View Full Version : ANA results
09-22-2006, 04:37 PM
I finally got my rheumatologist to tell me what my blood tests results were. Everyone on this site quotes an ANA number, but he only told me that 95% of my white blood cells were lupus cells. How does this relate to all the numbers that everyone else mentions? I get confused alot anyway, so any help would be appreciated.
09-22-2006, 05:43 PM
The only thing I can suggest is that your doctor may have been talking about an LE cell test. This is a test that was once used to help diagnose lupus, but has mostly been replaced by the ANA test now.
In 1948, a pathologist named Malcolm Hargreaves discovered the LE cell (Lupus Erythematosus cell), which was the first blood test used to help diagnose lupus. He found that 70-80% of patients with active SLE had these cells. An LE or "lupus cell" is a specific cell found in the blood specimens of many lupus patients. The LE cell is a white blood cell that has swallowed the nucleus of another white blood cell.
During the 1950s, researchers discovered that the LE cell was part of an antinuclear antibody (or ANA) reaction. This led to the development of other tests for autoantibodies. These are the tests that are primarily used today to diagnose lupus and other auto-immune disorders.
When the ANA test is negative but other symptoms
indicate SLE, the LE test is still used sometimes to help clarify the diagnosis. This test is considered to come up as positive in 90% of patients with active SLE. However, it can also be positive in other conditions such as scleroderma, RA, Mixed Connective Tissue Disease, in liver disease, and in people taking certain prescription medicines such as hydralazine. Since the LE cell test is not specific for SLE, it's rarely used
Saysusie or some of the other very knowledgeable folks on the forum may have better information for you, but that's my best guess as to what your doctor meant.
09-28-2006, 03:09 PM
Does this mean that it is possible that I don't have lupus or that it isn't serious? My physician suggested that I go to a rheumy after I had a high white blood cell count. The rheumy didn't seem to think I had lupus at first especially when he gave me a strength test and I pulled the little guy over. But when I went back with the tests he gave me and the distortion of my hands from six years back, he seemed to think that I had it. He did say that the tests on my kidneys and other organs were good. So that my main involvement was arthritis and the rash. This last episode my feet grew bunions and several other abnormalities. He is an older doctor so he didn't seem to take in what I consider brain fog.
09-29-2006, 03:12 PM
Your doctor will have to run several other tests before he can tell you if you have lupus and, if so, which type of lupus you may have. You could have Cutaneous Lupus: ACLE, SCLE, CCLE, or DLE/ Systemic Lupus: SLE/
Drug- Induced Lupus/ Overlap: RA, Myositis, Sjogren's, Scleroderma. Even within the same type of lupus, each case is unique, symptoms range from mild to severe and no two cases affect us in the same way.
The information that Marycain gave you is the closest explanation for LE Cells in the diagnosis of Lupus. The LE cell is a white blood cell that has swallowed the nucleus of another white blood cell.
There is a possibility that he might have been referring to Lupus T Cells: Patients with lupus produce antibodies against their own proteins. Patients also have immune T cells that produce a protein called IL-2, which normally usually protects against infection, at lower than typical levels. Sera from lupus patients contains antibodies that bind to T cells and activate a complex cellular signaling cascade that ultimately results in decreased IL-2 production. This deficiency in IL-2 could result in the autoantibody production that occurs in lupus.
Lupus T cells increase the production of an enzyme called cyclooxygenase 2 (COX-2), which helps trigger inflammation. The inflammatory process is a byproduct of the body's immune system, which fights infection and heals wounds and injuries: When an injury or an infection occurs, white blood cells are mobilized to rid the body of any foreign proteins, such as a virus.
The masses of blood cells that gather at the injured or infected site produce factors to repair wounds, clot the blood, and fight any infective agents. In the process the surrounding area becomes inflamed and some healthy tissue is injured. Under normal conditions, the immune system has other factors that control and limit this inflammatory process.
The Infection Fighters. The primary infection-fighting units are two types of white blood cells: lymphocytes and leukocytes.
