Saving Henry Read Online Free PDF Page B

uncomfortably high chance that we could have another baby with the disease. Although there was a 75 percent chance that our next baby would be healthy, our life experience taught us that statistics are predictions, not promises. After all, the chance of our having a baby with FA was 1 in 30,000. Once you hit a number like that, you stop taking comfort in the remoteness of a chance that something bad could happen.
    Through conversations with FARF leadership and our growing list of doctors, as well as our own research, Allen and I understood that Henry would need open-heart surgery at around six months of age and a bone-marrow transplant probably by the time he turnedfive. Though I was scared to death at the prospect of open-heart surgery, I understood that the bone-marrow transplant was the real challenge. Our best hope—if not our only one—that Henry would survive a transplant was if we could find a perfectly matched stem-cell donor. The only perfectly matched donors are siblings.
    At this time, in 1995, bone-marrow transplants from perfectly matched sibling donors had reported success rates of 85 percent. This meant that if we had another baby who did not inherit Fanconi anemia and whose bone marrow was compatible with Henry’s, then Henry would probably survive. When the baby was born, doctors could collect its umbilical-cord blood through a painless and harmless procedure, transplant it to Henry, and silence the most lethal threat to his life.
    In contrast, the success rate for a bone-marrow transplant from an unrelated donor—someone other than a sibling—was around 18 percent, meaning that without a sibling donor, Henry would probably die. At the time, no one with his type of FA had ever survived a transplant without a perfectly matched sibling donor.
    What this meant for us, in the simplest terms, was that Henry’s life depended on our having another baby with two critical characteristics: the baby had to be Fanconi anemia–free, and needed to be a human leukocyte antigen (HLA) match to Henry. HLA, also known as histocompatibility antigens, are genes that recognize whether a cell is foreign to the body. Any cell possessing an individual’s HLA type is recognized as belonging to that person, whereas a cell with a different HLA type is identified as an invader. Like all invaders, these cells are unwelcome, and the resulting internal battle can cause mild to great bodily harm and even death.
    HLA type is used to determine the compatibility of bone marrow, kidney, liver, pancreas, and heart for transplantation from one person to another. Compatibility between organ donor and recipient is judged by the number of HLA antigens found in the donor that areshared by the recipient. In 1995, bone-marrow-transplant compatibility was determined by six HLA antigens, including two each of HLA-A, HLA-B, and HLA-DR. Everyone acquires one set of three from each parent. Today, the testing is more sophisticated and the best donor would share eight antigens, which include HLA-C. The very best organ donor for Henry would be someone with the exact same HLA antigens. HLA type is inherited, and that is why siblings have the greatest likelihood of being perfectly matched at the HLA antigens and why they are therefore the ideal donors.
    Nothing was guaranteed. Because, like Fanconi anemia, HLA type is genetic, the chance of another baby being a perfect HLA match to Henry was just 25 percent. But Fanconi anemia further diminished those odds. If the sibling also had FA, he or she would not only be disqualified as a stem-cell donor but would also suffer from the disease, would probably experience significant birth defects, and eventually need a transplant from a healthy sibling. The probability that we would have a healthy baby who would also be an HLA match to Henry—the ideal-case scenario—was merely 18.75 percent, or one-quarter of the 75 percent chance that the baby would be healthy.
    In other words, it