The Hospitalist

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

New data on COVID-19 vaccines should serve as a “wake-up call” about the need to stop the spread of the SARS-CoV-2 virus among people and thus deprive it of opportunities to evolve its defenses, the top federal expert on infectious diseases said.

“The virus will continue to mutate and will mutate for its own selective advantage,” said Anthony S. Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, at a Friday news conference organized by the White House.

The continued transmission of SARS-CoV-2 “gives the virus the chance to adapt to the forces, in this case the immune response, that’s trying to get rid of it,” Dr. Fauci said. “That’s where you get mutations.”

Federal health officials are working to boost the U.S. supply of COVID-19 vaccines, even as signals emerge about the extent that the virus is already evolving.

Data released this week about the Janssen/Johnson & Johnson (J&J) and Novavax COVID-19 vaccines in late-stage development provides further evidence that they may not protect as well against emerging variants, Dr. Fauci said.

“Mutations that lead to different lineage do have clinical consequences,” he said, while also emphasizing that the emerging vaccines appear to confer broad protection. Dr. Fauci earlier in the day addressed the “messaging challenge” for clinicians and researchers in discussing the results of the J&J vaccine trial, which appear to fall short of those reported for the two vaccines already approved and in use in the United States. He noted the benefits of possibly soon having more authorized vaccines to combat COVID-19. But continued community spread of the infection will foster conditions that can undermine the vaccines’ effectiveness.

“Even though the long-range effect in the sense of severe disease is still handled reasonably well by the vaccines, this is a wake-up call to all of us,” Dr. Fauci said.

Pharmaceutical scientists and executives and government health officials will need to work together to continue to develop vaccines that can outwit the emerging variants, he said.

On Jan. 29, J&J reported that its highly anticipated single-dose vaccine had shown its worst results in South Africa where many cases of COVID-19 were caused by infection with a SARS-CoV-2 variant from the B.1.351 lineage. The overall efficacy was 66% globally, 72% in the United States, and 57% in South Africa against moderate to severe SARS-CoV-2, J&J said.

Novavax on Jan. 28 reported an efficacy rate for its COVID-19 vaccine of 49.4% from a clinical trial conducted in South Africa, compared with an 89.3% rate from a U.K. study. There already have been attempts to estimate how well the Pfizer/BioNTech and Moderna vaccines can handle new variants of the virus. They both have been granted emergency-use authorization by the U.S. Food and Drug Administration.
 

‘Genomic surveillance’

The Centers for Disease Control and Prevention on Thursday reported the first U.S.-documented cases of the B.1.351 variant of SARS-CoV-2 in South Carolina. On Jan. 26, the first confirmed U.S. case of a highly transmissible Brazilian coronavirus variant was detected in Minnesota, state health officials said.

The CDC’s stepped-up “genomic surveillance” will help keep clinicians and researchers aware of how SARS-CoV-2 is changing, Dr. Fauci said.

Speaking at the same White House news conference, CDC director Rochelle Walensky, MD, MPH, said the two South Carolina cases of the B.1.351 variant were reported in different parts of the state and not believed to be epidemiologically linked. The people involved “did not have any travel history,” she added.

The SARS-CoV-2 mutations were expected to emerge at some point, as with any virus, but their appearance underscores the need for people to remain vigilant about precautions that can stop its spread, Dr. Walensky said.

She and Dr. Fauci both stressed the need for continued use of masks and social distancing and urged people to get COVID-19 vaccines as they become available. Continued community spread of the virus allows this global health threat to keep replicating, and thus increases its chances to thwart medical interventions, Dr. Fauci said.

“The virus has a playing field, as it were, to mutate,” Dr. Fauci said. “If you stop that and stop the replication, the viruses cannot mutate if they don’t replicate.”

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

An international team of researchers studying COVID-19 has made a startling and pivotal discovery: The virus appears to cause the body to make weapons to attack its own tissues.

The finding could unlock a number of COVID-19’s clinical mysteries. They include the puzzling collection of symptoms that can come with the infection; the persistence of symptoms in some people for months after they clear the virus, a phenomenon dubbed long COVID-19; and why some children and adults have a serious inflammatory syndrome, called multisystem inflammatory syndrome in children (MIS-C) or MIS in adults (MIS-A), after their infections.

“It suggests that the virus might be directly causing autoimmunity, which would be fascinating,” says lead study author Paul Utz, MD, who studies immunology and autoimmunity at Stanford (Calif.) University.

The study also deepens the question of whether other respiratory viruses might also break the body’s tolerance to itself, setting people up for autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and lupus later in life.

Dr. Utz said he and his team are next going to study flu patients to see if that virus might also cause this phenomenon.

“My prediction is that it isn’t going to be specific just to SARS-CoV-2. I’m willing to bet that we will find this with other respiratory viruses,” he said.

The study comes on the heels of a handful of smaller, detailed investigations that have come to similar conclusions.

The study included data from more than 300 patients from four hospitals: two in California, one in Pennsylvania, and another in Germany.

Researchers used blood tests to study their immune responses as their infections progressed. Researchers looked for autoantibodies – weapons of the immune system that go rogue and launch an attack against the body’s own tissues. They compared these autoantibodies with those found in people who were not infected with the virus that causes COVID.

As previous studies have found, autoantibodies were more common after COVID – 50% of people hospitalized for their infections had autoantibodies, compared with less than 15% of those who were healthy and uninfected.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body.

“Their body is set up to get bad COVID, and it’s probably caused by the autoantibodies,” Dr. Utz said.

But in others, about 20% of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a preexisting condition.

Some of these were antibodies that attack key components of the immune system’s weapons against the virus, like interferon. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus’s ability to copy itself. Taking them out is a powerful evasive tactic, and previous studies have shown that people who are born with genes that cause them to have lower interferon function, or who make autoantibodies against these proteins, appear to be at higher risk for life-threatening COVID infections.

“It seems to give the virus a powerful advantage,” said study author, John Wherry, PhD, who directs the Institute for Immunology at the University of Pennsylvania, Philadelphia. “Now your immune system, instead of having a tiny little hill to climb, is staring at Mount Everest. That really is devious.”

In addition to those that sabotage the immune system, some people in the study had autoantibodies against muscles and connective tissues that are seen in some rare disorders.

Dr. Utz said they started the study after seeing COVID patients with strange collections of symptoms that looked more like autoimmune diseases than viral infections – skin rashes, joint pain, fatigue, aching muscles, brain swelling, dry eyes, blood that clots easily, and inflamed blood vessels.

“One thing that’s very important to note is that we don’t know if these patients are going to go on to develop autoimmune disease,” Dr. Utz said. “I think we’ll be able to answer that question in the next 6-12 months as we follow the long haulers and study their samples.”

Dr. Utz said it will be important to study autoantibodies in long haulers to see if they can identify exactly which ones seem to be at work in the condition. If you can catch them early, it might be possible to treat those at risk for enduring symptoms with drugs that suppress the immune system.

What this means, he said, is that COVID will be with us for a long, long time.

“We have to realize that there’s going to be long-term damage from this virus for the survivors. Not just the long haulers, but all the people who have lung damage and heart damage and everything else. We’re going to be studying this virus and it’s badness for decades,” Dr. Utz said.

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

Ceftolozane-tazobactam (C/T) was found effective for treating pneumonia, intra-abdominal, and urinary tract infections caused by Pseudomonas aeruginosa, according to the results of a retrospective, observational study conducted in critically ill patients.

The multicenter, observational study assessed 95 patients who received C/T for P. aeruginosa serious infections, according to a report published online in the International Journal of Antimicrobial Agents.

C/T is a novel beta-lactam/ beta-lactamase inhibitor combination active against gram-negative bacteria including P. aeruginosa, “This paper presents the largest real-life experience published on C/T therapy for treating serious P. aeruginosa infections according to researchers Barbara Balandin, MD, of the Hospital Universitario Puerta de Hierro, Majadahonda, Spain, and colleagues.

The main infections treated were nosocomial pneumonia (56.2%), intra-abdominal infection (10.5%), tracheobronchitis (8.4%), and urinary tract infection (6.3%). Most infections were complicated with sepsis (49.5%) or septic shock (45.3%), and bacteremia (10.5%).

A total of 46 episodes were treated with high-dose C/T (3 g every 8 hours), and 38 episodes were treated with standard dosage (1.5 g every 8 hours). Almost half (44.2%) of the patients were treated with C/T monotherapy, and the remaining group received combination therapy with other antibiotics, according to the researchers.

The primary outcome of the study was to assess the efficacy and toxicity of C/T therapy. The secondary outcome was to evaluate the risk factors for all-cause 30-day mortality from the first day of therapy.

Favorable results

Most of the infections (93.7%) were severe and included the presence of sepsis (49.5%) or septic shock (45.3%). Bacteremia was observed in 15 (15.7%) patients. Bacteremia was secondary to nosocomial pneumonia in eight cases, catheter infection in five, urinary tract infection in one, and soft tissue infection in one. According to their susceptibility profiles, 46 (48.4%) of the strains were classified as extensively drug-resistant (XDR) P. aeruginosa and 35 (36.5%) were multidrug-resistant (MDR) P. aeruginosa.

