Hemolytic disease of the newborn (ABO)

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ABO HDN
Specialty Hematology/pediatrics

In ABO hemolytic disease of the newborn (also known as ABO HDN) maternal IgG antibodies with specificity for the ABO blood group system pass through the placenta to the fetal circulation where they can cause hemolysis of fetal red blood cells which can lead to fetal anemia and HDN. In contrast to Rh disease, about half of the cases of ABO HDN occur in a firstborn baby and ABO HDN does not become more severe after further pregnancies.[ citation needed ]

Contents

The ABO blood group system is the best known surface antigen system, expressed on a wide variety of human cells. For Caucasian populations about one fifth of all pregnancies have ABO incompatibility between the fetus and the mother, but only a very small minority develop symptomatic ABO HDN. [1] The latter typically only occurs in mothers of blood group O, because they can produce enough IgG antibodies to cause hemolysis.[ citation needed ]

Although very uncommon, cases of ABO HDN have been reported in infants born to mothers with blood groups A [2] [3] and B. [4]

Presentation

Complications

Causes

Environmental exposure
Anti-A and anti-B antibodies are usually IgM and do not pass through the placenta, but some mothers "naturally" have IgG anti-A or IgG anti-B antibodies, which can pass through the placenta. Exposure to A-antigens and B-antigens, which are both widespread in nature, usually leads to the production of IgM anti-A and IgM anti-B antibodies but occasionally IgG antibodies are produced.[ citation needed ]
Fetal-maternal transfusion
Some mothers may be sensitized by fetal-maternal transfusion of ABO incompatible red blood and produce immune IgG antibodies against the antigen they do not have and their baby does. For example, when a mother of genotype OO (blood group O) carries a fetus of genotype AO (blood group A) she may produce IgG anti-A antibodies. The father will either have blood group A, with genotype AA or AO or, more rarely, have blood group AB, with genotype AB.[ citation needed ]
Blood transfusion
It would be very rare for ABO sensitization to be due to therapeutic blood transfusion as a great deal of effort and checking is done to ensure that blood is ABO compatible between the recipient and the donor.[ citation needed ]

Risk factors

In about a third of all ABO incompatible pregnancies maternal IgG anti-A or IgG anti-B antibodies pass through the placenta to the fetal circulation leading to a weakly positive direct Coombs test for the neonate's blood.[ citation needed ] However, ABO HDN is generally mild and short-lived and only occasionally severe because:

Diagnosis

Routine antenatal antibody screening blood tests (indirect Coombs test) do not screen for ABO HDN.[ citation needed ] If IgG anti-A or IgG anti-B antibodies are found in the pregnant woman's blood, they are not reported with the test results, because they do not correlate well with ABO HDN.[ citation needed ] Diagnosis is usually made by investigation of a newborn baby who has developed jaundice during the first week of life.

Testing

Treatment

The antibodies in ABO HDN cause anemia due to destruction of fetal red blood cells and jaundice due to the rise in blood levels of bilirubin a by-product of hemoglobin break down. If the anemia is severe, it can be treated with a blood transfusion, however this is rarely needed. On the other hand, neonates have underdeveloped livers that are unable to process large amounts of bilirubin and a poorly developed blood–brain barrier that is unable to block bilirubin from entering the brain. This can result in kernicterus if left unchecked. If the bilirubin level is sufficiently high as to cause worry, it can be lowered via phototherapy in the first instance or an exchange transfusion if severely elevated.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Blood type</span> Classification of blood based on antibodies and antigens on red blood cell surfaces

A blood type is a classification of blood, based on the presence and absence of antibodies and inherited antigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele and collectively form a blood group system.

Rh disease is a type of hemolytic disease of the fetus and newborn (HDFN). HDFN due to anti-D antibodies is the proper and currently used name for this disease as the Rh blood group system actually has more than 50 antigens and not only the D-antigen. The term "Rh Disease" is commonly used to refer to HDFN due to anti-D antibodies, and prior to the discovery of anti-Rho(D) immune globulin, it was the most common type of HDFN. The disease ranges from mild to severe, and occurs in the second or subsequent pregnancies of Rh-D negative women when the biologic father is Rh-D positive.

