Mother credits pioneering Kiwi doctor for her 'miracle baby'

By Martin Johnston

When Robyn McGregor was pregnant for the fifth time, the Kiwi doctor who led the world in fetal blood transfusions told her the prospects weren't good.

Robyn had produced three children but her fourth pregnancy ended in miscarriage.

With her fifth - whose 39-year-old result, Cathy, is now part of a follow-up study - potentially-fatal rhesus blood incompatibility was diagnosed. In this disorder, antibodies from the mother's immune system enter the fetus and attack the red blood cells, making the baby anaemic.

I'm not concerned about it [having a different heart structure] because I lead a very healthy lifestyle anyway
Cathy McGregor

Professor Sir William Liley, of National Women's Hospital in Auckland, had done the world's first successful blood transfusions into babies in the uterus more than a decade earlier, in 1963.

"Professor Liley looked after me at that stage. He said, 'Don't expect a live baby'. I had the highest level of antibodies that they had ever recorded. It was pretty grim for a while," Robyn recalls.

But with four blood transfusions while in her mother's uterus, five more when she was a newborn and another two in her first year of life, Cathy McGregor survived her eight-weeks-premature birth to become a healthy child and adult.

"She was my miracle baby," says Robyn, adding that she named her Catherine Florence. The second name was to honour the obstetrician who gave the intrauterine transfusions, Dr Florence Fraser.

Now aged 39, Cathy, an Auckland mother-of-two and clothing businesswoman, is taking part in a study of 95 people who, like her, suffered fetal anaemia and had blood transfusions.

Researchers at Auckland University's Liggins Institute were aware of animal evidence that fetal anaemia and transfusions led to changes in heart structure.

They tracked down people who had the condition and were treated with fetal blood transfusions between Liley's breakthrough in 1963, and 1992, tested them, and compared them with their siblings who did not have the condition.

There was no difference in the incidence of heart disease between the affected people and the siblings, which the researchers say is as expected because the affected group were younger when tested - they were between 18 and 47 - than the age at which heart disease usually appears.

But the structure of their hearts is different: they are smaller and thicker-walled. They have lower levels of HDL or so-called "good" cholesterol which is thought to help protect from heart-artery disease. Also, there were signs the inner lining of their blood vessels is working differently.

"We can't say whether the changes we saw will result in increased rates of heart disease when these people get older," says paediatrician Dr Alexandra Wallace, one of the researchers.

"They might have more heart disease as a group, or earlier onset of heart disease, or there may be no difference - their bodies might have managed to cope with and adapt to these differences."

Further follow up is planned when the participants are older.

Wallace says it is not known whether the cause of the affected people's different hearts is anaemia or transfusions, but anaemia is more likely because of the stress it places on the developing heart.

Cathy says it has not been unsettling to learn that her heart has developed different structures.

"I'm not concerned about it because I lead a very healthy lifestyle anyway."

The researchers say their findings, published in the Archives of Disease in Childhood, may be relevant for pre-term babies, as most develop anaemia soon after birth and some are treated with blood transfusions. Babies born small, either because they are born pre-term or had poor fetal growth, are at increased risk of heart-artery disease and other chronic diseases in adulthood.

What is rhesus blood type incompatibility
• Mother - Rh-negative. Fetus - Rh-positive
• The first such baby is unaffected, but during birth, some of its blood can sensitise the mother's immune system.
• She then produces antibodies which can attack fetal blood cells in subsequent Rh-incompatibility pregnancies, causing anaemia.
• Giving affected women immunoglobulin injections can prevent sensitisation.
• Untreated anaemia can lead to miscarriage, stillbirth, brain damage, deafness and blindness.
• Treating the anaemia can involve blood transfusions before and after birth, antibodies and ultraviolet light therapy.
• In New Zealand around 5000 Rh-positive babies a year are born to Rh-negative mothers. Around 750 babies a year need treatment.
• Auckland District Health Board gives blood transfusions in the uterus to about six babies a year, with between one and five transfusions each.

- NZ Herald

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