Lab result explainedInflammationLast updated November 11, 2026

ENA panel: anti-Smith, anti-RNP, SSA/Ro, SSB/La, Scl-70 and Jo-1 antibodies explained

Extractable nuclear antigen antibody panel (ENA panel) · ENA panel (reflex from a positive ANA; often with anti-dsDNA and complement) · reported in Antibody index (AI) or arbitrary units (AU/mL or U/mL) for each antibody; negative below 1.0 AI or below the kit's unit cut-off (often 20); line blots report negative, borderline, positive or strongly positive

An ENA panel measures antibodies against a group of proteins extracted from cell nuclei, the extractable nuclear antigens, and is the follow-up test that tells you what a positive ANA is actually reacting to. The standard panel reports six antibodies: anti-Smith (Sm), anti-U1-RNP, anti-SSA/Ro, anti-SSB/La, anti-Scl-70 (topoisomerase I) and anti-Jo-1, and many labs add anti-centromere, anti-ribosomal P or anti-chromatin. Each is reported as negative or positive, usually with a number such as an antibody index (negative below 1.0) or units (negative below about 20), and each points toward a particular connective tissue disease.

The point of the panel is pattern recognition. Anti-Smith is almost exclusive to lupus; high-titer anti-U1-RNP defines mixed connective tissue disease; anti-SSA/Ro and anti-SSB/La point to Sjögren's syndrome and to subacute cutaneous and neonatal lupus; anti-Scl-70 and anti-centromere divide systemic sclerosis into its diffuse and limited forms; anti-Jo-1 marks the antisynthetase syndrome of myositis and interstitial lung disease. None is a diagnosis on its own, and a positive result in someone with no symptoms is more often weak, non-specific binding than early disease.

The panel is usually run only when the ANA is positive, because ENA antibodies are uncommon when the ANA is negative, with two exceptions worth knowing: anti-SSA/Ro (especially its Ro52 component) and anti-Jo-1 target proteins that live partly in the cytoplasm and can be positive in people whose ANA screen is reported negative. Results typically take several days to two weeks. An equivocal or isolated low positive with no symptoms is usually repeated in 3 to 6 months rather than acted on.

ENA panel at a glance

What it is: a panel of antibodies to extractable nuclear antigens (Sm, U1-RNP, SSA/Ro, SSB/La, Scl-70, Jo-1, often centromere and others) ordered after a positive ANA to identify the likely connective tissue disease.
Normal: all antibodies negative, below the kit cut-off (often an index below 1.0 or under 20 units; line blots report 'negative').
Anti-Smith: lupus (highly specific, 20–30 percent sensitivity). Anti-U1-RNP: mixed connective tissue disease when high titer, also lupus. Anti-SSA/Ro and anti-SSB/La: Sjögren's syndrome, lupus, and neonatal lupus risk in pregnancy.
Anti-Scl-70: diffuse systemic sclerosis with lung fibrosis risk. Anti-centromere: limited systemic sclerosis. Anti-Jo-1: myositis with interstitial lung disease (antisynthetase syndrome).
A positive result without symptoms, especially a value just over the cut-off, is often non-specific; low positives occur in a few percent of healthy people on multiplex assays.
Next step: results are read with the ANA pattern and titer, anti-dsDNA, complement, blood counts, kidney and muscle tests and your symptoms, usually by a rheumatologist.

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What ENA panel measures

The extractable nuclear antigens are proteins and protein-RNA complexes that dissolve out of cell nuclei in saline, which is how they were first separated from DNA and histones in the 1960s. Sm and U1-RNP are parts of the spliceosome that processes messenger RNA; SSA/Ro (two unrelated proteins, Ro60 and Ro52) and SSB/La are involved in RNA quality control; Scl-70 is topoisomerase I, which unwinds DNA; Jo-1 is histidyl-tRNA synthetase, an enzyme of protein synthesis; and centromere proteins hold chromosomes together during cell division. Why the immune system targets these particular proteins in particular diseases is not fully understood, but the associations are strong enough to be built into the classification criteria for lupus, Sjögren's syndrome, systemic sclerosis and the myositis spectrum.

