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  • How a DNA test solved a medical mystery – and revealed a Duke doctor’s decades of deception

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    Summer McKesson struggled to breathe for years. Doctors told her it
    was because her blood would not stop clotting – and they couldn’t figure
    out why.

    A single clot alone can be lethal; but the recurring and
    unexplained clots that formed in McKesson’s heart and lungs were a
    medical mystery.

    After multiple surgeries to remove clots and scar
    tissue, McKesson traveled to the Mayo Clinic, where she sat in a
    conference room while renowned physicians and specialists worked through
    her case on a whiteboard.

    But even they were baffled.

    “To hear that even they had never seen it before,” she told CNN through tears, “I came back (home) just crushed at that point.”

    Desperate
    for answers, McKesson said she turned to 23andMe, hoping the DNA
    analysis service, which claims to offer insights into its clients’
    genetic health history, might unlock some clues to her condition.

    But
    her quest for answers would unearth a family secret – and a doctor’s
    decades-old deception that has ensnared multiple families across the
    country.

    Ask your parents about Dr. Peete

    McKesson
    never questioned her genetics – or considered 23andMe – until a team of
    surgeons performed an urgent, open-heart procedure in 2022 to remove
    clots from her heart and lungs.

    As she recovered, McKesson said her surgeon dropped another bomb.

    While
    operating, he’d noticed the connective tissue that supports her organs
    was stretchy and unusually fragile. He told her the complication –
    coupled with McKesson’s willowy build and Amazonian height – could be a
    sign of an inherited disorder called Marfan syndrome.

    His
    suspicions were correct. A geneticist confirmed McKesson’s diagnosis,
    and said her clotting disorder was also genetic, which ushered in a host
    of lifelong health challenges.

    Her heart would now need to be constantly monitored, and she will eventually need at least one more major heart surgery.

    But
    the diagnosis was puzzling for another reason: both of her conditions
    are genetic and, as far as she knew, no one else in her family had them.

    McKesson,
    43, said she didn’t have a full picture of her family’s health history
    because her father died when she was a teenager. So, she signed up for
    23andMe, submitted a DNA sample, and waited.

    The results arrived in her inbox in October 2023.

    “I
    was just sitting on my couch after work, and kind of quickly pulled up
    the results on my phone,” McKesson recalled. At first, she said, she was
    curious to learn more about her family’s ethnic background.

    “Growing
    up, I always was like … ‘I don’t look like any of y’all. No one has my
    nose. I’m a foot taller than everyone,’” she said, adding her family
    used to joke that she was adopted.

    While there weren’t many
    surprises in her family’s ancestry, McKesson said when she navigated to
    the “family members” section of the site, she drew up short:

    The test showed she had seven half-siblings.

    “I
    just remember being shocked and my mind just swirling,” she said. “I’m
    like, how is this possible? … Did my dad have another family or
    something?”

    Was she actually adopted? None of what she was learning made sense.

    She
    sent screenshots of the results to a trusted group of friends, and they
    discussed different theories. Then, later that night, she sent a
    message to her newly discovered half-siblings through the 23andMe
    website.

    “Humor has really gotten me through a lot of this,” McKesson said, so she opted for a lighter tone in her first note.

    She
    sent the same message to each name listed on the site. And then, she
    waited. It would take more than a month for anyone to respond.

    “I
    don’t want to cause any conflict,” one of them finally wrote, “but if
    you want to dig into this, I’d ask your parents if they went to see Dr.
    Peete.”

    A doctor’s decades of deception

    In
    1980, Laurie Kruppa and her husband, Doug, found themselves waiting for a
    fertility specialist named Dr. Charles Peete in a sterile exam room at
    Duke University Hospital.

    The couple wanted children, Laurie told
    CNN, but Doug had a vasectomy during a previous marriage, so her OB-GYN
    referred them to the physicians at Duke for fertility treatment.

    The
    1980s and ‘90s would prove to be a time of innovation in the fields of
    genetics and assisted reproductive technology. In 1978, a woman gave
    birth to a baby named Louise
    in the United Kingdom through in vitro fertilization, or IVF, making
    her the first child to be born through the novel procedure.

    But
    the Kruppas opted to use intrauterine insemination, or IUI, a procedure
    that had been around in some form for centuries but had only recently
    become common thanks to advances in freezing and banking sperm.

    During
    the procedure, a doctor places donor sperm directly into the patient’s
    uterus during ovulation, to increase the chances of conception.

    The
    Kruppas were instructed to bring $50 to each visit and, Laurie
    stressed, they were told the donor sperm would come from a resident in
    the university’s medical school.

    At each visit, Kruppa said she
    laid back on the table, placed her feet in the stirrups, and waited. And
    then, Peete would walk into the room.

    “He seemed nice enough and concerned, but we didn’t have a lot of interaction,” Kruppa recalled decades later.

    I would “wait 10 or 15 minutes, and then he’d come back and insert the sperm.”

    Kruppa
    said it took the couple seven attempts to conceive their eldest
    daughter. Two visits, less than a year later, to conceive their second
    daughter. And a single visit in 1984 to conceive their son.

    And for each child, Peete used his own sperm without her knowledge or consent.

    Revelations and revulsion

    It would be decades before the Kruppas would learn the truth about their children’s paternity.

