Avo blood group antigens. Plasma antigens

GENERAL PROVISIONS

The ABO blood group system consists of two group agglutinogens - A and B and two corresponding agglutinins in plasma - alpha (anti-A) and beta (anti-B). Various combinations of these antigens and antibodies form four blood groups: group 0(1) - both antigens are absent; group A (II) - only antigen A is present on red blood cells; group B (III) - only antigen B is present on erythrocytes; group AB (IV) - antigens A and B are present on red blood cells.

The uniqueness of the ABO system is that in the plasma of non-immunized people there are natural antibodies to an antigen that is not present on red blood cells: in people of group 0(1) - antibodies to A and B; in persons of group A (II) - anti-B antibodies; in persons of group B (III) - anti-A antibodies; persons of group AB(IV) do not have antibodies to antigens of the ABO system.

In the following text, anti-A and anti-B antibodies will be referred to as anti-A and anti-B.

Determination of the ABO blood group is carried out by identifying specific antigens and antibodies (double or cross reaction). Anti-A and anti-B are detected in serum using standard red blood cells A(II) and B(III). The presence or absence of antigens A and B on erythrocytes is determined using monoclonal or polyclonal antibodies (standard hemagglutinating sera) of appropriate specificity.

Determination of the blood group is carried out twice: the primary study - in the medical department (blood collection team); confirmatory research - in the laboratory department. The algorithm for conducting immunohematological laboratory tests during blood transfusion is presented in Fig. 18.1.

The result of determining the blood group is recorded in the upper right corner of the front sheet of the medical history or in the donor journal (card), indicating the date and signed by the doctor who made the determination.

In the north-west of Russia, the distribution of ABO blood groups in the population is as follows: group 0(I) - 35%; group A(II) - 35-40%; group B(III) - 15-20%; group AB (IV) - 5-10%.

It should be noted that there are different types (weak variants) of both antigen A (to a greater extent) and antigen B. The most common types of antigen A are A 1 and A 2. The prevalence of the A 1 antigen in individuals of groups A (II) and AB (IV) is 80%, and the A 2 antigen is about 20%. Blood samples containing A2 may contain anti-A1 antibodies that react with standard group A(II) red blood cells. The presence of anti-A 1 is detected by cross-determination of blood groups and during an individual compatibility test.

For differentiated determination of antigen A variants (A 1 and A 2), it is necessary to use specific reagents (phytohemagglutinins or monoclonal antibodies anti-A 1. Patients of groups A 2 (II) and A 2 B (IV) need to be transfused with erythrocyte-containing hemocomponents, respectively, of groups A 2 (II) and A 2 B (IV) Transfusions of washed erythrocytes may also be recommended: 0 (I) - patients with blood group A 2 (II) and B (III) - patients with blood group A; 2 B(II).

Table 18.4. Results of determining the ABO blood group
Research results						Group affiliation of the blood being tested
red blood cells with reagent			serum (plasma) with standard red blood cells
anti-AV	anti-A	anti-B	0(I)	A(II)	B (III)
-	-	-	-	+	+	0(I)
+	+	-	-	-	+	A(II)
+	-	+	-	+	-	B(III)
+	+	+	-	-	-	AB(IV)
Designations: + - presence of agglutination, - - absence of agglutination

Determination of blood group according to the ABO system

Blood groups are determined using standard sera (simple reaction) and standard red blood cells (double or cross reaction).

The blood group is determined by a simple reaction using two series of standard isohemagglutinating sera.

• Progress of determination [show] .

  Blood group determination is carried out in good lighting and temperature from + 15 to + 25 ° C on tablets. 0(1) is written on the left side of the tablet, A(II) in the middle, and B(III) on the right side. In the middle of the upper edge of the tablet, mark the donor's name or the number of the blood being tested. Use active standard sera of three groups (O, A, B) with a titer of at least 1:32, in two series. Serums are placed in special racks in two rows. Each serum has a labeled pipette. For additional control, group AB(IV) serum is used.

  One or two drops of standard sera are applied to the tablet in two rows: serum of group 0 (1) - on the left, serum of group A (II) - in the middle, serum of group B (III) - on the right.

  Drops of blood from a finger or test tube are applied with a pipette or glass rod near each drop of serum and mixed with a stick. The amount of blood should be 8-10 times less than serum. After mixing, the plate or tablet is gently rocked in the hands, which promotes faster and more precise agglutination of red blood cells. As agglutination occurs, but not earlier than after 3 minutes, one drop of 0.9% sodium chloride solution is added to the drops of serum with red blood cells where agglutination has occurred and observation is continued until 5 minutes have elapsed. After 5 minutes, read the reaction in transmitted light.

  If the agglutination is unclear, one drop of 0.9% sodium chloride solution is additionally added to the mixture of serum and blood, after which a conclusion about the group affiliation is given (Table 18.4).

• Reaction results [show] .
  1. The absence of agglutination in all three drops indicates that there is no agglutinogen in the blood being tested, that is, the blood belongs to group 0(I).
  2. The onset of agglutination in drops with serums 0(I) and B(III) indicates that there is agglutinogen A in the blood, that is, the blood belongs to group A(II).
  3. The presence of agglutination in drops with group 0(I) and A(II) sera indicates that the blood being tested contains agglutinogen B, that is, group B(III) blood.
  4. Agglutination in all three drops indicates the presence of agglutinogens A and B in the blood being tested, that is, the blood belongs to group AB (IV). However, in this case, given that agglutination with all sera is possible due to a nonspecific reaction, it is necessary to apply two or three drops of standard serum of group AB (IV) to the tablet or plate and add 1 drop of the test blood to them. The serum and blood are mixed and the reaction result is observed for 5 minutes.

     If agglutination does not occur, then the blood being tested is classified as group AB(IV). If agglutination appears with serum of group AB (IV), then the reaction is nonspecific. In case of weak agglutination and in all doubtful cases, the blood is retested with standard sera from other series.

Determination of ABO blood group by double reaction
(based on standard sera and standard erythrocytes)

Standard red blood cells are a 10-20% suspension of fresh native red blood cells (or preservative-washed test cells) of groups 0(I), A(II) and B(III) in a 0.9% sodium chloride solution or citrate-saline solution. Native standard red blood cells can be used within 2-3 days if they are stored in an isotonic saline solution at a temperature of +4°C. Preserved standard red blood cells are stored at +4°C for 2 months and washed from the preservative solution before use.

Ampules or vials with standard sera and standard red blood cells are placed in special racks with appropriate markings. To work with typing reagents, use dry, clean pipettes, separate for each reagent. To wash glass (plastic) rods and pipettes, prepare glasses with a 0.9% sodium chloride solution.

To determine the group, take 3-5 ml of blood into a test tube without a stabilizer. The blood should stand for 1.5-2 hours at a temperature of + 15-25 ° C.

• Progress of determination [show] .

  Two drops (0.1 ml) of standard sera of groups 0(I), A(II), B(III) of two series are applied to the tablet. Accordingly, each group of sera is given one small drop (0.01 ml) of standard erythrocytes of groups 0(I), A(II), B(III). One drop of test blood is added to standard sera, and two drops of test serum are added to standard erythrocytes. The amount of blood should be 8-10 times less than serum. The drops are mixed with a glass rod and, shaking the tablet in your hands for 5 minutes, monitor the onset of agglutination. If the agglutination is unclear, an additional drop of 0.9% sodium chloride solution (0.1 ml) is added to the mixture of serum and blood, after which a conclusion is made about the group affiliation (Table 18.4).

• Evaluation of the results of determining the ABO blood group [show] .
  1. The presence of agglutination with standard erythrocytes A and B and the absence of agglutination in three standard sera of two series indicates that the test serum contains both agglutinins - alpha and beta, and there are no agglutinogens in the test erythrocytes, that is, the blood belongs to group 0 (I) .
  2. The presence of agglutination with standard sera of groups 0(I), B(III) and with standard erythrocytes of group B(III) indicates that the test erythrocytes contain agglutinogen A, and the test serum contains agglutinin beta. Therefore, blood belongs to group A (II).
  3. The presence of agglutination with standard sera of groups 0(I), A(II) and with standard erythrocytes of group A(II) indicates that the test erythrocytes contain agglutinogen B, and the test serum contains agglutinin alpha. Therefore, the blood belongs to group B (III).
  4. The presence of agglutination with all standard sera and the absence of agglutination with all standard erythrocytes indicates that the erythrocytes under study contain both agglutinins, that is, the blood belongs to group AB (IV).

Determination of blood group
using anti-A and anti-B zoliclones

Anti-A and anti-B zoliclones (monoclonal antibodies to antigens A and B) are intended for determining the blood group of the human ABO system instead of standard isohemagglutinating sera. For each blood group determination, one series of anti-A and anti-B reagents is used.

• Progress of determination [show] .

  One large drop of anti-A and anti-B zoliclones (0.1 ml) is applied to the tablet (plate) under the appropriate inscriptions: “Anti-A” or “Anti-B”. One small drop of the blood being tested is placed nearby (the blood reagent ratio is 1:10), then the reagent and blood are mixed and the progress of the reaction is observed by gently shaking the tablet or plate.

  Agglutination with anti-A and anti-B coliclones usually occurs within the first 5-10 s. Observation should be carried out for 2.5 minutes, due to the possibility of a later onset of agglutination with red blood cells containing weak types of antigens A or B.

• An assessment of the results of the agglutination reaction with anti-A and anti-B cyclones is presented in table. 18.4, which also includes the results of determining agglutinins in donor serum using standard erythrocytes.

If spontaneous agglutination is suspected in persons with blood group AB(IV), a control study is performed with a 0.9% sodium chloride solution. The reaction must be negative.

Coliclones anti-A (pink) and anti-B (blue) are available in both native and lyophilized form in ampoules of 20, 50, 100 and 200 doses with a solvent attached to each ampoule, 2, 5, 10 , 20 ml respectively.

An additional control for the correct determination of the ABO blood group using anti-A and anti-B reagents is the monoclonal anti-AB reagent (Hematologist, Moscow). It is advisable to use the anti-AB reagent in parallel with both polyclonal immune sera and monoclonal reagents. As a result of the reaction with the anti-AB reagent, agglutination of erythrocytes of groups A (II), B (III) and AB (IV) develops; erythrocytes of group 0(I) have no agglutination.

