- Frequently Asked Questions About Antiphospholipid Syndrome
- What is antiphospholipid syndrome?
- What is a phospholipid?
- How was aPL discovered?
- Who gets APS?
- What happens if you have aPL?
- Frequently asked questions about antiphospholipid syndrome
- Cardiolipin Antibody Test: Normal Range + Test Results
- What is Cardiolipin?
- Structure of Cardiolipin
- Cardiolipin Antibodies
- Cardiolipin Antibody Testing
- Normal Range
- What Do Cardiolipin Antibody Test Results Mean?
- Antiphospholipid Antibodies
- Antiphospholipid Antibody Syndrome (APS)
- False-Positive Test for Syphilis
- Lupus Anticoagulant
- Anticardiolipin Antibody
- Anti-beta2 glycoprotein 1
- Cardiolipin IgG
Frequently Asked Questions About Antiphospholipid Syndrome
The SLE Workshop is a free support and education group held monthly for people with lupus and their families/friends. The HSS presentation from which this content was adapted was originally held on June 2, 2004. It has been periodically updated by the author.
What is antiphospholipid syndrome?
A syndrome is a collection of events or symptoms that constitutes a specific illness. Antiphospholipid syndrome (APS), also known as antiphospholipid antibody, anticardiolipin antibody, lupus anticoagulant, and Hughes’ syndrome, includes these symptoms:
- Repeated clotting in veins – such as a deep vein thrombosis (DVT) in an arm or a leg, or a pulmonary embolus (a blood clot in a lung) – or arteries (stroke, heart attack)
- Recurring pregnancy loss (miscarriage), usually in mid to late pregnancy rather than early pregnancy
- An antibody test that is strongly positive. A weakly positive test is common in otherwise normal people and is not enough to diagnose this syndrome
The above symptoms are specifically characteristic of APS. However, there are many other symptoms that people with APS may experience, including:
- Skin changes
- Low platelet count (insufficient amount of platelets in the blood)
- Some forms of heart, kidney and brain diseases
What is a phospholipid?
A phospholipid is a type of fat (“lipid” means fat) that contains phosphate. Phospholipids form the outside layer of all cells: those of humans, bacteria and viruses. Cardiolipin is a type of phospholipid.
The “cardio” part of this word comes from a phospholipid syphilis test, which used a chemical derived from a cow’s heart. (As will be discussed below, clinical tests for syphilis were key to the discovery of antiphospholipid antibodies.
) Another phospholipid sometimes used in testing is phosphatidylserine.
What are antiphospholipid antibodies (aPL), and how are they measured?
The general term antiphospholipid antibody (aPL) describes any of three antibodies measured in diagnosing or treating APS.
- Lupus anticoagulant (LAC) – An LAC test measures the effect that the antibody has on the time it takes blood to clot. If a patient's blood contains an antiphospholipid antibody (aPL), it will bind to phospholipids in a test tube, and the blood will not clot. Although a positive test is called “lupus anticoagulant,” the name comes from its confused history. It does not mean the patient has lupus, nor does it mean that the blood is prevented from clotting. In fact, in the body as opposed to the test tube, it clots too easily.
- Anticardiolipin (aCL) antibody is the most commonly measured antiphospholipid antibody.
- Anti-Beta-2-glycoprotein-I (aβ2GPI) measures the antibody to a specific protein (Beta-2-glycoprotein-I) that is required for aCL to bind to cardiolipin.
Anticardiolipin and aβ2GPI each have three subtypes: IgG, IgM, and IgA. These are all different types of immunoglobulin antibodies that people normally make.
When an infection (such as syphilis) is the reason a patient has a positive aPL test, the aPL is part of the body’s response to try to kill the infectious germ.
Some infections, as well as lupus, irritate certain types of blood cells and blood vessel cells.
A result is that the b2GP1 protein, which floats normally in the blood stream, recognizes that the irritated cells are abnormal, and “calls in” the antiphospholipid antibody, which starts the reaction that leads to blood clots.