Most US labs use multiplex bead immunoassays, chemiluminescence or ELISA for each antigen and report a number against a cut-off, with an equivocal zone just above it; some use line immunoblots that report bands as negative, borderline, positive or strongly positive. The older double immunodiffusion method detects only high-avidity antibodies and is less sensitive but more specific, and some rheumatologists still ask for it to confirm a surprising result. Because methods differ, antibody values are not comparable between labs and ENA titers are not usually tracked over time; anti-dsDNA, which is monitored serially, is a separate test.

Context shapes the interpretation. A high-titer speckled ANA with a positive anti-Smith or anti-U1-RNP, a centromere ANA pattern with anti-centromere, or a nucleolar pattern with anti-Scl-70 are internally consistent; a low-positive anti-Scl-70 with a negative ANA and no symptoms is almost always a false positive. The panel is not a screening test, and ordering it without a positive ANA or specific symptoms produces more false positives than true findings because these diseases are uncommon in the general population.

Normal range for ENA panel

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (Antibody index (AI) or arbitrary units (AU/mL or U/mL) for each antibody; negative below 1.0 AI or below the kit's unit cut-off (often 20); line blots report negative, borderline, positive or strongly positive)	Notes
All antibodies negative	Below the cut-off for each (index under 1.0, or under about 20 units; 'negative' on line blot)	Normal. Does not exclude connective tissue disease; a sizable share of people with lupus, Sjögren's or systemic sclerosis have a negative standard ENA.
Anti-Smith (Sm)	Positive points to systemic lupus erythematosus	Specificity above 95 percent but found in only 20 to 30 percent of people with lupus (higher in Black and Asian patients). Scores 6 points in the 2019 EULAR/ACR lupus criteria.
Anti-U1-RNP	Positive points to mixed connective tissue disease (high titer, required for that diagnosis) or lupus	Present in 25 to 40 percent of lupus; associated with Raynaud's, puffy fingers, myositis and pulmonary hypertension. Isolated anti-RNP without anti-Sm is the MCTD pattern.
Anti-SSA/Ro (Ro60 and Ro52)	Positive points to Sjögren's syndrome, lupus (including subacute cutaneous lupus) or, for Ro52 alone, myositis and interstitial lung disease	Found in 60 to 70 percent of Sjögren's and 30 to 40 percent of lupus. In pregnancy carries about a 2 percent risk of fetal heart block, 15 to 20 percent after a previously affected child.
Anti-SSB/La	Positive points to Sjögren's syndrome or lupus, nearly always alongside anti-SSA/Ro	Found in 30 to 50 percent of Sjögren's. Isolated anti-La without anti-Ro is rare and of doubtful significance.
Anti-Scl-70 (topoisomerase I)	Positive points to diffuse systemic sclerosis	Found in 20 to 40 percent of systemic sclerosis; associated with interstitial lung disease and more extensive skin involvement. Low positives on multiplex assays in people without symptoms are usually false positives.
Anti-Jo-1	Positive points to antisynthetase syndrome (myositis, interstitial lung disease, arthritis, 'mechanic's hands', Raynaud's, fever)	Found in 20 to 30 percent of polymyositis and dermatomyositis. Prompts a creatine kinase and lung assessment.
Anti-centromere (often added)	Positive points to limited cutaneous systemic sclerosis (formerly CREST)	Found in 60 to 80 percent of limited disease; associated with pulmonary arterial hypertension rather than lung fibrosis. Also seen in primary biliary cholangitis.
Anti-ribosomal P, anti-chromatin and others (extended panels)	Ribosomal P points to lupus (including neuropsychiatric lupus); chromatin/nucleosome to lupus and drug-induced lupus; PM-Scl and Ku to scleroderma-myositis overlap	Ordered selectively; interpretation is specialist territory.

Positive ENA antibody

A positive ENA antibody narrows the field. It tells your clinician which disease to look for, how to examine you and which organs to check: anti-Smith and anti-ribosomal P send attention to the kidneys, blood counts and nervous system; anti-SSA/Ro and anti-SSB/La to the eyes, mouth, salivary glands and, in pregnancy, the fetal heart; anti-Scl-70 and anti-centromere to the skin, lungs, esophagus, blood pressure and heart; anti-Jo-1 to the muscles and lungs; anti-U1-RNP to Raynaud's, swollen hands, muscles and pulmonary pressures. The strength of the result matters: a value many times the cut-off, or a strongly positive band on an immunoblot, is far more meaningful than one just over the line.