<span class="mw-page-title-main">Hemolytic disease of the newborn</span> Fetal and neonatal alloimmune blood condition

Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis, is an alloimmune condition that develops in a fetus at or around birth, when the IgG molecules produced by the mother pass through the placenta. Among these antibodies are some which attack antigens on the red blood cells in the fetal circulation, breaking down and destroying the cells. The fetus can develop reticulocytosis and anemia. The intensity of this fetal disease ranges from mild to very severe, and fetal death from heart failure can occur. When the disease is moderate or severe, many erythroblasts are present in the fetal blood, earning these forms of the disease the name erythroblastosis fetalis.

The direct and indirect Coombs tests, also known as antiglobulin test (AGT), are blood tests used in immunohematology. The direct Coombs test detects antibodies that are stuck to the surface of the red blood cells. Since these antibodies sometimes destroy red blood cells they can cause anemia; this test can help clarify the condition. The indirect Coombs test detects antibodies that are floating freely in the blood. These antibodies could act against certain red blood cells; the test can be carried out to diagnose reactions to a blood transfusion.

<span class="mw-page-title-main">Neonatal jaundice</span> Medical condition

Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. Other symptoms may include excess sleepiness or poor feeding. Complications may include seizures, cerebral palsy, or kernicterus.

Autoimmune hemolytic anemia (AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to an insufficient number of oxygen-carrying red blood cells in the circulation. The lifetime of the RBCs is reduced from the normal 100–120 days to just a few days in serious cases. The intracellular components of the RBCs are released into the circulating blood and into tissues, leading to some of the characteristic symptoms of this condition. The antibodies are usually directed against high-incidence antigens, therefore they also commonly act on allogenic RBCs. AIHA is a relatively rare condition, with an incidence of 5–10 cases per 1 million persons per year in the warm-antibody type and 0.45 to 1.9 cases per 1 million persons per year in the cold antibody type. Autoimmune hemolysis might be a precursor of later onset systemic lupus erythematosus.

Hemolytic disease of the newborn (anti-Kell1) is the second most common cause of severe hemolytic disease of the newborn (HDN) after Rh disease. Anti-Kell1 is becoming relatively more important as prevention of Rh disease is also becoming more effective.

Hemolytic disease of the newborn (anti-Rhc) can range from a mild to a severe disease. It is the third most common cause of severe HDN. Rh disease is the most common and hemolytic disease of the newborn (anti-Kell) is the second most common cause of severe HDN. It occurs more commonly in women who are Rh D negative.

The Kell antigen system is a human blood group system, that is, a group of antigens on the human red blood cell surface which are important determinants of blood type and are targets for autoimmune or alloimmune diseases which destroy red blood cells. The Kell antigens are K, k, Kpa, Kpb, Jsa and Jsb. The Kell antigens are peptides found within the Kell protein, a 93-kilodalton transmembrane zinc-dependent endopeptidase which is responsible for cleaving endothelin-3.

The Kidd antigen system are proteins found in the Kidd's blood group, which act as antigens, i.e., they have the ability to produce antibodies under certain circumstances. The Jk antigen is found on a protein responsible for urea transport in the red blood cells and the kidney. They are important in transfusion medicine. People with two Jk(a) antigens, for instance, may form antibodies against donated blood containing two Jk(b) antigens. This can lead to hemolytic anemia, in which the body destroys the transfused blood, leading to low red blood cell counts. Another disease associated with the Jk antigen is hemolytic disease of the newborn, in which a pregnant woman's body creates antibodies against the blood of her fetus, leading to destruction of the fetal blood cells. Hemolytic disease of the newborn associated with Jk antibodies is typically mild, though fatal cases have been reported.

Hemolytic disease of the newborn (anti-RhE) is caused by the anti-RhE antibody of the Rh blood group system. The anti-RhE antibody can be naturally occurring, or arise following immune sensitization after a blood transfusion or pregnancy.

Type II hypersensitivity, in the Gell and Coombs classification of allergic reactions, is an antibody mediated process in which IgG and IgM antibodies are directed against antigens on cells or extracellular material. This subsequently leads to cell lysis, tissue damage or loss of function through mechanisms such as

  1. complement activation via the classical complement pathway
  2. Antibody-dependent cellular cytotoxicity or
  3. anti-receptor activity.

Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia.

This page is currently under construction.