Sixty-eight (71.6%) patients presented a favorable clinical response, which was defined as a resolution of presenting symptoms and signs of the infection by the end of therapy. An unfavorable clinical response was considered as persistence or worsening of the presenting symptoms and signs or death occurring during treatment with no other cause identified. Death associated with infection was defined as persistence of signs and symptoms of P. aeruginosa infection during C/T therapy with no other cause identified.

Microbiological eradication was documented in 42.1% (40/95) of the episodes. However, the global ICU mortality was still high, at 36.5%, with mortality mainly related to the severity of the infection.

Mortality was found to be significantly correlated with the Charlson Comorbidity Index (5.7 vs. 4.3; P = .04) and the need for life-supporting therapies such as vasopressors (66.6% vs. 46.9%; P = .03) and renal replacement therapy (46.6% vs. 18.1%; P = .002). In addition, mortality was significantly associated with a higher sequential organ failure assessment (SOFA) score during C/T therapy (SOFA1, SOFA 3, and SOFA 7; P < .001).

No significant differences in outcomes were correlated with demographic features, type and severity of infection, and dose of C/T. Also, there were no differences seen in outcomes between patients treated with C/T monotherapy and combined therapy (30.9% vs. 30.1%; P = .55).

“The lack of a positive effect from combined therapy suggests that C/T monotherapy may be sufficient for treating P. aeruginosa isolates that are susceptible to that agent,” the researchers suggested. “This study shows that C/T appears to be a suitable, effective, and safe drug for treating severe infections due to P. aeruginosa, highlighting nosocomial pneumonia caused by MDR/XDR P. aeruginosa in ICU patients with multiple comorbidities, such as immunosuppression, and needing life-sustaining therapies,” they concluded.

The authors reported that they had no outside funding source and had no conflicts of interest.

[email protected]

Ceftolozane-tazobactam (C/T) was found effective for treating pneumonia, intra-abdominal, and urinary tract infections caused by Pseudomonas aeruginosa, according to the results of a retrospective, observational study conducted in critically ill patients.

The multicenter, observational study assessed 95 patients who received C/T for P. aeruginosa serious infections, according to a report published online in the International Journal of Antimicrobial Agents.

C/T is a novel beta-lactam/ beta-lactamase inhibitor combination active against gram-negative bacteria including P. aeruginosa, “This paper presents the largest real-life experience published on C/T therapy for treating serious P. aeruginosa infections according to researchers Barbara Balandin, MD, of the Hospital Universitario Puerta de Hierro, Majadahonda, Spain, and colleagues.

The main infections treated were nosocomial pneumonia (56.2%), intra-abdominal infection (10.5%), tracheobronchitis (8.4%), and urinary tract infection (6.3%). Most infections were complicated with sepsis (49.5%) or septic shock (45.3%), and bacteremia (10.5%).

A total of 46 episodes were treated with high-dose C/T (3 g every 8 hours), and 38 episodes were treated with standard dosage (1.5 g every 8 hours). Almost half (44.2%) of the patients were treated with C/T monotherapy, and the remaining group received combination therapy with other antibiotics, according to the researchers.

The primary outcome of the study was to assess the efficacy and toxicity of C/T therapy. The secondary outcome was to evaluate the risk factors for all-cause 30-day mortality from the first day of therapy.

Favorable results

Most of the infections (93.7%) were severe and included the presence of sepsis (49.5%) or septic shock (45.3%). Bacteremia was observed in 15 (15.7%) patients. Bacteremia was secondary to nosocomial pneumonia in eight cases, catheter infection in five, urinary tract infection in one, and soft tissue infection in one. According to their susceptibility profiles, 46 (48.4%) of the strains were classified as extensively drug-resistant (XDR) P. aeruginosa and 35 (36.5%) were multidrug-resistant (MDR) P. aeruginosa.

Sixty-eight (71.6%) patients presented a favorable clinical response, which was defined as a resolution of presenting symptoms and signs of the infection by the end of therapy. An unfavorable clinical response was considered as persistence or worsening of the presenting symptoms and signs or death occurring during treatment with no other cause identified. Death associated with infection was defined as persistence of signs and symptoms of P. aeruginosa infection during C/T therapy with no other cause identified.

Microbiological eradication was documented in 42.1% (40/95) of the episodes. However, the global ICU mortality was still high, at 36.5%, with mortality mainly related to the severity of the infection.

Mortality was found to be significantly correlated with the Charlson Comorbidity Index (5.7 vs. 4.3; P = .04) and the need for life-supporting therapies such as vasopressors (66.6% vs. 46.9%; P = .03) and renal replacement therapy (46.6% vs. 18.1%; P = .002). In addition, mortality was significantly associated with a higher sequential organ failure assessment (SOFA) score during C/T therapy (SOFA1, SOFA 3, and SOFA 7; P < .001).

No significant differences in outcomes were correlated with demographic features, type and severity of infection, and dose of C/T. Also, there were no differences seen in outcomes between patients treated with C/T monotherapy and combined therapy (30.9% vs. 30.1%; P = .55).

“The lack of a positive effect from combined therapy suggests that C/T monotherapy may be sufficient for treating P. aeruginosa isolates that are susceptible to that agent,” the researchers suggested. “This study shows that C/T appears to be a suitable, effective, and safe drug for treating severe infections due to P. aeruginosa, highlighting nosocomial pneumonia caused by MDR/XDR P. aeruginosa in ICU patients with multiple comorbidities, such as immunosuppression, and needing life-sustaining therapies,” they concluded.

The authors reported that they had no outside funding source and had no conflicts of interest.

[email protected]

Ceftolozane-tazobactam (C/T) was found effective for treating pneumonia, intra-abdominal, and urinary tract infections caused by Pseudomonas aeruginosa, according to the results of a retrospective, observational study conducted in critically ill patients.

The multicenter, observational study assessed 95 patients who received C/T for P. aeruginosa serious infections, according to a report published online in the International Journal of Antimicrobial Agents.

C/T is a novel beta-lactam/ beta-lactamase inhibitor combination active against gram-negative bacteria including P. aeruginosa, “This paper presents the largest real-life experience published on C/T therapy for treating serious P. aeruginosa infections according to researchers Barbara Balandin, MD, of the Hospital Universitario Puerta de Hierro, Majadahonda, Spain, and colleagues.

The main infections treated were nosocomial pneumonia (56.2%), intra-abdominal infection (10.5%), tracheobronchitis (8.4%), and urinary tract infection (6.3%). Most infections were complicated with sepsis (49.5%) or septic shock (45.3%), and bacteremia (10.5%).

A total of 46 episodes were treated with high-dose C/T (3 g every 8 hours), and 38 episodes were treated with standard dosage (1.5 g every 8 hours). Almost half (44.2%) of the patients were treated with C/T monotherapy, and the remaining group received combination therapy with other antibiotics, according to the researchers.

The primary outcome of the study was to assess the efficacy and toxicity of C/T therapy. The secondary outcome was to evaluate the risk factors for all-cause 30-day mortality from the first day of therapy.

Favorable results

Most of the infections (93.7%) were severe and included the presence of sepsis (49.5%) or septic shock (45.3%). Bacteremia was observed in 15 (15.7%) patients. Bacteremia was secondary to nosocomial pneumonia in eight cases, catheter infection in five, urinary tract infection in one, and soft tissue infection in one. According to their susceptibility profiles, 46 (48.4%) of the strains were classified as extensively drug-resistant (XDR) P. aeruginosa and 35 (36.5%) were multidrug-resistant (MDR) P. aeruginosa.

Sixty-eight (71.6%) patients presented a favorable clinical response, which was defined as a resolution of presenting symptoms and signs of the infection by the end of therapy. An unfavorable clinical response was considered as persistence or worsening of the presenting symptoms and signs or death occurring during treatment with no other cause identified. Death associated with infection was defined as persistence of signs and symptoms of P. aeruginosa infection during C/T therapy with no other cause identified.

Microbiological eradication was documented in 42.1% (40/95) of the episodes. However, the global ICU mortality was still high, at 36.5%, with mortality mainly related to the severity of the infection.

Mortality was found to be significantly correlated with the Charlson Comorbidity Index (5.7 vs. 4.3; P = .04) and the need for life-supporting therapies such as vasopressors (66.6% vs. 46.9%; P = .03) and renal replacement therapy (46.6% vs. 18.1%; P = .002). In addition, mortality was significantly associated with a higher sequential organ failure assessment (SOFA) score during C/T therapy (SOFA1, SOFA 3, and SOFA 7; P < .001).

No significant differences in outcomes were correlated with demographic features, type and severity of infection, and dose of C/T. Also, there were no differences seen in outcomes between patients treated with C/T monotherapy and combined therapy (30.9% vs. 30.1%; P = .55).

“The lack of a positive effect from combined therapy suggests that C/T monotherapy may be sufficient for treating P. aeruginosa isolates that are susceptible to that agent,” the researchers suggested. “This study shows that C/T appears to be a suitable, effective, and safe drug for treating severe infections due to P. aeruginosa, highlighting nosocomial pneumonia caused by MDR/XDR P. aeruginosa in ICU patients with multiple comorbidities, such as immunosuppression, and needing life-sustaining therapies,” they concluded.

