How is Polyagglutination resolved quizlet?
How is polyagglutination resolved? Serum from a group B individual contains anti-A. When A2 cells are added to serum and centrifuged, the cells with attached anti-A are removed from serum.
What is meant by Polyagglutination?
Polyagglutination is the term applied to red blood cells (RBCs) that are agglutinated by almost all samples of human sera from adults but not by autologous serum or sera of newborns. The polyagglutinable state may be transient or persistent.
What is Polyagglutination blood bank?
Polyagglutination is caused by changes in the RBC membrane that enable patient RBCs to agglutinate with normal human sera; this agglutination can interfere with blood bank testing. Depending on the cause, polyagglutination may or may not be the cause of RBC hemolysis.
What causes mixed field reactions in blood bank?
One of the potential causes of mixed field reactions on ABO and Rh typing is the presence within an individual of a chimeric state or mosaicism4,5. A chimera is present when two or more distinct cell populations containing genetic material from more than one zygote exist within an individual.
What is pseudo agglutination?
Medical Definition of pseudoagglutination : the forming of rouleaux by red blood cells.
What is TN activation?
T activation is the earliest known and the most common form of polyagglutination, a group of conditions character- ized by alterations in red blood cell (RBC) membrane glycoprotein structure in certain pathological states, result- ing in the agglutination of such transformed cells in the presence of most ABO compatible ...
What is TN Polyagglutination?
Tn polyagglutination syndrome is an acquired clonal disorder characterized by the polyagglutination of red blood cells by naturally occurring anti-Tn antibodies following exposure of the Tn antigen on the surface of erythrocytes.
What are lectins in blood bank?
Lectins are extracts made from the seeds of plants which have blood group specificity, i.e., they are proteins that combine specifically with sugars and act as if they were IgM antibodies. Lectins are used in blood banking as antisera for antigen typing red cells.
What is Rouleaux formation?
Rouleaux formation is the linking of RBCs into chains resembling stacks of coins. Some rouleaux is normal in dogs, and more occurs in normal cats. Increased rouleaux formation in canine blood smears is associated with an increase in fibrinogen or acute phase proteins and is usually seen in inflammatory diseases.
What happens when blood of different groups is mixed?
Blood Type Importance Now experts know that if you mix blood from two people with different blood types, the blood can clump, which may be fatal. That's because the person receiving the transfusion has antibodies that will actually fight the cells of the donor blood, causing a toxic reaction.
What are the common causes of discrepancies between cell grouping and reverse serum grouping?
1.2 Blood group discrepancies exist when the reaction in the forward group (red cells) does not match the reactions in the reverse grouping (plasma/serum), when expected reactions are weak or negative, or if the previous and current results do not match.
What is the most likely cause of the discrepancy between ABO antigens and antibodies?
Possible causes of an ABO discrepancy due to extra plasma reactivity include ABO subgroup, cold reactive alloantibody, cold reactive autoantibody, antibody to reagent constituent, transfusion of non-ABO-group–specific plasma components, infusion of IVIG, and post–stem cell transplant status.
What is TN Polyagglutination?
Tn polyagglutination syndrome is an acquired clonal disorder characterized by the polyagglutination of red blood cells by naturally occurring anti-Tn antibodies following exposure of the Tn antigen on the surface of erythrocytes.
What is Rouleaux formation?
Rouleaux formation is the linking of RBCs into chains resembling stacks of coins. Some rouleaux is normal in dogs, and more occurs in normal cats. Increased rouleaux formation in canine blood smears is associated with an increase in fibrinogen or acute phase proteins and is usually seen in inflammatory diseases.
What causes incomplete synthesis of N-glycans in congenital dyserythropoietic an?
Incomplete synthesis of N-glycans in congenital dyserythropoietic anemia type II caused by a defect in the gene encoding α-mannosidase II
What is the term for agglutination of RBCs?
Polyagglutination is the term applied to red blood cells (RBCs) that are agglutinated by almost all samples of human sera from adults but not by autologous serum or sera of newborns. The polyagglutinable state may be transient or persistent. Transient polyagglutinability results from the exposure of normally cryptic antigens by bacterial enzymatic activity during the course of an infectious process. RBCs are polyagglutinable because most sera from adults contain agglutinins for the exposed antigens. This type of polyagglutination can often be reproduced in vitro with bacterial culture fluids or isolated enzymes. Persistent polyagglutination may be a consequence of somatic mutation leading to a cellular lineage characterized by an enzyme deficiency that results in exposure of a normally cryptic antigen, Tn. Most human sera contain anti-Tn. Tn polyagglutination is regularly accompanied by leukopenia and thrombocytopenia and has been associated with leukemia. Other forms of persistent polyagglutination are due to the inheritance of rare blood groups or are associated with a hematologic dyscrasia.
