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Proclivity ID
18813001
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Specialty Focus
Psoriatic Arthritis
Spondyloarthropathies
Rheumatoid Arthritis
Osteoarthritis
Negative Keywords
gaming
gambling
compulsive behaviors
ammunition
assault rifle
black jack
Boko Haram
bondage
child abuse
cocaine
Daech
drug paraphernalia
explosion
gun
human trafficking
ISIL
ISIS
Islamic caliphate
Islamic state
mixed martial arts
MMA
molestation
national rifle association
NRA
nsfw
pedophile
pedophilia
poker
porn
pornography
psychedelic drug
recreational drug
sex slave rings
slot machine
terrorism
terrorist
Texas hold 'em
UFC
substance abuse
abuseed
abuseer
abusees
abuseing
abusely
abuses
aeolus
aeolused
aeoluser
aeoluses
aeolusing
aeolusly
aeoluss
ahole
aholeed
aholeer
aholees
aholeing
aholely
aholes
alcohol
alcoholed
alcoholer
alcoholes
alcoholing
alcoholly
alcohols
allman
allmaned
allmaner
allmanes
allmaning
allmanly
allmans
alted
altes
alting
altly
alts
analed
analer
anales
analing
anally
analprobe
analprobeed
analprobeer
analprobees
analprobeing
analprobely
analprobes
anals
anilingus
anilingused
anilinguser
anilinguses
anilingusing
anilingusly
anilinguss
anus
anused
anuser
anuses
anusing
anusly
anuss
areola
areolaed
areolaer
areolaes
areolaing
areolaly
areolas
areole
areoleed
areoleer
areolees
areoleing
areolely
areoles
arian
arianed
arianer
arianes
arianing
arianly
arians
aryan
aryaned
aryaner
aryanes
aryaning
aryanly
aryans
asiaed
asiaer
asiaes
asiaing
asialy
asias
ass
ass hole
ass lick
ass licked
ass licker
ass lickes
ass licking
ass lickly
ass licks
assbang
assbanged
assbangeded
assbangeder
assbangedes
assbangeding
assbangedly
assbangeds
assbanger
assbanges
assbanging
assbangly
assbangs
assbangsed
assbangser
assbangses
assbangsing
assbangsly
assbangss
assed
asser
asses
assesed
asseser
asseses
assesing
assesly
assess
assfuck
assfucked
assfucker
assfuckered
assfuckerer
assfuckeres
assfuckering
assfuckerly
assfuckers
assfuckes
assfucking
assfuckly
assfucks
asshat
asshated
asshater
asshates
asshating
asshatly
asshats
assholeed
assholeer
assholees
assholeing
assholely
assholes
assholesed
assholeser
assholeses
assholesing
assholesly
assholess
assing
assly
assmaster
assmastered
assmasterer
assmasteres
assmastering
assmasterly
assmasters
assmunch
assmunched
assmuncher
assmunches
assmunching
assmunchly
assmunchs
asss
asswipe
asswipeed
asswipeer
asswipees
asswipeing
asswipely
asswipes
asswipesed
asswipeser
asswipeses
asswipesing
asswipesly
asswipess
azz
azzed
azzer
azzes
azzing
azzly
azzs
babeed
babeer
babees
babeing
babely
babes
babesed
babeser
babeses
babesing
babesly
babess
ballsac
ballsaced
ballsacer
ballsaces
ballsacing
ballsack
ballsacked
ballsacker
ballsackes
ballsacking
ballsackly
ballsacks
ballsacly
ballsacs
ballsed
ballser
ballses
ballsing
ballsly
ballss
barf
barfed
barfer
barfes
barfing
barfly
barfs
bastard
bastarded
bastarder
bastardes
bastarding
bastardly
bastards
bastardsed
bastardser
bastardses
bastardsing
bastardsly
bastardss
bawdy
bawdyed
bawdyer
bawdyes
bawdying
bawdyly
bawdys
beaner
beanered
beanerer
beaneres
beanering
beanerly
beaners
beardedclam
beardedclamed
beardedclamer
beardedclames
beardedclaming
beardedclamly
beardedclams
beastiality
beastialityed
beastialityer
beastialityes
beastialitying
beastialityly
beastialitys
beatch
beatched
beatcher
beatches
beatching
beatchly
beatchs
beater
beatered
beaterer
beateres
beatering
beaterly
beaters
beered
beerer
beeres
beering
beerly
beeyotch
beeyotched
beeyotcher
beeyotches
beeyotching
beeyotchly
beeyotchs
beotch
beotched
beotcher
beotches
beotching
beotchly
beotchs
biatch
biatched
biatcher
biatches
biatching
biatchly
biatchs
big tits
big titsed
big titser
big titses
big titsing
big titsly
big titss
bigtits
bigtitsed
bigtitser
bigtitses
bigtitsing
bigtitsly
bigtitss
bimbo
bimboed
bimboer
bimboes
bimboing
bimboly
bimbos
bisexualed
bisexualer
bisexuales
bisexualing
bisexually
bisexuals
bitch
bitched
bitcheded
bitcheder
bitchedes
bitcheding
bitchedly
bitcheds
bitcher
bitches
bitchesed
bitcheser
bitcheses
bitchesing
bitchesly
bitchess
bitching
bitchly
bitchs
bitchy
bitchyed
bitchyer
bitchyes
bitchying
bitchyly
bitchys
bleached
bleacher
bleaches
bleaching
bleachly
bleachs
blow job
blow jobed
blow jober
blow jobes
blow jobing
blow jobly
blow jobs
blowed
blower
blowes
blowing
blowjob
blowjobed
blowjober
blowjobes
blowjobing
blowjobly
blowjobs
blowjobsed
blowjobser
blowjobses
blowjobsing
blowjobsly
blowjobss
blowly
blows
boink
boinked
boinker
boinkes
boinking
boinkly
boinks
bollock
bollocked
bollocker
bollockes
bollocking
bollockly
bollocks
bollocksed
bollockser
bollockses
bollocksing
bollocksly
bollockss
bollok
bolloked
bolloker
bollokes
bolloking
bollokly
bolloks
boner
bonered
bonerer
boneres
bonering
bonerly
boners
bonersed
bonerser
bonerses
bonersing
bonersly
bonerss
bong
bonged
bonger
bonges
bonging
bongly
bongs
boob
boobed
boober
boobes
boobies
boobiesed
boobieser
boobieses
boobiesing
boobiesly
boobiess
boobing
boobly
boobs
boobsed
boobser
boobses
boobsing
boobsly
boobss
booby
boobyed
boobyer
boobyes
boobying
boobyly
boobys
booger
boogered
boogerer
boogeres
boogering
boogerly
boogers
bookie
bookieed
bookieer
bookiees
bookieing
bookiely
bookies
bootee
booteeed
booteeer
booteees
booteeing
booteely
bootees
bootie
bootieed
bootieer
bootiees
bootieing
bootiely
booties
booty
bootyed
bootyer
bootyes
bootying
bootyly
bootys
boozeed
boozeer
boozees
boozeing
boozely
boozer
boozered
boozerer
boozeres
boozering
boozerly
boozers
boozes
boozy
boozyed
boozyer
boozyes
boozying
boozyly
boozys
bosomed
bosomer
bosomes
bosoming
bosomly
bosoms
bosomy
bosomyed
bosomyer
bosomyes
bosomying
bosomyly
bosomys
bugger
buggered
buggerer
buggeres
buggering
buggerly
buggers
bukkake
bukkakeed
bukkakeer
bukkakees
bukkakeing
bukkakely
bukkakes
bull shit
bull shited
bull shiter
bull shites
bull shiting
bull shitly
bull shits
bullshit
bullshited
bullshiter
bullshites
bullshiting
bullshitly
bullshits
bullshitsed
bullshitser
bullshitses
bullshitsing
bullshitsly
bullshitss
bullshitted
bullshitteded
bullshitteder
bullshittedes
bullshitteding
bullshittedly
bullshitteds
bullturds
bullturdsed
bullturdser
bullturdses
bullturdsing
bullturdsly
bullturdss
bung
bunged
bunger
bunges
bunging
bungly
bungs
busty
bustyed
bustyer
bustyes
bustying
bustyly
bustys
butt
butt fuck
butt fucked
butt fucker
butt fuckes
butt fucking
butt fuckly
butt fucks
butted
buttes
buttfuck
buttfucked
buttfucker
buttfuckered
buttfuckerer
buttfuckeres
buttfuckering
buttfuckerly
buttfuckers
buttfuckes
buttfucking
buttfuckly
buttfucks
butting
buttly
buttplug
buttpluged
buttpluger
buttpluges
buttpluging
buttplugly
buttplugs
butts
caca
cacaed
cacaer
cacaes
cacaing
cacaly
cacas
cahone
cahoneed
cahoneer
cahonees
cahoneing
cahonely
cahones
cameltoe
cameltoeed
cameltoeer
cameltoees
cameltoeing
cameltoely
cameltoes
carpetmuncher
carpetmunchered
carpetmuncherer
carpetmuncheres
carpetmunchering
carpetmuncherly
carpetmunchers
cawk
cawked
cawker
cawkes
cawking
cawkly
cawks
chinc
chinced
chincer
chinces
chincing
chincly
chincs
chincsed
chincser
chincses
chincsing
chincsly
chincss
chink
chinked
chinker
chinkes
chinking
chinkly
chinks
chode
chodeed
chodeer
chodees
chodeing
chodely
chodes
chodesed
chodeser
chodeses
chodesing
chodesly
chodess
clit
clited
cliter
clites
cliting
clitly
clitoris
clitorised
clitoriser
clitorises
clitorising
clitorisly
clitoriss
clitorus
clitorused
clitoruser
clitoruses
clitorusing
clitorusly
clitoruss
clits
clitsed
clitser
clitses
clitsing
clitsly
clitss
clitty
clittyed
clittyer
clittyes
clittying
clittyly
clittys
cocain
cocaine
cocained
cocaineed
cocaineer
cocainees
cocaineing
cocainely
cocainer
cocaines
cocaining
cocainly
cocains
cock
cock sucker
cock suckered
cock suckerer
cock suckeres
cock suckering
cock suckerly
cock suckers
cockblock
cockblocked
cockblocker
cockblockes
cockblocking
cockblockly
cockblocks
cocked
cocker
cockes
cockholster
cockholstered
cockholsterer
cockholsteres
cockholstering
cockholsterly
cockholsters
cocking
cockknocker
cockknockered
cockknockerer
cockknockeres
cockknockering
cockknockerly
cockknockers
cockly
cocks
cocksed
cockser
cockses
cocksing
cocksly
cocksmoker
cocksmokered
cocksmokerer
cocksmokeres
cocksmokering
cocksmokerly
cocksmokers
cockss
cocksucker
cocksuckered
cocksuckerer
cocksuckeres
cocksuckering
cocksuckerly
cocksuckers
coital
coitaled
coitaler
coitales
coitaling
coitally
coitals
commie
commieed
commieer
commiees
commieing
commiely
commies
condomed
condomer
condomes
condoming
condomly
condoms
coon
cooned
cooner
coones
cooning
coonly
coons
coonsed
coonser
coonses
coonsing
coonsly
coonss
corksucker
corksuckered
corksuckerer
corksuckeres
corksuckering
corksuckerly
corksuckers
cracked
crackwhore
crackwhoreed
crackwhoreer
crackwhorees
crackwhoreing
crackwhorely
crackwhores
crap
craped
craper
crapes
craping
craply
crappy
crappyed
crappyer
crappyes
crappying
crappyly
crappys
cum
cumed
cumer
cumes
cuming
cumly
cummin
cummined
cumminer
cummines
cumming
cumminged
cumminger
cumminges
cumminging
cummingly
cummings
cummining
cumminly
cummins
cums
cumshot
cumshoted
cumshoter
cumshotes
cumshoting
cumshotly
cumshots
cumshotsed
cumshotser
cumshotses
cumshotsing
cumshotsly
cumshotss
cumslut
cumsluted
cumsluter
cumslutes
cumsluting
cumslutly
cumsluts
cumstain
cumstained
cumstainer
cumstaines
cumstaining
cumstainly
cumstains
cunilingus
cunilingused
cunilinguser
cunilinguses
cunilingusing
cunilingusly
cunilinguss
cunnilingus
cunnilingused
cunnilinguser
cunnilinguses
cunnilingusing
cunnilingusly
cunnilinguss
cunny
cunnyed
cunnyer
cunnyes
cunnying
cunnyly
cunnys
cunt
cunted
cunter
cuntes
cuntface
cuntfaceed
cuntfaceer
cuntfacees
cuntfaceing
cuntfacely
cuntfaces
cunthunter
cunthuntered
cunthunterer
cunthunteres
cunthuntering
cunthunterly
cunthunters
cunting
cuntlick
cuntlicked
cuntlicker
cuntlickered
cuntlickerer
cuntlickeres
cuntlickering
cuntlickerly
cuntlickers
cuntlickes
cuntlicking
cuntlickly
cuntlicks
cuntly
cunts
cuntsed
cuntser
cuntses
cuntsing
cuntsly
cuntss
dago
dagoed
dagoer
dagoes
dagoing
dagoly
dagos
dagosed
dagoser
dagoses
dagosing
dagosly
dagoss
dammit
dammited
dammiter
dammites
dammiting
dammitly
dammits
damn
damned
damneded
damneder
damnedes
damneding
damnedly
damneds
damner
damnes
damning
damnit
damnited
damniter
damnites
damniting
damnitly
damnits
damnly
damns
dick
dickbag
dickbaged
dickbager
dickbages
dickbaging
dickbagly
dickbags
dickdipper
dickdippered
dickdipperer
dickdipperes
dickdippering
dickdipperly
dickdippers
dicked
dicker
dickes
dickface
dickfaceed
dickfaceer
dickfacees
dickfaceing
dickfacely
dickfaces
dickflipper
dickflippered
dickflipperer
dickflipperes
dickflippering
dickflipperly
dickflippers
dickhead
dickheaded
dickheader
dickheades
dickheading
dickheadly
dickheads
dickheadsed
dickheadser
dickheadses
dickheadsing
dickheadsly
dickheadss
dicking
dickish
dickished
dickisher
dickishes
dickishing
dickishly
dickishs
dickly
dickripper
dickrippered
dickripperer
dickripperes
dickrippering
dickripperly
dickrippers
dicks
dicksipper
dicksippered
dicksipperer
dicksipperes
dicksippering
dicksipperly
dicksippers
dickweed
dickweeded
dickweeder
dickweedes
dickweeding
dickweedly
dickweeds
dickwhipper
dickwhippered
dickwhipperer
dickwhipperes
dickwhippering
dickwhipperly
dickwhippers
dickzipper
dickzippered
dickzipperer
dickzipperes
dickzippering
dickzipperly
dickzippers
diddle
diddleed
diddleer
diddlees
diddleing
diddlely
diddles
dike
dikeed
dikeer
dikees
dikeing
dikely
dikes
dildo
dildoed
dildoer
dildoes
dildoing
dildoly
dildos
dildosed
dildoser
dildoses
dildosing
dildosly
dildoss
diligaf
diligafed
diligafer
diligafes
diligafing
diligafly
diligafs
dillweed
dillweeded
dillweeder
dillweedes
dillweeding
dillweedly
dillweeds
dimwit
dimwited
dimwiter
dimwites
dimwiting
dimwitly
dimwits
dingle
dingleed
dingleer
dinglees
dingleing
dinglely
dingles
dipship
dipshiped
dipshiper
dipshipes
dipshiping
dipshiply
dipships
dizzyed
dizzyer
dizzyes
dizzying
dizzyly
dizzys
doggiestyleed
doggiestyleer
doggiestylees
doggiestyleing
doggiestylely
doggiestyles
doggystyleed
doggystyleer
doggystylees
doggystyleing
doggystylely
doggystyles
dong
donged
donger
donges
donging
dongly
dongs
doofus
doofused
doofuser
doofuses
doofusing
doofusly
doofuss
doosh
dooshed
doosher
dooshes
dooshing
dooshly
dooshs
dopeyed
dopeyer
dopeyes
dopeying
dopeyly
dopeys
douchebag
douchebaged
douchebager
douchebages
douchebaging
douchebagly
douchebags
douchebagsed
douchebagser
douchebagses
douchebagsing
douchebagsly
douchebagss
doucheed
doucheer
douchees
doucheing
douchely
douches
douchey
doucheyed
doucheyer
doucheyes
doucheying
doucheyly
doucheys
drunk
drunked
drunker
drunkes
drunking
drunkly
drunks
dumass
dumassed
dumasser
dumasses
dumassing
dumassly
dumasss
dumbass
dumbassed
dumbasser
dumbasses
dumbassesed
dumbasseser
dumbasseses
dumbassesing
dumbassesly
dumbassess
dumbassing
dumbassly
dumbasss
dummy
dummyed
dummyer
dummyes
dummying
dummyly
dummys
dyke
dykeed
dykeer
dykees
dykeing
dykely
dykes
dykesed
dykeser
dykeses
dykesing
dykesly
dykess
erotic
eroticed
eroticer
erotices
eroticing
eroticly
erotics
extacy
extacyed
extacyer
extacyes
extacying
extacyly
extacys
extasy
extasyed
extasyer
extasyes
extasying
extasyly
extasys
fack
facked
facker
fackes
facking
fackly
facks
fag
faged
fager
fages
fagg
fagged
faggeded
faggeder
faggedes
faggeding
faggedly
faggeds
fagger
fagges
fagging
faggit
faggited
faggiter
faggites
faggiting
faggitly
faggits
faggly
faggot
faggoted
faggoter
faggotes
faggoting
faggotly
faggots
faggs
faging
fagly
fagot
fagoted
fagoter
fagotes
fagoting
fagotly
fagots
fags
fagsed
fagser
fagses
fagsing
fagsly
fagss
faig
faiged
faiger
faiges
faiging
faigly
faigs
faigt
faigted
faigter
faigtes
faigting
faigtly
faigts
fannybandit
fannybandited
fannybanditer
fannybandites
fannybanditing
fannybanditly
fannybandits
farted
farter
fartes
farting
fartknocker
fartknockered
fartknockerer
fartknockeres
fartknockering
fartknockerly
fartknockers
fartly
farts
felch
felched
felcher
felchered
felcherer
felcheres
felchering
felcherly
felchers
felches
felching
felchinged
felchinger
felchinges
felchinging
felchingly
felchings
felchly
felchs
fellate
fellateed
fellateer
fellatees
fellateing
fellately
fellates
fellatio
fellatioed
fellatioer
fellatioes
fellatioing
fellatioly
fellatios
feltch
feltched
feltcher
feltchered
feltcherer
feltcheres
feltchering
feltcherly
feltchers
feltches
feltching
feltchly
feltchs
feom
feomed
feomer
feomes
feoming
feomly
feoms
fisted
fisteded
fisteder
fistedes
fisteding
fistedly
fisteds
fisting
fistinged
fistinger
fistinges
fistinging
fistingly
fistings
fisty
fistyed
fistyer
fistyes
fistying
fistyly
fistys
floozy
floozyed
floozyer
floozyes
floozying
floozyly
floozys
foad
foaded
foader
foades
foading
foadly
foads
fondleed
fondleer
fondlees
fondleing
fondlely
fondles
foobar
foobared
foobarer
foobares
foobaring
foobarly
foobars
freex
freexed
freexer
freexes
freexing
freexly
freexs
frigg
frigga
friggaed
friggaer
friggaes
friggaing
friggaly
friggas
frigged
frigger
frigges
frigging
friggly
friggs
fubar
fubared
fubarer
fubares
fubaring
fubarly
fubars
fuck
fuckass
fuckassed
fuckasser
fuckasses
fuckassing
fuckassly
fuckasss
fucked
fuckeded
fuckeder
fuckedes
fuckeding
fuckedly
fuckeds
fucker
fuckered
fuckerer
fuckeres
fuckering
fuckerly
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Is pediatric subspecialty training financially worth it?

