What blood type is a person if their plasma contains only anti-a agglutinin?

Antigens

There are four major blood groups, A, B, AB, and O, determined by the presence or absence of A and B antigens on the surface of RBCs. Group A has only A antigen, group B carries B antigen, and group AB has both A and B antigens on the RBCs. Group O has neither A nor B antigen, but group O individuals have H antigen, which is the precursor substrate for A and B antigens. The A and B antigens are synthesized by transferase enzymes and differ only by the nature of the terminal carbohydrate to a d-galactose (Gal) residue that also has l-fucose (Fuc) in a 1-2 linkage of the N-linked oligosaccharides chain. N-acetyl-d-galactosamine is added by A-transferase, and d-galactose by B-transferase. Group O individuals have defective A or B transferases; therefore, no terminal carbohydrate is added, leaving H antigen, the terminal sugar of which is fucose, on the RBC. Some H antigen precursor remains on A and B RBCs in this order: A2 > B > A2B > A1 > A1B. In clinical practice, four ABO phenotypes (A, B, O, and AB) are discriminated. In addition, two common variations of group A, A1, and A2, can be distinguished. A1 and A2 phenotypes differ in the amount of A antigen on the RBCs (A2 has less than A1) and differ in carbohydrate branching structure. Approximately 80% of group A individuals are A1 and 20% are A2. In addition, there are other inherited phenotypes that have weaker expression of the specified antigen, e.g., A3, Ax, Ael, B3, B(A), and cisAB.

Rare are ‘Bombay’ (Oh) phenotype RBCs (first reported in Bombay, India), which lack the H antigen, and consequently, also lack A and B antigens. Of clinical relevance, potent anti-H with the same hemolytic potential as anti-A and anti-B can be produced by Bombay individuals, and they can only receive RBC transfusions from other people with the same Bombay type.

A or B antigen expression can weaken in patients with acute leukemia or stress hematopoiesis or occasionally during pregnancy. Chromosomal deletions or lesions that involve the ABO locus can result in the loss of transferase expression in the leukemic cell population.

ABO/Rh(D) Typing

Determination of the ABO blood group is performed in two steps: a forward and a reverse reaction. In the forward reaction, the presence of the A or/and B antigens is determined by mixing the RBCs to be tested with anti-A and anti-B reagents. If there is a reaction with only anti-A, then the patient has the A antigen on the red cells. His or her ABO blood group is A. If there is reaction with anti-B, then the patient has the B antigen. His or her blood group is B. If there is reaction with both anti-A and anti-B, then the patient has both AB antigens. His or her ABO blood group is AB. If there is no reaction, then the patient has neither A or B antigens. Thus his or her ABO blood group is O.

In the reverse reaction, the serum of the patient is mixed with reagent RBCs of A1 and B types to detect the presence of anti-A1 and anti-B antibodies. If there is reaction with A1 cells, then the patient has an anti-A1 antibody. If the patient has anti-A1 antibody, then he/she cannot have the A antigen. If there is reaction with B cells, then the patient has anti-B antibody. If the patient has anti-B antibody, then he/she cannot have the B antigen. Thus an individual with blood group A will have anti-B antibody. An individual with blood group B will have anti-A1 antibody. An individual with blood group AB will have none of the antibodies, and finally an individualwith blood group O will have both the antibodies. If the forward and the reverse reaction lead to different conclusions regarding the ABO type, reaction strength is weaker than expected, and/or the historical blood type does not match the current one, the cause for the discrepancy must be fully investigated for a final interpretation of the ABO blood group type.

“Rh typing” is a misnomer because it does not involve phenotyping for all major antigens belonging to the Rh system, but only for the D antigen, the most immunogenic of all. The Rh or D type is determined in a similar was as the forward ABO typing, using anti-D reagent. Blood donors who type Rh-negative (D-negative) are further tested to detect the presence of so-called weak D antigen (Du) using more sensitive methods, such as the presence of antihuman globulin (AHG), which acts as an enhancer of the reaction between the D antigen and the anti-D reagent.