Neonates are defined as babies up to 28 days after birth. Most extremely preterm babies require at least one red cell transfusion; this is partly due to the amount of blood removed with blood samples compared to the baby's total blood volume and partly due to anemia of prematurity. Most transfusions are given as small volume top-up transfusions to increase the baby's hemoglobin above a certain pre-defined level, or because the baby is unwell due to the anemia. Possible side-effects of anemia in babies can be poor growth, lethargy and episodes of apnea. Exchange blood transfusion is used to treat a rapidly rising bilirubin that does not respond to treatment with phototherapy or intravenous immunoglobulin. This is usually due to hemolytic disease of the newborn, but may also be due to other causes, e.g., G6PD deficiency.

Rh factor testing, also known as Rhesus factor testing, is the procedure of determining the rhesus D status of an individual.

An Intrauterine transfusion (IUT) is a procedure that provides blood to a fetus, most commonly through the umbilical cord. It is used in cases of severe fetal anemia, such as when fetal red blood cells are being destroyed by maternal antibodies. IUTs are performed by perinatologists at hospitals or specialized centers.

<span class="mw-page-title-main">Ruth Darrow</span> American pathologist

Ruth Renter Darrow (1895–1956) was an American pathologist who was the first to identify the cause of hemolytic disease of the newborn (HDN). In 1938, three years prior to the discovery of antibodies against the Rh antigen, Darrow correctly hypothesized that the disease was caused by destruction of red blood cells due to antibodies in the mother's blood. Darrow's research was inspired by her personal experiences with the disease.

<span class="mw-page-title-main">Blood compatibility testing</span> Testing to identify incompatibilities between blood types

Blood compatibility testing is conducted in a medical laboratory to identify potential incompatibilities between blood group systems in blood transfusion. It is also used to diagnose and prevent some complications of pregnancy that can occur when the baby has a different blood group from the mother. Blood compatibility testing includes blood typing, which detects the antigens on red blood cells that determine a person's blood type; testing for unexpected antibodies against blood group antigens ; and, in the case of blood transfusions, mixing the recipient's plasma with the donor's red blood cells to detect incompatibilities (crossmatching). Routine blood typing involves determining the ABO and RhD type, and involves both identification of ABO antigens on red blood cells and identification of ABO antibodies in the plasma. Other blood group antigens may be tested for in specific clinical situations.

Hemolytic jaundice, also known as prehepatic jaundice, is a type of jaundice arising from hemolysis or excessive destruction of red blood cells, when the byproduct bilirubin is not excreted by the hepatic cells quickly enough. Unless the patient is concurrently affected by hepatic dysfunctions or is experiencing hepatocellular damage, the liver does not contribute to this type of jaundice.

