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azzed
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bullturds
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cocaine
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cocainees
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crackwhore
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cum
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cumsluted
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cunthunterer
cunthunteres
cunthuntering
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cunthunters
cunting
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cuntlicked
cuntlicker
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dagos
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damn
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damneder
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dickbag
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dickbags
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dickdippered
dickdipperer
dickdipperes
dickdippering
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dicker
dickes
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dickfaceed
dickfaceer
dickfacees
dickfaceing
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dickflippered
dickflipperer
dickflipperes
dickflippering
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dickheaded
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dickheadser
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dingleed
dingleer
dinglees
dingleing
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dipship
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dipshipes
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dizzyed
dizzyer
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dizzying
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dizzys
doggiestyleed
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dopeyer
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drunker
drunkes
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dumass
dumassed
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dumasses
dumassing
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dumasss
dumbass
dumbassed
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dumbassing
dumbassly
dumbasss
dummy
dummyed
dummyer
dummyes
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dyke
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dykeer
dykees
dykeing
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erotic
eroticed
eroticer
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erotics
extacy
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extacying
extacyly
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extasy
extasyed
extasyer
extasyes
extasying
extasyly
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facked
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faged
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fagged
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faggoted
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fagoted
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faiged
faiger
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faigts
fannybandit
fannybandited
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fannybandits
farted
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fartknockered
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fartly
farts
felch
felched
felcher
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fellateer
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fellateing
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fellatio
fellatioed
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feltched
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floozy
floozyed
floozyer
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foad
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freexes
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friggaer
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fuckined
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fuckinged
fuckinger
fuckinges
fuckinging
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fuckings
fuckining
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Why patients should ditch cloth masks
Are you still wearing a cloth face mask?
Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.
For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.
KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.
Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.
But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.
In fact, public health experts have been urging stronger mask protection for months.
“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”
Here’s what to know about these protective masks.
They’re necessary
Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.
The quality of a mask also matters a lot, said Dr. Wen.
“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”
If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”
But people should wear a 3-ply surgical mask at the very least.
Three-ply surgical and N95 mask qualities
With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.
“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”
Another important tip on 3-ply surgical masks and N95s: These masks are reusable.
But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
Protection first
For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.
But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”
Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.
“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”
“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”
For more information on where to find 3-ply surgical masks and N95s, check here or here to start.
A version of this article first appeared on WebMD.com.
Are you still wearing a cloth face mask?
Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.
For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.
KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.
Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.
But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.
In fact, public health experts have been urging stronger mask protection for months.
“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”
Here’s what to know about these protective masks.
They’re necessary
Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.
The quality of a mask also matters a lot, said Dr. Wen.
“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”
If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”
But people should wear a 3-ply surgical mask at the very least.
Three-ply surgical and N95 mask qualities
With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.
“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”
Another important tip on 3-ply surgical masks and N95s: These masks are reusable.
But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
Protection first
For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.
But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”
Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.
“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”
“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”
For more information on where to find 3-ply surgical masks and N95s, check here or here to start.
A version of this article first appeared on WebMD.com.
Are you still wearing a cloth face mask?
Amid the rapidly spreading Omicron variant, experts stress that we all should swap cloth masks for N95 respirators or 3-ply surgical masks.
For background: N95 respirators are tightly fitting masks that cover your mouth and nose and help prevent contact with droplets and tiny particles in the air from people talking, coughing, sneezing, and spreading in other ways. Usually worn by health care workers and first responders, these masks can filter up to 95% of air droplets and particles, according to the CDC.
KN95 and KN94 masks are similar but are designed to meet international standards, unlike N95s that are approved by the Centers for Disease Control and Prevention’s National Institute for Occupational Safety and Health.
Meanwhile, a 3-ply surgical mask is a looser-fitting mask that can help prevent contact with infected droplets in the air.
But recommendations to opt for N95 and 3-ply surgical masks over cloth masks are nothing new, says Leana Wen, MD, an emergency doctor and public health professor at George Washington University, Washington.
In fact, public health experts have been urging stronger mask protection for months.
“It’s not just with Omicron that we need better masks, it was with Delta, it was with Alpha before that,” Dr. Wen said. “We have known for many months that COVID-19 is airborne, and therefore, a simple cloth mask is not going to cut it.”
Here’s what to know about these protective masks.
They’re necessary
Omicron is spreading much faster than previous COVID-19 variants. As it’s up to three times as likely to spread as the Delta variant, mask-wearing is paramount right now, says Anita Gupta, DO, an adjunct assistant professor of anesthesiology and critical care medicine and pain medicine at Johns Hopkins University, Baltimore.
The quality of a mask also matters a lot, said Dr. Wen.
“Double masking, including a well-fitting cloth mask on top of a surgical mask, adds additional protection,” she said. “Ideally, though, people should be wearing an N95, KN95, or KF94 when in indoor settings around other people with unknown vaccination status.”
If wearing an N95 mask causes extreme discomfort, wear it in high-risk settings where there are lots of people, like crowded restaurants and busy commuter trains, says Dr. Wen. “If you’re in a grocery store, there’s plenty of space and ventilation. You may not need an N95. I recommend that people obtain different masks and practice with them in low-risk settings before they go out in public in a high-risk setting.”
But people should wear a 3-ply surgical mask at the very least.
Three-ply surgical and N95 mask qualities
With 3-ply surgical masks, the fit of the mask is often more of an issue than its comfort, Dr. Wen said. But there are ways to adjust these masks, especially for those who have smaller heads.
“You can put a rubber band around the ear loops and make them a bit tighter,” said Dr. Wen. “Some people have found that using pins in their hair, that’s another way of keeping the loops in place.”
Another important tip on 3-ply surgical masks and N95s: These masks are reusable.
But how many times you should use them varies, Dr. Wen said. “As an example, if you are sweating a lot, and the mask is now really damp. Or putting it in your purse or backpack, and now it’s misshapen, and you cannot get it back to fit on your face, then it’s time to throw it away.”
Protection first
For some, cloth masks became somewhat of a statement, with people sporting logos of their favorite NFL team, or maybe even a fun animal print.
But you should always keep in mind the purpose of wearing a mask, Dr. Wen said. “Mask wearing is very functional and is about reducing your likelihood of contracting COVID. People should also use whatever methods inspire them, too, but for me, it’s purely a functional exercise.”
Mask wearing is not always enjoyable, but it remains critical in keeping people safe from COVID-19, especially the elderly and other high-risk people, Gupta says.
“There is lots of research and experts working hard to stop COVID-19,” she says. “It is important for all of us to remember that wearing a mask alone doesn’t make us safe.”
“We all need to keep washing our hands frequently and maintaining a distance from people, as well.”
For more information on where to find 3-ply surgical masks and N95s, check here or here to start.
A version of this article first appeared on WebMD.com.
COVID-19–positive or exposed? What to do next
With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?
New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.
This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
If you have tested positive for COVID-19, what do you do next?
“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)
Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.
Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5 days.
Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.
According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
If you have been exposed to someone with COVID-19, what do you do next?
“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.
For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.
On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.
But if someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
When should the person who has been exposed get tested?
After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”
Testing should be done by those exposed at least once, Dr. Adalja said.
“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
At what point can the infected person mingle safely with others?
“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”
A version of this article first appeared on WebMD.com.
With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?
New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.
This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
If you have tested positive for COVID-19, what do you do next?
“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)
Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.
Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5 days.
Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.
According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
If you have been exposed to someone with COVID-19, what do you do next?
“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.
For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.
On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.
But if someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
When should the person who has been exposed get tested?
After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”
Testing should be done by those exposed at least once, Dr. Adalja said.
“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
At what point can the infected person mingle safely with others?
“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”
A version of this article first appeared on WebMD.com.
With new cases of COVID-19 skyrocketing to more than 240,000 a day recently in the U.S., many people are facing the same situation: A family member or friend tests positive or was exposed to someone who did, and the holiday gathering, visit, or return to work is just days or hours away. Now what?
New guidance issued Dec. 27 by the Centers for Disease Control and Prevention shortens the recommended isolation and quarantine period for the general population, coming after the agency shortened the isolation period for health care workers.
This news organization reached out to two infectious disease specialists to get answers to questions that are frequently asked in these situations.
If you have tested positive for COVID-19, what do you do next?
“If you have tested positive, you are infected. At the moment, you are [either] symptomatically affected or presymptomatically infected,’’ said Paul A. Offit, MD, director of the Vaccine Education Center and professor of pediatrics at Children’s Hospital of Philadelphia. At that point, you need to isolate for 5 days, according to the new CDC guidance. (That period has been shortened from 10 days.)
Isolation means separating the infected person from others. Quarantine refers to things you should do if you’re exposed to the virus or you have a close contact infected with COVID-19.