    During
    those years, Kruppa said she and her husband had moved their family
    from North Carolina to Ohio and debated whether they should even tell
    their kids they were donor-conceived.

    “We thought maybe the two
    girls were definitely related because they came 16 months apart. So, we
    just thought maybe it was a resident that was still there,” Kruppa said.

    “My son was born two and a half years later, so we thought it had to be somebody different.”

    After
    years of keeping their secret, Kruppa said the rising popularity of
    consumer DNA products eventually forced their hand. They revealed the
    news to their children during a family vacation.

    “They all reacted very well,” Kruppa said of her kids. “They’ve never not thought that (Doug) was their dad.”

    But
    they also joined 23andMe and began doing their own research. Kruppa
    said her middle child was the first to discover their connection to
    Peete. Out of the blue, her daughter asked what hospital her parents
    used and if Kruppa remembered the name of her doctor.

    Then, the
    kids called another family meeting and revealed what Peete had done to
    their parents. Initially, Kruppa said, “I was really glad they were all
    true siblings.”

    It took her months to fully process what Peete’s actions meant for her – and over time, she became angry.

    “When
    I started thinking, I got much more upset about the ethics of it,” she
    said. “I’m pretty sure he was my father’s age … This is like getting
    raped by your father.”

    As the Kruppas’ children were grappling
    with the truth about their paternity, Jim Harris was in North Carolina
    exchanging emails with a newfound half-sibling on 23andMe.

    Less
    than a year after his father died from cancer, Harris said his mom
    called and insisted they meet to discuss something important.

    “She
    drops this bomb that, my dad never wanted to tell me this, but they
    couldn’t conceive at the time, and they went to a fertility clinic at
    Duke University.

    “It was early 1977,” he said, “and they got a sperm donor.”

    Coming
    so soon on the heels of his father’s death, Harris said the confession
    caused him to spiral. He was raised as an only child, but 23andMe
    revealed he had multiple half-siblings.

    And Harris said his conversations with one sibling in particular stood out.

    At
    first, the woman was confused about their shared genetics, then
    curious. Maybe she was also donor-conceived, and their parents had used
    the same donor, she suggested.

    But when Harris started researching the woman’s maiden name, he discovered her father was Dr. Peete. He sent her a message.

    To Harris, the conclusion was clear: His mom’s doctor had used his own sperm instead of a donor’s.

    It
    took Peete’s daughter days to respond to the revelation, and when she
    did, she admitted to being “stunned, shocked and completely baffled.”

    “It
    didn’t even cross my mind that my dad would’ve been the donor, because
    my dad was the most honorable human being,” she wrote, “… being a part
    of whatever or however this happened just doesn’t add up.”

    But as they continued to exchange messages, she later noted how Jim looked a lot like her father.

    “I think there is more to this story we may never really know,” she said.

    The country doctor

    Dr.
    Charles Henry Peete Jr. died in 2013 at the age of 89. CNN reached out
    to his immediate family multiple times during the reporting of this
    story, but did not hear back.

    A public obituary posted online
    describes Peete as a “compassionate country doctor,” who discovered his
    passion for medicine by observing his father, the town physician.

    Peete
    graduated from Harvard Medical School in 1947 and, according to the
    obituary, he completed a residency in obstetrics, gynecology and
    endocrinology before accepting a position as an assistant professor and
    physician at Duke in 1956.

    Decades later, in the late 1970s, Peete
    would become one of Dr. Ken Fortier’s attending physicians and his
    mentor during his gynecology and gynecological surgery residency at
    Duke.

    “He was very calm and composed,” Fortier recalled. “He was
    superb technically as a surgeon. He made things look easy that others
    might struggle with.”

    Peete, he said, was the type of person who was “quietly there in the background, but they’re always there when you need (them).”

    At
    the time, Fortier told CNN, it was widely known that residents and
    medical students – especially those specializing in obstetrics and
    gynecology – were often tapped to donate sperm.

    “There wasn’t
    anything taboo about it,” he said. “There were people in the department
    who specialized in infertility that tended to have a kind of cadre of
    donors, and they usually were the best people that were generally
    healthy.”

    But when he learned, through CNN, that his mentor and
    colleague had fathered the children of some of his patients, Fortier
    searched for the right words.

    “The idea … the thought of using one’s own sperm … that surprised me,” he said.

    When fertility treatment becomes fraud

    Among
    the earliest publicized cases of intrauterine insemination (IUI) in the
    United States was an act of what’s come to be known as “fertility
    fraud” – when a physician deliberately misrepresents the origin of donor
    sperm or eggs, oftentimes using his own sample instead to impregnate a
    patient.

    In 1909, a physician in Minnesota wrote a letter to the
    editor of a medical publication describing an “artificial impregnation”
    he said he’d witnessed 25 years earlier – in 1884 – while attending
    medical school in Philadelphia.

    “At the time the procedure was so
    novel, so peculiar in its human ethics, that the six young men of the
    senior class who (witnessed) the operation were pledged to absolute
    secrecy,” author A.D. Hard wrote.

    A wealthy couple had
    visited the hospital to learn why they were struggling to conceive. Hard
    said the husband was deemed sterile and one of the medical students
    joked that the only way his wife could get pregnant was with “a hired
    man.”