A positive ENA does not by itself diagnose anything. Each of these diseases is classified on a combination of symptoms, examination, imaging and laboratory findings, and the antibody is one component. Anti-SSA/Ro is the clearest example: it is present in a majority of people with Sjögren's syndrome but also in a third of lupus patients, in some with myositis or systemic sclerosis, and in perhaps 1 percent of healthy people, most of whom never develop disease. The disease associations in the table are probabilities, not certainties.

Isolated low positives are common enough to deserve their own interpretation. Multiplex and ELISA platforms detect weak binding that the older immunodiffusion method would have called negative, and a single low-positive antibody with a negative ANA and no symptoms is, in most studies, a false positive or a finding of no clinical consequence. Such results are usually repeated in 3 to 6 months, ideally with an ANA by immunofluorescence, and the person is reassured if nothing has changed.

Common causes

Systemic lupus erythematosus (anti-Sm, anti-U1-RNP, anti-SSA/Ro, anti-SSB/La, anti-ribosomal P, anti-chromatin)
Lupus produces the widest range of ENA antibodies. Anti-Smith is nearly specific to it, anti-U1-RNP accompanies anti-Sm in many patients, anti-Ro marks the photosensitive subacute cutaneous form, and anti-ribosomal P is linked to neuropsychiatric lupus and hepatitis.
Mixed connective tissue disease (high-titer anti-U1-RNP)
An overlap of lupus, systemic sclerosis and myositis features with Raynaud's and puffy hands, defined by a high anti-U1-RNP titer in the absence of anti-Sm. Pulmonary arterial hypertension is the main long-term risk and is screened for by echocardiography.
Sjögren's syndrome (anti-SSA/Ro, anti-SSB/La)
Dry eyes and mouth from immune attack on tear and salivary glands, often with joint pain, fatigue, a positive rheumatoid factor and high IgG. Anti-Ro is positive in 60 to 70 percent and is a criterion for classification; anti-La almost always accompanies it.
Systemic sclerosis (anti-Scl-70, anti-centromere, anti-RNA polymerase III)
Anti-Scl-70 goes with the diffuse form, rapid skin thickening and interstitial lung disease; anti-centromere with the limited form, long-standing Raynaud's, telangiectasia, calcinosis and pulmonary arterial hypertension; anti-RNA polymerase III (not on all panels) with scleroderma renal crisis.
Myositis and antisynthetase syndrome (anti-Jo-1, Ro52, PM-Scl, Mi-2)
Anti-Jo-1 identifies a cluster of muscle inflammation, interstitial lung disease, arthritis, fever, Raynaud's and cracked 'mechanic's hands'; lung disease may precede weakness. Ro52 often travels with Jo-1 and signals more severe lung involvement.
Neonatal lupus and congenital heart block (maternal anti-SSA/Ro, anti-SSB/La)
The antibodies cross the placenta and in about 2 percent of pregnancies damage the fetal cardiac conduction system between 18 and 26 weeks, or cause a transient rash and liver or blood-count changes in the newborn. The mother may be entirely well; this is often how her antibody is found.
Low-level and non-specific positives
Automated assays return weak positives in roughly 2 to 5 percent of healthy people, more often with age and in women, and in people with unrelated illnesses. A value just over the cut-off, a negative ANA by immunofluorescence and no symptoms point to this explanation.
Drug-induced autoimmunity and infections
Hydralazine, procainamide, minocycline, isoniazid and TNF inhibitors produce ANA with anti-histone or anti-chromatin antibodies, occasionally with low-level ENA reactivity; hepatitis C, HIV, EBV, parvovirus B19 and endocarditis can do the same transiently. Repeat testing after recovery or drug withdrawal usually shows them fading.
Relatives of people with autoimmune disease and overlap syndromes
First-degree relatives of people with lupus or Sjögren's carry ENA antibodies more often than the general population without necessarily developing disease, and people with one autoimmune disease (thyroiditis, primary biliary cholangitis, autoimmune hepatitis) have higher rates of incidental anti-Ro or anti-centromere positivity.