Lymphocytes include two subtypes known as T-cell s and B-cells. Both types of cells are designed to recognize foreign invaders, antigens, and to launch an offensive or defensive action against them:
B-cells produce antibodies when confronted with an antigen coming from outside the cell. Antibodies are separate agents that can either ride along with a B-cell or travel on their own designed to attack the antigen. The B-cell then develops a "memory" to remember that specific antigen and alert the immune system if it detects it again.
T-cells also have special receptors attached to their surface that recognize specific antigens. T-cells, however, are further categorized as killer T-cells or helper T-cells (TH cells). Killer T-cells directly attack antigens, such as viruses, that occur in any cells that contains a nucleus. Helper T-cells recognize antigens, but their role is two fold. They stimulate B-cells and other white cells to attack the antigen. They also produce cytokines, powerful immune factors that have an important role in the inflammatory process . Helper T-Cells. The actions of the helper T-cells are of special interest in this process. For some unknown reason, the T-cells become overactive and mistake the body's own cells as an antigen and trigger a series of immune responses to destroy the false enemy. TH-cells stimulate B-cells to produce antibodies. In this case, however they appear to direct the B-cells to produce autoantibodies, which are directed against the body's own cells. Antibodies come in five types: IgM, IgG, IgA, IgD, or IgE. The autoantibody in SLE appears to be derived from IgG.
Autoantibodies. In the majority of patients with SLE, antinuclear antibodies (ANA) are the specific autoantibodies that attack the nucleus and DNA of the patient's healthy cells. Experts have identified two subtypes of ANA that are specific only to SLE patients:
Anti-DNA. An autoantibody called anti-double stranded DNA (anti-ds DNA) may play a critical role in the process. A 2001 study suggested that these antibodies specifically attack a protein in the kidney called alpha-actinin, which researchers suspect may also occur in other tissues that are affected by SLE, such as in the skin, joints, and brain. A subset of anti-DNA has also been found to target nerve-cell receptors in the brains of SLE patients.
Anti-Sm antibodies. Other autoantibodies may also be involved:
Anti-Ro (SSA). These autoantibodies may be involved in the sun-sensitivity experienced by SLE patients.
Antiphospholipid antibodies. About half of SLE patients also have these antibodies. They attack phospholipids, fatty compounds found in cell membranes throughout the body. Antiphospholipid antibodies increase the risks for blood clots and may be responsible for narrowing of and irregularities in blood vessels and low blood cell counts. Antiphospholipid antibodies are linked with miscarriage, kidney, heart, cerebral, and eye problems in SLE patients.
Cytokines. TH-cells also secrete or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are indispensable for healing. If overproduced, however, they can cause serious damage, including inflammation and cellular injury. They can cause inflammation that occurs in parts of the body beyond the joints, which can produce fever, shock, and even organ damage, such as the liver. Specific cytokines called interferons and interleukins play a critical role in SLE by regulating the secretion of autoantibodies by B-cells. Researchers are currently interested in interferon alpha; some scientists believe high levels of this cytokine may underlie the autoimmune response in SLE.
Complement. Another immune factor of high interest in SLE is complement. This is comprised of more than 30 proteins and is important for defending and regulating the immune response against foreign cells. Inherited deficiencies in certain complement components (C1q, C1r, C1s, C4, and C2) have long been associated with SLE. Deficiencies may contribute to SLE in the following manner:
Complement may protect against autoimmune disease by normalizing apoptosis, the natural process by which cells self-destruct. In their absence, then, apoptosis goes awry and leads to the release of nucleosomes (collections of DNA and protein) that, in turn, trigger the destructive SLE antinuclear autoantibodies. Complement components are also necessary for clearing molecular rubble called immune complex. This is the end product of the previous intense immune activity. It consists of autoantibodies and antigens, leftover debris when the battle is over. In the absence of complement, this debris accumulates and is deposited in the kidneys, blood vessels, joints, and other sites where it further incites the immune system to produce inflammation and tissue damage.