    “The woman was chloroformed and with a hard rubber syringe
    some fresh semen from the best-looking member of the class was deposited
    in the uterus, and the cervix slightly plugged with gauze,” Hard wrote.

    The professor, he said, later confessed his actions to the woman’s husband.

    “Strange as it may seem, the man was delighted with the idea,” Hard wrote.

    Both the doctor and the professor agreed to never tell the man’s wife, he said.

    Today, these actions – and those of Dr. Peete – would be deemed not only unethical, but an act of medical malpractice.

    Informed
    consent – or the idea patients have the right to make independent and
    informed decisions about their own bodies and healthcare outcomes – is a
    cornerstone of modern medicine.

    In using his own sperm without his patients’ knowledge, experts told CNN, Peete violated that central covenant.

    “If
    he said, ‘we’re using a resident’s sperm,’ and it was his own sperm,
    that’s very problematic,” said Dr. Robert Klitzman, director of Columbia
    University’s Masters of Bioethics program and author of the book
    “Designing Babies.”

    “The standard (of care) should be to tell people where the sperm is coming from,” he said, “Even back then.”

    But Peete is far from the only doctor to have committed this type of deception. In 1992, Cecil Jacobson
    was convicted of 52 counts of fraud and perjury for inseminating his
    patients with his own sperm and was sent to prison. And the advent of
    consumer DNA products has led to numerous claims of fertility fraud over
    the years.

    For all its focus on creating life, the US fertility
    industry remains underregulated, Klitzman said. While many countries
    have pushed to limit or outright prohibit anonymous sperm donations,
    Klitzman noted the US does not have similar laws.

    “There are many
    things that we look at now with an ethical understanding of the full
    harms, risks, benefits … and think – what were they thinking back then?”
    Klitzman said.

    Peete ‘forever changed my life’

    That
    question haunts Peete’s progeny. Did he use his own sperm because there
    was a shortage? Or was this ego? Some kind of God complex that drove
    him to essentially commit medical fraud?

    For McKesson, the
    rationale for Peete’s actions is secondary to their repercussions.
    Learning the truth of her paternity has sparked something of an
    existential crisis, she said.

    “Ultimately, the hardest thing to
    process once you started putting the pieces together was that I was a
    product of a crime, that I was the product of medical rape,” she said.

    Both
    McKesson’s clotting disorder and Marfan syndrome are genetic, meaning
    one of her biological parents either passed on the traits, or it’s what
    scientists describe as a “new mutation.”

    Our DNA consists of
    billions of letters that combine to form a unique word: You. But
    sometimes, as the genetic code from each parent divides and replicates,
    changes are made. Scientists call these mutations.

    “Most mutations
    have no meaning,” Klitzman said, “but occasionally one does and that’s
    the so-called ‘de novo,’ – a new mutation.”

    These mutations can be spontaneous, but the paternal age of a sperm donor can also be a factor. A study published earlier this month in Nature revealed genetic risks for children increase as fathers age.

    Peete would have been approaching 60 at the time McKesson was conceived.

    When
    she learned Peete was her biological father, McKesson said she reached
    out to his family for more information on his health but did not hear
    back.

    “I’ve never blamed his family for anything, I mean, they
    didn’t ask for any of this either,” McKesson said.” But “let’s just say
    (Marfan syndrome) doesn’t run in his family – it could also come from
    the fact that he was older.”

    Without further insights into her paternal health history, McKesson admitted she doesn’t have a way to be sure.

    “I’ve just had to accept that this chapter is never going to be closed,” she said. “It’s just forever changed my life.”

    Still,
    McKesson said, because genetic impacts can span generations, she’s been
    vocal about her conditions with her half-siblings, encouraging anyone
    she meets to get themselves – and their children – tested.

    At McKesson’s insistence, Harris, who is 6’7”, was also tested for Marfan syndrome, but he was negative.

    Thus
    far, McKesson said Peete is believed to have fathered at least 12
    children outside of his immediate family over more than 20 years.

    But,
    she added, that number is solely based on those who have submitted DNA
    samples to consumer DNA sites like 23andMe and Ancestry.

    And with 23andMe filing for bankruptcy earlier this year, her chances of finding any additional siblings may be dwindling.

    A matter of life and death

    Since
    learning the truth of what happened, both Kruppa and McKesson said they
    have separately been in contact with Duke University, where Peete was
    employed.

    In emails reviewed by CNN, the university appeared
    initially to be responsive. A lawyer was hired to contact Peete’s
    previous clients and investigate his actions, and, at Kruppa’s
    instigation, the university now also offers an ethics course that
    addresses fertility fraud.

    For a time, McKesson said, the
    university also appeared to be mediating conversations between Peete’s
    victims and his immediate family.

    But when she continued to insist
    the Peete family provide more insight into the doctor’s genetic and
    medical history, they stopped responding.

    When reached for comment
    on this story, Duke Health officials said in a statement its program is
    built on a “commitment to operating within the highest ethical and
    legal standards in the field.”

    “We have been made aware of
    unacceptable actions by an individual that occurred in our program in
    the early days of fertility care during the late 1970s and early 1980s,”
    the statement said. “The unacceptable actions could not happen today at
    Duke Health and should never have happened.”

    CNN also reached out to the legal team that investigated Peete’s actions but did not receive a response.