What is pneumonia with hemolysis caused by?
Severe pneumonia with hemolysis caused by neuraminidase. Detection of cryptantigens by indirect immunofluorescent technic
What is the state in which an individual's red blood cells are agglutinated by all sera regardless?
The state in which an individual's red blood cells are agglutinated by all sera regardless of blood type is called: polyagglutination. All of the following are tests performed in the blood bank to classify subgroups of A except: LISS enhancement. All of the following may depress antigen expression except:
What happens when A2 cells are added to serum and centrifuged?
Serum from a group B individual contains anti-A. When A2 cells are added to serum and centrifuged, the cells with attached anti-A are removed from serum. What is the name of this technique?
What is polyagglutination in blood?
Polyagglutination (PA) is the agglutination of red cells with all human serum except own. Exposure of crypt antigens over red blood cells due to the action of glycosylated enzymes causes polyagglutination. Many bacterial or viral infections activate these enzymes. The major variants of PA are the T cryptic antigens like T, Tn, Tk, Th, and Tx. The other lesser prevalent types are Cad, HEMPAS, NOR, and Hyde Park Polyagglutination. [ 1, 2] There were few case reports on PA, but information on healthy individuals with PA is scarce. Here, we report a case of PA detected in a healthy blood donor.
Is polyagglutination a rare disease?
Nowadays, polyagglutination is rarely detected due to the use of monoclonal antisera. Our case report describes the presence of Tn polyagglutination in a healthy adult blood donor with no prior history of any infection in the recent past.
Is PA a rare occurrence?
Although PA is a rare occurrence, it needs particular emphasis on identification. It appears to be a clueless situation, primarily in incompatible cross-match despite negative antibody screening, DAT, and the auto-control. Hence, an algorithm could be developed ( Fig. 1) and included in the SOP in the immunohematology laboratory to identify and resolve PA for the transfusion of cross-match compatible blood units.
How long does erythrocyte polyagglutination last?
In two children with bowel disorders, erythrocyte T-polyagglutination persisted for 12 months in one case and for seven months in the other. Both cultures required both transfusions to support surgery. Washed red cell concentrates were transfused instead of whole blood to prevent dangerous destruction of T-transformed erythrocytes by anti-T antibodies normally present in the plasma of blood donors.
What is the term for agglutination of RBCs?
Polyagglutination is the term applied to red blood cells (RBCs) that are agglutinated by almost all samples of human sera from adults but not by autologous serum or sera of newborns. The polyagglutinable state may be transient or persistent. Transient polyagglutinability results from the exposure of normally cryptic antigens by bacterial enzymatic activity during the course of an infectious process. RBCs are polyagglutinable because most sera from adults contain agglutinins for the exposed antigens. This type of polyagglutination can often be reproduced in vitro with bacterial culture fluids or isolated enzymes. Persistent polyagglutination may be a consequence of somatic mutation leading to a cellular lineage characterized by an enzyme deficiency that results in exposure of a normally cryptic antigen, Tn. Most human sera contain anti-Tn. Tn polyagglutination is regularly accompanied by leukopenia and thrombocytopenia and has been associated with leukemia. Other forms of persistent polyagglutination are due to the inheritance of rare blood groups or are associated with a hematologic dyscrasia.
Why are serological results discrepancies?
Laboratory professionals, consultants, and treating physicians may encounter discrepancies in serological testing results for numerous reasons; identifying the reason (s) for the presence of an unexpected antibody or antigen can be challenging. A question-based approach can be useful in identifying the underlying cause of the discrepancy. We describe a new approach to serological problems in a transfusion-service laboratory. The approach we outline herein is targeted towards a general transfusion medicine service, rather than a center that offers complex antibody investigations using specialized techniques. This question-based problem-solving approach considers patient factors including diagnosis, transfusion history, previous pregnancies, and medication history, along with serological test results: ABO and Rh groups, direct and indirect antiglobulin tests, reacting temperature of the antibody, effect of enzyme treatment of cells, strength of reactivity, and antibody reactivity with umbilical cord cells. We also demonstrate the usefulness of this approach through a case scenario.
Is Tn polyagglutination a rare disorder?