Under the new CDC guidelines, after the 5-day isolation, if the infected person then has no symptoms, he or she can leave isolation and then wear a mask for 5 days.
Those who test positive also need to tell their close contacts they are positive, said Amesh Adalja, MD, a senior scholar at the Johns Hopkins Center for Health Security.
According to the CDC, the change to a shortened quarantine time is motivated by science ‘’demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of the illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after.”
If you have been exposed to someone with COVID-19, what do you do next?
“If they are vaccinated and boosted, the guidance says there is no need to quarantine,” Dr. Adalja said. But the CDC guidance does recommend these people wear a well-fitting mask at all times when around others for 10 days after exposure.
For everyone else, including the unvaccinated and those who are more than 6 months out from their second Pfizer or Moderna vaccine dose, or more than 2 months from their J&J dose, the CDC recommends a quarantine for 5 days – and wearing a mask for the 5 days after that.
On a practical level, Dr. Adalja said he thinks those who are vaccinated but not boosted could also skip the quarantine and wear a mask for 10 days. Dr. Offit agrees. Because many people exposed have trouble quarantining, Dr. Offit advises those exposed who can’t follow that guidance to be sure to wear a mask for 10 days when indoors. The CDC guidance also offers that as another strategy – that if a 5-day quarantine is not feasible, the exposed person should wear a mask for 10 days when around others.
But if someone who was exposed gets symptoms, that person then enters the infected category and follows that guidance, Dr. Offit said.
When should the person who has been exposed get tested?
After the exposure, ‘’you should probably wait 2-3 days,” Dr. Offit said. “The virus has to reproduce itself.”
Testing should be done by those exposed at least once, Dr. Adalja said.
“But there’s data to support daily testing to guide their activities, but this is not CDC guidance. Home tests are sufficient for this purpose.”
At what point can the infected person mingle safely with others?
“Technically, if asymptomatic, 10 days without a mask, 5 days with a mask,” said Dr. Adalja. “I think this could also be guided with home test negativity being a gauge [as to whether to mingle].”
A version of this article first appeared on WebMD.com.
COVID-19 antigen tests may be less sensitive to Omicron: FDA
Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.
Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.
The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.
The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.
Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.
“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
Testing still important
The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.
They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.
The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.
An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.
The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.
The agency said that it will provide updated information and any needed recommendations when appropriate.
A version of this article first appeared on Medscape.com.
Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.
Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.
The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.
The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.
Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.
“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
Testing still important
The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.
They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.
The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.
An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.
The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.
The agency said that it will provide updated information and any needed recommendations when appropriate.
A version of this article first appeared on Medscape.com.
Rapid antigen tests for COVID-19 might be less effective at detecting the Omicron variant that is spreading rapidly across the United States, according to the Food and Drug Administration.
Early data suggest that COVID-19 antigen tests “do detect the Omicron variant but may have reduced sensitivity,” the FDA said in a statement posted Dec. 28 on its website.
The FDA is working with the National Institutes of Health’s Rapid Acceleration of Diagnostics (RADx) initiative to assess the performance of antigen tests with patient samples that have the Omicron variant.
The potential for antigen tests to be less sensitive for the Omicron variant emerged in tests using patient samples containing live virus, “which represents the best way to evaluate true test performance in the short term,” the FDA said.
Initial laboratory tests using heat-activated (killed) virus samples found that antigen tests were able to detect the Omicron variant.
“It is important to note that these laboratory data are not a replacement for clinical study evaluations using patient samples with live virus, which are ongoing. The FDA and RADx are continuing to further evaluate the performance of antigen tests using patient samples with live virus,” the FDA said.
Testing still important
The agency continues to recommend use of antigen tests as directed in the authorized labeling and in accordance with the instructions included with the tests.
They note that antigen tests are generally less sensitive and less likely to pick up very early infections, compared with molecular tests.
The FDA continues to recommend that an individual with a negative antigen test who has symptoms or a high likelihood of infection because of exposure follow-up with a molecular test to determine if they have COVID-19.
An individual with a positive antigen test should self-isolate and seek follow-up care with a health care provider to determine the next steps.
The FDA, with partners and test developers, are continuing to evaluate test sensitivity, as well as the best timing and frequency of antigen testing.
The agency said that it will provide updated information and any needed recommendations when appropriate.
A version of this article first appeared on Medscape.com.
Coronavirus can spread to heart, brain days after infection
The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.
The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.
“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.
“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”
The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.
“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.
“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”
Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.
“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.
A version of this article first appeared on WebMD.com.
The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.
The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.
“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.
“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”
The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.
“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.
“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”
Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.
“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.
A version of this article first appeared on WebMD.com.
The coronavirus that causes COVID-19 can spread to the heart and brain within days of infection and can survive for months in organs, according to a new study by the National Institutes of Health.
The virus can spread to almost every organ system in the body, which could contribute to the ongoing symptoms seen in “long COVID” patients, the study authors wrote. The study is considered one of the most comprehensive reviews of how the virus replicates in human cells and persists in the human body. It is under review for publication in the journal Nature.
“This is remarkably important work,” Ziyad Al-Aly, MD, director of the Clinical Epidemiology Center at the Veterans Affairs St. Louis Health Care System, told Bloomberg News. Dr. Al-Aly wasn’t involved with the NIH study but has researched the long-term effects of COVID-19.
“For a long time now, we have been scratching our heads and asking why long COVID seems to affect so many organ systems,” he said. “This paper sheds some light and may help explain why long COVID can occur even in people who had mild or asymptomatic acute disease.”
The NIH researchers sampled and analyzed tissues from autopsies on 44 patients who died after contracting the coronavirus during the first year of the pandemic. They found persistent virus particles in multiple parts of the body, including the heart and brain, for as long as 230 days after symptoms began. This could represent infection with defective virus particles, they said, which has also been seen in persistent infections among measles patients.
“We don’t yet know what burden of chronic illness will result in years to come,” Raina MacIntyre, PhD, a professor of global biosecurity at the University of New South Wales, Sydney, told Bloomberg News.
“Will we see young-onset cardiac failure in survivors or early-onset dementia?” she asked. “These are unanswered questions which call for a precautionary public health approach to mitigation of the spread of this virus.”
Unlike other COVID-19 autopsy research, the NIH team had a more comprehensive postmortem tissue collection process, which typically occurred within a day of the patient’s death, Bloomberg News reported. The researchers also used a variety of ways to preserve tissue to figure out viral levels. They were able to grow the virus collected from several tissues, including the heart, lungs, small intestine, and adrenal glands.
“Our results collectively show that, while the highest burden of SARS-CoV-2 is in the airways and lung, the virus can disseminate early during infection and infect cells throughout the entire body, including widely throughout the brain,” the study authors wrote.
A version of this article first appeared on WebMD.com.
Omega-3 supplementation improves sleep, mood in breast cancer patients on hormone therapy
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
FROM RESEARCHSQUARE
What causes cancer? There’s a lot we don’t know
People with cancer are often desperate to know what caused their disease. Was it something they did? Something they could have prevented?
In a recent analysis, experts estimated that about 40% of cancers can be explained by known, often modifiable risk factors. Smoking and obesity represent the primary drivers, though a host of other factors – germline mutations, alcohol, infections, or environmental pollutants like asbestos – contribute to cancer risk as well.
But what about the remaining 60% of cancers?
The study suggests that, And a small but significant number may simply be caused by chance.
Here’s what experts suspect those missing causes might be, and why they can be so difficult to confirm.
Possibility 1: Known risk factors contribute more than we realize
For certain factors, a straight line can be drawn to cancer.
Take smoking, for instance. Decades of research have helped scientists clearly delineate tobacco’s carcinogenic effects. Researchers have pinpointed a unique set of mutations in the tumors of smokers that can be seen when cells grown in a dish are exposed to the carcinogens present in tobacco.
In addition, experts have been able to collect robust data from epidemiologic studies on smoking prevalence as well as associated cancer risks and deaths, in large part because an individual’s lifetime tobacco exposure is fairly easy to measure.
“The evidence for smoking is incredibly consistent,” Paul Brennan, PhD, a cancer epidemiologist at the World Health Organization’s International Agency for Research on Cancer, said in an interview.
For other known risk factors, such as obesity and air pollution, many more questions than answers remain.
Because of the limitations in how such factors are measured, we are likely downplaying their effects, said Richard Martin, PhD, a professor of clinical epidemiology at the University of Bristol (England).
Take obesity. Excess body weight is associated with an increased risk of at least 13 cancers. Although risk estimates vary by study and cancer type, according to a global snapshot from 2012, being overweight or obese accounted for about 4% of all cancers worldwide – 1% in low-income countries and as high as 8% in high-income countries.
However, Dr. Brennan believes “we have underestimated the effect of obesity [on cancer].”