    In the US, 14 states
    have passed laws against so-called fertility fraud. North Carolina,
    where Dr. Peete was employed, does not yet have a statute against it.

    Both
    McKesson and Kruppa said they have separately considered lawsuits. But,
    given the lack of regulation over the US fertility industry, and the
    fact that Peete has died, they feel their options are limited.

    McKesson said it’s “pretty impossible for the victims to have any sort of justice in this situation.”

    Still,
    she told CNN, she was most disappointed by how both the Peete family
    and Duke University have responded to the situation – especially
    considering that, at least in her case, it could be a matter of life and
    death.

    “I felt like this was a chance for them to step up and be
    involved in doing the right thing, and they’ve chosen not to,” she said.

    “The
    patients that were impacted and their families deserve to know that
    they may have had a crime committed against them and be acknowledged –
    and to know their family medical history to the extent that that’s
    possible.”

    For a while, McKesson said, she would research her
    newfound siblings to see what traits they have in common. She has the
    same smile as one of Peete’s daughters, she said. And both McKesson and
    Harris are slim and tall.

    But she said she’s decided to speak out
    now because she’s concerned other siblings might also unknowingly be
    living with a life-threatening genetic disorder.

    With treatment, a person diagnosed with Marfan syndrome can expect to live as long as someone without the disease.

    But left untreated, the average life expectancy is 45 years.

    “My
    hope in sharing my story is that if I have any other half-siblings out
    there, that I could save their life by knowing my medical history,” she
    said.

    “I’m trying to do the right thing.”

    CNN’s Ryan Young and Meridith Edwards contributed to this report.

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  • Venice Canal assault victim files $5-million claim against the city of Los Angeles

    Venice Canal assault victim files $5-million claim against the city of Los Angeles

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    A woman who was attacked and sexually assaulted while out for a walk on the Venice Canals in April has filed a $5-million claim against the city of Los Angeles, charging that the government was derelict in its duty to provide safe streets and protect its citizens.

    Mary Klein, 55, who suffered a savage beating that left her with missing teeth and a blood clot in her brain, was attacked around 10:30 p.m. April 6 as she strolled through the upscale seaside neighborhood. Another woman, Sarah Alden, 53, was also attacked that night and later died.

    Police later arrested Anthony Francisco Jones, 29; he was charged with two counts of forcible rape, murder, attempted murder, mayhem, torture and sodomy by use of force. He pleaded not guilty to the charges.

    The Times does not normally identify victims of sexual assault, but Klein came forward to share her story, saying people should take it as a wake-up call that more social services are needed for people suffering from mental illness and more police protection is needed for everyone.

    “That’s why all this crime is happening — we’re ignoring the extreme mental health crisis going on in our streets,” she said this summer.

    In filing her claim, Klein said she is trying to drive home the point that the government must do more to protect its citizens. The attack on her, she said, has turned her into an activist for public safety.

    Los Angeles City officials could not immediately be reached for comment on the claim.

    Klein filmed herself walking up to Los Angeles City Hall on Friday to submit her claim, speaking into the camera as the government buildings loomed behind her. A claim against the city can be a precursor to a lawsuit.

    “There is a dereliction of duty by the government in Los Angeles, in California,” she says in her video. “A dereliction of duty to protect its citizens from the criminals and also to fund the police correctly.”

    “I have lifelong damages to my jaw, my brain, blood clotting in my brain, due to a transient attacking me on an un-patrolled street in Venice,” she said. The street, she said, “was dark, no lighting, a public street where numerous incidents of violent crime and murder have occurred, and still absolutely no police presence on the street.”

    “That’s not the police’s fault,” she said. “That’s the people who defund the police.”

    In an interview, she said she was appreciative of Los Angeles officials, including Mayor Karen Bass, the City Council and the Los Angeles Police Department. She said she supports Bass’s goal to expand the LAPD by 1,000 officers.

    “This is not about City Hall,” she said. “I see them doing a lot of work to help the community.” But the government as a whole must do more, she said.

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    Jessica Garrison

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  • The Enigma of ‘Heat-Related’ Deaths

    The Enigma of ‘Heat-Related’ Deaths

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    The autopsy should have been a piece of cake. My patient had a history of widely metastatic cancer, which was pretty straightforward as far as causes of death go. Entering the various body cavities, my colleague and I found what we anticipated: Nearly every organ was riddled with tumors. But after we had completed the work, I realized that I knew why the patient had died, but not why he’d died that day. We found no evidence of a heart attack or blood clot or ruptured bowel. Nothing to explain his sudden demise. Yes, he had advanced cancer—but he’d been living with that cancer the day before he died, and over many weeks and months preceding. I asked my colleague what he thought. Perhaps there had been some subtle change in the patient’s blood chemistry, or in his heart’s electrical signaling, that we simply couldn’t see? “I guess the patient just up and died,” he said.

    I’m a hospital pathologist; my profession is one of many trying to explain the end of life. In that role, I have learned time and again that even the most thorough medical exams leave behind uncertainty. Take the current spate of heat-related fatalities brought on by a summer of record-breaking temperatures. Residents of Phoenix endured a month of consecutive 110-degree days. People have been literally sizzling on sidewalks. And news organizations are taking note of what is said to be a growing body count: 39 heat deaths in Maricopa County, Arizona; 10 in Laredo, Texas. But the precision of these figures is illusory. Cause of death cannot be measured as exactly as the temperature, and what qualifies as “heat-related” will always be a judgment call: Some people die from heat; others just up and die when it happens to be hot.

