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Chromatin antibody: Make sure you know your labs

posted in Diagnosing Lupus on May 5, 2021 by

Donald Thomas

Updated February 15, 2025

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Some systemic lupus erythematosus (SLE) are positive for anti-chromatin antibodies. This is an interesting antibody that has some interesting properties, and this article goes into detail about anti-chromatin antibodies and their significance in SLE patients.

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NOTE: Johns Hopkins University Press, publisher of The Lupus Encyclopedia, is a nonprofit publisher. If you purchase JHUP books, like The Lupus Encyclopedia, you support projects like Project MUSE.

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Know your labs when you have lupus

Anti-chromatin antibodies attach to chromatin in lupus patients

Chromatin is our DNA packaged up nice and neat with other proteins such as histone and RNA. It protects our DNA. Photo: at Wikipedia.com from the NIH

Chromatin Antibody (Also called Anti-Chromatin Antibody; anti-chromatin antibody, chromatin nucleosomal antibody; nucleosome antibody).

Bottom lines:
– Elevated anti-chromatin antibodies are fairly specific for people who have lupus, but can occasionally be seen in other autoimmune disorders. They are related to anti-dsDNA antibodies.
–  They are rare in healthy people
– They may possibly increase the risk of having lupus kidney inflammation (lupus nephritis), however, having them does not mean you will get nephritis. Just make sure to have a urine sample checked regularly
– In some people, they can fluctuate with disease activity and help monitor how someone with systemic lupus erythematosus (SLE) is responding to therapy. 

I recommend that all patients get copies of their labs so they can understand more about their lupus. If you are chromatin antibody positive, then read this article to learn more.

What are anti-chromatin antibodies and what do they mean?

Chromatin refers to the complex of DNA and other proteins that form chromosomes inside the nuclei of cells. About 60% to 70% of people who have SLE are positive for these antibodies, and they appear more commonly in SLE than in other systemic autoimmune diseases. Initial studies suggested that patients with SLE who are positive for chromatin antibody may have an increased risk for developing inflammation of the kidneys (lupus nephritis); however, this has been questioned in subsequent studies.

​Sometimes it can be difficult to tell if a patient may have SLE or Sjögren’s when they first come to a rheumatologist. One study showed that if that patient is positive for chromatin antibody and negative for SSA antibody, they most likely have SLE as their diagnosis. In some people with SLE, chromatin antibodies fluctuate with disease activity, decreasing in value when there is better control of lupus and increasing when it is worse. Chromatin antibodies can also occur in other systemic autoimmune diseases, including drug-induced lupus, mixed connective tissue disease, and scleroderma.

For more in-depth information on autoantibodies like anti-chromatin and lupus:

Read chapter 4 of The Lupus Encyclopedia, edition 2

Look up your symptoms, conditions, and medications in the Index of The Lupus Encyclopedia

If you enjoy the information from The Lupus Encyclopedia, please click the “SUPPORT” button at the top of the page to learn how you can help. 

What are your comments and opinions?

If you have lupus, what has your experience been? What do you recommend for other patients?

Do you have any questions to ask Dr. Thomas?

Please click on “Leave a Comment” above to comment.

Please support “The Lupus Encyclopedia” blog post page

Click on “SUPPORT” at the top of the page to learn how you can support “The Lupus Encyclopedia“

Author

Don Thomas, MD, author of “The Lupus Encyclopedia” and “The Lupus Secrets”

REFERENCES:

– The above excerpt comes from “The Lupus Encyclopedia” prior to printing of the second edition
– Mehra, S., & Fritzler, M. J. (2014). The spectrum of anti-chromatin/nucleosome autoantibodies: independent and interdependent biomarkers of disease. Journal of immunology research, 2014, 368274. https://doi.org/10.1155/2014/368274

For more in-depth information on Chromatin antibody: Make sure you know your labs:

Read more in The Lupus Encyclopedia, edition 2

Look up your symptoms, conditions, and medications in the Index of The Lupus Encyclopedia

If you enjoy the information from The Lupus Encyclopedia, please click the “SUPPORT” button at the top of the page to learn how you can help. 

What are your comments and opinions?

If you have lupus, what has your experience been? What do you recommend for other patients?

Do you have any questions to ask Dr. Thomas?

Please click on “Leave a Comment” above to comment.