ERRORS IN DETERMINING GROUP MEMBERSHIP

Errors in determining blood groups can depend on three reasons:

1. technical;
2. inferiority of standard sera and standard erythrocytes;
3. biological characteristics of the blood being tested.

Errors due to technical reasons include:

• a) incorrect placement of serums on the plate;
• b) incorrect quantitative ratios of serum and erythrocytes;
• c) the use of insufficiently clean tablets and other objects that come into contact with blood. There should be a separate pipette for each serum; To wash pipettes, only 0.9% sodium chloride solution should be used;
• d) incorrect recording of the blood being tested;
• e) failure to comply with the required time for the agglutination reaction; in case of haste, when the reaction is taken into account before 5 minutes have elapsed, agglutination may not occur if there are weak agglutinogens in the blood being tested; if the reaction is overexposed for more than 5 minutes, droplets may dry out from the edges, simulating agglutination, which will also lead to an erroneous conclusion;
• f) absence of agglutination due to high (above 25°C) ambient temperature. To avoid this mistake, it is advisable to use specially prepared serums for working in hot climates; carry out the determination of blood groups on a plate or plastic tray, the outer surface of the bottom of which is immersed in cold water.
• g) improper centrifugation: insufficient centrifugation can lead to a false negative result, and excessive centrifugation can lead to a false positive result.

Errors depending on the use of inferior standard sera and standard erythrocytes:

• a) weak standard sera with a titer lower than 1:32 or expired can cause late and weak agglutination;
• b) the use of unsuitable standard sera or erythrocytes that were prepared unsterilely and insufficiently preserved leads to the occurrence of nonspecific “bacterial” agglutination.

Errors depending on the biological characteristics of the blood being tested:

Errors depending on the biological characteristics of the red blood cells being studied:

• a) late and weak agglutination is explained by “weak” forms of antigens, erythrocytes, and more often by the presence of a weak agglutinogen A 2 in groups A and AB. At the same time, in the case of determining the blood group without testing the serum for the presence of agglutinins (simple reaction), errors may occur, as a result of which blood of group A 2 B is defined as group B (III), and blood A 2 - as group 0 (I). Therefore, in order to avoid errors, determination of the blood group of both donors and recipients must be carried out using standard red blood cells (double or cross reaction). To identify agglutinogen A 2, it is recommended to repeat the study with other types (series) of reagents, using other laboratory glassware, increasing the reaction registration time.

  Specific reagents for clarifying the blood group in the presence of weak variants of the A antigen (A 1, A 2, A 3) using the direct agglutination reaction are the anti-A cl zolicone and the anti-A reagent).

• b) “panagglutination” or “autoagglutination”, that is, the ability of blood to give the same nonspecific agglutination with all sera and even with its own. The intensity of such a reaction weakens after 5 minutes, while true agglutination increases. It is most often found in hematological, oncological patients, burnt patients, etc. For control, it is recommended to evaluate whether agglutination of the tested red blood cells occurs in standard serum of group AB (IV) and physiological solution.

  The blood group during “panagglutination” can be determined after washing the red blood cells three times. To eliminate nonspecific agglutination, the tablet is placed in a thermostat at a temperature of +37°C for 5 minutes, after which the nonspecific agglutination disappears, but the true one remains. It is advisable to repeat the determination using monoclonal antibodies and Coombs test.

  In the case where washing of red blood cells does not give the desired result, it is necessary to re-take a blood sample into a pre-warmed test tube, place the sample in a thermal container to maintain a temperature of +37°C and deliver it to the laboratory for analysis. Blood group determination must be performed at a temperature of +37°C, for which preheated reagents, saline solution and a tablet are used.

• c) red blood cells of the tested blood form “coin columns”, which can be mistaken for agglutinates during macroscopic examination. Adding 1-2 drops of isotonic sodium chloride solution followed by gentle rocking of the tablet, as a rule, destroys the “coin columns”.
• d) mixed or incomplete agglutination: some of the red blood cells agglutinate, and some remain free. It is observed in patients of groups A(II), B(III) and AB(IV) after bone marrow transplantation or during the first three months after blood transfusion of group 0(I). The heterogeneity of peripheral blood erythrocytes is clearly verified in the DiaMed gel test.

Errors depending on the biological characteristics of the serum being tested:

• a) detection of antibodies of a different specificity during routine testing is the result of previous sensitization. It is advisable to determine the specificity of antibodies and select typed red blood cells without the antigen to which immunization has been detected. The immunized recipient is required to individually select compatible donor blood;
• b) if the formation of “coin columns” of standard erythrocytes in the presence of the test serum is detected, it is advisable to confirm the abnormal result using standard erythrocytes of group 0 (I). To differentiate “coin columns” and true agglutinates, add 1-2 drops of isotonic sodium chloride solution and shake the tablet, while the “coin columns” are destroyed;
• c) absence of anti-A or anti-B antibodies. Possible in newborns and patients with suppressed humoral immunity;
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LITERATURE [show] .

1. Immunological selection of donor and recipient for blood transfusions, its components and bone marrow transplants / Comp. Shabalin V.N., Serova L.D., Bushmarina T.D. and others - Leningrad, 1979. - 29 p.
2. Kaleko S. P., Serebryannaya N. B., Ignatovich G. P. et al. Allosensitization during hemocomponent therapy and optimization of the selection of histocompatible donor-recipient pairs in military medical institutions / Methodological. recommendations. - St. Petersburg, 1994. - 16 p.
3. Practical transfusiology / Ed. Kozinets G.I., Biryukova L.S., Gorbunova N.A. and others - Moscow: Triada-T, 1996. - 435 p.
4. Guide to military transfusiology / Ed. E. A. Nechaev. - Moscow, 1991. - 280 p.
5. Guide to Transfusion Medicine / Ed. E. P. Svedentsova. - Kirov, 1999.- 716 p.
6. Rumyantsev A.G., Agranenko V.A. Clinical transfusiology. - M.: GEOTAR MEDICINE, 1997. - 575 p.
7. Shevchenko Yu.L., Zhiburt E.B., Safe blood transfusion: A guide for doctors. - St. Petersburg: Peter, 2000. - 320 p.
8. Shevchenko Yu.L., Zhiburt E.B., Serebryannaya N.B. Immunological and infectious safety of hemocomponent therapy. - St. Petersburg: Nauka, 1998. - 232 p.
9. Shiffman F.J. Pathophysiology of blood / Transl. from English - M. - St. Petersburg: BINOM Publishing House - Nevsky Dialect, 2000. - 448 p.
10. Blood transfusion in Clinical Medicine / Ed. P.L.Mollison, C.P. Engelfriet, M. Contreras.- Oxford, 1988.- 1233 p.

Source: Medical laboratory diagnostics, programs and algorithms. Ed. prof. Karpishchenko A.I., St. Petersburg, Intermedica, 2001

This system is the main one that determines the compatibility or incompatibility of transfused blood. It includes two genetically determined important antigens: A and B - and two types of antibodies to them, agglutinins a and b. Combinations of agglutinogens and agglutinins determine 4 groups of the ABO system. This system is the only one where non-immune people have natural antibodies to the missing antigen in their plasma. Agglutinogen A in most people is well expressed (has great antigenic power): with anti-A antibodies (a), it gives a pronounced reaction of erythrocyte agglutination. In approximately 12% of individuals of groups A(11) and AB(IV), the antigen has weak antigenic properties; it is designated as A2 antigen. Thus, there is a group of antigens A: A1 (strong) and weaker A2, A3, A4, etc. The existence of weak A antigens should be remembered when determining blood groups, since red blood cells with such antigens are capable of giving only late and weak agglutination, which may lead to errors. Weak variants of the B antigen are very rare. Antibodies of the ABO system a (anti-A) and b (anti-B) are a normal property of blood plasma that does not qualitatively change during a person’s life, and and b are complete, cold antibodies. In most cases, they are not found in newborns and appear during the first three months of life or even a year. Group agglutinins reach full development by the age of 18, and in old age their titer (level) decreases, which is also observed in immunodeficiency states. In addition to the normally existing (natural) group antibodies a and b, in some cases immune antibodies anti-A and anti-B arise. The most common reason for this is pregnancy, in which the mother and fetus have different blood groups, more often if the mother is group 1(0), the fetus is 11(A) or W(B). Determination of blood type is necessary for compatible blood transfusion. In this case, it is necessary to adhere to the rule: the donor's red blood cells should not contain an antigen corresponding to the recipient's antibodies, i.e. A and a, B and c, since otherwise there will be massive destruction of the injected red blood cells by the patient's antibodies - hemolysis, which can lead to the death of the recipient. Group antibodies of the donor can be ignored, since they are diluted by the recipient's plasma. Therefore, type O(I) blood, which does not contain agglutinogens, can be transfused to people of any blood group. Persons with blood type 0(1) are considered “universal donors”. Blood of group A(P) can be transfused into recipients of group A(P) and group AB(IV), which do not have agglutinins in the plasma. Blood of group B(III) can be transfused to persons with group B(III) and AB(IV).

Determination of blood groups of the ABO system is carried out using the following methods.

I. Determination of blood group using standard isohemagglutinating sera. With this method, the presence or absence of agglutinogens is determined in the blood and, based on this, a conclusion is made about the group affiliation of the blood being tested.

2. Determination of blood group using a cross method, i.e., simultaneously using standard isohemagglutinating sera and standard erythrocytes. With this method, as with the first, the presence or absence of agglutinogens is determined and, in addition, using standard red blood cells, the presence or absence of group agglutinins is determined.

3. Determination of blood group using monoclonal antibodies (COLICLONS).

ERRORS IN DETERMINING BLOOD TYPES

Technical errors. Violation of the stated rules for determining blood groups can lead to incorrect assessment of the reaction results. Deviations from the rules may include:

Use of low-quality standard serums or red blood cells (expired expiration date, contamination with them, drying of serums);

Mixing up blood samples;

Incorrect placement of standard sera or focytes in racks;

Incorrect order of applying standard reagents to the plate;

Incorrect serum to red blood cell ratio (not 10:1);

Study at a temperature of less than 15 ° C (cold agglutination occurs) or more than 25 ° C (agglutination slows down);

Failure to comply with the time required for the reaction (5 minutes);

Do not add saline solution followed by rocking the plate;

Do not use a control reaction with ABo(IV) group serum;

Use of dirty or wet pipettes, sticks, plates.

