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Q: Why is O the most common blood type when it is recessive?
Krishna: Blood type is inherited. O type is the most common despite being a recessive gene because it is more highly expressed in the gene pool, while type A and type B are dominant (and type AB is codominant) but are less common because they are less expressed in the gene pool.
Q: Can two parents with O blood type have a child with A?
ABO incompatibility in the newborn generally presents as neonatal jaundice due to a Coombs positive hemolytic anemia and occurs in 0.5-1% of newborns. In contrast to the severe intrauterine or neonatal hemolytic anemia associated with Rh sensitization, clinically important neonatal anemia due to ABO incompatibility occurs infrequently. The major clinical issue with HDN due to ABO incompatibility is jaundice.
Several reasons have been proposed to account for lack of intrauterine hemolysis due to ABO incompatibility. These include less well developed A and B antigens on fetal red blood cells to stimulate maternal antibody production, and the ubiquitous distribution of A and B antigens in other tissues resulting in fewer antibodies that cross the placenta to bind to antigens on fetal red cells. The most important reason that ABO incompatibility does not cause hydrops fetalis is that naturally occurring anti-A and anti-B antibodies are IgM and do not cross the placenta.
It is estimated that <1% of type-O mothers have clinically significant anti-A or anti-B antibody which is IgG. ABO incompatibility with transplacental transfer of IgG anti-A antibody, or more commonly, anti-B antibody has rarely been reported in association with intrauterine hemolysis leading to hydrops fetalis. It should be noted that other causes of nonimmune hydrops fetalis have not been systematically excluded in these case reports. The most likely explanation for these rare cases is that exposure to antigens similar to the A or B antigen may occur from sources other than the fetus and stimulates IgG production in the mother. For example, an antigen similar to the B antigen is found in E.coli, and exposure to this organism may stimulate production of IgG anti-B antibody in type O individuals.
In contrast to Rh incompatibility, which tends to become more severe with each subsequent Rh positive pregnancy, ABO incompatibility does not demonstrate any consistent pattern. Thus, the patient’s first offspring may have clinically important hemolytic disease of the newborn due to ABO incompatibility, while subsequent newborns may be unaffected or very mildly affected. Because of the rarity of severe intrauterine hemolysis due to ABO incompatibility, assessment for intrauterine fetal anemia is not recommended based on the mother having type O blood. Measurement of IgG anti-A and anti-B antibody may be considered part of the evaluation of unexplained signs of fetal anemia such as ascites or hydrops when the mother is type O. Collecting a cord blood sample at birth for blood type and direct antibody testing should be considered when the mother is type O and a previous child had hemolytic disease of the newborn due to ABO incompatibility.
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ABO incompatibility (1) is the most common maternal-fetal blood group incompatibility and the most common cause of haemolytic disease of the newborn (HDN).
ABO incompatibility is one of the diseases which can cause jaundice. ABO incompatibility happens when a mother's blood type is O, and her baby's blood type is A or B. The mother's immune system may react and make antibodies against her baby's red blood cells.
The expression of ABO incompatibility in most of the cases is mild due to the lower expression of A and B Antigens on fetal red cells. ABO incompatibility has affected the first pregnancy and is milder in the subsequent pregnancies.
ABO incompatibility in the newborn generally presents as neonatal jaundice .
In contrast to Rh incompatibility, which tends to become more severe with each subsequent Rh positive pregnancy, ABO incompatibility does not demonstrate any consistent pattern. Thus, the patient’s first offspring may have clinically important haemolytic disease of the newborn due to ABO incompatibility, while subsequent newborns may be unaffected or very mildly affected.
ABO incompatibility is treated in newborns by light therapy (phototherapy). On rare occasions an exchange transfusion may be necessary. Full recovery usually occurs with no lasting repercussions (1).
It can persist up to 12 weeks after birth.
Usually, hospital-born babies will be checked for jaundice within 72 hours of being born during the newborn physical examination.
But you should keep an eye out for the symptoms of jaundice after you return home because it can sometimes take up to a week to appear. When you're at home with your baby, look out for yellowing of their skin or the whites of their eyes. Gently pressing your fingers on the tip of their nose or on their forehead can make it easier for you to spot any yellowing.You should also check your baby's urine and poo. Your baby may have jaundice if their urine is yellow (a newborn baby's urine should be colourless) or their poo is pale (it should be yellow or orange). If your baby has jaundice, their skin will look slightly yellow. The yellowing of the skin usually starts on the head and face, before spreading to the chest and stomach.
About 60 percent of full-term infants also develop the condition. Severe cases can cause brain damage if untreated.
Jaundice is caused by too much bilirubin in the blood. This is known as hyperbilirubinaemia.
Bilirubin is a yellow substance produced when red blood cells, which carry oxygen around the body, are broken down, in this case because of the attack.
The bilirubin travels in the bloodstream to the liver. The liver changes the form of the bilirubin so it can be passed out of the body in poo.
But if there's too much bilirubin in the blood or the liver can't get rid of it, the excess bilirubin causes jaundice.
Jaundice is common in newborn babies because babies have a high number of red blood cells in their blood, which are broken down and replaced frequently.
A newborn baby's liver isn't fully developed, so it's less effective at processing the bilirubin and removing it from the blood.
This means the level of bilirubin in babies can be about twice as high as in adults.
By the time a baby is around 2 weeks old, they're producing less bilirubin and their liver is more effective at removing it from the body.
This means the jaundice often corrects itself by this point without causing any harm.
If your baby's bilirubin level is high, the most commonly used treatment is phototherapy (bright light therapy). It does not contain rays that would harm your baby. Phototherapy is very safe and effective and is only available in hospital.
Phototherapy works by changing the bilirubin in the skin into a form that will not cause deafness or brain damage. Your baby needs phototherapy until the level of bilirubin has dropped to a safer level. Your baby needs regular blood tests to measure the bilirubin level. Babies usually have phototherapy treatment for 48 hours, but often longer for bilirubin levels that remain high.
(Normal indirect bilirubin would be under 5.2 mg/dL within the first 24 hours of birth. But many newborns have some kind of jaundice and bilirubin levels that rise above 5 mg/dL within the first few days after birth. Jaundice is considered pathologic if it presents within the first 24 hours after birth, the total serum bilirubin level rises by more than 5 mg per dL (86 mol per L) per day or is higher than 17 mg per dL (290 mol per L), or an infant has signs and symptoms suggestive of serious illness). (3)
Usually, phototherapy is the only medical treatment needed. A small number of babies with severe jaundice need blood transfusions to replace red blood cells that have been used up, and to dilute out the bilirubin (2).
Footnotes:
© 2025 Created by Dr. Krishna Kumari Challa.
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