Determination of the weak D is required only for blood donors to establish the true D status and is performed by testing patient’s RBCs IgG anti-D in AHG phase. If the weak D testing is positive, the Rh(D) type is interpreted as Rh(D)-positive, and if negative, the Rh(D) type is interpreted as a true negative. The weak D status is neither required nor routinely determined in recipients since Rh(D)-negative blood is safe to be transfused regardless of the true Rh(D) status of recipient. The presence of other antigens belonging to the Rh blood group is not determined for routine transfusions.

Blood Groups

The A blood group has a gene (A-transferase) which expresses antigen A; a gene in the AB blood group expresses both the A and B antigens for the genes (A-transferase and B-transferase) (Figure 4.7); and in the B blood group, the B-transferase gene expresses antigen B. Antigens A and B are chemically arranged from antigen H by H-transferase. The gene that determines an ABO blood group is located on chromosome 9. The gene coding for antigen H is located on chromosome 19, and transforms the H-transferase precursor to antigen H. This gene is not expressed in people with the Bombay blood type. Besides classification of the ABO blood group system, there are other blood group systems based on Rhesus factor, Lewis and MN blood groups. The distribution of ABO blood groups differs greatly by area and ethnicity; for example, about 40% of Japanese people have the A blood group, 30% O, 20% B and 10% AB, whereas 90% or more of native South Americans are blood group O, and this figure may exceed 99% depending on the area. A relationship between the ABO blood group and illness was noticed in 1980. An outline was published in the scientific journal Nature in 2000, and completed by the Human Genome Project (International Human Genome Sequencing Consortium, 2000). A weak correlation was found between ABO blood group and Helicobacter pylori infection. In contrast, there is a close relation between the Lewis secretory form and H. pylori infection. Bone marrow transplantation can change a recipient’s ABO blood group. For example, the ABO blood group of the late Ichikawa Danjuro XII, who had myelocytic leukemia, changed following bone marrow transplantation.

Diagnosis

Laboratory evaluation for vWD requires several assays to quantitate vWF and characterize its structure and function. Many variables affect vWF assay results, including the patient’s ABO blood type. Persons of blood group AB have 60% to 70% higher vWF levels than those of blood group O. Thus some laboratories interpret vWF levels referenced to specific normal ranges for blood types.

Clinical conditions and disorders with elevated vWF levels include pregnancy (third trimester), collagen vascular disorders, postoperative period, liver disease, and disseminated intravascular coagulation. Low levels are seen in hypothyroidism and the first 4 days of the menstrual cycle.

Symptoms are modified by medications like aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), which can exacerbate the bleeding; oral contraceptives can decrease the bleeding in women with vWD by increasing vWF levels. vWF levels in African American women are 15% higher than in white women. Clinical symptoms and family history are important for establishing the diagnosis of vWD, and a single test is sometimes not sufficient to rule out the diagnosis.

Initial work-up should include a complete blood count, aPTT, PT, fibrinogen level, or thrombin time. These tests do not rule out vWD but help rule out thrombocytopenia or factor deficiency as the cause for bleeding. The closure times on the PFA-100, which has replaced the bleeding time as a screening test in some centers, may be prolonged. The aPTT in vWD is only abnormal when factor VIII is sufficiently reduced.

Specific tests for vWD include ristocetin cofactor assay, a factor VIII activity, and vWF antigen (vWF Ag) assay. The ristocetin cofactor activity measures induced binding of vWF to platelet glycoprotein Ib and is the best functional assay of vWF activity. Multimer analysis is done by agarose gel electrophoresis using anti-vWF polyclonal antibody and is available at reference laboratories. Collagen binding assay and genotyping, especially for type 2 vWD, are new tests available to assist with the diagnosis.

In type 1 vWD, the vWF is subnormal in amount, with normal multimer structure. Those with types 2A and 2B vWD lack the HMW multimers. In type 2B, the vWF has a heightened affinity for platelets, often resulting in some degree of thrombocytopenia from platelet aggregation. A useful laboratory test for type 2B is the low-dose ristocetin-induced platelet aggregation (RIPA) assay.

In type 3 (severe) vWD, the affected person has inherited a gene for type 1 vWD from each parent, resulting in very low levels (3%) of vWF (and low factor VIII, because there is no vWF to protect factor VIII from proteolytic degradation). Less commonly, a person with type 3 is doubly heterozygous.Table 4 provides a quick overview of the laboratory findings in the different variants of vWD.