In all cases of unclear or questionable results, it is necessary to re-determine the blood group by cross-testing using standard sera from other series.

Errors associated with the biological characteristics of the blood being tested.

Incorrect identification of group A 2 and A 2 B. Red blood cells with weak antigen A form small, slowly appearing agglutinates with antiserum. The reaction can be taken into account as negative, i.e. group A 2 is mistakenly registered as O(1), and A 2 B as B(III). The risk of such an error is especially high in the simultaneous presence of technical errors (the ratio of serum to red blood cells is 10:1, the temperature is above 25 ° C, the results are taken into account earlier than 5 minutes).

Errors associated with the presence of nonspecific agglutinability of the studied erythrocytes. This phenomenon is observed in patients with malignant tumors, leukemia, sepsis, burns, liver cirrhosis, autoimmune hemolytic anemia and is caused by dysproteinemia. Detects the presence of nonspecific agglutination by control with ABO (IV) group serum. In these cases, it is necessary to re-determine group membership using a cross-sectional method. In drops where agglutination is observed, you can add saline solution heated to 37°C. If necessary, you can wash the red blood cells under study with warm (37°C) saline and determine the blood type again.

Errors associated with the presence of extraagglutinins. In the blood serum of individuals of groups A2(P) and A2B(IV), antibodies to the A1 antigen - a1 - are found in approximately 1% of cases. This complicates the determination of blood group by the cross method, since the serum of such individuals agglutinates standard red blood cells of group A(P), i.e., manifests itself as serum of group 0(1).

In some diseases, a decrease in the agglutinability of erythrocytes, especially group A(P), is observed.

In immunodeficiency states, elderly people experience a decrease in the level of group agglutinins.

In all cases of obtaining a questionable result, the determination of blood group should be repeated using a cross-sectional method using sera of higher activity.

18. Antigens of the Rh system. Rh system groups. Clinical significance. Methods for determining Rh antigens and possible errors.

Rh antigens are the second most important in transfusion practice after ABO blood groups. During the period of active introduction of blood transfusions into the clinic, the number of post-transfusion complications after repeated transfusions of blood compatible with ABO antigens has increased significantly. The Rh system includes six antigens, to designate which two nomenclatures are used in parallel: Wiener (Rh 0, rh", rh", Hr 0, hr", hr"); Fischer and Reis (D, C, E, d, c, e).

Rh 0 - D, rh" - C, rh" - E, Hr 0 - d, hr" - c, hr" - e.

Since the Rho(D) antigen is the most active in this system, it is called the Rh factor. It is depending on the presence or absence of this factor that people are divided into Rh-positive (Rh+) and Rh-negative (Rh-). This division is accepted only in relation to recipients. Antigens rh"(C) and rh"(E) are less active than Rho(D), but antibodies to them can also be produced in people who do not contain antigens C and E in their red blood cells. Therefore, the requirements for red blood cells from Rh negative donors are more stringent. Red blood cells should not contain not only antigen D, but also C and E. Antigens Hro(d), hr"(c), hr"(e) are characterized by low activity, although hr"(c) antibodies can cause isoimmunological conflicts. 1-3% of Rh-positive individuals have a weak variant of the D - D antigen in their erythrocytes, which determines the presence of small, questionable agglutination when determining the Rh factor. In these cases, the Rh factor of the recipient's or pregnant woman's blood is indicated as Rh negative (Rh-), and the Rh factor of the donor's blood is indicated as Rh positive (Rh+). Transfusion of blood with antigen D to Rh-negative recipients is not allowed. Rh antigens are formed at 8-10 weeks of embryogenesis, and their antigenicity can even exceed the activity of antigens in adults. The Rh system, unlike the ABO system, does not have natural antibodies. Anti-Rhesus antibodies arise only after immunization of an Rh-negative organism as a result of a transfusion of Rh-positive blood or pregnancy with an Rh-positive fetus. In the body of sensitized individuals, antibodies to Rh antigens persist for several years, sometimes throughout life. In most cases, the titer of anti-Rhesus antibodies gradually decreases, but again increases sharply when Rh-positive blood enters the body again. Rh antibodies differ in specificity (anti-D, anti-III C, etc.) and in serological properties (complete and incomplete). Full antibodies cause agglutination of red blood cells in a saline environment at room temperature. For agglutination to occur under the influence of incomplete antibodies, special conditions are required: elevated temperature, colloidal medium (gelatin, whey protein). Complete antibodies (IgM) are synthesized at the beginning of the immune reaction and soon disappear from the blood. Incomplete antibodies (IgG, IgA) appear later, take a long time to synthesize and cause the development of hemolytic disease in newborns, as they pass through the placenta and damage fetal cells.

Determination of Rh blood

The method for determining the Rh factor depends on the form of Rh antibodies in the standard serum and the method of its preparation. The anti-rhesus serum is accompanied by accompanying instructions describing the method for which this series of serum is intended.

For each study, a control must be placed to check the specificity and activity of anti-Rhesus serum. For control, standard Rh-positive erythrocytes of group 0(1) or the same group as the blood being tested are used, and standard Rh-negative erythrocytes must be of the same group as the blood being tested.

When determining Rh status by two series of standard sera in cases where they are used by different methods, the result is taken into account as true if it coincides in both series of studies after checking control samples confirming the specificity and activity of each series of anti-Rhesus serum, i.e. in the absence agglutination with standard Rh-negative erythrocytes of the same group and the presence of agglutination with standard Rh-positive erythrocytes of the same group or group 0(1) and in control samples without anti-Rhesus serum (reagent). If a weak or questionable reaction is observed when determining Rh status, then the person’s blood should be re-examined with the same and other series of anti-Rhesus serum and it is advisable to include serum containing complete antibodies. If all series of sera containing incomplete antibodies also give a weak or questionable reaction, and the reaction with complete antibodies is negative, this means that the red blood cells contain a weak type of rhesus antigen, the so-called factor D u. In these cases, the Rh-type of the patient's or pregnant woman's blood is indicated as Rh-negative (Rh-), and the Rh-type of the donor's blood as Rh-positive (Rh+), thus preventing the transfusion of his blood to Rh-negative recipients.

Determination of the Rh factor can also be carried out using the following methods.

Determination of the Rh factor Rh 0 (D) by a conglutination reaction using gelatin (in a test tube heated to 46-48 ° C).

Determination of the Rh factor Rho(D) by a conglutination reaction in a serum medium on a heated plane.

Determination of the Rh factor Rh 0 (D) by an agglutination reaction in a saline medium in small test tubes. The agglutination reaction in a saline medium is suitable only for working with serum containing complete Rh antibodies.

Determination of Rh factor Rh 0 (D) using monoclonal antibodies.

Determination of the Rh factor Rho(D) using an indirect Coombs test.

19 Anemia. Classification and brief description. Etiology and pathogenesis of anemia. Anemia (from the Greek anemia - lack of blood) is a large group of diseases that is characterized by a decrease in the amount of hemoglobin or hemoglobin and red blood cells per unit volume of blood. Anemia differs in etiology, development mechanisms, clinical and hematological picture, so there are many different classifications, but they are not perfect enough. L.I. Idelson proposed a working classification of anemia for clinicians: 1) acute posthemorrhagic anemia; 2) iron deficiency anemia; 3) anemia associated with impaired synthesis or utilization of porphyrins (sideroblastic); 4) anemia associated with impaired DNA and RNA synthesis (megaloblastic); 5) hemolytic anemia; 6) anemia associated with inhibition of proliferation of bone marrow cells (hypoplastic, aplastic); 7) anemia associated with the replacement of hematopoietic bone marrow by a tumor process (metaplastic).

Anemia can be either an independent disease or a concomitant symptom or complication of certain internal diseases, infectious diseases and oncological diseases. There are multifactorial anemias, that is, of mixed origin, for example: hemolytic anemia with iron deficiency, aplastic anemia with a hemolytic component, etc.

Depending on:

1) the values ​​of the color indicator distinguish between anemia:

Normochromic (color index 0.9-1.1);

Hypochromic (color index less than 0.85);

Hyperchromic (color index greater than 1.15);

2) the average diameter of red blood cells:

Normocytic (average erythrocyte diameter 7.2-7.5 µm)

Microcytic (the average diameter of red blood cells is less than 6.5 microns),

Macrocytic (the average diameter of red blood cells is more than 8.0 microns),

Megalocytic (the average diameter of erythrocytes is more than 12 microns);

3) the average volume of erythrocytes in femtoliters (fl, 1 fl is equal to 1 micron 3):

Normocytic (average erythrocyte volume 87±5 fL);

Microcytic (average red blood cell volume less than 80 fL);

Macrocytic (the average volume of red blood cells is more than 95 fL);

4) the level of reticulocytes in peripheral blood.

Regenerative (reticulocyte count 0.5-5%);

Hyperregenerative (the number of reticulocytes is more than 5%);

Hypo- and aregenerative (the number of reticulocytes is reduced or absent, despite severe anemia).

The reticulocyte level is an indicator of the regenerative function of the bone marrow in relation to erythropoiesis.

Normochromic anemias include acute posthemorrhagic (in the first days after blood loss), hypo- and aplastic, non-spherocytic hemolytic, autoimmune hemolytic, metaplastic (with leukemia, multiple myeloma, etc.), as well as anemia developing with endocrine disorders (hypofunction of the adrenal glands), kidney diseases, chronic infections.

Hypochromic anemias include iron deficiency, sideroblastic, some myelotoxic, and hemolytic (thalassemia).

B12-(folate)-deficiency and some hemolytic anemias are hyperchromic (hereditary microspherocytosis, if microspherocytes predominate among the red blood cells in the smear). Sometimes vitamin B1 2 deficiency anemia is normochromic.

Normocytic include acute posthemorrhagic, aplastic, autoimmune hemolytic anemia, etc.