    Mortality is contested ground, a place where different types of knowledge are in conflict. In Clark County, Nevada, for example, coroners spend weeks investigating possible heat-related deaths. Families are interviewed, death scenes are inspected, and medical tests are performed. The coroner must factor in all of these sources of information because no single autopsy finding can definitively diagnose a heat fatality. A victim may be found to have suffered from hyperthermia—an abnormally high body temperature—or they may be tossed into the more subjective bucket of those who died from ”environmental heat stress.”

    Very few deaths undergo such an extensive forensic examination in the first place. Most of the time, the circumstances appear straightforward—a 75-year-old has a stroke; a smoker succumbs to an exacerbation of his chronic lung disease—and the patient’s primary-care doctor or hospital physician completes the death certificate on their own. But heat silently worsens many preexisting conditions; oppressive temperatures can cause an already dysfunctional organ to fail. A recent study out of China estimated that mortality from heart attacks can rise as much as 74 percent during a severe, several-day heat wave. Another study from the U.S. found that even routine temperature fluctuations can subtly alter kidney function, cholesterol levels, and blood counts. Physicians can’t easily tease out these influences. If an elderly man on a park bench suddenly slouches over from a heart attack in 90-degree weather, it’s hard to say for sure whether the heat was what did him in. Epidemiologists must come to the rescue, using statistics to uncover those hidden causes at the population level. This bird’s-eye view shows a simple fact: Bad weather means more death. But it still doesn’t tell us what to think about the man on the bench.

    Read: America is failing to protect workers from extreme heat

    Research (and common sense) tells us that some individuals are going to be especially vulnerable to climate risks. Poverty, physical labor, substandard housing, advanced age, and medical comorbidities all put one in greater danger of experiencing heat-related illness. The weather has a way of kicking you while you’re down, and the wealthy and able-bodied are better able to dodge the blows. A financial struggle as small as an unpaid $51 portion of an electricity bill can prove deadly in the summer. In the autopsies I’ve performed, a patient’s family, medical record, and living situation often told a story of long-term social neglect. But there was no place on the death certificate for me to describe these tragic circumstances. There was certainly no checkbox to indicate that climate change contributed to a fatality. Such matters were out of my jurisdiction.

    The public-health approach to assessing deaths has its own problems. Mostly it’s confusing. Reams of scientific studies have reported on hundreds of different risk factors for mortality. Sultry weather appears to be dangerous, but so do skipping breakfast, taking naps, and receiving care from a male doctor. Researchers have declared just about everything a major killer. A few months ago, the surgeon general announced that feeling disconnected is as deadly as smoking up to 15 cigarettes a day. The FDA commissioner has said that misinformation is the nation’s leading cause of premature death. And is poverty or medical error the fourth-leading cause? I can’t keep track.

    With so many mortality statistics at our disposal, which ones get emphasized can be more a matter of politics than science. Liberals see the current heat wave—and its wave of heat-related deaths—as an urgent call to action to combat climate change, while conservatives dismiss this concern as a mental disorder. A recent Wall Street Journal op-ed concluded that worrying about climate change is irrational, because “if heat waves were as deadly as the press proclaims, Homo sapiens couldn’t have survived thousands of years without air conditioning.” (Humans survived thousands of years without penicillin, but syphilis was still a net negative.) Similarly, when COVID became the third-leading cause of death in the U.S., pandemic skeptics said it was a fiction: Victims were dying “with COVID,” not “from COVID.” Because many people who died of SARS-CoV-2 had underlying risk factors, some politicians and doctors brushed off the official numbers as hopelessly confounded. Who could say whether the virus had killed anyone at all?

    Read: Summer in the South is becoming unbearable

    The dismissal of COVID’s carnage was mostly cynical and unscientific. But it’s true that death certificates paint one picture of the pandemic, and excess-death calculations paint another. Scientists will be debating COVID’s exact body count for decades. Fatalities from heat are subject to similar ambiguities, even as their determination comes with real-world consequences. In June, for example, officials from Multnomah County, Oregon—where Portland is located—sued oil and gas producers over the effects of a 2021 heat wave that resulted in 69 heat-related deaths, as officially recorded. This statistic will likely be subjected to intense cross-examination. The pandemic showed us that casting doubt on the deceased is a convenient strategy.

    No matter how we count the bodies, extreme weather leads to suffering—especially among the most vulnerable members of society. A lot of people have already perished during this summer’s heat wave. Their passing is more than a coincidence—not all of them just up and died.

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    Benjamin Mazer

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  • Race, Income Can Determine Blood Cancer Outcomes, Studies Show

    Race, Income Can Determine Blood Cancer Outcomes, Studies Show

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    By Ernie Mundell 

    HealthDay Reporter

    MONDAY, Dec. 12, 2022 (HealthDay News) — If someone is stricken with a blood cancer or life-threatening clot, they’ll probably fare better if they are white and wealthy, three new studies show.
     

