If you have been Rh-sensitized in the past, it is very important to be closely monitored by an experienced OB/GYN during any future pregnancy with an Rh-positive partner; as the fetus is more likely to be classified as Rh-Positive (Rh+/-). The Rh-sensitized immune system of the mother is now poised and ready, may quickly recognize the Rh-Positive Red Blood Cells of the Fetus.  It may quickly develop IgG antibodies, which can cross the placenta and destroy the fetal red blood cells that the mother's body sees as "foreign" invaders.  This immune system response can result in fetal disease, also known as Rh-Disease, Erthroblastosis or Hemolytic Disease of the Newborn; which can be mild to severe and in extreme cases can cause death.  Once a woman is Rh-sensitized, the condition may produce more serious problems in each subsequent Rh-Positive pregnancy with an Rh-Positive Partner.

Below are the common “Levels” referred to, when discussing Rh-Disease and the extent of damage it can cause to the developing fetus.

 In addition to the major ABO and Rh blood group antigens, there are numerous other minor RBC blood group antigens that are less common, these include Kell, Kidd, Duffy, and other Rh antigens. Antibodies to these antigens are only produced by the body when exposed to them through blood transfusion or when an expectant mother is exposed to fetal red blood cells during pregnancy.

When a person with a RBC antibody is exposed to RBCs bearing the "foreign" antigen, whether by a transfusion or pregnancy, the RBC antibodies may attach to the specific antigens on the foreign RBCs and target those RBCs for destruction. Depending on the antigen and antibody involved and the quantity of RBCs damaged, it can cause an immune reaction ranging from mild to severe, even deadly.

The RhoGAM shot used in Rh incompatible pregnancies to stop the mother's immune reaction to the foreign Rh+ fetal red blood cells.  RhoGAM is most effective in preventing sensitization from the main Rh blood group system and it's two most common gene loci (RHD and RHCE). The Rh antigen of greatest importance is the D antigen, it's a combination of the Rh alleles that are inherited from each parent. If both D genes are inherited, the individual is said to be homozygous Rh-positive (Rh+/+). If one D gene is inherited, the blood type will be Rh positive and the individual is said to be heterozygous due to the deletion of one D gene from one chromosome (Rh+/-). If neither D gene is present, the individual will be Rh-negative (Rh-/-). Total absence of both the RHD & RHCE genes results in the condition known as Rh null & it's very rare!

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BACKGROUND Cell-free fetal nucleic acids (cffNA) can be detected in the maternal circulation during pregnancy, potentially offering an excellent method for early non-invasive prenatal diagnosis (NIPD) of the genetic status of a fetus. Using molecular techniques, fetal DNA and RNA can be detected from 5 weeks gestation and are rapidly cleared from the circulation following birth.

RESULTS Cell-free fetal DNA comprises only 3–6% of the total circulating cell-free DNA, therefore diagnoses are primarily limited to those caused by paternally inherited sequences as well as conditions that can be inferred by the unique gene expression patterns in the fetus and placenta. Broadly, the potential applications of this technology fall into two categories: first, high genetic risk families with inheritable monogenic diseases, including sex determination in cases at risk of X-linked diseases and detection of specific paternally inherited single gene disorders; and second, routine antenatal care offered to all pregnant women, including prenatal screening/diagnosis for aneuploidy, particularly Down syndrome (DS), and diagnosis of Rhesus factor status in RhD negative women. Already sex determination and Rhesus factor diagnosis are nearing translation into clinical practice for high-risk individuals.

CONCLUSIONS The analysis of cffNA may allow NIPD for a variety of genetic conditions and may in future form part of national antenatal screening programmes for DS and other common genetic disorders.

In a given month the chances of conception are low for a healthy women but that the mother’s blood type could also decrease or increase her chances of having a baby is not what was known till now. Recently a study in US has shown that women who have a blood type O have lesser number of eggs and poor egg qualities than others, making conception more difficult for them.

It was found that women who had a blood type O had a higher level of “follicle stimulating hormone” (FSH) than those with type A. This hormone, according to fertility experts, is produced in the body to stimulate the follicles in the ovaries and ask them to produce more eggs. The higher percentage of this hormone thus indicates that the body has low number of eggs.

Usually in women aged between 30 and 40 when the eggs have reduced, the FSH is higher to stimulate the ovaries to produce more eggs. The researchers found that women with blood type O had an FSH level mostly higher than the threshold level of 10. This was higher than any other blood type.

