Pediatric News

Because of significant reduction in delivery of recommended childhood immunization during the pandemic, there is a risk for resurgence of vaccine preventable infections, including measles, pertussis, and polio, which can result in significant morbidity and mortality in children, reported Amy G. Feldman, MD, of Children’s Hospital Colorado, Aurora, and associates.

Yangna/Thinkstock

Will loss of herd immunity lead to vaccine deserts?

When asked to comment, pediatric infectious disease specialist Christopher J. Harrison, MD, said, “My concern is that we may see expansion of what I call ‘vaccine deserts.’ Vaccine deserts occur in underserved communities, areas with pockets of vaccine-hesitant families or among selected groups with difficult access to health care. These vaccine deserts have held a higher density of vulnerables due to low vaccine uptake, often giving rise to outbreaks of vaccine-preventable diseases, e.g., measles, mumps, pertussis. They are usually due to an index case arriving from another vaccine desert (a developing country or a developed country, U.S. or foreign) where the disease is still endemic or pockets of vaccine hesitancy/refusal exist. When detected, local outbreaks result in rapid responses from public/private health collaborations that limit the outbreak. But what if vaccine deserts became more generalized in the U.S. because of loss of vaccine-induced herd immunity in many more or larger areas of our communities because of pandemic-driven lack of vaccinations? That pandemic-driven indirect damage would further stress the health care system and the economy. And it may first show up in the older children whose vaccines were deferred in the first 4-6 months of the pandemic.”

Dr. Feldman and associates cited findings from a collaborative survey conducted by UNICEF, the World Health Organization, Gavi the Vaccine Alliance, the CDC, the Sabin Vaccine Institute, and the Johns Hopkins Bloomberg School of Public Health, which found that immunization programs experienced moderate to severe disruptions or terminations in at least 68 of 129 low and middle-income countries surveyed. According to the WHO, CDC, Red Cross, and GAVI, 94 million people presently are estimated to be at risk as a consequence of not receiving their measles vaccines following the suspensions.

“These national and international declines in routine immunizations have placed the global community at significant risk for outbreaks of vaccine-preventable infections (VPIs) including measles, polio, and pertussis, diseases which are more deadly, more contagious and have a higher reproductive factor (R0) amongst children than COVID-19,” the authors observed.

Dr. Feldman and associates outlined the horrible devastation that these VPI can cause in children, including significantly higher morbidity and mortality than adults, especially among those with immunodeficiencies. Neurologic deficits, paralysis, intellectual disabilities, and vision and hearing loss are just some of the permanent effects conveyed. “It is concerning to imagine how measles could spread across the United States when social distancing restriction[s] are relaxed and unvaccinated children return to school and usual community engagement,” they noted.
 

Collaborative engagement key to course correction

The authors found that primary care providers and public health communities are working not only to restore vaccine administration but also to restore confidence that vaccine delivery is safe in spite of COVID. In addition to recommending specific risk mitigation strategies for clinicians, they also suggested individual practitioners use electronic health records to identify patients with COVID-related lapses in vaccination, employ electronic health record–based parent notification of overdue immunizations, and offer distance-friendly vaccination options that include parking lot or drive-up window vaccine delivery.

Additionally, Dr. Feldman and colleagues recommended that local, state, regional, and national health systems use public service announcements via television and digital as well as social media platforms to convey important messages about the considerable health risks associated with vaccine avoidance and the availability of free or reduced-cost vaccination programs through the federally funded Vaccines For Children program for parents out of work or without insurance. Equally important is messaging around encouraging vaccine opportunities during all health care visits, whether they be subspecialty, urgent care, emergency room, or inpatient visits. In areas where access to clinics is limited, they urged the use of mobile clinics as well as additional focus on providing medical homes to children with poor access to care.

“A partial but expanding safety net may be developing spontaneously, i.e., practices and clinics based on a patient-centered medical home (PCMH) model,” noted Dr. Harrison, professor of pediatrics, University of Missouri-Kansas City, in an interview. “When lagging vaccinations were reported in mid-2020, we checked with a local hospital–based urban clinic and two suburban private practices modeled on PCMH. Each had noted a drastic drop in well checks in the first months of the pandemic. But with ill visits nearly nonexistent, they doubled down on maintaining health maintenance visits. Even though staff and provider work hours were limited, and families were less enthusiastic about well checks, momentum appears to have grown so that, by later in 2020, vaccine uptake rates were again comparable to 2019. So, some already seem to have answered the call, but practices/clinics remain hampered by months of reduced revenue needed to support staff, providers, PPE supplies, and added infection control needs,” he said.The study was funded by the Agency for Healthcare Research Quality. Dr. Isakov disclosed relationships with various pharmaceutical companies outside the submitted work. The other authors had no relevant disclosures. Dr. Harrison’s institution receives grant funding from GSK, Merck, and Pfizer for pediatric vaccine trials and pneumococcal seroprevalence studies on which he is an investigator.

pdnews@mdedge.com

Because of significant reduction in delivery of recommended childhood immunization during the pandemic, there is a risk for resurgence of vaccine preventable infections, including measles, pertussis, and polio, which can result in significant morbidity and mortality in children, reported Amy G. Feldman, MD, of Children’s Hospital Colorado, Aurora, and associates.

Yangna/Thinkstock

Will loss of herd immunity lead to vaccine deserts?

When asked to comment, pediatric infectious disease specialist Christopher J. Harrison, MD, said, “My concern is that we may see expansion of what I call ‘vaccine deserts.’ Vaccine deserts occur in underserved communities, areas with pockets of vaccine-hesitant families or among selected groups with difficult access to health care. These vaccine deserts have held a higher density of vulnerables due to low vaccine uptake, often giving rise to outbreaks of vaccine-preventable diseases, e.g., measles, mumps, pertussis. They are usually due to an index case arriving from another vaccine desert (a developing country or a developed country, U.S. or foreign) where the disease is still endemic or pockets of vaccine hesitancy/refusal exist. When detected, local outbreaks result in rapid responses from public/private health collaborations that limit the outbreak. But what if vaccine deserts became more generalized in the U.S. because of loss of vaccine-induced herd immunity in many more or larger areas of our communities because of pandemic-driven lack of vaccinations? That pandemic-driven indirect damage would further stress the health care system and the economy. And it may first show up in the older children whose vaccines were deferred in the first 4-6 months of the pandemic.”

Dr. Feldman and associates cited findings from a collaborative survey conducted by UNICEF, the World Health Organization, Gavi the Vaccine Alliance, the CDC, the Sabin Vaccine Institute, and the Johns Hopkins Bloomberg School of Public Health, which found that immunization programs experienced moderate to severe disruptions or terminations in at least 68 of 129 low and middle-income countries surveyed. According to the WHO, CDC, Red Cross, and GAVI, 94 million people presently are estimated to be at risk as a consequence of not receiving their measles vaccines following the suspensions.

“These national and international declines in routine immunizations have placed the global community at significant risk for outbreaks of vaccine-preventable infections (VPIs) including measles, polio, and pertussis, diseases which are more deadly, more contagious and have a higher reproductive factor (R0) amongst children than COVID-19,” the authors observed.

Dr. Feldman and associates outlined the horrible devastation that these VPI can cause in children, including significantly higher morbidity and mortality than adults, especially among those with immunodeficiencies. Neurologic deficits, paralysis, intellectual disabilities, and vision and hearing loss are just some of the permanent effects conveyed. “It is concerning to imagine how measles could spread across the United States when social distancing restriction[s] are relaxed and unvaccinated children return to school and usual community engagement,” they noted.
 

Collaborative engagement key to course correction

The authors found that primary care providers and public health communities are working not only to restore vaccine administration but also to restore confidence that vaccine delivery is safe in spite of COVID. In addition to recommending specific risk mitigation strategies for clinicians, they also suggested individual practitioners use electronic health records to identify patients with COVID-related lapses in vaccination, employ electronic health record–based parent notification of overdue immunizations, and offer distance-friendly vaccination options that include parking lot or drive-up window vaccine delivery.

Additionally, Dr. Feldman and colleagues recommended that local, state, regional, and national health systems use public service announcements via television and digital as well as social media platforms to convey important messages about the considerable health risks associated with vaccine avoidance and the availability of free or reduced-cost vaccination programs through the federally funded Vaccines For Children program for parents out of work or without insurance. Equally important is messaging around encouraging vaccine opportunities during all health care visits, whether they be subspecialty, urgent care, emergency room, or inpatient visits. In areas where access to clinics is limited, they urged the use of mobile clinics as well as additional focus on providing medical homes to children with poor access to care.