Microcytic anemia includes iron deficiency and sideroblastic anemia, macrocytic anemia includes vigamin B12 (folate) deficiency anemia, etc.

Regenerative anemias include posthemorrhagic anemia; hyperregenerative - hemolytic anemia, especially the condition after a hemolytic crisis; to hypo- and aregenerative - hypoplastic, aplastic anemia.

The bone marrow reacts to the development of iron deficiency and hemolytic anemia with irritation and red sprout hyperplasia. With hypoplastic anemia, there is a progressive decline in erythropoiesis up to its complete depletion.

20. Laboratory diagnostics of iron-saturated and iron-unsaturated anemia. Iron deficiency anemia. Types of iron deficiency. Laboratory tests reflecting iron deficiency in the body. Picture of peripheral blood and bone marrow in IDA. Laboratory diagnosis of sideroblastic anemia. Metabolism and role of iron in the body

Iron is of great importance for the body; it is part of hemoglobin, myoglobin, and respiratory enzymes. It is distributed among fixed assets.

Hemoglobin fund. Hemoglobin iron makes up 60-65% of the total iron content in the body.

Emergency Fund. This is the iron of ferritin and hemosiderin, which are deposited in the liver, spleen, bone marrow, and muscles. Makes up 30-40% of the iron level in the body. Ferritin is a water-soluble complex of ferric iron and apoferritin protein, containing 20% ​​iron. It is a labile fraction of the iron reserve fund. If necessary, it is easily used for the needs of erythropoiesis. Hemosiderin is a water-insoluble protein, similar in composition to ferritin, but contains a larger amount of iron - 25-30%. It is a stable, firmly fixed fraction of iron reserves in the body.

The transport fund is represented by iron bound to the transport protein transferrin. Constitutes 1% of the iron content in the body.

The tissue fund is represented by iron, iron-containing enzymes (cytochromes, peroxidase, etc.), myoglobin. Constitutes 1% of the iron content in the body.

The total iron content in the body of adults is 4-5 g. It enters the body with the diet. Contained in products of animal and plant origin (meat, especially beef, liver, eggs, legumes, apples, dried apricots, etc.). Iron is absorbed much better from animal products than from plant products, since it is contained in them in the form of heme. Thus, 20-25% of the iron contained in them is absorbed from meat, 11% from fish, and 3-5% from plant products. Ascorbic acid and organic acids (citric, malic, etc.) promote iron absorption; tannin and high fat content in the diet inhibit absorption. The absorption of iron from foods is limited. 2-2.5 mg of iron is absorbed per day; for a short time after severe bleeding, up to 3 mg of iron can be absorbed. The main amount of iron is absorbed in the duodenum and in the initial part of the jejunum. A small amount of iron can be absorbed in all parts of the small intestine.

Iron absorption occurs in two stages: 1) the intestinal mucosa captures iron supplied with the diet; 2) iron from the intestinal mucosa passes into the blood, is loaded onto transferrin and delivered to places of use and depot. Transferrin also transfers iron from its funds and cells of the phagocytic mononuclear lear system, in which destruction of red blood cells occurs, to the bone marrow, where it is partially used for the synthesis of hemoglobin, and partially deposited in the form of iron reserves, as well as to other iron storage sites. Typically, 1/3 of transferrin is bound to iron. It is called bound transferrin or serum iron. Normal serum iron levels in men and women are 13-30 and 12-25 µmol/l, respectively. The portion of transferrin not bound to iron is called free transferrin or unsaturated, latent serum iron-binding capacity. The maximum amount of iron that transferrin could attach before its saturation is designated as the total iron-binding capacity of serum (TIBC) (normally 30-85 µmol/l). The difference between TIBC and serum iron values ​​reflects the latent iron-binding capacity, and the ratio of serum iron to TIBC, expressed as a percentage, reflects the percentage of transferrin saturation with iron (normal 16-50%). To judge the amount of iron reserves in the body, the following is carried out:

Study of serum ferritin levels using radioimmunoassay methods;

Desferal test. Desferal (desferoxamine) is a complexone that, after being introduced into the body, selectively binds to iron reserves, i.e., ferritin iron, and removes it in the urine. The patient is injected intramuscularly with 500 mg of desferal once, daily urine is collected and the iron content in it is determined. After administration of desferal, 0.8 to 1.2 mg of iron is normally excreted in the urine, while in patients with iron deficiency anemia or in the presence of hidden iron deficiency, the amount of iron excreted in the urine sharply decreases;

Counting the number of sideroblasts in the bone marrow puncture, and siderocytes in the peripheral blood. Sideroblasts are normoblasts, i.e., nucleated cells of the red row, in the cytoplasm of which blue granules of iron reserves - ferritin - are detected. Normally, 20-40% of normoblasts are sideroblasts. Siderocytes are red blood cells in which ferritin granules are found. Normally in the peripheral blood: up to 1% siderocytes. Ferritin granules in sideroblasts and siderocytes are revealed by special staining with Prussian blue.

The body is characterized by physiological losses of iron in urine, feces, bile, exfoliated cells of the intestinal mucosa, with sweat, when cutting hair and nails. Women lose iron with their periods.

The development of iron deficiency anemia is preceded by hidden (latent) iron deficiency. Patients develop complaints and clinical signs characteristic of iron deficiency pyaemia, but less pronounced (weakness, moderate pallor of the skin and visible mucous membranes, headaches, palpitations, often perversion of taste and smell, dry skin, brittle nails, etc.). The examination does not yet reveal changes in the content of hemoglobin, red blood cells and other indicators of peripheral blood. But disturbances in iron metabolism are detected: serum iron decreases, total and latent iron-binding abilities of serum increase, the percentage of transferrin saturation decreases, and the level of iron reserves decreases. This is sideropenia without anemia. Hidden iron deficiency can develop at any age, and women, adolescents and children are especially likely to suffer from it. If hidden iron deficiency is not compensated, but deepens, iron deficiency anemia develops.

Although all polymorphism- the result of differences in DNA sequence, some polymorphic loci have been studied by testing for changes in the proteins encoded by these alleles, rather than by examining differences in the DNA sequence of the alleles themselves. It is believed that any individual is likely heterozygous for alleles defining structurally different polypeptides at approximately 20% of all loci; when comparing individuals from different ethnic groups, polymorphism is found in an even larger proportion of proteins.

Thus, within human species There is a striking degree of biochemical individuality in the characteristics of enzymes and other gene products. Moreover, because the products of many biochemical pathways interact, it is plausible to assume that each individual, regardless of health status, has unique, genetically determined biochemical characteristics and thus responds uniquely to environmental, dietary, and pharmacological influences.

This is the concept of chemical individuality, first put forward a century ago by the remarkable British physician Archibald Garrod, turned out to be correct.

Here we will discuss several polymorphisms of medical importance: blood groups ABO and Rh factor Rh (important in determining compatibility for blood transfusions) and MHC (playing an important role in organ and tissue transplantation). Studying changes in proteins, rather than in the DNA that encodes them, has real benefits; after all, it is the different protein products of different polymorphic alleles that are often responsible for different phenotypes and therefore determine how genetic changes at a locus affect organism-environment interactions.

Blood groups and their polymorphisms

The first examples are genetically predetermined protein changes so-called blood group antigens were found in red blood cells. A large number of polymorphisms are known in human blood components, especially in the ABO and Rh antigens of erythrocytes. In particular, the ABO and Rh systems are important in blood transfusion, tissue and organ transplantation, and hemolytic disease of the newborn.

ABO blood group system

Human blood may belong to one of four groups, according to the presence on the surface of red blood cells of two antigens, A and B, and the presence in the plasma of two corresponding antibodies, anti-A and anti-B. There are four main phenotypes: 0, A, B and AB. People with group A have antigen A on their red blood cells, with group B they have antigen B, with group AB they have both antigens A and B, and finally with group 0 they do not have any antigen.

One of the characteristics AVO groups does not apply to other blood group systems - it is a reciprocal relationship between the presence of antigens on red blood cells and antibodies in the serum. When red blood cells lack A antigen, the serum contains anti-A antibodies; when B antigen is absent, the serum contains anti-B antibodies. The reason for the reciprocal relationship is unknown, but it is believed that the formation of anti-A and anti-B antibodies is a response to the presence of A- and B-like antigens in the environment (for example, in bacteria).

They are determined by a locus on chromosome 9. Alleles A, B and 0 at this locus are a classic example of multiallelicism, when three alleles, two of which (A and B) are inherited as codominant, and the third (0) as a recessive trait, determine four phenotypes. Antigens A and B are determined by the action of alleles A and B on the surface glycoprotein of erythrocytes, called antigen H.

The specificity of antigens is determined by the terminal carbohydrates added to the substrate H. The B allele encodes a glycosyltransferase that preferentially recognizes the sugar D-galactose and adds it to the end of the oligosaccharide chain contained in the H antigen, thereby creating the B antigen. The A allele encodes a slightly different form of the enzyme that recognizes and adding N-acetylgalactosamine to the substrate instead of D-galactose, thereby creating antigen A. The third allele, 0, encodes a mutant version of transferase that does not have transferase activity and does not affect the substrate H.

Molecular differences in the gene identified glycosyltransferases, responsible for alleles A, B, and 0. A sequence of four different nucleotides that differs between alleles A and B results in amino acid changes that alter the specificity of the glycosyltransferase. Allele 0 has a single-nucleotide deletion in the coding region of the ABO gene, causing a frameshift mutation and inactivating transferase activity in people with group 0. Now that the DNA sequences are known, determination of group membership in the ABO system can be done directly at the level of the genotype, rather than the phenotype, especially when there are technical difficulties in serological analysis, which often happens in judicial practice or when establishing paternity.

The video shows the technique for determining blood group using standard sera:

Primary medical significance AVO systems- in blood transfusion and tissue or organ transplantation. The ABO blood group system has compatible and incompatible combinations. A compatible combination is when the donor's red blood cells do not carry the A or B antigen corresponding to the antibody in the recipient's serum. Although there are theoretically "universal" donors (group 0) and "universal" recipients (group AB), the patient is transfused with blood from his own ABO group except in emergency situations.