Please support “The Lupus Encyclopedia” blog post page

Click on “SUPPORT” at the top of the page to learn how you can support “The Lupus Encyclopedia“

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24 Comments

  1. Which medications can cause chromatin antibodies? Which medications can cause drug-induced lupus?

  2. You stated, “ Chromatin antibodies can also occur in other systemic autoimmune diseases, including drug-induced lupus, …” So I’m assuming that’s what the previous commenter was referring to. I’m curious as well. I had completely normal bloodwork, then 2 weeks later had high ANA and Ant-chromatin. My rheumatologist doesn’t seem concerned because I don’t have any concerning symptoms. She believes it may be drug induced as I was on antibiotics for over a year for recurring UTI’s. Since then I’ve dealt with various pains s I it does seem to be since taking all these different antibiotics. She ran my blood work again 2 months later and the ANA and antichromatin levels dropped. She says they normally see numbers go up, not come down… not sure how accurate that is. Anyway, I’m terrified after doing research so I’m having her tests everything I can think of before asking her to put me on meds. Or is it possible to manage without meds? How do you know if it’s affecting your organs? When should I be concerned about a diagnosis if I’m not having typical symptoms?

    • Shawna: So sorry to hear of your predicament. The “unknown” and gray areas can be some of the most anxiety provoking.

      I’ll start that anti-chromatin is rarely seen in healthy individuals. So, if I have a patient who had a positive ANA then a positive anti-chromatin… they must have had something going on to make the physicians wonder about the possibility of a systemic autoimmune disease like lupus or Sjogren’s disease. Otherwise, it should not have been tested. If there is not a definitive diagnosis, I’d want to follow the patient closely with a history, physical exam and labs for CBC, chem, random urine protein/creatinine ratio, urinalysis, anti-dsDNA (chromatin is very closely related to this antibody), C3, and C4. I’d make sure that these were checked at least once: CH50, ENA, direct Coomb’s antibody, anticardiolipin antibody, lupus anticoagulant, beta-2 glycoprotein-I antibody, ribosomal-P antibody, ENA, RF, CCP, and an SPEP. I would also consider ordering the AVISE Lupus Test. If your doctor doesn’t order this… you could download the order form, find out what lab is the closest to you on the lab locator on their website, and ask your doc if it would be OK for them to order (if you fill out the paperwork ahead of time, this should be pretty easy. There is no way for me to conjecture otherwise without being your physician. I sure hope they figure things out for you.

      Donald Thomas, MD

  3. Is it possible to have lupus if you are symptomatic with matching criteria with a negative ANA titer but significantly elevated Chromatin antibody test?

    • Dear Jessica: Thanks for reading my post and commenting.

      1. Anything is possible. I’ve seen it all over 30 years. We know that autoantibodies can occur many years before SLE occurs. Scientists are now working on lab tests that may be able to identify patients with SLE years before our current ability; so hopefully this will improve in the future.
      2. However, we can also have false positive anti-chromatin antibodies. This is more likely to happen in an ANA-negative patient who has no symptoms of SLE.

      Recommend: learn the symptoms of lupus, Sjogren’s disease, and RA … if any occur in the future, get reevaluated.

      Good luck,

      Donald Thomas, MD

  4. Does a high positive anti-chromatin, positive ANA, RNP (anti-U1 and anti-U2) specifically correlate to lupus? The patient experiences myositis-like symptoms on one side of the body. Patient has high creatinine. Would this indicate MCTD and therefore no concern for lupus? Should further testing on kidney function be done?

    • Deniece: This constellation of antibodies is not specific for lupus, myositis, nor MCTD. All of these can have these antibodies. All of these can cause muscle inflammation as well (myositis). If someone has nonspecific findings that can be seen in more than one CTD and does not satisfy classification criteria for either one, yet has evidence for a CTD, most of use would use a diagnosis of undifferentiated connective tissue disease (UCTD) yet still offer treatment targeted at the manifestations (most commonly hydroxychloroquine). Regarding a high serum creatinine, I’d absolutely want to know the eGFR, urinalysis and random urine protein to creatinine ratio. Note that some drugs can also cause a high creatinine in the absence of kidney disease (this includes hydroxychloroquine and Bactrim, famotidine, and fenofibrate).