Liver Transplantation in ABO-Nonidentical Recipients

Matching donor livers with recipients for ABO blood groups to avoid damage from natural blood group antibodies is not difficult. The blood groups are evenly distributed among liver donors and liver transplant candidates (Table 74-1). The less common blood groups B and AB constitute only approximately 10% and 3% of donors and candidates, respectively. Thus, the donor pool is considerably more limited for patients with these less common types. ABO-incompatible transplants have been performed in emergency situations when a compatible donor is not available, and unlike the outcome of other ABO-incompatible organ transplants, hyperacute rejection of the ABO-incompatible liver rarely occurs.13 Even in cases when there was a hyperacute rejection, the process proceeded at a slower pace than for kidneys.

Although hyperacute rejection is rare, the literature shows that ABO-identical liver transplants have had the best prospects for survival. Initially, a large retrospective study of 671 liver transplants performed in Pittsburgh,14 of which 91 were ABO compatible and 31 were incompatible, revealed a substantially higher graft failure rate among the ABO-nonidentical grafts. The authors recommended that the use of ABO-nonidentical grafts should be limited to small children for whom few suitable donors were available or to patients in urgent need of transplantation. This policy has been largely followed with respect to ABO. Rydberg15 reviewed the results of 400 ABO-incompatible liver transplantations performed between 1986 and 2000 and reported in 24 different studies and concluded that ABO-incompatible liver transplantations were substantially less successful than ABO-compatible liver transplants. Rydberg noted that children younger than 3 years whose immature immune system may be more forgiving than that of adults might be an exception to this trend.

Recent data from the United Network for Organ Sharing (UNOS) Organ Procurement and Transplantation Network (OPTN) (Fig. 74-1) also show that recipients of ABO-compatible or ABO-incompatible livers between 1995 and 2000 had poorer outcomes than recipients of ABO-identical organs. The graft survival rates at 6 months ranged from 83% for ABO-identical to 76% for ABO-compatible and 66% for ABO-incompatible livers. Five years after transplantation the differences in graft survival rates remained essentially the same, suggesting that the deleterious effect of ABO differences manifests early within the first year after transplantation and that there is no additional long-term disadvantage associated with ABO-nonidentical transplants. Thus, liver graft survival rates for recent ABO-incompatible transplants performed at centers throughout the United States was approximately 15% lower at 5 years than from ABO-compatible donors overall. It is noteworthy that among these 25,507 deceased donor liver transplants performed in the United States between 1995 and 2000, ABO nonidentical transplants were not common. Only 9% of liver transplants were performed from ABO-nonidentical but compatible donors, and fewer than 2% were from ABO-incompatible donors.

The often urgent nature of ABO-compatible and -incompatible transplants could explain the poorer outcomes in these combinations. However, two early studies compared ABO-identical, -compatible, and-incompatible transplants done in urgent situations and found that the 35% to 45% lower 2-year survival rate of ABO-incompatible grafts was not a result of the emergency conditions under which the transplantation was performed.16,17 In fact, the incompatible grafts in each case were lost early and immunoglobulin and complement components were readily identified on sinusoidal cells and arterial endothelium, indicating a clear humoral component to the graft failures. This conclusion was supported by a subsequent analysis comparing 31 ABO-incompatible transplants with 199 ABO-compatible emergency transplants at the University of California at Los Angeles (UCLA),18 which revealed a significantly increased incidence of rejection, thrombosis, and biliary stricture among incompatible graft recipients, resulting in a 20% lower 1-year graft survival rate. Most recently, a study of 229 highly urgent liver transplantations in Scandinavia19 noted that patients who received an ABO-identical graft had significantly higher patient survival rates than did those who received ABO-compatible (n = 76) or -incompatible livers (n = 10). In this study, which included transplants performed in five countries during 1990 to 2001, the authors noted that the outcomes for highly urgent transplants had improved during the course of the study, but that ABO compatibility produced superior results throughout.