“A partial but expanding safety net may be developing spontaneously, i.e., practices and clinics based on a patient-centered medical home (PCMH) model,” noted Dr. Harrison, professor of pediatrics, University of Missouri-Kansas City, in an interview. “When lagging vaccinations were reported in mid-2020, we checked with a local hospital–based urban clinic and two suburban private practices modeled on PCMH. Each had noted a drastic drop in well checks in the first months of the pandemic. But with ill visits nearly nonexistent, they doubled down on maintaining health maintenance visits. Even though staff and provider work hours were limited, and families were less enthusiastic about well checks, momentum appears to have grown so that, by later in 2020, vaccine uptake rates were again comparable to 2019. So, some already seem to have answered the call, but practices/clinics remain hampered by months of reduced revenue needed to support staff, providers, PPE supplies, and added infection control needs,” he said.The study was funded by the Agency for Healthcare Research Quality. Dr. Isakov disclosed relationships with various pharmaceutical companies outside the submitted work. The other authors had no relevant disclosures. Dr. Harrison’s institution receives grant funding from GSK, Merck, and Pfizer for pediatric vaccine trials and pneumococcal seroprevalence studies on which he is an investigator.

pdnews@mdedge.com

Because of significant reduction in delivery of recommended childhood immunization during the pandemic, there is a risk for resurgence of vaccine preventable infections, including measles, pertussis, and polio, which can result in significant morbidity and mortality in children, reported Amy G. Feldman, MD, of Children’s Hospital Colorado, Aurora, and associates.

Yangna/Thinkstock

Will loss of herd immunity lead to vaccine deserts?

When asked to comment, pediatric infectious disease specialist Christopher J. Harrison, MD, said, “My concern is that we may see expansion of what I call ‘vaccine deserts.’ Vaccine deserts occur in underserved communities, areas with pockets of vaccine-hesitant families or among selected groups with difficult access to health care. These vaccine deserts have held a higher density of vulnerables due to low vaccine uptake, often giving rise to outbreaks of vaccine-preventable diseases, e.g., measles, mumps, pertussis. They are usually due to an index case arriving from another vaccine desert (a developing country or a developed country, U.S. or foreign) where the disease is still endemic or pockets of vaccine hesitancy/refusal exist. When detected, local outbreaks result in rapid responses from public/private health collaborations that limit the outbreak. But what if vaccine deserts became more generalized in the U.S. because of loss of vaccine-induced herd immunity in many more or larger areas of our communities because of pandemic-driven lack of vaccinations? That pandemic-driven indirect damage would further stress the health care system and the economy. And it may first show up in the older children whose vaccines were deferred in the first 4-6 months of the pandemic.”

Dr. Feldman and associates cited findings from a collaborative survey conducted by UNICEF, the World Health Organization, Gavi the Vaccine Alliance, the CDC, the Sabin Vaccine Institute, and the Johns Hopkins Bloomberg School of Public Health, which found that immunization programs experienced moderate to severe disruptions or terminations in at least 68 of 129 low and middle-income countries surveyed. According to the WHO, CDC, Red Cross, and GAVI, 94 million people presently are estimated to be at risk as a consequence of not receiving their measles vaccines following the suspensions.

“These national and international declines in routine immunizations have placed the global community at significant risk for outbreaks of vaccine-preventable infections (VPIs) including measles, polio, and pertussis, diseases which are more deadly, more contagious and have a higher reproductive factor (R0) amongst children than COVID-19,” the authors observed.

Dr. Feldman and associates outlined the horrible devastation that these VPI can cause in children, including significantly higher morbidity and mortality than adults, especially among those with immunodeficiencies. Neurologic deficits, paralysis, intellectual disabilities, and vision and hearing loss are just some of the permanent effects conveyed. “It is concerning to imagine how measles could spread across the United States when social distancing restriction[s] are relaxed and unvaccinated children return to school and usual community engagement,” they noted.
 

Collaborative engagement key to course correction

The authors found that primary care providers and public health communities are working not only to restore vaccine administration but also to restore confidence that vaccine delivery is safe in spite of COVID. In addition to recommending specific risk mitigation strategies for clinicians, they also suggested individual practitioners use electronic health records to identify patients with COVID-related lapses in vaccination, employ electronic health record–based parent notification of overdue immunizations, and offer distance-friendly vaccination options that include parking lot or drive-up window vaccine delivery.

Additionally, Dr. Feldman and colleagues recommended that local, state, regional, and national health systems use public service announcements via television and digital as well as social media platforms to convey important messages about the considerable health risks associated with vaccine avoidance and the availability of free or reduced-cost vaccination programs through the federally funded Vaccines For Children program for parents out of work or without insurance. Equally important is messaging around encouraging vaccine opportunities during all health care visits, whether they be subspecialty, urgent care, emergency room, or inpatient visits. In areas where access to clinics is limited, they urged the use of mobile clinics as well as additional focus on providing medical homes to children with poor access to care.

“A partial but expanding safety net may be developing spontaneously, i.e., practices and clinics based on a patient-centered medical home (PCMH) model,” noted Dr. Harrison, professor of pediatrics, University of Missouri-Kansas City, in an interview. “When lagging vaccinations were reported in mid-2020, we checked with a local hospital–based urban clinic and two suburban private practices modeled on PCMH. Each had noted a drastic drop in well checks in the first months of the pandemic. But with ill visits nearly nonexistent, they doubled down on maintaining health maintenance visits. Even though staff and provider work hours were limited, and families were less enthusiastic about well checks, momentum appears to have grown so that, by later in 2020, vaccine uptake rates were again comparable to 2019. So, some already seem to have answered the call, but practices/clinics remain hampered by months of reduced revenue needed to support staff, providers, PPE supplies, and added infection control needs,” he said.The study was funded by the Agency for Healthcare Research Quality. Dr. Isakov disclosed relationships with various pharmaceutical companies outside the submitted work. The other authors had no relevant disclosures. Dr. Harrison’s institution receives grant funding from GSK, Merck, and Pfizer for pediatric vaccine trials and pneumococcal seroprevalence studies on which he is an investigator.

pdnews@mdedge.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 .

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 .

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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

HIV-positive patients who are adherent with antiretroviral medications are achieving undetectable or very low levels of HIV viremia and living longer. In response, clinical care is continually adapting to the dramatically altered natural history of disease.

Today, the cutting edge of clinical care overlaps with primary care. The clinical vanguard addresses the medical vulnerabilities of patients with HIV, seeking to eliminate preventable morbidity and premature death. Among this clinical vanguard is the screening for and prevention of anal cancer. With the increased longevity of people living with HIV and the nearly universal exposure to human papillomavirus (HPV), there is now potential for progression to mucosal cellular dysplasia and eventual malignancy.

We know that prevention is possible because of the example of cervical cancer, the etiology of which is exposure to oncogenic serotypes of HPV (16 and 18 are most common). Screenings for cervical cancer (regular clinical examinations and Pap smears) and treatments to eliminate high-grade dysplasia have decreased the incidence rate by over 50% since the 1970s. Vaccination against HPV has been available since 2006 and offers the prospect of preventing HPV-associated malignancies, including head and neck cancer, in future decades.

However, rates of anal cancer are increasing. The CDC estimates that about 4,700 new cases of HPV-associated anal cancers are diagnosed in women and about 2,300 are diagnosed in men each year in the United States. Anal cancer rates in individuals with HIV have increased in the era of effective antiretrovirals and greater longevity. The highest rates, at 95 per 100,000, are in HIV-positive men who have sex with men. Very similar rates were noted in a more recent study that found increased risk with advancing age and in those with an AIDS diagnosis.
 

All patients with HIV should be screened

The New York State AIDS Institute Clinical Guidelines Program recommends screening for anal dysplasia in all patients with HIV. A proactive approach similar to cervical cancer screening is appropriate and includes measures easily implemented by all clinicians.

• History: Assess for rectal symptoms, anal pain, discharge, and lumps.
• Physical exam: Assess for presence of perianal lesions; perform a thorough digital rectal exam.
• Anal Pap test for anal cytology: Insert a Dacron swab moistened with tap water about 3 inches into the anal canal, applying pressure to lateral anal walls and rotating the swab. Then remove and place the swab into liquid cytology solution, shake vigorously for a full 30 seconds, and assess for any dysplasia (high-grade squamous intraepithelial lesion, low-grade intraepithelial lesion, atypical squamous cells of undetermined significance), which would warrant further evaluation by high-resolution anoscopy (HRA).

High-resolution anoscopy

HRA for anal dysplasia corresponds to colposcopy for cervical dysplasia. The ability to treat and eliminate high-risk precursor lesions interrupts the progression to malignancy. The efficacy of this strategy is being evaluated in a National Institutes of Health prospective trial called the Anchor Study. The epidemiology of HPV; the clinical horror of witnessing the painful, preventable deaths of young patients with well-controlled HIV caused by anal cancer; and the example of controlling cervical cancer have motivated my practice to assure comprehensive care for our patients.

Unfortunately, establishing HRA in one’s practice is challenging. Barriers to practice include the expense of required equipment and the absence of consensus on specific products. In addition, hands-on precepting to ease newcomers to competence is not generally available. Considerable skill is required for complete visualization of the anal transformative zone in the folds of the anal canal, and recognizing high-risk lesions requires study and accumulated experience. The International Anal Neoplasia Society is a useful resource that also offers a training course. We are invited to train ourselves, and to rely on the eventual feedback of biopsy results and the forbearance of our early patients.