A key reason, he said, is most studies use body mass index to determine whether someone is overweight or obese, but BMI is a poor measure of body fat. BMI does not differentiate between fat and muscle, which means two people with the same height and weight can have the same BMI, even if one is an athlete who eats lean meats and vegetables while the other lives a sedentary life and consumes large quantities of processed foods and alcohol.
On top of that, studies often only calculate a person’s BMI once, and a single measurement can’t tell you how a person’s weight has fluctuated in recent years or across different stages of their life. However, recent analyses suggest that obesity status over time may be more relevant to cancer risk than one-off measures.
In addition, many studies now suggest that alterations to our gut microbes and high blood insulin level – often seen in people who are overweight or obese – may increase the risk of cancer and speed the growth of tumors.
When these additional factors are considered, the impact of excess body fat may ultimately play a much more significant role in cancer risk. In fact, according to Dr. Brennan, “if we estimate [the effects of obesity] properly, it might at some point become the main cause of cancer.”
Possibility 2: Environmental or lifestyle factors remain under the radar
Researchers have linked many substances we consume or are exposed to in our daily lives – air pollution, toxins from industrial waste, and highly processed foods – to cancer. But the extent or contribution of potential carcinogens in our surroundings, particularly those found almost everywhere at low levels, is still largely unknown.
One simple reason is the effects of many of these substances remain difficult to assess. For instance, it is much harder to study the impact of pollutants found in food or water, in which a given population will share similar exposure levels versus tobacco, where it is possible to compare a person who smokes a pack of cigarettes a day with a person who does not smoke.
“If you’ve got exposures that are ubiquitous, it can be difficult to discern their [individual] roles,” Dr. Martin said. “There are many causes that we [likely] don’t really know because everyone has been exposed.”
On the flip side, some carcinogenic substances that people encounter for limited periods might be missed if studies are not performed at the time of exposure.
“What’s in the body at age 40 may not reflect what you were exposed at age 5-10 on the playground or soccer field,” said Graham Colditz, MD, PhD, an epidemiologist and public health expert at Washington University, St. Louis. “The technology keeps changing so we can get better measures of what you’ve got exposure to today, but how that relates to 5, 10, 15 years ago is probably very variable.”
In addition, researchers have found that many carcinogens do not cause specific mutations in a cell’s DNA; rather, studies suggest that most carcinogens lead to cancer-promoting changes in cells, such as inflammation.
“We need to think of how potential carcinogens are causing cancer,” Dr. Brennan said. Instead of provoking mutations, potential carcinogens may use a “whole other kind of pathway.” When, for instance, inflammation becomes chronic, it may spur a cascade of events that ultimately leads to cancer.
Finally, not much is known about what causes cancers in low- and middle-income countries. Most of the research to date has been in high-income countries, such the United States, Australia, and parts of Europe.
“There’s a real lack of robust epidemiological studies in other parts of the world, Latin America, Africa, parts of Asia,” Marc Gunter, PhD, a molecular epidemiologist at the IARC, told this news organization.
Possibility 3: Some cancers occur by chance
When it comes to cancer risk, an element of chance may be at play. Cancer can occur in individuals who have very little exposure to known carcinogens or have no family history of cancer.
“We all know there are people who get cancer who eat very healthy diets, are never overweight, and never smoke,” Dr. Gunter said. “Then there are people on the other end of the extreme who don’t get cancer.”
But what fraction of cancers are attributable to chance?
A controversial 2017 study published in Science suggested that, based on the rate of cell turnover in healthy tissues in the lung, pancreas, and other parts of the body, only about one-third of cancers could be linked to environmental or genetic factors. The rest, the authors claimed, occurred because of random mutations that accumulated in a person’s DNA – in other words, bad luck.
That study brought on a flood of criticism from scientists who pointed to serious flaws in the work that led the researchers to significantly overestimate the share of chance-related cancers.
The actual proportion of cancers that occur by chance is much lower, according to Dr. Brennan. “If you look at international comparisons [of cancer rates] and take a conservative estimate, you see that maybe 10% or 15% of cancers are really chance.”
Whether some cancers are caused by bad luck or undiscovered risk factors remains an open question.
But the bottom line is many unknown causes of cancer are likely environmental or lifestyle related, which means that, in theory, they can be altered, even prevented.
“There is always going to be some element of chance, but you can modify your chance, depending on your lifestyle and maybe other factors, which we don’t fully understand yet,” Dr. Gunter said.
The good news is that, when it comes to prevention, there are many ways to modify our behaviors – such as consuming fewer processed meats, going for a daily walk, or getting vaccinated against cancer-causing viruses – to improve our chances of living cancer free. And as scientists better understand more about what causes cancer, possibilities for prevention will only grow.
“There is a constant, slow growth [in knowledge] that is lowering the overall risk of cancer,” Dr. Brennan said. “We’re never going to eliminate cancer, but we will be able to control it as a disease.”
A version of this article first appeared on Medscape.com.
People with cancer are often desperate to know what caused their disease. Was it something they did? Something they could have prevented?
In a recent analysis, experts estimated that about 40% of cancers can be explained by known, often modifiable risk factors. Smoking and obesity represent the primary drivers, though a host of other factors – germline mutations, alcohol, infections, or environmental pollutants like asbestos – contribute to cancer risk as well.
But what about the remaining 60% of cancers?
The study suggests that, And a small but significant number may simply be caused by chance.
Here’s what experts suspect those missing causes might be, and why they can be so difficult to confirm.
Possibility 1: Known risk factors contribute more than we realize
For certain factors, a straight line can be drawn to cancer.
Take smoking, for instance. Decades of research have helped scientists clearly delineate tobacco’s carcinogenic effects. Researchers have pinpointed a unique set of mutations in the tumors of smokers that can be seen when cells grown in a dish are exposed to the carcinogens present in tobacco.
In addition, experts have been able to collect robust data from epidemiologic studies on smoking prevalence as well as associated cancer risks and deaths, in large part because an individual’s lifetime tobacco exposure is fairly easy to measure.
“The evidence for smoking is incredibly consistent,” Paul Brennan, PhD, a cancer epidemiologist at the World Health Organization’s International Agency for Research on Cancer, said in an interview.
For other known risk factors, such as obesity and air pollution, many more questions than answers remain.
Because of the limitations in how such factors are measured, we are likely downplaying their effects, said Richard Martin, PhD, a professor of clinical epidemiology at the University of Bristol (England).
Take obesity. Excess body weight is associated with an increased risk of at least 13 cancers. Although risk estimates vary by study and cancer type, according to a global snapshot from 2012, being overweight or obese accounted for about 4% of all cancers worldwide – 1% in low-income countries and as high as 8% in high-income countries.
However, Dr. Brennan believes “we have underestimated the effect of obesity [on cancer].”
A key reason, he said, is most studies use body mass index to determine whether someone is overweight or obese, but BMI is a poor measure of body fat. BMI does not differentiate between fat and muscle, which means two people with the same height and weight can have the same BMI, even if one is an athlete who eats lean meats and vegetables while the other lives a sedentary life and consumes large quantities of processed foods and alcohol.
On top of that, studies often only calculate a person’s BMI once, and a single measurement can’t tell you how a person’s weight has fluctuated in recent years or across different stages of their life. However, recent analyses suggest that obesity status over time may be more relevant to cancer risk than one-off measures.
In addition, many studies now suggest that alterations to our gut microbes and high blood insulin level – often seen in people who are overweight or obese – may increase the risk of cancer and speed the growth of tumors.
When these additional factors are considered, the impact of excess body fat may ultimately play a much more significant role in cancer risk. In fact, according to Dr. Brennan, “if we estimate [the effects of obesity] properly, it might at some point become the main cause of cancer.”
Possibility 2: Environmental or lifestyle factors remain under the radar
Researchers have linked many substances we consume or are exposed to in our daily lives – air pollution, toxins from industrial waste, and highly processed foods – to cancer. But the extent or contribution of potential carcinogens in our surroundings, particularly those found almost everywhere at low levels, is still largely unknown.
One simple reason is the effects of many of these substances remain difficult to assess. For instance, it is much harder to study the impact of pollutants found in food or water, in which a given population will share similar exposure levels versus tobacco, where it is possible to compare a person who smokes a pack of cigarettes a day with a person who does not smoke.
“If you’ve got exposures that are ubiquitous, it can be difficult to discern their [individual] roles,” Dr. Martin said. “There are many causes that we [likely] don’t really know because everyone has been exposed.”
On the flip side, some carcinogenic substances that people encounter for limited periods might be missed if studies are not performed at the time of exposure.