    The ongoing impact of patient race and income to medical outcomes was in the spotlight Saturday in New Orleans at the annual meeting of the American Society of Hematology (ASH).

    In one study, a team led by Dr. Matthew Maurer, of the Mayo Clinic in Rochester, Minn., looked at who got enrolled (or didn’t) in clinical trials for new treatments against a blood cancer known as diffuse large B-cell lymphoma (DLBCL).

    It’s the most common form of lymphoma in the United States. According to ASH, existing therapies help cure about 60% of patients, but another 40% may not be helped.

    So, enrollment in clinical trials can be crucial for some patients. The Mayo study examined data on enrollment in DLBCL trials from eight large academic medical centers across America.

    It found that 76% of enrollees were white.

    Results from lab tests were key to getting accepted into the trials, but Black or Hispanic Americans were much less likely to meet those lab-based criteria than were whites, the research showed.

    That means trial organizers may need to take a closer look at lab-based eligibility criteria to help level the playing field for entry into future clinical trials. “These exclusion criteria are not impacting everyone equally – they’re impacting minorities more than white non-Hispanic patients,” Maurer said in an ASH news release.

    Stem cell transplant disparities

    Another study looked at stem cell transplants that in many cases can cure a blood cancer. The procedures necessitate finding a donor (often a family member) with the same blood antigen proteins as the patient.

    If such a donor can’t be found, doctors can still perform the transplant, but it often uses cells that are “half-matched” and come from either umbilical cord blood or less-than-ideally matched family members or others. These transplants leave patients more vulnerable to dangerous immune reactions and require more intense follow-up care.

    The study was led by Dr. Warren Fingrut, of the Cord Blood Transplantation Program at Memorial Sloan Kettering Cancer Center in New York City. Looking at records from 372 people who underwent stem cell transplants at the center between 2020 and 2022, his team found that while only about one-quarter (24%) of patients with European (typically white) ancestry had to undergo the less well-matched form of transplant, that number rose to 58% among patients who were not of European descent.

    The likelihood of a more complex stem cell transplant being needed rose even higher if the minority patient also came from a low-income household, the investigators found.

    “Our transplant program is very committed to extending transplant access to minority populations, but our study highlights that many of these patients are both receiving the most complex transplants and facing significant socioeconomic challenges,” Fingrut said in the ASH news release. “Our findings show that addressing financial hardship will be critical to extend transplant access, especially to patients from minority groups.”

    Advanced treatments for a dangerous clot

    In a third study, researchers found that race and income seemed to matter when U.S. patients were hit by potentially life-threatening clots in the lungs known as pulmonary embolisms.

    Non-white and poorer patients were “significantly less likely to receive the most advanced therapies and more likely to die after suffering a pulmonary embolism,” the ASH news release noted.

    The study involved data on more than 1 million U.S. patients hospitalized with a dangerous clot in the lungs between 2016 and 2018. Over 66,000 had the most severe, life-threatening form of pulmonary embolism.

    Compared to white patients, Asian patients were 24% less likely to receive advanced therapies when hit by a severe form of pulmonary embolism, and they were 50% more likely to die, reported a team led by Dr. Mary Cushman, of the Larner College of Medicine at the University of Vermont.

    Likewise, Black patients in the same situation were 13% less likely to get the best treatments compared to white patients, and were 11% more likely to die. Hispanic patients were also 10% more likely to die from their embolism than white people were, the investigators found.

    Money and insurance also mattered: Folks insured via Medicaid or Medicare were 30% less likely to get an advanced therapy compared to the privately insured, the study found. And people who placed in the lowest one-quarter with regards to income were 9% more likely to die from their clot compared to folks placing in the top quarter of income.

    “Many people die of pulmonary embolism every year,” Cushman noted in the ASH news release. “It’s preventable and it’s certainly treatable. We need to think about what we can do in hospitals to make sure that care is equitable.”

    “I hope that clinicians will think about these findings in terms of how they take care of patients every day, and try their best to recognize their unconscious biases,” she added. “Clinicians need to look at the patient in front of them and remember that regardless of their social class or the color of their skin, they should be treated the same as everybody else.”

    Experts note that studies presented at medical meetings should be considered preliminary until published in a peer-reviewed journal.

    More information

    Find out more about blood cancers at the American Cancer Society.

     

     

    SOURCE: American Society of Hematology, news release, Dec. 10, 2022

     

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  • What Doctors Still Don’t Understand About Long COVID

    What Doctors Still Don’t Understand About Long COVID

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    As a pulmonary specialist, I spend most of my clinical time in the hospital—which, during pandemic surges, has meant many long days treating critically ill COVID-19 patients in the ICU. But I also work in an outpatient clinic, where I also treat those same sorts of patients after they’re discharged: people who survived weeks-long hospitalizations but have been dealing ever since with lung damage. Such patients often face the same social and economic factors that made them vulnerable to COVID-19 to begin with, and they require attentive care.

    Patients like these undoubtedly suffer what researchers have been calling post-acute sequelae of SARS-CoV-2, or PASC—which, according to one highly publicized recent CDC study, afflicts some 20 percent of COVID-19 survivors ages 18 to 64. Other studies have yielded lower estimates of the condition also called long COVID, and while differences in study methodology account for some of this variability, there’s a more fundamental issue eluding efforts to uncover the one “true” estimate of the likelihood of this condition. Quite simply, long COVID isn’t any one thing.