The expanding scope of our medical practices must shift to meet the evolving needs of the growing population of virologically suppressed patients who are living longer. HIV care involves curing life-threatening opportunistic infections, encouraging antiretroviral adherence, and providing comprehensive care – which now includes preventing anal cancer.

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

Smartphone “addiction” may explain poor sleep quality in a significant proportion of young adults, new research suggests.

maewjpho/Thinkstock

Investigators found that almost 40% of adults aged 18-30 years who self-reported excessive smartphone use also reported poor sleep.

“Our study provides further support to the growing body of evidence that smartphone addiction has a deleterious impact on sleep,” wrote the researchers.

The study was published online March 2 in Frontiers of Psychiatry.
 

Not a clinical diagnosis

Smartphone addiction is not formally recognized as a clinical diagnosis, but it’s an “active” area of research, lead investigator Ben Carter, PhD, King’s College London, noted in the report.

In a cross-sectional survey, 1,043 college students (aged 18-30 years, 73% women) completed the 10-question validated Smartphone Addiction Scale Short Version (SAS-SV) and the adapted Pittsburgh Sleep Quality Score Index.

On the SAS-SV, 406 students (38.9%) reported “addiction” to their smartphones. This estimated prevalence is consistent with other reported studies in young adult populations globally, which is in the range of 30%-45%, the researchers noted.

Overall, 61.6% of participants surveyed reported poor sleep; among those who reported smartphone addiction, 68.7% had poor sleep quality, vs. 57.1% of those who did not report smartphone addiction.

In multivariable analysis that adjusted for a variety of relevant factors, among those for whom there was evidence of smartphone addiction, the odds of poor sleep were increased by 41% (adjusted odds ratio [aOR] = 1.41; 95% confidence interval, 1.06-1.87, P = .018).

The findings also suggest that a greater amount of time spent using the phone and greater use late at night can raise the risk for smartphone addiction.

“Should smartphone addiction become firmly established as a focus of clinical concern, those using their phones after midnight or using their phones for four or more hours per day are likely to be at high risk, and should guide administration of the SAS-SV,” the researchers wrote.
 

Caveats, cautions, and concerns

Reached for comment, Paul Weigle, MD, psychiatrist with Hartford HealthCare and Hartford (Conn.) Hospital, and member of the American Academy of Child and Adolescent Psychiatry, said the finding of a relationship between addictive smartphone usage and poor sleep quality is not surprising.

“Great increases in adolescent screen media habits in recent decades have seen a concurrent increase in rates of insomnia among this population,” he said in an interview.

Dr. Weigle also noted that young people who use the phone excessively often do so in bed, “which decreases sleep onset by disrupting conditioning (the tendency for our bodies to relate bed with sleep) and by increasing physiological arousal, which makes it more difficult to fall asleep. The blue light from smartphones used at night disrupts our body’s natural circadian rhythms, confusing our brains regarding whether it is night or day, and further worsens sleep.”

Dr. Weigle said in an interview that some of his patients come to him seeking sleep medications, although the best treatment is to perform a “smartphone-ectomy” every evening.

Teenage patients will “beg, borrow, or steal” to be allowed to keep their phones by the bed with the promise not to use them overnight. Three-quarters of the time, when the parents are able to charge the phone in another room, “the sleep problem resolves,” Dr. Weigle said.

One caveat, he said, is that it’s “somewhat unclear whether this is best classified as an addiction or simply a seriously problematic habit. Either way, this type of habit causes a great deal of distress and dysfunction in the lives of those it affects, so it is important to understand,” he said.

In a statement, Bob Patton, PhD, lecturer in clinical psychology, University of Surrey, Guildford, England, noted that this is a cross-sectional study “and as such cannot lead to any firm conclusions about phone usage as the cause of reduced sleep quality.

“It does, however, provide some compelling evidence,” Dr. Patton said, “that the nature of smartphone usage and its related consequences are important considerations in addressing the emerging phenomenon of ‘smartphone addiction.’ ”

Also weighing in, Andrew Przybylski, PhD, director of research, Oxford (England) Internet Institute, University of Oxford, said the study is “the latest, among many dozens of others, to study so-called ‘smartphone addiction,’ a condition which is not recognized by any global health body and is not a psychiatric disorder.

“The study is a correlational analysis of a sample of participants recruited on university campuses and therefore only reflects the experiences of those who had the purpose of the study explained to them. It can say nothing about behaviors in the general population,” Dr. Przybylski said in a statement.

“Readers should be cautious of making any firm conclusions about the impact of smartphone use in the general population, or the idea that they’re addictive in any objective sense, on the basis of this work,” he added. The study had no specific funding. Dr. Carter, Dr. Weigle, Dr. Patton, and Dr. Przybylski have disclosed no relevant financial relationships.

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

Smartphone “addiction” may explain poor sleep quality in a significant proportion of young adults, new research suggests.

maewjpho/Thinkstock

Investigators found that almost 40% of adults aged 18-30 years who self-reported excessive smartphone use also reported poor sleep.

“Our study provides further support to the growing body of evidence that smartphone addiction has a deleterious impact on sleep,” wrote the researchers.

The study was published online March 2 in Frontiers of Psychiatry.
 

Not a clinical diagnosis

Smartphone addiction is not formally recognized as a clinical diagnosis, but it’s an “active” area of research, lead investigator Ben Carter, PhD, King’s College London, noted in the report.

In a cross-sectional survey, 1,043 college students (aged 18-30 years, 73% women) completed the 10-question validated Smartphone Addiction Scale Short Version (SAS-SV) and the adapted Pittsburgh Sleep Quality Score Index.

On the SAS-SV, 406 students (38.9%) reported “addiction” to their smartphones. This estimated prevalence is consistent with other reported studies in young adult populations globally, which is in the range of 30%-45%, the researchers noted.

Overall, 61.6% of participants surveyed reported poor sleep; among those who reported smartphone addiction, 68.7% had poor sleep quality, vs. 57.1% of those who did not report smartphone addiction.

In multivariable analysis that adjusted for a variety of relevant factors, among those for whom there was evidence of smartphone addiction, the odds of poor sleep were increased by 41% (adjusted odds ratio [aOR] = 1.41; 95% confidence interval, 1.06-1.87, P = .018).

The findings also suggest that a greater amount of time spent using the phone and greater use late at night can raise the risk for smartphone addiction.

“Should smartphone addiction become firmly established as a focus of clinical concern, those using their phones after midnight or using their phones for four or more hours per day are likely to be at high risk, and should guide administration of the SAS-SV,” the researchers wrote.
 

Caveats, cautions, and concerns

Reached for comment, Paul Weigle, MD, psychiatrist with Hartford HealthCare and Hartford (Conn.) Hospital, and member of the American Academy of Child and Adolescent Psychiatry, said the finding of a relationship between addictive smartphone usage and poor sleep quality is not surprising.

“Great increases in adolescent screen media habits in recent decades have seen a concurrent increase in rates of insomnia among this population,” he said in an interview.

Dr. Weigle also noted that young people who use the phone excessively often do so in bed, “which decreases sleep onset by disrupting conditioning (the tendency for our bodies to relate bed with sleep) and by increasing physiological arousal, which makes it more difficult to fall asleep. The blue light from smartphones used at night disrupts our body’s natural circadian rhythms, confusing our brains regarding whether it is night or day, and further worsens sleep.”

Dr. Weigle said in an interview that some of his patients come to him seeking sleep medications, although the best treatment is to perform a “smartphone-ectomy” every evening.

Teenage patients will “beg, borrow, or steal” to be allowed to keep their phones by the bed with the promise not to use them overnight. Three-quarters of the time, when the parents are able to charge the phone in another room, “the sleep problem resolves,” Dr. Weigle said.

One caveat, he said, is that it’s “somewhat unclear whether this is best classified as an addiction or simply a seriously problematic habit. Either way, this type of habit causes a great deal of distress and dysfunction in the lives of those it affects, so it is important to understand,” he said.

In a statement, Bob Patton, PhD, lecturer in clinical psychology, University of Surrey, Guildford, England, noted that this is a cross-sectional study “and as such cannot lead to any firm conclusions about phone usage as the cause of reduced sleep quality.

“It does, however, provide some compelling evidence,” Dr. Patton said, “that the nature of smartphone usage and its related consequences are important considerations in addressing the emerging phenomenon of ‘smartphone addiction.’ ”

Also weighing in, Andrew Przybylski, PhD, director of research, Oxford (England) Internet Institute, University of Oxford, said the study is “the latest, among many dozens of others, to study so-called ‘smartphone addiction,’ a condition which is not recognized by any global health body and is not a psychiatric disorder.

“The study is a correlational analysis of a sample of participants recruited on university campuses and therefore only reflects the experiences of those who had the purpose of the study explained to them. It can say nothing about behaviors in the general population,” Dr. Przybylski said in a statement.