“What’s in the body at age 40 may not reflect what you were exposed at age 5-10 on the playground or soccer field,” said Graham Colditz, MD, PhD, an epidemiologist and public health expert at Washington University, St. Louis. “The technology keeps changing so we can get better measures of what you’ve got exposure to today, but how that relates to 5, 10, 15 years ago is probably very variable.”
In addition, researchers have found that many carcinogens do not cause specific mutations in a cell’s DNA; rather, studies suggest that most carcinogens lead to cancer-promoting changes in cells, such as inflammation.
“We need to think of how potential carcinogens are causing cancer,” Dr. Brennan said. Instead of provoking mutations, potential carcinogens may use a “whole other kind of pathway.” When, for instance, inflammation becomes chronic, it may spur a cascade of events that ultimately leads to cancer.
Finally, not much is known about what causes cancers in low- and middle-income countries. Most of the research to date has been in high-income countries, such the United States, Australia, and parts of Europe.
“There’s a real lack of robust epidemiological studies in other parts of the world, Latin America, Africa, parts of Asia,” Marc Gunter, PhD, a molecular epidemiologist at the IARC, told this news organization.
Possibility 3: Some cancers occur by chance
When it comes to cancer risk, an element of chance may be at play. Cancer can occur in individuals who have very little exposure to known carcinogens or have no family history of cancer.
“We all know there are people who get cancer who eat very healthy diets, are never overweight, and never smoke,” Dr. Gunter said. “Then there are people on the other end of the extreme who don’t get cancer.”
But what fraction of cancers are attributable to chance?
A controversial 2017 study published in Science suggested that, based on the rate of cell turnover in healthy tissues in the lung, pancreas, and other parts of the body, only about one-third of cancers could be linked to environmental or genetic factors. The rest, the authors claimed, occurred because of random mutations that accumulated in a person’s DNA – in other words, bad luck.
That study brought on a flood of criticism from scientists who pointed to serious flaws in the work that led the researchers to significantly overestimate the share of chance-related cancers.
The actual proportion of cancers that occur by chance is much lower, according to Dr. Brennan. “If you look at international comparisons [of cancer rates] and take a conservative estimate, you see that maybe 10% or 15% of cancers are really chance.”
Whether some cancers are caused by bad luck or undiscovered risk factors remains an open question.
But the bottom line is many unknown causes of cancer are likely environmental or lifestyle related, which means that, in theory, they can be altered, even prevented.
“There is always going to be some element of chance, but you can modify your chance, depending on your lifestyle and maybe other factors, which we don’t fully understand yet,” Dr. Gunter said.
The good news is that, when it comes to prevention, there are many ways to modify our behaviors – such as consuming fewer processed meats, going for a daily walk, or getting vaccinated against cancer-causing viruses – to improve our chances of living cancer free. And as scientists better understand more about what causes cancer, possibilities for prevention will only grow.
“There is a constant, slow growth [in knowledge] that is lowering the overall risk of cancer,” Dr. Brennan said. “We’re never going to eliminate cancer, but we will be able to control it as a disease.”
A version of this article first appeared on Medscape.com.
People with cancer are often desperate to know what caused their disease. Was it something they did? Something they could have prevented?
In a recent analysis, experts estimated that about 40% of cancers can be explained by known, often modifiable risk factors. Smoking and obesity represent the primary drivers, though a host of other factors – germline mutations, alcohol, infections, or environmental pollutants like asbestos – contribute to cancer risk as well.
But what about the remaining 60% of cancers?
The study suggests that, And a small but significant number may simply be caused by chance.
Here’s what experts suspect those missing causes might be, and why they can be so difficult to confirm.
Possibility 1: Known risk factors contribute more than we realize
For certain factors, a straight line can be drawn to cancer.
Take smoking, for instance. Decades of research have helped scientists clearly delineate tobacco’s carcinogenic effects. Researchers have pinpointed a unique set of mutations in the tumors of smokers that can be seen when cells grown in a dish are exposed to the carcinogens present in tobacco.
In addition, experts have been able to collect robust data from epidemiologic studies on smoking prevalence as well as associated cancer risks and deaths, in large part because an individual’s lifetime tobacco exposure is fairly easy to measure.
“The evidence for smoking is incredibly consistent,” Paul Brennan, PhD, a cancer epidemiologist at the World Health Organization’s International Agency for Research on Cancer, said in an interview.
For other known risk factors, such as obesity and air pollution, many more questions than answers remain.
Because of the limitations in how such factors are measured, we are likely downplaying their effects, said Richard Martin, PhD, a professor of clinical epidemiology at the University of Bristol (England).
Take obesity. Excess body weight is associated with an increased risk of at least 13 cancers. Although risk estimates vary by study and cancer type, according to a global snapshot from 2012, being overweight or obese accounted for about 4% of all cancers worldwide – 1% in low-income countries and as high as 8% in high-income countries.
However, Dr. Brennan believes “we have underestimated the effect of obesity [on cancer].”
A key reason, he said, is most studies use body mass index to determine whether someone is overweight or obese, but BMI is a poor measure of body fat. BMI does not differentiate between fat and muscle, which means two people with the same height and weight can have the same BMI, even if one is an athlete who eats lean meats and vegetables while the other lives a sedentary life and consumes large quantities of processed foods and alcohol.
On top of that, studies often only calculate a person’s BMI once, and a single measurement can’t tell you how a person’s weight has fluctuated in recent years or across different stages of their life. However, recent analyses suggest that obesity status over time may be more relevant to cancer risk than one-off measures.
In addition, many studies now suggest that alterations to our gut microbes and high blood insulin level – often seen in people who are overweight or obese – may increase the risk of cancer and speed the growth of tumors.
When these additional factors are considered, the impact of excess body fat may ultimately play a much more significant role in cancer risk. In fact, according to Dr. Brennan, “if we estimate [the effects of obesity] properly, it might at some point become the main cause of cancer.”
Possibility 2: Environmental or lifestyle factors remain under the radar
Researchers have linked many substances we consume or are exposed to in our daily lives – air pollution, toxins from industrial waste, and highly processed foods – to cancer. But the extent or contribution of potential carcinogens in our surroundings, particularly those found almost everywhere at low levels, is still largely unknown.
One simple reason is the effects of many of these substances remain difficult to assess. For instance, it is much harder to study the impact of pollutants found in food or water, in which a given population will share similar exposure levels versus tobacco, where it is possible to compare a person who smokes a pack of cigarettes a day with a person who does not smoke.
“If you’ve got exposures that are ubiquitous, it can be difficult to discern their [individual] roles,” Dr. Martin said. “There are many causes that we [likely] don’t really know because everyone has been exposed.”
On the flip side, some carcinogenic substances that people encounter for limited periods might be missed if studies are not performed at the time of exposure.
“What’s in the body at age 40 may not reflect what you were exposed at age 5-10 on the playground or soccer field,” said Graham Colditz, MD, PhD, an epidemiologist and public health expert at Washington University, St. Louis. “The technology keeps changing so we can get better measures of what you’ve got exposure to today, but how that relates to 5, 10, 15 years ago is probably very variable.”
In addition, researchers have found that many carcinogens do not cause specific mutations in a cell’s DNA; rather, studies suggest that most carcinogens lead to cancer-promoting changes in cells, such as inflammation.
“We need to think of how potential carcinogens are causing cancer,” Dr. Brennan said. Instead of provoking mutations, potential carcinogens may use a “whole other kind of pathway.” When, for instance, inflammation becomes chronic, it may spur a cascade of events that ultimately leads to cancer.
Finally, not much is known about what causes cancers in low- and middle-income countries. Most of the research to date has been in high-income countries, such the United States, Australia, and parts of Europe.
“There’s a real lack of robust epidemiological studies in other parts of the world, Latin America, Africa, parts of Asia,” Marc Gunter, PhD, a molecular epidemiologist at the IARC, told this news organization.
Possibility 3: Some cancers occur by chance
When it comes to cancer risk, an element of chance may be at play. Cancer can occur in individuals who have very little exposure to known carcinogens or have no family history of cancer.
“We all know there are people who get cancer who eat very healthy diets, are never overweight, and never smoke,” Dr. Gunter said. “Then there are people on the other end of the extreme who don’t get cancer.”
But what fraction of cancers are attributable to chance?
A controversial 2017 study published in Science suggested that, based on the rate of cell turnover in healthy tissues in the lung, pancreas, and other parts of the body, only about one-third of cancers could be linked to environmental or genetic factors. The rest, the authors claimed, occurred because of random mutations that accumulated in a person’s DNA – in other words, bad luck.
That study brought on a flood of criticism from scientists who pointed to serious flaws in the work that led the researchers to significantly overestimate the share of chance-related cancers.
The actual proportion of cancers that occur by chance is much lower, according to Dr. Brennan. “If you look at international comparisons [of cancer rates] and take a conservative estimate, you see that maybe 10% or 15% of cancers are really chance.”