The authors reported that they had no outside funding source and had no conflicts of interest.

[email protected]

Background: Delirium is a common disorder in hospitalized adults and is associated with poor outcomes. Antipsychotics are used clinically to treat delirium, but benefits and harms remain unclear.

Limitations include heterogeneous use of agents, routes, dose, and measurement tools, which limits generalization of evidence. Multiple RCTs excluded patients with underlying cardiac and neurologic conditions that likely led to underrepresentation of harm in routine use. Insufficient evidence still exists for multiple clinically relevant outcomes including long-term cognitive function.

Bottom line: Evidence from several studies does not support the use of haloperidol or newer antipsychotics to treat delirium.

Citation: Nikooie R et al. Antipsychotics for delirium treatment in adults: A systematic review. Ann Intern Med. 2019 Oct 1;171(7):485-95.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Delirium is a common disorder in hospitalized adults and is associated with poor outcomes. Antipsychotics are used clinically to treat delirium, but benefits and harms remain unclear.

Limitations include heterogeneous use of agents, routes, dose, and measurement tools, which limits generalization of evidence. Multiple RCTs excluded patients with underlying cardiac and neurologic conditions that likely led to underrepresentation of harm in routine use. Insufficient evidence still exists for multiple clinically relevant outcomes including long-term cognitive function.

Bottom line: Evidence from several studies does not support the use of haloperidol or newer antipsychotics to treat delirium.

Citation: Nikooie R et al. Antipsychotics for delirium treatment in adults: A systematic review. Ann Intern Med. 2019 Oct 1;171(7):485-95.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Delirium is a common disorder in hospitalized adults and is associated with poor outcomes. Antipsychotics are used clinically to treat delirium, but benefits and harms remain unclear.

Limitations include heterogeneous use of agents, routes, dose, and measurement tools, which limits generalization of evidence. Multiple RCTs excluded patients with underlying cardiac and neurologic conditions that likely led to underrepresentation of harm in routine use. Insufficient evidence still exists for multiple clinically relevant outcomes including long-term cognitive function.

Bottom line: Evidence from several studies does not support the use of haloperidol or newer antipsychotics to treat delirium.

Citation: Nikooie R et al. Antipsychotics for delirium treatment in adults: A systematic review. Ann Intern Med. 2019 Oct 1;171(7):485-95.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

COVID-19 infection altered the gut microbiota of adult patients and caused depletion of several types of bacteria with known immunomodulatory properties, based on data from a cohort study of 100 patients with confirmed COVID-19 infections from two hospitals.

“As the GI tract is the largest immunological organ in the body and its resident microbiota are known to modulate host immune responses, we hypothesized that the gut microbiota is associated with host inflammatory immune responses in COVID19,” wrote Yun Kit Yeoh, PhD, of the Chinese University of Hong Kong, and colleagues.

In a study published in Gut, the researchers investigated patient microbiota by collecting blood, stool, and patient records between February and May 2020 from 100 confirmed SARS-CoV-2–infected patients in Hong Kong during hospitalization, as well as follow-up stool samples from 27 patients up to 30 days after they cleared the COVID-19 virus; these observations were compared with 78 non–COVID-19 controls.

Overall, 274 stool samples were sequenced. Samples collected from patients during hospitalization for COVID-19 were compared with non–COVID-19 controls. The presence of phylum Bacteroidetes was significantly higher in COVID-19 patients compared with controls (23.9% vs. 12.8%; P < .001), as were Actinobacteria (26.1% vs. 19.0%; P < .001).

After controlling for antibiotics, the investigators found that “differences between cohorts were primarily linked to enrichment of taxa such as Parabacteroides, Sutterella wadsworthensis, and Bacteroides caccae and depletion of Adlercreutzia equolifaciens, Dorea formicigenerans, and Clostridium leptum in COVID-19 relative to non-COVID-19” (P < .05). In addition, Faecalibacterium prausnitzii and Bifidobacterium bifidum were negatively correlated with COVID-19 severity after investigators controlled for patient age and antibiotic use (P < .05).

The researchers also examined bacteria in COVID-19 patients and controls in the context of cytokines and other inflammatory markers. “We hypothesized that these compositional changes play a role in exacerbating disease by contributing to dysregulation of the immune response,” they said.

In fact, species depleted in COVID-19 patients including included B. adolescentis, E. rectale, and F. prausnitzii were negatively correlated with inflammatory markers including CXCL10, IL-10, TNF-alpha, and CCL2.

In addition, 42 stool samples from 27 patients showed significantly distinct gut microbiota from controls up to 30 days (median, 6 days) after virus clearance, regardless of antibiotics use (P < .05), the researchers said.
 

Long-term data needed

The study findings were limited by several factors, including the potential confounding of microbial signatures associated with COVID-19 because of heterogeneous patient management in the clinical setting and the potential that gut microbiota reflects a patient’s health with no impact on disease severity, as well as lack of data on the role of antibiotics for severe and critical patients, the researchers noted. In addition, “gut microbiota composition is highly heterogeneous across human populations and changes in compositions reported here may not necessarily be reflected in patients with COVID-19 from other biogeographies,” they wrote.

The “longer follow-up of patients with COVID-19 (e.g., 3 months to 1 year after clearing the virus) is needed to address questions related to the duration of gut microbiota dysbiosis post recovery, link between microbiota dysbiosis and long-term persistent symptoms, and whether the dysbiosis or enrichment/depletion of specific gut microorganisms predisposes recovered individuals to future health problems,” they wrote.

However, the results suggest a likely role for gut microorganisms in host inflammatory responses to COVID-19 infection, and “underscore an urgent need to understand the specific roles of gut microorganisms in human immune function and systemic inflammation,” they concluded.
 

More than infectious

“A growing body of evidence suggests that severity of illness from COVID-19 is largely determined by the patient’s aberrant immune response to the virus,” Jatin Roper, MD, of Duke University, Durham, N.C., said in an interview. “Therefore, a critical question is: What patient factors determine this immune response? The gut microbiota closely interact with the host immune system and are altered in many immunological diseases,” he said. “Furthermore, the SARS-CoV-2 virus infects enterocytes in the intestine and causes symptomatic gastrointestinal disease in a subset of patients. Therefore, understanding a possible association between gut microbiota and COVID-19 may reveal microbial species involved in disease pathogenesis,” he emphasized.   

In the current study, “I was surprised to find that COVID-19 infection is associated with depletion of immunomodulatory gut bacteria,” said Dr. Roper. “An open question is whether these changes are caused by the SARS-CoV-2 virus and then result in altered immune response. Alternatively, the changes in gut microbiota may be a result of the immune response or other changes associated with the disease,” he said.

“COVID-19 is an immunological disease, not just an infectious disease,” explained Dr. Roper. “The gut microbiota may play an important role in the pathogenesis of the disease. Thus, specific gut microbes could one day be analyzed to risk stratify patients, or even modified to treat the disease,” he noted.
 

Beyond COVID-19

“Given the impact of the gut microbiota on health and disease, as well as the impact of diseases on the microbiota, I am not at all surprised to find that there were significant changes in the microbiota of COVID-19 patients and that these changes are associated with inflammatory cytokines, chemokines, and blood markers of tissue damage,” said Anthony Sung, MD, also of Duke University.

According to Dr. Sung, researchers have already been investigating possible connections between gut microbiota and other conditions such as Alzheimer’s disease, and it’s been hypothesized that these connections are mediated by interactions between the gut microbiota and the immune system.

“While this is an important paper in our understanding of COVID-19, and highlights the microbiome as a potential therapeutic target, we need to conduct clinical trials of microbiota-based interventions before we can fully realize the clinical implications of these findings,” he said.

The study was supported by the Health and Medical Research Fund, the Food and Health Bureau, The Government of the Hong Kong Special Administrative Region, and donations from Hui Hoy & Chow Sin Lan Charity Fund Limited, Pine and Crane Company Limited, Mr. Hui Ming, and The D.H. Chen Foundation. The researchers had no financial conflicts to disclose. Dr. Roper and Dr. Sung had no financial conflicts to disclose.

COVID-19 infection altered the gut microbiota of adult patients and caused depletion of several types of bacteria with known immunomodulatory properties, based on data from a cohort study of 100 patients with confirmed COVID-19 infections from two hospitals.

“As the GI tract is the largest immunological organ in the body and its resident microbiota are known to modulate host immune responses, we hypothesized that the gut microbiota is associated with host inflammatory immune responses in COVID19,” wrote Yun Kit Yeoh, PhD, of the Chinese University of Hong Kong, and colleagues.

In a study published in Gut, the researchers investigated patient microbiota by collecting blood, stool, and patient records between February and May 2020 from 100 confirmed SARS-CoV-2–infected patients in Hong Kong during hospitalization, as well as follow-up stool samples from 27 patients up to 30 days after they cleared the COVID-19 virus; these observations were compared with 78 non–COVID-19 controls.

Overall, 274 stool samples were sequenced. Samples collected from patients during hospitalization for COVID-19 were compared with non–COVID-19 controls. The presence of phylum Bacteroidetes was significantly higher in COVID-19 patients compared with controls (23.9% vs. 12.8%; P < .001), as were Actinobacteria (26.1% vs. 19.0%; P < .001).

