What the lab technician sees under the microscope when testing a patient for anti-SSA antibodies. These are human epithelial cells to which blood was added from a patient who has anti-SSA antibodies, proving that that person is positive for anti-SSA. Photo credit below
Know your labs, such as the anti-SSA test when you have lupus!
The anti-SSA test is also called SSA antibody I recommend that all lupus patients get copies of their labs every time they are done. Look up any abnormal results from a reliable source to know what they mean. If you cannot find a reliable source, then ask your doctor.
Remember… Knowledge is Power!
So, let’s talk about anti-SSA (also called anti-Ro).
Anti-SSA is measured as a blood test in red-top tubes
Anti-SSA antibody:Also called Anti-Sjögren’s Syndrome A, Sjögren’s Anti-SS-A, Ro Antibody
Why is anti-SSA also called anti-Ro?
Anti-SSA and anti-SSB antibodies were first discovered in 1961 in people who had Sjögren’s syndrome. This systemic autoimmune disorder attacks the body’s moisture-producing glands, commonly causing dry eyes and dry mouth. The medical terms for them are “Sjögren’s syndrome-A” and “Sjögren’s syndrome-B” antibodies (or SSA and SSB for short). In 1969, another laboratory described antibodies in people who had lupus and named them anti-Ro and anti-La. “Ro” and “La” were the first two letters of the last names of the lupus patients in whom the antibodies were initially found (Robert and Lane respectively, according to Dubois’ Lupus 9th edition). Researchers later showed that anti-SSA was the same as anti-Ro and that anti-SSB was the same as anti-La. These terms are now interchangeable, with anti-SSA meaning the same thing as anti-Ro and anti-SSB meaning the same thing as anti-La.
How often does it occur?
Anti-SSA is more commonly positive in SLE patients than anti-SSB. SSA is positive in 20% to 60% of people who have SLE (depending on the patient population and the laboratory method used to detect the antibodies). Anywhere from 75% to 95% of people who have Sjögren’s syndrome are positive for this antibody. It can be present in any of the systemic autoimmune diseases and nonautoimmune conditions.
Subacute cutaneous lupus erythematosus (papulosquamous or psoriasiform type) in a systemic lupus patient with high positive anti-SSA (photo by Don Thomas, MD, shared with patient’s signed permission)
Some things may occur more often in people positive for anti-SSA antibodies:
People who have SLE (systemic lupus erythematosus) and are anti-SSA positive have an increased risk of developing rashes with sun exposure (especially subacute cutaneous lupus), inflammation of the lungs (pneumonitis), shrinking lung syndrome, inflammation of the liver (hepatitis), inflammation of the pancreas (pancreatitis), inflammation of the heart (myocarditis), low platelet counts (thrombocytopenia), low lymphocyte counts (lymphopenia), and an overlap syndrome with Sjögren’s.
IMPORTANT NOTE: From the list above, the most important ones are sun-sensitive rash and Sjögren’s. Most do not develop the other problems, but are listed for your knowledge. Your doctor will monitor your liver enzymes and blood counts (hopefully every 3 months) and make sure to let your doctor know if you get chest pain, shortness of breath, bruising, rash, dry mouth or dry eyes.
Anti-SSA positive patients should particularly avoid ultraviolet light and become UV protection fanatics. Please download and follow my UV protection handout from this page:
https:///www.lupusencyclopedia.com/lupus-secrets.html
ANA-negative SLE patients and anti-SSA
Although it is rare, some people who have SLE and are negative for ANA are positive for SSA antibody. If someone is thought to have SLE, but their ANA is negative, doctors should check for SSA antibodies. A newer ANA test, called “HEp-2000 ANA” (by a laboratory called Immuno Concepts in Sacramento, California), may be better at showing ANA positivity in these patients who are SSA antibody positive.
Anti-SSA can become positive years before SLE occurs
SSA antibody can be positive in someone many years before they develop lupus or Sjögren’s. It is one of the earliest antibodies to appear in many patients. This was figured out from blood samples of Army soldiers at the old Walter Reed Army Medical Center (Washington, DC) where I did my rheumatology fellowship.
It is essential that people found to have a positive SSA antibody (but not have evidence of having lupus, Sjögren’s, or any associated disease) be checked regularly by a doctor. I recommend that people in this situation learn what the symptoms of lupus and Sjögren’s are, and if any occur, to see a rheumatologist right away. Also, it is a good idea to see a rheumatologist regularly (such as once or twice a year) to have a proper physical examination and labs done. SLE can be potentially diagnosed by blood work (such as finding low blood counts or protein in the urine), yet the person may feel perfectly fine. The faster a proper diagnosis is made, the better the person usually does. Of course, someone who is SSA antibody positive may never develop any disease with it, but it better to be safe. I’d also recommend that someone in this category (antibody positive but no disease) avoid all potential triggers that may cause lupus (see table 3.1).