Whether some cancers are caused by bad luck or undiscovered risk factors remains an open question.
But the bottom line is many unknown causes of cancer are likely environmental or lifestyle related, which means that, in theory, they can be altered, even prevented.
“There is always going to be some element of chance, but you can modify your chance, depending on your lifestyle and maybe other factors, which we don’t fully understand yet,” Dr. Gunter said.
The good news is that, when it comes to prevention, there are many ways to modify our behaviors – such as consuming fewer processed meats, going for a daily walk, or getting vaccinated against cancer-causing viruses – to improve our chances of living cancer free. And as scientists better understand more about what causes cancer, possibilities for prevention will only grow.
“There is a constant, slow growth [in knowledge] that is lowering the overall risk of cancer,” Dr. Brennan said. “We’re never going to eliminate cancer, but we will be able to control it as a disease.”
A version of this article first appeared on Medscape.com.
COVID booster protection may wane in about 10 weeks, new data show
new data from Britain.
, according toU.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.
“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”
Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.
Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)
Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.
The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.
“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.
The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.
A version of this article first appeared on WebMD.com.
new data from Britain.
, according toU.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.
“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”
Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.
Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)
Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.
The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.
“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.
The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.
A version of this article first appeared on WebMD.com.
new data from Britain.
, according toU.K. health officials shared the data just before Christmas and noted that there haven’t been enough severe cases of the Omicron variant to calculate how well boosters protect against severe disease. But they believe the extra shots provide significant protection against hospitalization and death.
“It will be a few weeks before effectiveness against severe disease with Omicron can be estimated,” U.K. Health Security Agency officials wrote in the report. “However, based on experience with previous variants, this is likely to be substantially higher than the estimates against symptomatic disease.”
Since countries began reporting Omicron cases in November, multiple studies have suggested the variant is better at escaping antibodies from vaccination and previous infection, according to the New York Times. The U.K. report adds to that, noting that both the initial vaccine series and booster doses were less effective and faded faster against the Omicron variant than the Delta variant.
Among those who received two doses of the AstraZeneca vaccine, a booster of the Pfizer or Moderna vaccine was 60% effective at preventing symptomatic disease 2 to 4 weeks after the shot. But after 10 weeks, the Pfizer booster was 35% effective, and the Moderna booster was 45% effective. (The AstraZeneca vaccine is not authorized in the United States, but the Johnson & Johnson shot uses a similar technology, the New York Times reported.)
Among those who received three Pfizer doses, vaccine effectiveness was 70% about a week after the booster but dropped to 45% after 10 weeks. At the same time, those who received an initial two-dose series of the Pfizer vaccine and then a Moderna booster seemed to have 75% effectiveness up to 9 weeks.
The report was based on an analysis of 148,000 Delta cases and 68,000 Omicron cases in the United Kingdom through Dec. 20. So far, the U.K. health officials wrote, Omicron infections appear to be less severe and less likely to lead to hospitalization than Delta infections. At that time, 132 people with lab-confirmed Omicron had been admitted to hospitals, and 14 deaths had been reported among ages 52-96.
“This analysis is preliminary because of the small numbers of Omicron cases currently in hospital and the limited spread of Omicron into older age groups as yet,” the report said.
The reinfection rate has also increased for the Omicron variant, the report found. Among the 116,000 people who had an Omicron infection, about 11,000 -- or 9.5% -- were linked to a previously confirmed infection, which is likely an undercount of reinfections. In the data analyzed, 69 Omicron cases were a third episode of COVID-19 infection, and 290 cases occurred 60-89 days after a first infection.
A version of this article first appeared on WebMD.com.
Remdesivir may keep unvaccinated out of the hospital: Study
The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.
Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.
All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.
An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.
The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.
Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.
“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”
Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.
Gilead released the study findings in September.
A version of this article first appeared on WebMD.com.
The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.
Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.
All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.
An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.
The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.
Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.
“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”
Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.
Gilead released the study findings in September.
A version of this article first appeared on WebMD.com.
The antiviral remdesivir, an intravenous drug given mostly to seriously ill COVID-19 patients in hospitals, could keep unvaccinated people who become infected out of the hospital if given on an outpatient basis, a new study says.
Researchers studied 562 unvaccinated people from September 2020 to April 2021, according to the study published in the New England Journal of Medicine. The study determined the risk of hospitalization or death was 87% lower in study participants who were given remdesivir than participants who received a placebo.
All participants were at high risk of developing severe COVID-19 because of their age – they were over 60 – or because they had an underlying medical condition such as diabetes or obesity.
An important caveat: The findings are based on data collected before the Delta variant surged in the summer of 2021 or the Omicron variant surged late in the year, the Washington Post reported.
The new study says the drug could be helpful in keeping vaccinated as well as unvaccinated people out of the hospital – an important factor as the Omicron surge threatens to overwhelm health systems around the world.
Remdesivir could be a boon for COVID-19 patients in parts of the world that don’t have vaccines or for patients with immunocompromised systems.
“These data provide evidence that a 3-day course of remdesivir could play a critical role in helping COVID-19 patients stay out of the hospital,” Robert L. Gottlieb, MD, PhD, the therapeutic lead for COVID-19 research at Baylor Scott & White Health in Dallas, said in a news release from Gilead Pharmaceuticals. “While our hospitals are ready to assist patients in need, prevention and early intervention are preferable to reduce the risk of disease progression and allow patients not requiring oxygen to recover from home when appropriate.”
Remdesivir was the first antiviral for COVID-19 authorized by the Food and Drug Administration. It was given to then-President Donald Trump when he was hospitalized with COVID-19 in October 2020.
Gilead released the study findings in September.
A version of this article first appeared on WebMD.com.
New studies suggest Omicron infections are less severe than Delta ones
People who get COVID-19 infections caused by the Omicron variant are less likely to need hospital care, compared with those infected by the Delta variant, according to two large new studies from the U.K. and South Africa.
The findings, which were released ahead of peer review, add to previous glimmers of evidence suggesting that Omicron – while extremely contagious -– may result in less severe symptoms than its predecessors.
“This is helping us quantify how much less severe Omicron is than Delta, and it appears to be between 40 to 75% reduced risk of hospitalizations, adjusted for many factors, which is very good,” said Eric Topol, MD, the editor-in-chief of Medscape and a cardiologist at Scripps Research Translational Institute in La Jolla, CA.
The first analysis, which was done by the World Health Organization Collaborating Centre for Infectious Disease Modelling and Imperial College London, found that overall, people infected by Omicron had about a 20% reduced risk of needing any hospital care for their infections and a 40% lower risk of an overnight hospital stay, compared to those infected with Delta.
Meanwhile, people who were re-infected – meaning they caught Omicron after recovering from a previous COVID-19 infection – had a 50%-60% lower risk of needing hospital care, likely reflecting the benefits of having some prior immunity against the same family of viruses.
The study included everyone with polymerase chain reaction-confirmed COVID-19 in the U.K. during the first 2 weeks of December – roughly 56,000 Omicron cases and 269,000 Delta infections.
The second study, from researchers at the National Institute for Communicable Diseases in South Africa, included more than 29,000 COVID-19 cases that had lab results highly suggestive of Omicron infections. Compared to people infected with the Delta variant, those with presumed Omicron infections were about 70% less likely to have severe disease.
While the news is hopeful for individuals, on a population level, health care systems may still be stressed, the study authors warned.
“Given the high transmissibility of the Omicron virus, there remains the potential for health services to face increasing demand if Omicron cases continue to grow at the rate that has been seen in recent weeks,” said study author Neil Ferguson, PhD, who studies how infectious diseases spread at Imperial College London.
The study authors say their findings are specific to the U.K. and South Africa, where substantial portions of the population have some immune protection from past infection. In other words, they may not apply to countries where fewer people have been vaccinated or recovered from a bout with COVID-19.
A version of this article first appeared on WebMD.com.
People who get COVID-19 infections caused by the Omicron variant are less likely to need hospital care, compared with those infected by the Delta variant, according to two large new studies from the U.K. and South Africa.
The findings, which were released ahead of peer review, add to previous glimmers of evidence suggesting that Omicron – while extremely contagious -– may result in less severe symptoms than its predecessors.
“This is helping us quantify how much less severe Omicron is than Delta, and it appears to be between 40 to 75% reduced risk of hospitalizations, adjusted for many factors, which is very good,” said Eric Topol, MD, the editor-in-chief of Medscape and a cardiologist at Scripps Research Translational Institute in La Jolla, CA.
The first analysis, which was done by the World Health Organization Collaborating Centre for Infectious Disease Modelling and Imperial College London, found that overall, people infected by Omicron had about a 20% reduced risk of needing any hospital care for their infections and a 40% lower risk of an overnight hospital stay, compared to those infected with Delta.