After controlling for antibiotics, the investigators found that “differences between cohorts were primarily linked to enrichment of taxa such as Parabacteroides, Sutterella wadsworthensis, and Bacteroides caccae and depletion of Adlercreutzia equolifaciens, Dorea formicigenerans, and Clostridium leptum in COVID-19 relative to non-COVID-19” (P < .05). In addition, Faecalibacterium prausnitzii and Bifidobacterium bifidum were negatively correlated with COVID-19 severity after investigators controlled for patient age and antibiotic use (P < .05).

The researchers also examined bacteria in COVID-19 patients and controls in the context of cytokines and other inflammatory markers. “We hypothesized that these compositional changes play a role in exacerbating disease by contributing to dysregulation of the immune response,” they said.

In fact, species depleted in COVID-19 patients including included B. adolescentis, E. rectale, and F. prausnitzii were negatively correlated with inflammatory markers including CXCL10, IL-10, TNF-alpha, and CCL2.

In addition, 42 stool samples from 27 patients showed significantly distinct gut microbiota from controls up to 30 days (median, 6 days) after virus clearance, regardless of antibiotics use (P < .05), the researchers said.
 

Long-term data needed

The study findings were limited by several factors, including the potential confounding of microbial signatures associated with COVID-19 because of heterogeneous patient management in the clinical setting and the potential that gut microbiota reflects a patient’s health with no impact on disease severity, as well as lack of data on the role of antibiotics for severe and critical patients, the researchers noted. In addition, “gut microbiota composition is highly heterogeneous across human populations and changes in compositions reported here may not necessarily be reflected in patients with COVID-19 from other biogeographies,” they wrote.

The “longer follow-up of patients with COVID-19 (e.g., 3 months to 1 year after clearing the virus) is needed to address questions related to the duration of gut microbiota dysbiosis post recovery, link between microbiota dysbiosis and long-term persistent symptoms, and whether the dysbiosis or enrichment/depletion of specific gut microorganisms predisposes recovered individuals to future health problems,” they wrote.

However, the results suggest a likely role for gut microorganisms in host inflammatory responses to COVID-19 infection, and “underscore an urgent need to understand the specific roles of gut microorganisms in human immune function and systemic inflammation,” they concluded.
 

More than infectious

“A growing body of evidence suggests that severity of illness from COVID-19 is largely determined by the patient’s aberrant immune response to the virus,” Jatin Roper, MD, of Duke University, Durham, N.C., said in an interview. “Therefore, a critical question is: What patient factors determine this immune response? The gut microbiota closely interact with the host immune system and are altered in many immunological diseases,” he said. “Furthermore, the SARS-CoV-2 virus infects enterocytes in the intestine and causes symptomatic gastrointestinal disease in a subset of patients. Therefore, understanding a possible association between gut microbiota and COVID-19 may reveal microbial species involved in disease pathogenesis,” he emphasized.   

In the current study, “I was surprised to find that COVID-19 infection is associated with depletion of immunomodulatory gut bacteria,” said Dr. Roper. “An open question is whether these changes are caused by the SARS-CoV-2 virus and then result in altered immune response. Alternatively, the changes in gut microbiota may be a result of the immune response or other changes associated with the disease,” he said.

“COVID-19 is an immunological disease, not just an infectious disease,” explained Dr. Roper. “The gut microbiota may play an important role in the pathogenesis of the disease. Thus, specific gut microbes could one day be analyzed to risk stratify patients, or even modified to treat the disease,” he noted.
 

Beyond COVID-19

“Given the impact of the gut microbiota on health and disease, as well as the impact of diseases on the microbiota, I am not at all surprised to find that there were significant changes in the microbiota of COVID-19 patients and that these changes are associated with inflammatory cytokines, chemokines, and blood markers of tissue damage,” said Anthony Sung, MD, also of Duke University.

According to Dr. Sung, researchers have already been investigating possible connections between gut microbiota and other conditions such as Alzheimer’s disease, and it’s been hypothesized that these connections are mediated by interactions between the gut microbiota and the immune system.

“While this is an important paper in our understanding of COVID-19, and highlights the microbiome as a potential therapeutic target, we need to conduct clinical trials of microbiota-based interventions before we can fully realize the clinical implications of these findings,” he said.

The study was supported by the Health and Medical Research Fund, the Food and Health Bureau, The Government of the Hong Kong Special Administrative Region, and donations from Hui Hoy & Chow Sin Lan Charity Fund Limited, Pine and Crane Company Limited, Mr. Hui Ming, and The D.H. Chen Foundation. The researchers had no financial conflicts to disclose. Dr. Roper and Dr. Sung had no financial conflicts to disclose.

COVID-19 infection altered the gut microbiota of adult patients and caused depletion of several types of bacteria with known immunomodulatory properties, based on data from a cohort study of 100 patients with confirmed COVID-19 infections from two hospitals.

“As the GI tract is the largest immunological organ in the body and its resident microbiota are known to modulate host immune responses, we hypothesized that the gut microbiota is associated with host inflammatory immune responses in COVID19,” wrote Yun Kit Yeoh, PhD, of the Chinese University of Hong Kong, and colleagues.

In a study published in Gut, the researchers investigated patient microbiota by collecting blood, stool, and patient records between February and May 2020 from 100 confirmed SARS-CoV-2–infected patients in Hong Kong during hospitalization, as well as follow-up stool samples from 27 patients up to 30 days after they cleared the COVID-19 virus; these observations were compared with 78 non–COVID-19 controls.

Overall, 274 stool samples were sequenced. Samples collected from patients during hospitalization for COVID-19 were compared with non–COVID-19 controls. The presence of phylum Bacteroidetes was significantly higher in COVID-19 patients compared with controls (23.9% vs. 12.8%; P < .001), as were Actinobacteria (26.1% vs. 19.0%; P < .001).

After controlling for antibiotics, the investigators found that “differences between cohorts were primarily linked to enrichment of taxa such as Parabacteroides, Sutterella wadsworthensis, and Bacteroides caccae and depletion of Adlercreutzia equolifaciens, Dorea formicigenerans, and Clostridium leptum in COVID-19 relative to non-COVID-19” (P < .05). In addition, Faecalibacterium prausnitzii and Bifidobacterium bifidum were negatively correlated with COVID-19 severity after investigators controlled for patient age and antibiotic use (P < .05).

The researchers also examined bacteria in COVID-19 patients and controls in the context of cytokines and other inflammatory markers. “We hypothesized that these compositional changes play a role in exacerbating disease by contributing to dysregulation of the immune response,” they said.

In fact, species depleted in COVID-19 patients including included B. adolescentis, E. rectale, and F. prausnitzii were negatively correlated with inflammatory markers including CXCL10, IL-10, TNF-alpha, and CCL2.

In addition, 42 stool samples from 27 patients showed significantly distinct gut microbiota from controls up to 30 days (median, 6 days) after virus clearance, regardless of antibiotics use (P < .05), the researchers said.
 

Long-term data needed

The study findings were limited by several factors, including the potential confounding of microbial signatures associated with COVID-19 because of heterogeneous patient management in the clinical setting and the potential that gut microbiota reflects a patient’s health with no impact on disease severity, as well as lack of data on the role of antibiotics for severe and critical patients, the researchers noted. In addition, “gut microbiota composition is highly heterogeneous across human populations and changes in compositions reported here may not necessarily be reflected in patients with COVID-19 from other biogeographies,” they wrote.

The “longer follow-up of patients with COVID-19 (e.g., 3 months to 1 year after clearing the virus) is needed to address questions related to the duration of gut microbiota dysbiosis post recovery, link between microbiota dysbiosis and long-term persistent symptoms, and whether the dysbiosis or enrichment/depletion of specific gut microorganisms predisposes recovered individuals to future health problems,” they wrote.

However, the results suggest a likely role for gut microorganisms in host inflammatory responses to COVID-19 infection, and “underscore an urgent need to understand the specific roles of gut microorganisms in human immune function and systemic inflammation,” they concluded.
 

More than infectious

“A growing body of evidence suggests that severity of illness from COVID-19 is largely determined by the patient’s aberrant immune response to the virus,” Jatin Roper, MD, of Duke University, Durham, N.C., said in an interview. “Therefore, a critical question is: What patient factors determine this immune response? The gut microbiota closely interact with the host immune system and are altered in many immunological diseases,” he said. “Furthermore, the SARS-CoV-2 virus infects enterocytes in the intestine and causes symptomatic gastrointestinal disease in a subset of patients. Therefore, understanding a possible association between gut microbiota and COVID-19 may reveal microbial species involved in disease pathogenesis,” he emphasized.   

In the current study, “I was surprised to find that COVID-19 infection is associated with depletion of immunomodulatory gut bacteria,” said Dr. Roper. “An open question is whether these changes are caused by the SARS-CoV-2 virus and then result in altered immune response. Alternatively, the changes in gut microbiota may be a result of the immune response or other changes associated with the disease,” he said.

“COVID-19 is an immunological disease, not just an infectious disease,” explained Dr. Roper. “The gut microbiota may play an important role in the pathogenesis of the disease. Thus, specific gut microbes could one day be analyzed to risk stratify patients, or even modified to treat the disease,” he noted.
 