Permanent presence anti-A And anti-B antibodies explain the failure of many early blood transfusion attempts because these antibodies can cause rapid destruction of ABO-incompatible cells. When transplanting tissues and organs, successful engraftment requires compatibility of the donor and recipient according to the ABO and HLA group (described later).

Rh blood group system

According to clinical Rh system value comparable to the ABO system due to its role in the development of hemolytic disease of the newborn and in incompatibility with blood transfusions. The name Rh comes from the Rhesus monkeys used in the experiments that led to the discovery of the system. Simply put, the population is divided into Rh-positive individuals who express in their erythrocytes the Rh D antigen, a polypeptide encoded by the gene (RHD) on chromosome 1, and Rh-negative individuals who do not express this antigen. A negative Rh phenotype is usually caused by homozygosity for a nonfunctional allele of the RHD gene. The frequency of Rh-negative individuals varies greatly among different ethnic groups. For example, 17% of whites and 7% of African Americans are Rh negative, compared with only 0.5% of Japanese.

Hemolytic disease of newborns and blood types

The main clinical significance of the system Rh- that Rh-negative individuals can easily form anti-Rh antibodies after encountering Rh-positive red blood cells. This becomes a problem when an Rh-negative mother carries an Rh-positive fetus. Normally, during pregnancy, small amounts of fetal blood cross the placental barrier and enter the maternal bloodstream. If the mother is Rh negative and the fetus is Rh positive, the mother produces antibodies that return to the fetus and damage its red blood cells, causing hemolytic disease of the newborn with serious consequences.

U Rh-negative pregnant women the risk of immunization with Rh-positive fetal erythrocytes can be minimized by the administration of anti-Rhesus immunoglobulin at 28-32 weeks of gestation and additionally shortly after birth. Human anti-Rhesus immunoglobulin removes Rh-positive fetal cells from the mother's bloodstream before they sensitize her. Anti-Rhesus immune globulin is also administered after miscarriage, abortion, or invasive procedures such as IVS or amniocentesis, in cases where Rh-positive fetal cells enter the maternal bloodstream. The discovery of the Rh system and its role in the development of hemolytic disease of the newborn is an important contribution of genetics to medicine.

Functions. Blood groups are genetically inherited characteristics that do not change during life under natural conditions. A blood group is a specific combination of surface antigens of erythrocytes (agglutinogens) of the ABO system. Determination of group membership is widely used in clinical practice during the transfusion of blood and its components, in gynecology and obstetrics when planning and managing pregnancy. The AB0 blood group system is the main system that determines the compatibility and incompatibility of transfused blood, because its constituent antigens are the most immunogenic. A feature of the AB0 system is that in the plasma of non-immune people there are natural antibodies to an antigen that is absent on red blood cells. The AB0 blood group system consists of two group erythrocyte agglutinogens (A and B) and two corresponding antibodies - plasma agglutinins alpha (anti-A) and beta (anti-B). Various combinations of antigens and antibodies form 4 blood groups:

• Group 0(I) - there are no group agglutinogens on red blood cells, alpha and beta agglutinins are present in the plasma.
• Group A (II) - red blood cells contain only agglutinogen A, agglutinin beta is present in the plasma;
• Group B (III) - red blood cells contain only agglutinogen B, plasma contains agglutinin alpha;
• Group AB (IV) - antigens A and B are present on red blood cells, plasma does not contain agglutinins.

Determination of blood groups is carried out by identifying specific antigens and antibodies (double method, or cross reaction).

Blood incompatibility is observed if the red blood cells of one blood carry agglutinogens (A or B), and the plasma of another blood contains the corresponding agglutinins (alpha or beta), and an agglutination reaction occurs.

Transfusion of red blood cells, plasma and especially whole blood from a donor to a recipient must be strictly observed in group compatibility. To avoid incompatibility between the blood of the donor and the recipient, it is necessary to accurately determine their blood groups using laboratory methods. It is best to transfuse blood, red blood cells and plasma of the same group as determined for the recipient. In emergency cases, group 0 red blood cells (but not whole blood!) can be transfused into recipients with other blood groups; Group A red blood cells can be transfused into recipients with blood group A and AB, and red blood cells from a group B donor can be transfused into group B and AB recipients.

Blood group compatibility cards (agglutination is indicated by a + sign):

Donor blood	Recipient's blood

Donor's red blood cells	Recipient's blood

Group agglutinogens are found in the stroma and membrane of erythrocytes. Antigens of the ABO system are detected not only on red blood cells, but also on cells of other tissues or can even be dissolved in saliva and other body fluids. They develop in the early stages of intrauterine development, and are already found in significant quantities in the newborn. The blood of newborn children has age-related characteristics - characteristic group agglutinins may not yet be present in the plasma, which begin to be produced later (constantly detected after 10 months) and the determination of the blood group in newborns in this case is carried out only by the presence of antigens of the ABO system.

In addition to situations involving the need for blood transfusion, determination of blood type, Rh factor, and the presence of alloimmune anti-erythrocyte antibodies should be carried out during planning or during pregnancy to identify the likelihood of an immunological conflict between mother and child, which can lead to hemolytic disease of the newborn.

Hemolytic disease of the newborn

Hemolytic jaundice of newborns, caused by an immunological conflict between mother and fetus due to incompatibility of erythrocyte antigens. The disease is caused by incompatibility of the fetus and mother for D-Rhesus or ABO antigens, less often there is incompatibility for other Rhesus (C, E, c, d, e) or M-, M-, Kell-, Duffy-, Kidd- antigens. Any of these antigens (usually D-Rh antigen), penetrating into the blood of a Rh-negative mother, causes the formation of specific antibodies in her body. The latter enter the fetal blood through the placenta, where they destroy the corresponding antigen-containing red blood cells. Predispose to the development of hemolytic disease of the newborn is impaired placental permeability, repeated pregnancies and blood transfusions to a woman without taking into account the Rh factor, etc. With early manifestations of the disease, an immunological conflict can be the cause of premature birth or miscarriages.

There are varieties (weak variants) of antigen A (to a greater extent) and less frequently of antigen B. As for antigen A, there are options: “strong” A1 (more than 80%), weak A2 (less than 20%), and even weaker ones (A3 , A4, Ah - rarely). This theoretical concept is important for blood transfusion and can cause accidents when assigning donor A2 (II) to group 0 (I) or donor A2B (IV) to group B (III), since the weak form of antigen A sometimes causes errors in the determination blood groups of the ABO system. Correct identification of weak A antigen variants may require repeated testing with specific reagents.

A decrease or complete absence of natural agglutinins alpha and beta is sometimes noted in immunodeficiency states:

• neoplasms and blood diseases - Hodgkin's disease, multiple myeloma, chronic lymphatic leukemia;
• congenital hypo- and agammaglobulinemia;
• in young children and the elderly;
• immunosuppressive therapy;
• severe infections.

Difficulties in determining the blood group due to suppression of the hemagglutination reaction also arise after the introduction of plasma substitutes, blood transfusion, transplantation, septicemia, etc.

Inheritance of blood groups

The patterns of inheritance of blood groups are based on the following concepts. There are three possible variants (alleles) at the ABO gene locus - 0, A and B, which are expressed in an autosomal codominant manner. This means that individuals who have inherited genes A and B express the products of both of these genes, resulting in the AB (IV) phenotype. Phenotype A (II) can be present in a person who has inherited from parents either two genes A, or genes A and 0. Accordingly, phenotype B (III) - when inheriting either two genes B, or B and 0. Phenotype 0 (I) appears when inheritance of two genes 0. Thus, if both parents have blood group II (genotypes AA or A0), one of their children may have the first group (genotype 00). If one of the parents has blood type A(II) with a possible genotype AA and A0, and the other has B(III) with a possible genotype BB or B0, children can have blood groups 0(I), A(II), B(III) ) or AB (!V).

• Hemolytic disease of newborns (detection of incompatibility between the blood of mother and fetus according to the AB0 system);
• Preoperative preparation;
• Pregnancy (preparation and follow-up of pregnant women with negative Rh factor)

Preparation for the study: not required

If necessary (detection of the A2 subtype), additional testing is carried out using specific reagents.

Execution time: 1 day

Research result:

• 0 (I) - first group,
• A (II) - second group,
• B (III) - third group,
• AB (IV) - fourth blood group.

When subtypes (weak variants) of group antigens are identified, the result is given with an appropriate comment, for example, “a weakened variant A2 has been identified, individual selection of blood is required.”

Rh factor Rh

The main surface erythrocyte antigen of the Rh system, by which a person’s Rh status is assessed.

Functions. Rh antigen is one of the erythrocyte antigens of the Rh system, located on the surface of erythrocytes. There are 5 main antigens in the Rh system. The main (most immunogenic) antigen is Rh (D), which is usually referred to as the Rh factor. The red blood cells of approximately 85% of people carry this protein, so they are classified as Rh positive (positive). 15% of people do not have it and are Rh negative (Rh negative). The presence of the Rh factor does not depend on group membership according to the AB0 system, does not change throughout life, and does not depend on external reasons. It appears in the early stages of intrauterine development, and is already found in a significant amount in the newborn. Determination of Rh blood is used in general clinical practice during transfusion of blood and its components, as well as in gynecology and obstetrics when planning and managing pregnancy.

Incompatibility of blood according to the Rh factor (Rh conflict) during blood transfusion is observed if the donor's red blood cells carry Rh agglutinogen, and the recipient is Rh negative. In this case, the Rh-negative recipient begins to produce antibodies directed against the Rh antigen, leading to the destruction of red blood cells. Transfusion of red blood cells, plasma and especially whole blood from a donor to a recipient must be strictly observed compatibility not only with blood type, but also with Rh factor. The presence and titer of antibodies to the Rh factor and other alloimmune antibodies already present in the blood can be determined by specifying the “anti-Rh (titer)” test.

Determination of blood type, Rh factor, and the presence of alloimmune anti-erythrocyte antibodies should be carried out when planning or during pregnancy to identify the likelihood of an immunological conflict between mother and child, which can lead to hemolytic disease of the newborn. The occurrence of Rh conflict and the development of hemolytic disease of newborns is possible if the pregnant woman is Rh negative and the fetus is Rh positive. If the mother is Rh + and the fetus is Rh negative, there is no danger of hemolytic disease for the fetus.