Meanwhile, people who were re-infected – meaning they caught Omicron after recovering from a previous COVID-19 infection – had a 50%-60% lower risk of needing hospital care, likely reflecting the benefits of having some prior immunity against the same family of viruses.
The study included everyone with polymerase chain reaction-confirmed COVID-19 in the U.K. during the first 2 weeks of December – roughly 56,000 Omicron cases and 269,000 Delta infections.
The second study, from researchers at the National Institute for Communicable Diseases in South Africa, included more than 29,000 COVID-19 cases that had lab results highly suggestive of Omicron infections. Compared to people infected with the Delta variant, those with presumed Omicron infections were about 70% less likely to have severe disease.
While the news is hopeful for individuals, on a population level, health care systems may still be stressed, the study authors warned.
“Given the high transmissibility of the Omicron virus, there remains the potential for health services to face increasing demand if Omicron cases continue to grow at the rate that has been seen in recent weeks,” said study author Neil Ferguson, PhD, who studies how infectious diseases spread at Imperial College London.
The study authors say their findings are specific to the U.K. and South Africa, where substantial portions of the population have some immune protection from past infection. In other words, they may not apply to countries where fewer people have been vaccinated or recovered from a bout with COVID-19.
A version of this article first appeared on WebMD.com.
People who get COVID-19 infections caused by the Omicron variant are less likely to need hospital care, compared with those infected by the Delta variant, according to two large new studies from the U.K. and South Africa.
The findings, which were released ahead of peer review, add to previous glimmers of evidence suggesting that Omicron – while extremely contagious -– may result in less severe symptoms than its predecessors.
“This is helping us quantify how much less severe Omicron is than Delta, and it appears to be between 40 to 75% reduced risk of hospitalizations, adjusted for many factors, which is very good,” said Eric Topol, MD, the editor-in-chief of Medscape and a cardiologist at Scripps Research Translational Institute in La Jolla, CA.
The first analysis, which was done by the World Health Organization Collaborating Centre for Infectious Disease Modelling and Imperial College London, found that overall, people infected by Omicron had about a 20% reduced risk of needing any hospital care for their infections and a 40% lower risk of an overnight hospital stay, compared to those infected with Delta.
Meanwhile, people who were re-infected – meaning they caught Omicron after recovering from a previous COVID-19 infection – had a 50%-60% lower risk of needing hospital care, likely reflecting the benefits of having some prior immunity against the same family of viruses.
The study included everyone with polymerase chain reaction-confirmed COVID-19 in the U.K. during the first 2 weeks of December – roughly 56,000 Omicron cases and 269,000 Delta infections.
The second study, from researchers at the National Institute for Communicable Diseases in South Africa, included more than 29,000 COVID-19 cases that had lab results highly suggestive of Omicron infections. Compared to people infected with the Delta variant, those with presumed Omicron infections were about 70% less likely to have severe disease.
While the news is hopeful for individuals, on a population level, health care systems may still be stressed, the study authors warned.
“Given the high transmissibility of the Omicron virus, there remains the potential for health services to face increasing demand if Omicron cases continue to grow at the rate that has been seen in recent weeks,” said study author Neil Ferguson, PhD, who studies how infectious diseases spread at Imperial College London.
The study authors say their findings are specific to the U.K. and South Africa, where substantial portions of the population have some immune protection from past infection. In other words, they may not apply to countries where fewer people have been vaccinated or recovered from a bout with COVID-19.
A version of this article first appeared on WebMD.com.
Hyperprolactinemia – When, why, and how to evaluate prolactin
Because of the increasing popularity and success of in vitro fertilization, the field of reproductive endocrinology and infertility has steadily morphed toward the treatment of infertility. Nevertheless, a physician board certified in reproductive endocrinology and infertility is the referring physician of choice regarding prolactin disorders and gynecologists should be familiar with the symptoms and sequela of prolactin elevations. This month’s column will address when to obtain a serum prolactin and how to appropriately manage hyperprolactinemia.
Of all the anterior pituitary hormones (adrenocorticotropic hormone, follicle-stimulating hormone, growth hormone, luteinizing hormone, prolactin, thyroid-stimulating hormone ), prolactin is the only one under tonic inhibition by dopamine. Disturbances in this dopaminergic pathway result in elevated serum prolactin. The normal range for prolactin is approximately 5-20 ng/mL.
In the nonpregnant state, little is known regarding the purpose of prolactin, which is produced by the anterior pituitary cluster of cells called lactotrophs. To prepare the breast for postpartum lactation, increases in prolactin are necessary and sustained throughout pregnancy. Second to pregnancy, amenorrhea can occur in 10%-20% of cases of hyperprolactinemia. Outside of pregnancy, elevations in prolactin result in hypogonadism, through gonadotropin-releasing hormone suppression, resulting in infertility (48%), headache (39%), oligomenorrhea (29%) and galactorrhea (24%).1 Most hypogonadal symptoms are more likely to occur with prolactin levels greater than 100 ng/mL, whereas infertility and ovulation dysfunction can occur with mild to moderate hyperprolactinemia, respectively. Prolonged amenorrhea can risk bone mineral density loss.
While the focus of our discussion is the effect of prolactin on women, men with hyperprolactinemia can experience hypogonadotropic hypogonadism with resultant decreased libido, impotence, infertility, gynecomastia, or, rarely, galactorrhea.2
The three Ps – physiological, pharmacologic, pathological
Physiological causes of hyperprolactinemia include rising estradiol during the late follicular phase and into the secretory phase of the menstrual cycle or while taking combined oral contraception, nipple stimulation, pregnancy, lactation, meals, sleep, and stress.
Drugs can interrupt the dopaminergic pathway, thereby elevating serum prolactin but usually not above 100 ng/mL, except for the antipsychotic drug risperidone, which can cause marked elevation up to 300 or even 400 ng/mL. Medications that can cause hyperprolactinemia are estrogens, neuroleptic drugs such as risperidone, metoclopramide, antidepressant drugs, cimetidine, methyldopa, and verapamil.
A pituitary MRI can diagnose an adenoma, that is, a collection of cells in the pituitary that are responsible for hyperprolactinemia and is named based on its size. Microadenomas are less than 1 cm and are typically associated with serum prolactin values below 200 ng/mL. Macroadenomas can worsen while a patient is on combined oral contraception and during pregnancy; fortunately, this is not the case with a microadenoma.
Hypothyroidism can elevate serum prolactin since thyrotropin releasing hormone is known to stimulate prolactin secretion.3 Consequently, when a patient presents with both hypothyroidism and hyperprolactinemia, thyroid replacement should be initiated for thyroid regulation and potential restoration of prolactin levels. If hyperprolactinemia persists, then further evaluation is required. Chronic renal impairment can also elevate prolactin levels due to decreased clearance.
Management
The appropriate evaluation of hyperprolactinemia consists of a history to disclose medications, identify galactorrhea, and visual changes. Because of an adenoma compressing the optic chiasm, partial blindness may occur where vision is lost in the outer half of both the right and left visual field, called bitemporal hemianopsia. Mild elevations in prolactin should be tested at a time when physiological influences are at a minimum, that is, during menses, fasting, and in late morning.4 Persistent elevations should be appropriately evaluated rather than by using the empiric “shotgun” approach of prescribing a dopamine agonist. Laboratory testing for repeated elevations in prolactin includes a pituitary MRI looking for a mass in the hypothalamic-pituitary region that interrupts dopamine suppression.
Treatment of hyperprolactinemia begins with a dopamine agonist and is indicated when there is hypogonadism or intolerable galactorrhea. Cabergoline is the first choice because of effectiveness (reduced adenoma size in greater than 90% of patients) and lesser side effects, particularly nausea, than bromocriptine. Dopamine agonists, such as bromocriptine and cabergoline, belong to the category of ergot-derived dopamine agonists and have been used to treat Parkinson’s disease. At high doses used to treat Parkinson’s, cabergoline is associated with an increased risk of valvular heart disease. In the United States, pergolide was voluntarily withdrawn from the market in March 2007 because of this risk. At the lower doses generally used for the treatment of hyperprolactinemia, cabergoline is probably not associated with excess risk.5
Newer dopamine agonists are known as nonergot. These are pramipexole, ropinirole, rotigotine, and apomorphine. They have not been associated with a risk of heart damage and can be prescribed.
The initial prescribing dose of cabergoline should be 0.25 mg twice a week or 0.5 mg once a week. If bromocriptine is used, the starting dose is 1.25 mg after dinner or at bedtime for 1 week, then increasing to 1.25 mg twice a day (after breakfast and after dinner or at bedtime to reduce nausea and fatigue). After 1 month of a dopamine agonist, the patient should be evaluated for side effects and a serum prolactin level should be obtained. With a normal prolactin level, gonadal function will probably return within a few months. The dopamine agonist should typically be discontinued with pregnancy as pregnancy increases prolactin physiologically.
