SAN DIEGO — Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

Daryl Leja, National Human Genome Research Institute

• Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
• Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
• Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
• Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

SAN DIEGO — Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

Daryl Leja, National Human Genome Research Institute

• Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
• Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
• Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
• Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

SAN DIEGO — Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

Daryl Leja, National Human Genome Research Institute

• Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
• Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
• Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
• Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

RIO DE JANEIRO — The addition of daratumumab to lenalidomide maintenance therapy following autologous stem cell transplant (ASCT) significantly improves rates of achieving minimal residual disease (MRD) negativity and progression-free survival (PFS) among patients newly diagnosed with multiple myeloma (MM), new research showed.

“To date, no randomized trial has directly compared daratumumab-based maintenance therapy vs standard of care lenalidomide maintenance, which is the focus of our trial,” said first author Ashraf Z. Badros, MD, a professor of medicine at the Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland Medical Center, Baltimore, in presenting the findings at the International Myeloma Society (IMS) 2024.

“These results support the addition of daratumumab not only to induction/consolidation but also to standard of care lenalidomide maintenance for these patients,” he said of the study, which was published concurrently in the journal Blood.

Despite ongoing advancements in regimens for induction, consolidation, and maintenance posttransplant, most patients with MM eventually relapse, driving continuing efforts to optimize treatment strategies and improve long-term outcomes.

While daratumumab, an anti-CD38 monoclonal antibody, is approved in induction and consolidation with ASCT for patients with newly diagnosed MM, the authors sought to investigate the potential benefits of adding it to the standard-of-care therapy lenalidomide in maintenance therapy.

For the phase 3 AURIGA trial, they recruited 200 patients with newly diagnosed MM within 12 months of induction therapy and 6 months of ASCT.

The patients, who were all anti-CD38 naive, received at least four induction cycles, had at least a very good partial response, and were MRD positive following ASCT.

They were randomized 1:1 to receive 28-day lenalidomide maintenance cycles either with (n = 99) or without (n = 101) subcutaneous daratumumab for at least 36 cycles or until disease progression, unacceptable toxicity, or withdrawal.

The patients had similar baseline demographic characteristics; their median age was about 62 years, and 25.3% in the daratumumab and 23.5% in the no-daratumumab group had ISS stage III disease. At the time of diagnosis, 23.9% and 16.9%, respectively, had high cytogenic risk.

Overall, patients received a median of five induction cycles prior to entering the study.

For the primary endpoint, the rate of conversion from MRD positive to MRD negative (at a sensitivity of 10-5 using next-generation sequencing) by 12 months was significantly higher in the daratumumab group than in the lenalidomide-only group, at 50.5% vs 18.8% (odds ratio [OR], 4.51; P < .0001).

A similar benefit with the daratumumab group was observed across all clinically relevant subgroups, including patients with high-risk disease.

The MRD-negative conversion rate was similar at the 10-6 threshold (23.2% vs 5%; OR, 5.97; P = .0002).

At a median follow-up of 32.3 months, the overall rates of MRD negativity were 60.6% and 27.7%, with and without daratumumab, respectively (OR, 4.12; P < .0001)

The achievement of complete response or better also was significantly greater with daratumumab (75.8% vs 61.4%; OR, 2.00; P = .0255).

Likewise, PFS favored daratumumab (hazard ratio, 0.53), and the estimated 30-month PFS rates were 82.7% and 66.4%, respectively.

The daratumumab group received more maintenance cycles than the lenalidomide-only group (median of 33 vs 21.5), and it had higher rates of completion of 12 cycles (88.5% vs 78.6%). Dr. Badros noted that the main reason for discontinuation of therapy in the no-daratumumab arm was disease progression.

Consistent with previous studies, daratumumab was associated with more grade 3/4 treatment-emergent adverse events (TEAEs), occurring in 74.0% patients vs 67.3% patients not receiving daratumumab, including infections (18.8% vs 13.3%), cytopenia (54.2% vs 46.9%), and neutropenia (46.9% vs 41.8%). Dr. Badros noted the significantly longer time of treatment in the daratumumab arm (30 months vs 20 months).

Serious TEAEs occurred in 30.2% daratumumab patients and 22.4% no-daratumumab patients, and fatal TEAEs occurred in 2.1% and 1.0% patients, respectively.

