the autoantibody repertoire often broadens to include anti‑Sm, anti‑dsDNA, and anti‑RNP. Because no single assay reliably predicts flares or organ involvement, SLE monitoring remains multifaceted and incorporates ANA with other autoantibodies and routine clinical measures, tailored to the patient. Drug‑induced lupus arises during exposure to certain medications—most commonly procainamide and hydralazine, but also some ACE inhibitors, beta‑blockers, isoniazid, minocycline, sulfasalazine, hydrochlorothiazide, and others—and presents with features that resemble idiopathic SLE. ANA is detectable in most affected patients. In symptomatic individuals taking these agents, ANA testing helps evaluate for drug‑induced lupus. After complete discontinuation of the offending drug, both clinical manifestations and immunologic abnormalities typically resolve; a follow‑up ANA that reverts to negative supports this diagnosis. Low‑titer ANA occurs in a portion of healthy individuals (about 3% to 5%, and up to 10% to 37% among those older than 65 years). Positive ANA in the absence of autoimmune symptoms should be interpreted in conjunction with historical, clinical, and additional laboratory data.