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Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

 

 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

 

 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Pursuing fellowship training is often financially costly in terms of lifetime earnings, compared with starting a career as a general pediatrician immediately after residency, a report suggests.

Researchers found that most pediatric subspecialists – including those practicing neurology, pulmonology, and adolescent medicine – do not see a financial return from additional training because of the delays in receiving increased compensation and the repayment of educational debt.

“Most pediatric subspecialists don’t experience a relative increase in compensation after training compared to a general pediatrician, so there isn’t a financial benefit to additional training,” lead author Eva Catenaccio, MD, from the division of pediatric neurology, department of neurology, Johns Hopkins University, Baltimore, told this news organization.

The findings, published online March 8 in Pediatrics, contribute to the ongoing debate about the length of pediatric fellowship training programs. The data also provide evidence for the potential effect of a pediatric subspecialty loan repayment program.
 

Pediatric subspecialty training rarely pays off

However, not all practitioners in pediatric subspecialties would find themselves in the red relative to their generalist peers. Three subspecialties had a positive financial return: cardiology, critical care, and neonatology. Dr. Catenaccio explained that this may be because these subspecialties tend to be “inpatient procedure oriented, which are often more [lucrative] than outpatient cognitive–oriented subspecialties, such as pediatric infectious diseases, endocrinology, or adolescent medicine.”

Enrolling in a pediatric fellowship program resulted in lifetime financial returns that ranged from an increase of $852,129 for cardiology, relative to general pediatrics, to a loss of $1,594,366 for adolescent medicine, researchers found.

For the study, researchers calculated the financial returns of 15 pediatric subspecialties – emergency medicine, neurology, cardiology, critical care, neonatology, hematology and oncology, pulmonology, hospitalist medicine, allergy and immunology, gastroenterology, rheumatology, nephrology, adolescent medicine, infectious diseases, and endocrinology – in comparison with returns of private practice general pediatrics on the basis of 2018-2019 data on fellowship stipends, compensation, and educational debt.

They obtained most of the data from the Association of American Medical Colleges Survey of Resident/Fellow Stipends and Benefits, AAMC’s annual Medical School Faculty Salary Report, and the AAMC Medical School Graduation Questionnaire.

Richard Mink, MD, department of pediatrics, Harbor-UCLA Medical Center, Torrance, Calif., noted that it would have been helpful to have also compared the lifetime earnings of practitioners in pediatric subspecialties to academic general pediatricians and not just those in private practice.
 

The financial gap has worsened

To better understand which aspects of fellowship training have the greatest effect on lifetime compensation, Dr. Catenaccio and colleagues evaluated the potential effects of shortening fellowship length, eliminating school debt, and implementing a federal loan repayment plan. These changes enhanced the returns of cardiology, critical care, and neonatology – subspecialties that had already seen financial returns before these changes – and resulted in a positive financial return for emergency medicine.

The changes also narrowed the financial gap between subspecialties and general pediatrics. However, the remaining subspecialties still earned less than private practice pediatrics.

The new study is an update to a 2011 report, which reflected 2007-2008 data for 11 subspecialties. This time around, the researchers included the subspecialty of hospitalist medicine, which was approved as a board-certified subspecialty by the American Board of Pediatrics in 2014, as well as neurology, allergy and immunology, and adolescent medicine.

“I was most surprised that the additional pediatric subspecialties we included since the 2011 report followed the same general trend, with pediatric subspecialty training having a lower lifetime earning potential than general pediatrics,” Dr. Catenaccio said.

Comparing results from the two study periods showed that the financial gap between general pediatrics and subspecialty pediatrics worsened over time. For example, the financial return for pediatric endocrinology decreased an additional $500,000 between 2007 and 2018.

The researchers believe a combination of increased educational debt burden, slow growth in compensation, and changing interest rates over time have caused the financial differences between general pediatrics and subspecialty pediatrics to become more pronounced.
 

 

 

‘Pediatric subspecialty training is worth it!’

Despite the financial gaps, Dr. Catenaccio and colleagues say pediatric subspecialty training is still worthwhile but that policymakers should address these financial differences to help guide workforce distribution in a way that meets the needs of patients.

“I think pediatric subspecialty training is worth it,” said Dr. Catenaccio, who’s pursuing pediatric subspecialty training. “There are so many factors that go into choosing a specialty or subspecialty in medicine, including the desire to care for a particular patient population, interest in certain diseases or organ systems, lifestyle considerations, and research opportunities.”

But it’s also important for trainees to be aware of economic considerations in their decision-making.

Dr. Mink, who wrote an accompanying commentary, agrees that young clinicians should not make career decisions on the basis of metrics such as lifetime earning measures.

“I think people who go into pediatrics have decided that money is not the driving force,” said Dr. Mink. He noted that pediatricians are usually not paid well, compared with other specialists. “To me the important thing is you have to like what you’re doing.”

2020 study found that trainees who chose a career in pediatric pulmonology, a subspecialty, said that financial considerations were not the driving factor in their decision-making. Nevertheless, Dr. Mink also believes young clinicians should take into account their educational debt.

The further widening of the financial gap between general pediatrics and pediatric subspecialties could lead to shortages in the pediatric subspecialty workforce.

The authors and Dr. Mink have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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To improve psoriatic arthritis outcomes, address common comorbidities

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Only about 30% or fewer of patients with psoriatic arthritis (PsA) on therapy achieve disease remission by any definition. One reason for this may be inadequate attention to common comorbid conditions, Alexis Ogdie, MD, MSCE, declared at the 2021 Rheumatology Winter Clinical Symposium.

Courtesy Dr. Alexis Ogdie
Dr. Alexis Ogdie

“I believe that addressing off-target aspects of disease is really important to improving the patient experience of their disease. We might need to target these directly in order to improve outcomes,” said Dr. Ogdie, a rheumatologist and epidemiologist at the University of Pennsylvania, Philadelphia, who coauthored the current American College of Rheumatology/National Psoriasis Foundation PsA guidelines.

Since rheumatologists are by now well informed about the increased cardiovascular risk associated with PsA, she focused on two common comorbidities that get less attention, both of which are associated with worse clinical outcomes in PsA: obesity and mental health issues.
 

Anxiety and depression

Dr. Ogdie was first author of a large, population-based, longitudinal cohort study of cause-specific mortality in 8,706 U.K. patients with PsA, 41,752 with RA, and more than 81,000 controls. Particularly striking was the finding of elevated mortality because of suicide in the rheumatic disease patients: a 203% increased risk in the PsA population, compared with the general population, and a 147% greater risk in patients with RA.

Overall, 30%-40% of PsA patients have comorbid depression and/or anxiety.

“That’s pretty striking. It’s also true for rheumatoid arthritis and axial spondyloarthritis. And if you’re depressed, you’re much less likely to respond to therapy in the way that we are measuring response to therapy,” Dr. Ogdie said.

Her approach to screening for depression and anxiety in her PsA patients, and indeed in all her other patients, is to begin by normalizing the topic, explaining to them that these affective disorders are common among patients with these disorders. She lets her patients know they can talk to her about it. And she informs them that, while effective treatment of their rheumatic disease may improve their depression or anxiety, managing those is also important for improving their disease. Additionally, understanding whether depression is present is important prior to prescribing certain medications. Apremilast (Otezla), for example, can worsen preexisting depression.



“Ask about signs and symptoms of depression,” Dr. Ogdie urged her colleagues. “I do this at every single visit in my review of symptoms. This is one I don’t skip. I ask: ‘Do you have any symptoms of depression or anxiety?’ ”

Structured evidence-based screening tools, many of which are well suited for completion during a patient’s preappointment check-in survey, include the Patient Health Questionnaire–2, the PHQ-9, the Patient-Reported Outcomes Measure Information System–10, PROMIS–Depression, and Routine Assessment of Patient Index Data 3.

“I also really like the PROMIS-29. It covers many domains of interest: depression and anxiety, sleep, fatigue, pain, physical function. It gives a lot of information about what’s going on in a patient’s life right now,” according to the rheumatologist.