“Overall, there were no new safety concerns for daratumumab,” he said.

The authors noted that the requirement that patients be anti-CD38 naive was partially because of “the D-VRd [daratumumab combined with bortezomib, lenalidomide, and dexamethasone] regimen gaining popularity and increased utilization in the myeloma community for transplant-eligible patients with NDMM, even before the publication of the long-term results of the randomized GRIFFIN and PERSEUS studies.”

A key question, remarked Joseph Mikhael, MD, who is chief medical officer of the International Myeloma Foundation, from the audience, is how applicable the findings are in the modern environment, where most patients now have indeed had prior anti-CD38 treatment.

In response, Dr. Badros explained that “I think this is an important study because it is probably one of the few studies that separates the impact of daratumumab-lenalidomide without prior daratumumab use.”

Dr. Badros noted that results from the PERSEUS trial, of D-VRd, show MRD-positive to MRD-negative conversion rates that are similar to the current trial; “therefore, I really don’t think that using daratumumab up front will prevent using it as maintenance,” he said. “If anything, it actually improves outcomes.”

The findings from continuous treatment “are an important reminder that high-risk patients do not do well if you stop treatment,” he said.

Further commenting on the research at the meeting, María-Victoria Mateos, MD, PhD, an associate professor of medicine at the University of Salamanca in Spain, noted that “the unmet need in maintenance is to upgrade the quality of the response and to increase the conversion of MRD-positivity to MRD negative in order to delay the progression of the disease and prolong the overall survival.”

Regarding the AURIGA trial, “this is very interesting data about the role of daratumumab-lenalidomide maintenance in patients who are MRD positive after autologous stem cell transplantation.”

“What is more important is we are progressing in response-adaptive therapy, and we are generating very useful information to possibly make the majority of patients become MRD negative.

“Developing early endpoints as surrogate markers for long-term outcomes and overall survival is critically important,” she added. “Otherwise, trials may continue for more than 15 years.”

The study was sponsored by Janssen Biotech. Dr. Badros reported relationships with Bristol-Myers Squibb, BeiGene, Roche, Jansen, and GSK. Mateos disclosed ties with AbbVie, Amgen, Bristol-Myers Squibb, GSK, Kite, Johnson & Johnson, Oncopeptides, Pfizer, Regeneron, Roche, and Sanofi.

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

RIO DE JANEIRO — The addition of daratumumab to lenalidomide maintenance therapy following autologous stem cell transplant (ASCT) significantly improves rates of achieving minimal residual disease (MRD) negativity and progression-free survival (PFS) among patients newly diagnosed with multiple myeloma (MM), new research showed.

“To date, no randomized trial has directly compared daratumumab-based maintenance therapy vs standard of care lenalidomide maintenance, which is the focus of our trial,” said first author Ashraf Z. Badros, MD, a professor of medicine at the Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland Medical Center, Baltimore, in presenting the findings at the International Myeloma Society (IMS) 2024.

“These results support the addition of daratumumab not only to induction/consolidation but also to standard of care lenalidomide maintenance for these patients,” he said of the study, which was published concurrently in the journal Blood.

Despite ongoing advancements in regimens for induction, consolidation, and maintenance posttransplant, most patients with MM eventually relapse, driving continuing efforts to optimize treatment strategies and improve long-term outcomes.

While daratumumab, an anti-CD38 monoclonal antibody, is approved in induction and consolidation with ASCT for patients with newly diagnosed MM, the authors sought to investigate the potential benefits of adding it to the standard-of-care therapy lenalidomide in maintenance therapy.

For the phase 3 AURIGA trial, they recruited 200 patients with newly diagnosed MM within 12 months of induction therapy and 6 months of ASCT.

The patients, who were all anti-CD38 naive, received at least four induction cycles, had at least a very good partial response, and were MRD positive following ASCT.

They were randomized 1:1 to receive 28-day lenalidomide maintenance cycles either with (n = 99) or without (n = 101) subcutaneous daratumumab for at least 36 cycles or until disease progression, unacceptable toxicity, or withdrawal.

The patients had similar baseline demographic characteristics; their median age was about 62 years, and 25.3% in the daratumumab and 23.5% in the no-daratumumab group had ISS stage III disease. At the time of diagnosis, 23.9% and 16.9%, respectively, had high cytogenic risk.