Hemolytic disease of the fetus and newborns- hemolytic jaundice of newborns, caused by an immunological conflict between mother and fetus due to incompatibility of erythrocyte antigens. The disease can be caused by incompatibility of the fetus and mother for D-Rhesus or ABO antigens, less often there is incompatibility for other Rhesus (C, E, c, d, e) or M-, N-, Kell-, Duffy-, Kidd antigens (according to statistics, 98% of cases of hemolytic disease of newborns are associated with D - Rh antigen). Any of these antigens, penetrating into the blood of a Rh-negative mother, causes the formation of specific antibodies in her body. The latter enter the fetal blood through the placenta, where they destroy the corresponding antigen-containing red blood cells. Predisposition to the development of hemolytic disease of newborns is impaired placental permeability, repeated pregnancies and blood transfusions to a woman without taking into account the Rh factor, etc. With early manifestations of the disease, an immunological conflict can cause premature birth or repeated miscarriages.

Currently, there is a possibility of medical prevention of the development of Rh conflict and hemolytic disease of newborns. All Rh-negative women during pregnancy should be under medical supervision. It is also necessary to monitor the level of Rh antibodies over time.

There is a small category of Rh-positive individuals who are able to form anti-Rh antibodies. These are individuals whose red blood cells are characterized by significantly reduced expression of the normal Rh antigen on the membrane (“weak” D, Dweak) or expression of an altered Rh antigen (partial D, Dpartial). In laboratory practice, these weak variants of the D antigen are combined into the Du group, the frequency of which is about 1%.

Recipients containing Du antigen should be classified as Rh-negative and should be transfused only with Rh-negative blood, since normal D antigen can cause an immune response in such individuals. Donors with the Du antigen qualify as Rh-positive donors, since transfusion of their blood can cause an immune response in Rh-negative recipients, and in the case of previous sensitization to the D antigen, severe transfusion reactions.

Inheritance of the Rh blood factor.

The laws of inheritance are based on the following concepts. The gene encoding the Rh factor D (Rh) is dominant, the allelic gene d is recessive (Rh-positive people can have the DD or Dd genotype, Rh-negative people can only have the dd genotype). A person receives 1 gene from each parent - D or d, and thus has 3 genotype options - DD, Dd or dd. In the first two cases (DD and Dd), a blood test for Rh factor will give a positive result. Only with the dd genotype will a person have Rh negative blood.

Let's consider some variants of the combination of genes that determine the presence of the Rh factor in parents and children

• 1) The father is Rh positive (homozygote, genotype DD), the mother is Rh negative (genotype dd). In this case, all children will be Rh positive (100% probability).
• 2) The father is Rh positive (heterozygote, genotype Dd), the mother is Rh negative (genotype dd). In this case, the probability of having a child with negative or positive Rh is the same and equal to 50%.
• 3) The father and mother are heterozygotes for this gene (Dd), both are Rh positive. In this case, it is possible (with a probability of about 25%) to give birth to a child with negative Rh.

Indications for the purpose of analysis:

• Determination of transfusion compatibility;
• Hemolytic disease of newborns (detection of incompatibility of the blood of mother and fetus according to the Rh factor);
• Preoperative preparation;
• Pregnancy (prevention of Rh conflict).

Preparation for the study: not required.

Material for research: whole blood (with EDTA)

Determination method: Filtration of blood samples through a gel impregnated with monoclonal reagents - agglutination + gel filtration (cards, crossover method).

Execution time: 1 day

Interpretation of results:

The result is given in the form:
Rh + positive Rh - negative
When weak subtypes of antigen D (Du) are detected, a comment is issued: “a weak Rh antigen (Du) has been detected, it is recommended to transfuse Rh-negative blood if necessary.”

Anti-Rh (alloimmune antibodies to the Rh factor and other erythrocyte antigens)

Antibodies to the clinically most important erythrocyte antigens, primarily the Rh factor, indicating the body's sensitization to these antigens.

Functions. Rh antibodies belong to the so-called alloimmune antibodies. Alloimmune anti-erythrocyte antibodies (to the Rh factor or other erythrocyte antigens) appear in the blood under special conditions - after a transfusion of immunologically incompatible donor blood or during pregnancy, when fetal red blood cells carrying paternal antigens that are immunologically foreign to the mother penetrate through the placenta into the woman’s blood. Non-immune Rh-negative people do not have antibodies to the Rh factor. In the Rh system, there are 5 main antigens, the main (most immunogenic) is antigen D (Rh), which is usually referred to as the Rh factor. In addition to the Rh system antigens, there are a number of clinically important erythrocyte antigens to which sensitization can occur, causing complications during blood transfusion. The method of screening blood for the presence of alloimmune anti-erythrocyte antibodies, used in INVITRO, allows, in addition to antibodies to the Rh factor RH1(D), to detect alloimmune antibodies to other erythrocyte antigens in the test serum.

The gene encoding the Rh factor D (Rh) is dominant, the allelic gene d is recessive (Rh-positive people can have the DD or Dd genotype, Rh-negative people can only have the dd genotype). During pregnancy of a Rh-negative woman with a Rh-positive fetus, the development of an immunological conflict between mother and fetus due to the Rh factor is possible. Rh conflict can lead to miscarriage or the development of hemolytic disease of the fetus and newborns. Therefore, determination of blood type, Rh factor, as well as the presence of alloimmune anti-erythrocyte antibodies should be carried out when planning or during pregnancy to identify the likelihood of an immunological conflict between mother and child. The occurrence of Rh conflict and the development of hemolytic disease of newborns is possible if the pregnant woman is Rh negative and the fetus is Rh positive. If the mother has a positive Rh antigen and the fetus is negative, a conflict regarding the Rh factor does not develop. The incidence of Rh incompatibility is 1 case in 200-250 births.

Hemolytic disease of the fetus and newborns is hemolytic jaundice of newborns, caused by an immunological conflict between mother and fetus due to incompatibility of erythrocyte antigens. The disease is caused by incompatibility of the fetus and mother for D-Rhesus or ABO (group) antigens, less often there is incompatibility for other Rhesus (C, E, c, d, e) or M-, M-, Kell-, Duffy- , Kidd antigens. Any of these antigens (usually D-Rh antigen), penetrating into the blood of a Rh-negative mother, causes the formation of specific antibodies in her body. The penetration of antigens into the maternal bloodstream is facilitated by infectious factors that increase the permeability of the placenta, minor injuries, hemorrhages and other damage to the placenta. The latter enter the fetal blood through the placenta, where they destroy the corresponding antigen-containing red blood cells. Predisposition to the development of hemolytic disease of newborns is impaired placental permeability, repeated pregnancies and blood transfusions to a woman without taking into account the Rh factor, etc. With early manifestations of the disease, an immunological conflict can cause premature birth or miscarriages.

During the first pregnancy with a Rh-positive fetus, a pregnant woman with Rh "-" has a 10-15% risk of developing a Rh conflict. The first meeting of the mother's body with a foreign antigen occurs, the accumulation of antibodies occurs gradually, starting from approximately 7-8 weeks of pregnancy. The risk of incompatibility increases with each subsequent pregnancy with a Rh-positive fetus, regardless of how it ended (induced abortion, miscarriage or childbirth, surgery for an ectopic pregnancy), with bleeding during the first pregnancy, with manual separation of the placenta, and also if childbirth is carried out by caesarean section or accompanied by significant blood loss. with transfusions of Rh-positive blood (if they were carried out even in childhood). If a subsequent pregnancy develops with an Rh-negative fetus, incompatibility does not develop.

All pregnant women with Rh "-" are placed on special registration in the antenatal clinic and dynamic monitoring of the level of Rh antibodies is carried out. For the first time, an antibody test must be taken from the 8th to the 20th week of pregnancy, and then periodically check the antibody titer: once a month until the 30th week of pregnancy, twice a month until the 36th week and once a week until the 36th week. Termination of pregnancy at less than 6-7 weeks may not lead to the formation of Rh antibodies in the mother. In this case, during a subsequent pregnancy, if the fetus has a positive Rh factor, the probability of developing immunological incompatibility will again be 10-15%.

Testing for alloimmune anti-erythrocyte antibodies is also important in general preoperative preparation, especially for people who have previously received blood transfusions.

Indications for the purpose of analysis:

• Pregnancy (prevention of Rh conflict);
• Monitoring of pregnant women with negative Rh factor;
• Miscarriage;
• Hemolytic disease of newborns;
• Preparation for blood transfusion.

Preparation for the study: not required.
Material for research: whole blood (with EDTA)

Determination method: agglutination + gel filtration method (cards). Incubation of standard typed erythrocytes with the test serum and filtration by centrifugation of the mixture through a gel impregnated with a polyspecific antiglobilin reagent. Agglutinated red blood cells are detected on the surface of the gel or in its thickness.

The method uses suspensions of erythrocytes from group 0(1) donors, typed according to erythrocyte antigens RH1(D), RH2(C), RH8(Cw), RH3(E), RH4(c), RH5(e), KEL1( K), KEL2(k), FY1(Fy a) FY2(Fy b), JK (Jk a), JK2(Jk b), LU1 (Lu a), LU2 (LU b), LE1 (LE a), LE2 (LE b), MNS1(M), MNS2 (N), MNS3 (S), MNS4(s), P1 (P).

Execution time: 1 day

When alloimmune anti-erythrocyte antibodies are detected, their semi-quantitative determination is carried out.
The result is given in titers (the maximum dilution of the serum at which a positive result is still detected).

Units of measurement and conversion factors: U/ml

Reference values: negative.

Positive result: Sensitization to Rh antigen or other erythrocyte antigens.

Some life situations (upcoming surgery, pregnancy, desire to become a donor, etc.) require an analysis, which we are accustomed to simply calling “blood type.” Meanwhile, in the broad understanding of this term, there is some inaccuracy here, since most of us mean the well-known erythrocyte AB0 system, described in 1901 by Landsteiner, but do not know about it and therefore say “blood test for group”, thus separating another important system.