    From the April 2021 issue: Unlocking the mysteries of long COVID

    The wide spectrum of conditions that fall under the umbrella of long COVID impedes researchers’ ability to interpret estimates of national prevalence based on surveys of symptoms, which conflate different problems with different causes. More importantly, however, an incomplete and constrained perspective on what long COVID is or isn’t limits Americans’ understanding of who is suffering and why, and of what we can do to improve patients’ lives today.

    The cases of long COVID that turn up in news reports, the medical literature, and in the offices of doctors like me fall into a few rough (and sometimes overlapping) categories. The first seems most readily explainable: the combination of organ damage, often profound physical debilitation, and poor mental health inflicted by severe pneumonia and resultant critical illness. This serious long-term COVID-19 complication gets relatively little media attention despite its severity. The coronavirus can cause acute respiratory distress syndrome, the gravest form of pneumonia, which can in turn provoke a spiral of inflammation and injury that can end up taking down virtually every organ. I have seen many such complications in the ICU: failing hearts, collapsed lungs, failed kidneys, brain hemorrhages, limbs cut off from blood flow, and more. More than 7 million COVID-19 hospitalizations occurred in the United States before the Omicron wave, suggesting that millions could be left with damaged lungs or complications of critical illness. Whether these patients’ needs for care and rehabilitation are being adequately (and equitably) met is unclear: Ensuring that they are is an urgent priority.

    Recently, a second category of long COVID has made headlines. It includes the new onset of recognized medical conditions—like heart disease, a stroke, or a blood clot—after a mild COVID-19 infection. It might seem odd that an upper respiratory tract infection could trigger a heart attack. Yet this pattern has been well described after other common respiratory-virus infections, particularly influenza. Similarly, various types of infections can lead to blood clots in the legs, which can travel (dangerously) to the lungs. Respiratory infections are not hermetically sealed from the rest of the body; acute inflammation arising in one location can sometimes have consequences elsewhere.

    But mild COVID-19 is so common that measuring the prevalence of such complications—which also regularly occur in people without COVID-19—can be tricky. Well-controlled investigations are needed to disentangle causation and correlation, particularly because social disadvantage is associated both with COVID exposure and illnesses of basically every organ system. Some such studies, which analyzed giant electronic-health-record databases, have suggested that even mild COVID-19 is at least correlated with a startlingly wide spectrum of seemingly every illness, including diabetes, asthma, and kidney failure; basically every type of heart disease; alcohol-, benzodiazepine-, and opioid-use disorders; and much more.

    To be clear, this research generally suggests that such complications occur far less often after mild COVID-19 cases than severe ones, and the extent to which the coronavirus causes each such complication remains unclear. In other words, we can surmise that at least some of these complications (particularly vascular complications, which have been well-described in many studies) are likely a consequence of COVID-19, but we can’t say with certainty how many. And more importantly, we don’t yet understand why some people with mild COVID recover easily while others go on to experience such complications. However, an estimated 81 percent of Americans have now been infected at least once, so the public-health ramifications are large even if COVID causes only some of the aforementioned recognized diseases, and even if our individual risk of complications after a mild infection is modest. Regardless of cause, patients who do develop any such chronic diseases require attentive, ongoing medical care—a challenge in a nation where 30 million are uninsured and even more underinsured.

    Another category of long COVID is something rather more quotidian, if still very distressing for those experiencing it: respiratory symptoms that last longer than expected after an acute upper-respiratory infection caused by the coronavirus, but that are not associated with lung damage, critical illness, or a new diagnosis like a heart attack or diabetes. Symptoms such as shortness of breath and chest pain are common months after run-of-the-mill pneumonia unconnected to the coronavirus, for instance, while many patients who contract non-COVID-related upper respiratory infections subsequently report a protracted cough or a lingering loss of their sense of smell. That a COVID-related airway infection sometimes has similar consequences only stands to reason.

    Read: Long-haulers are fighting for their future

    However, none of these may be what most people think of when long COVID is invoked. Some may even argue that such syndromes are not, in fact, long COVID at all, even if they cause long-term suffering. “Long Covid is not a condition for which there are currently accepted objective diagnostic tests or biomarkers,” wrote Steven Phillips and Michelle Williams in the New England Journal of Medicine. “It is not blood clots, myocarditis, multisystem inflammatory disease, pneumonia, or any number of well-characterized conditions caused by Covid-19.” Instead, for some the term may invoke a chronic illness—a complex of numerous unexplained, potentially debilitating symptoms—even among those who may barely have felt sick with COVID in the acute phase. Symptoms may vary widely, and include severe fatigue, cognitive issues often described as brain fog, shortness of breath, “internal tremors,” gastrointestinal problems, palpitations, dizziness, and many other issues around the body—all typically following a mild acute respiratory infection. If the other forms of long COVID seem more easily explainable, this type is often characterized as a medical mystery.