Overall, patients received a median of five induction cycles prior to entering the study.

For the primary endpoint, the rate of conversion from MRD positive to MRD negative (at a sensitivity of 10-5 using next-generation sequencing) by 12 months was significantly higher in the daratumumab group than in the lenalidomide-only group, at 50.5% vs 18.8% (odds ratio [OR], 4.51; P < .0001).

A similar benefit with the daratumumab group was observed across all clinically relevant subgroups, including patients with high-risk disease.

The MRD-negative conversion rate was similar at the 10-6 threshold (23.2% vs 5%; OR, 5.97; P = .0002).

At a median follow-up of 32.3 months, the overall rates of MRD negativity were 60.6% and 27.7%, with and without daratumumab, respectively (OR, 4.12; P < .0001)

The achievement of complete response or better also was significantly greater with daratumumab (75.8% vs 61.4%; OR, 2.00; P = .0255).

Likewise, PFS favored daratumumab (hazard ratio, 0.53), and the estimated 30-month PFS rates were 82.7% and 66.4%, respectively.

The daratumumab group received more maintenance cycles than the lenalidomide-only group (median of 33 vs 21.5), and it had higher rates of completion of 12 cycles (88.5% vs 78.6%). Dr. Badros noted that the main reason for discontinuation of therapy in the no-daratumumab arm was disease progression.

Consistent with previous studies, daratumumab was associated with more grade 3/4 treatment-emergent adverse events (TEAEs), occurring in 74.0% patients vs 67.3% patients not receiving daratumumab, including infections (18.8% vs 13.3%), cytopenia (54.2% vs 46.9%), and neutropenia (46.9% vs 41.8%). Dr. Badros noted the significantly longer time of treatment in the daratumumab arm (30 months vs 20 months).

Serious TEAEs occurred in 30.2% daratumumab patients and 22.4% no-daratumumab patients, and fatal TEAEs occurred in 2.1% and 1.0% patients, respectively.

“Overall, there were no new safety concerns for daratumumab,” he said.

The authors noted that the requirement that patients be anti-CD38 naive was partially because of “the D-VRd [daratumumab combined with bortezomib, lenalidomide, and dexamethasone] regimen gaining popularity and increased utilization in the myeloma community for transplant-eligible patients with NDMM, even before the publication of the long-term results of the randomized GRIFFIN and PERSEUS studies.”

A key question, remarked Joseph Mikhael, MD, who is chief medical officer of the International Myeloma Foundation, from the audience, is how applicable the findings are in the modern environment, where most patients now have indeed had prior anti-CD38 treatment.

In response, Dr. Badros explained that “I think this is an important study because it is probably one of the few studies that separates the impact of daratumumab-lenalidomide without prior daratumumab use.”

Dr. Badros noted that results from the PERSEUS trial, of D-VRd, show MRD-positive to MRD-negative conversion rates that are similar to the current trial; “therefore, I really don’t think that using daratumumab up front will prevent using it as maintenance,” he said. “If anything, it actually improves outcomes.”

The findings from continuous treatment “are an important reminder that high-risk patients do not do well if you stop treatment,” he said.

Further commenting on the research at the meeting, María-Victoria Mateos, MD, PhD, an associate professor of medicine at the University of Salamanca in Spain, noted that “the unmet need in maintenance is to upgrade the quality of the response and to increase the conversion of MRD-positivity to MRD negative in order to delay the progression of the disease and prolong the overall survival.”

Regarding the AURIGA trial, “this is very interesting data about the role of daratumumab-lenalidomide maintenance in patients who are MRD positive after autologous stem cell transplantation.”

“What is more important is we are progressing in response-adaptive therapy, and we are generating very useful information to possibly make the majority of patients become MRD negative.

“Developing early endpoints as surrogate markers for long-term outcomes and overall survival is critically important,” she added. “Otherwise, trials may continue for more than 15 years.”

The study was sponsored by Janssen Biotech. Dr. Badros reported relationships with Bristol-Myers Squibb, BeiGene, Roche, Jansen, and GSK. Mateos disclosed ties with AbbVie, Amgen, Bristol-Myers Squibb, GSK, Kite, Johnson & Johnson, Oncopeptides, Pfizer, Regeneron, Roche, and Sanofi.

