Positive AntiNuclear Antibody (ANA) SS-B/La

By | September 21, 2012

Positive AntiNuclear Antibody (ANA)  SS-B/LaI failed a test yesterday, a blood test. This is the third to show positive for the antinuclear antibody (ANA) known as anti SS-B/La. This means my immune system is attacking a protein inside the nucleus of my own cells. This is bad.  Fortunately, I do not also have the SS-A antibody, which probably indicates I don’t have Lupus (SLE) or Sjögren’s syndrome. What caused this problem and how do I fix it? The first step is to gather information, as many clues as possible…

Sjögren syndrome type B antigen (SS-B) also known as Lupus La protein is a protein that in humans is encoded by the SSB gene.[1]

La is involved in diverse aspects of RNA metabolism, including binding and protecting 3-prime UUU (OH) elements of newly RNA polymerase III-transcribed RNA, processing 5-prime and 3-prime ends of pre-tRNA precursors, acting as an RNA chaperone, and binding viral RNAs associated with hepatitis C virus. La protein was originally defined by its reactivity with autoantibodies from patients with Sjögren’s syndrome and systemic lupus erythematosus.[1][2]

Sjögren syndrome antigen B has been shown to interact with nucleolin.[3]


… data suggest that SS-B/La belongs to a large family of RNA-binding proteins which includes heterogeneous nuclear RNPs, nucleolin, mRNA polyadenylate binding protein, and small nuclear RNPs.

The La/SSB antigen appears to be a nuclear phosphoprotein with a molecular weight of 48 kD and is complexed with the Ro particle [26]. In addition to other functions, the La protein serves as a termination factor for RNA polymerase III [27].

  • It is unusual to encounter sera that contain anti-La/SSB activity without demonstrable antibodies to Ro/SSA in patients with SLE or Sjögren’s syndrome.
  • Isolated anti-La/SSB antibody activity has been seen in some patients with primary biliary cirrhosis and autoimmune hepatitis.
  • Antibodies to the La/SSB antigen are present in 70 to 95 percent of patients with primary Sjögren’s syndrome, and in 10 to 35 percent of patients with SLE, and are occasionally seen in patients with cutaneous LE, scleroderma disorders, and rheumatoid arthritis [10,17]


I take the flax oil daily and have no dry eye problems when I do that, but long term, I’d like to reverse the problem. What are the options? One site recommends going vegetarian:

… Mammalian tissue from food such as beef, veal, pork, cheese, milk, and ice cream is remarkably similar, at a molecular level, to your own tissue. So eating animal food may provoke an autoimmune flare. This is why I highly recommend adopting a vegetarian diet for those who have been diagnosed with an autoimmune disorder.

The best choices for oils in autoimmune disease are flax, olive, and coconut. Human clinical studies have also shown that fish oil can induce clinical remission of MS, rheumatoid arthritis, and other inflammatory diseases such as ulcerative colitis and psoriasis. Look for a fish oil that is cold-pressed, and take at least 2,000 mg daily of mixed DHA and EPA.

Antioxidants are also important in reversing immune system confusion, but they must be taken synergistically. Vitamin E taken alone can potentially oxidize because it’s a polyunsaturated fat. To prevent oxidation, take vitamin E in conjunction with vitamin C and selenium. To halt and maybe even reverse your autoimmune process, take vitamin E in high doses of up to 1,600 IUs per day, with 3—5 g of vitamin C and 400 mcg of selenium.

via Better Nutrition Magazine :: Supplements, Nutrition, Recipes, Personal Care :: Columns :: Ask the Naturopath.

The Weston A Price people would disagree, but how many people have they cured of autoimmune problems? Where is the documentation of any such claims? If I do have autoimmune hepatitis, how is that cured?