Beyond COVID-19

“Given the impact of the gut microbiota on health and disease, as well as the impact of diseases on the microbiota, I am not at all surprised to find that there were significant changes in the microbiota of COVID-19 patients and that these changes are associated with inflammatory cytokines, chemokines, and blood markers of tissue damage,” said Anthony Sung, MD, also of Duke University.

According to Dr. Sung, researchers have already been investigating possible connections between gut microbiota and other conditions such as Alzheimer’s disease, and it’s been hypothesized that these connections are mediated by interactions between the gut microbiota and the immune system.

“While this is an important paper in our understanding of COVID-19, and highlights the microbiome as a potential therapeutic target, we need to conduct clinical trials of microbiota-based interventions before we can fully realize the clinical implications of these findings,” he said.

The study was supported by the Health and Medical Research Fund, the Food and Health Bureau, The Government of the Hong Kong Special Administrative Region, and donations from Hui Hoy & Chow Sin Lan Charity Fund Limited, Pine and Crane Company Limited, Mr. Hui Ming, and The D.H. Chen Foundation. The researchers had no financial conflicts to disclose. Dr. Roper and Dr. Sung had no financial conflicts to disclose.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

The COVID-19 variants that have emerged in the United Kingdom, Brazil, South Africa and now Southern California are eliciting two notably distinct responses from U.S. public health officials.

janiecbros/iStock/Getty Images Plus

First, broad concern. A variant that wreaked havoc in the United Kingdom, leading to a spike in cases and hospitalizations, is surfacing in a growing number of places in the United States. During the week of Jan. 24, another worrisome variant seen in Brazil surfaced in Minnesota. If these or other strains significantly change the way the virus transmits and attacks the body, as scientists fear they might, they could cause yet another prolonged surge in illness and death in the U.S., even as cases have begun to plateau and vaccines are rolling out.

On the other hand, variants aren’t novel or even uncommon in viral illnesses. The viruses that trigger common colds and flus regularly evolve. Even if a mutated strain of SARS-CoV-2, the virus that causes COVID-19, makes it more contagious or makes people sicker, the basic public health response stays the same: Monitor the virus, and any mutations, as it moves across communities. Use masking, testing, physical distancing, and quarantine to contain the spread.

The problem is that the U.S. has struggled with every step of its public health response in its first year of battle against COVID-19. And that raises the question of whether the nation will devote the attention and resources needed to outflank the virus as it evolves.

Researchers are quick to stress that a coronavirus mutation in itself is no cause for alarm. In the course of making millions and billions of copies as part of the infection process, small changes to a virus’s genome happen all the time as a function of evolutionary biology.

“The word ‘variant’ and the word ‘mutation’ have these scary connotations, and they aren’t necessarily scary,” said Kelly Wroblewski, director of infectious disease programs for the Association of Public Health Laboratories.

When a mutation rings public health alarms, it’s typically because it has combined with other mutations and, collectively, changed how the virus behaves. At that point, it may be named a variant. A variant can make a virus spread faster, or more easily jump between species. It can make a virus more successful at making people sicker, or change how our immune systems respond.

SARS-CoV-2 has been mutating for as long as we’ve known about it; mutations were identified by scientists throughout 2020. Though relevant scientifically – mutations can actually be helpful, acting like a fingerprint that allows scientists to track a virus’s spread – the identified strains mostly carried little concern for public health.

Then came the end of the year, when several variants began drawing scrutiny. One of the most concerning, first detected in the United Kingdom, appears to make the virus more transmissible. Emerging evidence suggests it also could be deadlier, though scientists are still debating that.

We know more about the U.K. variant than others not because it’s necessarily worse, but because the British have one of the best virus surveillance programs in the world, said William Hanage, PhD, an epidemiologist and a professor at Harvard University.

By contrast, the U.S. has one of the weakest genomic surveillance programs of any rich country, Dr. Hanage said. “As it is, people like me cobble together partnerships with places and try and beg them” for samples, he said on a recent call with reporters.

Other variant strains were identified in South Africa and Brazil, and they share some mutations with the U.K. variant. That those changes evolved independently in several parts of the world suggests they might present an evolutionary advantage for the virus. Yet another strain was recently identified in Southern California and flagged due to its increasing presence in hard-hit cities like Los Angeles.

The Southern California strain was detected because a team of researchers at Cedars-Sinai, a hospital and research center in Los Angeles, has unfettered access to patient samples. They were able to see that the strain made up a growing share of cases at the hospital in recent weeks, as well as among the limited number of other samples haphazardly collected at a network of labs in the region.

Not only does the U.S. do less genomic sequencing than most wealthy countries, but it also does its surveillance by happenstance. That means it takes longer to detect new strains and draw conclusions about them. It’s not yet clear, for example, whether that Southern California strain was truly worthy of a press release.

Vast swaths of America’s privatized and decentralized system of health care aren’t set up to send samples to public health or academic labs. “I’m more concerned about the systems to detect variants than I am these particular variants,” said Mark Pandori, PhD, director of Nevada’s public health laboratory and associate professor at the University of Nevada-Reno School of Medicine.

Limited genomic surveillance of viruses is yet another side effect of a fragmented and underfunded public health system that’s struggled to test, track contacts and get COVID-19 under control throughout the pandemic, Ms. Wroblewski said.

The nation’s public health infrastructure, generally funded on a disease-by-disease basis, has decent systems set up to sequence flu, foodborne illnesses and tuberculosis, but there has been no national strategy on COVID-19. “To look for variants, it needs to be a national picture if it’s going to be done well,” Ms. Wroblewski said.

The Biden administration has outlined a strategy for a national response to COVID-19, which includes expanded surveillance for variants.

So far, vaccines for COVID-19 appear to protect against the known variants. Moderna has said its vaccine is effective against the U.K. and South African strains, though it yields fewer antibodies in the face of the latter. The company is working to develop a revised dose of the vaccine that could be added to the current two-shot regimen as a precaution.

But a lot of damage can be done in the time it will take to roll out the current vaccine, let alone an update.

Even with limited sampling, the U.K. variant has been detected in more than two dozen U.S. states, and the Centers for Disease Control and Prevention has warned it could be the predominant strain in the U.S. by March. When it took off in the United Kingdom at the end of last year, it caused a swell in cases, overwhelmed hospitals, and led to a holiday lockdown. Whether the U.S. faces the same fate could depend on which strains it is competing against, and how the public behaves in the weeks ahead.

Already risky interactions among people could, on average, get a little riskier. Many researchers are calling for better masks and better indoor ventilation. But any updates on recommendations likely would play at the margins. Even if variants spread more easily, the same recommendations public health experts have been espousing for months – masking, physical distancing, and limiting time indoors with others – will be the best way to ward them off, said Kirsten Bibbins-Domingo, MD, a physician and professor at the University of California, San Francisco.

“It’s very unsexy what the solutions are,” Dr. Bibbins-Domingo said. “But we need everyone to do them.”

That doesn’t make the task simple. Masking remains controversial in many states, and the public’s patience for maintaining physical distance has worn thin.

Adding to the concerns: Though case numbers stabilized in many parts of the U.S. in January, they have stabilized at rates many times what they were during previous periods in the pandemic or in other parts of the world. Having all that virus in so many bodies creates more opportunities for new mutations and new variants to emerge.

“If we keep letting this thing sneak around, it’s going to get around all the measures we take against it, and that’s the worst possible thing,” said Nevada’s Dr. Pandori.

Compared with less virulent strains, a more contagious variant likely will require that more people be vaccinated before a community can see the benefits of widespread immunity. It’s a bleak outlook for a nation already falling behind in the race to vaccinate enough people to bring the pandemic under control.

“When your best solution is to ask people to do the things that they don’t like to do anyway, that’s very scary,” said Dr. Bibbins-Domingo.
 

This story was produced by KHN, which publishes California Healthline, an editorially independent service of the California Health Care Foundation.

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Experts discuss how to best protect people with diabetes from serious COVID-19 outcomes in a newly published article that summarizes in-depth discussions on the topic from a conference held online last year.

Lead author and Diabetes Technology Society founder and director David C. Klonoff, MD, said in an interview: “To my knowledge this is the largest article or learning that has been written anywhere ever about the co-occurrence of COVID-19 and diabetes and how COVID-19 affects diabetes ... There are a lot of different dimensions.” 

The 37-page report covers all sessions from the Virtual International COVID-19 and Diabetes Summit, held Aug. 26-27, 2020, which had 800 attendees from six continents, on topics including pathophysiology and COVID-19 risk factors, the impact of social determinants of health on diabetes and COVID-19, and psychological aspects of the COVID-19 pandemic for people with diabetes.

The freely available report was published online Jan. 21 in the Journal of Diabetes Science and Technology by Jennifer Y. Zhang of the Diabetes Technology Society, Burlingame, Calif., and colleagues.

Other topics include medications and vaccines, outpatient diabetes management during the COVID-19 pandemic and the growth of telehealth, inpatient management of diabetes in patients with or without COVID-19, ethical considerations, children, pregnancy, economics of care for COVID-19, government policy, regulation of tests and treatments, patient surveillance/privacy, and research gaps and opportunities.