Around 2% of anti-SSA women can have a baby with “neonatal lupus.” Make sure to have your obstetrician check a fetal heart check starting at around 16 weeks
Important pregnancy information about anti-SSA:
One of the most important potential problems is that this antibody can cross through the placenta and enter the fetus of a woman who is positive for this antibody. These antibodies can potentially cause tissue damage in the unborn baby’s heart or skin (called neonatal lupus) whose mother is anti-SSA positive. Fortunately, this occurs in only about one out of fifty mothers who are positive for anti-SSA.
However, suppose a mother with SSA antibody has one child with neonatal lupus. In that case, her chances of each subsequent baby having neonatal lupus are approximately 20%.
Source of text:
from “The Lupus Encyclopedia” preliminary write up for the upcoming 2nd edition, by Don Thomas, MD and Johns Hopkins University Press
References for the above can be found under chapter 4 here:
https:///www.lupusencyclopedia.com/references.html
Photo credit (1st photo of lab test HeP immunofluorescence of anti-SSA test = from www.wikipedia.com article on Anti-SSA/anti-Ro antibodies, photo by Simon Caulton
Have you seen cases where the SSA antibodies show up after having lupus for several years? I was found to have positive antiphospholipid and anti ds dna antibodies back in 2019, and my SSA and SSB antibodies were negative at the time. But, in the past month I’ve started to notice my eyes and mouth feeling drier, and sometimes my jaw/salivary gland areas feel sore, so I’ve been wondering whether I should have the SSA and SSB checked again. Or would it not change management whether I have overlapping Sjogrens or not because I already get the regular “lupus labs” and see a rheumatologist every three months? They are already pretty sure I have overlapping SSc along with lupus. The prospect of adding a third systemic disorder to my list is kind of depressing.
Great question, showing quite a bit of knowledge since you added “or would it not change management.” It probably would not change management since Sjogren’s overlap can occur in the absence of anti-SSA. However, if you are of child-bearing age, it would be important if you were going to consider getting pregnant in the future.
Of note, scleroderma overlap absolutely can cause dry mouth and eyes. This happens frequently due to scarring of the glands. This is a very different cause than the inflammatory cause from Sjogren’s. In a patient with SLE/SSc overlap syndrome with negative anti-SSA, the scleroderma would be the more likely cause.
However, following all the advice for dry mouth and dry eyes from the Sjogren’s Foundation at Sjogrens.org can be very helpful.
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My Ana and double stranded DNA wen away after years of being positive but now I have positive anti chromatin. I can’t find much information on this lab
This is an unusual circumstance. ANA and anti-dsDNA becoming negative is a great prognostic sign. However, we do not really know if becoming chromatin antibody positive changes things. Anti-chromatin antibody is very closely related to anti-DNA antibodies. One could theorize that the anti-dsDNA becoming negative is the most important thing and that the anti-chromatin antibody is simply a less specific “equivalent.” If I had to bet or theorize, I would think this is overall a good thing…. I hope you do well… Donald Thomas, MD
If you have a positive ANA. ANA titer of 1:1280 and tested postive for SS-A (antibody only) no others. And you have clinical symptoms more consistent with Lupus rather than Sjorgren’s is that enough to diagnose Lupus? I don’t have the dry eye, mouth, and other gland issues that come with Sjorgen’s.
Brandi: SLE and Sjogren’s has a ton in common. Even many of their immunologic abnormalities are very similar. It can sometimes be difficult to tell the difference between one or the other or if someone has both (SLE with Sjogren’s disease overlap). One out of three SLE patients are anti-SSA positive; 60-70% of Sjogren’s patients are as well. I have many SLE patients who are anti-SSA positive and who do not have Sjogren’s. However, it does increase the risk for developing Sjogren’s disease, sun sensitive rashes, congenital heart block, neonatal lupus, heart inflammation, etc, so those are the things you want to keep in mind (though most of our anti-SSA positive patients do not get these (except the photosensitivity is incredibly common).
I am SSA positive (went from 3.6 down to 3). ANA went negative. Low complement C4, low ceruloplasmin, slightly low iron. Tingling in hands and feet. Migraines. Sore wrists. No swelling. Nursing an 11 month old. Dizzy upon standing. No other clinical symptoms. Should I pursue liver studies / tilt table? EKG is fine. Haven’t done SFN biopsy. Halter monitor fine
Julia: With anti-SSA and low C4 complement, I’d have a high suspicion for the possibility of an autoimmune disorder. If I discovered that the tingling is peripheral neuropathy on EMG and there is no other cause, then at least an undifferentiated connective tissue disease would be entertained. Just from what you tell me, and EMG/NCS of the hands and feet, and possibly a Tilt Test (autonomic dysfunction is underdiagnosed) would be considered in one of my patients. We know from the 2003 Arbuckle study that anti-SSA could appear 5-7 years before a diagnosis of systemic lupus. Don’t stop seeking answers. I wish our diagnostic tests were more advanced than they are. Too many patients end up with no answer for too long of a time….
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