“Readers should be cautious of making any firm conclusions about the impact of smartphone use in the general population, or the idea that they’re addictive in any objective sense, on the basis of this work,” he added. The study had no specific funding. Dr. Carter, Dr. Weigle, Dr. Patton, and Dr. Przybylski have disclosed no relevant financial relationships.

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

Smartphone “addiction” may explain poor sleep quality in a significant proportion of young adults, new research suggests.

maewjpho/Thinkstock

Investigators found that almost 40% of adults aged 18-30 years who self-reported excessive smartphone use also reported poor sleep.

“Our study provides further support to the growing body of evidence that smartphone addiction has a deleterious impact on sleep,” wrote the researchers.

The study was published online March 2 in Frontiers of Psychiatry.
 

Not a clinical diagnosis

Smartphone addiction is not formally recognized as a clinical diagnosis, but it’s an “active” area of research, lead investigator Ben Carter, PhD, King’s College London, noted in the report.

In a cross-sectional survey, 1,043 college students (aged 18-30 years, 73% women) completed the 10-question validated Smartphone Addiction Scale Short Version (SAS-SV) and the adapted Pittsburgh Sleep Quality Score Index.

On the SAS-SV, 406 students (38.9%) reported “addiction” to their smartphones. This estimated prevalence is consistent with other reported studies in young adult populations globally, which is in the range of 30%-45%, the researchers noted.

Overall, 61.6% of participants surveyed reported poor sleep; among those who reported smartphone addiction, 68.7% had poor sleep quality, vs. 57.1% of those who did not report smartphone addiction.

In multivariable analysis that adjusted for a variety of relevant factors, among those for whom there was evidence of smartphone addiction, the odds of poor sleep were increased by 41% (adjusted odds ratio [aOR] = 1.41; 95% confidence interval, 1.06-1.87, P = .018).

The findings also suggest that a greater amount of time spent using the phone and greater use late at night can raise the risk for smartphone addiction.

“Should smartphone addiction become firmly established as a focus of clinical concern, those using their phones after midnight or using their phones for four or more hours per day are likely to be at high risk, and should guide administration of the SAS-SV,” the researchers wrote.
 

Caveats, cautions, and concerns

Reached for comment, Paul Weigle, MD, psychiatrist with Hartford HealthCare and Hartford (Conn.) Hospital, and member of the American Academy of Child and Adolescent Psychiatry, said the finding of a relationship between addictive smartphone usage and poor sleep quality is not surprising.

“Great increases in adolescent screen media habits in recent decades have seen a concurrent increase in rates of insomnia among this population,” he said in an interview.

Dr. Weigle also noted that young people who use the phone excessively often do so in bed, “which decreases sleep onset by disrupting conditioning (the tendency for our bodies to relate bed with sleep) and by increasing physiological arousal, which makes it more difficult to fall asleep. The blue light from smartphones used at night disrupts our body’s natural circadian rhythms, confusing our brains regarding whether it is night or day, and further worsens sleep.”

Dr. Weigle said in an interview that some of his patients come to him seeking sleep medications, although the best treatment is to perform a “smartphone-ectomy” every evening.

Teenage patients will “beg, borrow, or steal” to be allowed to keep their phones by the bed with the promise not to use them overnight. Three-quarters of the time, when the parents are able to charge the phone in another room, “the sleep problem resolves,” Dr. Weigle said.

One caveat, he said, is that it’s “somewhat unclear whether this is best classified as an addiction or simply a seriously problematic habit. Either way, this type of habit causes a great deal of distress and dysfunction in the lives of those it affects, so it is important to understand,” he said.

In a statement, Bob Patton, PhD, lecturer in clinical psychology, University of Surrey, Guildford, England, noted that this is a cross-sectional study “and as such cannot lead to any firm conclusions about phone usage as the cause of reduced sleep quality.

“It does, however, provide some compelling evidence,” Dr. Patton said, “that the nature of smartphone usage and its related consequences are important considerations in addressing the emerging phenomenon of ‘smartphone addiction.’ ”

Also weighing in, Andrew Przybylski, PhD, director of research, Oxford (England) Internet Institute, University of Oxford, said the study is “the latest, among many dozens of others, to study so-called ‘smartphone addiction,’ a condition which is not recognized by any global health body and is not a psychiatric disorder.

“The study is a correlational analysis of a sample of participants recruited on university campuses and therefore only reflects the experiences of those who had the purpose of the study explained to them. It can say nothing about behaviors in the general population,” Dr. Przybylski said in a statement.

“Readers should be cautious of making any firm conclusions about the impact of smartphone use in the general population, or the idea that they’re addictive in any objective sense, on the basis of this work,” he added. The study had no specific funding. Dr. Carter, Dr. Weigle, Dr. Patton, and Dr. Przybylski have disclosed no relevant financial relationships.

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.

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.

A wide variety of medications exists for treating hyperhidrosis, a dermatologist told colleagues, but before prescribing anything to a pediatric patient, he recommended, ask the patient a simple question: “What bothers you the most?”

The answer will provide guidance for developing a step-by-step treatment strategy and help provide the patient “a set of realistic expectations in terms of what the response will look like,” George Hightower, MD, PhD, a pediatric dermatologist at Rady Children’s Hospital and the University of California, San Diego, said at MedscapeLive’s Women’s & Pediatric Dermatology Seminar.

A similar question-based approach will help guide therapy for patients with hidradenitis suppurativa (HS), he said.

With regards to hyperhidrosis, Dr. Hightower said that patients most commonly complain that their underarms are too smelly, too sweaty, and red, itchy, or painful. Causes, he said, can include irritation/contact dermatitis, folliculitis, and seborrheic dermatitis, as well as hyperhidrosis or HS.

Primary focal axillary hyperhidrosis is defined as focal, visible, excessive sweating for at least 6 months without an apparent cause plus at least two of the following characteristics: Sweating is bilateral and relatively symmetric, it impairs daily activities, it starts before the age of 25 with at least one episode per week (many patients have it daily), a family history of idiopathic hyperhidrosis is present, and focal sweating does not occur during sleep.

Secondary hyperhidrosis can be linked to other conditions, such as a spinal column injury, Dr. Hightower noted.

The first step on the treatment ladder is topical 20% aluminum chloride, which is available over the counter. This should be applied nightly for 1 week then every 1-2 weeks, Dr. Hightower recommended. All of his patients with hyperhidrosis have had at least one trial of this treatment.

The next option is daily topical treatment with 2.4% glycopyrronium tosylate (Qbrexza) cloths, approved by the Food and Drug Administration in 2018 for primary axillary hyperhidrosis in patients aged 9 and older. According to the prescribing information, dry mouth was by far the most common treatment-associated adverse effect in clinical trials (24% versus almost 6% among those on vehicle). As for skin reactions, erythema occurred in about 17% of both the intervention and vehicle groups, and burning/stinging occurred in 14% of those on treatment and almost 17% of those on vehicle.

“If they’re not able to get access to the cloths due to [insurance] coverage issues, or they don’t allow them to reach the clinical endpoint desired, then I use an oral daily glycopyrrolate pill,” Dr. Hightower said.

He recommends 1 mg to 6 mg daily of the anticholinergic drug, which has been used off-label for hyperhidrosis for several years. A 2012 study of 31 children with hyperhidrosis, he noted, supported the use of the drug. The retrospective study found that 90% of the patients, at a mean daily dose of 2 mg, experienced improvements, reported as major in 71%. In addition, patients experienced improvement within hours of taking the medication, and benefits disappeared within a day of stopping the medication. In the study, patients were on the treatment for an average of 2.1 years, and 29% experienced side effects, which were dose related; the most common were dry mouth in 26% and dry eyes in 10%.

According to goodrx.com, a month’s supply of 2 mg of the drug costs as little as $13 with a discount or coupon.

The next steps in treatment are procedural interventions such as microwave-based therapies.

Dr. Hightower said that patients should be advised that treatment may take years, and to encourage them to return for follow-up. He suggested this helpful message: “We’re still trying to find the best treatment for you, and we’ll need to see you back in the office.”
 

Hidradenitis suppurativa

Dr. Hightower said that too often, HS goes undiagnosed for a significant period of time, preventing patients from seeing a dermatologist for treatment. Hallmarks of HS include inflammatory nodules, abscesses, and scarring, he said. “It can be disfiguring, painful, embarrassing, and associated with significantly decreased quality of life. Early recognition in terms of making and solidifying the diagnosis is important so we can prevent further worsening of the disease.”

The goal of treatment include preventing scars and unnecessary emergency department visits, and stopping flares from worsening, Dr. Hightower said. For specifics, he pointed to clinical management guidelines released by the United States and Canadian hidradenitis suppurativa foundations in 2019.

Make sure to set individualized treatment goals and understand the impact of treatment on the patient’s interactions with family, school, and peers, he said. And keep in mind that “parent-defined goals may be different from patient-defined goals.”

Dr. Hightower reported no relevant disclosures. MedscapeLive and this news organization are owned by the same parent company

A wide variety of medications exists for treating hyperhidrosis, a dermatologist told colleagues, but before prescribing anything to a pediatric patient, he recommended, ask the patient a simple question: “What bothers you the most?”

