Uninsured, undocumented immigrants often go to the emergency room for treatment. Since 1986 the federal government has required that patients in the emergency room receive care, regardless of their immigration status or ability to pay.

But caring for chronic conditions such as kidney disease or cancer in the emergency room is expensive. So some states are quietly expanding access for undocumented immigrants to obtain medical treatment beyond the ER.

One of those states is Washington, where an undocumented immigrant named Gonzalo lives with his wife, Ricarda.

Gonzalo is really sick.

“I can’t enjoy the day — go out — because I’m always unwell,” he said in an interview in Spanish.

Gonzalo moved to the U.S. from Mexico about 30 years ago. He’s 60 years old. We’re not using his last name because of his immigration status.

Ten years ago, Gonzalo’s kidneys failed. Since then, he’s gotten sicker and sicker. Five years ago, he had to quit his job as a painter.

“I used to pay the rent. I paid for everything, and we didn’t lack anything,” he said. “But I got sick and everything changed.”

Now, Gonzalo and his wife live with one of their daughters in her apartment south of Seattle.

Across the country, there are about 6,500 undocumented immigrants with kidney failure, according to the National Institutes of Health. What kind of care they get depends on where they live.

In most states, they can only get dialysis in hospital emergency rooms.

That means, every couple of weeks, they go to the hospital when so many toxins have built up in their body it’s life-threatening. Usually, they have to stay overnight so they can be dialyzed twice. That costs nearly $300,000 per person every year.

So seven states, including Washington, have a different system.

“The state of Washington has something called AEM,” said Leah Haseley, a nephrologist — a kidney doctor — in Seattle. She’s talking about Alien Emergency Medical, part of Washington’s Medicaid.

“AEM pays for two things,” she explained. “They pay for dialysis for undocumented people, and they pay for chemotherapy for cancer treatment for undocumented people as well.”

Regular dialysis costs about a quarter of what emergency dialysis does — but it’s controversial.

“The first time that you show up at a hospital with kidney failure, that’s an emergency,” said Matthew O’Brien, with the Federation for American Immigration Reform, a group that advocates for stricter immigration laws. “After that, it’s a chronic condition, and we don’t believe that it’s appropriate to reward lawbreakers with benefits at the expense of U.S. taxpayers.”

But there are others who say even regularly scheduled dialysis isn’t enough: undocumented immigrants who qualify should be given kidney transplants, because the cost of a transplant is less than the ongoing costs of regular or emergency dialysis. But, without health insurance, few undocumented immigrants can afford a transplant.

In 2015, Illinois became the first state with a system for paying for organ transplants for undocumented immigrants.

Dr. David Ansell was a prominent advocate for the change.

“In about a year and a half the cost for a transplant pays itself back,” he said, “but also people can go back to work and contribute to the state.”

So far, more than 200 undocumented immigrants in Illinois have been given access to organ transplants, with their insurance premiums paid for by a non-profit. Now, Dr. Ansell and other public health advocates hope to see a similar program at the national level.

Many who oppose this say, with limited organs available, they should be reserved for citizens and legal immigrants.

But Dr. Ansell says, in Illinois, 75 percent of kidney transplants for undocumented immigrants come from donations from their own family — a much higher rate than the rest of the population.

“If you’re undocumented in Illinois, you can get a driver’s license, and disproportionately the Latino community is signing up to donate their organs,” Dr. Ansell added. “It’s a simple matter of ethics and fairness.”

He said, since Illinois started paying for the transplants, the total number of organs available has increased, because so many more Latinos have signed up for organ donation.

Overall in the US, studies have found that undocumented immigrants donate 2 to 3% of all organs.

Back in the Seattle area, Gonzalo says all three of his daughters are willing to give him a kidney, but he has no way to pay for the transplant.

That’s why his wife, Ricarda, says she’s taken to buying lottery tickets.

She said in Spanish, “I’ve told my husband, ‘If I win the lottery, I won’t think twice. I’m going to get you a kidney.'”

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Imagine yourself stuck in the hospital.

Would you rather your doctors be well-rested, with a limit on how many hours they can work? Or would you rather they work longer shifts, seeing you through the critical hours of your illness and with fewer handoffs of your care?

That’s the choice being reexamined after a study published in March in the The New England Journal of Medicine found that longer shifts for medical residents were just as safe as shorter shifts.

The results, which support an earlier study that also found no association between shift length and patient safety, have led some physicians to suggest that the issue of how long residents should work has now been “laid to rest.”

University of Pennsylvania’s Dr. David Asch, one of the study’s lead investigators, said in a statement that despite concern about lengthy shifts for residents, “they really don’t seem to have an effect on any important domains.”

Sixty-three internal medicine residency programs participated in the latest study. Half of the programs adhered to limits on how long residents could work. First-year residents were restricted to 16-hour shifts, while more senior residents could work up to 28 hours. For the other half, there was no limit on how long residents could work.