Treatment of a macroadenoma is essential when the tumor is large enough to cause neurologic symptoms, such as visual impairment or headache, and is preferable when it is invasive or when there are enlarging microadenomas since they are likely to continue to grow and become symptomatic. About 95% of microadenomas have not been shown to increase in size during 4-6 years of observation.6
Transsphenoidal surgery should be considered when there is:
- Persistent hyperprolactinemia and/or size of the adenoma, with associated symptoms or signs despite several months of dopamine agonist treatment at high doses.
- Presence of a giant lactotroph adenoma (e.g., >3 cm) with pregnancy desired including those whose adenoma responds to a dopamine agonist – to avoid significant growth during pregnancy while off medication.
Data from over 6,000 pregnancies suggest that the administration of bromocriptine during the first month of pregnancy does not harm the fetus.7
Discontinuing treatment
Three scenarios may allow for cessation of dopamine agonist therapy. The first is when a patient has had a normal serum prolactin test following 2 years of low-dose dopamine agonist. Another is the patient who had hyperprolactinemia and a microadenoma that responded to treatment with a normal prolactin level and no further evidence of an adenoma by MRI for at least 2 years. Lastly, the patient who had a macroadenoma prior to treatment and a subsequent normal serum prolactin level without an adenoma for at least 2 years.
Like the management of thyroid dysfunction, our field must be aware of prolactin disorders for early detection, prompt referral, and appropriate management to minimize long-term consequences.
Dr. Trolice is director of Fertility CARE – The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
References
1. Bayrak A et al. Fertil Steril. 2005 Jul;84(1):181-5.
2. Carter JN et al. N Engl J Med. 1978 Oct 19;299(16):847-52.
3. Sachson R et al. N Engl J Med. 1972;287:972.
4. Singh SP and Singh TP. Ann Endocrinol (Paris). 1984;45(2):137-41.
5. Valassi E et al. J Clin Endocrinol Metab. 2010 Mar;95(3):1025-33.
6. Sisam DA et al. Fertil Steril. 1987 Jul;48(1):67-71.
7. Molitch ME. Best Pract Res Clin Endocrinol Metab. 2011 Dec;25(6):885-96.
Because of the increasing popularity and success of in vitro fertilization, the field of reproductive endocrinology and infertility has steadily morphed toward the treatment of infertility. Nevertheless, a physician board certified in reproductive endocrinology and infertility is the referring physician of choice regarding prolactin disorders and gynecologists should be familiar with the symptoms and sequela of prolactin elevations. This month’s column will address when to obtain a serum prolactin and how to appropriately manage hyperprolactinemia.
Of all the anterior pituitary hormones (adrenocorticotropic hormone, follicle-stimulating hormone, growth hormone, luteinizing hormone, prolactin, thyroid-stimulating hormone ), prolactin is the only one under tonic inhibition by dopamine. Disturbances in this dopaminergic pathway result in elevated serum prolactin. The normal range for prolactin is approximately 5-20 ng/mL.
In the nonpregnant state, little is known regarding the purpose of prolactin, which is produced by the anterior pituitary cluster of cells called lactotrophs. To prepare the breast for postpartum lactation, increases in prolactin are necessary and sustained throughout pregnancy. Second to pregnancy, amenorrhea can occur in 10%-20% of cases of hyperprolactinemia. Outside of pregnancy, elevations in prolactin result in hypogonadism, through gonadotropin-releasing hormone suppression, resulting in infertility (48%), headache (39%), oligomenorrhea (29%) and galactorrhea (24%).1 Most hypogonadal symptoms are more likely to occur with prolactin levels greater than 100 ng/mL, whereas infertility and ovulation dysfunction can occur with mild to moderate hyperprolactinemia, respectively. Prolonged amenorrhea can risk bone mineral density loss.
While the focus of our discussion is the effect of prolactin on women, men with hyperprolactinemia can experience hypogonadotropic hypogonadism with resultant decreased libido, impotence, infertility, gynecomastia, or, rarely, galactorrhea.2
The three Ps – physiological, pharmacologic, pathological
Physiological causes of hyperprolactinemia include rising estradiol during the late follicular phase and into the secretory phase of the menstrual cycle or while taking combined oral contraception, nipple stimulation, pregnancy, lactation, meals, sleep, and stress.
Drugs can interrupt the dopaminergic pathway, thereby elevating serum prolactin but usually not above 100 ng/mL, except for the antipsychotic drug risperidone, which can cause marked elevation up to 300 or even 400 ng/mL. Medications that can cause hyperprolactinemia are estrogens, neuroleptic drugs such as risperidone, metoclopramide, antidepressant drugs, cimetidine, methyldopa, and verapamil.
A pituitary MRI can diagnose an adenoma, that is, a collection of cells in the pituitary that are responsible for hyperprolactinemia and is named based on its size. Microadenomas are less than 1 cm and are typically associated with serum prolactin values below 200 ng/mL. Macroadenomas can worsen while a patient is on combined oral contraception and during pregnancy; fortunately, this is not the case with a microadenoma.
Hypothyroidism can elevate serum prolactin since thyrotropin releasing hormone is known to stimulate prolactin secretion.3 Consequently, when a patient presents with both hypothyroidism and hyperprolactinemia, thyroid replacement should be initiated for thyroid regulation and potential restoration of prolactin levels. If hyperprolactinemia persists, then further evaluation is required. Chronic renal impairment can also elevate prolactin levels due to decreased clearance.
Management
The appropriate evaluation of hyperprolactinemia consists of a history to disclose medications, identify galactorrhea, and visual changes. Because of an adenoma compressing the optic chiasm, partial blindness may occur where vision is lost in the outer half of both the right and left visual field, called bitemporal hemianopsia. Mild elevations in prolactin should be tested at a time when physiological influences are at a minimum, that is, during menses, fasting, and in late morning.4 Persistent elevations should be appropriately evaluated rather than by using the empiric “shotgun” approach of prescribing a dopamine agonist. Laboratory testing for repeated elevations in prolactin includes a pituitary MRI looking for a mass in the hypothalamic-pituitary region that interrupts dopamine suppression.
Treatment of hyperprolactinemia begins with a dopamine agonist and is indicated when there is hypogonadism or intolerable galactorrhea. Cabergoline is the first choice because of effectiveness (reduced adenoma size in greater than 90% of patients) and lesser side effects, particularly nausea, than bromocriptine. Dopamine agonists, such as bromocriptine and cabergoline, belong to the category of ergot-derived dopamine agonists and have been used to treat Parkinson’s disease. At high doses used to treat Parkinson’s, cabergoline is associated with an increased risk of valvular heart disease. In the United States, pergolide was voluntarily withdrawn from the market in March 2007 because of this risk. At the lower doses generally used for the treatment of hyperprolactinemia, cabergoline is probably not associated with excess risk.5
Newer dopamine agonists are known as nonergot. These are pramipexole, ropinirole, rotigotine, and apomorphine. They have not been associated with a risk of heart damage and can be prescribed.
The initial prescribing dose of cabergoline should be 0.25 mg twice a week or 0.5 mg once a week. If bromocriptine is used, the starting dose is 1.25 mg after dinner or at bedtime for 1 week, then increasing to 1.25 mg twice a day (after breakfast and after dinner or at bedtime to reduce nausea and fatigue). After 1 month of a dopamine agonist, the patient should be evaluated for side effects and a serum prolactin level should be obtained. With a normal prolactin level, gonadal function will probably return within a few months. The dopamine agonist should typically be discontinued with pregnancy as pregnancy increases prolactin physiologically.
Treatment of a macroadenoma is essential when the tumor is large enough to cause neurologic symptoms, such as visual impairment or headache, and is preferable when it is invasive or when there are enlarging microadenomas since they are likely to continue to grow and become symptomatic. About 95% of microadenomas have not been shown to increase in size during 4-6 years of observation.6
Transsphenoidal surgery should be considered when there is:
- Persistent hyperprolactinemia and/or size of the adenoma, with associated symptoms or signs despite several months of dopamine agonist treatment at high doses.
- Presence of a giant lactotroph adenoma (e.g., >3 cm) with pregnancy desired including those whose adenoma responds to a dopamine agonist – to avoid significant growth during pregnancy while off medication.
Data from over 6,000 pregnancies suggest that the administration of bromocriptine during the first month of pregnancy does not harm the fetus.7
Discontinuing treatment
Three scenarios may allow for cessation of dopamine agonist therapy. The first is when a patient has had a normal serum prolactin test following 2 years of low-dose dopamine agonist. Another is the patient who had hyperprolactinemia and a microadenoma that responded to treatment with a normal prolactin level and no further evidence of an adenoma by MRI for at least 2 years. Lastly, the patient who had a macroadenoma prior to treatment and a subsequent normal serum prolactin level without an adenoma for at least 2 years.