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

RIO DE JANEIRO — The addition of daratumumab to lenalidomide maintenance therapy following autologous stem cell transplant (ASCT) significantly improves rates of achieving minimal residual disease (MRD) negativity and progression-free survival (PFS) among patients newly diagnosed with multiple myeloma (MM), new research showed.

“To date, no randomized trial has directly compared daratumumab-based maintenance therapy vs standard of care lenalidomide maintenance, which is the focus of our trial,” said first author Ashraf Z. Badros, MD, a professor of medicine at the Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland Medical Center, Baltimore, in presenting the findings at the International Myeloma Society (IMS) 2024.

“These results support the addition of daratumumab not only to induction/consolidation but also to standard of care lenalidomide maintenance for these patients,” he said of the study, which was published concurrently in the journal Blood.

Despite ongoing advancements in regimens for induction, consolidation, and maintenance posttransplant, most patients with MM eventually relapse, driving continuing efforts to optimize treatment strategies and improve long-term outcomes.

While daratumumab, an anti-CD38 monoclonal antibody, is approved in induction and consolidation with ASCT for patients with newly diagnosed MM, the authors sought to investigate the potential benefits of adding it to the standard-of-care therapy lenalidomide in maintenance therapy.

For the phase 3 AURIGA trial, they recruited 200 patients with newly diagnosed MM within 12 months of induction therapy and 6 months of ASCT.

The patients, who were all anti-CD38 naive, received at least four induction cycles, had at least a very good partial response, and were MRD positive following ASCT.

They were randomized 1:1 to receive 28-day lenalidomide maintenance cycles either with (n = 99) or without (n = 101) subcutaneous daratumumab for at least 36 cycles or until disease progression, unacceptable toxicity, or withdrawal.

The patients had similar baseline demographic characteristics; their median age was about 62 years, and 25.3% in the daratumumab and 23.5% in the no-daratumumab group had ISS stage III disease. At the time of diagnosis, 23.9% and 16.9%, respectively, had high cytogenic risk.

Overall, patients received a median of five induction cycles prior to entering the study.

For the primary endpoint, the rate of conversion from MRD positive to MRD negative (at a sensitivity of 10-5 using next-generation sequencing) by 12 months was significantly higher in the daratumumab group than in the lenalidomide-only group, at 50.5% vs 18.8% (odds ratio [OR], 4.51; P < .0001).

A similar benefit with the daratumumab group was observed across all clinically relevant subgroups, including patients with high-risk disease.

The MRD-negative conversion rate was similar at the 10-6 threshold (23.2% vs 5%; OR, 5.97; P = .0002).

At a median follow-up of 32.3 months, the overall rates of MRD negativity were 60.6% and 27.7%, with and without daratumumab, respectively (OR, 4.12; P < .0001)

The achievement of complete response or better also was significantly greater with daratumumab (75.8% vs 61.4%; OR, 2.00; P = .0255).

Likewise, PFS favored daratumumab (hazard ratio, 0.53), and the estimated 30-month PFS rates were 82.7% and 66.4%, respectively.

The daratumumab group received more maintenance cycles than the lenalidomide-only group (median of 33 vs 21.5), and it had higher rates of completion of 12 cycles (88.5% vs 78.6%). Dr. Badros noted that the main reason for discontinuation of therapy in the no-daratumumab arm was disease progression.

Consistent with previous studies, daratumumab was associated with more grade 3/4 treatment-emergent adverse events (TEAEs), occurring in 74.0% patients vs 67.3% patients not receiving daratumumab, including infections (18.8% vs 13.3%), cytopenia (54.2% vs 46.9%), and neutropenia (46.9% vs 41.8%). Dr. Badros noted the significantly longer time of treatment in the daratumumab arm (30 months vs 20 months).

Serious TEAEs occurred in 30.2% daratumumab patients and 22.4% no-daratumumab patients, and fatal TEAEs occurred in 2.1% and 1.0% patients, respectively.

“Overall, there were no new safety concerns for daratumumab,” he said.

The authors noted that the requirement that patients be anti-CD38 naive was partially because of “the D-VRd [daratumumab combined with bortezomib, lenalidomide, and dexamethasone] regimen gaining popularity and increased utilization in the myeloma community for transplant-eligible patients with NDMM, even before the publication of the long-term results of the randomized GRIFFIN and PERSEUS studies.”