The researchers focused on patients’ mortality rates. They found that the number of patients who died within 30 days of admission to the hospital was similar between the two groups. Though the study didn’t examine medical errors directly, the implication is that the rate of medical error was also similar.

The findings are reassuring, given what we know about the effects of sleep deprivation on cognitive performance. Some studies have found that sleep deprivation can lead to a similar level of impairment as heavy drinking.

Concerns about exhausted physicians in training have been around since at least 1984, when a college freshman named Libby Zion died in a New York hospital from an error made by a sleep-deprived resident. After a high-profile investigation, New York state instituted the first limits on how long physicians in training could work — no more than 24 hours in a shift, and no more than 80 hours in a week. These limits were extended to all residency programs in 2003 and strengthened in 2011.

It seemed like a prudent change. As many have argued, we don’t let our pilots fly without adequate rest.

But some physicians challenged the limits, pointing out that we had no direct evidence to support the change. It had simply never been studied.

Shift limits could have unintended consequences. For example, shorter shifts mean more handoffs between physicians, during which important information can sometimes be lost.

Does the latest study mean that strict limits on shift length should be rolled back, since they’ve not been proven to help patients? Or is there more to the story than medical errors and patient safety?

Just as sleep deprivation has been shown to impair cognition, so too has it been found to dampen empathy for others.

Studies show that a single night of sleep deprivation interferes with our ability to perceive emotions in others and compromises our ability to empathize. Longer periods of sleep deprivation reduce measures of emotional intelligence and interpersonal functioning.

One of the darkest moments of my medical training came at the end of a 28-hour call in the ICU. Firefighters had rescued a woman from a house fire, badly burned and barely alive. She was at the threshold of death when she arrived. Her suffering must have been unbearable, but I’m ashamed to say that all I could think about was how long her death paperwork would keep me awake.

I don’t think I’m alone in finding that sleep deprivation warps my ability to provide compassionate care. In 2002, researchers at the University of Pennsylvania surveyed residents before and after their first year of training. The prevalence of chronic sleep deprivation soared from 9% to 43%. Emotional exhaustion rose from 8.5% to 68%, and measures of empathy dropped 10%-15%.

We can’t say how these changes affected patients, but it’s no stretch to imagine that they were probably harmful to the patient-physician relationship. They were certainly harmful to the residents — the prevalence of depression increased from 4.3% to nearly 30% by year’s end, and burnout leaped from 4% to 55%.

Skeptics about shift limits may point out that both groups in The New England Journal of Medicine study got a similar amount of sleep, when averaged over time. But participants in the group without shift limits were nearly 2.5 times more likely to be dissatisfied with their amount of time for rest and with their overall well-being. They were also more likely to report that patient safety and the quality of their education had suffered as a result of the longer hours.

In 2017, after the publication of an earlier study showing no association between shift length and patient safety, the governing body of graduate medical education backtracked on shift limits. Maximum shift length for first-year residents was increased from 16 to 24 hours, and more shift-to-shift variation was permitted for senior residents, as long as the 80-hour weekly cap was maintained when averaged over four weeks.

It was an important development, according to Asch and his colleagues, because it seemed that educational policy would finally be based on evidence rather than opinion.

Moving toward evidence-based policy in medical education makes sense. After all, as Asch pointed out, we would never approve a new drug without strong evidence supporting its use.

But it’s my view that using these studies to justify further loosening work-hour restrictions doesn’t make sense. This new study provides strong evidence that shorter shifts are just as safe for patients as longer shifts.

Given what we know about the effects of sleep deprivation on emotional capacity and residents’ well-being, why would we relax work limits again without proof that doing so would cause no harm?

Clayton Dalton is a resident physician at Massachusetts General Hospital in Boston.

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Scientists are gearing up a major study to find out whether a drug can silence the gene that causes a devastating illness called Huntington’s disease.

This development follows the discovery that the experimental drug reduced levels of the damaged protein that causes this mind-robbing ailment. The new study will determine whether that drug can also stop progression of the disease.

It is also another sign that drugs built with DNA, or its cellular collaborator RNA, can be powerful tools for tempering diseases that until now have seemed out of reach.

Huntington’s disease is an apt target because it’s caused by a single mutated gene. It also a frightening and devastating disease.

The symptoms “are like having Alzheimer’s, Parkinson’s and ALS [Lou Gehrig’s disease] simultaneously, when it’s in full swing,” says Jeanette Garcia, a 57-year-old advocate in San Jose, Calif.

If one of your parents has Huntington’s disease, there’s a 50-50 chance you will get it, too. About 30,000 people in the United States carry the deadly gene.

Garcia and her nine siblings lost their mother to the disease. They know the terrible odds. When they get together for family reunions and talk turns to Huntington’s, “it is all of a sudden this terrifying prospect we’re all faced with,” she says.