Like the management of thyroid dysfunction, our field must be aware of prolactin disorders for early detection, prompt referral, and appropriate management to minimize long-term consequences.
Dr. Trolice is director of Fertility CARE – The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
References
1. Bayrak A et al. Fertil Steril. 2005 Jul;84(1):181-5.
2. Carter JN et al. N Engl J Med. 1978 Oct 19;299(16):847-52.
3. Sachson R et al. N Engl J Med. 1972;287:972.
4. Singh SP and Singh TP. Ann Endocrinol (Paris). 1984;45(2):137-41.
5. Valassi E et al. J Clin Endocrinol Metab. 2010 Mar;95(3):1025-33.
6. Sisam DA et al. Fertil Steril. 1987 Jul;48(1):67-71.
7. Molitch ME. Best Pract Res Clin Endocrinol Metab. 2011 Dec;25(6):885-96.
Because of the increasing popularity and success of in vitro fertilization, the field of reproductive endocrinology and infertility has steadily morphed toward the treatment of infertility. Nevertheless, a physician board certified in reproductive endocrinology and infertility is the referring physician of choice regarding prolactin disorders and gynecologists should be familiar with the symptoms and sequela of prolactin elevations. This month’s column will address when to obtain a serum prolactin and how to appropriately manage hyperprolactinemia.
Of all the anterior pituitary hormones (adrenocorticotropic hormone, follicle-stimulating hormone, growth hormone, luteinizing hormone, prolactin, thyroid-stimulating hormone ), prolactin is the only one under tonic inhibition by dopamine. Disturbances in this dopaminergic pathway result in elevated serum prolactin. The normal range for prolactin is approximately 5-20 ng/mL.
In the nonpregnant state, little is known regarding the purpose of prolactin, which is produced by the anterior pituitary cluster of cells called lactotrophs. To prepare the breast for postpartum lactation, increases in prolactin are necessary and sustained throughout pregnancy. Second to pregnancy, amenorrhea can occur in 10%-20% of cases of hyperprolactinemia. Outside of pregnancy, elevations in prolactin result in hypogonadism, through gonadotropin-releasing hormone suppression, resulting in infertility (48%), headache (39%), oligomenorrhea (29%) and galactorrhea (24%).1 Most hypogonadal symptoms are more likely to occur with prolactin levels greater than 100 ng/mL, whereas infertility and ovulation dysfunction can occur with mild to moderate hyperprolactinemia, respectively. Prolonged amenorrhea can risk bone mineral density loss.
While the focus of our discussion is the effect of prolactin on women, men with hyperprolactinemia can experience hypogonadotropic hypogonadism with resultant decreased libido, impotence, infertility, gynecomastia, or, rarely, galactorrhea.2
The three Ps – physiological, pharmacologic, pathological
Physiological causes of hyperprolactinemia include rising estradiol during the late follicular phase and into the secretory phase of the menstrual cycle or while taking combined oral contraception, nipple stimulation, pregnancy, lactation, meals, sleep, and stress.
Drugs can interrupt the dopaminergic pathway, thereby elevating serum prolactin but usually not above 100 ng/mL, except for the antipsychotic drug risperidone, which can cause marked elevation up to 300 or even 400 ng/mL. Medications that can cause hyperprolactinemia are estrogens, neuroleptic drugs such as risperidone, metoclopramide, antidepressant drugs, cimetidine, methyldopa, and verapamil.
A pituitary MRI can diagnose an adenoma, that is, a collection of cells in the pituitary that are responsible for hyperprolactinemia and is named based on its size. Microadenomas are less than 1 cm and are typically associated with serum prolactin values below 200 ng/mL. Macroadenomas can worsen while a patient is on combined oral contraception and during pregnancy; fortunately, this is not the case with a microadenoma.
Hypothyroidism can elevate serum prolactin since thyrotropin releasing hormone is known to stimulate prolactin secretion.3 Consequently, when a patient presents with both hypothyroidism and hyperprolactinemia, thyroid replacement should be initiated for thyroid regulation and potential restoration of prolactin levels. If hyperprolactinemia persists, then further evaluation is required. Chronic renal impairment can also elevate prolactin levels due to decreased clearance.
Management
The appropriate evaluation of hyperprolactinemia consists of a history to disclose medications, identify galactorrhea, and visual changes. Because of an adenoma compressing the optic chiasm, partial blindness may occur where vision is lost in the outer half of both the right and left visual field, called bitemporal hemianopsia. Mild elevations in prolactin should be tested at a time when physiological influences are at a minimum, that is, during menses, fasting, and in late morning.4 Persistent elevations should be appropriately evaluated rather than by using the empiric “shotgun” approach of prescribing a dopamine agonist. Laboratory testing for repeated elevations in prolactin includes a pituitary MRI looking for a mass in the hypothalamic-pituitary region that interrupts dopamine suppression.
Treatment of hyperprolactinemia begins with a dopamine agonist and is indicated when there is hypogonadism or intolerable galactorrhea. Cabergoline is the first choice because of effectiveness (reduced adenoma size in greater than 90% of patients) and lesser side effects, particularly nausea, than bromocriptine. Dopamine agonists, such as bromocriptine and cabergoline, belong to the category of ergot-derived dopamine agonists and have been used to treat Parkinson’s disease. At high doses used to treat Parkinson’s, cabergoline is associated with an increased risk of valvular heart disease. In the United States, pergolide was voluntarily withdrawn from the market in March 2007 because of this risk. At the lower doses generally used for the treatment of hyperprolactinemia, cabergoline is probably not associated with excess risk.5
Newer dopamine agonists are known as nonergot. These are pramipexole, ropinirole, rotigotine, and apomorphine. They have not been associated with a risk of heart damage and can be prescribed.
The initial prescribing dose of cabergoline should be 0.25 mg twice a week or 0.5 mg once a week. If bromocriptine is used, the starting dose is 1.25 mg after dinner or at bedtime for 1 week, then increasing to 1.25 mg twice a day (after breakfast and after dinner or at bedtime to reduce nausea and fatigue). After 1 month of a dopamine agonist, the patient should be evaluated for side effects and a serum prolactin level should be obtained. With a normal prolactin level, gonadal function will probably return within a few months. The dopamine agonist should typically be discontinued with pregnancy as pregnancy increases prolactin physiologically.
Treatment of a macroadenoma is essential when the tumor is large enough to cause neurologic symptoms, such as visual impairment or headache, and is preferable when it is invasive or when there are enlarging microadenomas since they are likely to continue to grow and become symptomatic. About 95% of microadenomas have not been shown to increase in size during 4-6 years of observation.6
Transsphenoidal surgery should be considered when there is:
- Persistent hyperprolactinemia and/or size of the adenoma, with associated symptoms or signs despite several months of dopamine agonist treatment at high doses.
- Presence of a giant lactotroph adenoma (e.g., >3 cm) with pregnancy desired including those whose adenoma responds to a dopamine agonist – to avoid significant growth during pregnancy while off medication.
Data from over 6,000 pregnancies suggest that the administration of bromocriptine during the first month of pregnancy does not harm the fetus.7
Discontinuing treatment
Three scenarios may allow for cessation of dopamine agonist therapy. The first is when a patient has had a normal serum prolactin test following 2 years of low-dose dopamine agonist. Another is the patient who had hyperprolactinemia and a microadenoma that responded to treatment with a normal prolactin level and no further evidence of an adenoma by MRI for at least 2 years. Lastly, the patient who had a macroadenoma prior to treatment and a subsequent normal serum prolactin level without an adenoma for at least 2 years.
Like the management of thyroid dysfunction, our field must be aware of prolactin disorders for early detection, prompt referral, and appropriate management to minimize long-term consequences.
Dr. Trolice is director of Fertility CARE – The IVF Center in Winter Park, Fla., and professor of obstetrics and gynecology at the University of Central Florida, Orlando.
References
1. Bayrak A et al. Fertil Steril. 2005 Jul;84(1):181-5.
2. Carter JN et al. N Engl J Med. 1978 Oct 19;299(16):847-52.
3. Sachson R et al. N Engl J Med. 1972;287:972.
4. Singh SP and Singh TP. Ann Endocrinol (Paris). 1984;45(2):137-41.
5. Valassi E et al. J Clin Endocrinol Metab. 2010 Mar;95(3):1025-33.
6. Sisam DA et al. Fertil Steril. 1987 Jul;48(1):67-71.
7. Molitch ME. Best Pract Res Clin Endocrinol Metab. 2011 Dec;25(6):885-96.