Symptoms that can go with it

Often none when a single antibody is weakly positive
Dry, gritty eyes and a dry mouth, difficulty swallowing dry food, swollen salivary glands (anti-SSA/Ro, anti-SSB/La)
Joint pain and swelling, mouth ulcers, a photosensitive rash, fatigue and hair loss (anti-Sm, anti-RNP, anti-Ro)
Fingers turning white and blue in the cold, puffy fingers, tight shiny skin on the hands and face, fingertip ulcers (anti-Scl-70, anti-centromere, anti-RNP)
Heartburn and difficulty swallowing from a stiff esophagus (systemic sclerosis)
Breathlessness on exertion or a dry cough from interstitial lung disease or pulmonary hypertension (anti-Scl-70, anti-Jo-1, anti-centromere, anti-RNP)
Weakness climbing stairs or lifting the arms, muscle aching and cracked skin on the sides of the fingers (anti-Jo-1)
Foamy urine, swelling, confusion or seizures when lupus involves the kidneys or nervous system (anti-Sm, anti-ribosomal P)

Read it alongside

ANA with pattern and titer — the screen that precedes the panel; the pattern (speckled, homogeneous, centromere, nucleolar) should match the ENA result, and a mismatch prompts a repeat.
Anti-dsDNA — equally specific for lupus and, unlike the ENA antibodies, useful for monitoring disease activity over time.
Complement C3 and C4 — low levels indicate active immune-complex disease, mainly lupus, and are part of the lupus criteria.
Rheumatoid factor and total IgG — raised in 60 to 80 percent of Sjögren's syndrome, where a high IgG (hypergammaglobulinemia) is typical.
Creatine kinase — raised with muscle inflammation; checked when anti-Jo-1, anti-RNP or anti-PM-Scl is positive or weakness is reported.
CBC with differential and platelets — cytopenias accompany lupus and mixed connective tissue disease.
Urinalysis, urine albumin-to-creatinine ratio and creatinine — kidney involvement in lupus and, rarely, scleroderma renal crisis.
ESR and CRP — the ESR tracks activity in these diseases, while CRP is often normal in lupus and Sjögren's and rises with infection or serositis.

What usually happens next

Your clinician will match the positive antibody to your symptoms and examination, usually with an ANA pattern, anti-dsDNA, complement, CBC, creatinine, urinalysis and creatine kinase, and refer you to rheumatology if a connective tissue disease is likely.
An isolated low positive with no symptoms is usually repeated in 3 to 6 months, ideally with an ANA by immunofluorescence, rather than acted on; many have faded or stay unchanged without disease.
Specific antibodies trigger specific checks: pulmonary function tests and a chest CT for anti-Scl-70 or anti-Jo-1; an echocardiogram for anti-centromere or anti-RNP; an eye examination and salivary gland assessment for anti-Ro/La; a baseline blood pressure and kidney function for systemic sclerosis.
If you are pregnant or planning pregnancy and anti-SSA/Ro or anti-SSB/La is positive, tell your obstetrician: fetal heart monitoring by serial echocardiography between about 16 and 26 weeks is standard, and hydroxychloroquine lowers the recurrence risk of heart block.
Ask which method your lab used and whether an unexpected result can be confirmed by a second method, since multiplex and immunoblot assays occasionally disagree.

Diet, lifestyle and natural levers with evidence

What can move ENA panel once the cause is known. Nothing here replaces finding the cause.

Nothing natural changes an ENA antibody result

Strong evidence

ENA antibodies, once established, persist for years at a similar level regardless of diet, supplements or lifestyle, and no human study has shown any food, herb or supplement turning one negative. They are also not generally monitored over time, so a later 'lower' value usually reflects assay variation. The levers below concern what the result means and the course of the diseases behind it.

Getting the test in the right context

Strong evidence

The predictive value of a positive ENA depends on why it was ordered. In people with a positive ANA and specific symptoms, a positive anti-Sm, anti-Scl-70 or anti-Jo-1 is highly likely to be real; ordered as a screen for fatigue or aches with a negative ANA, most positives are false. Recent viral infection, endocarditis, hepatitis C, and drugs such as hydralazine, minocycline, procainamide and TNF inhibitors can all produce transient autoantibodies, so a repeat 3 to 6 months after recovery or drug withdrawal is more informative than any intervention.