A key question, remarked Joseph Mikhael, MD, who is chief medical officer of the International Myeloma Foundation, from the audience, is how applicable the findings are in the modern environment, where most patients now have indeed had prior anti-CD38 treatment.

In response, Dr. Badros explained that “I think this is an important study because it is probably one of the few studies that separates the impact of daratumumab-lenalidomide without prior daratumumab use.”

Dr. Badros noted that results from the PERSEUS trial, of D-VRd, show MRD-positive to MRD-negative conversion rates that are similar to the current trial; “therefore, I really don’t think that using daratumumab up front will prevent using it as maintenance,” he said. “If anything, it actually improves outcomes.”

The findings from continuous treatment “are an important reminder that high-risk patients do not do well if you stop treatment,” he said.

Further commenting on the research at the meeting, María-Victoria Mateos, MD, PhD, an associate professor of medicine at the University of Salamanca in Spain, noted that “the unmet need in maintenance is to upgrade the quality of the response and to increase the conversion of MRD-positivity to MRD negative in order to delay the progression of the disease and prolong the overall survival.”

Regarding the AURIGA trial, “this is very interesting data about the role of daratumumab-lenalidomide maintenance in patients who are MRD positive after autologous stem cell transplantation.”

“What is more important is we are progressing in response-adaptive therapy, and we are generating very useful information to possibly make the majority of patients become MRD negative.

“Developing early endpoints as surrogate markers for long-term outcomes and overall survival is critically important,” she added. “Otherwise, trials may continue for more than 15 years.”

The study was sponsored by Janssen Biotech. Dr. Badros reported relationships with Bristol-Myers Squibb, BeiGene, Roche, Jansen, and GSK. Mateos disclosed ties with AbbVie, Amgen, Bristol-Myers Squibb, GSK, Kite, Johnson & Johnson, Oncopeptides, Pfizer, Regeneron, Roche, and Sanofi.

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

Further data from the FLOW study were presented during the 2024 congress of the European Association for the Study of Diabetes (EASD) in Madrid. The FLOW study was originally presented in May at the European Renal Association’s 2024 congress in Stockholm. It was the first dedicated kidney outcomes trial to examine a GLP-1 receptor agonist. 

The FLOW study demonstrated significant kidney, cardiovascular, and mortality benefits with semaglutide 1 mg once weekly in patients with type 2 diabetes and chronic kidney disease (CKD). This study has elevated semaglutide to a new pillar of care for the management of diabetic kidney disease (DKD) alongside RAAS inhibitors, SGLT2 inhibitors, and finerenone. 

At first, whether the benefits of semaglutide were independent of baseline SGLT2 inhibitor use was uncertain. The data presented at the EASD congress, however, appeared to confirm the additive benefits of semaglutide, when combined with SGLT2 inhibitor use, in patients with DKD. The authors did acknowledge that study power was limited, given the low use of SGLT2 inhibitors at trial recruitment (no licensed SGLT2 inhibitor was available for CKD at that point), so small, clinically relevant interactions may not have been detected.

So, what are the implications of the FLOW study for primary care?

DKD is a common clinical challenge in primary care; a national diabetes audit in the United Kingdom suggested that over 40% of patients with type 2 diabetes had kidney disease. Moreover, DKD is the most common cause of kidney failure in adults starting renal replacement therapy in the United Kingdom.

Residual renal risk in patients with DKD persists despite optimal use of guideline-directed medical therapy (GDMT) with RAAS inhibitors, SGLT2 inhibitors, and finerenone, as demonstrated in the many landmark kidney outcomes trials over the past 25 years.

So, a new pillar of GDMT is welcome, but I am worried that this widened choice of therapies may worsen therapeutic inertia; baseline use of the newer DKD therapies (specifically SGLT2 inhibitors and finerenone) remains low. 

In addition, during the EASD FLOW session, Katherine Tuttle, MD, executive director for research at Providence Inland Northwest Health Services in Spokane, Washington, presented data from the US CURE-CKD registry study showing that baseline ACE inhibitor/ARB use of about 70% dropped to 50% after just 90 days. Baseline use of SGLT2 inhibitors was only about 6% and dropped to 5% after 90 days.