“A comprehensive report like this is so important because it covers such a wide range of topics that are all relevant when it comes to protecting patients with diabetes during a pandemic. Our report aims to bring together all these different aspects of policy during the pandemic, patient physiology, and patient psychology, so I hope it will be widely read and widely appreciated,” Ms. Zhang said in an interview.

Two important clinical trends arising as a result of the pandemic – the advent of telehealth in diabetes management and the use of continuous glucose monitoring (CGM) in hospital – are expected to continue even after COVID-19 abates, said Dr. Klonoff, medical director of the Diabetes Research Institute at Mills-Peninsula Medical Center, San Mateo, Calif.


 

Telehealth in diabetes here to stay, in U.S. at least  

Dr. Klonoff noted that with diabetes telehealth, or “telediabetes” as it’s been dubbed, by using downloaded device data patients don’t have to travel, pay for parking, or take as much time off work. “There are advantages ... patients really like it,” he said.

And for health care providers, an advantage of remote visits is that the clinician can look at the patient while reviewing the patient’s data. “With telehealth for diabetes, the patient’s face and the software data are right next to each other on the same screen. Even as I’m typing I’m looking at the patient ... I consider that a huge advantage,” Dr. Klonoff said.

Rule changes early in the pandemic made the shift to telehealth in the United States possible, he said.

“Fortunately, Medicare and other payers are covering telehealth. It used to be there was no coverage, so that was a damper. Now that it’s covered I don’t think that’s going to go back. Everybody likes it,” he said. 
 

CGM in hospitals helps detect hypoglycemia on wards

Regarding the increase of inpatient CGM (continuous glucose monitoring) prompted by the need to minimize patient exposure of nursing staff during the pandemic and the relaxing of Food and Drug Administration rules about its use, Dr. Klonoff said this phenomenon has led to two other positive developments.

“For FDA, it’s actually an opportunity to see some data collected. To do a clinical trial [prior to] March 2020 you had to go through a lot of processes to do a study. Once it becomes part of clinical care, then you can collect a lot of data,” he noted.   

Moreover, Dr. Klonoff said there’s an important new area where hospital use of CGM is emerging: detection of hypoglycemia on wards.

“When a patient is in the ICU, if they become hypoglycemic or hyperglycemic it will likely be detected. But on the wards, they simply don’t get the same attention. Just about every doctor has had a case where somebody drifted into hypoglycemia that wasn’t recognized and maybe even died,” he explained.

If, however, “patients treated with insulin could all have CGMs that would be so useful. It would send out an alarm. A lot of times people don’t eat when you think they will. Suddenly the insulin dose is inappropriate and the nurse didn’t realize. Or, if IV nutrition stops and the insulin is given [it can be harmful].”

Another example, he said, is a common scenario when insulin is used in patients who are treated with steroids. “They need insulin, but then the steroid is decreased and the insulin dose isn’t decreased fast enough. All those situations can be helped with CGM.”

Overall, he concluded, COVID-19 has provided many lessons, which are “expanding our horizons.”

Ms. Zhang has reported no relevant financial relationships. Dr. Klonoff has reported being a consultant for Dexcom, EOFlow, Fractyl, Lifecare, Novo Nordisk, Roche Diagnostics, Samsung, and Thirdwayv.

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

Although not correlated with each other, increased levels of circulating neprilysin and corin concentrations correlate with increased risk of cardiovascular death and heart failure hospitalizations in chronic heart failure (CHF) patients, according to prospective analysis involving 1,009 HF patients.

This implies that these enzymes might have value for individualizing care, including treatment of patients in heart failure with preserved ejection fraction (HFpEF), reported a team of investigators led by D.H. Frank Gommans, MD, PhD, department of cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.

When followed for up to 7 years and after adjustment for differences in sex and age, the highest risk for the primary composite endpoint of cardiovascular (CV) death and heart failure hospitalization was observed in those with both high soluble neprilysin (sNEP) and high soluble corin (sCOR). The lowest risk was observed in the group with low levels of both enzymes.

The data suggest that monitoring these enzymes might provide “a step toward individualized CHF patient management,” Dr. Gommans reported in JACC Heart Failure, the adjusted hazard ratio for elevated sNEP and sCOR translated into a greater than 50% increase in the composite primary endpoint relative to low levels of both (HR, 1.56; P = .003). After a “comprehensive multivariable analysis,” the increased risk remained substantial and significant (HR, 1.41; P = .03).

In the natriuretic peptide pathway, which has long been recognized as a mediator of vasodilation, venous compliance, diuresis, and other processes dysregulated in heart failure, NEP and COR are “key mediators,” according to the investigators, who cited previously published studies. More attention has turned to these enzymes as potential biomarkers in the context of the PARADIGM trial, which associated an angiotensin-receptor neprilysin inhibitor (ARNI) with a survival benefit in CHF.

The observational study consisted of CHF patients attending a heart failure clinic and who were ARNI naive at inclusion. On the basis of circulating enzyme measurements undertaken from blood samples employing standard techniques, they were stratified into four groups. Those with low levels of both enzymes served as the reference. They were compared with those with low sNEP and high sCOR, those with high sNEP and low sCOR, and those with high levels of both enzymes.

Over the course of a median 4.5 years of follow-up, there were 511 deaths, of which 54% were from a CV cause. There were also 331 heart failure hospitalizations. In all, 449 patients reached the primary composite endpoint.

When compared with the group with low sNEP and low sCOR, an elevation in either enzyme was associated with a numerically but not significantly greater hazard ratio for the primary composite endpoint. The lack of correlation in the elevation of these two enzymes suggests each provides different prognostic information, although it appears that both must be considered together to predict outcomes.

Clinically, stratification of these enzymes might be most useful in HFpEF patients. Relative to the separation of event curves in the CHF patients with reduced ejection fraction (HFrEF), the divergence in the event curves for HFpEF were greater. In addition, event curves separated from the reference in HFpEF patients but not the HFrEF patients if either enzyme was elevated.

Asked if these data hold particular promise for monitoring and individualizing therapy in HFpEF patients, Dr. Gommans said yes. Although he cautioned that this was an observational study and that the differences between the HFpEF and HFrEF should be considered exploratory, he agreed that components of the natriuretic peptide pathway have particular potential to provide new prognostic information and individualize care in HFpEF, where therapeutic options remain limited.

Stratification of natriuretic peptide enzymes in this group might “present as an interesting alternative to ejection fraction” for prognosis and the consideration of treatment choices, he suggested.

Although further validation of the prognostic importance of sNEP and sCOR is needed, according to Dr. Gommans, he foresees the potential of therapeutic trials based on elevated levels of these enzymes. For example, he speculated that these levels might distinguish HFpEF patients who could benefit from a first-line ARNI.

In an accompanying editorial, significant doubts were expressed about simple measurements of sNEP and sCOR concentrations to predict clinical course or guide treatment decisions. The authors of the editorial agreed this is an important area of study but warned of its complexity.

“Concentrations of circulating neprilysin have been shown to correlate poorly with neprilysin activity. Thus the rate of natriuretic peptide degradation by neprilysin cannot be determined solely by measuring circulating levels,” cautioned Peder L. Myhre, MD, PhD, who is a cardiology fellow at Akershus University Hospital in Nordbyhagen, Norway, and postdoc researcher at the University of Oslo.

“Accordingly, concentrations of neprilysin and corin cannot alone be used to predict response to therapies interacting with these peptides,” he added. He agreed that neprilysin and corin might be appropriate biomarkers in CHF, but he thinks the focus must be on their enzymatic activity, not their circulating levels.

“Measuring the enzymatic activity may be a feasible strategy, but this remains to be seen,” he said.

Dr. Gommans reported a financial relationship with Novartis. Dr. Myhre reported financial relationships with Amgen, Novartis, and Novo Nordisk.

Although not correlated with each other, increased levels of circulating neprilysin and corin concentrations correlate with increased risk of cardiovascular death and heart failure hospitalizations in chronic heart failure (CHF) patients, according to prospective analysis involving 1,009 HF patients.

This implies that these enzymes might have value for individualizing care, including treatment of patients in heart failure with preserved ejection fraction (HFpEF), reported a team of investigators led by D.H. Frank Gommans, MD, PhD, department of cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.

When followed for up to 7 years and after adjustment for differences in sex and age, the highest risk for the primary composite endpoint of cardiovascular (CV) death and heart failure hospitalization was observed in those with both high soluble neprilysin (sNEP) and high soluble corin (sCOR). The lowest risk was observed in the group with low levels of both enzymes.

The data suggest that monitoring these enzymes might provide “a step toward individualized CHF patient management,” Dr. Gommans reported in JACC Heart Failure, the adjusted hazard ratio for elevated sNEP and sCOR translated into a greater than 50% increase in the composite primary endpoint relative to low levels of both (HR, 1.56; P = .003). After a “comprehensive multivariable analysis,” the increased risk remained substantial and significant (HR, 1.41; P = .03).

In the natriuretic peptide pathway, which has long been recognized as a mediator of vasodilation, venous compliance, diuresis, and other processes dysregulated in heart failure, NEP and COR are “key mediators,” according to the investigators, who cited previously published studies. More attention has turned to these enzymes as potential biomarkers in the context of the PARADIGM trial, which associated an angiotensin-receptor neprilysin inhibitor (ARNI) with a survival benefit in CHF.