The answer will provide guidance for developing a step-by-step treatment strategy and help provide the patient “a set of realistic expectations in terms of what the response will look like,” George Hightower, MD, PhD, a pediatric dermatologist at Rady Children’s Hospital and the University of California, San Diego, said at MedscapeLive’s Women’s & Pediatric Dermatology Seminar.

A similar question-based approach will help guide therapy for patients with hidradenitis suppurativa (HS), he said.

With regards to hyperhidrosis, Dr. Hightower said that patients most commonly complain that their underarms are too smelly, too sweaty, and red, itchy, or painful. Causes, he said, can include irritation/contact dermatitis, folliculitis, and seborrheic dermatitis, as well as hyperhidrosis or HS.

Primary focal axillary hyperhidrosis is defined as focal, visible, excessive sweating for at least 6 months without an apparent cause plus at least two of the following characteristics: Sweating is bilateral and relatively symmetric, it impairs daily activities, it starts before the age of 25 with at least one episode per week (many patients have it daily), a family history of idiopathic hyperhidrosis is present, and focal sweating does not occur during sleep.

Secondary hyperhidrosis can be linked to other conditions, such as a spinal column injury, Dr. Hightower noted.

The first step on the treatment ladder is topical 20% aluminum chloride, which is available over the counter. This should be applied nightly for 1 week then every 1-2 weeks, Dr. Hightower recommended. All of his patients with hyperhidrosis have had at least one trial of this treatment.

The next option is daily topical treatment with 2.4% glycopyrronium tosylate (Qbrexza) cloths, approved by the Food and Drug Administration in 2018 for primary axillary hyperhidrosis in patients aged 9 and older. According to the prescribing information, dry mouth was by far the most common treatment-associated adverse effect in clinical trials (24% versus almost 6% among those on vehicle). As for skin reactions, erythema occurred in about 17% of both the intervention and vehicle groups, and burning/stinging occurred in 14% of those on treatment and almost 17% of those on vehicle.

“If they’re not able to get access to the cloths due to [insurance] coverage issues, or they don’t allow them to reach the clinical endpoint desired, then I use an oral daily glycopyrrolate pill,” Dr. Hightower said.

He recommends 1 mg to 6 mg daily of the anticholinergic drug, which has been used off-label for hyperhidrosis for several years. A 2012 study of 31 children with hyperhidrosis, he noted, supported the use of the drug. The retrospective study found that 90% of the patients, at a mean daily dose of 2 mg, experienced improvements, reported as major in 71%. In addition, patients experienced improvement within hours of taking the medication, and benefits disappeared within a day of stopping the medication. In the study, patients were on the treatment for an average of 2.1 years, and 29% experienced side effects, which were dose related; the most common were dry mouth in 26% and dry eyes in 10%.

According to goodrx.com, a month’s supply of 2 mg of the drug costs as little as $13 with a discount or coupon.

The next steps in treatment are procedural interventions such as microwave-based therapies.

Dr. Hightower said that patients should be advised that treatment may take years, and to encourage them to return for follow-up. He suggested this helpful message: “We’re still trying to find the best treatment for you, and we’ll need to see you back in the office.”
 

Hidradenitis suppurativa

Dr. Hightower said that too often, HS goes undiagnosed for a significant period of time, preventing patients from seeing a dermatologist for treatment. Hallmarks of HS include inflammatory nodules, abscesses, and scarring, he said. “It can be disfiguring, painful, embarrassing, and associated with significantly decreased quality of life. Early recognition in terms of making and solidifying the diagnosis is important so we can prevent further worsening of the disease.”

The goal of treatment include preventing scars and unnecessary emergency department visits, and stopping flares from worsening, Dr. Hightower said. For specifics, he pointed to clinical management guidelines released by the United States and Canadian hidradenitis suppurativa foundations in 2019.

Make sure to set individualized treatment goals and understand the impact of treatment on the patient’s interactions with family, school, and peers, he said. And keep in mind that “parent-defined goals may be different from patient-defined goals.”

Dr. Hightower reported no relevant disclosures. MedscapeLive and this news organization are owned by the same parent company

A wide variety of medications exists for treating hyperhidrosis, a dermatologist told colleagues, but before prescribing anything to a pediatric patient, he recommended, ask the patient a simple question: “What bothers you the most?”

The answer will provide guidance for developing a step-by-step treatment strategy and help provide the patient “a set of realistic expectations in terms of what the response will look like,” George Hightower, MD, PhD, a pediatric dermatologist at Rady Children’s Hospital and the University of California, San Diego, said at MedscapeLive’s Women’s & Pediatric Dermatology Seminar.

A similar question-based approach will help guide therapy for patients with hidradenitis suppurativa (HS), he said.

With regards to hyperhidrosis, Dr. Hightower said that patients most commonly complain that their underarms are too smelly, too sweaty, and red, itchy, or painful. Causes, he said, can include irritation/contact dermatitis, folliculitis, and seborrheic dermatitis, as well as hyperhidrosis or HS.

Primary focal axillary hyperhidrosis is defined as focal, visible, excessive sweating for at least 6 months without an apparent cause plus at least two of the following characteristics: Sweating is bilateral and relatively symmetric, it impairs daily activities, it starts before the age of 25 with at least one episode per week (many patients have it daily), a family history of idiopathic hyperhidrosis is present, and focal sweating does not occur during sleep.

Secondary hyperhidrosis can be linked to other conditions, such as a spinal column injury, Dr. Hightower noted.

The first step on the treatment ladder is topical 20% aluminum chloride, which is available over the counter. This should be applied nightly for 1 week then every 1-2 weeks, Dr. Hightower recommended. All of his patients with hyperhidrosis have had at least one trial of this treatment.

The next option is daily topical treatment with 2.4% glycopyrronium tosylate (Qbrexza) cloths, approved by the Food and Drug Administration in 2018 for primary axillary hyperhidrosis in patients aged 9 and older. According to the prescribing information, dry mouth was by far the most common treatment-associated adverse effect in clinical trials (24% versus almost 6% among those on vehicle). As for skin reactions, erythema occurred in about 17% of both the intervention and vehicle groups, and burning/stinging occurred in 14% of those on treatment and almost 17% of those on vehicle.

“If they’re not able to get access to the cloths due to [insurance] coverage issues, or they don’t allow them to reach the clinical endpoint desired, then I use an oral daily glycopyrrolate pill,” Dr. Hightower said.

He recommends 1 mg to 6 mg daily of the anticholinergic drug, which has been used off-label for hyperhidrosis for several years. A 2012 study of 31 children with hyperhidrosis, he noted, supported the use of the drug. The retrospective study found that 90% of the patients, at a mean daily dose of 2 mg, experienced improvements, reported as major in 71%. In addition, patients experienced improvement within hours of taking the medication, and benefits disappeared within a day of stopping the medication. In the study, patients were on the treatment for an average of 2.1 years, and 29% experienced side effects, which were dose related; the most common were dry mouth in 26% and dry eyes in 10%.

According to goodrx.com, a month’s supply of 2 mg of the drug costs as little as $13 with a discount or coupon.

The next steps in treatment are procedural interventions such as microwave-based therapies.

Dr. Hightower said that patients should be advised that treatment may take years, and to encourage them to return for follow-up. He suggested this helpful message: “We’re still trying to find the best treatment for you, and we’ll need to see you back in the office.”
 

Hidradenitis suppurativa

Dr. Hightower said that too often, HS goes undiagnosed for a significant period of time, preventing patients from seeing a dermatologist for treatment. Hallmarks of HS include inflammatory nodules, abscesses, and scarring, he said. “It can be disfiguring, painful, embarrassing, and associated with significantly decreased quality of life. Early recognition in terms of making and solidifying the diagnosis is important so we can prevent further worsening of the disease.”

The goal of treatment include preventing scars and unnecessary emergency department visits, and stopping flares from worsening, Dr. Hightower said. For specifics, he pointed to clinical management guidelines released by the United States and Canadian hidradenitis suppurativa foundations in 2019.

Make sure to set individualized treatment goals and understand the impact of treatment on the patient’s interactions with family, school, and peers, he said. And keep in mind that “parent-defined goals may be different from patient-defined goals.”

Dr. Hightower reported no relevant disclosures. MedscapeLive and this news organization are owned by the same parent company

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.

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.

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.

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.

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.

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.

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.

Skin microbiome therapy to protect against Staphylococcus aureus in patients with atopic dermatitis (AD) proved safe in a phase 1 randomized clinical trial that also demonstrated “encouraging clinical and mechanistic results,” Richard L. Gallo, MD, PhD, and his coinvestigators have reported in Nature Medicine.

Findings from the 1-week, 54-patient trial of a topical formulation containing Staphylococcus hominis A9 (ShA9) offer evidence that the strain directly kills S. aureus, inhibits the production of S. aureus–generated toxins, and enables expansion of a healthy bacterial community, “allowing the rest of the microbiome to start to recover to normal,” Dr. Gallo, professor and chairman of the department of dermatology at the University of California, San Diego, said in an interview.

