Ryan Dant was born with a rare disease that was expected to end his life by age 10
Two clinical trials have resulted in therapies to help Ryan and other patients live longer
On Saturday, 29-year-old Ryan Dant walked across the stage in his cap and gown as he graduated from his dream school, the University of Louisville.
It’s remarkable because Ryan wasn’t expected to attend college, let alone the school whose logo he wore on T-shirts and basketball jerseys as a toddler. Because underneath that cap and gown, medications are circulating through his entire body to make this moment possible. Because his parents never gave up, even when they heard there was no chance.
It’s remarkable because Ryan is still alive, despite being born with a death sentence in his genes.
The normal beginnings of rare disease
His father, Mark Dant, likes to say that Ryan was born with a love for baseball. The night before his birth, his parents went to a Texas Rangers game.
The healthy, beautiful boy was born in 1988, weighing 8 pounds, 13 ounces. He was perfect, Mark said. At the age of 3, he could throw a baseball so hard that his mom, Jeanne, made a “no ball in the house” rule. Every night, Ryan would watch baseball games with his family on TV, cheering on Rangers pitcher Nolan Ryan. He loved the fact that he could see his own name on the back of the baseball player’s jersey.
Before enrolling him in day care at age 3, Jeanne took Ryan to the pediatrician. What was supposed to be a routine checkup revealed that Ryan’s liver and spleen were too large, and the Dants were referred to a geneticist. Mark, who had just made lieutenant at the police department in Carrollton, Texas, didn’t believe anything was wrong with his son. He didn’t go with them to see the geneticist. But two weeks later, tests confirmed the diagnosis.
The geneticist said Ryan had a rare genetic disorder called mucopolysaccharidosis I, or MPS I, with a wide-range of symptoms affecting multiple systems in the body. The mutation forms in a gene that makes an enzyme that helps break down byproducts of chemical reactions in cells. The enzyme can’t be produced, leading to a buildup of this byproduct that can cause damage to cells, tissues and organs.
It explained why his spleen and liver were enlarged; the buildup made them 2½ times larger than normal.
The geneticist told the Dants that Ryan would die by the time he was 10 or 12. Over time, they would see him change. He would be in a lot of pain, possibly go blind and deaf, suffer a stiffening and curling of the muscles in his limbs that would put him a wheelchair. He would decline mentally.
Soon, he would lose the ability to play baseball.
Mark Dant pressed the doctor, asking about research or medications.
” ‘You have to understand, your son has a disease that is so rare that there aren’t many scientists working on it,’ ” he recalls the doctor saying. “He was telling us to take him home and love him, because he wouldn’t be around long.”
MPS I affects one in 100,000 children globally, according to the National Organization for Rare Diseases.
The Dants immediately decided not to tell Ryan; he was too young to understand. They cried in the hallway before taking him home. That became the new normal for them: crying at night, separately, after Ryan