I suspect that much of this reduction in prescribing of ACE inhibitors/ARBs will have been in response to an acute dip in estimated glomerular filtration rate (eGFR) or hyperkalemia, which has been a perennial challenge with RAAS inhibitor use in primary care. Ongoing education in primary care is required to manage hyperkalemia and reductions in eGFR after RAAS inhibitor initiation to prevent premature cessation of these foundational therapies. 

On a positive note, there was no acute dip in eGFR after prescribing semaglutide in DKD. This observation will be reassuring for primary care and hopefully prevent unnecessary cessation of therapy.

Also reassuring was the lack of difference in diabetic retinopathy adverse events between the semaglutide and placebo groups. These events raised concerns about semaglutide following the SUSTAIN-6 CVOT study and have affected attitudes in primary care. But the rapidity and magnitude of improvement in glycemic control with semaglutide was believed to be the underlying issue, rather than semaglutide itself. A similar phenomenon has been observed with insulin. The ongoing FOCUS study is exploring the long-term effects of semaglutide on diabetic retinopathy in patients with type 2 diabetes. This study will hopefully provide a definite answer to this issue.

Another useful message from the FLOW study for primary care is the utility of semaglutide for glucose-lowering in the context of CKD. A1c was 0.81% lower in the semaglutide group compared with the placebo group in participants with eGFRs as low as 25 mL/min/1.73 m². It is well established that SGLT2 inhibitors have negligible glucose-lowering effects once eGFR drops below 45 mL/min/1.73 m². Indeed, my usual practice in CKD, if additional glucose-lowering is required once renal protection has been established with an SGLT2 inhibitor, was to add a GLP-1 receptor agonist. It is reassuring to have my clinical practice ratified by the FLOW study.

Semaglutide also helpfully provides an alternative therapeutic option for patients who do not tolerate SGLT2 inhibitors because of, for example, recurrent mycotic genital infections or polyuria, or for those in whom SGLT2 inhibitors are contraindicated, such as patients who have experienced an unprovoked episode of diabetic ketoacidosis. Many of these patients still require cardiovascular and kidney protection, so the FLOW study gives me a viable evidence-based alternative.

As a class, semaglutide and GLP-1 receptor agonists are, of course, not without side effects. Gastrointestinal side effects are the most common, and this finding was echoed in the FLOW study. Gastrointestinal disorders led to permanent treatment discontinuation in 4.5% of the semaglutide group compared with 1.1% of the placebo group. The overall safety profile of semaglutide was favorable, however. 

Gastrointestinal side effects can be particularly concerning in the context of CKD because of the possibility of clinical dehydration and acute kidney injury with persistent vomiting or diarrhea. Patient education is particularly important when using GLP-1 receptor agonists in this group of individuals. Reassuringly, there was no imbalance in dehydration and acute kidney injury between trial arms in the FLOW study. 

Notably, past studies have suggested that patients with CKD are more likely to experience gastrointestinal side effects with GLP-1 receptor agonists; in these patients, the usual mantra of GLP-1 receptor agonist prescribing is particularly important: Start low, go slow.

Finally, medication adherence is a challenge with multiple pillars of GDMT: These evidence-based disease-modifying therapies work only if our patients take them regularly. My senior partner had a lovely turn of phrase when reviewing patients with multiple long-term conditions; he would always start the consultation by asking individuals which medications they were not taking regularly. 

Overall, the FLOW study confirms semaglutide’s position as a new therapeutic pillar for DKD. This treatment will help address the residual renal risk for patients with DKD despite optimal use of GDMT. However, education and support will be required in primary care to prevent worsening therapeutic inertia.
 

Kevin Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, UK, has disclosed the following relevant financial relationships: Received speaker fees from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Dexcom; Daiichi Sankyo; Lilly; Menarini; Novartis; Novo Nordisk; Roche Diagnostics; Embecta; Roche Diabetes Care. Received honoraria for participation in advisory boards from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Lilly; Menarini; Novartis; Roche Diabetes Care; Roche Diagnostics; Sanofi. Received funding for conference registration and subsistence from: Menarini; Daiichi Sankyo.