The observational study consisted of CHF patients attending a heart failure clinic and who were ARNI naive at inclusion. On the basis of circulating enzyme measurements undertaken from blood samples employing standard techniques, they were stratified into four groups. Those with low levels of both enzymes served as the reference. They were compared with those with low sNEP and high sCOR, those with high sNEP and low sCOR, and those with high levels of both enzymes.

Over the course of a median 4.5 years of follow-up, there were 511 deaths, of which 54% were from a CV cause. There were also 331 heart failure hospitalizations. In all, 449 patients reached the primary composite endpoint.

When compared with the group with low sNEP and low sCOR, an elevation in either enzyme was associated with a numerically but not significantly greater hazard ratio for the primary composite endpoint. The lack of correlation in the elevation of these two enzymes suggests each provides different prognostic information, although it appears that both must be considered together to predict outcomes.

Clinically, stratification of these enzymes might be most useful in HFpEF patients. Relative to the separation of event curves in the CHF patients with reduced ejection fraction (HFrEF), the divergence in the event curves for HFpEF were greater. In addition, event curves separated from the reference in HFpEF patients but not the HFrEF patients if either enzyme was elevated.

Asked if these data hold particular promise for monitoring and individualizing therapy in HFpEF patients, Dr. Gommans said yes. Although he cautioned that this was an observational study and that the differences between the HFpEF and HFrEF should be considered exploratory, he agreed that components of the natriuretic peptide pathway have particular potential to provide new prognostic information and individualize care in HFpEF, where therapeutic options remain limited.

Stratification of natriuretic peptide enzymes in this group might “present as an interesting alternative to ejection fraction” for prognosis and the consideration of treatment choices, he suggested.

Although further validation of the prognostic importance of sNEP and sCOR is needed, according to Dr. Gommans, he foresees the potential of therapeutic trials based on elevated levels of these enzymes. For example, he speculated that these levels might distinguish HFpEF patients who could benefit from a first-line ARNI.

In an accompanying editorial, significant doubts were expressed about simple measurements of sNEP and sCOR concentrations to predict clinical course or guide treatment decisions. The authors of the editorial agreed this is an important area of study but warned of its complexity.

“Concentrations of circulating neprilysin have been shown to correlate poorly with neprilysin activity. Thus the rate of natriuretic peptide degradation by neprilysin cannot be determined solely by measuring circulating levels,” cautioned Peder L. Myhre, MD, PhD, who is a cardiology fellow at Akershus University Hospital in Nordbyhagen, Norway, and postdoc researcher at the University of Oslo.

“Accordingly, concentrations of neprilysin and corin cannot alone be used to predict response to therapies interacting with these peptides,” he added. He agreed that neprilysin and corin might be appropriate biomarkers in CHF, but he thinks the focus must be on their enzymatic activity, not their circulating levels.

“Measuring the enzymatic activity may be a feasible strategy, but this remains to be seen,” he said.

Dr. Gommans reported a financial relationship with Novartis. Dr. Myhre reported financial relationships with Amgen, Novartis, and Novo Nordisk.

Although not correlated with each other, increased levels of circulating neprilysin and corin concentrations correlate with increased risk of cardiovascular death and heart failure hospitalizations in chronic heart failure (CHF) patients, according to prospective analysis involving 1,009 HF patients.

This implies that these enzymes might have value for individualizing care, including treatment of patients in heart failure with preserved ejection fraction (HFpEF), reported a team of investigators led by D.H. Frank Gommans, MD, PhD, department of cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.

When followed for up to 7 years and after adjustment for differences in sex and age, the highest risk for the primary composite endpoint of cardiovascular (CV) death and heart failure hospitalization was observed in those with both high soluble neprilysin (sNEP) and high soluble corin (sCOR). The lowest risk was observed in the group with low levels of both enzymes.

The data suggest that monitoring these enzymes might provide “a step toward individualized CHF patient management,” Dr. Gommans reported in JACC Heart Failure, the adjusted hazard ratio for elevated sNEP and sCOR translated into a greater than 50% increase in the composite primary endpoint relative to low levels of both (HR, 1.56; P = .003). After a “comprehensive multivariable analysis,” the increased risk remained substantial and significant (HR, 1.41; P = .03).

In the natriuretic peptide pathway, which has long been recognized as a mediator of vasodilation, venous compliance, diuresis, and other processes dysregulated in heart failure, NEP and COR are “key mediators,” according to the investigators, who cited previously published studies. More attention has turned to these enzymes as potential biomarkers in the context of the PARADIGM trial, which associated an angiotensin-receptor neprilysin inhibitor (ARNI) with a survival benefit in CHF.

The observational study consisted of CHF patients attending a heart failure clinic and who were ARNI naive at inclusion. On the basis of circulating enzyme measurements undertaken from blood samples employing standard techniques, they were stratified into four groups. Those with low levels of both enzymes served as the reference. They were compared with those with low sNEP and high sCOR, those with high sNEP and low sCOR, and those with high levels of both enzymes.

Over the course of a median 4.5 years of follow-up, there were 511 deaths, of which 54% were from a CV cause. There were also 331 heart failure hospitalizations. In all, 449 patients reached the primary composite endpoint.

When compared with the group with low sNEP and low sCOR, an elevation in either enzyme was associated with a numerically but not significantly greater hazard ratio for the primary composite endpoint. The lack of correlation in the elevation of these two enzymes suggests each provides different prognostic information, although it appears that both must be considered together to predict outcomes.

Clinically, stratification of these enzymes might be most useful in HFpEF patients. Relative to the separation of event curves in the CHF patients with reduced ejection fraction (HFrEF), the divergence in the event curves for HFpEF were greater. In addition, event curves separated from the reference in HFpEF patients but not the HFrEF patients if either enzyme was elevated.

Asked if these data hold particular promise for monitoring and individualizing therapy in HFpEF patients, Dr. Gommans said yes. Although he cautioned that this was an observational study and that the differences between the HFpEF and HFrEF should be considered exploratory, he agreed that components of the natriuretic peptide pathway have particular potential to provide new prognostic information and individualize care in HFpEF, where therapeutic options remain limited.

Stratification of natriuretic peptide enzymes in this group might “present as an interesting alternative to ejection fraction” for prognosis and the consideration of treatment choices, he suggested.

Although further validation of the prognostic importance of sNEP and sCOR is needed, according to Dr. Gommans, he foresees the potential of therapeutic trials based on elevated levels of these enzymes. For example, he speculated that these levels might distinguish HFpEF patients who could benefit from a first-line ARNI.

In an accompanying editorial, significant doubts were expressed about simple measurements of sNEP and sCOR concentrations to predict clinical course or guide treatment decisions. The authors of the editorial agreed this is an important area of study but warned of its complexity.

“Concentrations of circulating neprilysin have been shown to correlate poorly with neprilysin activity. Thus the rate of natriuretic peptide degradation by neprilysin cannot be determined solely by measuring circulating levels,” cautioned Peder L. Myhre, MD, PhD, who is a cardiology fellow at Akershus University Hospital in Nordbyhagen, Norway, and postdoc researcher at the University of Oslo.

“Accordingly, concentrations of neprilysin and corin cannot alone be used to predict response to therapies interacting with these peptides,” he added. He agreed that neprilysin and corin might be appropriate biomarkers in CHF, but he thinks the focus must be on their enzymatic activity, not their circulating levels.

“Measuring the enzymatic activity may be a feasible strategy, but this remains to be seen,” he said.

Dr. Gommans reported a financial relationship with Novartis. Dr. Myhre reported financial relationships with Amgen, Novartis, and Novo Nordisk.

Background: Resumption of AC or AP therapy for patients following a GIB represents a common clinical challenge. Interruption of these medications following a GIB is associated with increased risk of macrovascular events, thrombosis, morbidity, and death. Prior studies have found inconsistent risk of rebleeding and death with resumption of these therapies following GIB. Little evidence exists for long-term outcomes and optimal timing of AC and AP resumption.

Although resumption of AC or AP following a GIB increased bleeding risk, this may be outweighed by reductions in ischemic events and death if these agents are continued. For hospitalist clinicians, this remains a nuanced and patient-centered decision.

Interpretation is limited by variability in GIB location, agents used, and timing of resumption. Also, the study population included a limited number of elderly patients with multiple comorbidities and high overall death rate.

Bottom line: Resuming AC and AP medications following gastrointestinal bleeding doubled the rebleeding risk but lowered the risk of ischemic events and death, compared with the discontinuation of these medications.

Citation: Sostres C et al. Risk of rebleeding, vascular events and death after gastrointestinal bleeding in anticoagulant and/or antiplatelet users. Aliment Pharmcol Ther. 2019 Oct;50:919-29.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Resumption of AC or AP therapy for patients following a GIB represents a common clinical challenge. Interruption of these medications following a GIB is associated with increased risk of macrovascular events, thrombosis, morbidity, and death. Prior studies have found inconsistent risk of rebleeding and death with resumption of these therapies following GIB. Little evidence exists for long-term outcomes and optimal timing of AC and AP resumption.