      Donald Thomas, MD

  5. Just got test results.
    SM/RNP ab 8.0 high,
    Sjogrens Ab SSA 8.0 high,
    Chromatin ab 3.3 high.
    Everything else in normal range or negative
    Is this Lupus (SLE) ??
    Thanks in advance

    • Lisa: Anti-Sm/RNP is more closely related to anti-RNP antibody than to anti-Smith. This combo (Sm/RNP, SSA, chromatin) can be seen in most of the systemic autoimmune diseases (SLE, Sjogren’s disease, polymyositis, scleroderma). These labs had to be ordered for other reasons (arthritis, Raynaud’s, low blood counts etc)… your doc would have to put all of it together to help figure out. If you have dry mouth or eyes, then Sjogren’s would definitely need to be considered. Good luck!

      Donald Thomas, MD

  6. My daughter who’s 7 years old. She has some concerning symptoms that seem to come and go.

    She was tested and they found:
    Abnormal c4
    Lower normal C3
    Homogeneous pattern
    1:160
    POS ANA
    POS Anti Chromatin

    I’m being told this is not enough to diagnose. I’m extremely frustrated for her. I do think it’s early lupus and not the full blown disease. How do we test children and why is t this enough to at minimum…put her in a case study?

    • Amber: Sorry to hear you daughter is going though this. It has to be worrisome as the parent.
      If the C4 is high instead of low, then it is unhelpful (even a common cold can do that). If it is low, then that is significant and significantly increases the chances of this being associated with some disorder.
      If it is high, this entire pattern can be seen with too many things, including infections like parvovirus infection and hence the doctors’ reluctance to diagnose a specific disease.

      If it were my daughter, I’d ask for the AVISE Exagen CTD and Lupus AVISE testing (some of the most sensitive and specific tests there are for these disorders. Even if your doctor doesn’t do them in their office, they can order it and you can find a lab close to you. Read my ANA lab workup post and it gives specific instructions.

      https://www.lupusencyclopedia.com/ana-positive-how-to-get-a-lupus-diagnosis/

      Good luck. I hope it is something that just goes away on its own.

      Donald Thomas, MD

  7. I just received my blood work back from a positive ANA result.

    Spin test included speckled pattern 1:8
    Spindle Apparatus Pattern 1:160
    Anti-Cardiolipin Ab, IgM 18
    C3 185
    Anti-Chromatin Ab, IgG 23

    All other tests were normal.
    Symptoms include dry mouth, imbalance, fatigue

    Does this mean lupus?

    • Dear Sher: It all depends upon what else is going on.

      For example, Sjogren’s disease patients can be chromatin antibody positive as well. Your rheumatologist will need to put the pieces of the puzzle together … good luck!

      Donald Thomas, MD

  8. Hi Don- so happy to have found this site. I have been treated for SLEs since 2012 although I’ve had symptoms since the early 90’s when I was in college ( I was told I had a million different thing wrong with me & I was depressed & had anxiety, you know how that goes). I was tested in my early 20’s by a Rheum due to severe joint pain & inflammation & again in my early 30’s due to a Malar rash I’ve had since all my symptoms started. Both time nothing showed up in my blood.

    In 2011 I wasted my fatigue & all over pain was fibromyalgia but in 2012 I started getting fevers every day, double vision, crippling joint pain & the Malar rash has been there since college. I finally tested ANA positive 1:80 speckled pattern but serum negative for everything else. I was given Plaquenil and my PCP (and the Rheum I saw) felt that given all of my symptoms plus the ANA that felt that an SLE dx was appropriate. The Plaquenil stopped the fevers and 90% of the joint pain as well as improved the rash (at the time).

    However, 12 years later I’m significantly more affected by my symptoms and the Plaquenil isn’t enough. I know feel the joint pain in my feet as well as my hands and I need to get steroid injections in my back every year or I can’t function. The fevers come back occasionally and the fatigue is overwhelming. I’m now also experiencing new symptoms, hair loss, discoid rashes on my chest and face, constant abdominal pain and headaches. I had to medically retire in 2017 because I could no longer work full time.