The main thing is to regularly screen for anxiety and depression and then refer symptomatic patients for further assessment and treatment. This is not something that all rheumatologists have been trained to do.

 

 

Obesity

Dr. Ogdie was lead author of a national CORRONA Registry study which concluded that obese patients with PsA were only half as likely to achieve remission on a tumor necrosis factor (TNF) inhibitor, compared with nonobese patients. She believes the same holds true for all other types of therapy: Across the board, obesity is associated with a poor response. And obesity is much more common in PsA patients than the general population in every age group. Moreover, obesity is associated with risk factors for cardiovascular disease and is associated with fatty liver disease, two other major comorbid conditions in the PsA population.

The CORRONA Registry findings are supportive of an earlier Italian prospective, observational study of 135 obese and an equal number of normal-weight PsA patients, all of whom started on a TNF inhibitor and were followed for 24 months. In a multivariate-adjusted analysis, obesity was independently associated with a 390% higher risk of not achieving minimal disease activity.

The same Italian group subsequently conducted a prospective dietary intervention study in 138 overweight or obese patients with PsA starting anti-TNF therapy. A total of 59% of participants randomized to either of the two dietary interventions experienced at least a 5% weight loss at 6 months. The key study finding: Compared with the subjects with less than 5% weight loss, those with 5%-10% weight loss were 275% more likely to achieve minimal disease activity at 6 months, and in those with greater than 10% weight loss the likelihood of attaining minimal disease activity increased by 567%.

“We’re talking about a disease where treatments tested in clinical trials have odds ratios in the 1.2 range, compared with other therapies, so this is a really striking difference,” she observed.

Several studies have demonstrated that obesity in psoriasis patients is a risk factor for developing PsA. Recently, U.K. investigators took things a step further, reporting in a huge observational study that obese or overweight psoriasis patients who reduced their body mass index over a 10-year period had a corresponding reduction in the risk of developing PsA, compared with overweight or obese psoriasis patients whose BMI remained steady over the same period.



What’s needed now is access to programs to help patients with PsA lose weight. Health insurers are often unwilling to provide coverage. “We have a really tough time getting the patients in to see a nutritionist unless they’re willing to pay out of pocket,” Dr. Ogdie said.

Physical activity is an important element in successful weight loss. It also is recommended in practice guidelines for patients with inflammatory arthritis because of its salutary effects on disease activity scores, pain and stiffness, sleep, and quality of life. But a recent survey conducted by Dr. Ogdie and coworkers concluded that patients with PsA and other forms of inflammatory arthritis don’t receive much exercise guidance from their rheumatologists. About 60% of subjects were inactive. Those who were physically active typically engaged in aerobic exercise but were much less likely to do the other guideline-recommended forms of exercise, namely flexibility, balance, and resistance training. The patients’ report of low engagement of their physicians “suggests an opportunity for more prescriptive exercise discussions,” according to the investigators.

Diabetes, a critical risk factor for cardiovascular disease, occurs at an increased incidence in PsA. This was demonstrated in a U.K. cohort study coauthored by Dr. Ogdie. The study, which included nearly 4,200 individuals with PsA, concluded that they had a 43% greater incidence of diabetes than the general population in an analysis adjusted for body mass index, smoking, alcohol use, and demographics.

New-onset diabetes can be readily picked up by rheumatologists based upon the laboratory work they often order at patient office visits, or during their review of symptoms, she noted, and added that the U.S. Preventive Services Task Force recommends ordering a hemoglobin A1c test every 3 years.

Dr. Ogdie reported receiving research grants and/or consulting fees from numerous pharmaceutical companies. Her research is also funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Psoriasis Foundation.

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Only about 30% or fewer of patients with psoriatic arthritis (PsA) on therapy achieve disease remission by any definition. One reason for this may be inadequate attention to common comorbid conditions, Alexis Ogdie, MD, MSCE, declared at the 2021 Rheumatology Winter Clinical Symposium.

Courtesy Dr. Alexis Ogdie
Dr. Alexis Ogdie

“I believe that addressing off-target aspects of disease is really important to improving the patient experience of their disease. We might need to target these directly in order to improve outcomes,” said Dr. Ogdie, a rheumatologist and epidemiologist at the University of Pennsylvania, Philadelphia, who coauthored the current American College of Rheumatology/National Psoriasis Foundation PsA guidelines.

Since rheumatologists are by now well informed about the increased cardiovascular risk associated with PsA, she focused on two common comorbidities that get less attention, both of which are associated with worse clinical outcomes in PsA: obesity and mental health issues.
 

Anxiety and depression

Dr. Ogdie was first author of a large, population-based, longitudinal cohort study of cause-specific mortality in 8,706 U.K. patients with PsA, 41,752 with RA, and more than 81,000 controls. Particularly striking was the finding of elevated mortality because of suicide in the rheumatic disease patients: a 203% increased risk in the PsA population, compared with the general population, and a 147% greater risk in patients with RA.

Overall, 30%-40% of PsA patients have comorbid depression and/or anxiety.

“That’s pretty striking. It’s also true for rheumatoid arthritis and axial spondyloarthritis. And if you’re depressed, you’re much less likely to respond to therapy in the way that we are measuring response to therapy,” Dr. Ogdie said.

Her approach to screening for depression and anxiety in her PsA patients, and indeed in all her other patients, is to begin by normalizing the topic, explaining to them that these affective disorders are common among patients with these disorders. She lets her patients know they can talk to her about it. And she informs them that, while effective treatment of their rheumatic disease may improve their depression or anxiety, managing those is also important for improving their disease. Additionally, understanding whether depression is present is important prior to prescribing certain medications. Apremilast (Otezla), for example, can worsen preexisting depression.



“Ask about signs and symptoms of depression,” Dr. Ogdie urged her colleagues. “I do this at every single visit in my review of symptoms. This is one I don’t skip. I ask: ‘Do you have any symptoms of depression or anxiety?’ ”

Structured evidence-based screening tools, many of which are well suited for completion during a patient’s preappointment check-in survey, include the Patient Health Questionnaire–2, the PHQ-9, the Patient-Reported Outcomes Measure Information System–10, PROMIS–Depression, and Routine Assessment of Patient Index Data 3.

“I also really like the PROMIS-29. It covers many domains of interest: depression and anxiety, sleep, fatigue, pain, physical function. It gives a lot of information about what’s going on in a patient’s life right now,” according to the rheumatologist.

The main thing is to regularly screen for anxiety and depression and then refer symptomatic patients for further assessment and treatment. This is not something that all rheumatologists have been trained to do.

 

 

Obesity

Dr. Ogdie was lead author of a national CORRONA Registry study which concluded that obese patients with PsA were only half as likely to achieve remission on a tumor necrosis factor (TNF) inhibitor, compared with nonobese patients. She believes the same holds true for all other types of therapy: Across the board, obesity is associated with a poor response. And obesity is much more common in PsA patients than the general population in every age group. Moreover, obesity is associated with risk factors for cardiovascular disease and is associated with fatty liver disease, two other major comorbid conditions in the PsA population.

The CORRONA Registry findings are supportive of an earlier Italian prospective, observational study of 135 obese and an equal number of normal-weight PsA patients, all of whom started on a TNF inhibitor and were followed for 24 months. In a multivariate-adjusted analysis, obesity was independently associated with a 390% higher risk of not achieving minimal disease activity.

The same Italian group subsequently conducted a prospective dietary intervention study in 138 overweight or obese patients with PsA starting anti-TNF therapy. A total of 59% of participants randomized to either of the two dietary interventions experienced at least a 5% weight loss at 6 months. The key study finding: Compared with the subjects with less than 5% weight loss, those with 5%-10% weight loss were 275% more likely to achieve minimal disease activity at 6 months, and in those with greater than 10% weight loss the likelihood of attaining minimal disease activity increased by 567%.

“We’re talking about a disease where treatments tested in clinical trials have odds ratios in the 1.2 range, compared with other therapies, so this is a really striking difference,” she observed.

Several studies have demonstrated that obesity in psoriasis patients is a risk factor for developing PsA. Recently, U.K. investigators took things a step further, reporting in a huge observational study that obese or overweight psoriasis patients who reduced their body mass index over a 10-year period had a corresponding reduction in the risk of developing PsA, compared with overweight or obese psoriasis patients whose BMI remained steady over the same period.



What’s needed now is access to programs to help patients with PsA lose weight. Health insurers are often unwilling to provide coverage. “We have a really tough time getting the patients in to see a nutritionist unless they’re willing to pay out of pocket,” Dr. Ogdie said.

Physical activity is an important element in successful weight loss. It also is recommended in practice guidelines for patients with inflammatory arthritis because of its salutary effects on disease activity scores, pain and stiffness, sleep, and quality of life. But a recent survey conducted by Dr. Ogdie and coworkers concluded that patients with PsA and other forms of inflammatory arthritis don’t receive much exercise guidance from their rheumatologists. About 60% of subjects were inactive. Those who were physically active typically engaged in aerobic exercise but were much less likely to do the other guideline-recommended forms of exercise, namely flexibility, balance, and resistance training. The patients’ report of low engagement of their physicians “suggests an opportunity for more prescriptive exercise discussions,” according to the investigators.

Diabetes, a critical risk factor for cardiovascular disease, occurs at an increased incidence in PsA. This was demonstrated in a U.K. cohort study coauthored by Dr. Ogdie. The study, which included nearly 4,200 individuals with PsA, concluded that they had a 43% greater incidence of diabetes than the general population in an analysis adjusted for body mass index, smoking, alcohol use, and demographics.

New-onset diabetes can be readily picked up by rheumatologists based upon the laboratory work they often order at patient office visits, or during their review of symptoms, she noted, and added that the U.S. Preventive Services Task Force recommends ordering a hemoglobin A1c test every 3 years.

Dr. Ogdie reported receiving research grants and/or consulting fees from numerous pharmaceutical companies. Her research is also funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Psoriasis Foundation.

Only about 30% or fewer of patients with psoriatic arthritis (PsA) on therapy achieve disease remission by any definition. One reason for this may be inadequate attention to common comorbid conditions, Alexis Ogdie, MD, MSCE, declared at the 2021 Rheumatology Winter Clinical Symposium.

Courtesy Dr. Alexis Ogdie
Dr. Alexis Ogdie

“I believe that addressing off-target aspects of disease is really important to improving the patient experience of their disease. We might need to target these directly in order to improve outcomes,” said Dr. Ogdie, a rheumatologist and epidemiologist at the University of Pennsylvania, Philadelphia, who coauthored the current American College of Rheumatology/National Psoriasis Foundation PsA guidelines.

Since rheumatologists are by now well informed about the increased cardiovascular risk associated with PsA, she focused on two common comorbidities that get less attention, both of which are associated with worse clinical outcomes in PsA: obesity and mental health issues.
 

Anxiety and depression

Dr. Ogdie was first author of a large, population-based, longitudinal cohort study of cause-specific mortality in 8,706 U.K. patients with PsA, 41,752 with RA, and more than 81,000 controls. Particularly striking was the finding of elevated mortality because of suicide in the rheumatic disease patients: a 203% increased risk in the PsA population, compared with the general population, and a 147% greater risk in patients with RA.

Overall, 30%-40% of PsA patients have comorbid depression and/or anxiety.

“That’s pretty striking. It’s also true for rheumatoid arthritis and axial spondyloarthritis. And if you’re depressed, you’re much less likely to respond to therapy in the way that we are measuring response to therapy,” Dr. Ogdie said.

Her approach to screening for depression and anxiety in her PsA patients, and indeed in all her other patients, is to begin by normalizing the topic, explaining to them that these affective disorders are common among patients with these disorders. She lets her patients know they can talk to her about it. And she informs them that, while effective treatment of their rheumatic disease may improve their depression or anxiety, managing those is also important for improving their disease. Additionally, understanding whether depression is present is important prior to prescribing certain medications. Apremilast (Otezla), for example, can worsen preexisting depression.



“Ask about signs and symptoms of depression,” Dr. Ogdie urged her colleagues. “I do this at every single visit in my review of symptoms. This is one I don’t skip. I ask: ‘Do you have any symptoms of depression or anxiety?’ ”

Structured evidence-based screening tools, many of which are well suited for completion during a patient’s preappointment check-in survey, include the Patient Health Questionnaire–2, the PHQ-9, the Patient-Reported Outcomes Measure Information System–10, PROMIS–Depression, and Routine Assessment of Patient Index Data 3.

“I also really like the PROMIS-29. It covers many domains of interest: depression and anxiety, sleep, fatigue, pain, physical function. It gives a lot of information about what’s going on in a patient’s life right now,” according to the rheumatologist.

The main thing is to regularly screen for anxiety and depression and then refer symptomatic patients for further assessment and treatment. This is not something that all rheumatologists have been trained to do.

 

 

Obesity

Dr. Ogdie was lead author of a national CORRONA Registry study which concluded that obese patients with PsA were only half as likely to achieve remission on a tumor necrosis factor (TNF) inhibitor, compared with nonobese patients. She believes the same holds true for all other types of therapy: Across the board, obesity is associated with a poor response. And obesity is much more common in PsA patients than the general population in every age group. Moreover, obesity is associated with risk factors for cardiovascular disease and is associated with fatty liver disease, two other major comorbid conditions in the PsA population.

The CORRONA Registry findings are supportive of an earlier Italian prospective, observational study of 135 obese and an equal number of normal-weight PsA patients, all of whom started on a TNF inhibitor and were followed for 24 months. In a multivariate-adjusted analysis, obesity was independently associated with a 390% higher risk of not achieving minimal disease activity.

The same Italian group subsequently conducted a prospective dietary intervention study in 138 overweight or obese patients with PsA starting anti-TNF therapy. A total of 59% of participants randomized to either of the two dietary interventions experienced at least a 5% weight loss at 6 months. The key study finding: Compared with the subjects with less than 5% weight loss, those with 5%-10% weight loss were 275% more likely to achieve minimal disease activity at 6 months, and in those with greater than 10% weight loss the likelihood of attaining minimal disease activity increased by 567%.