From the patient's point of view, all of these measures are equivalent: They all test for antiphospholipid antibodies.
In terms of predicting health outcomes and the development of APS, the LAC test is more powerful than the aCL or aβ2GPI tests. Among the aCL or aβ2GPI antibody tests, the IgG subtype is more powerful than IgM, which is more powerful than IgA.
For each of these antibody tests, a strongly positive test suggests a worse patient outcome than a weakly positive test.
How was aPL discovered?
In the early 1900s, when a blood test for syphilis became available, doctors recognized that some people had false-positive test results for syphilis, meaning that they tested positive even though they did not actually have the disease. At the time, this was just considered a medical curiosity. It was not recognized as having clinical importance.
But during the 1940s and 1950s, medical practitioners concluded that the false-positive syphilis test results occurred most often in patients with systemic lupus erythematosus (usually called just lupus or SLE). Today, a false-positive syphilis test result is a clue to a possible diagnosis of lupus.
However, it does not make a conclusive diagnosis of lupus, nor does it – by itself – indicate a diagnosis of APS.
In the 1950s and 1960s it became understood that the false-positive syphilis test result was associated with LAC and its blood clotting abnormalities. In 1983, three lupus researchers in London with ties to HSS – Graham Hughes, Azzudin Gharavi and E.
Nigel Harris – developed a much simpler test (now called the aCL ELISA) to replace the cumbersome test for LAC. They tested their SLE patients and found that aCL occurred in patients with spontaneous blood clots and with pregnancy losses.
They shared the test with other investigators, including HSS physicians, and by 1985 we and others confirmed their findings.
Until 1989, doctors thought that APS was a subtype of lupus. However, by then enough recorded cases of APS in people without lupus led British, Australian, Italian, and Dutch investigators to argue that APS should be considered a separate illness.
They further argued that the name “primary antiphospholipid syndrome” (PAPS) should be used to describe APS in patients who do not have lupus, and “secondary antiphospholipid syndrome (sAPS) be used to describe APS in patients who do have lupus.
In 1990, the Beta-2-glycoprotein-I (aβ2GPI) was discovered, the importance of which was reviewed above.
Who gets APS?
There are differences between those who get SLE and those who get APS. Whereas 90% of the people who develop SLE are women, with APS, if you count only the people who develop blood clots, and do not count women who have problems with their pregnancies, about 50% of people with APS are women.
But, if you do count people who develop blood clots as well as those who have pregnancy problems, about 70% of APS patients are women. SLE is most frequent in people of African descent, next most frequent in Asians and Hispanics, and least frequent in people of European descent.
By contrast, APS is seen more in those of European and Asian descent than in people of African descent. About one third of lupus patients have aPL.
What happens if you have aPL?
The main symptom is blood clots. The antibody may be in the blood stream for years before anything happens, and some people with these antibodies are well for their entire lives.
What causes the clotting? One theory is that the antibody itself irritates the cells on the inside of blood vessels. Another theory is that an infection irritates the cells and attracts the antibody.
Regardless which theory is correct, the result is that a clot forms.
The antibody runs in families and is often found in families of patients who have SLE or PAPS. In other words, if either SLE or PAPS is present in the family, the lihood of a blood relative having aPL is increased. Women develop the antibody more often than men, but it is not known why. It is also not known what causes the antibody to appear in the first place.
Two different theories explain why people develop the antiphospholipid antibody. The first is that an infection causes people to make the antibody but that nothing happens until something else, such as an injury or another infection, triggers the disease.
The second theory states that the antiphospholipid antibody is normally present in the body in small quantities and is used to remove old and dying cells. People with APS may make too much of the antibody or may make an abnormal antibody. Or, in some cases, it may be that the b2GP1 that ties aPL to the targeted irritated cells is abnormal.
In some APS patients, it may be that the cells which are irritated are the underlying problem and the aPL antibodies are trying (unsuccessfully) to correct the situation.
Although blood clotting is the chief health risk of APS, in pregnant women the antibody damages the placenta, starving the fetus by cutting off the blood supply that feeds it.