Sun protection in anti-Ro and lupus-related disease

Moderate evidence

Anti-SSA/Ro is strongly linked to photosensitive subacute cutaneous lupus, and ultraviolet light triggers both skin lesions and systemic flares by releasing nuclear antigens from damaged skin cells. In controlled studies, daily broad-spectrum SPF 50 sunscreen prevented UV-induced lesions in people with cutaneous lupus, and sun protection is a standard EULAR recommendation. It changes the disease course, not the antibody.

Stopping smoking

Moderate evidence

Smoking is associated with more active cutaneous lupus and a roughly twofold lower chance of responding to hydroxychloroquine in meta-analyses, with more digital ulcers and worse vascular disease in systemic sclerosis, and with a higher risk of developing rheumatoid arthritis and lupus in the first place. Ex-smokers approach never-smokers on most of these measures within a few years of quitting.

When to see a clinician promptly

Emergency in systemic sclerosis (anti-Scl-70 or anti-RNA polymerase III): a sudden rise in blood pressure (above about 150/85 mmHg or 20 mmHg over your usual) with headache, visual disturbance, breathlessness or reduced urine, which may be scleroderma renal crisis and needs same-day treatment to protect the kidneys.
New or worsening breathlessness on exertion or a persistent dry cough with anti-Scl-70, anti-Jo-1, anti-RNP or anti-centromere, which can be interstitial lung disease or pulmonary hypertension and is more treatable early.
Progressive muscle weakness, difficulty swallowing or a creatine kinase several times normal with anti-Jo-1 or anti-RNP.
A fingertip ulcer that is not healing, or a finger that stays white, blue or numb for more than a few hours, in anyone with Raynaud's and a positive antibody.
If you are pregnant with anti-SSA/Ro or anti-SSB/La and have not yet been offered fetal heart monitoring, or if fetal movements fall.
Foamy urine, swelling, fever, chest pain on breathing, confusion or seizures with lupus-associated antibodies (anti-Sm, anti-RNP, anti-ribosomal P).

Frequently asked questions

What does a positive ENA panel mean?

It means antibodies against one or more specific nuclear proteins were detected, and which one tells your clinician what to look for: anti-Smith or anti-ribosomal P for lupus, high anti-RNP for mixed connective tissue disease, anti-SSA/Ro and anti-SSB/La for Sjögren's syndrome or lupus, anti-Scl-70 or anti-centromere for systemic sclerosis and anti-Jo-1 for myositis with lung disease. None is a diagnosis on its own. The strength of the result, the ANA pattern and above all your symptoms and examination decide what it means.

What is the anti-Smith antibody and is it always lupus?

Anti-Smith targets proteins of the spliceosome, the machinery that edits messenger RNA. It is one of the most specific lupus antibodies, found in well under 5 percent of people without lupus, which is why it scores as highly as anti-dsDNA in the classification criteria. It is not sensitive, however: only 20 to 30 percent of lupus patients have it. A clearly positive anti-Sm almost always indicates lupus or a lupus overlap; a value barely over the cut-off on a multiplex assay with no symptoms is repeated and sometimes confirmed by immunodiffusion before it is believed.

What do SSA and SSB antibodies mean?

Anti-SSA/Ro and anti-SSB/La are the antibodies of Sjögren's syndrome, present in 60 to 70 percent and 30 to 50 percent of patients respectively, and also occur in a third of people with lupus, particularly the photosensitive subacute cutaneous form. Anti-La almost never appears without anti-Ro. Their most important practical consequence is in pregnancy, where they cross the placenta and cause congenital heart block in about 2 percent of pregnancies and neonatal lupus rash in a few percent more; women who carry them are offered fetal heart monitoring.

Can an ENA panel be positive if the ANA is negative?

Occasionally. Anti-SSA/Ro, especially the Ro52 component, and anti-Jo-1 target proteins found partly in the cytoplasm, so the standard ANA screen on HEp-2 cells can miss them, and solid-phase ANA screens miss some antibodies that immunofluorescence would catch. If a positive ENA accompanies a negative ANA, a repeat ANA by immunofluorescence and attention to cytoplasmic staining usually resolve it. A low-positive anti-Scl-70 or anti-Sm with a negative immunofluorescence ANA and no symptoms is most often a false positive.

I have a positive anti-RNP. Do I have mixed connective tissue disease?