Tn polyagglutination syndrome is a rare disorder that has been reported on only a few occasions in the literature, and, to the best of our knowledge, never before in the context of febrile neutropenia. We report the case of a 26-year-old Caucasian woman who presented to our emergency department complaining of a persistent fever over the previous three days. She had a history of long-standing refractory pancytopenia with multi-lineage dysplasia and severe neutropenia, but she had rarely experienced infection. The results of a physical examination and multiple laboratory tests were unremarkable. While investigating the possible causes of the refractory, long-standing pancytopenia, the possibility of a polyagglutinable state was suggested. Blood samples were sent to the laboratory for an analysis of mixed-field seed lectin agglutination assay. A serum lectin panel confirmed the final diagnosis of Tn-activation. We should include Tn-activation in our differential whenever we encounter cases of refractory long-standing idiopathic cytopenias and inconclusive bone marrow results displaying multi-lineage dysplasia. Novel genetic techniques have recently revealed the interesting pathophysiology of this phenomenon. The recognition and inclusion of Tn polyagglutination syndrome in our differential diagnoses has important clinical implications, given its main associated features, such as severe thrombocytopenia and neutropenia, which are usually linked to a benign clinical course and prognosis. Increased awareness of the polyagglutinable disorders will potentially decrease the need for invasive and costly medical interventions and also raises the need for monitoring of this specific sub-set of patients. In addition, the study of the expression and implications of Tn, and other similar antigens, offers a fascinating perspective for the study of its role in the diagnosis, prognosis and immunotherapy of solid tumors and hematological malignancies. The infrequency with which Tn polyagglutination syndrome is encountered, its clinical features and its pathophysiology make it a formidable diagnostic challenge.
Is Tn polyagglutination associated with leukemia?
A case of Tn polyagglutinability in a patient with acute myelomonocy tic leukemia is described. This represents the third report in which Tn polyagglutination has been associated with a leukemic state. Serologic recognition of Tn polyagglutination and probable causes are discussed. Known cases of Tn-polyagglutinability are reviewed.
What is polyagglutination in RBC?
Polyagglutination is the term applied to RBC that are agglutinated by almost all samples of human sera from adults, but not by autologous serum or sera of newborns [ 1 – 3] (Figure 2 ). Previously, all cases of TnP, and many other polyagglutinable phenomenons, were diagnosed during infancy or at the moment when a blood group classification for a transfusion was made, as former techniques of hemoclassification were performed using human adult serum containing multiple antibodies. However, current blood grouping practice uses murine diluted monoclonal antibody re-agents that do not include any other potentially pro-agglutinating immunoglobulins (Ig), thus denying the opportunity to recognize polyagglutinable cells and their implications [ 4, 5 ]. This has been reflected in a lack of reports about this condition over the last 30 years.
What causes Tn antigen?
Tn antigen is caused by a hemizygous pleiotropic somatic mutation or gene suppression in adults at the pluripotent stem cell level , creating an abnormal clone in expansion through an autoimmune process, in which it is hypothesized that the patient's Natural Killer cells (NK) target the O-glycans of the normal blood cells and selectively destroy the normal blood cell population. This leads to the loss of anti-Tn and possibly the multi-lineage dysplasia and subsequent cytopenias [ 8 ].
How to diagnose TNP?
A diagnosis of TnP is made using mixed-field seed lectin agglutination. Lectin typing reagents contain proteins that recognize specific carbohydrates on RBC membranes, causing their direct agglutination. Positive agglutination reactions following exposure of the patient's red blood cells to specific lectins derived from seeds of Dolichos biflorus, Glycine soja and Salvia sclerea plant species are considered as pathognomonic for diagnosis (Table 1 ). The only exception occurs in patients with blood group A, due to its chemical similarity with the Tn antigen [ 1 – 5, 9 ]; monoclonal anti-Tn reagents are available for these cases [ 9 ]. Many other types of agglutination have been described in the literature. Most of them are transient and related to episodes of acute infection where bacterial enzymes (for example, neuraminidase and endoβ-galactosidase) expose such antigens (T, Th, Tk, TX, VA). There are some other inherited types of agglutination whose frequency has not been established (Cad [Sda], HEMPAS, NOR, Hyde Park, Tr) [ 9 – 11 ].
Is Tn polyagglutination syndrome rare?
Tn polyagglutination syndrome is a rare disorder that has been reported on only a few occasions in the literature, and, to the best of our knowledge, never before in the context of febrile neutropenia.