“We’re talking about a disease where treatments tested in clinical trials have odds ratios in the 1.2 range, compared with other therapies, so this is a really striking difference,” she observed.

Several studies have demonstrated that obesity in psoriasis patients is a risk factor for developing PsA. Recently, U.K. investigators took things a step further, reporting in a huge observational study that obese or overweight psoriasis patients who reduced their body mass index over a 10-year period had a corresponding reduction in the risk of developing PsA, compared with overweight or obese psoriasis patients whose BMI remained steady over the same period.



What’s needed now is access to programs to help patients with PsA lose weight. Health insurers are often unwilling to provide coverage. “We have a really tough time getting the patients in to see a nutritionist unless they’re willing to pay out of pocket,” Dr. Ogdie said.

Physical activity is an important element in successful weight loss. It also is recommended in practice guidelines for patients with inflammatory arthritis because of its salutary effects on disease activity scores, pain and stiffness, sleep, and quality of life. But a recent survey conducted by Dr. Ogdie and coworkers concluded that patients with PsA and other forms of inflammatory arthritis don’t receive much exercise guidance from their rheumatologists. About 60% of subjects were inactive. Those who were physically active typically engaged in aerobic exercise but were much less likely to do the other guideline-recommended forms of exercise, namely flexibility, balance, and resistance training. The patients’ report of low engagement of their physicians “suggests an opportunity for more prescriptive exercise discussions,” according to the investigators.

Diabetes, a critical risk factor for cardiovascular disease, occurs at an increased incidence in PsA. This was demonstrated in a U.K. cohort study coauthored by Dr. Ogdie. The study, which included nearly 4,200 individuals with PsA, concluded that they had a 43% greater incidence of diabetes than the general population in an analysis adjusted for body mass index, smoking, alcohol use, and demographics.

New-onset diabetes can be readily picked up by rheumatologists based upon the laboratory work they often order at patient office visits, or during their review of symptoms, she noted, and added that the U.S. Preventive Services Task Force recommends ordering a hemoglobin A1c test every 3 years.

Dr. Ogdie reported receiving research grants and/or consulting fees from numerous pharmaceutical companies. Her research is also funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the National Psoriasis Foundation.

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Close joint health monitoring essential with new hemophilia therapies

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Novel therapies have transformed the treatment of hemophilia in recent decades, but these new approaches also raise new challenges for clinicians who monitor joint health in persons with hemophilia, a specialist said.

“Patient-reported outcomes should be combined with other, more objective outcome measures for joint health monitoring, and joint ultrasound is a promising tool for objective joint health monitoring, although, due to its relatively recent introduction in clinical practice, we lack objective data and standardization,” said Roberta Gualtierotti, MD, PhD, from the Università Degli Studi of Milan.

She reviewed the challenges and approaches to monitoring joint health in persons with hemophilia during the annual congress of the European Association for Haemophilia and Allied Disorders.

Over the last decades the target of hemophilia treatment has shifted from prolonging survival to improving joint health and quality of life, and care has improved with the introduction of novel therapies such as extended half-life replacement products, nonreplacement therapies, and gene therapy, she noted.

However, “due to different pharmacodynamics and pharmacokinetics profiles, the currently available therapies cannot be compared to each other on several levels,” Dr. Gualtierotti said.

Laboratory monitoring of replacement therapies with standard coagulation assays may be unreliable, and depending on the mechanism of action and type of administration of nonreplacement agents, patients may experience breakthrough bleeding, especially after traumatic injury, she said.

Until the specific noncoagulatory effects of factor VIII on bone and joint health is better understood, close monitoring of patients will be required, she added.
 

Outcome measures

Subjective measures of joint health include patient-reported bleeding rates and health-related quality of life. These are practical for home management, but patients may not be able to distinguish symptoms of acute joint bleeding from chronic arthritis pain, with the potential for either under- or overtreatment, and subjective reporting is likely to miss subclinical bleeding that can occur even when patients are on prophylaxis.

Health-related quality of life tools, whether generic or specific for hemophilia, are not sensitive to small improvements, and they are not always used in routine clinical practice.

Objective measures include physical examination with scoring according to the World Federation of Hemophilia (Gilbert Scale) score or Hemophilia Joint Health Score, but these measures have limited ability to identify early or subclinical joint abnormalities.

“Therefore, joint physical examination on its own is not a sufficient measure of treatment efficacy, and it should be used in combination with other tools more objective, such as imaging,” Dr. Gualtierotti said.
 

Get the picture?

Imaging with x-rays, MRI, and, recently in some centers, point-of-care ultrasound can provide clinicians with important real-time information about the joint stability and health.

Point-of-care ultrasound in particular offers promise as a practical tool, with no ionizing radiation and high sensitivity for synovial hyperplasia subclinical joint effusion. It’s relatively inexpensive, can be used to image multiple joints, and allows for ease of follow-up, she said. The technique requires specialized training, however, and there is a lack of prospective data about its utility in hemophilia.

Various ultrasound scoring systems have been proposed, and home-based ultrasound is currently being explored in several clinical trials, Dr. Gualtierotti noted.

Other avenues for remote joint health monitoring under consideration are serum or synovial biomarkers for joint bleeding and arthropathy that could be employed at bedside or at home, smartphone apps for breakthrough bleeding and patient-reported outcomes, and sensors for detecting abnormalities in gait that may signal joint dysfunction, she said.
 

 

 

Best practice

In the question-and-answer session following the talk, Fernando Zikan, MD, from the Federal University of Rio de Janeiro noted that, “in underdeveloped countries, we still find it very difficult to guide good practices for joint health control by the patient and family members. Which strategy do you think is fundamental for the patient to feel safe to notice changes in his body?”

“It would be useful to educate patients to come to the center whenever the patient has trauma and whenever an increase in his physical activity occurs. If this is far, a bedside ultrasound evaluation by the general practitioner could help avoid joint damage. Finally, a correct rehabilitation is fundamental,” Dr. Gualtierotti replied.

Asked by several others whether she used ultrasound in her daily practice, Dr. Gualtierotti said that “we use joint ultrasound in our clinical practice in the regular annual check-up examination and whenever the patient suspects and reports hemarthrosis.”

Dr. Gualtierotti reported participation in advisory boards for Biomarin, Pfizer, Bayer, and Takeda, and in educational seminars sponsored by Pfizer, Sobi, and Roche. She has received support for congress travel and/or attendance by Bayer and Pfizer. Dr. Zikan reported no relevant disclosures.

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Novel therapies have transformed the treatment of hemophilia in recent decades, but these new approaches also raise new challenges for clinicians who monitor joint health in persons with hemophilia, a specialist said.

“Patient-reported outcomes should be combined with other, more objective outcome measures for joint health monitoring, and joint ultrasound is a promising tool for objective joint health monitoring, although, due to its relatively recent introduction in clinical practice, we lack objective data and standardization,” said Roberta Gualtierotti, MD, PhD, from the Università Degli Studi of Milan.

She reviewed the challenges and approaches to monitoring joint health in persons with hemophilia during the annual congress of the European Association for Haemophilia and Allied Disorders.

Over the last decades the target of hemophilia treatment has shifted from prolonging survival to improving joint health and quality of life, and care has improved with the introduction of novel therapies such as extended half-life replacement products, nonreplacement therapies, and gene therapy, she noted.

However, “due to different pharmacodynamics and pharmacokinetics profiles, the currently available therapies cannot be compared to each other on several levels,” Dr. Gualtierotti said.

Laboratory monitoring of replacement therapies with standard coagulation assays may be unreliable, and depending on the mechanism of action and type of administration of nonreplacement agents, patients may experience breakthrough bleeding, especially after traumatic injury, she said.

Until the specific noncoagulatory effects of factor VIII on bone and joint health is better understood, close monitoring of patients will be required, she added.
 

Outcome measures

Subjective measures of joint health include patient-reported bleeding rates and health-related quality of life. These are practical for home management, but patients may not be able to distinguish symptoms of acute joint bleeding from chronic arthritis pain, with the potential for either under- or overtreatment, and subjective reporting is likely to miss subclinical bleeding that can occur even when patients are on prophylaxis.

Health-related quality of life tools, whether generic or specific for hemophilia, are not sensitive to small improvements, and they are not always used in routine clinical practice.

Objective measures include physical examination with scoring according to the World Federation of Hemophilia (Gilbert Scale) score or Hemophilia Joint Health Score, but these measures have limited ability to identify early or subclinical joint abnormalities.

“Therefore, joint physical examination on its own is not a sufficient measure of treatment efficacy, and it should be used in combination with other tools more objective, such as imaging,” Dr. Gualtierotti said.
 

Get the picture?

Imaging with x-rays, MRI, and, recently in some centers, point-of-care ultrasound can provide clinicians with important real-time information about the joint stability and health.

Point-of-care ultrasound in particular offers promise as a practical tool, with no ionizing radiation and high sensitivity for synovial hyperplasia subclinical joint effusion. It’s relatively inexpensive, can be used to image multiple joints, and allows for ease of follow-up, she said. The technique requires specialized training, however, and there is a lack of prospective data about its utility in hemophilia.

Various ultrasound scoring systems have been proposed, and home-based ultrasound is currently being explored in several clinical trials, Dr. Gualtierotti noted.

Other avenues for remote joint health monitoring under consideration are serum or synovial biomarkers for joint bleeding and arthropathy that could be employed at bedside or at home, smartphone apps for breakthrough bleeding and patient-reported outcomes, and sensors for detecting abnormalities in gait that may signal joint dysfunction, she said.
 

 

 

Best practice

In the question-and-answer session following the talk, Fernando Zikan, MD, from the Federal University of Rio de Janeiro noted that, “in underdeveloped countries, we still find it very difficult to guide good practices for joint health control by the patient and family members. Which strategy do you think is fundamental for the patient to feel safe to notice changes in his body?”

“It would be useful to educate patients to come to the center whenever the patient has trauma and whenever an increase in his physical activity occurs. If this is far, a bedside ultrasound evaluation by the general practitioner could help avoid joint damage. Finally, a correct rehabilitation is fundamental,” Dr. Gualtierotti replied.

Asked by several others whether she used ultrasound in her daily practice, Dr. Gualtierotti said that “we use joint ultrasound in our clinical practice in the regular annual check-up examination and whenever the patient suspects and reports hemarthrosis.”

Dr. Gualtierotti reported participation in advisory boards for Biomarin, Pfizer, Bayer, and Takeda, and in educational seminars sponsored by Pfizer, Sobi, and Roche. She has received support for congress travel and/or attendance by Bayer and Pfizer. Dr. Zikan reported no relevant disclosures.

 

Novel therapies have transformed the treatment of hemophilia in recent decades, but these new approaches also raise new challenges for clinicians who monitor joint health in persons with hemophilia, a specialist said.

“Patient-reported outcomes should be combined with other, more objective outcome measures for joint health monitoring, and joint ultrasound is a promising tool for objective joint health monitoring, although, due to its relatively recent introduction in clinical practice, we lack objective data and standardization,” said Roberta Gualtierotti, MD, PhD, from the Università Degli Studi of Milan.

She reviewed the challenges and approaches to monitoring joint health in persons with hemophilia during the annual congress of the European Association for Haemophilia and Allied Disorders.

Over the last decades the target of hemophilia treatment has shifted from prolonging survival to improving joint health and quality of life, and care has improved with the introduction of novel therapies such as extended half-life replacement products, nonreplacement therapies, and gene therapy, she noted.

However, “due to different pharmacodynamics and pharmacokinetics profiles, the currently available therapies cannot be compared to each other on several levels,” Dr. Gualtierotti said.

Laboratory monitoring of replacement therapies with standard coagulation assays may be unreliable, and depending on the mechanism of action and type of administration of nonreplacement agents, patients may experience breakthrough bleeding, especially after traumatic injury, she said.

Until the specific noncoagulatory effects of factor VIII on bone and joint health is better understood, close monitoring of patients will be required, she added.
 

Outcome measures

Subjective measures of joint health include patient-reported bleeding rates and health-related quality of life. These are practical for home management, but patients may not be able to distinguish symptoms of acute joint bleeding from chronic arthritis pain, with the potential for either under- or overtreatment, and subjective reporting is likely to miss subclinical bleeding that can occur even when patients are on prophylaxis.

Health-related quality of life tools, whether generic or specific for hemophilia, are not sensitive to small improvements, and they are not always used in routine clinical practice.

Objective measures include physical examination with scoring according to the World Federation of Hemophilia (Gilbert Scale) score or Hemophilia Joint Health Score, but these measures have limited ability to identify early or subclinical joint abnormalities.

“Therefore, joint physical examination on its own is not a sufficient measure of treatment efficacy, and it should be used in combination with other tools more objective, such as imaging,” Dr. Gualtierotti said.
 

Get the picture?

Imaging with x-rays, MRI, and, recently in some centers, point-of-care ultrasound can provide clinicians with important real-time information about the joint stability and health.

Point-of-care ultrasound in particular offers promise as a practical tool, with no ionizing radiation and high sensitivity for synovial hyperplasia subclinical joint effusion. It’s relatively inexpensive, can be used to image multiple joints, and allows for ease of follow-up, she said. The technique requires specialized training, however, and there is a lack of prospective data about its utility in hemophilia.

Various ultrasound scoring systems have been proposed, and home-based ultrasound is currently being explored in several clinical trials, Dr. Gualtierotti noted.

Other avenues for remote joint health monitoring under consideration are serum or synovial biomarkers for joint bleeding and arthropathy that could be employed at bedside or at home, smartphone apps for breakthrough bleeding and patient-reported outcomes, and sensors for detecting abnormalities in gait that may signal joint dysfunction, she said.
 

 

 

Best practice

In the question-and-answer session following the talk, Fernando Zikan, MD, from the Federal University of Rio de Janeiro noted that, “in underdeveloped countries, we still find it very difficult to guide good practices for joint health control by the patient and family members. Which strategy do you think is fundamental for the patient to feel safe to notice changes in his body?”