Anticoagulating medication heparin and aspirin protect the blood supply, giving the fetus an 80% to 90% chance of survival.
This is markedly better than the 20% survival rate in the 1980s, before APS was known to medical science.
Even with better fetal survival rates and heparin treatment, pregnancies are not always normal in people with APS. Although a normal pregnancy lasts 40 weeks (producing babies bigger than 6 pounds), in APS, premature deliveries (30 to 35 weeks, with babies weighing between 3 to 5 pounds) regularly occur. Once born, however, the babies do fine.
Mouse models can be used to study the antibody. New studies in mice suggest that different forms of treatment that focus on the complement system (a part of the immune system that amplifies its abilities under certain conditions) and other processes – rather than on clotting – may be more effective. HSS rheumatologist Dr. Jane Salmon is a leader in this work.
Warfarin (Coumadin) can prevent blood clots. This medication is commonly used for people with strokes and heart attacks. Aspirin and hydroxychloroquine (Plaquenil) may help. The new, oral anticoagulant drugs rivaroxaban [Xarelto] and apixaban [Eliquis] do not work, and should not be used. In serious cases, an experimental therapy, intravenous immunoglobulin, is helpful.
A rare complication of APS, called catastrophic APS (CAPS), consists of very rapid clotting throughout the body. It is life-threatening and demands immediate in-hospital treatment. This article describes this illness and its treatment.
Frequently asked questions about antiphospholipid syndrome
Q. Does antiphospholipid syndrome turn into lupus (SLE)?
Q. Does antiphospholipid syndrome cause hardening of the arteries?
Doctors used to think so, but now it is pretty clear that there is no correlation between APS and hardening of the arteries.
Q. Does antiphospholipid syndrome cause heart valve disease?
The answer is yes in a small number of patients. Some SLE patients without APS also develop leaking heart valve disease, but it appears to occur more often in those with APS. It is not clear why this happens.
Q. Is antiphospholipid syndrome caused by infection?
Scientists are looking into this. So far, researchers have been able to produce the antibody by certain infections only in mice.
Q. What is the relationship between lupus and antiphospholipid syndrome?
About 30% of lupus patients test positive for antiphospholipid antibody. It is not known why. About half of patients with APS have SLE.
Q. Why don’t people with primary antiphospholipid syndrome (PAPS) have lupus as well?
It is not known why.
There are good treatments for antiphospholipid syndrome, but better ones are needed. Doctors can prevent blood clots in people at risk, but we would to do so in a much safer and more effective fashion than we can right now. Also, we can save most pregnancies, but many are premature. Researchers continue to explore new and imaginative treatments for this disease.
Cardiolipin Antibody Test: Normal Range + Test Results
Cardiolipin is a key component in the structure of mitochondria. However, the body sometimes creates antibodies that mistakenly attack this compound. Find out what the cardiolipin antibody test is and what the results can mean.
What is Cardiolipin?
Cardiolipin is an important component found in mitochondria. Mitochondria are special structures found in the body’s cells that are responsible for producing energy .
More specifically, cardiolipin is a phospholipid (a type of fat) that helps form the inner wall (otherwise known as the membrane) of the mitochondria structure .
As a part of the membrane of mitochondria, cardiolipin has several functions, including regulating various proteins and triggering apoptosis, which is the process that eliminates and recycles old and damaged cells [1, 2].
Structure of Cardiolipin
Many of the effects of cardiolipin are due to its unique structure.
For example, cardiolipin contains more fatty acids than most other phospholipids. The fatty acids make cardiolipin cone-shaped, allowing it to interact with many proteins .
The structure of cardiolipin is also able to change, allowing it to adapt into different shapes .
Sometimes, the immune system may produce antibodies that mistakenly attack the body’s own cardiolipins. These cardiolipin antibodies may cause several negative health effects, including increased risk for blood clots and pregnancy complications .