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

Further data from the FLOW study were presented during the 2024 congress of the European Association for the Study of Diabetes (EASD) in Madrid. The FLOW study was originally presented in May at the European Renal Association’s 2024 congress in Stockholm. It was the first dedicated kidney outcomes trial to examine a GLP-1 receptor agonist. 

The FLOW study demonstrated significant kidney, cardiovascular, and mortality benefits with semaglutide 1 mg once weekly in patients with type 2 diabetes and chronic kidney disease (CKD). This study has elevated semaglutide to a new pillar of care for the management of diabetic kidney disease (DKD) alongside RAAS inhibitors, SGLT2 inhibitors, and finerenone. 

At first, whether the benefits of semaglutide were independent of baseline SGLT2 inhibitor use was uncertain. The data presented at the EASD congress, however, appeared to confirm the additive benefits of semaglutide, when combined with SGLT2 inhibitor use, in patients with DKD. The authors did acknowledge that study power was limited, given the low use of SGLT2 inhibitors at trial recruitment (no licensed SGLT2 inhibitor was available for CKD at that point), so small, clinically relevant interactions may not have been detected.

So, what are the implications of the FLOW study for primary care?

DKD is a common clinical challenge in primary care; a national diabetes audit in the United Kingdom suggested that over 40% of patients with type 2 diabetes had kidney disease. Moreover, DKD is the most common cause of kidney failure in adults starting renal replacement therapy in the United Kingdom.

Residual renal risk in patients with DKD persists despite optimal use of guideline-directed medical therapy (GDMT) with RAAS inhibitors, SGLT2 inhibitors, and finerenone, as demonstrated in the many landmark kidney outcomes trials over the past 25 years.

So, a new pillar of GDMT is welcome, but I am worried that this widened choice of therapies may worsen therapeutic inertia; baseline use of the newer DKD therapies (specifically SGLT2 inhibitors and finerenone) remains low. 

In addition, during the EASD FLOW session, Katherine Tuttle, MD, executive director for research at Providence Inland Northwest Health Services in Spokane, Washington, presented data from the US CURE-CKD registry study showing that baseline ACE inhibitor/ARB use of about 70% dropped to 50% after just 90 days. Baseline use of SGLT2 inhibitors was only about 6% and dropped to 5% after 90 days.

I suspect that much of this reduction in prescribing of ACE inhibitors/ARBs will have been in response to an acute dip in estimated glomerular filtration rate (eGFR) or hyperkalemia, which has been a perennial challenge with RAAS inhibitor use in primary care. Ongoing education in primary care is required to manage hyperkalemia and reductions in eGFR after RAAS inhibitor initiation to prevent premature cessation of these foundational therapies. 

On a positive note, there was no acute dip in eGFR after prescribing semaglutide in DKD. This observation will be reassuring for primary care and hopefully prevent unnecessary cessation of therapy.

Also reassuring was the lack of difference in diabetic retinopathy adverse events between the semaglutide and placebo groups. These events raised concerns about semaglutide following the SUSTAIN-6 CVOT study and have affected attitudes in primary care. But the rapidity and magnitude of improvement in glycemic control with semaglutide was believed to be the underlying issue, rather than semaglutide itself. A similar phenomenon has been observed with insulin. The ongoing FOCUS study is exploring the long-term effects of semaglutide on diabetic retinopathy in patients with type 2 diabetes. This study will hopefully provide a definite answer to this issue.

Another useful message from the FLOW study for primary care is the utility of semaglutide for glucose-lowering in the context of CKD. A1c was 0.81% lower in the semaglutide group compared with the placebo group in participants with eGFRs as low as 25 mL/min/1.73 m². It is well established that SGLT2 inhibitors have negligible glucose-lowering effects once eGFR drops below 45 mL/min/1.73 m². Indeed, my usual practice in CKD, if additional glucose-lowering is required once renal protection has been established with an SGLT2 inhibitor, was to add a GLP-1 receptor agonist. It is reassuring to have my clinical practice ratified by the FLOW study.

Semaglutide also helpfully provides an alternative therapeutic option for patients who do not tolerate SGLT2 inhibitors because of, for example, recurrent mycotic genital infections or polyuria, or for those in whom SGLT2 inhibitors are contraindicated, such as patients who have experienced an unprovoked episode of diabetic ketoacidosis. Many of these patients still require cardiovascular and kidney protection, so the FLOW study gives me a viable evidence-based alternative.

