Joshua Bright for The New York Times
Ryan Eisner, who survived sepsis, outside his parents' home in Bayside, Queens. It is unknown why the drug that saved him failed with others.
Five doctors hovered at the bed of Ryan Eisner, a cloud of white coats throwing a dark shadow over the star college athlete.
Astonished, then frozen with dread, his father, Mitchell Eisner, watched from a few feet away, holding the bundle of clothes he had just picked up from their home in Bayside, Queens. When he had left less than an hour earlier, there had been no such bedside commotion. Ryan Eisner, a junior at Drew University who was the starting guard on the basketball team, had come down with a bad dose of pneumonia at the beginning of October 2007. But surely the infection would clear up in a few days, and he'd be back on the court.
Then, everything changed.
"I said, 'What's going on?' " his father recalled. "The doctor in charge turned to me and said: 'You'd better start praying. He's going to die.' I said, 'When?' He goes, 'Anytime.' They told me he had gone into septic shock."
Responding to the infection in his lungs, Ryan Eisner's own body had begun to kill him. His immune system, having lost the ability to tell friend from foe, to distinguish invading pathogens from his own tissues, had switched on the self-destructive force that is broadly known as sepsis. Once it starts, every white blood cell in the body is activated, "turning them into uncontrolled roving gangs of street fighters," as Dr. Kevin J. Tracey, a neurosurgeon and immunologist, wrote in "Fatal Sequence: The Killer Within," a book on sepsis.
A leading cause of death in hospitals, sepsis often brings on shock — a drastic drop in blood pressure, often followed by organ failure. When sepsis is identified early, patients have a better chance of survival. But Mr. Eisner was beyond that point. He was gravely ill, and there was hardly anything to stop a person in his condition from getting worse.
A study published this week said that nearly every one of 150 proposed drugs for sepsis had failed in clinical trials, even though tests of mice had suggested they would help. Billions of dollars and years of research had been invested, and apparently wasted, by assuming the mouse's genetic wiring was near enough to a human's as to make no difference. But the genetic gears of mice do work differently.
At the same time, Mr. Eisner's case draws, in crude strokes, the unmapped terrain. Having decoded the human genome, researchers are finding many mechanisms of life to be stubbornly inscrutable, much as each generation of astrophysicists who expand the map of the cosmos must reach for new theories to explain the universe. Whether in outer space or inner space, using giant telescopes or precision molecular assays, we find that the mysteries of how things work have gotten deeper.
Mr. Eisner was sedated and put on a respirator. By the next morning, different things were going wrong every hour with his blood and his organs. The doctors told his father there was little they could do. They could try a risky drug, Xigris, the marketing of which had been the source of much controversy. It was expensive, they explained, and had side effects, including bleeding, that could accelerate his son's decline. "It was the only hope," Mitchell Eisner said.
The drug was flown in. It worked. In effect, it broke the destructive looping in his immune system. The young Mr. Eisner returned to play basketball and graduate on time.
A year later, Eli Lilly & Company, the makers of Xigris, pulled it from the market, saying that it was not improving the survival of sepsis patients. In the study published this week, it was listed among the failed drugs. Sometimes, though, it worked. So far, no one has figured out an ironclad way of forecasting which patients would be helped.
Dr. Tracey's research in the 1980s at Cornell University Medical College showed how a compound called TNF produced by everyone's immune system could send the body into shock. He said that successful drugs were created without knowing the genetic control switches. A mouse can show what works, even if no one knows why, he said. "I may not know what a genomic response means to my patient, but I know that if their blood pressure is 20 because of too much TNF, then we should give anti-TNF," said Dr. Tracey, now the president of the Feinstein Institute for Medical Research at North Shore-Long Island Jewish Health System.
Still, it remains a mystery why Mr. Eisner got so sick from his pneumonia, and why Xigris helped him — and not others — recover. The bad news is that mice cannot provide that valuable information. "I just know," Mr. Eisner said, "that I wouldn't be here without it."
E-mail: dwyer@nytimes.com
Twitter: @jimdwyernyt
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