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During the past 20 years, Dr Eric Daiter has successfully helped thousands of couples that have suffered through the grief and emotional trauma of a pregnancy loss. If you have questions about miscarriage or you just want to find a compassionate infertility specialist to guide you, Dr Eric Daiter would be happy to help (in his Edison, NJ office or on the telephone). It is easy, just call us at 908 226 0250 to set up an appointment (leave a message with your name and number if we are unable to get to the phone and someone will call you back).


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Immunologic Problems

Case: 26 year old G5 S5 with “unexplained recurrent pregnancy loss” after a thorough basic evaluation, is interested in pursuing tests to identify a possible immunologic basis for her losses.

Question: Is testing for NK cells useful?

Answer: Natural Killer (NK) cells are a sub population of lymphocytes that are predominantly used in nonadaptive immunity to identify foreign material and destroy or remove it. NK cells are found in various tissues, including the maternal uterus (womb) and the placenta (cells derived from the growing embryo and fetus). NK cells may be “activated” to kill or destroy foreign material by various factors (cytokines or molecular intercellular messengers) and may be suppressed by T suppressor cells (a different type of lymphocyte cells).

Cell surface antigens (components of the cell surface membrane that can elicit an immune response) can serve as markers for a particular type of cell. The CD (cluster designation) antigen that is often used to identify NK cells is CD 56, which is an antigen that is found on all NK cells.

Case: 26 year old G5 S5 with “unexplained recurrent pregnancy loss” after a thorough basic evaluation, is interested in pursuing tests to identify a possible immunologic basis for her pregnancy losses.

Question: Is testing for anti thyroid antibodies useful in this situation, if the serum TSH concentration (which had been performed to look for a cause of a subtle ovulation dysfunction) has been normal?

Answer: Antibodies are produced in large quantities by B lymphocytes that differentiate (mature) into plasma cells. The antibodies can then mediate adaptive humoral (blood) immunity by attaching to specific cell surface antigens (molecules on a cell surface membrane that can elicit an immune response) as a signal to the other components of the immune system that the antigen is “foreign” and should be destroyed or removed.

When a person produces antibodies that attach to, and then trigger an attack on, one’s own tissues then this is referred to as “auto immune disease.” In this situation, one’s immune system attacks one’s own tissues as though they are “foreign” rather than “self.”

Autoimmune disorders seem to occur in clusters, in which a person may concurrently attack the thyroid with anti thyroid antibodies while simultaneously attacking another tissue with antibodies specifically directed against that type of tissue.

One type of autoimmune disorder may be a direct immunologic attack on placental tissue (tissue derived from the embryo or fetus) within the uterus. At this time, the only tests for autoimmune disease that are known to cause recurrent pregnancy losses are those identifying the antiphospholipid syndrome. In the antiphospholipid syndrome, this autoimmune disorder leads to abnormal blood clotting which then leads to destruction of the pregnancy. If the antiphospholipid syndrome tests are normal on the basic evaluation, it is certainly possible that other autoimmune disorders remain important.

Many reproductive endocrinologists use the presence of anti thyroid antibodies as a general marker of autoimmune disease, which can then reflect an increased probability of having an autoimmune cause for recurrent pregnancy losses. In fact, several small clinical trials have consistently demonstrated an association between the presence of anti thyroid antibodies and (otherwise unexplained) recurrent pregnancy loss.

Case: 25 year old G3 S3 with (significantly) elevated anti cardiolipin antibodies.

Question: Should treatment be suggested and what treatment options are available for the antiphospholipid syndrome?

Answer: Women with untreated antiphospholipid syndrome have a poor chance of a delivering a viable full term fetus (baby). The pregnancy loss rate has been reported to be as high as 96% for women with untreated antiphospholipid syndrome and recurrent pregnancy loss.

Treatment alternatives include low dose (baby) aspirin (81 mg) daily by mouth starting at least 10 days prior to ovulation, heparin, prednisone (or other glucocorticoid) and/or immunoglobulins intravenously. Care should be taken to inform the patient that she should absolutely not replace low dose aspirin with regular strength aspirin (325 mg) since these two different strengths have very different biological actions.

The low dose aspirin treatment hopes to decrease blood clot formation, theoretically by increasing the prostacyclin to thromboxane ratio in the circulation. This treatment is often considered to have a minimal to mild effect on the antiphospholipid syndrome and many reproductive immunologists couple the low dose aspirin treatment with one of the other (more aggressive but higher risk) treatment alternatives.

In a reproductive endocrinology office that primarily focuses on clinical infertility (such as my own office) I believe that low dose aspirin has little risk and potential benefit. Therefore, I am willing to initiate this treatment alone to determine whether the couple is then able to carry a pregnancy to term. Before initiating treatment, I advise the couple that they should consider a reproductive immunology consultation in a local academic center since their treatment at such an institution may be more aggressive. If the patient has a loss on the low dose aspirin, then I encourage the couple to consider adding heparin or glucocorticoids in a research (academic) setting where their clinical status and outcome can be more appropriately monitored.

Case: 26 year old G5 S5 with unexplained recurrent pregnancy loss after a thorough basic evaluation, is interested in pursuing tests to identify a possible immunologic basis for her losses.

Question: Is testing for HLA DQ alpha and beta genotypes useful?

Answer: Alloimmune dysfunction occurs when there is a disruption in the normal immunologic response to nonself tissue. The genetic makeup of a pregnancy is not entirely maternal, so the uterus must confer immunologic privilege to this tissue in order for it to be accepted (and grow) within the uterus. One possible class of immunologic abnormality that might be associated with recurrent pregnancy loss involves a breach in immunologic privilege.

HLA (human lymphocyte antigen) genotypes are genes (chromosomal material) that encode antigens (immunologicially reactive molecules) that are used by an individual’s immune system to distinguish tissues as self or foreign. There is a persistent theory that when there is abundant sharing between the HLA genotypes (such as HLA DQ Alpha) within the maternal (mother’s) and the paternal (father’s) chromosomes, then there may be an increased risk of alloimmune recurrent pregnancy loss.

There are currently no generally accepted and reliable tests for alloimmune causes of recurrent pregnancy loss. Therefore, this category remains predominantly a diagnosis of exclusion. I have not found there to be a benefit in obtaining this testing for the evaluation of recurrent pregnancy loss.

Case: 26 year old G5 S5 with “unexplained recurrent pregnancy loss” after a thorough basic evaluation, is interested in pursuing tests to identify a possible immunologic basis for her pregnancy losses.

Question: Is testing for antibodies directed at each (or any) of the specific phospholipids useful, if the screening antiphospholipid antibody tests have been normal?

Answer: Phospholipids are normally a major component of the human cell membrane. Antibodies directed against these phospholipid molecules have been strongly associated with recurrent pregnancy loss, thrombosis of (blood clotting within) the placenta, and reduced placental size.

Generally, screening tests for antiphospholipid antibodies may be divided into either direct assays that detect antibodies against phospholipids or blood clotting tests that rely on (antibody free) phospholipids in order to obtain a normal result.

If a patient is screened for the antiphospholipid syndrome using both a blood clotting test (such as the activated partial thromboplastin time or the dilute Russell viper venom time) and direct antibody test panels (to detect anti cardiolipin antibodies and any of a panel of antibodies against various phospholipids), a normal result does not require further testing for antibodies directed against specific phospholipids (such as anti phosphotidyl-serine antibodies).

To my understanding, once a diagnosis of the antiphospholipid syndrome has been established further definition of which specific types of antibodies are excessive is also not clinically relevant since this additional information would not change the management (recommended treatments).

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