“It would be useful to educate patients to come to the center whenever the patient has trauma and whenever an increase in his physical activity occurs. If this is far, a bedside ultrasound evaluation by the general practitioner could help avoid joint damage. Finally, a correct rehabilitation is fundamental,” Dr. Gualtierotti replied.

Asked by several others whether she used ultrasound in her daily practice, Dr. Gualtierotti said that “we use joint ultrasound in our clinical practice in the regular annual check-up examination and whenever the patient suspects and reports hemarthrosis.”

Dr. Gualtierotti reported participation in advisory boards for Biomarin, Pfizer, Bayer, and Takeda, and in educational seminars sponsored by Pfizer, Sobi, and Roche. She has received support for congress travel and/or attendance by Bayer and Pfizer. Dr. Zikan reported no relevant disclosures.

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JAMA editor resigns over controversial podcast

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Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.



Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

A version of this article first appeared on WebMD.com .

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Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.



Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

A version of this article first appeared on WebMD.com .

Edward H. Livingston, MD, has resigned as deputy editor of JAMA after he and the journal faced significant backlash over a February 2021 podcast that questioned the existence of structural racism.

JAMA editor in chief Howard Bauchner, MD, apologized to JAMA staff and stakeholders and asked for and received Dr. Livingston’s resignation, according to a statement from AMA CEO James Madara.

More than 2,000 people have signed a petition on Change.org calling for an investigation at JAMA over the podcast, called “Structural Racism for Doctors: What Is It?”

It appears they are now getting their wish. Dr. Bauchner announced that the journal’s oversight committee is investigating how the podcast and a tweet promoting the episode were developed, reviewed, and ultimately posted.

“This investigation and report of its findings will be thorough and completed rapidly,” Dr. Bauchner said.

Dr. Livingston, the host of the podcast, has been heavily criticized across social media. During the podcast, Dr. Livingston, who is White, said: “Structural racism is an unfortunate term. Personally, I think taking racism out of the conversation will help. Many of us are offended by the concept that we are racist.”

The audio of the podcast has been deleted from JAMA’s website. In its place is audio of a statement from Dr. Bauchner. In his statement, which he released last week, he said the comments in the podcast, which also featured Mitch Katz, MD, were “inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA.”

Dr. Katz is an editor at JAMA Internal Medicine and CEO of NYC Health + Hospitals in New York.



Also deleted was a JAMA tweet promoting the podcast episode. The tweet said: “No physician is racist, so how can there be structural racism in health care? An explanation of the idea by doctors for doctors in this user-friendly podcast.”

The incident was met with anger and confusion in the medical community.

Herbert C. Smitherman, MD, vice dean of diversity and community affairs at Wayne State University, Detroit, noted after hearing the podcast that it was a symptom of a much larger problem.

“At its core, this podcast had racist tendencies. Those attitudes are why you don’t have as many articles by Black and Brown people in JAMA,” he said. “People’s attitudes, whether conscious or unconscious, are what drive the policies and practices which create the structural racism.”

Dr. Katz responded to the backlash last week with the following statement: “Systemic racism exists in our country. The disparate effects of the pandemic have made this painfully clear in New York City and across the country.

“As clinicians, we must understand how these structures and policies have a direct impact on the health outcomes of the patients and communities we serve. It is woefully naive to say that no physician is a racist just because the Civil Rights Act of 1964 forbade it, or that we should avoid the term ‘systematic racism’ because it makes people uncomfortable. We must and can do better.”

JAMA, an independent arm of the AMA, is taking other steps to address concerns. Its executive publisher, Thomas Easley, held an employee town hall this week, and said JAMA acknowledges that “structural racism is real, pernicious, and pervasive in health care.” The journal is also starting an “end-to-end review” of all editorial processes across all JAMA publications. Finally, the journal will also create a new associate editor’s position who will provide “insight and counsel” on racism and structural racism in health care.

A version of this article first appeared on WebMD.com .

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Don’t discontinue osteoporosis meds for COVID-19 vaccines, expert guidance says

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COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

Dr. Suzanne Jan De Beur

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

  • Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
  • Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
  • Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
  • Teriparatide and abaloparatide should be continued.
  • Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
  • Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

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COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

Dr. Suzanne Jan De Beur

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

  • Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
  • Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
  • Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
  • Teriparatide and abaloparatide should be continued.
  • Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
  • Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

COVID-19 vaccines are safe and effective for patients taking osteoporosis medications, according to joint guidance from six endocrine and osteoporosis societies and foundations.

Dr. Suzanne Jan De Beur

They noted, though, that some timing modifications with certain medications should be considered to help distinguish between adverse events from the medication versus the vaccine.

The American Society for Bone and Mineral Research “is an international organization, so we brought together our sister societies that have a vested interested in bone health. Vaccination is happening worldwide, and we wanted to present a united front and united recommendations about how to handle osteoporosis medications appropriately during vaccination,” said Suzanne Jan De Beur, MD, who is president of ASBMR and an associate professor of medicine at Johns Hopkins University, Baltimore.

There has been quite a lot of concern from the community about vaccine and medications, from both physicians and patients wondering whether treatments and vaccines should occur in a certain order, and whether there should be a time gap between the two, said Dr. Jan De Beur. “There was a dearth of information about the best practices for osteoporosis treatment management during vaccination, and we didn’t want people missing their opportunity for a vaccine, and we also didn’t want them unnecessarily delaying their osteoporosis treatment.”

There is no evidence that osteoporosis therapies affect the risk or severity of COVID-19 disease, nor do they appear to change the disease course. Osteoporosis itself does not appear associated with increased risk of infection or severe outcomes, so patients with osteoporosis do not need to be prioritized for vaccination based on that condition alone.

There is no evidence that osteoporosis therapies affect the safety or efficacy of vaccination, but given that vaccine availability is currently inconsistent, patients may need to make temporary changes to their osteoporosis regimens to ensure they can receive vaccine when it is available, such as ensuring a delay between medication and vaccination injections.

A key reason for a delay between injectable or infusion medications and a vaccine is to distinguish between adverse events that could occur, so that an adverse reaction to vaccine isn’t mistaken for an adverse reaction to a drug. Nevertheless, the real world is messy. Dr. Jan De Beur noted a recent patient who arrived at her clinic for an injectable treatment who had just received a COVID-19 vaccination that morning. “We decided to put the injection in the other arm, rather than reschedule the person and put them through the risk of coming back. We could distinguish between injection-site reactions, at least,” she said.

copyright DesignPics/Thinkstock

No changes should be made to general bone health therapies, such as calcium and vitamin D supplementation, weight-bearing exercises, and maintenance of a balanced diet.

The guidance includes some recommendations for specific osteoporosis medications.

  • Oral bisphosphonates: Alendronate, risedronate, and ibandronate should be continued.
  • Intravenous bisphosphonates: a 7-day interval (4-day minimum) is recommended between intravenous bisphosphonate (zoledronic acid and ibandronate) infusion and COVID-19 vaccination in order to distinguish potential autoimmune or inflammatory reactions that could be attributable to either intravenous bisphosphonate or the vaccine.
  • Denosumab: There should be a 4- to 7-day delay between denosumab infusion and COVID-19 vaccination to account for injection-site reactions. Another option is to have denosumab injected into the contralateral arm or another site like the abdomen or upper thigh, if spacing the injections is not possible. In any case, denosumab injections should be performed within 7 months of the previous dose.
  • Teriparatide and abaloparatide should be continued.
  • Romosozumab: There should be a 4- to 7-day delay between a romosozumab injection and COVID-19 vaccine, or romosozumab can be injected in the abdomen (with the exception of a 2-inch area around the naval) or thigh if spacing is not possible.
  • Raloxifene should be continued in patients receiving COVID-19 vaccination.

Guidance signatories include ASBMR, the American Association of Clinical Endocrinology, the Endocrine Society, the European Calcified Tissue Society, the National Osteoporosis Foundation, and the International Osteoporosis Foundation.

Dr. Jan De Beur has no relevant financial disclosures.

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Inpatient sodium imbalances linked to adverse COVID-19 outcomes

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Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Dr. Steven Q. Simpson

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

 

 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Dr. Steven Q. Simpson

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

 

 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

 

Both high and low serum sodium levels are associated with adverse outcomes for hospitalized patients with COVID-19, new research suggests.

In the retrospective study of 488 patients hospitalized with COVID-19 at one of two London hospitals between February and May 2020, hypernatremia (defined as serum sodium level >145 mmol/L) at any time point during hospital stay was associated with a threefold increase in inpatient mortality.

Hyponatremia (serum sodium level <135 mmol/L) was associated with twice the likelihood of requiring advanced ventilatory support. In-hospital mortality was also increased among patients with hypovolemic hyponatremia.

“Serum sodium values could be used in clinical practice to identify patients with COVID-19 at high risk of poor outcomes who would benefit from more intensive monitoring and judicious rehydration,” Ploutarchos Tzoulis, MD, PhD, and colleagues wrote in their article, which was published online on Feb. 24, 2021, in the Journal of Clinical Endocrinology and Metabolism.

The findings will be presented at the upcoming news conference held by the Endocrine Society
 

Should sodium be included in a risk calculator for COVID-19?

Dr. Tzoulis, professor of endocrinology at the University College London Medical School, said in an interview that “sodium could be incorporated in risk calculators across other routine biomarkers, such as white cell count, lymphocytes, and CRP [C-reactive protein], in order to provide a tool for dynamic risk stratification throughout the clinical course of COVID-19 and assist clinical decision-making.”

Moreover, he said, “we should follow less conservative strategies in the rate and amount of fluid resuscitation in order to prevent hypernatremia, which is induced by negative fluid balance and can often be iatrogenic.”

Dr. Steven Q. Simpson

Asked to comment, Steven Q. Simpson, MD, professor of medicine in the division of pulmonary, critical care, and sleep medicine at the University of Kansas, Kansas City, said that the article is missing key results that would assist in interpreting of the findings.

“Data regarding diuretic use and sparing of fluid administration are not in the paper. ... It is simply not possible to tell whether serum sodium is a ‘predictor’ ... or if it is a side effect of other issues or actions taken by physicians in patients who are progressing poorly.

“To say that sodium needs to be included in a risk calculator is to subtly suggest that there is some causal association with mortality, and that has quite clearly not been established,” stressed Dr. Simpson, who is president of the American College of Chest Physicians but was not speaking for the organization.

He added: “The data are interesting, but not actionable. It is common practice in critical care medicine to adjust water and salt intake to maintain serum sodium within the normal range, so the paper really doesn’t change any behavior.”

Dr. Tzoulis said in an interview that, despite not having electronic medical record data on diuretic use or fluid input and output, “our acute physicians and intensivists at both study sites have been adamant that they’ve not routinely used diuretics in COVID-19 patients. Diuretics have been sparingly used in our cohort, and also the frequency of pulmonary edema was reported as below 5%.”

Regarding volume of fluid intake, Dr. Tzoulis noted, “At our hospital sites, the strategy has been that of cautious fluid resuscitation. In fact, the amount of fluid given has been reported by our physicians and intensivists as ‘on purpose much more conservative than the usual one adopted in patients with community-acquired pneumonia at risk of respiratory failure.’ ”
 

 

 

Hyper- and hyponatremia linked to adverse COVID-19 outcomes

In the study, 5.3% of the 488 patients had hypernatremia at hospital presentation, and 24.6% had hyponatremia. Of note, only 19% of those with hyponatremia underwent laboratory workup to determine the etiology. Of those, three quarters had hypovolemic hyponatremia, determined on the basis of a urinary sodium cutoff of 30 mmol/L.

The total in-hospital mortality rate was 31.1%. There was a strong, although nonsignificant, trend toward higher mortality in association with sodium status at admission. Death rates were 28.4%, 30.8%, and 46.1% for those who were normonatremic, hyponatremic, and hypernatremic, respectively (P = .07). Baseline serum sodium levels didn’t differ between survivors (137 mmol/L) and nonsurvivors (138 mmol/L).

In multivariable analysis, the occurrence of hypernatremia at any point during the first 5 days in the hospital was among three independent risk factors for higher in-hospital mortality (adjusted hazard ratio, 2.74; P = .02). The other risk factors were older age and higher CRP level.

Overall, hyponatremia was not associated with death (P = .41).

During hospitalization, 37.9% of patients remained normonatremic; 36.9% experienced hyponatremia; 10.9% had hypernatremia; and 14.3% had both conditions at some point during their stay.

In-hospital mortality was 21% among those with normonatremia, compared with 56.6% for those with hypernatremia (odds ratio, 3.05; P = .0038) and 45.7% for those with both (OR, 2.25; P < .0001).

The 28.3% mortality rate in the overall group that experienced hyponatremia didn’t differ significantly from the 21.1% in the normonatremic group (OR, 1.34; P = .16). However, the death rate was 40.9% among the subgroup that developed hypovolemic hyponatremia, significantly higher than the normonatremic group (OR, 2.59, P = .0017).

The incidence of hyponatremia decreased from 24.6% at admission to 14.1% 5 days later, whereas the frequency of hypernatremia rose from 5.3% to 13.8%.
 

Key finding: Link between hospital-acquired hypernatremia and death

“The key novel finding of our study was that hospital-acquired hypernatremia, rather than hypernatremia at admission, was a predictor for in-hospital mortality, with the worst prognosis being reported in patients with the largest increase in serum sodium in the first 5 days of hospitalization,” noted Dr. Tzoulis and colleagues.

Hypernatremia was present in 29.6% of nonsurvivors, compared with 5.2% in survivors.

Among 120 patients with hyponatremia at admission, 31.7% received advanced respiratory support, compared with 17.5% and 7.7% of those with normonatremia or hypernatremia, respectively (OR, 2.18; P = .0011).

In contrast, there was no difference in the proportions needing ventilatory support between those with hypernatremia and those with normonatremia (16.7% vs. 12.4%; OR, 1.44; P = .39).