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Have you heard of Anti-G Blood?
Anti-G and Immune Tolerance in Pregnancy

Download the PDF Explanation

The Fallacy of Pooling Heterogeneous Data

When related to the Rh-Factor and pregnancy, a person who is heterozygous is recessively carrying an Rh-Negative factor. They are in fact, Rh+/- people.
This study explains WHY you cannot get true results when you are pooling or combining the Rh+/- population into the Rh+ group.
You can print the study below but in layman's terms; let's say we have a Chicken and a Duck that we are studying, as well as their heterozygous offspring that we'll call a CHUCK!  If we are looking for differences, similarities and trends; would it be fair to add the CHUCK to the Category of Chickens or Ducks? No!  It would skew the results, as some CHUCKS may be more Chicken like and others more Duck like; the animal would be non-comparable to either main category. It is my hope that somebody will start to get the control groups straight before continuing to conduct studies that START OFF wrong!

after Rh-Sensitization!

Today there are procedures and precautions used to help prevent Rh-Disease from affecting the unborn fetus in a post Rh-sensitization pregnancy.

Unfortunately, some woman do become Rh-sensitized and fear that they may not be able to have another healthy pregnancy come to term.  Some of the information can be confusing or not explained well and lead to a person not having a full understanding of their situation.  Once Rh-sensitized, the immune response that causes Rh-disease can only occur again in Rh-Positive Pregnancies.

On a website recently reviewed, I noticed that when explaining Rh-sensitization it states, “The baby growing inside the Rh-negative mother may have Rh-positive blood, inherited from the father.  Statistically, at least 50% of the children born to an Rh-negative mother and Rh-positive father will be Rh-positive”. 

This is my opinion is an example of an explanation that leads to confusion for most people.   Our blood type is NOT inherited from  our mother OR father.  We each receive one blood type letter and one Rh factor from EACH parent and we all end up with two.  A person who is Type O- is really Type OO-/-, as they received one type (O) and one (Rh-) Factor from each parent. While the statistics may be spot on, we clearly do not actually inherit our blood type from one parent or the other, but from BOTH!

One  major misunderstanding made by most people, is that all Rh-positve people are Rh+/+.  However, there are many people in the population who are called Rh+ but who are really Rh+/-. These people are heterozygous, which means they possess two different forms of a particular gene, one inherited from each parent. A person who is heterozygous is called a heterozygote or a gene carrier. When talking about the Rh-Factor, it would actually make the person (Rh+/-) or an Rh- recessive gene carrier.

Unfortunately, we do not usually know our recessive traits unless closely investigated by familial history or extensive testing is performed.  This results in statistics like, “at least 50% of children born to an Rh-negative mother and an Rh-negative father will be Rh-positive”, as stated on the site referenced above.

As science advances, there are new and upcoming possible solutions to this issue for Rh-sensitized and Rh-incompatible couples.  According to Dr. Kenneth Moise, “We really are interested in trying to get rid of the maternal antibody, that's the problem. If we could get a mother to drop her titers before she became pregnant through some sort of immunomodulation, we think that would ultimately be the correct way to treat this disease”.  However, he states that the studies are still in the early stages.   He also mentions that in some situations even today, through genetic engineering, they are now able to offer some unique therapies to the father or to the couple that are in fact heterozygous or Rh+/-.  Dr. Moise explains that if the father is heterozygous, that means that although he is called Rh positive, he is actually Rh+/-.  As a recessive gene carrier he has a 50-50 chance of in fact fathering an affected offspring, and if that offspring happens to be Rh negative, that offspring has no effects of the disease and he'll be fine. However, if in fact the father passes his dominant Rh+ factor, the fetus will obviously be affected.

Furthermore, Dr. Moise states, “We are now able to do genetic engineering with in vitro fertilization with the egg cells and test those embryos to see if they're Rh negative or Rh positive”. Once separated they would then only place the Rh-negative embryos in the uterus to guarantee the couple an unaffected pregnancy. He states that while he believes it's been attempted once, it was unsuccessful and to his knowledge, no one has yet to do it with success. However, there are said to be several couples who have very bad Rh disease, a heterozygous paternal genotype & they are considering this therapy. Hopefully, they will soon have more success with finding a fix to this often heart breaking situation.

ScienceDaily (Nov. 19, 2008) — The “Rhesus” blood group is well-known from the public for its importance in the field of transfusion medicine.

For several years, researchers from ULB have been studying Rhesus factors. These factors belong to a family comprising five proteins, three of which are present at the red cell surface (RhCE, RhD and RhAG) and determine the Rhesus blood group, and two others (RhBG and RhCG) which are found in various organs including the kidney, the liver and the male genital tract. 
In 2000, this research group proposes that Rhesus factors play a role in the transport of ammonium in mammals, a process also remaining unknown in animals. This hypothesis was tested by Dr. Sophie Biver during her doctoral thesis performed in the Laboratory of Biology of Development (Profs Josiane and Claude Szpirer, also at IBMM, ULB), in collaboration with the group of Dr. Marini.
The basic idea is simple: to generate mice deprived of the RHCG gene (the one expressed in the kidney) in order to determine if as proposed, these mice would present anomalies related to a defect in ammonium transport, and in particular to a defect in ammonium excretion in the urine.