Autoimmune hepatitis is a disease characterized by chronic inflammation of the liver… , which can range from mild to severe. … The exact mechanism whereby the body’s own immune system attacks the liver is not yet known. It appears that certain types of white blood cells (the type of blood cell that usually fights infection), in addition to attacking foreign substances (e.g. germs and viruses) misread liver cells as foreign substances and start attacking these cells. The type of damage that follows is known as chronic hepatitis. A number of other conditions can cause identical patterns of liver damage. … It is absolutely not contagious. It is generally not considered an inherited disease but a tendency to autoimmune diseases may run in some families. That is, children of patients with autoimmune hepatitis may be at slightly increased risk of developing autoimmune diseases of the thyroid or liver or arthritis. The risk, however, is only slightly greater than the normal population … Blood tests will almost always reveal elevations of ALT and AST enzymes that the liver makes. In addition, other blood tests will reveal antibodies directed against parts of different cells, such as anti-smooth muscle antibody and antinuclear factor. Your doctor, on examining you, may find abnormalities suggestive of chronic liver disease such as a large liver, jaundice, and certain signs noticeable on the skin…. milk thistle or its active ingredient, silymarin, has been studied, and has no beneficial effect. Standard treatments such as prednisone have been proven to delay or prevent progression to cirrhosis and thus save lives. It is ill-advised to delay or not take standard treatments in the hope that alternative remedies may work …Since we do not know exactly what causes autoimmune hepatitis, we do not yet have a medical cure for the condition.

via Liver.CA

“We don’t know yet” is not an acceptable answer to me. I’ll have to keep looking. Probably a virus.  I’m consulting a Rheumatologist, who probably won’t have any ideas about a cure, but at least I can check out the liver infection idea and then move on. Another clue:

SSB (La) antibody is seen in 50-60% of Sjögren syndrome cases and is specific if it is the only ENA antibody present. Fifteen-25% of patients with systemic lupus erythematosus (SLE) and 5-10% of patients with progressive systemic sclerosis (PSS) also have this antibody.

What is progressive systemic sclerosis?

Scleroderma is a connective tissue disease that involves changes in the skin, blood vessels, muscles, and internal organs. It is a type of autoimmune disorder, a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue. …  The cause of scleroderma is unknown. People with this condition have a buildup of a substance called collagen in the skin and other organs. This buildup leads to the symptoms of the disease. The disease usually affects people 30 to 50 years old. … Some people with scleroderma have a history of being around silica dust and polyvinyl chloride, but most do not.

Where I have this one or not, my problem may be due to poisoning by plastics or some dental adhesive. I drink out of plastic bottles every day and have for years, but I use type 1 polyethylene instead of type 3 which is PVC/vinyl. I was tested for SS-B in the past. It was negative on 2/8/2010 and positive 5/23/2012 so what happened during those years? 9/11 attacks, changed cologne, had dental work, a friend with Lupus …

What I don’t understand, really, is why my body keeps making this particular ANA. Once your body learns to make a particular anti-nuclear antibody, you just keep making it? That seems unlikely. Is the anti-SSB always in response to an actual SSB/La protein being present in the nucleus of a person’s cells? Or is there some toxin/virus in my system that is causing me to produce the attack chemical which then mistakenly attacks my own cells?

STEP 1: My nutritionist has been telling me to give up plastic bottles! Okay, okay, starting today, no more water from plastic bottles. I’ll use stainless steel for a few years and see if that makes a difference.

Water is often bottled in #1 PET or PETE bottles (polyethylene terephthalate), which may or may not leach DEHA, a known carcinogen, into the water. Experts agree that you should not re-use #1 plastic bottles. Plastics numbered 3, 6 and 7 are worse; they contain Bisphenol A (BPA), which is suspected of causing neurological and behavioral problems in fetuses and children. BPA mimics the female hormone estrogen, which may have detrimental effects, including cancer of the brain, breast, and prostate, on the female reproductive system and the immune system in adults. … Water is often bottled in #1 PET or PETE bottles (polyethylene terephthalate), which may or may not leach DEHA, a known carcinogen, into the water. Experts agree that you should not re-use #1 plastic bottles. Plastics numbered 3, 6 and 7 are worse; they contain Bisphenol A (BPA), which is suspected of causing neurological and behavioral problems in fetuses and children. BPA mimics the female hormone estrogen, which may have detrimental effects, including cancer of the brain, breast, and prostate, on the female reproductive system and the immune system in adults.


What’s the problem with #1 plastic bottles?