Cardiolipin antibodies (also known as anticardiolipin antibodies) are associated with a number of health conditions, some of which include :
- Antiphospholipid syndrome
- Systemic lupus erythematosus
- Behçet’s disease
However, the presence of cardiolipin antibodies in the blood does not necessarily indicate a problem. According to some estimates, cardiolipin antibodies can be detected in about 1% to 5% of healthy people .
Cardiolipin Antibody Testing
A cardiolipin antibody test detects cardiolipin antibodies in the blood. The test requires a blood sample that is usually taken from a vein in the arm.
This test is typically performed when a patient experiences unexplained blood clots, recurrent miscarriages, or autoimmune disease symptoms .
There are actually three types of cardiolipin antibodies — IgG, IgM, and IgA .
The types most commonly tested for are IgG and IgM as those two are the most strongly associated with autoimmune diseases. IgA may be tested if results for the other two types are negative, but there is still a clinical suspicion that cardiolipin antibodies are involved .
Cardiolipin antibodies may be transient, meaning they may be detectable at one point, but not later on. If someone tests positive for cardiolipin antibodies on an initial test, a second test may be performed later to confirm that the antibodies are persistent .
In addition, healthy individuals can test positive for cardiolipin antibodies .
Normal ranges can vary between laboratories due to differences in equipment, techniques, and chemicals used. If your results are outside of the normal range, it may not necessarily mean there is something wrong. However, a normal result also doesn’t mean a particular medical condition is absent. Always talk with your doctor to learn more about your test results.
Cardiolipin antibody tests are usually reported as a positive or negative result.
However, a higher concentration of antibodies may be a strong indication of autoimmune disease .
Tests can measure IgG (GPL) or IgM (MPL), which may have different cut-off points to be considered positive or negative .
Several different manufacturers offer cardiolipin tests, so the interpretation of results highly depends on the type of test used .
For example, some types may consider GPL or MPL values greater than 5 to be a positive result. However, other types of tests require a value greater than 10 to be considered a positive result .
What Do Cardiolipin Antibody Test Results Mean?
Always talk with your doctor to learn more about your test results.
The results of a cardiolipin antibody test are either positive or negative.
A negative result means no cardiolipin antibody was detected in the blood. However, cardiolipin antibodies may take some time to develop in those with autoimmune disorders .
A positive result means that cardiolipin antibody was detected in the blood. As mentioned earlier, the presence of cardiolipin antibodies may indicate several diseases, such as:
- Antiphospholipid syndrome (APS)
- Systemic lupus erythematosus (SLE)
- Behçet’s disease
The cardiolipin antibody test is often performed in patients who experience unexplained blood clots or recurrent miscarriages. This is because autoimmune disorders APS and SLE can alter the blood’s ability to clot, which can lead to thrombosis (blood clots) and pregnancy complications .
Other types of tests may be performed to confirm the diagnosis of a disorder.
However, positive test results don’t necessarily indicate a health problem. Many healthy individuals test positive for cardiolipin antibodies .
Additionally, infections or certain medications (such as phenytoin or valproate) can cause a temporary increase in cardiolipin antibodies .
Antiphospholipid antibodies are antibodies directed against phosphorus-fat components of your cell membranes called phospholipids, certain blood proteins that bind with phospholipids, and the complexes formed when proteins and phospholipids bind.
Approximately 50% of people with lupus possesses these antibodies, and over a twenty-year period of time, one half of lupus patients with one of these antibodies—the lupus anticoagulant—will experience a blood clot.
People without lupus can also have antiphospholipid antibodies.
The most commonly discussed antiphospholipid antibodies are the lupus anticoagulant (LA) and anticardiolipin antibody (aCL). These two antibodies are often found together, but can also be detected alone in an individual.
Other antiphospholipid antibodies include anti-beta 2 glycoprotein 1 (anti-ß2 GPI), anti-prothrombin, and the “false-positive” test for syphilis.
other antibodies involved in lupus that are directed against self (auto-antibodies), antiphospholipid antibodies can come and go or increase and decrease.