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Jeanette Garcia discovered through genetic testing that she is going to develop Huntington’s disease, eventually.

Courtesy of Jeanette Garcia

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Courtesy of Jeanette Garcia

Garcia decided to take the genetic test for this condition in 2008 and found out she had inherited the damaged gene. She’s recently been seeing the first signs of the illness, including involuntary movements, which she noticed when watching a video of herself, “and I went, ‘Holy crap, OK here we go.’ “

But her disease is emerging at what could be a fortunate moment. She’s heading off to a neurologist to see if she would qualify for a study that is generating a lot of excitement.

Last year, drugmaker Roche’s Genentech unit said that an experimental drug sharply reduced the amount of illness-inducing protein measured in people’s spinal fluid. The results of that study, involving 46 patients, were published Monday by the New England Journal of Medicine.

The protein isn’t eliminated entirely with the experimental drug, but animal experiments suggest that reducing it significantly could be enough to stave off symptoms.

The researchers are now about to launch a trial involving 660 volunteers with early symptoms of the disease, to see if the drug, called RG6042, can slow or stop Huntington’s progression.

“It’s so exciting,” Garcia says. “I want to be a part of it.”

This study marks a milestone for Huntington’s disease. More than 25 years ago, a scientist named Nancy Wexler was able to identify the errant gene that causes the disease by painstakingly studying families in a region of Venezuela where the disease is nearly epidemic.

Her finding was one of the early, great successes in tracking down disease genes. But it has taken all the intervening years to develop this promising angle of attack.

One huge advance has been the development of methods to silence a damaged gene, so cells don’t convert those errant instructions into dangerous proteins, such as the one that causes the symptoms of Huntington’s.

Scientists have developed several methods to jam this signal. The Roche drug uses a custom-built piece of genetic material called an antisense oligonucleotide to block the process. Other advanced research projects aimed at Huntington’s and other diseases use a technique called RNA interference to accomplish a similar result.

Another major challenge has been to figure out how to get the drug into the brain. Scientists at Ionis Pharmaceuticals in San Diego figured out how to make that happen with the antisense oligonucleotide targeting Huntington’s.

The answer turned out to be injecting it into spinal fluid, which circulates up and down the spine and into the brain. “The drug could actually transfer quite readily to the brain and then sink into the target brain tissue,” says Dr. Scott Schobel, who heads the research effort on this drug at Roche, which is co-developing the experimental drug with Ionis.

Roche started recruiting patients for this study in January, but halted the trial to redesign it, after discovering the drug didn’t need to be injected as often as they had planned.

“We’re going to get back up and running over the next several weeks to months,” Schobel says.

The study is supposed to follow patients for 25 months, which should be enough time to determine whether people’s symptoms are held in check by the treatment.

George Yohrling, a scientist at the Huntington’s Disease Society of America, says his main concern is whether the experimental drug will penetrate deeply enough into the brain to stop the disease.

If not, he says other treatments under development could succeed in that regard. One strategy is to use viruses to deliver one of these gene-silencing drugs.

“A lot of different approaches are being worked on in different stages of drug discovery across the world,” Yohrling says. “It’s really quite exciting.”

This development follows more than 20 years of boom-and-bust excitement about gene-silencing strategies.

“Initially there was wild enthusiasm,” says Dr. Judy Lieberman, a professor of pediatrics at Harvard Medical School. “There were literally hundreds of biotech companies formed to do that.”

But they quickly hit technical and scientific roadblocks, she says, “and eventually almost all of them about abandoned these efforts.”

As scientists gradually worked their way through these challenges, Huntington’s disease emerged as an appealing target, despite being a rare disease with a far smaller potential market than, for example, a drug for Alzheimer’s disease.

The first antisense oligonucleotide to be approved as a drug by the Food and Drug Administration treats an even rarer condition, called spinal muscular atrophy. And there are now competitive products targeting that disease, thanks in part to the financial incentives drug companies get to develop drugs for “orphan” diseases. (The drugs are also extraordinarily expensive).

Drug developers are also aware that this strategy could be useful for common disorders, such as high cholesterol. That’s an active area for drug development.

Drug companies would jump on an opportunity to develop a drug for Alzheimer’s or autism, Yohrling says, if only they could identify a straightforward target gene to disrupt. That strategy “now makes the ‘undruggable’ druggable,” he says.

But that’s getting ahead of the story. Before the FDA even considers approving a treatment for Huntington’s, Roche will have to demonstrate that its experimental drug is safe and effective.

Garcia is eager to help them make that case, by joining the study if she can, and encouraging others to do the same. She says she can’t even let herself hope that the treatment will work for her. She’s thinking of her four children and six grandchildren.

She has a grandson who was born blind and is also at risk for Huntington’s, she says. “I’m just not going to stop because I don’t want him to have to deal with this.”

You can contact NPR Science Correspondent Richard Harris at rharris@npr.org.

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