“And perhaps most exciting,” Dr. Gallo added, is the finding that the subset of patients with AD who were most responsive to the ShA9 compound – approximately two-thirds of the participants who were randomized to receive it – showed improvement in local EASI (Eczema Area and Severity Index) and SCORAD (Scoring Atopic Dermatitis) scores used to assess inflammation. Plans are underway for a larger and longer trial, he said.

S. aureus commonly colonizes patients with AD and exacerbates disease by causing inflammation. In recent years, Dr. Gallo and other investigators have come to believe that AD is a cyclic disease in which the skin’s microbiome affects the host, and the host affects the microbiome. The goal of bacteriotherapy is to break the cycle of S. aureus colonization and improve the skin immune and barrier dysfunction characteristics of AD, Dr. Gallo said.

ShA9, a bacterium isolated from healthy human skin, was chosen as a potential topical therapy for AD based on its capacity both to selectively kill S. aureus and to inhibit toxin production by S. aureus. Dr. Gallo’s team’s preclinical work involved screening thousands of isolates of coagulase-negative staphylococci for gene products that perform these two functions by expressing both antimicrobial peptides (AMPs) and autoinducing peptides (AIPs), the latter of which inhibit the S. aureus quorum-sending system that leads to toxin production. Most patients with AD lack protective strains of coagulase-negative staphylococci, including S. hominis, prior research has found.

The double-blind phase 1 trial randomized 54 adults with moderate-severe AD affecting the ventral forearms in a 2:1 fashion to receive the proprietary lyophilized preparation of ShA9 or an ShA9-free formulation twice daily for 1 week. All participants were culture positive for S. aureus.

Clinical assessments and skin swabs were obtained before and within an hour after the first application of day 1, and swabs were collected on days 4 and 7 within 4 hours of the first application.

Blinded physician assessments and skin swabs were also obtained at 24, 48, and 96 hours after the final dose on day 7.

Based on structured daily diaries, there were no serious adverse events, and significantly fewer adverse events in those treated with ShA9, compared with the vehicle alone; 55.6% versus 83.3%, respectively, were considered to have adverse events.

The adverse event–reporting system captured the normal fluctuation of eczema and considered any report of fluctuation above baseline to be an adverse event. “Patients treated with the [placebo formulation] had the expected high frequency of itching, burning, and pain that you see with AD but it was encouraging that the frequency of reporting these events was significantly less in those treated with the active [formulation],” Dr. Gallo said in the interview.

Their report describes a decrease in S. aureus in participants treated with ShA9, and increases in ShA9 DNA. Not all S. aureus strains were directly killed by ShA9, but all strains had reduced expression of mRNA for psm-alpha, an important virulence factor. That reduced expression correlated with ShA9 AIPs and improved EASI scores, the latter of which was observed in a post-hoc analysis. “Participants with S. aureus not killed by ShA9 were still sensitive to inhibition of toxin production, a mechanistic outcome that predicted clinical improvement in mice and may require longer therapy to observe clinical improvement in humans,” the investigators wrote.

Local eczema severity was not significantly different between the bacteriotherapy and control groups. But the post-hoc analysis showed that after 7 days of treatment, and up to 4 days after treatment was discontinued, the patients with S. aureus that was sensitive to killing by ShA9 (21 out of 35 total who received the bacteriotherapy) showed improvement in EASI and SCORAD scores, compared with control patients.

Future research will assess the compound in both S. aureus culture-positive and culture-negative patients, and in patients with mild disease, Dr. Gallo said.

The trial was conducted at USCD and the National Jewish Health General Clinical Research Center in Denver, and was sponsored by the National Institute of Allergy and Infectious Diseases. The ShA9 formulation and related technology are licensed to MatriSys Bioscience, of which Dr. Gallo is the cofounder and an advisory board member. Dr. Gallo holds equity interest in the company.

Skin microbiome therapy to protect against Staphylococcus aureus in patients with atopic dermatitis (AD) proved safe in a phase 1 randomized clinical trial that also demonstrated “encouraging clinical and mechanistic results,” Richard L. Gallo, MD, PhD, and his coinvestigators have reported in Nature Medicine.

Findings from the 1-week, 54-patient trial of a topical formulation containing Staphylococcus hominis A9 (ShA9) offer evidence that the strain directly kills S. aureus, inhibits the production of S. aureus–generated toxins, and enables expansion of a healthy bacterial community, “allowing the rest of the microbiome to start to recover to normal,” Dr. Gallo, professor and chairman of the department of dermatology at the University of California, San Diego, said in an interview.

“And perhaps most exciting,” Dr. Gallo added, is the finding that the subset of patients with AD who were most responsive to the ShA9 compound – approximately two-thirds of the participants who were randomized to receive it – showed improvement in local EASI (Eczema Area and Severity Index) and SCORAD (Scoring Atopic Dermatitis) scores used to assess inflammation. Plans are underway for a larger and longer trial, he said.

S. aureus commonly colonizes patients with AD and exacerbates disease by causing inflammation. In recent years, Dr. Gallo and other investigators have come to believe that AD is a cyclic disease in which the skin’s microbiome affects the host, and the host affects the microbiome. The goal of bacteriotherapy is to break the cycle of S. aureus colonization and improve the skin immune and barrier dysfunction characteristics of AD, Dr. Gallo said.

ShA9, a bacterium isolated from healthy human skin, was chosen as a potential topical therapy for AD based on its capacity both to selectively kill S. aureus and to inhibit toxin production by S. aureus. Dr. Gallo’s team’s preclinical work involved screening thousands of isolates of coagulase-negative staphylococci for gene products that perform these two functions by expressing both antimicrobial peptides (AMPs) and autoinducing peptides (AIPs), the latter of which inhibit the S. aureus quorum-sending system that leads to toxin production. Most patients with AD lack protective strains of coagulase-negative staphylococci, including S. hominis, prior research has found.

The double-blind phase 1 trial randomized 54 adults with moderate-severe AD affecting the ventral forearms in a 2:1 fashion to receive the proprietary lyophilized preparation of ShA9 or an ShA9-free formulation twice daily for 1 week. All participants were culture positive for S. aureus.

Clinical assessments and skin swabs were obtained before and within an hour after the first application of day 1, and swabs were collected on days 4 and 7 within 4 hours of the first application.

Blinded physician assessments and skin swabs were also obtained at 24, 48, and 96 hours after the final dose on day 7.

Based on structured daily diaries, there were no serious adverse events, and significantly fewer adverse events in those treated with ShA9, compared with the vehicle alone; 55.6% versus 83.3%, respectively, were considered to have adverse events.

The adverse event–reporting system captured the normal fluctuation of eczema and considered any report of fluctuation above baseline to be an adverse event. “Patients treated with the [placebo formulation] had the expected high frequency of itching, burning, and pain that you see with AD but it was encouraging that the frequency of reporting these events was significantly less in those treated with the active [formulation],” Dr. Gallo said in the interview.

Their report describes a decrease in S. aureus in participants treated with ShA9, and increases in ShA9 DNA. Not all S. aureus strains were directly killed by ShA9, but all strains had reduced expression of mRNA for psm-alpha, an important virulence factor. That reduced expression correlated with ShA9 AIPs and improved EASI scores, the latter of which was observed in a post-hoc analysis. “Participants with S. aureus not killed by ShA9 were still sensitive to inhibition of toxin production, a mechanistic outcome that predicted clinical improvement in mice and may require longer therapy to observe clinical improvement in humans,” the investigators wrote.

Local eczema severity was not significantly different between the bacteriotherapy and control groups. But the post-hoc analysis showed that after 7 days of treatment, and up to 4 days after treatment was discontinued, the patients with S. aureus that was sensitive to killing by ShA9 (21 out of 35 total who received the bacteriotherapy) showed improvement in EASI and SCORAD scores, compared with control patients.

Future research will assess the compound in both S. aureus culture-positive and culture-negative patients, and in patients with mild disease, Dr. Gallo said.

The trial was conducted at USCD and the National Jewish Health General Clinical Research Center in Denver, and was sponsored by the National Institute of Allergy and Infectious Diseases. The ShA9 formulation and related technology are licensed to MatriSys Bioscience, of which Dr. Gallo is the cofounder and an advisory board member. Dr. Gallo holds equity interest in the company.

Skin microbiome therapy to protect against Staphylococcus aureus in patients with atopic dermatitis (AD) proved safe in a phase 1 randomized clinical trial that also demonstrated “encouraging clinical and mechanistic results,” Richard L. Gallo, MD, PhD, and his coinvestigators have reported in Nature Medicine.

Findings from the 1-week, 54-patient trial of a topical formulation containing Staphylococcus hominis A9 (ShA9) offer evidence that the strain directly kills S. aureus, inhibits the production of S. aureus–generated toxins, and enables expansion of a healthy bacterial community, “allowing the rest of the microbiome to start to recover to normal,” Dr. Gallo, professor and chairman of the department of dermatology at the University of California, San Diego, said in an interview.