Mediocre Plastic: (contains BPA which is released over time)
#1 Recycling symbol– Designed for one-time use only. Also labeled as PETE (Polyethyl Tetra Ethelene)
This is the type of bottle that water is usually sold in. Do not refill this bottle – the chemical bond breaks down over time, and then can transfer BPA into the liquid. Many people who are concerned about the environmental impact of using a bottle only once and then throwing it away will refill #1 bottles. We don’t recommend this because over time, as they are tumbled around in your car, become dented, etc. BPA is released. We suggest you avoid buying #1 bottles whenever possible, and switch to refillable stainless steel or glass bottles, a much better alternative for both you and the environment.


Could long term BPA exposure trigger the SS-B ANA?

More notes:

It is poorly understood how ANCA are developed, although several hypotheses have been suggested. There is probably a genetic contribution, particularly in genes controlling the level of immune response – although genetic susceptibility is likely to be linked to an environmental factor, some possible factors including vaccination or exposure to silicates. Two possible mechanisms of ANCA development are postulated, although neither of these theories answers the question of how the different ANCA specificities are developed, and there is much research still being undertaken on the development of ANCA.[3]


5 thoughts on “Positive AntiNuclear Antibody (ANA) SS-B/La

  1. Leslie

    I too have the Ssb positive twice in last yr & not ssa also one positive ANA .. Love to know how you are doing now.

  2. yasisaber

    I have the Positive SSB too without ant SSA, My symptoms are extreme fatigue and bruising , block nose and itchy ears, but no dry mouth or dry eye. Most of the articles are about SSA and SSB together. So please let me know about your progress

    1. Xeno Post author

      I often have a stuffy nose and use a saline nasal rinse to help that. This positive ANA hasn’t gone away yet and now I have also tested positive for pancreatic Islet Cell Antibody (IA-2), so I’m killing off my pancreas slowly and without enough insulin production my blood sugar gets dangerously high. This sugar causes damage to small blood vessels and various symptoms, some of which, like a potential diabetic coma, are life threatening. Get checked for IA-2 if you have only SSB to be sure you don’t have adult onset diabetes. I’m thin by the way, and don’t have any other diabetes risk factors.


      A 66-year-old Taiwanese male received blood transfusions during coronary artery bypass surgery in 1987. Serum specimens, obtained as part of a study on post-transfusion hepatitis, demonstrated that the patient had no evidence of hepatitis C prior to transfusion, but developed acute HCV infection after transfusion. One year later, the patient, who had no personal or family history of diabetes, presented with diabetic ketoacidosis, and tests for C-peptide confirmed that he had Type 1 DM. Testing of pre- and post-operative serum specimens demonstrated that the patient developed positive tests for islet cell and glutamic acid decarboxylase antibodies 4 weeks after transfusion, concurrent with the development of acute HCV infection.

      The simultaneous development of HCV infection and diabetes-related autoantibodies suggest a relationship between HCV and Type 1 DM.”



      Since the hepatitis C virus (HCV) was identified, numerous epidemiological studies have reported a higher prevalence of type 2 diabetes mellitus (DM2) in subjects infected by HCV (1-3). Although the initial associations of diabetes and liver disease were made in subjects with advanced liver disease (1-4), more recent reports have described an increase in DM2 before the development of advanced liver cirrhosis (5). Furthermore, the epidemiological link has been established between DM2 and HCV infection, rather than other causes of liver diseases, such as hepatitis B viral infection (HBV) and alcohol abuse (6). The increase in the number of cases of DM2 among people infected by HCV has been reported to be as much as four times higher than in the general population (7). Other factors, such as obesity, which is characterized by a high body mass index (BMI); advanced age and family history of diabetes, are also associated with the higher incidence of diabetes in the HCV-infected population (8-10).

      In addition to infection by HCV, other viral agents such as coxsackie virus, congenital rubella and cytomegalovirus have been proposed as being capable of triggering the development of diabetes mellitus type 1 (DM1) or juvenile diabetes mellitus (11-13). It is unclear as to why some patients with HCV infection develop diabetes. However, it is tempting to speculate that the HCV infection is able to trigger autoimmune mechanism(s) against the insulin producing pancreatic beta cells in susceptible individuals.