Acute kidney injury occurred in 181 patients (37.1%). It was not related to serum sodium concentration at any time point.

Dr. Tzoulis and Dr. Simpson disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Delay surgery by 7 weeks after COVID-19 diagnosis, study shows

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Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

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Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

  • 0 to 2 weeks – 9.1% mortality.
  • 3 to 4 weeks – 6.9%.
  • 5 to 6 weeks – 5.5%.
  • 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

 

 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

A version of this article first appeared on Medscape.com.

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Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

BraunS/Getty Images

Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

  • 0 to 2 weeks – 9.1% mortality.
  • 3 to 4 weeks – 6.9%.
  • 5 to 6 weeks – 5.5%.
  • 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

 

 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

A version of this article first appeared on Medscape.com.

Seven weeks appears to be the ideal amount of time to delay surgery, when possible, after someone tests positive for COVID-19, researchers in the United Kingdom report.

BraunS/Getty Images

Risk for death was about 3.5 to 4 times higher in the first 6 weeks after surgery among more than 3,000 people with a preoperative COVID-19 diagnosis compared with patients without COVID-19. After 7 weeks, the 30-day mortality rate dropped to a baseline level.

The study was published online March 9 in Anaesthesia.

Surgery should be further delayed for people who remain symptomatic at 7 weeks post diagnosis, lead author Dmitri Nepogodiev, MBChB, said in an interview.

“In this group we recommend waiting until COVID-19 symptoms resolve, if possible. However, our study did not capture specific data on long COVID … so we are unable to make specific recommendations for this group,” said Dr. Nepogodiev, research fellow at the NIHR Global Health Research Unit on Global Surgery at the University of Birmingham (England).

“This should be an area for future research,” he added.

The international, multicenter, prospective cohort study is notable for its sheer size – more than 15,000 investigators reported outcomes for 140,231 surgical patients from 1,674 hospitals across 116 countries. In total, 2.2% of these patients tested positive for SARS-CoV-2 prior to surgery.

Surgery of any type performed in October 2020 was assessed. A greater proportion of patients with a preoperative COVID-19 diagnosis had emergency surgery, 44%, compared with 30% of people who never had a COVID-19 diagnosis.

Most patients were asymptomatic at the time of surgery, either because they never experienced COVID-19 symptoms or their symptoms resolved. The 30-day mortality rate was the primary outcome.
 

Death rates among surgical patients with preoperative COVID-19 diagnosis

Comparing the timing of surgery after COVID-19 diagnosis vs. 30-day mortality yielded the following results:

  • 0 to 2 weeks – 9.1% mortality.
  • 3 to 4 weeks – 6.9%.
  • 5 to 6 weeks – 5.5%.
  • 7 weeks or longer – 2.0%..

For comparison, the 30-day mortality rate for surgical patients without a preoperative COVID-19 diagnosis was 1.4%. A COVID-19 diagnosis more than 7 weeks before surgery did not make a significant difference on outcomes.
 

The ‘why’ remains unknown

The reasons for the association between a COVID-19 diagnosis and higher postoperative death rates remain unknown. However, Dr. Nepogodiev speculated that it could be related to “some degree of lung injury, even if patients are initially asymptomatic.”

Intubation and mechanical ventilation during surgery could exacerbate the existing lung injury, he said, thereby leading to more severe COVID-19.

In fact, Dr. Nepogodiev and colleagues found that postoperative pulmonary complications followed a pattern similar to the findings on death. They reported higher rates of pneumonia, acute respiratory distress syndrome, and unexpected reventilation in the first 6 weeks following a COVID-19 diagnosis. Again, at 7 weeks and beyond, the rates returned to be relatively the same as those for people who never had COVID-19.

“Waiting for 7 or more weeks may allow time for the initial COVID-19 injury to resolve,” Dr. Nepogodiev said.
 

 

 

‘An important study’

“This is an important study of postoperative mortality among patients recovered from COVID-19,” Adrian Diaz, MD, MPH, said in an interview when asked to comment.

The large cohort and numerous practice settings are among the strengths of the research, said Dr. Diaz, of the University of Michigan Institute for Healthcare Policy and Innovation in Ann Arbor. He was lead author of a June 2020 review article on elective surgery in the time of COVID-19, published in The American Journal of Surgery.

“As with nearly all studies of this nature, results must be interpreted on a case-by-case basis for individual patients. However, this study does add important information for patients and providers in helping them have an informed discussion on the timing of surgery,” said Dr. Diaz, a fellow in the Center for Healthcare Outcomes and Policy and a resident in general surgery at the Ohio State University, Columbus.

Dr. Nepogodiev and colleagues included both urgent and elective surgeries in the study. Dr. Diaz said this was a potential limitation because emergency operations “should never be delayed, by definition.” Lack of indications for the surgeries and information on cause of death were additional limitations.

Future research should evaluate any benefit in delaying surgery longer than 7 or more weeks, Dr. Diaz added, perhaps looking specifically at 10, 12, or 14 weeks, or considering outcomes as a continuous variable. This would help health care providers “garner more insight into risk and benefits of delaying surgery beyond 7 weeks.”

Dr. Nepogodiev and Dr. Diaz disclosed no relevant financial relationships. The study had multiple funding sources, including the National Institute for Health Research Global Health Research Unit, the Association of Upper Gastrointestinal Surgeons, the British Association of Surgical Oncology, and Medtronic.

A version of this article first appeared on Medscape.com.

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Nearly 20% of lupus patients have severe infection in first decade after diagnosis

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People with systemic lupus erythematosus (SLE) experienced significantly higher rates of first severe infections, a higher number of severe infections overall, and greater infection-related mortality, compared with controls, based on data from a population-based cohort study of more than 30,000 individuals.

Infections remain a leading cause of morbidity and early mortality in patients with SLE, wrote Kai Zhao, MSc, of Arthritis Research Canada, Richmond, and colleagues. However, “limitations from existing studies including selected samples, small sizes, and prevalent cohorts can negatively affect the accuracy of both the absolute and relative risk estimates of infections in SLE at the population level,” they said.

In a study published in Rheumatology, the researchers identified 5,169 people newly diagnosed with SLE between Jan. 1, 1997, and March 31, 2015, and matched them with 25,845 non-SLE controls using an administrative health database of all health care services funded in British Columbia during the time period. The investigators said the study is the first “to evaluate the risk of severe infections in a large population-based and incident SLE cohort.”

The average age of the patients was 46.9 at the time of their index SLE diagnosis, and 86% were women. The average follow-up period was approximately 10 years.



The primary outcome was the first severe infection after the onset of SLE that required hospitalization or occurred in the hospital setting. A total of 955 (18.5%) first severe infections occurred in the SLE group, compared with 1,988 (7.7%) in the controls, for incidence rates of 19.7 events per 1,000 person-years and 7.6 events per 1,000 person-years, respectively, yielding an 82% increased risk of severe infection for SLE patients after adjustment for confounding baseline factors.

Secondary outcomes of the total number of severe infections and infection-related mortality both showed significant increases in SLE patients, compared with controls. The total number of severe infections in the SLE and control groups was 1,898 and 3,114, respectively, with an adjusted risk ratio of 2.07.

As for mortality, a total of 539 deaths occurred in SLE patients during the study period, and 114 (21%) were related to severe infection. A total of 1,495 deaths occurred in the control group, including 269 (18%) related to severe infection. The adjusted hazard ratio was 1.61 after adjustment for confounding baseline variables.

The risks for first severe infection, total number of severe infections, and infection-related mortality were “independent of traditional risk factors for infection and the results remain robust in the presence of an unmeasured confounder (smoking) and competing risk of death,” the researchers said. Reasons for the increased risk are uncertain, but likely result from intrinsic factors such as immune system dysfunction and extrinsic factors such as the impact of immunosuppressive medications. “Future research can focus on quantifying the relative contributions of these intrinsic and extrinsic factors on the increased infection risk in SLE patients,” they added.

The study findings were limited by several factors linked to the observational design, including possible misdiagnosis of SLE and inaccurate measure of SLE onset, the researchers noted. In addition, no data were available for certain confounders such as smoking and nonhospitalized infections, they said.



However, the results were strengthened by the large size and general population and the use of sensitivity analyses, they noted. For SLE patients, “increased awareness of the risk of infections can identify their early signs and potentially prevent hospitalizations,” and clinicians can promote infection prevention strategies, including vaccinations when appropriate, they added.

Based on their findings, “we recommend a closer surveillance for severe infections in SLE patients and risk assessment for severe infections for SLE patients after diagnosis,” the researchers emphasized. “Further studies are warranted to further identify risk factors for infections in SLE patients to develop personalized treatment regimens and to select treatment in practice by synthesizing patient information,” they concluded.

The study was supported by the Canadian Institutes for Health Research. The researchers had no financial conflicts to disclose.

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People with systemic lupus erythematosus (SLE) experienced significantly higher rates of first severe infections, a higher number of severe infections overall, and greater infection-related mortality, compared with controls, based on data from a population-based cohort study of more than 30,000 individuals.

Infections remain a leading cause of morbidity and early mortality in patients with SLE, wrote Kai Zhao, MSc, of Arthritis Research Canada, Richmond, and colleagues. However, “limitations from existing studies including selected samples, small sizes, and prevalent cohorts can negatively affect the accuracy of both the absolute and relative risk estimates of infections in SLE at the population level,” they said.

In a study published in Rheumatology, the researchers identified 5,169 people newly diagnosed with SLE between Jan. 1, 1997, and March 31, 2015, and matched them with 25,845 non-SLE controls using an administrative health database of all health care services funded in British Columbia during the time period. The investigators said the study is the first “to evaluate the risk of severe infections in a large population-based and incident SLE cohort.”

The average age of the patients was 46.9 at the time of their index SLE diagnosis, and 86% were women. The average follow-up period was approximately 10 years.



The primary outcome was the first severe infection after the onset of SLE that required hospitalization or occurred in the hospital setting. A total of 955 (18.5%) first severe infections occurred in the SLE group, compared with 1,988 (7.7%) in the controls, for incidence rates of 19.7 events per 1,000 person-years and 7.6 events per 1,000 person-years, respectively, yielding an 82% increased risk of severe infection for SLE patients after adjustment for confounding baseline factors.

Secondary outcomes of the total number of severe infections and infection-related mortality both showed significant increases in SLE patients, compared with controls. The total number of severe infections in the SLE and control groups was 1,898 and 3,114, respectively, with an adjusted risk ratio of 2.07.

As for mortality, a total of 539 deaths occurred in SLE patients during the study period, and 114 (21%) were related to severe infection. A total of 1,495 deaths occurred in the control group, including 269 (18%) related to severe infection. The adjusted hazard ratio was 1.61 after adjustment for confounding baseline variables.

The risks for first severe infection, total number of severe infections, and infection-related mortality were “independent of traditional risk factors for infection and the results remain robust in the presence of an unmeasured confounder (smoking) and competing risk of death,” the researchers said. Reasons for the increased risk are uncertain, but likely result from intrinsic factors such as immune system dysfunction and extrinsic factors such as the impact of immunosuppressive medications. “Future research can focus on quantifying the relative contributions of these intrinsic and extrinsic factors on the increased infection risk in SLE patients,” they added.

The study findings were limited by several factors linked to the observational design, including possible misdiagnosis of SLE and inaccurate measure of SLE onset, the researchers noted. In addition, no data were available for certain confounders such as smoking and nonhospitalized infections, they said.



However, the results were strengthened by the large size and general population and the use of sensitivity analyses, they noted. For SLE patients, “increased awareness of the risk of infections can identify their early signs and potentially prevent hospitalizations,” and clinicians can promote infection prevention strategies, including vaccinations when appropriate, they added.

Based on their findings, “we recommend a closer surveillance for severe infections in SLE patients and risk assessment for severe infections for SLE patients after diagnosis,” the researchers emphasized. “Further studies are warranted to further identify risk factors for infections in SLE patients to develop personalized treatment regimens and to select treatment in practice by synthesizing patient information,” they concluded.

The study was supported by the Canadian Institutes for Health Research. The researchers had no financial conflicts to disclose.

People with systemic lupus erythematosus (SLE) experienced significantly higher rates of first severe infections, a higher number of severe infections overall, and greater infection-related mortality, compared with controls, based on data from a population-based cohort study of more than 30,000 individuals.

Infections remain a leading cause of morbidity and early mortality in patients with SLE, wrote Kai Zhao, MSc, of Arthritis Research Canada, Richmond, and colleagues. However, “limitations from existing studies including selected samples, small sizes, and prevalent cohorts can negatively affect the accuracy of both the absolute and relative risk estimates of infections in SLE at the population level,” they said.

In a study published in Rheumatology, the researchers identified 5,169 people newly diagnosed with SLE between Jan. 1, 1997, and March 31, 2015, and matched them with 25,845 non-SLE controls using an administrative health database of all health care services funded in British Columbia during the time period. The investigators said the study is the first “to evaluate the risk of severe infections in a large population-based and incident SLE cohort.”

The average age of the patients was 46.9 at the time of their index SLE diagnosis, and 86% were women. The average follow-up period was approximately 10 years.



The primary outcome was the first severe infection after the onset of SLE that required hospitalization or occurred in the hospital setting. A total of 955 (18.5%) first severe infections occurred in the SLE group, compared with 1,988 (7.7%) in the controls, for incidence rates of 19.7 events per 1,000 person-years and 7.6 events per 1,000 person-years, respectively, yielding an 82% increased risk of severe infection for SLE patients after adjustment for confounding baseline factors.

Secondary outcomes of the total number of severe infections and infection-related mortality both showed significant increases in SLE patients, compared with controls. The total number of severe infections in the SLE and control groups was 1,898 and 3,114, respectively, with an adjusted risk ratio of 2.07.

As for mortality, a total of 539 deaths occurred in SLE patients during the study period, and 114 (21%) were related to severe infection. A total of 1,495 deaths occurred in the control group, including 269 (18%) related to severe infection. The adjusted hazard ratio was 1.61 after adjustment for confounding baseline variables.