    The issue is my PCP and the original Rheum have retired and I’m having a terrible time finding a new Rheum who will acknowledge that I have SLE or that it’s active. My most recent bloodwork shows the ANA unchanged (Titer 1:80) along with all the other SLE markers negative except a high Anti-Chromatin. In my research it appears that that is a marker for SLE, however the last Rheum I spoke to said that wasn’t true & when I pointed out that I had learned about it via medical journals & studies he said I shouldn’ trust them. He then asked me if I had a traumatic childhood and told me to get a therapist! The reason I chose him was because he is young & I felt like I wouldn’t have o worry about being treated like I was in the 90’s- being told it was all in my head. He had my test results in front of him & could seee my butterfly rash & discoid rash on my chest. He also said he wanted to reduce my Plaquenil dose Fromm 400 mg a day to 200 mg a day. That’s when I got up and left because that is the only thing that helps me at all.

    I greatly apologize for the length of my post but I’m so frustrated because I’m at a loss as my condition worsens & I can’t find anyone to help me, Am I crazy in asserting to a Rheum that given my bloodwork and symptoms and response to the Plaquenil I clearly hav SLE and therefore further treatment options should be explored?

    Any thoughts are greatly appreciated and you’re offering such an amazing service to those of us stuck on auto-immune roller coaster with no help

    Liz

    • Liz: So sorry to hear this and not an uncommon story. So common that I made a note to do a blog post soon on “What to do if a rheumatologist doesn’t believe you have SLE”.

      One of the most important is to get all your labs and rheumatologist notes from the time of your initial diagnosis.

      Having photos of the original rashes to show is also very helpful. However, few people realize it is a good idea to save them for the future “just in case.”

      Good luck and I hope you do well.

      Look out for my new blog post in the next few weeks.

      Donald Thomas, MD

  9. Hi! I have positive ANA (1:1280 speckled), Raynaud’s, suspected malar rash (photosensitive, butterfly shape, but not confirmed by derm), low WBC, low C3, low C4, anti-chromatin antibodies, but negative ds-DNA and no joint pain (all other bloodwork normal). Rheumatologist suspects early lupus. I am so confused, though, why I have no joint pain or ds-DNA. Does this make sense at all?

    • Amy: This is why we have classification criteria for SLE and why anti-dsDNA is only one of many possible criteria. Every SLE patient is different. 10% have no joint pain, 30-50% are anti-dsDNA negative. There are very few things that cause Raynaud’s, malar rash, leukopenia, hypocomplementemia, and +ANA/chromatin antibodies: SLE would be by far the most common cause. If there is any doubt whatsoever: what would I do? … I’d see derm ASAP, take all this information, and just make sure the rash is not rosacea or seborrheic dermatitis etc and if not… start on hydroxychloroquine, UV light protection etc ASAP.

      Good luck and I hope you do well.
      If you do have SLE, I recommend: https://www.lupusencyclopedia.com/how-to-succeed-after-lupus-diagnosis/

      Donald Thomas, MD

    • Would a result of Antichromatin antibodies <0.2 be considered a positive result?

      • Marcy: This would be a negative result. Reading lab report results can be confusing.

        Dr T

  10. These are my results and a doctor who is not my PC but part of my plan said I may not have Lupus. It’s confusing. Can you help me interpret this.
    SYSTEMIC LUPUS ERYTHEMATOSUS (SLE), DISEASE ACTIVITY PANEL

    DNA (DS) ANTIBODY: < 1

    CHROMATIN (NUCLEOSOMAL) ANTIBODY: 2.0 POS (this one is positve)

    COMPLEMENT COMPONENT C3C: 100

    COMPLEMENT COMPONENT C4C: 19

  11. Thank you for this information. I am in the process of a concrete diagnosis of autoimmune hepatitis. Elevated LVTs, liver biopsy showed inflammation and necrosis. No cancer. However, my other autoimmune levels are also reactive. In the past I had Hashimoto’s Disease resulting in thyroid cancer/thyroidectomy, so I read I am prone to other autoimmune issues.

    Chromatin Antibody IgG: 34 (high)
    dsDNS Ab IgG: 25 (high)
    Immunoglobulin G, serum: 1656 mg/dl (high)

    for the AIH:
    Smooth muscle Ab, IgG titer: <1:20
    ANA detected, homogeneous pattern, titer 1:1280
    Mitochondrial M2 Ab, IgG: 10.8 and currently 9.0
    F-Actin Antibody IgG: 61 (high)

    thank you for any information

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