References

  1. ↑ "Archived copy". Archived from the original on 2005-03-01. Retrieved 2007-12-09.{{cite web}}: CS1 maint: archived copy as title (link)[ full citation needed ]
  2. ↑ Wang, Michael; Hays, Taru; Ambruso, Dan R.; Silliman, Christopher C.; Dickey, William C. (2005). "Hemolytic disease of the newborn caused by a high titer anti-group B IgG from a group a mother". Pediatric Blood & Cancer. 45 (6): 861–2. doi:10.1002/pbc.20503. PMID   16007582. S2CID   44546304.
  3. ↑ Jeon, H; Calhoun, B; Pothiawala, M; Herschel, M; Baron, B. W. (2000). "Significant ABO hemolytic disease of the newborn in a group B infant with a group A2 mother". Immunohematology. 16 (3): 105–8. doi: 10.21307/immunohematology-2019-587 . PMID   15373613. S2CID   38090703.
  4. ↑ Haque, K. M.; Rahman, M (2000). "An unusual case of ABO-haemolytic disease of the newborn". Bangladesh Medical Research Council Bulletin. 26 (2): 61–4. PMID   11508073.
  5. 1 2 3 4 5 6 Murray, N. A; Roberts, I. A G (2007). "Haemolytic disease of the newborn". Archives of Disease in Childhood: Fetal and Neonatal Edition. 92 (2): F83–8. doi:10.1136/adc.2005.076794. PMC   2675453 . PMID   17337672.
  6. ↑ Shapiro, Steven M (2004). "Definition of the Clinical Spectrum of Kernicterus and Bilirubin-Induced Neurologic Dysfunction (BIND)". Journal of Perinatology. 25 (1): 54–9. doi:10.1038/sj.jp.7211157. PMID   15578034. S2CID   19663259.
  7. ↑ Blair, Eve; Watson, Linda (2006). "Epidemiology of cerebral palsy". Seminars in Fetal and Neonatal Medicine. 11 (2): 117–25. doi:10.1016/j.siny.2005.10.010. PMID   16338186.
  8. ↑ Lande, Lottie (1948). "Clinical signs and development of survivors of kernicterus due to Rh sensitization". The Journal of Pediatrics. 32 (6): 693–705. doi:10.1016/S0022-3476(48)80225-8. PMID   18866937.
  9. 1 2 3 4 Koenig, J. M.; Christensen, R. D. (1989). "Neutropenia and thrombocytopenia in infants with Rh hemolytic disease". The Journal of Pediatrics. 114 (4 Pt 1): 625–31. doi:10.1016/s0022-3476(89)80709-7. PMID   2494315.
  10. 1 2 Lalezari, P; Nussbaum, M; Gelman, S; Spaet, T. H. (1960). "Neonatal neutropenia due to maternal isoimmunization". Blood. 15 (2): 236–43. doi: 10.1182/blood.V15.2.236.236 . PMID   14413526.
  11. 1 2 Rath, M. E. A.; Smits-Wintjens, V. E. H. J.; Oepkes, D.; Walther, F. J.; Lopriore, E. (2013). "Iron status in infants with alloimmune haemolytic disease in the first three months of life". Vox Sanguinis. 105 (4): 328–33. doi:10.1111/vox.12061. PMID   23802744. S2CID   24789324.
  12. ↑ Mitchell, S; James, A (1999). "Severe late anemia of hemolytic disease of the newborn". Paediatrics & Child Health. 4 (3): 201–3. doi:10.1093/pch/4.3.201. PMC   2828194 . PMID   20212966.
  13. ↑ Al-Alaiyan, S.; Al Omran, A. (1999). "Late hyporegenerative anemia in neonates with rhesus hemolytic disease". Journal of Perinatal Medicine. 27 (2): 112–5. doi:10.1515/JPM.1999.014. PMID   10379500. S2CID   32155893.
  14. 1 2 Bethesda DL (2005). "Hemolytic disease of the newborn". Blood Groups and Red Cell Antigens. National Center for Biotechnology Information.
  15. ↑ Heddle, N. M.; Wentworth, P.; Anderson, D. R.; Emmerson, D.; Kelton, J. G.; Blajchman, M. A. (1995). "Three examples of Rh haemolytic disease of the newborn with a negative direct antiglobulin test". Transfusion Medicine. 5 (2): 113–6. doi:10.1111/j.1365-3148.1995.tb00197.x. PMID   7655573. S2CID   21936425.
  16. 1 2 3 Hemolytic Disease of Newborn~workup at eMedicine
  17. ↑ Arora, Satyam; Doda, Veena; Maria, Arti; Kotwal, Urvershi; Goyal, Saurabh (2015). "Maternal anti-M induced hemolytic disease of newborn followed by prolonged anemia in newborn twins". Asian Journal of Transfusion Science. 9 (1): 98–101. doi: 10.4103/0973-6247.150968 . PMC   4339947 . PMID   25722586.
  18. ↑ "Archived copy" (PDF). Archived from the original (PDF) on 2021-03-09. Retrieved 2017-02-15.{{cite web}}: CS1 maint: archived copy as title (link)[ full citation needed ]
  19. 1 2 3 American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. (2004). "Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation". Pediatrics. 114 (1): 297–316. doi:10.1542/peds.114.1.297. PMID   15231951.
  20. ↑ Onesimo, Roberta; Rizzo, Daniela; Ruggiero, Antonio; Valentini, Piero (2010). "Intravenous Immunoglobulin therapy for anti-E hemolytic disease in the newborn". The Journal of Maternal-Fetal & Neonatal Medicine. 23 (9): 1059–61. doi:10.3109/14767050903544751. PMID   20092394. S2CID   25144401.
  21. ↑ Gottstein, R (2003). "Systematic review of intravenous immunoglobulin in haemolytic disease of the newborn". Archives of Disease in Childhood: Fetal and Neonatal Edition. 88 (1): F6–10. doi:10.1136/fn.88.1.F6. PMC   1755998 . PMID   12496219.
  22. ↑ Hemolytic Disease of Newborn~followup at eMedicine
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