The risks for first severe infection, total number of severe infections, and infection-related mortality were “independent of traditional risk factors for infection and the results remain robust in the presence of an unmeasured confounder (smoking) and competing risk of death,” the researchers said. Reasons for the increased risk are uncertain, but likely result from intrinsic factors such as immune system dysfunction and extrinsic factors such as the impact of immunosuppressive medications. “Future research can focus on quantifying the relative contributions of these intrinsic and extrinsic factors on the increased infection risk in SLE patients,” they added.

The study findings were limited by several factors linked to the observational design, including possible misdiagnosis of SLE and inaccurate measure of SLE onset, the researchers noted. In addition, no data were available for certain confounders such as smoking and nonhospitalized infections, they said.



However, the results were strengthened by the large size and general population and the use of sensitivity analyses, they noted. For SLE patients, “increased awareness of the risk of infections can identify their early signs and potentially prevent hospitalizations,” and clinicians can promote infection prevention strategies, including vaccinations when appropriate, they added.

Based on their findings, “we recommend a closer surveillance for severe infections in SLE patients and risk assessment for severe infections for SLE patients after diagnosis,” the researchers emphasized. “Further studies are warranted to further identify risk factors for infections in SLE patients to develop personalized treatment regimens and to select treatment in practice by synthesizing patient information,” they concluded.

The study was supported by the Canadian Institutes for Health Research. The researchers had no financial conflicts to disclose.

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Bone loss common in kidney stone patients, yet rarely detected

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Almost one in four men and women diagnosed with kidney stones have osteoporosis or a history of fracture at the time of their diagnosis, yet fewer than 10% undergo bone mineral density (BMD) screening, a retrospective analysis of a Veterans Health Administration database shows.

kgerakis/Getty Images

Because the majority of those analyzed in the VA dataset were men, this means that middle-aged and older men with kidney stones have about the same risk for osteoporosis as postmenopausal women do, but BMD screening for such men is not currently recommended, the study notes.

“These findings suggest that the risk of osteoporosis or fractures in patients with kidney stone disease is not restricted to postmenopausal women but is also observed in men, a group that is less well recognized to be at risk,” Calyani Ganesan, MD, of Stanford (Calif.) University and colleagues say in their article, published online March 3 in the Journal of Bone and Mineral Research.

“We hope this work raises awareness regarding the possibility of reduced bone strength in patients with kidney stones, [and] in our future work, we hope to identify which patients with kidney stones are at higher risk for osteoporosis or fracture to help guide bone density screening efforts by clinicians in this population,” Dr. Ganesan added in a statement.
 

VA dataset: Just 9.1% had DXA after kidney stone diagnosed

A total of 531,431 patients with a history of kidney stone disease were identified in the VA dataset. Of these, 23.6% either had been diagnosed with osteoporosis or had a history of fracture around the time of their kidney stone diagnosis. The most common diagnosis was a non-hip fracture, seen in 19% of patients, Dr. Ganesan and colleagues note, followed by osteoporosis in 6.1%, and hip fracture in 2.1%.

The mean age of the patients who concurrently had received a diagnosis of kidney stone disease and osteoporosis or had a fracture history was 64.2 years. In this cohort, more than 91% were men. The majority of the patients were White.



Among some 462,681 patients who had no prior history of either osteoporosis or fracture before their diagnosis of kidney stones, only 9.1% had undergone dual-energy x-ray absorptiometry (DXA) screening for BMD in the 5 years after their kidney stone diagnosis.

“Of those who completed DXA ... 20% were subsequently diagnosed with osteoporosis,” the authors note – 19% with non-hip fracture, and 2.4% with hip fracture.

Importantly, 85% of patients with kidney stone disease who were screened with DXA and were later diagnosed with osteoporosis were men.

“Given that almost 20% of patients in our cohort had a non-hip fracture, we contend that osteoporosis is underdiagnosed and undertreated in older men with kidney stone disease,” the authors stress.

Perform DXA screen in older men, even in absence of hypercalciuria

The authors also explain that the most common metabolic abnormality associated with kidney stones is high urine calcium excretion, or hypercalciuria.

“In a subset of patients with kidney stones, dysregulated calcium homeostasis may be present in which calcium is resorbed from bone and excreted into the urine, which can lead to osteoporosis and the formation of calcium stones,” they explain.

However, when they carried out a 24-hour assessment of urine calcium excretion on a small subset of patients with kidney stones, “we found no correlation between osteoporosis and the level of 24-hour urine calcium excretion,” they point out.

Even when the authors excluded patients who were taking a thiazide diuretic – a class of drugs that decreases urine calcium excretion – there was no correlation between osteoporosis and the level of 24-hour urine calcium excretion.

The investigators suggest it is possible that, in the majority of patients with kidney stones, the cause of hypercalciuria is more closely related to overabsorption of calcium from the gut, not to overresorption of calcium from the bone.

“Nonetheless, our findings indicate that patients with kidney stone disease could benefit from DXA screening even in the absence of hypercalciuria,” they state.

“And our findings provide support for wider use of bone mineral density screening in patients with kidney stone disease, including middle-aged and older men, for whom efforts to mitigate risks of osteoporosis and fractures are not commonly emphasized,” they reaffirm.

The study was funded by the VA Merit Review and the National Institute of Diabetes and Digestive and Kidney Diseases. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Almost one in four men and women diagnosed with kidney stones have osteoporosis or a history of fracture at the time of their diagnosis, yet fewer than 10% undergo bone mineral density (BMD) screening, a retrospective analysis of a Veterans Health Administration database shows.

kgerakis/Getty Images

Because the majority of those analyzed in the VA dataset were men, this means that middle-aged and older men with kidney stones have about the same risk for osteoporosis as postmenopausal women do, but BMD screening for such men is not currently recommended, the study notes.

“These findings suggest that the risk of osteoporosis or fractures in patients with kidney stone disease is not restricted to postmenopausal women but is also observed in men, a group that is less well recognized to be at risk,” Calyani Ganesan, MD, of Stanford (Calif.) University and colleagues say in their article, published online March 3 in the Journal of Bone and Mineral Research.

“We hope this work raises awareness regarding the possibility of reduced bone strength in patients with kidney stones, [and] in our future work, we hope to identify which patients with kidney stones are at higher risk for osteoporosis or fracture to help guide bone density screening efforts by clinicians in this population,” Dr. Ganesan added in a statement.
 

VA dataset: Just 9.1% had DXA after kidney stone diagnosed

A total of 531,431 patients with a history of kidney stone disease were identified in the VA dataset. Of these, 23.6% either had been diagnosed with osteoporosis or had a history of fracture around the time of their kidney stone diagnosis. The most common diagnosis was a non-hip fracture, seen in 19% of patients, Dr. Ganesan and colleagues note, followed by osteoporosis in 6.1%, and hip fracture in 2.1%.

The mean age of the patients who concurrently had received a diagnosis of kidney stone disease and osteoporosis or had a fracture history was 64.2 years. In this cohort, more than 91% were men. The majority of the patients were White.



Among some 462,681 patients who had no prior history of either osteoporosis or fracture before their diagnosis of kidney stones, only 9.1% had undergone dual-energy x-ray absorptiometry (DXA) screening for BMD in the 5 years after their kidney stone diagnosis.

“Of those who completed DXA ... 20% were subsequently diagnosed with osteoporosis,” the authors note – 19% with non-hip fracture, and 2.4% with hip fracture.

Importantly, 85% of patients with kidney stone disease who were screened with DXA and were later diagnosed with osteoporosis were men.

“Given that almost 20% of patients in our cohort had a non-hip fracture, we contend that osteoporosis is underdiagnosed and undertreated in older men with kidney stone disease,” the authors stress.

Perform DXA screen in older men, even in absence of hypercalciuria

The authors also explain that the most common metabolic abnormality associated with kidney stones is high urine calcium excretion, or hypercalciuria.

“In a subset of patients with kidney stones, dysregulated calcium homeostasis may be present in which calcium is resorbed from bone and excreted into the urine, which can lead to osteoporosis and the formation of calcium stones,” they explain.

However, when they carried out a 24-hour assessment of urine calcium excretion on a small subset of patients with kidney stones, “we found no correlation between osteoporosis and the level of 24-hour urine calcium excretion,” they point out.

Even when the authors excluded patients who were taking a thiazide diuretic – a class of drugs that decreases urine calcium excretion – there was no correlation between osteoporosis and the level of 24-hour urine calcium excretion.

The investigators suggest it is possible that, in the majority of patients with kidney stones, the cause of hypercalciuria is more closely related to overabsorption of calcium from the gut, not to overresorption of calcium from the bone.

“Nonetheless, our findings indicate that patients with kidney stone disease could benefit from DXA screening even in the absence of hypercalciuria,” they state.

“And our findings provide support for wider use of bone mineral density screening in patients with kidney stone disease, including middle-aged and older men, for whom efforts to mitigate risks of osteoporosis and fractures are not commonly emphasized,” they reaffirm.

The study was funded by the VA Merit Review and the National Institute of Diabetes and Digestive and Kidney Diseases. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Almost one in four men and women diagnosed with kidney stones have osteoporosis or a history of fracture at the time of their diagnosis, yet fewer than 10% undergo bone mineral density (BMD) screening, a retrospective analysis of a Veterans Health Administration database shows.

kgerakis/Getty Images

Because the majority of those analyzed in the VA dataset were men, this means that middle-aged and older men with kidney stones have about the same risk for osteoporosis as postmenopausal women do, but BMD screening for such men is not currently recommended, the study notes.

“These findings suggest that the risk of osteoporosis or fractures in patients with kidney stone disease is not restricted to postmenopausal women but is also observed in men, a group that is less well recognized to be at risk,” Calyani Ganesan, MD, of Stanford (Calif.) University and colleagues say in their article, published online March 3 in the Journal of Bone and Mineral Research.

“We hope this work raises awareness regarding the possibility of reduced bone strength in patients with kidney stones, [and] in our future work, we hope to identify which patients with kidney stones are at higher risk for osteoporosis or fracture to help guide bone density screening efforts by clinicians in this population,” Dr. Ganesan added in a statement.
 

VA dataset: Just 9.1% had DXA after kidney stone diagnosed

A total of 531,431 patients with a history of kidney stone disease were identified in the VA dataset. Of these, 23.6% either had been diagnosed with osteoporosis or had a history of fracture around the time of their kidney stone diagnosis. The most common diagnosis was a non-hip fracture, seen in 19% of patients, Dr. Ganesan and colleagues note, followed by osteoporosis in 6.1%, and hip fracture in 2.1%.

The mean age of the patients who concurrently had received a diagnosis of kidney stone disease and osteoporosis or had a fracture history was 64.2 years. In this cohort, more than 91% were men. The majority of the patients were White.



Among some 462,681 patients who had no prior history of either osteoporosis or fracture before their diagnosis of kidney stones, only 9.1% had undergone dual-energy x-ray absorptiometry (DXA) screening for BMD in the 5 years after their kidney stone diagnosis.

“Of those who completed DXA ... 20% were subsequently diagnosed with osteoporosis,” the authors note – 19% with non-hip fracture, and 2.4% with hip fracture.

Importantly, 85% of patients with kidney stone disease who were screened with DXA and were later diagnosed with osteoporosis were men.

“Given that almost 20% of patients in our cohort had a non-hip fracture, we contend that osteoporosis is underdiagnosed and undertreated in older men with kidney stone disease,” the authors stress.

Perform DXA screen in older men, even in absence of hypercalciuria

The authors also explain that the most common metabolic abnormality associated with kidney stones is high urine calcium excretion, or hypercalciuria.

“In a subset of patients with kidney stones, dysregulated calcium homeostasis may be present in which calcium is resorbed from bone and excreted into the urine, which can lead to osteoporosis and the formation of calcium stones,” they explain.

However, when they carried out a 24-hour assessment of urine calcium excretion on a small subset of patients with kidney stones, “we found no correlation between osteoporosis and the level of 24-hour urine calcium excretion,” they point out.

Even when the authors excluded patients who were taking a thiazide diuretic – a class of drugs that decreases urine calcium excretion – there was no correlation between osteoporosis and the level of 24-hour urine calcium excretion.

The investigators suggest it is possible that, in the majority of patients with kidney stones, the cause of hypercalciuria is more closely related to overabsorption of calcium from the gut, not to overresorption of calcium from the bone.

“Nonetheless, our findings indicate that patients with kidney stone disease could benefit from DXA screening even in the absence of hypercalciuria,” they state.

“And our findings provide support for wider use of bone mineral density screening in patients with kidney stone disease, including middle-aged and older men, for whom efforts to mitigate risks of osteoporosis and fractures are not commonly emphasized,” they reaffirm.

The study was funded by the VA Merit Review and the National Institute of Diabetes and Digestive and Kidney Diseases. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Myth busting: SARS-CoV-2 vaccine

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MYTH: I shouldn’t get the vaccine because of potential long-term side effects

We know that 68 million people in the United States and 244 million people worldwide have already received messenger RNA (mRNA) SARS-CoV-2 vaccines (Pfizer/BioNTech and Moderna). So for the short-term side effects we already know more than we would know about most vaccines.

Dr. Michael E. Pichichero

What about the long-term side effects? There are myths that these vaccines somehow could cause autoimmunity. This came from three publications where the possibility of mRNA vaccines to produce autoimmunity was brought up as a discussion point.1-3 There was no evidence given in these publications, it was raised only as a hypothetical possibility.

There’s no evidence that mRNA or replication-defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) produce autoimmunity. Moreover, the mRNA and replication-defective DNA, once it’s inside of the muscle cell, is gone within a few days. What’s left after ribosome processing is the spike (S) protein as an immunogen. We’ve been vaccinating with proteins for 50 years and we haven’t seen autoimmunity.
 