    Teasing apart which kind of long COVID a person has is important, both to advance our understanding of the illness and to best care for people. Yet lumping and splitting varieties of long COVID into categories is not easy. A given patient’s case might have features of more than one of the types that I’ve described here. Some patient advocates and researchers have tended to exclude patients in the first category—that is, survivors of protracted critical illness—from their conception of COVID long-haulers. I would argue that, insofar as we define long COVID as lasting damage and symptoms imposed by SARS-CoV-2, the full variety of severe long-term manifestations should be included in its scope. “Clinical phenotyping” studies now under way may eventually help scientists and doctors better understand the needs of different types of patients, but patients in all categories deserve better care today.

    The biological mechanisms by which an acute coronavirus upper respiratory infection might lead to a bewildering range of chronic, burdensome symptoms even in the aftermath of mild infections are debated. Some scientists, for instance, believe that the virus causes an autoimmune disease akin to lupus. Meanwhile, one group of researchers has argued that even a mild respiratory infection from SARS-CoV-2 causes tiny clots to block tiny blood vessels all over the body, depriving tissues of oxygen throughout the body. Still others believe that the coronavirus causes a chronic infection, as such viruses as HIV or hepatitis C do. Meanwhile, some have emphasized the possibility of structural brain damage. While some published studies have provided support for each theory, none has been adequately validated as a central unifying thesis. Each is, however, worth continuing to explore.

    A recently published investigation, conducted at the National Institutes of Health, suggests that clinicians and scientists should consider additional possibilities as potential drivers of symptoms for at least some patients. The researchers found far higher levels of physical symptoms and mental distress among subjects who had had COVID (many with long COVID) than among those who had not. Yet symptoms could not be explained by basically any test results: Researchers found effectively no substantive differences in markers of inflammation or immune activation, in objective neurocognitive testing, or in heart, lung, liver, or kidney function. And yet these patients were suffering from such symptoms as fatigue, shortness of breath, concentration and memory problems, chest pain, and more. Notably, researchers did not identify viral persistence in the bodies of patients reporting troublesome symptoms.

    What this means in practice is that there are some people suffering from long COVID symptoms without evidence of structural damage to the body, autoimmunity, or chronic infection. Psychosocial strain and suffering, moreover, appears common in this population. Even pointing this out is sensitive territory—it leads some people to wrongly suggest that long COVID is less severe or concerning than those suffering from it describe, or even to question the reality of the illness. And, understandably, the invocation of psychosocial factors as potential contributing factors to suffering for some individuals may make patients feel as though they are being second-guessed. The reality, though, is that psychosocial strain is an important driver of physical symptoms and suffering—one that clinicians should treat with empathy. All suffering, after all, is ultimately produced and perceived in one place: our brain.

    Severe depression, for instance, can inflict debilitating and severe physical symptoms of every sort, including crushing fatigue and withering brain fog, and is itself linked to having had COVID-19. And notably, a recent study in JAMA Psychiatry found that pre-infection psychosocial distress—e.g. depression, anxiety, or loneliness—was associated with a 30–50 percent increase in the risk of long COVID among those infected, even after adjustment for various factors. A false separation of brain and body has long plagued medicine, but it does not reflect biological reality: After all, diverse neuropsychiatric processes are associated with numerous “physical” changes, ranging from reduced blood flow to the brain to high (or low) levels of the stress hormone cortisol.

    Illnesses of any cause that result in protracted time off one’s feet can also instigate (likely in conjunction with other factors) reversible cardiovascular deconditioning, wherein the blood volume contracts and the amount of blood ejected by the heart with each squeeze falls—changes that can lead to a racing heart rate or faintness when standing, as decades of studies have shown. Diverse neurological symptoms can also be produced by a glitch in the function rather than the structure of the brain—or what has been described as problems of brain “software” rather than “hardware”—resulting in conditions known as functional neurological disorders. Similar glitches, known as functional respiratory disorders, can disturb our breathing patterns or cause shortness of breath, even when our lungs are structurally normal. My point is not to speculate on some overarching hypothesis to explain all symptoms among all patients with long COVID. The whole point is that there’s unlikely to be just one. And there is still much to learn.

    Research is underway to better understand this spectrum of illnesses, and their causes. But whichever diverse factors might be contributing to patients’ symptoms, we can take steps—both among clinicians and as a society—to improve lives now. Social supports can be as important as medical interventions: For those unable to work, qualification for disability assistance should not depend on a particular lab or lung-function test result. All patients with long-COVID symptoms deserve and require high-quality medical care without onerous cost barriers that may bankrupt them, which further compounds suffering. Universal healthcare is, that is to say, desperately needed to respond to this pandemic and its aftermath.

    Additionally, while no specific long-COVID medications have emerged, some treatments may be helpful for improving certain symptoms regardless of the specific type of illness, such as physical rehabilitative treatments for those with shortness of breath or reduced exercise tolerance. Ensuring universal access to such specialized rehabilitative care is essential as we enter the next stage of this pandemic. So is helping patients avoid the emerging cottage industry of dodgy providers hawking unproven long-COVID therapies. Health-care professionals also need more education about the broad spectrum of COVID-19-related issues, both to improve care and reduce stigmatization of patients with all types of this illness.

    Read: The pandemic after the pandemic

    Doctors and scientists still have much to learn about symptoms that continue—or first turn up—months or weeks after an initial COVID infection. What’s clear today is that long COVID can be many different things. That may confound our efforts to categorize it and discuss its implications, but the sheer variety should not get in the way of care for all who are suffering.

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    Adam Gaffney

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