The presence of an antiphospholipid antibody such as the lupus anticoagulant and anticardiolipin antibody in an individual is associated with a predisposition for blood clots.
Blood clots can form anywhere in the body and can lead to stroke, gangrene, heart attack, and other serious complications.
In people with lupus, the risk of clotting does not necessarily correlate with disease activity, so the presence of these antibodies can cause problems even when a person’s lupus is in control.
Complications of antiphospolipid antibodies in lupus include fetal loss and/or miscarriages, blood clots of the veins or arteries (thromboses), low platelet counts (autoimmune thrombocytopenia), strokes, transient ischemic attacks (stroke warnings), Libman-Sacks endocarditis (formation of a clot on a specific heart valve), pulmonary emboli, and pulmonary hypertension.
Many people with antiphospholipid antibodies have a purple or reddish lacy pattern just under their skin known as livedo. This pattern is especially apparent on the extremities (i.e., the arms and legs).
It is important to realize, however, that having livedo does not necessarily mean one has antiphospholipid antibodies; rather, doctors acknowledge a correlation between the two conditions.
Livedo can be associated with other diseases of the blood vessels, but in fact, many perfectly healthy women also experience the condition.
Antiphospholipid Antibody Syndrome (APS)
Individuals who experience complications from antiphospholipid antibodies are diagnosed with Antiphospholipid Antibody Syndrome (APS). This condition can occur both in people with lupus and those without lupus. Fifty percent of people with lupus have APS.
The presence of one or more clinical episodes of thromboses (blood clots) and/or complications during pregnancy, such as miscarriage or premature birth, in conjunction with a significant level of anticardiolipin antibodies, antiphospholipid antibodies, and/or anti-ß2 GPI anti- antibodies usually indicates the presence of APS.
When APS is the sole diagnosis, and no other connective tissue diseases are present, APS is often said to be the primary diagnosis; when APS is present in association with lupus or another connective tissue disease, APS is said to be “secondary.
” This classification is controversial, however, because some people with primary APS (about 8%) later develop lupus, suggesting a connection between the two conditions.
False-Positive Test for Syphilis
In the 1940s, when it was common for people to have premarital exams, doctors realized that some women with lupus tested positive for syphilis. Further studies indicated that 1 in 5 people with lupus had a false-positive syphilis test.
The syphilis test of those days—the Wasserman test—was dependant on an antibody found in syphilis patients called reagin. The substance to which this antibody reacts is cardiolipin, so the individuals with a false-positive syphilis test actually had a form of anticardiolipin antibodies.
The false-positive syphilis test was the first recognized test for antiphospholipid antibodies, but it is now known that people can have antiphospholipid antibodies without having a false-positive syphilis test and vice versa.
The false-positive test is not associated with an increased risk of blood clots in all medical studies performed in the past, but certain studies, including the Johns Hopkins Lupus Cohort, suggest that there is a connection.
The false-positive syphilis test was one of the first three recognized indications of antiphospholipid antibodies. The other two were the lupus anticoagulant and anticardiolipin antibody.
In the late 1940s, it was found that an antibody present in some lupus patients prolonged a clotting test dependent on phospholipids. For this reason, it was thought that this antibody increased the tendency to bleed, and thus it was deemed the lupus anticoagulant.
However, this name is now recognized as a misnomer for two reasons. First, the term “anticoagulant” is a false label, since lupus anticoagulant actually increases the ability of the blood to clot.
Second, the term “lupus” in the name of the antibody is misleading, since more than half of all people who possess this antibody do not have lupus.
Tests called coagulation tests are used to detect the lupus anticoagulant (LA). Remember that even though the lupus anticoagulant causes the blood to clot more easily in vivo (i.e., in a person’s body), they actually cause prolonged clotting times in vitro (i.e., in a test tube). Therefore, if it takes more time than normal for the blood to clot, the lupus anticoagulant is usually suspected.