MYTH: The vaccines aren’t safe because they were developed so quickly

These vaccines were developed at “warp speed” – that doesn’t mean they were developed without all the same safety safeguards that the Food and Drug Administration requires. The reason it happened so fast is because the seriousness of the pandemic allowed us, as a community, to enroll the patients into the studies fast. In a matter of months, we had all the studies filled. In a normal circumstance, that might take 2 or 3 years. And all of the regulatory agencies – the National Institutes of Health, the FDA, the Centers for Disease Control and Prevention – were ready to take the information and put a panel of specialists together and immediately review the data. No safety steps were missed. The same process that’s always required of phase 1, of phase 2, and then at phase 3 were accomplished.

The novelty of these vaccines was that they could be made so quickly. Messenger RNA vaccines can be made in a matter of days and then manufactured in a matter of 2 months. The DNA vaccines has a similar timeline trajectory.
 

MYTH: There’s no point in getting the vaccines because we still have to wear masks

Right now, out of an abundance of caution, until it’s proven that we don’t have to wear masks, it’s being recommended that we do so for the safety of others. Early data suggest that this will be temporary. In time, I suspect it will be shown that, after we receive the vaccine, it will be shown that we are not contagious to others and we’ll be able to get rid of our masks.

MYTH: I already had COVID-19 so I don’t need the vaccine

Some people have already caught the SARS-CoV-2 virus that causes this infection and so they feel that they’re immune and they don’t need to get the vaccine. Time will tell if that’s the case. Right now, we don’t know for sure. Early data suggest that a single dose of vaccine in persons who have had the infection may be sufficient. Over time, what happens in the vaccine field is we measure the immunity from the vaccine, and from people who’ve gotten the infection, and we find that there’s a measurement in the blood that correlates with protection. Right now, we don’t know that correlate of protection level. So, out of an abundance of caution, it’s being recommended that, even if you had the disease, maybe you didn’t develop enough immunity, and it’s better to get the vaccine than to get the illness a second time.

 

 

MYTH: The vaccines can give me SARS-CoV-2 infection

The new vaccines for COVID-19, released under emergency use Authorization, are mRNA and DNA vaccines. They are a blueprint for the Spike (S) protein of the virus. In order to become a protein, the mRNA, once it’s inside the cell, is processed by ribosomes. The product of the ribosome processing is a protein that cannot possibly cause harm as a virus. It’s a little piece of mRNA inside of a lipid nanoparticle, which is just a casing to protect the mRNA from breaking down until it’s injected in the body. The replication defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) are packaged inside of virus cells (adenoviruses). The DNA vaccines involve a three-step process:

  • 1. The adenovirus, containing replication-defective DNA that encodes mRNA for the Spike (S) protein, is taken up by the host cells where it must make its way to the nucleus of the muscle cell.
  • 2. The DNA is injected into the host cell nucleus and in the nucleus the DNA is decoded to an mRNA.
  • 3. The mRNA is released from the nucleus and transported to the cell cytoplasm where the ribosomes process the mRNA in an identical manner as mRNA vaccines.

MYTH: The COVID-19 vaccines can alter my DNA

The mRNA and replication-defective DNA vaccines never interact with your DNA. mRNA vaccines never enter the nucleus. Replication-defective DNA vaccines cannot replicate and do not interact with host DNA. The vaccines can’t change your DNA.

Here is a link to YouTube videos I made on this topic: https://youtube.com/playlist?list=PLve-0UW04UMRKHfFbXyEpLY8GCm2WyJHD.

Dr. Michael E. Pichichero receives his first injection of the Moderna vaccine in January 2021.

Here is a photo of me receiving my first SARS-CoV-2 shot (Moderna) in January 2021. I received my second shot in February. I am a lot less anxious. I hope my vaccine card will be a ticket to travel in the future.

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts of interest to report.

References

1. Peck KM and Lauring AS. J Virol. 2018. doi: 10.1128/JVI.01031-17.

2. Pepini T et al. J Immunol. 2017 May 15. doi: 10.4049/jimmunol.1601877.

3. Theofilopoulos AN et al. Annu Rev Immunol. 2005. doi: 10.1146/annurev.immunol.23.021704.115843.

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MYTH: I shouldn’t get the vaccine because of potential long-term side effects

We know that 68 million people in the United States and 244 million people worldwide have already received messenger RNA (mRNA) SARS-CoV-2 vaccines (Pfizer/BioNTech and Moderna). So for the short-term side effects we already know more than we would know about most vaccines.

Dr. Michael E. Pichichero

What about the long-term side effects? There are myths that these vaccines somehow could cause autoimmunity. This came from three publications where the possibility of mRNA vaccines to produce autoimmunity was brought up as a discussion point.1-3 There was no evidence given in these publications, it was raised only as a hypothetical possibility.

There’s no evidence that mRNA or replication-defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) produce autoimmunity. Moreover, the mRNA and replication-defective DNA, once it’s inside of the muscle cell, is gone within a few days. What’s left after ribosome processing is the spike (S) protein as an immunogen. We’ve been vaccinating with proteins for 50 years and we haven’t seen autoimmunity.
 

MYTH: The vaccines aren’t safe because they were developed so quickly

These vaccines were developed at “warp speed” – that doesn’t mean they were developed without all the same safety safeguards that the Food and Drug Administration requires. The reason it happened so fast is because the seriousness of the pandemic allowed us, as a community, to enroll the patients into the studies fast. In a matter of months, we had all the studies filled. In a normal circumstance, that might take 2 or 3 years. And all of the regulatory agencies – the National Institutes of Health, the FDA, the Centers for Disease Control and Prevention – were ready to take the information and put a panel of specialists together and immediately review the data. No safety steps were missed. The same process that’s always required of phase 1, of phase 2, and then at phase 3 were accomplished.

The novelty of these vaccines was that they could be made so quickly. Messenger RNA vaccines can be made in a matter of days and then manufactured in a matter of 2 months. The DNA vaccines has a similar timeline trajectory.
 

MYTH: There’s no point in getting the vaccines because we still have to wear masks

Right now, out of an abundance of caution, until it’s proven that we don’t have to wear masks, it’s being recommended that we do so for the safety of others. Early data suggest that this will be temporary. In time, I suspect it will be shown that, after we receive the vaccine, it will be shown that we are not contagious to others and we’ll be able to get rid of our masks.

MYTH: I already had COVID-19 so I don’t need the vaccine

Some people have already caught the SARS-CoV-2 virus that causes this infection and so they feel that they’re immune and they don’t need to get the vaccine. Time will tell if that’s the case. Right now, we don’t know for sure. Early data suggest that a single dose of vaccine in persons who have had the infection may be sufficient. Over time, what happens in the vaccine field is we measure the immunity from the vaccine, and from people who’ve gotten the infection, and we find that there’s a measurement in the blood that correlates with protection. Right now, we don’t know that correlate of protection level. So, out of an abundance of caution, it’s being recommended that, even if you had the disease, maybe you didn’t develop enough immunity, and it’s better to get the vaccine than to get the illness a second time.

 

 

MYTH: The vaccines can give me SARS-CoV-2 infection

The new vaccines for COVID-19, released under emergency use Authorization, are mRNA and DNA vaccines. They are a blueprint for the Spike (S) protein of the virus. In order to become a protein, the mRNA, once it’s inside the cell, is processed by ribosomes. The product of the ribosome processing is a protein that cannot possibly cause harm as a virus. It’s a little piece of mRNA inside of a lipid nanoparticle, which is just a casing to protect the mRNA from breaking down until it’s injected in the body. The replication defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) are packaged inside of virus cells (adenoviruses). The DNA vaccines involve a three-step process:

  • 1. The adenovirus, containing replication-defective DNA that encodes mRNA for the Spike (S) protein, is taken up by the host cells where it must make its way to the nucleus of the muscle cell.
  • 2. The DNA is injected into the host cell nucleus and in the nucleus the DNA is decoded to an mRNA.
  • 3. The mRNA is released from the nucleus and transported to the cell cytoplasm where the ribosomes process the mRNA in an identical manner as mRNA vaccines.

MYTH: The COVID-19 vaccines can alter my DNA

The mRNA and replication-defective DNA vaccines never interact with your DNA. mRNA vaccines never enter the nucleus. Replication-defective DNA vaccines cannot replicate and do not interact with host DNA. The vaccines can’t change your DNA.

Here is a link to YouTube videos I made on this topic: https://youtube.com/playlist?list=PLve-0UW04UMRKHfFbXyEpLY8GCm2WyJHD.

Dr. Michael E. Pichichero receives his first injection of the Moderna vaccine in January 2021.

Here is a photo of me receiving my first SARS-CoV-2 shot (Moderna) in January 2021. I received my second shot in February. I am a lot less anxious. I hope my vaccine card will be a ticket to travel in the future.

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts of interest to report.

References

1. Peck KM and Lauring AS. J Virol. 2018. doi: 10.1128/JVI.01031-17.

2. Pepini T et al. J Immunol. 2017 May 15. doi: 10.4049/jimmunol.1601877.

3. Theofilopoulos AN et al. Annu Rev Immunol. 2005. doi: 10.1146/annurev.immunol.23.021704.115843.

 

MYTH: I shouldn’t get the vaccine because of potential long-term side effects

We know that 68 million people in the United States and 244 million people worldwide have already received messenger RNA (mRNA) SARS-CoV-2 vaccines (Pfizer/BioNTech and Moderna). So for the short-term side effects we already know more than we would know about most vaccines.

Dr. Michael E. Pichichero

What about the long-term side effects? There are myths that these vaccines somehow could cause autoimmunity. This came from three publications where the possibility of mRNA vaccines to produce autoimmunity was brought up as a discussion point.1-3 There was no evidence given in these publications, it was raised only as a hypothetical possibility.

There’s no evidence that mRNA or replication-defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) produce autoimmunity. Moreover, the mRNA and replication-defective DNA, once it’s inside of the muscle cell, is gone within a few days. What’s left after ribosome processing is the spike (S) protein as an immunogen. We’ve been vaccinating with proteins for 50 years and we haven’t seen autoimmunity.
 

MYTH: The vaccines aren’t safe because they were developed so quickly

These vaccines were developed at “warp speed” – that doesn’t mean they were developed without all the same safety safeguards that the Food and Drug Administration requires. The reason it happened so fast is because the seriousness of the pandemic allowed us, as a community, to enroll the patients into the studies fast. In a matter of months, we had all the studies filled. In a normal circumstance, that might take 2 or 3 years. And all of the regulatory agencies – the National Institutes of Health, the FDA, the Centers for Disease Control and Prevention – were ready to take the information and put a panel of specialists together and immediately review the data. No safety steps were missed. The same process that’s always required of phase 1, of phase 2, and then at phase 3 were accomplished.

The novelty of these vaccines was that they could be made so quickly. Messenger RNA vaccines can be made in a matter of days and then manufactured in a matter of 2 months. The DNA vaccines has a similar timeline trajectory.
 

MYTH: There’s no point in getting the vaccines because we still have to wear masks

Right now, out of an abundance of caution, until it’s proven that we don’t have to wear masks, it’s being recommended that we do so for the safety of others. Early data suggest that this will be temporary. In time, I suspect it will be shown that, after we receive the vaccine, it will be shown that we are not contagious to others and we’ll be able to get rid of our masks.

MYTH: I already had COVID-19 so I don’t need the vaccine

Some people have already caught the SARS-CoV-2 virus that causes this infection and so they feel that they’re immune and they don’t need to get the vaccine. Time will tell if that’s the case. Right now, we don’t know for sure. Early data suggest that a single dose of vaccine in persons who have had the infection may be sufficient. Over time, what happens in the vaccine field is we measure the immunity from the vaccine, and from people who’ve gotten the infection, and we find that there’s a measurement in the blood that correlates with protection. Right now, we don’t know that correlate of protection level. So, out of an abundance of caution, it’s being recommended that, even if you had the disease, maybe you didn’t develop enough immunity, and it’s better to get the vaccine than to get the illness a second time.

 

 

MYTH: The vaccines can give me SARS-CoV-2 infection

The new vaccines for COVID-19, released under emergency use Authorization, are mRNA and DNA vaccines. They are a blueprint for the Spike (S) protein of the virus. In order to become a protein, the mRNA, once it’s inside the cell, is processed by ribosomes. The product of the ribosome processing is a protein that cannot possibly cause harm as a virus. It’s a little piece of mRNA inside of a lipid nanoparticle, which is just a casing to protect the mRNA from breaking down until it’s injected in the body. The replication defective DNA vaccines (AstraZeneca/Oxford and Johnson & Johnson) are packaged inside of virus cells (adenoviruses). The DNA vaccines involve a three-step process:

  • 1. The adenovirus, containing replication-defective DNA that encodes mRNA for the Spike (S) protein, is taken up by the host cells where it must make its way to the nucleus of the muscle cell.
  • 2. The DNA is injected into the host cell nucleus and in the nucleus the DNA is decoded to an mRNA.
  • 3. The mRNA is released from the nucleus and transported to the cell cytoplasm where the ribosomes process the mRNA in an identical manner as mRNA vaccines.

MYTH: The COVID-19 vaccines can alter my DNA

The mRNA and replication-defective DNA vaccines never interact with your DNA. mRNA vaccines never enter the nucleus. Replication-defective DNA vaccines cannot replicate and do not interact with host DNA. The vaccines can’t change your DNA.

Here is a link to YouTube videos I made on this topic: https://youtube.com/playlist?list=PLve-0UW04UMRKHfFbXyEpLY8GCm2WyJHD.

Dr. Michael E. Pichichero receives his first injection of the Moderna vaccine in January 2021.

Here is a photo of me receiving my first SARS-CoV-2 shot (Moderna) in January 2021. I received my second shot in February. I am a lot less anxious. I hope my vaccine card will be a ticket to travel in the future.

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He has no conflicts of interest to report.

References

1. Peck KM and Lauring AS. J Virol. 2018. doi: 10.1128/JVI.01031-17.

2. Pepini T et al. J Immunol. 2017 May 15. doi: 10.4049/jimmunol.1601877.

3. Theofilopoulos AN et al. Annu Rev Immunol. 2005. doi: 10.1146/annurev.immunol.23.021704.115843.

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