Liver allocation algorithms often provide for mandatory sharing of livers for highly urgent patients, allowing ABO-compatible and even ABO-incompatible offers. However, such prioritizations may disadvantage other less urgent patients, particularly blood group O patients. Eurotransplant reported a simulation study that suggests that a restricted ABO matching policy provides the optimal balance for both urgent and elective patients from the allocation perspective. Under this system, blood group O livers are offered to blood group O or B patients and blood group A livers are offered to blood group A or AB patients.20 The UNOS in the United States uses a similar policy. Blood group O livers are allocated first to blood group O patients, then livers are allocated to blood group B patients who are ranked according to their medical condition. A point system is used to promote ABO-identical combinations over ABO-compatible and ABO-incompatible transplantations.

Despite the poorer survival rates for ABO-incompatible transplantations, many survive and function well. This observation contrasts sharply with the results for inadvertent ABO-incompatible kidney transplants, nearly all of which have failed very early after the transplant.21 When ABO-incompatible transplants are performed inadvertently or in urgent situations, there is no time to assess the suitability of the recipient to receive an incompatible organ. However, the results of ABO-incompatible transplantations might be improved when the incompatibility is anticipated and the recipient can be conditioned in advance.

Acquired Blood Group Chimerism

Acquired blood group chimerism is medically induced and can be a transient phenomenon or a permanent state. Transient blood group chimerism is the most common type of blood group chimerism. It happens following transfusion of ABO-compatible, but not ABO-specific, red blood cells. The ABO blood group system has four distinct phenotypes: A, B, AB, and O. Red cells with the blood groups A, B, and AB carry distinct carbohydrate antigens on their surface; red cells with blood group O carry none. The plasma carries ABO red cell antibodies or agglutinins that are specific for the ABO blood antigens that are lacking. That is, a blood group A person has antibodies directed against the B antigen (anti-B antibodies). So long as blood is provided that is ABO compatible for transfusion, it does not need to be ABO identical. For example, patients with blood groups O, A, B, and AB can all safely receive blood group O red cell products for transfusion (see chart below).

Patient ABO blood typeAcceptable red cell product ABO typeOOAA or OBB or OABAB, A, B, or O

This biological compatibility allows patients in need of emergent transfusion, such as after a traumatic event, to safely receive blood group O cells (universal donor). This is standard practice for hospitals treating trauma victims. Following ABO-compatible (but not identical) transfusion, patients with A, B, or AB blood types will display more than one blood type when tested; thus, a blood group chimera is transiently created. As the transfused red cells live their normal life span of approximately 120 days, they will be removed from circulation and the patient will return to their natural blood type. Genetic testing of the patient during this time can elucidate the patient’s true ABO blood type, if it is necessary to determine for the purposes of clinical care.

Treatment-related blood group chimerism can also occur following ABO-incompatible hematopoietic (blood) stem cell transplant, which is reserved for the treatment of hematological malignancy, such as leukemia, or for inherited disorders, such as sickle-cell disease. In stem cell transplantation, blood stem cells are collected from a stem cell donor or umbilical cord blood donor and transfused into a patient following a conditioning regimen. Selection of the stem cell or umbilical cord blood donor is based on the human leukocyte antigen (HLA), or tissue typing, in an attempt to find the closest match available to achieve the best results. The donor may not have an identical ABO type as the patient. Thus, following engraftment of the new donor cells into the patient, the blood type of the donor and the patient will both be present; thus, a blood group chimera has been created. Months after successful hematopoietic stem cell transplant, the patient’s blood type will shift to be completely that of the donor.

There are several ways in which blood group chimerism may be created: through inheritance of more than one cell lineage in embryonic development or through medical therapy. No matter what the mechanism, blood group chimerism will often be detected when testing the blood for the purposes of medical care, usually in preparation for a blood transfusion. If more than one red blood cell population is encountered, an investigation to determine the underlying cause is necessary. Discrepant results in the blood bank can delay the availability of blood for transfusion.