I hope that this has been helpful
Peace and Blessings
09-29-2006, 03:55 PM
It might be helpful to see a foot specialist to make sure that what you are describing as bunions actually are. Bunions occur in the joint that connects your big toe to the base of the foot - they can run in families, but are usually caused by poorly fitting shoes. But some people with rheumatoid arthritis can develop joint deformities that affect their toes, so you really should see a specialist to make sure, especially since you have some deformities in your hands. Rheumatoid arthritis can cause symptoms a lot like lupus. If not treated, it can cause joint damage and deformity.
If you are not sure what your doctor's diagnosis is, you should schedule an appointment to talk with him. Ask him to explain to you in plain, non-medical language what he thinks is wrong, and what treatment he suggests. It might help to take someone with you, especially if you have a problem with confusion or brain fog. Brain fog is very common in lupus patients, so don't feel like you are alone in this. A lot of us share this problem.
09-30-2006, 06:08 PM
Thank you SaySusie, that helps me understand the process better. As far as the bunions are concerned, fifteen years ago I had the bunions removed that I was born with. Those grew off the side of my foot as if I was trying to grow a toe there. One of my daughters inherited that same deformity. These new bunions are bony etrusicians that have occured since the flare that finally was diagnosed as lupus. Six years ago a differant doctor looked at my hands when they became deformed and did a blood test. His diagnosis was that it wasn't rheumatiod arthritis. My concern was that I would lose the use of my hands, and his advise was use it or lose it. Anyway, my middle finger on my left hand, had the upper tip rotate from the knuckle enough to make it look almost as if it is going sideways. Since that time however, my hands only ache when the weather changes or it rains or whenever. What I did then was bind my hands to enable me to keep using them, which is pretty much what I did with my joints this time trying to keep them from going to far out of whack. It wasn't where the bunions occured that hurt this time it was my arch, so it is possible that in the effort to keep using that foot I did create the bunions, but I believe that it also kept my foot from becoming more altered than it did.
10-06-2006, 08:59 AM
Is it possible to have negative tests and still have lupus? i have a cousin who experiences malar rash, achy joints, extreme fatigue, weakened immune system, bruising, colitis and she's had pericarditis and a wierd 2-day stroke that shot pains in her head and weakened her left side for about two days. They ruled out leukemia and a ton of other things, but the tests for Lupus came back negative. Our grandma died of kidney failure (back in the 1940's) and had early onsite arthritis, so we figured she died of lupus.
Just how accurate are these tests for lupus?
10-06-2006, 09:24 AM
But it is possible to have ANA-negative lupus, although it's pretty rare - I think the statistics are fewer than 5% of lupus patients are ANA negative. Part of the problem is that a lot of the symptoms of lupus - pain, fatigue, joint aches, etc. - can be caused by other auto-immune diseases as well as conditions like fibromyalgia and chronic fatigue syndrome. Many people with lupus develop pericarditis, but it's also common in people with respiratory problems too. A condition called rosacea can look a lot like a malar rash and sometimes even doctors have trouble telling the difference. That's part of the reason why lupus is so hard to diagnose - many of the symptoms are not specific to lupus.
Even when the ANA test is negative, lupus patients can have other antibodies like ds-dna, anti-smith, anti-ro, etc., so it's important to do a complete antibody panel when the symptoms look like lupus. If all the tests for antibody subsets are negative, it's unlikely she has lupus, because autoimmunity is the hallmark of lupus.
She should definitely be tested for lyme disease, beause in its late stages it can cause symptoms a lot like lupus, including a rash and neurologic problems. MS is also a condition that can cause lupus-like symptoms.
There is a really good book called THE LUPUS BOOK, by Dr. Daniel Wallace, that explains the process of lupus diagnosis, and many of the diseases that mimic lupus. It's available in many public libraries, and also in book stores and Amazon. If there is one book I think every lupus patient should own, that would be it. It has a section on ANA negative lupus.
10-07-2006, 01:15 PM
I am not saying that I completely understand what you are saying, but I have two doctors that believe that I have lupus and I guess that will have to do.
10-07-2006, 01:26 PM
Hi, oldgal. I think we got our wires crossed - my last post was talking about littlered's cousin, who has symptoms but no diagnosis. I guess we should have started a new topic, sorry for confusing you.