“And perhaps most exciting,” Dr. Gallo added, is the finding that the subset of patients with AD who were most responsive to the ShA9 compound – approximately two-thirds of the participants who were randomized to receive it – showed improvement in local EASI (Eczema Area and Severity Index) and SCORAD (Scoring Atopic Dermatitis) scores used to assess inflammation. Plans are underway for a larger and longer trial, he said.

S. aureus commonly colonizes patients with AD and exacerbates disease by causing inflammation. In recent years, Dr. Gallo and other investigators have come to believe that AD is a cyclic disease in which the skin’s microbiome affects the host, and the host affects the microbiome. The goal of bacteriotherapy is to break the cycle of S. aureus colonization and improve the skin immune and barrier dysfunction characteristics of AD, Dr. Gallo said.

ShA9, a bacterium isolated from healthy human skin, was chosen as a potential topical therapy for AD based on its capacity both to selectively kill S. aureus and to inhibit toxin production by S. aureus. Dr. Gallo’s team’s preclinical work involved screening thousands of isolates of coagulase-negative staphylococci for gene products that perform these two functions by expressing both antimicrobial peptides (AMPs) and autoinducing peptides (AIPs), the latter of which inhibit the S. aureus quorum-sending system that leads to toxin production. Most patients with AD lack protective strains of coagulase-negative staphylococci, including S. hominis, prior research has found.

The double-blind phase 1 trial randomized 54 adults with moderate-severe AD affecting the ventral forearms in a 2:1 fashion to receive the proprietary lyophilized preparation of ShA9 or an ShA9-free formulation twice daily for 1 week. All participants were culture positive for S. aureus.

Clinical assessments and skin swabs were obtained before and within an hour after the first application of day 1, and swabs were collected on days 4 and 7 within 4 hours of the first application.

Blinded physician assessments and skin swabs were also obtained at 24, 48, and 96 hours after the final dose on day 7.

Based on structured daily diaries, there were no serious adverse events, and significantly fewer adverse events in those treated with ShA9, compared with the vehicle alone; 55.6% versus 83.3%, respectively, were considered to have adverse events.

The adverse event–reporting system captured the normal fluctuation of eczema and considered any report of fluctuation above baseline to be an adverse event. “Patients treated with the [placebo formulation] had the expected high frequency of itching, burning, and pain that you see with AD but it was encouraging that the frequency of reporting these events was significantly less in those treated with the active [formulation],” Dr. Gallo said in the interview.

Their report describes a decrease in S. aureus in participants treated with ShA9, and increases in ShA9 DNA. Not all S. aureus strains were directly killed by ShA9, but all strains had reduced expression of mRNA for psm-alpha, an important virulence factor. That reduced expression correlated with ShA9 AIPs and improved EASI scores, the latter of which was observed in a post-hoc analysis. “Participants with S. aureus not killed by ShA9 were still sensitive to inhibition of toxin production, a mechanistic outcome that predicted clinical improvement in mice and may require longer therapy to observe clinical improvement in humans,” the investigators wrote.

Local eczema severity was not significantly different between the bacteriotherapy and control groups. But the post-hoc analysis showed that after 7 days of treatment, and up to 4 days after treatment was discontinued, the patients with S. aureus that was sensitive to killing by ShA9 (21 out of 35 total who received the bacteriotherapy) showed improvement in EASI and SCORAD scores, compared with control patients.

Future research will assess the compound in both S. aureus culture-positive and culture-negative patients, and in patients with mild disease, Dr. Gallo said.

The trial was conducted at USCD and the National Jewish Health General Clinical Research Center in Denver, and was sponsored by the National Institute of Allergy and Infectious Diseases. The ShA9 formulation and related technology are licensed to MatriSys Bioscience, of which Dr. Gallo is the cofounder and an advisory board member. Dr. Gallo holds equity interest in the company.

Officials have previously linked being overweight or obese to a greater risk for more severe COVID-19. A report today from the U.S. Centers for Disease Control and Prevention adds numbers and some nuance to the association.

Data from nearly 150,000 U.S. adults hospitalized with COVID-19 nationwide indicate that risk for more severe disease outcomes increases along with body mass index (BMI). The risk of COVID-19–related hospitalization and death associated with obesity was particularly high among people younger than 65.

“As clinicians develop care plans for COVID-19 patients, they should consider the risk for severe outcomes in patients with higher BMIs, especially for those with severe obesity,” the researchers note. They add that their findings suggest “progressively intensive management of COVID-19 might be needed for patients with more severe obesity.”

People with COVID-19 close to the border between a healthy and overweight BMI – from 23.7 kg/m² to 25.9 kg/m² – had the lowest risks for adverse outcomes.

The study was published online today in Morbidity and Mortality Weekly Report.
 

Greater need for critical care

The risk of ICU admission was particularly associated with severe obesity. For example, those with a BMI in the 40-44.9 kg/m² category had a 6% increased risk, which jumped to 16% higher among those with a BMI of 45 or greater.

Compared to people with a healthy BMI, the need for invasive mechanical ventilation was 12% more likely among overweight adults with a BMI of 25-29.2. The risked jumped to 108% greater among the most obese people, those with a BMI of 45 or greater, lead CDC researcher Lyudmyla Kompaniyets, PhD, and colleagues reported.

Moreover, the risks for hospitalization and death increased in a dose-response relationship with obesity.

For example, risks of being hospitalized were 7% greater for adults with a BMI between 30 and 34.9 and climbed to 33% greater for those with a BMI of 45. Risks were calculated as adjusted relative risks compared with people with a healthy BMI between 18.5 and 24.9.

Interestingly, being underweight was associated with elevated risk for COVID-19 hospitalization as well. For example, people with a BMI of less than 18.5 had a 20% greater chance of admission vs. people in the healthy BMI range. Unknown underlying medical conditions or issues related to nutrition or immune function could be contributing factors, the researchers note.
 

Elevated risk of dying

The risk of death in adults with obesity ranged from 8% higher in the 30-34.9 range up to 61% greater for those with a BMI of 45.

Chronic inflammation or impaired lung function from excess weight are possible reasons that higher BMI imparts greater risk, the researchers note.

The CDC researchers evaluated 148,494 adults from 238 hospitals participating in PHD-SR database. Because the study was limited to people hospitalized with COVID-19, the findings may not apply to all adults with COVID-19.

Another potential limitation is that investigators were unable to calculate BMI for all patients in the database because about 28% of participating hospitals did not report height and weight.

The study authors had no relevant financial relationships to disclose. 

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

Officials have previously linked being overweight or obese to a greater risk for more severe COVID-19. A report today from the U.S. Centers for Disease Control and Prevention adds numbers and some nuance to the association.

Data from nearly 150,000 U.S. adults hospitalized with COVID-19 nationwide indicate that risk for more severe disease outcomes increases along with body mass index (BMI). The risk of COVID-19–related hospitalization and death associated with obesity was particularly high among people younger than 65.

“As clinicians develop care plans for COVID-19 patients, they should consider the risk for severe outcomes in patients with higher BMIs, especially for those with severe obesity,” the researchers note. They add that their findings suggest “progressively intensive management of COVID-19 might be needed for patients with more severe obesity.”

People with COVID-19 close to the border between a healthy and overweight BMI – from 23.7 kg/m² to 25.9 kg/m² – had the lowest risks for adverse outcomes.

The study was published online today in Morbidity and Mortality Weekly Report.
 

Greater need for critical care

The risk of ICU admission was particularly associated with severe obesity. For example, those with a BMI in the 40-44.9 kg/m² category had a 6% increased risk, which jumped to 16% higher among those with a BMI of 45 or greater.

Compared to people with a healthy BMI, the need for invasive mechanical ventilation was 12% more likely among overweight adults with a BMI of 25-29.2. The risked jumped to 108% greater among the most obese people, those with a BMI of 45 or greater, lead CDC researcher Lyudmyla Kompaniyets, PhD, and colleagues reported.

Moreover, the risks for hospitalization and death increased in a dose-response relationship with obesity.

For example, risks of being hospitalized were 7% greater for adults with a BMI between 30 and 34.9 and climbed to 33% greater for those with a BMI of 45. Risks were calculated as adjusted relative risks compared with people with a healthy BMI between 18.5 and 24.9.

Interestingly, being underweight was associated with elevated risk for COVID-19 hospitalization as well. For example, people with a BMI of less than 18.5 had a 20% greater chance of admission vs. people in the healthy BMI range. Unknown underlying medical conditions or issues related to nutrition or immune function could be contributing factors, the researchers note.
 

Elevated risk of dying

The risk of death in adults with obesity ranged from 8% higher in the 30-34.9 range up to 61% greater for those with a BMI of 45.

Chronic inflammation or impaired lung function from excess weight are possible reasons that higher BMI imparts greater risk, the researchers note.