Karl Landsteiner, who was awarded the Nobel Prize for this discovery, continued to work throughout his life on the search for other antigens located on the surface of red blood cells, and in 1940 the world learned about the existence of the Rhesus system, which ranks second in importance. In addition, scientists in 1927 found protein substances isolated in the erythrocyte systems - MNs and Pp. At that time, this was a huge breakthrough in medicine, because people suspected that it could lead to the death of the body, and that someone else’s blood could save a life, so they attempted to transfuse it from animals to humans and from humans to humans. Unfortunately, success did not always come, but science has confidently moved forward to the present day We only talk about blood group out of habit, meaning the AB0 system.

What is a blood type and how did it become known?

Determination of blood group is based on the classification of genetically determined individually specific proteins of all tissues of the human body. These organ-specific protein structures are called antigens(alloantigens, isoantigens), but they should not be confused with antigens specific to certain pathological formations (tumors) or proteins that cause infections that enter the body from the outside.

The antigenic set of tissues (and blood, of course), given from birth, determines the biological individuality of a particular individual, which can be a person, any animal, or a microorganism, that is, isoantigens characterize group-specific characteristics that make it possible to distinguish these individuals within their species.

The alloantigenic properties of our tissues began to be studied by Karl Landsteiner, who mixed the blood (erythrocytes) of people with the sera of other people and noticed that in some cases, red blood cells stick together (agglutination), while in others the color remains homogeneous. True, at first the scientist found 3 groups (A, B, C), the 4th blood group (AB) was discovered later by the Czech Jan Jansky. In 1915, the first standard sera containing specific antibodies (agglutinins) that determine group affiliation were already obtained in England and America. In Russia, the blood group according to the AB0 system began to be determined in 1919, but digital designations (1, 2, 3, 4) were introduced into practice in 1921, and a little later they began to use alphanumeric nomenclature, where antigens were designated by Latin letters (A and B), and antibodies - Greek (α and β).

It turns out there are so many of them...

To date, immunohematology has been replenished with more than 250 antigens located on erythrocytes. The main erythrocyte antigen systems include:

These systems, in addition to transfusiology (blood transfusion), where the main role still belongs to AB0 and Rh, most often remind of themselves in obstetric practice(miscarriages, stillbirths, birth of children with severe hemolytic disease), however, it is not always possible to determine erythrocyte antigens of many systems (except AB0, Rh), which is due to the lack of typing sera, the obtaining of which requires large material and labor costs. Thus, when we talk about blood groups 1, 2, 3, 4, we mean the main antigenic system of erythrocytes, called the AB0 system.

Table: possible combinations of AB0 and Rh (blood groups and Rh factors)

In addition, approximately from the middle of the last century, antigens began to be discovered one after another:

1. Platelets, which in most cases repeated the antigenic determinants of erythrocytes, but with a lesser degree of severity, which makes it difficult to determine the blood group on platelets;
2. Nuclear cells, primarily lymphocytes (HLA - histocompatibility system), which have opened up wide opportunities for organ and tissue transplantation and solving some genetic problems (hereditary predisposition to a certain pathology);
3. Plasma proteins (the number of described genetic systems has already exceeded a dozen).

The discoveries of many genetically determined structures (antigens) made it possible not only to take a different approach to determining the blood group, but also to strengthen the position of clinical immunohematology in terms of combating various pathological processes, made it possible to safely, as well as transplant organs and tissues.

Main system dividing people into 4 groups

The group affiliation of erythrocytes depends on group-specific antigens A and B (agglutinogens):

• Containing protein and polysaccharides;
• Closely associated with the stroma of red blood cells;
• Not related to hemoglobin, which is not involved in any way in the agglutination reaction.

By the way, agglutinogens can be found on other blood cells (platelets, leukocytes) or in tissues and body fluids (saliva, tears, amniotic fluid), where they are detected in much smaller quantities.

Thus, antigens A and B can be found on the stroma of a particular person’s red blood cells(together or separately, but always forming a pair, for example, AB, AA, A0 or BB, B0) or they cannot be found there at all (00).

In addition, globulin fractions (agglutinins α and β) float in the blood plasma. compatible with the antigen (A with β, B with α), called natural antibodies.

Obviously, in the first group, which does not contain antigens, both types of group antibodies will be present - α and β. In the fourth group, normally there should not be any natural globulin fractions, because if this is allowed, antigens and antibodies will begin to stick together: α will agglutinate (glue) A, and β, respectively, B.

Depending on combinations of options and the presence of certain antigens and antibodies, the group affiliation of human blood can be represented in the following form:

• 1 blood group 0αβ(I): antigens – 00(I), antibodies – α and β;
• Blood group 2 Aβ(II): antigens – AA or A0(II), antibodies – β;
• Blood group 3 Bα(III): antigens – BB or B0(III), antibodies – α
• 4 blood group AB0(IV): antigens only A and B, no antibodies.

The reader may be surprised to learn that there is a blood type that does not fit this classification . It was discovered in 1952 by a Bombay resident, which is why it is called “Bombay”. Antigenic-serological variant of red blood cells type « Bombay» does not contain antigens of the AB0 system, and in the serum of such people, along with natural antibodies α and β, anti-H are detected(antibodies directed at substance H, differentiating antigens A and B and preventing their presence on the stroma of red blood cells). Subsequently, “Bombay” and other rare types of group affiliation were found in different parts of the planet. Of course, you cannot envy such people, because in the event of massive blood loss, they need to look for a life-saving environment all over the globe.

Ignorance of the laws of genetics can cause tragedy in the family

The blood group of each person according to the AB0 system is the result of inheriting one antigen from the mother and another from the father. Receiving hereditary information from both parents, a person in his phenotype has half of each of them, that is, the blood group of the parents and the child is a combination of two characteristics, and therefore may not coincide with the blood group of the father or mother.

Discrepancies between the blood groups of parents and the child give rise to doubts and suspicions of their spouse’s infidelity in the minds of some men. This happens due to the lack of basic knowledge of the laws of nature and genetics, therefore, in order to avoid tragic mistakes on the part of the male sex, whose ignorance often breaks happy family relationships, we consider it necessary to once again explain where a child’s blood group according to the AB0 system comes from and give examples of expected results.

Option 1. If both parents have blood type O: 00(I) x 00(I), then the child will only have the first 0(I) group, all others are excluded. This happens because the genes that synthesize antigens of the first blood group - recessive, they can only manifest themselves in homozygous a state when no other gene (dominant) is suppressed.

Option 2. Both parents have the second group A (II). However, it can be either homozygous, when two characters are the same and dominant (AA), or heterozygous, represented by a dominant and recessive variant (A0), so the following combinations are possible here:

• AA(II) x AA(II) → AA(II);
• AA(II) x A0(II) → AA(II);
• A0(II) x A0(II) → AA(II), A0(II), 00(I), that is, with such a combination of parental phenotypes, both the first and second groups are probable, third and fourth are excluded.

Option 3. One of the parents has the first group 0(I), the other has the second:

• AA(II) x 00(I) → A0(II);
• A0(II) x 00(I) → A0 (II), 00(I).

Possible groups for a child are A(II) and 0(I), excluded – B(III) and AB(IV).

Option 4. In the case of a combination of two third groups inheritance will go according to option 2: possible membership would be the third or first group, whereas the second and fourth will be excluded.

Option 5. When one of the parents has the first group, and the second the third, inheritance is similar option 3– the child has possible B(III) and 0(I), but excluded A(II) and AB(IV) .

Option 6. Parent groups A(II) and B(III ) when inherited, they can give any group affiliation of the AB0 system(1, 2, 3, 4). The emergence of 4 blood groups is an example codominant inheritance when both antigens in the phenotype are equal and equally manifest themselves as a new trait (A + B = AB):

• AA(II) x BB(III) → AB(IV);
• A0(II) x B0(III) → AB(IV), 00(I), A0(II), B0(III);
• A0(II) x BB(III) → AB(IV), B0(III);
• B0(III) x AA(II) → AB(IV), A0(II).

Option 7. When combining the second and fourth groups possible for parents second, third and fourth groups in a child, the first one is excluded:

• AA(II) x AB(IV) → AA(II), AB(IV);
• A0(II) x AB(IV) → AA(II), A0(II), B0(III), AB(IV).

Option 8. A similar situation arises in the case of a combination of the third and fourth groups: A(II), B(III) and AB(IV) will be possible, and the first is excluded.

• BB (III) x AB (IV) → BB (III), AB (IV);
• B0(III) x AB(IV) → A0(II), ВB(III), B0(III), AB(IV).

Option 9 – most interesting. Parents have blood groups 1 and 4 as a result, the child develops a second or third blood group, but never – first and fourth:

• AB(IV) x 00(I);
• A + 0 = A0(II);
• B + 0 = B0 (III).

Table: child’s blood type based on parents’ blood groups

Obviously, the statement that parents and children have the same group membership is a fallacy, because genetics obeys its own laws. As for determining the child’s blood type based on the group affiliation of the parents, this is only possible if the parents have the first group, that is, in this case, the appearance of A (II) or B (III) will exclude biological paternity or motherhood. The combination of the fourth and first groups will lead to the emergence of new phenotypic characteristics (group 2 or 3), while the old ones will be lost.

Boy, girl, group compatibility

If in the old days, for the birth of an heir in the family, the reins were placed under the pillow, but now everything is put on an almost scientific basis. Trying to deceive nature and “order” the sex of the child in advance, future parents perform simple arithmetic operations: divide the father’s age by 4, and the mother’s by 3, whoever has the larger remainder wins. Sometimes this coincides, and sometimes it disappoints, so what is the probability of getting the desired gender using calculations - official medicine does not comment, so it is up to everyone to calculate or not, but the method is painless and absolutely harmless. You can try, what if you get lucky?

for reference: what really affects the gender of the child is the combination of X and Y chromosomes

But the compatibility of the parents’ blood type is a completely different matter, not in terms of the child’s gender, but in the sense of whether he will be born at all. The formation of immune antibodies (anti-A and anti-B), although rare, can interfere with the normal course of pregnancy (IgG) and even breastfeeding (IgA). Fortunately, the AB0 system does not interfere with reproduction processes so often, which cannot be said about the Rh factor. It can cause miscarriage or the birth of babies with, the best consequence of which is deafness, and in the worst case, the child cannot be saved at all.