The activated partial thromboplastin time (aPTT) is often used to test for LA. If this test is normal, more sensitive coagulation tests are performed, including the modified Russell viper venom time (RVVT), platelet neutralization procedure (PNP), and kaolin clotting time (KCT). Normally, two of these tests (the apt and the RVVT) are performed to detect whether lupus anticoagulant is present.
Even though the false-positive syphilis test and the lupus anticoagulant were identified in the 1940s, the link between these entities was not investigated until the 1980s, when a researcher at the Graham Hughes laboratory in Britain named Nigel Harris began looking at antibodies to the phospholipid antigens.
Harris realized that cardiolipin was a major element of the false-positive syphilis test, and he developed a more specific test for the antibody. He also determined that the presence of these anticardiolipin antibodies was associated with recurrent thromboses (blood clots) and pregnancy losses.
Others in Hughes’ laboratory began to publish studies showing the link between anticardiolipin antibodies and stroke, deep vein thrombosis (DVT), recurrent pregnancy loss, livedo, seizures, and other conditions.
In fact, what we now know as antiphospholipid syndrome was known as the anticardiolipin syndrome even though other antiphospholipids, namely the lupus anticoagulant, were known to produce similar effects.
There are different classes (isotypes) of anticardiolipin antibody, namely IgG, IgM, and IgA. IgG is the anticardiolipin antibody type most associated with complications.
An enzyme-linked immunosorbent assay (ELISA) is used to test for anticardiolipin antibodies. One can test for all isotypes at once, or they can be detected separately.
High levels of the IgM isotype are associated with autoimmune hemolytic anemia, a condition in which an individual’s immune system attacks their red blood cells.
Anti-beta2 glycoprotein 1
Beta2 glycoprotein 1 is the protein in the body to which anticardiolipin antibodies bind, and it is also possible to measure antibodies to beta2 glycoprotein 1.
An individual can be positive for anticardiolipin antibodies and negative for anti-ß2 GPI and vice versa, and detection of anti-ß2 GPI is not yet part of routine testing done for patients with an increased lihood of blood clots.
- “Antiphospholipid Antibodies.” Lab Tests Online. 3 June 2009. American Association for Clinical Chemistry. 6 July 2009 .
- “Blood Tests.” The Lupus Site. 6 July 2009 .
- “Cardiolipin Antibodies.” Lab Tests Online. 3 June 2009. American Association for Clinical Chemistry. 6 July 2009 .
- “Laboratory Tests.” Lupus Foundation of America. 6 July 2009 .
- Laboratory Tests for Lupus.” Lupus Foundation of America. 12 July 2009 .
- “Lupus Anticoagulant.” Lab Tests Online. 3 June 2009. American Association for Clinical Chemistry. 6 July 2009 .
- Wallace, Daniel J. The Lupus Book: A Guide for Patients and Their Families. 1st ed. New York: Oxford University Press, 1995.
- Wallace, Daniel J., and Bevra Hannahs Hahn, eds. Dubois’ Lupus Erythematosus. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
|Plasma Separator Tube 4.5 mL|
Alternate Collection Media:
Call laboratory for additional acceptable specimen collection containers.
3.0 mL whole blood from light green top tube or TWO Microtainer® devices.
24 hrs/day, 7 days a week, including holidays.
Turn Around Time:
2 hours (upon receipt in laboratory)
Reference range and methodology changed effective March 11, 2014. Negative: < 20 U/mL Positive: 20 U/mL or greater
Reference ranges are standardized to the 99th percentile cutoff as described by the Miyakis/Sapporo criteria (ref 1). A positive of 20 U/mL or greater exceeds the 99th percentile and can fulfill the laboratory portion of the criteria needed for diagnosis of antiphospholipid syndrome (see below).
The antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by the main clinical features of venous and/or arterial thrombosis (intravascular blood clotting), thrombocytopenia, recurrent fetal loss, and moderate-to-high titers of antiphospholipid (aPL) antibodies, lupus anticoagulant, anti-cardiolipin antibodies, and anti-beta-2-glycoprotein I antibodies (refs 1-2). aPL antibodies are autoantibodies that react with negatively-charged phospholipids such as cardiolipin. They are often found in the sera of patients with systemic lupus erythematosus and related diseases and are typical for the development of secondary APS. The presence of antiphospholipid antibodies in patients with no other autoimmune disease is characteristic of primary APS. Anti-cardiolipin antibodies are found in 80-90% of patients with APS. However, the presence of anti-cardiolipin antibodies are not specific to APS, because these antibodies may be detected in other autoimmune diseases, following administration of certain drugs, and in the aftermath of infectious disease (e.g., hepatitis C, syphilis, and infectious mononucleosis). Beta-2-glycoprotein I, also known as apolipoprotein H, inhibits the intrinsic coagulation pathway and is involved in the regulation of blood coagulation. Beta-2-glycoprotein I has been shown to be the primary autoantigen for anti-cardiolipin antibodies. Antibodies to beta-2-glycoprotein I are more specific to APS than anti-cardiolipin antibodies. Due to the heterogenous nature of aPL antibodies, combined measurements of anti-cardiolipin and anti-beta-2-glycoprotein I antibodies may provide better sensitivity than either assay alone. The criteria for defining APS as described by the Miyakis/Sapporo criteria (International Consensus Statement on an Update of the Classification Criteria for Definite Antiphospholipid Syndrome, Journal of Thrombosis and Hemostasis 2006; 4:295-306) are as follows: Clinical criteria: 1. Vascular thrombosis One or more clinical episodes of arterial, venous or small vessel thrombosis 2. Pregnancy morbidity (a) One or more unexplained deaths of a morphologically normal fetus at or beyond the 10th week of gestation (b) One or more pre-term births of a morphologically normal neonate before the 34th week of gestation because of: (i) eclampsia or severe pre-eclampsia or (ii) recognized features of placental insufficiency (c) Three or more unexplained consecutive spontaneous miscarriages before the 10th week of gestation, with maternal anatomic or hormonal abnormalities and paternal and maternal chromosomal causes excluded Laboratory criteria: 1. Lupus anticoagulant present in plasma, on two or more occasions at least 12 weeks apart 2. Anticardiolipin antibody of immunoglobulin IgG and/or IgM isotype in serum or plasma, present in medium or high titer (i.e. >40GPL units or MPL units, or > the 99th percentile), on two or more occasions, at least 12 weeks apart 3. Anti-beta-2-glycoprotein I antibody of IgG and/or IgM isotype in serum or plasma (in titer >the 99th percentile), present on two or more occasions at least 12 weeks apart APS is present if at least one of the clinical criteria and one of the laboratory criteria above are met. The presence of IgG antibodies to cardiolipin or beta-2-glycoprotein I at levels greater than 99th percentile is part of the SLICC (Systemic Lupus International Collaborating Clinics) Classification Criteria for Systemic Lupus Erythematosus immunologic criteria (ref. 3). References: 1. International Consensus Statement on an Update of the Classification Criteria for Definite Antiphospholipid Syndrome, Journal of Thrombosis and Hemostasis 2006; 4:295-306. 2. Devreese K and Hoylaerts M. Clinical Chemistry 2010; 56:930-940. 3. Petri M et al. Arthritis and Rheumatism 2012; 64(8):2677-2686.
Multiplex Flow Immunoassay
Centrifuge at a speed and time necessary to get barrier separation of plasma/serum and cells within 1 hour of collection. Send specimen in original tube. Do Not transfer to another tube.
Each sample must be labeled with at least TWO full patient identifiers (First/Last Name & DOB are sufficient for non-UIHC affiliated clients) to avoid sample rejection/delays.
All sample storage requirements are intended for delivery to UIHC within 24 hours of collection for testing. If samples won't arrive in this time period, please call the UIHC Core Lab for alternative storage/shipping instructions (319-356-3527).
Place labeled specimen into zip-lock type biohazard bag; seal bag.Place completed requisition into outside pocket of bag.
Transport in cooler with refrigerated coolant packs.