Breast and Other Gynecologic Cancers

The following articles represent a sampler of the advances in understanding relationships between ABH antigens, secretor status, and the incidence and prognosis of different gynecologic-related cancers. In 2009 a correlation between breast cancer in Greek women and ABO blood group was published. One hundred sixty-six female patients with breast cancer were examined. They revealed that blood group A is more often associated with ductal breast cancer (49.6%), in contrast to the other blood groups, and particularly to blood group AB (3.6%). The relative risk of metastasis in Rh (−) patients was 4.2 times higher than that in Rh (+) patients. Consequentially, blood group A, and particularly A (−), has the worst prognosis of all.126

Breast cancer researchers have given the aberrant glycosylation moiety T/Tn antigen the moniker “ligand-like complex” (LLC). By virtue of altered antigenicity, LLC allows for both metastatic egress from the regional lymph nodes and detachment from the extracellular matrix and thus is associated with cancers of poor prognosis.127 We believe that LLC may well be the “A-like,” pancarcinoma cross-reacting antigen. Observation of the GalNac-binding lectin from the Roman snail, Helix pomatia agglutinin, appears to identify this oligosaccharide128; there have been separate reports that “Springer’s vaccine” (human group O RBC membrane–derived T/Tn antigen containing traces of phosphoglycolipid A hyperantigen) has had significant effect as an immune modulator in breast carcinoma of even advanced stage.129

A study of epithelial ovarian cancer incidence and its association to ABO blood groups and risk was performed in 2010 at Harvard and analyzed data from 49,153 women in the Nurses’ Health Study. Compared with women with blood group O, women with blood group AB or B had a nonsignificant 38% increase in ovarian cancer incidence, whereas blood group A was not associated with risk. Combining blood groups AB and B, they observed a statistically significant positive association with presence versus absence of the B antigen for the serous invasive subtype and overall. In this large, prospective cohort of women, the presence of the B antigen was positively associated with ovarian cancer incidence, whereas blood group A was not associated with the same risk.130

Another interesting, yet not definitive, association is presented between invasive squamous cell carcinoma (SCC) of the vulva and ABO blood groups. The distribution of ABO blood group for 33 women diagnosed with invasive SCC of the vulva was determined. ABO blood group was also recorded for 100 female patients (controls) who underwent a gynecologic procedure for a nonneoplastic process during the same period. A trend was identified for women with invasive SCC of the vulva to have blood group type A, but this did not determine a definitive association between blood group type A, or any other blood group, and vulvar SCC.131

ABO blood group system

The ABO blood group system is the first described of the human blood groups based upon carbohydrate alloantigens present on red cell membranes. Anti-A or anti-B isoagglutinins (alloantibodies) are present only in the blood sera of individuals not possessing that specificity. This serves as the basis for grouping humans into phenotypes designated A, B, AB, and O. Blood group methodology to determine the ABO blood type makes use of the agglutination reaction. Table 15.2 shows ABO blood group antigens, antibodies, and the front and back typing.

Table 15.2. ABO blood group antigens, antibodies and grouping by front and back typing

Front typingBack typingReaction of cells tested withReaction of serum tested againstBlood typeErythrocyte surface antigenAntibody in serumAnti-AAnti-BA cellsB cellsO cellsAA antigenAnti-B+00+0BB antigenAnti-A0++00ABA, B antigensNo antibody++000OH antigenBoth anti-A and anti-B00++0

The ABO system remains the most important in the transfusion of blood and is also critical in organ transplantation. Table 15.3 gives the suggested ABO group selection order for transfusion of erythrocytes and plasma. Epitopes of the ABO system are found on oligosaccharide terminal sugars. The genes designated as A/B, Se, H, and Le govern the formation of these epitopes and of the Lewis (Le) antigens. The two precursor substances type I and type II differ only in that the terminal galactose is joined to the penultimate N-acetylglucosamine in the b 1–3 linkage in type I chains, but in the b 1–4 linkage in type II chains.

Table 15.3. Suggested ABO group selection order for transfusion of erythrocytes and plasma

Component ABO group1st choice2nd choice3rd choice4th choiceRecipient ABO groupRBCPlasmaRBCPlasmaRBCPlasmaRBCPlasmaABABABA(A)B(B)O(O)AAAOAB(B)(O)BBBOAB(A)(O)OOOABAB

What blood type has only agglutinin A?

What does it mean when blood agglutinates with anti

What blood type has only anti