      The mechanisms proposed for the development of DM1 following viral infection are generally based on findings of specific humoral and cellular immunity against viral antigens as well as insulin producing pancreatic cells in some diabetic children (11-15). In HCV infection, the use of interferon alfa, a well-known immune enhancer for the treatment of HCV infection, has been observed to be associated with the development of diabetes (16, 17). Contrary to DM1 that occurs mainly in children, the diabetes associated with HCV infection has so far been observed mainly in adults (1-3). This may be due to the low incidence of HCV infection in children since the mechanisms of infection by HCV are associated with adult lifestyle. For example, sharing needles by intravenous drug users, tattooing and sexually transmitted diseases (18-20). Furthermore, risks for transmission of HCV infection in children, such as blood transfusion, have been dramatically reduced since the introduction of the screening tests for HCV antibodies in blood donors.

      Presently, it is unknown what may make an individual susceptible to the development of diabetes after a viral infection. A genetic susceptibility for the development of DM1 has been well documented in some individuals (21). Whatever the trigger mechanism(s) for the development of diabetes in susceptible individuals, DM1 or insulin dependent diabetes has been associated with genetic markers known as human hystocompatibility antigens (HLA). Resistance to the development of diabetes has also been associated with HLA antigens.

      A better understanding of the immunogenetics of HCV infection is needed. During the last few years, we have learned that the viral and clinical outcome of HCV infection is associated with the HLA type of the individual. Most HCV infected individuals develop chronic HCV infection, which is characterized by the presence of the HCV ribonucleic acid (RNA) in the blood and a high probability for the development of chronic liver disease including liver cirrhosis and liver cancer. However, some 20-30% of the infected individuals develop an immune response that is able to spontaneously overcome the infection (22, 23). These individuals become negative for HCV RNA and do not develop HCV-associated liver diseases. All of the above findings suggest that the genetic makeup of an individual is a determining factor in the outcome of the HCV infection, in which the development of diabetes is one of the possible outcomes.


      Try some Camel Milk:

      Camel milk has been widely used in a number of countries as a food additive and for curing some commonly occurring diseases. Recently, camel milk has been deeply studied for its special properties because of higher hepatoprotective, insulin like and antibacterial activities. These properties distinguish camel milk from milk of other animals. The present study was carried out to investigate the protective effects of camel milk against CCl4-induced hepatotoxicity which lead to biochemical alterations in liver function of male albino wister rats. White albino male rats (200-250 g) were divided into 5 groups, a normal control water group, a control camel milk group and three CCl4-intoxicated groups treated with or without camel milk. Protective roles of camel milk were analyzed by assaying the liver function parameters as serum aminotransferases, alkaline phosphatase, serum proteins and cholesterol levels. Histopathological examinations were also studied in all groups of rats by microscopy. Data showed that intraperitoneal administration of CCl4 (1 mL kg-1 b.wt.) resulted in statistically significant increase in the serum levels of aminotransferases and change in serum protein, albumin and cholesterol levels which approach to normal levels after the treatment with raw camel milk.

      Furthermore, histopathological studies reveal that camel milk treatments significantly reduce the incidence of liver lesions induced by CCl4. Our findings demonstrate that CCl4 exposure alters liver function biochemical parameters, which shift towards normal values after treatment with camel milk. So camel milk has a good potent for curing some liver diseases.


      1. Jeremy

        I have had symptoms of type 1 ,getting tested right now.Oddly enough the doc had ssb and ssa done prior to me requesting type 1 diabetes test. my ssb came out positive but not ssa.He didnt even mention it,seems like he was in a hurry.thats beside the point though.but anywho, Im pretty sure its type 1 ,my father had the same diabetes.Im glad i caught this on time,because doctors dont.Ill let you know my results

  3. Robert

    I found this page because I also am positive for SSb and negative for SSa. I care because I have symptoms of Sogrens. Evidently you do not have any symptoms that concern you so I don’t know why you care about the positive SSb. Depending on the lab there a lot of false positives for SSb. http://www.ncbi.nlm.nih.gov/pubmed/25735642

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