Although resumption of AC or AP following a GIB increased bleeding risk, this may be outweighed by reductions in ischemic events and death if these agents are continued. For hospitalist clinicians, this remains a nuanced and patient-centered decision.

Interpretation is limited by variability in GIB location, agents used, and timing of resumption. Also, the study population included a limited number of elderly patients with multiple comorbidities and high overall death rate.

Bottom line: Resuming AC and AP medications following gastrointestinal bleeding doubled the rebleeding risk but lowered the risk of ischemic events and death, compared with the discontinuation of these medications.

Citation: Sostres C et al. Risk of rebleeding, vascular events and death after gastrointestinal bleeding in anticoagulant and/or antiplatelet users. Aliment Pharmcol Ther. 2019 Oct;50:919-29.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Resumption of AC or AP therapy for patients following a GIB represents a common clinical challenge. Interruption of these medications following a GIB is associated with increased risk of macrovascular events, thrombosis, morbidity, and death. Prior studies have found inconsistent risk of rebleeding and death with resumption of these therapies following GIB. Little evidence exists for long-term outcomes and optimal timing of AC and AP resumption.

Although resumption of AC or AP following a GIB increased bleeding risk, this may be outweighed by reductions in ischemic events and death if these agents are continued. For hospitalist clinicians, this remains a nuanced and patient-centered decision.

Interpretation is limited by variability in GIB location, agents used, and timing of resumption. Also, the study population included a limited number of elderly patients with multiple comorbidities and high overall death rate.

Bottom line: Resuming AC and AP medications following gastrointestinal bleeding doubled the rebleeding risk but lowered the risk of ischemic events and death, compared with the discontinuation of these medications.

Citation: Sostres C et al. Risk of rebleeding, vascular events and death after gastrointestinal bleeding in anticoagulant and/or antiplatelet users. Aliment Pharmcol Ther. 2019 Oct;50:919-29.

Dr. Berry is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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

Hospitalist Sarah Stone, MD, arrived for her day shift at Sharp Chula Vista one day in late December. The ICU and hospital wards were still overflowing with COVID-19 patients. But over the previous couple of months, she’d also seen more and more recovered patients presenting with a myriad of symptoms: pulmonary emboli, cardiomyopathy, a shocking case of aspergillosis, and those rare cases of “long COVID,” the patients who just can’t get better.

This morning it was a woman in her 30s. She felt fine, but 2 weeks after recovering from COVID-19, she had unexplained bruising on her arm, a petechiae rash on her legs, and her gums were bleeding. Once admitted to the emergency department, her platelet count of 5000/mm³ was a dead giveaway of immune thrombocytopenic purpura (ITP).

In Dr. Stone’s experience, new and otherwise unexplained symptoms so soon post COVID-19 can’t be written off as a coincidence without some additional consideration. But a quick preliminary search of the literature during her rounds came up almost empty. She found one report with three cases of post-COVID-19 ITP. But other online resources made no mention of it. Kenneth Johnson, MD, the hematologist/oncologist consulting on the new case, told Dr. Stone he’d seen one other case of post-COVID-19 ITP only earlier that month. Dr. Stone called a sister hospital. They’d seen one other case just weeks before.

“I was surprised to find just three cases in the literature when we had seen three among us in a matter of weeks,” Dr. Stone said in an interview. Something was missing.
 

A missing link

ITP is caused by an immune reaction against a patient’s own platelets. Platelet numbers drop, causing easy bruising, bleeding gums, and internal bleeding. Acute cases can usually be resolved within 3 months, but for some patients the condition can be extended or even chronic.

“We know that infections like influenza can cause ITP, so in this light, [COVID-19-associated ITP] might not be surprising,” Gerard Jansen, MD, PhD, an internist and hematologist in Rotterdam, the Netherlands, said in an interview.

Dr. Jansen and colleagues recorded three cases of post-COVID-19 ITP in May 2020 – the report Dr. Stone had found during her shift. Two patients developed ITP several weeks after COVID-19 and responded to treatment with corticosteroids and intravenous immunoglobulin G (IVIG). The third patient, however, died of intracerebral bleeding while still battling COVID-19. He was retrospectively diagnosed with COVID-19-associated ITP.

A deeper dive into the literature uncovers additional case reports from India, France, the United Kingdom, Turkey, and one from China as early as January 2020. A September 2020 review of ITP secondary to COVID-19 included 23 papers and a total of 45 patients. The review authors noted that more than 70% of cases occurred in patients who were aged over 50 years and 75% had had moderate to severe COVID-19 infections. However, the sample size of 45 is too small to definitively describe what’s happening in the overall population.

ITP’s link to COVID-19 gained a media spotlight after the Miami obstetrician, Gregory Michael, MD, developed ITP days after getting the Pfizer COVID-19 vaccine. In early January, after 2 weeks in the ICU, Dr. Michael died of a hemorrhagic stroke caused by the low platelet count.

Pfizer said in a statement that the company is “actively investigating” the case, “but we don’t believe at this time that there is any direct connection to the vaccine.” Other experts have said the timing, particularly in a relatively young and healthy man, means a link to the vaccine is possible or even likely, but final results won›t be known until the Centers for Disease Control and Prevention finishes its investigation.

But “it is quite unusual to die from ITP,” San Diego hematologist Dr. Johnson said in an interview. In his more than 20 years of practice, he has never had a patient die from the condition.

For his part, Dr. Jansen, the hematologist in Rotterdam, said that at this point we just don’t know if there’s a link between the vaccine and ITP. Both infection and drugs are well established causes of ITP, so with that general mechanism or pathology in mind it makes sense that COVID-19 and the vaccine could instigate ITP. But it would be very difficult to prove in just one instance, he said. And considering the millions who have thus far received the vaccine without incident, and the known risks and dangers of COVID-19, “we still advise to vaccinate,” he said.
 

The number of cases is underestimated

Since his original case report in May, Dr. Jansen has seen five or so additional cases. But the causal link between the coronavirus and the hematologic symptoms is still undefined. “We don’t know much about platelet counts in COVID-19 at all,” he said. It could be that COVID-19 somehow inhibits platelet production or that it kills existing platelets. Whatever the exact relationship to the virus, Dr. Jansen expects that the true number of COVID-19-related ITP cases is higher than current estimates suggest.

One reason it isn’t coming up more often, Dr. Jansen said, may be that the cause of ITP in COVID-19 patients is hard to pin down. In the case report from May, Dr. Jansen and colleagues wrote: “And there are numerous other factors that can cause thrombocytopenia where COVID is concerned. For instance the coagulation activation by COVID‐19 infection leading to disseminated intravascular coagulation (DIC) and subsequent thrombocytopenia. Also, treatments for COVID‐19, including heparin, azithromycin and hydroxychloroquine, may lead to thrombocytopenia.”

Tracking and understanding COVID-19-associated ITP first requires the extensive process of elimination needed to diagnose it.

In addition, drugs used to treat COVID-19 could be masking COVID-19-related ITP. “Dexamethasone is a mainstay of COVID treatment. And it’s how we treat ITP,” Dr. Johnson said, which means physicians may be treating ITP without even registering it. And that’s one hypothesis for why Dr. Stone and Dr. Johnson didn’t see a case until 9 months into the pandemic.

Treating COVID-19-associated ITP also has its challenges, particularly in patients who develop it during an acute COVID-19 infection and are at risk for both internal bleeding and thrombosis. This was the case for the third patient in Dr. Jansen’s case report. The patient developed a pulmonary embolism and had a falling platelet count. He was given a platelet infusion and then an anticoagulant for the thrombosis. But a retrospective look at the case revealed the transfusion “did not increase numbers at all – which suggests ITP,” Dr. Jansen said. Intracerebral bleeding was the cause of death.

That’s why “it’s important to be aware of this phenomenon,” Dr. Jansen said of COVID-19-associated ITP. If a transfusion is unsuccessful, consider that the patient may have ITP and adjust. Dr. Johnson hasn’t had to treat a patient battling both complications simultaneously but says the ideal course of action would be to raise platelets with steroids and IVIG and then give the anticoagulant once the platelet count is higher. But reality is rarely ideal. Often these two treatments will have to be given concurrently since the patient faces two life-threatening risks, he said. “It’s a very challenging situation,” he said.

The good news is that standard treatments for ITP seem to work for COVID-19-associated ITP. The 30-year-old patient of Dr. Stone and Dr. Johnson responded so well to intravenous steroids that IVIG was unnecessary. She’s now on a slow prednisone taper and maintains platelet counts at 114,000/mm³ at her weekly follow-up appointments with Dr. Johnson.

Meanwhile, Dr. Jansen’s two other patients, now nearly a year out of treatment, require no additional medication. One of the patients is fully recovered and, though the other still has lower than normal platelet counts, she has no bleeding symptoms and her platelet counts remain stable. Still, Dr. Jansen is anxious for more data looking at the platelet counts in every COVID-19 patient and to combine findings from existing COVID-19-associated ITP patients.

For Dr. Stone, she says she’s added one COVID-19-associated complication to her belt. One less aftereffect will catch her off guard. And she wants others to have the same information.

“It’s just a little bit daunting. We don’t know how bad post-COVID will be,” she said. “There’s so many levels to this disease. Some people deal with it for so long and some people just get better and move on – we think ... so far.”
 

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