Not necessarily. Anti-U1-RNP occurs in 25 to 40 percent of people with lupus, in some with systemic sclerosis and myositis, and at low level in some healthy people. Mixed connective tissue disease requires a high titer of anti-U1-RNP without anti-Smith plus a characteristic combination of Raynaud's, swollen hands, arthritis, myositis and lung involvement. Your clinician will look for those features and, if the titer is high, arrange an echocardiogram and lung function tests because pulmonary hypertension is the main risk.

What does anti-Scl-70 positive mean?

Anti-Scl-70 (anti-topoisomerase I) is the antibody of diffuse cutaneous systemic sclerosis, found in 20 to 40 percent of people with systemic sclerosis and strongly associated with interstitial lung disease, so a true positive leads to lung function tests, a high-resolution chest CT and regular monitoring. Its specificity is high when the ANA shows a nucleolar or fine speckled pattern and you have Raynaud's or skin changes. Low positives on multiplex assays in people with none of these are common and are usually false; they are repeated rather than acted on.

Are ENA antibodies dangerous in pregnancy?

Most are not, but anti-SSA/Ro and anti-SSB/La are, because they can affect the fetal heart. Congenital heart block develops in about 2 percent of pregnancies in antibody-positive women and in 15 to 20 percent of those who have already had an affected child; it usually starts between 18 and 26 weeks and is screened for by serial fetal echocardiography. Hydroxychloroquine during pregnancy reduced recurrence to about 7 percent in a prospective study. Systemic sclerosis and lupus antibodies matter indirectly, through the disease activity and organ involvement they signal.

How long do ENA panel results take and do I need to fast?

No fasting or special preparation is needed; the sample is ordinary serum drawn with the ANA or reflexed from it. Because the panel is usually run in batches at a reference laboratory, results take several days to about two weeks. Tell the lab about recent infections and all medicines, since some drugs induce autoantibodies, and ask that any surprising positive be repeated or confirmed by a second method.

References

ANA (antinuclear antibody) test. MedlinePlus, US National Library of Medicine (2023)View source
Agmon-Levin N, Damoiseaux J, Kallenberg C, et al.. International recommendations for the assessment of autoantibodies to cellular antigens referred to as anti-nuclear antibodies. Annals of the Rheumatic Diseases (2014)
Damoiseaux J, Andrade LEC, Carballo OG, et al.. Clinical relevance of HEp-2 indirect immunofluorescent patterns: the International Consensus on ANA patterns (ICAP) perspective. Annals of the Rheumatic Diseases (2019)
Kavanaugh A, Tomar R, Reveille J, Solomon DH, Homburger HA. Guidelines for clinical use of the antinuclear antibody test and tests for specific autoantibodies to nuclear antigens. Archives of Pathology & Laboratory Medicine (2000)
Aringer M, Costenbader K, Daikh D, et al.. 2019 European League Against Rheumatism/American College of Rheumatology classification criteria for systemic lupus erythematosus. Arthritis & Rheumatology (2019)
Shiboski CH, Shiboski SC, Seror R, et al.. 2016 American College of Rheumatology/European League Against Rheumatism classification criteria for primary Sjögren's syndrome. Arthritis & Rheumatology (2017)
van den Hoogen F, Khanna D, Fransen J, et al.. 2013 classification criteria for systemic sclerosis: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis & Rheumatism (2013)
Nihtyanova SI, Denton CP. Autoantibodies as predictive tools in systemic sclerosis. Nature Reviews Rheumatology (2010)
Buyon JP, Hiebert R, Copel J, et al.. Autoimmune-associated congenital heart block: demographics, mortality, morbidity and recurrence rates obtained from a national neonatal lupus registry. Journal of the American College of Cardiology (1998)
Izmirly PM, Costedoat-Chalumeau N, Pisoni CN, et al.. Maternal use of hydroxychloroquine is associated with a reduced risk of recurrent anti-SSA/Ro-antibody-associated cardiac manifestations of neonatal lupus. Circulation (2012)
Satoh M, Chan EK, Ho LA, et al.. Prevalence and sociodemographic correlates of antinuclear antibodies in the United States. Arthritis & Rheumatism (2012)
Mixed connective tissue disease (MCTD). Merck Manual Professional Version (2024)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.