The CDC researchers evaluated 148,494 adults from 238 hospitals participating in PHD-SR database. Because the study was limited to people hospitalized with COVID-19, the findings may not apply to all adults with COVID-19.

Another potential limitation is that investigators were unable to calculate BMI for all patients in the database because about 28% of participating hospitals did not report height and weight.

The study authors had no relevant financial relationships to disclose. 

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

Officials have previously linked being overweight or obese to a greater risk for more severe COVID-19. A report today from the U.S. Centers for Disease Control and Prevention adds numbers and some nuance to the association.

Data from nearly 150,000 U.S. adults hospitalized with COVID-19 nationwide indicate that risk for more severe disease outcomes increases along with body mass index (BMI). The risk of COVID-19–related hospitalization and death associated with obesity was particularly high among people younger than 65.

“As clinicians develop care plans for COVID-19 patients, they should consider the risk for severe outcomes in patients with higher BMIs, especially for those with severe obesity,” the researchers note. They add that their findings suggest “progressively intensive management of COVID-19 might be needed for patients with more severe obesity.”

People with COVID-19 close to the border between a healthy and overweight BMI – from 23.7 kg/m² to 25.9 kg/m² – had the lowest risks for adverse outcomes.

The study was published online today in Morbidity and Mortality Weekly Report.
 

Greater need for critical care

The risk of ICU admission was particularly associated with severe obesity. For example, those with a BMI in the 40-44.9 kg/m² category had a 6% increased risk, which jumped to 16% higher among those with a BMI of 45 or greater.

Compared to people with a healthy BMI, the need for invasive mechanical ventilation was 12% more likely among overweight adults with a BMI of 25-29.2. The risked jumped to 108% greater among the most obese people, those with a BMI of 45 or greater, lead CDC researcher Lyudmyla Kompaniyets, PhD, and colleagues reported.

Moreover, the risks for hospitalization and death increased in a dose-response relationship with obesity.

For example, risks of being hospitalized were 7% greater for adults with a BMI between 30 and 34.9 and climbed to 33% greater for those with a BMI of 45. Risks were calculated as adjusted relative risks compared with people with a healthy BMI between 18.5 and 24.9.

Interestingly, being underweight was associated with elevated risk for COVID-19 hospitalization as well. For example, people with a BMI of less than 18.5 had a 20% greater chance of admission vs. people in the healthy BMI range. Unknown underlying medical conditions or issues related to nutrition or immune function could be contributing factors, the researchers note.
 

Elevated risk of dying

The risk of death in adults with obesity ranged from 8% higher in the 30-34.9 range up to 61% greater for those with a BMI of 45.

Chronic inflammation or impaired lung function from excess weight are possible reasons that higher BMI imparts greater risk, the researchers note.

The CDC researchers evaluated 148,494 adults from 238 hospitals participating in PHD-SR database. Because the study was limited to people hospitalized with COVID-19, the findings may not apply to all adults with COVID-19.

Another potential limitation is that investigators were unable to calculate BMI for all patients in the database because about 28% of participating hospitals did not report height and weight.

The study authors had no relevant financial relationships to disclose. 

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

The U.S. Food and Drug Administration has granted emergency use authorization (EUA) for the Cue COVID-19 Test for Home and Over The Counter Use (Cue OTC Test, Cue Health).

The Cue OTC Test is the first molecular diagnostic test available to consumers without a prescription.

The test detects genetic material from SARS-CoV-2 present in the nostrils and delivers results in about 20 minutes to the user’s mobile smart device via the Cue Health app.

In testing, the Cue OTC Test correctly identified 96% of positive nasal swab samples from individuals known to have symptoms and correctly identified 100% of positive samples from individuals without symptoms.

The test is intended for use in people aged 2 years and older with and without symptoms.

“With this authorization, consumers can purchase and self-administer one of the easiest, fastest, and most accurate tests without a prescription,” Clint Sever, cofounder and chief product officer of Cue Health, said in a news release.

“This FDA authorization will help us improve patient outcomes with a solution that provides the accuracy of central lab tests, with the speed and accessibility required to address emergent global health issues,” he said.

Cue Health expects to produce more than 100,000 single-use test kits per day by this summer. Dena Cook, the company’s chief communications officer, told this news organization that the company hasn’t announced pricing information yet, but the price will be “comparable” to other price points and other products on the market.  

“The FDA continues to prioritize the availability of more at-home testing options in response to the pandemic,” Jeff Shuren, MD, JD, director of the FDA’s Center for Devices and Radiological Health, said in a statement.

“Cue COVID-19 Test for Home and Over-the-Counter Use provides access to accurate and reliable testing at home, without a prescription. The FDA will continue to work collaboratively with test developers to advance effective testing options for doctors, clinicians, and the public,” he said.

In June, the FDA granted an EUA to Cue Health’s COVID-19 test for use in clinical and point-of-care settings.

The test is currently being used in hospitals, physicians’ offices, and dental clinics, as well as schools, essential businesses, nursing homes, and other congregate-care facilities. The test is also being distributed through a program led by the U.S. Department of Defense and the U.S. Department of Health & Human Services across several states.

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

The U.S. Food and Drug Administration has granted emergency use authorization (EUA) for the Cue COVID-19 Test for Home and Over The Counter Use (Cue OTC Test, Cue Health).

The Cue OTC Test is the first molecular diagnostic test available to consumers without a prescription.

The test detects genetic material from SARS-CoV-2 present in the nostrils and delivers results in about 20 minutes to the user’s mobile smart device via the Cue Health app.

In testing, the Cue OTC Test correctly identified 96% of positive nasal swab samples from individuals known to have symptoms and correctly identified 100% of positive samples from individuals without symptoms.

The test is intended for use in people aged 2 years and older with and without symptoms.

“With this authorization, consumers can purchase and self-administer one of the easiest, fastest, and most accurate tests without a prescription,” Clint Sever, cofounder and chief product officer of Cue Health, said in a news release.

“This FDA authorization will help us improve patient outcomes with a solution that provides the accuracy of central lab tests, with the speed and accessibility required to address emergent global health issues,” he said.

Cue Health expects to produce more than 100,000 single-use test kits per day by this summer. Dena Cook, the company’s chief communications officer, told this news organization that the company hasn’t announced pricing information yet, but the price will be “comparable” to other price points and other products on the market.  

“The FDA continues to prioritize the availability of more at-home testing options in response to the pandemic,” Jeff Shuren, MD, JD, director of the FDA’s Center for Devices and Radiological Health, said in a statement.

“Cue COVID-19 Test for Home and Over-the-Counter Use provides access to accurate and reliable testing at home, without a prescription. The FDA will continue to work collaboratively with test developers to advance effective testing options for doctors, clinicians, and the public,” he said.

In June, the FDA granted an EUA to Cue Health’s COVID-19 test for use in clinical and point-of-care settings.

The test is currently being used in hospitals, physicians’ offices, and dental clinics, as well as schools, essential businesses, nursing homes, and other congregate-care facilities. The test is also being distributed through a program led by the U.S. Department of Defense and the U.S. Department of Health & Human Services across several states.

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

The U.S. Food and Drug Administration has granted emergency use authorization (EUA) for the Cue COVID-19 Test for Home and Over The Counter Use (Cue OTC Test, Cue Health).

The Cue OTC Test is the first molecular diagnostic test available to consumers without a prescription.

The test detects genetic material from SARS-CoV-2 present in the nostrils and delivers results in about 20 minutes to the user’s mobile smart device via the Cue Health app.

In testing, the Cue OTC Test correctly identified 96% of positive nasal swab samples from individuals known to have symptoms and correctly identified 100% of positive samples from individuals without symptoms.

The test is intended for use in people aged 2 years and older with and without symptoms.

“With this authorization, consumers can purchase and self-administer one of the easiest, fastest, and most accurate tests without a prescription,” Clint Sever, cofounder and chief product officer of Cue Health, said in a news release.

“This FDA authorization will help us improve patient outcomes with a solution that provides the accuracy of central lab tests, with the speed and accessibility required to address emergent global health issues,” he said.

Cue Health expects to produce more than 100,000 single-use test kits per day by this summer. Dena Cook, the company’s chief communications officer, told this news organization that the company hasn’t announced pricing information yet, but the price will be “comparable” to other price points and other products on the market.  

“The FDA continues to prioritize the availability of more at-home testing options in response to the pandemic,” Jeff Shuren, MD, JD, director of the FDA’s Center for Devices and Radiological Health, said in a statement.

“Cue COVID-19 Test for Home and Over-the-Counter Use provides access to accurate and reliable testing at home, without a prescription. The FDA will continue to work collaboratively with test developers to advance effective testing options for doctors, clinicians, and the public,” he said.

In June, the FDA granted an EUA to Cue Health’s COVID-19 test for use in clinical and point-of-care settings.

The test is currently being used in hospitals, physicians’ offices, and dental clinics, as well as schools, essential businesses, nursing homes, and other congregate-care facilities. The test is also being distributed through a program led by the U.S. Department of Defense and the U.S. Department of Health & Human Services across several states.

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