Group affiliation and pregnancy

Determination of blood group according to the AB0 and Rhesus (Rh) systems is a mandatory procedure when registering for pregnancy.

In the case of a negative Rh factor in the expectant mother and the same result in the future father of the child, there is no need to worry, since the baby will also have a negative Rh factor.

A “negative” woman should not immediately panic when first(abortions and miscarriages are also considered) pregnancy. Unlike the AB0 (α, β) system, the Rhesus system does not have natural antibodies, so the body only recognizes “foreign”, but does not react to it in any way. Immunization will occur during childbirth, therefore, so that the woman’s body does not “remember” the presence of foreign antigens (Rh factor is positive), a special anti-Rhesus serum is administered to the postpartum woman on the first day after birth, protecting subsequent pregnancies. In the case of strong immunization of a “negative” woman with a “positive” antigen (Rh+), compatibility for conception is in great question, therefore, despite long-term treatment, the woman is plagued by failures (miscarriages). A woman’s body, which has a negative Rhesus, having once “remembered” someone else’s protein (“memory cell”), will respond with the active production of immune antibodies during subsequent meetings (pregnancy) and will in every possible way reject it, that is, its own desired and long-awaited child, if it turns out to be positive Rh factor.

Compatibility for conception should sometimes be kept in mind in relation to other systems. By the way, AB0 is quite loyal to the presence of strangers and rarely gives immunization. However, there are known cases of the emergence of immune antibodies in women during ABO-incompatible pregnancy, when a damaged placenta allows fetal red blood cells to enter the mother’s blood. It is generally accepted that women are most likely to be isoimmunized by vaccinations (DTP), which contain group-specific substances of animal origin. First of all, this feature was noticed in substance A.

Probably, second place after the Rhesus system in this regard can be given to the histocompatibility system (HLA), and then - Kell. In general, each of them is capable of sometimes presenting a surprise. This happens because the body of a woman who has a close relationship with a certain man, even without pregnancy, reacts to his antigens and produces antibodies. This process is called sensitization. The only question is to what level sensitization will reach, which depends on the concentration of immunoglobulins and the formation of antigen-antibody complexes. With a high titer of immune antibodies, compatibility for conception is in great doubt. Rather, we will be talking about incompatibility, which requires enormous efforts of doctors (immunologists, gynecologists), unfortunately, often in vain. A decrease in titer over time is also of little reassurance; the “memory cell” knows its task...

Video: pregnancy, blood type and Rh conflict

Compatible blood transfusion

In addition to compatibility for conception, no less important is transfusion compatible, where the ABO system plays a dominant role (transfusion of blood incompatible with the ABO system is very dangerous and can lead to death!). Often a person believes that the 1st (2, 3, 4) blood group of him and his neighbor must necessarily be the same, that the first will always suit the first, the second - the second, and so on, and in case of certain circumstances they (neighbors) can help each other to a friend. It would seem that a recipient with blood group 2 should accept a donor of the same group, but this is not always the case. The thing is that antigens A and B have their own varieties. For example, antigen A has the most allospecific variants (A 1, A 2, A 3, A 4, A 0, A X, etc.), but B is slightly inferior (B 1, B X, B 3, B weak, etc. .), that is, it turns out that these options may simply not be compatible, even though when testing blood for group the result will be A (II) or B (III). Thus, taking into account such heterogeneity, one can imagine how many varieties a blood group 4 can have, containing both A and B antigens?

The statement that blood type 1 is the best, as it suits everyone without exception, and blood type 4 can accept anyone, is also outdated. For example, some people with blood type 1 are for some reason called “dangerous” universal donors. And the danger lies in the fact that without having antigens A and B on their erythrocytes, the plasma of these people contains a large titer of natural antibodies α and β, which, entering the bloodstream of the recipient of other groups (except the first), begin to agglutinate the antigens located there (A and/or IN).

compatibility of blood groups during transfusion

Currently, transfusions of mixed blood groups are not practiced, with the exception of only some cases of transfusions that require special selection. Then the first Rh-negative blood group is considered universal, the red blood cells of which are washed 3 or 5 times to avoid immunological reactions. The first blood group with positive Rh can be universal only in relation to Rh(+) red blood cells, that is, after determining for compatibility and washing of red blood cells can be transfused to a Rh-positive recipient with any group of the AB0 system.

The most common group in the European territory of the Russian Federation is considered to be the second - A (II), Rh (+), the rarest is blood group 4 with negative Rh. In blood banks, the attitude towards the latter is especially reverent, because a person with a similar antigenic composition should not die just because, if necessary, they will not find the required amount of red blood cells or plasma. By the way, plasmaAB(IV) Rh(-) is suitable for absolutely everyone, since it contains nothing (0), but this question is never considered due to the rare occurrence of blood group 4 with negative Rhesus.

How is blood type determined?

Blood group determination according to the AB0 system can be done by taking a drop from your finger. By the way, every health worker who has a diploma of higher or secondary medical education should be able to do this, regardless of their profile. As for other systems (Rh, HLA, Kell), a blood test for the group is taken from a vein and, following the procedure, the affiliation is determined. Such studies are already within the competence of a laboratory diagnostics physician, and immunological typing of organs and tissues (HLA) generally requires special training.

A blood group test is done using standard serums, manufactured in special laboratories and meeting certain requirements (specificity, titer, activity), or using zoliclones, obtained in the factory. In this way, the group affiliation of red blood cells is determined ( direct method). To eliminate errors and gain complete confidence in the reliability of the results obtained, the blood type is determined at blood transfusion stations or in the laboratories of surgical and, especially, obstetric hospitals cross method, where serum is used as the test sample, and specially selected standard red blood cells go as a reagent. By the way, In newborns, it is very difficult to determine group affiliation using a cross-sectional method; although agglutinins α and β are called natural antibodies (given from birth), they begin to be synthesized only from six months and accumulate by 6-8 years.

Blood type and character

Does blood type affect character and is it possible to predict in advance what can be expected from a one-year-old pink-cheeked toddler in the future? Official medicine considers group affiliation from such a perspective with little or no attention paid to these issues. A person has many genes, as well as group systems, so one can hardly expect the fulfillment of all the predictions of astrologers and determine the character of a person in advance. However, some coincidences cannot be ruled out, because some predictions do come true.

prevalence of blood groups in the world and the characters attributed to them

So, astrology says that:

1. Carriers of the first blood group are brave, strong, purposeful people. Leaders by nature, possessing irrepressible energy, they not only achieve great heights themselves, but also carry others along with them, that is, they are wonderful organizers. At the same time, their character is not without negative traits: they can suddenly flare up and show aggression in a fit of anger.
2. The second blood group are people who are patient, balanced, calm, slightly shy, empathetic and taking everything to heart. They are distinguished by homeliness, thriftiness, the desire for comfort and coziness, however, stubbornness, self-criticism and conservatism interfere with solving many professional and everyday problems.
3. The third blood type suggests a search for the unknown, a creative impulse, harmonious development, communication skills. With such a character, he could move mountains, but bad luck - poor tolerance of routine and monotony does not allow this. Holders of group B (III) quickly change their mood, show inconsistency in their views, judgments, and actions, and dream a lot, which prevents them from achieving their intended goal. And their goals change quickly...
4. With regard to individuals with the fourth blood group, astrologers do not support the version of some psychiatrists who claim that among its owners there are the most maniacs. People who study the stars agree that the 4th group has collected the best features of the previous ones, and therefore has a particularly good character. Leaders, organizers, with enviable intuition and sociability, representatives of the AB (IV) group, at the same time, are indecisive, contradictory and original, their mind is constantly fighting with their heart, but on which side will victory be a big question mark.

Of course, the reader understands that all this is very approximate, because people are so different. Even identical twins show some kind of individuality, at least in character.

Nutrition and diet by blood type

The concept of a blood group diet owes its appearance to the American Peter D’Adamo, who at the end of the last century (1996) published a book with recommendations for proper nutrition depending on group affiliation according to the AB0 system. At the same time, this fashion trend penetrated into Russia and was classified as alternative.

According to the vast majority of doctors with medical education, this direction is unscientific and contradicts established ideas based on numerous studies. The author shares the view of official medicine, so the reader has the right to choose who to believe.

• The statement that at first all people had only the first group, its owners “hunters living in a cave”, mandatory meat eaters having a healthy digestive tract can be safely questioned. Group substances A and B were identified in preserved tissues of mummies (Egypt, America), which are more than 5000 years old. Proponents of the concept of “Eat Right for Your Type” (the title of D’Adamo’s book) do not point out that the presence of O(I) antigens is considered a risk factor for diseases of the stomach and intestines(peptic ulcer), in addition, carriers of this group more often than others have problems with blood pressure ( ).
• Holders of the second group were recognized as clean by Mr. D’Adamo vegetarians. Considering that this group affiliation is prevalent in Europe and in some areas reaches 70%, one can imagine the outcome of mass vegetarianism. Probably, mental hospitals will be overcrowded, because modern man is an established predator.

Unfortunately, the blood group A(II) diet does not draw the attention of those interested to the fact that people with this antigenic composition of erythrocytes make up the majority of patients , . It happens to them more often than others. So maybe a person should work in this direction? Or at least keep in mind the risk of such problems?

Food for thought

An interesting question: when should a person switch to the recommended blood type diet? From birth? During puberty? In the golden years of youth? Or when old age comes knocking? Here you have the right to choose, we just want to remind you that children and adolescents cannot be deprived of essential microelements and vitamins, you cannot prefer one and ignore the other.

Young people like some things and don’t like others, but if a healthy person is ready, only after reaching adulthood, to follow all dietary recommendations in accordance with their group affiliation, then this is his right. I would just like to note that, in addition to the antigens of the AB0 system, there are other antigenic phenotypes that exist in parallel, but also contribute to the life of the human body. Ignore them or keep them in mind? Then diets also need to be developed for them, and it is not a fact that they will coincide with current trends promoting healthy eating for certain categories of people with one or another group affiliation. For example, the leukocyte HLA system is more closely associated with various diseases than others; it can be used to calculate in advance a hereditary predisposition to a particular pathology. So why not engage in just such, more realistic prevention immediately with the help of food?

Video: the secrets of human blood groups