As a class, semaglutide and GLP-1 receptor agonists are, of course, not without side effects. Gastrointestinal side effects are the most common, and this finding was echoed in the FLOW study. Gastrointestinal disorders led to permanent treatment discontinuation in 4.5% of the semaglutide group compared with 1.1% of the placebo group. The overall safety profile of semaglutide was favorable, however. 

Gastrointestinal side effects can be particularly concerning in the context of CKD because of the possibility of clinical dehydration and acute kidney injury with persistent vomiting or diarrhea. Patient education is particularly important when using GLP-1 receptor agonists in this group of individuals. Reassuringly, there was no imbalance in dehydration and acute kidney injury between trial arms in the FLOW study. 

Notably, past studies have suggested that patients with CKD are more likely to experience gastrointestinal side effects with GLP-1 receptor agonists; in these patients, the usual mantra of GLP-1 receptor agonist prescribing is particularly important: Start low, go slow.

Finally, medication adherence is a challenge with multiple pillars of GDMT: These evidence-based disease-modifying therapies work only if our patients take them regularly. My senior partner had a lovely turn of phrase when reviewing patients with multiple long-term conditions; he would always start the consultation by asking individuals which medications they were not taking regularly. 

Overall, the FLOW study confirms semaglutide’s position as a new therapeutic pillar for DKD. This treatment will help address the residual renal risk for patients with DKD despite optimal use of GDMT. However, education and support will be required in primary care to prevent worsening therapeutic inertia.
 

Kevin Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, UK, has disclosed the following relevant financial relationships: Received speaker fees from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Dexcom; Daiichi Sankyo; Lilly; Menarini; Novartis; Novo Nordisk; Roche Diagnostics; Embecta; Roche Diabetes Care. Received honoraria for participation in advisory boards from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Lilly; Menarini; Novartis; Roche Diabetes Care; Roche Diagnostics; Sanofi. Received funding for conference registration and subsistence from: Menarini; Daiichi Sankyo.

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

Further data from the FLOW study were presented during the 2024 congress of the European Association for the Study of Diabetes (EASD) in Madrid. The FLOW study was originally presented in May at the European Renal Association’s 2024 congress in Stockholm. It was the first dedicated kidney outcomes trial to examine a GLP-1 receptor agonist. 

The FLOW study demonstrated significant kidney, cardiovascular, and mortality benefits with semaglutide 1 mg once weekly in patients with type 2 diabetes and chronic kidney disease (CKD). This study has elevated semaglutide to a new pillar of care for the management of diabetic kidney disease (DKD) alongside RAAS inhibitors, SGLT2 inhibitors, and finerenone. 

At first, whether the benefits of semaglutide were independent of baseline SGLT2 inhibitor use was uncertain. The data presented at the EASD congress, however, appeared to confirm the additive benefits of semaglutide, when combined with SGLT2 inhibitor use, in patients with DKD. The authors did acknowledge that study power was limited, given the low use of SGLT2 inhibitors at trial recruitment (no licensed SGLT2 inhibitor was available for CKD at that point), so small, clinically relevant interactions may not have been detected.

So, what are the implications of the FLOW study for primary care?

DKD is a common clinical challenge in primary care; a national diabetes audit in the United Kingdom suggested that over 40% of patients with type 2 diabetes had kidney disease. Moreover, DKD is the most common cause of kidney failure in adults starting renal replacement therapy in the United Kingdom.

Residual renal risk in patients with DKD persists despite optimal use of guideline-directed medical therapy (GDMT) with RAAS inhibitors, SGLT2 inhibitors, and finerenone, as demonstrated in the many landmark kidney outcomes trials over the past 25 years.

So, a new pillar of GDMT is welcome, but I am worried that this widened choice of therapies may worsen therapeutic inertia; baseline use of the newer DKD therapies (specifically SGLT2 inhibitors and finerenone) remains low. 

In addition, during the EASD FLOW session, Katherine Tuttle, MD, executive director for research at Providence Inland Northwest Health Services in Spokane, Washington, presented data from the US CURE-CKD registry study showing that baseline ACE inhibitor/ARB use of about 70% dropped to 50% after just 90 days. Baseline use of SGLT2 inhibitors was only about 6% and dropped to 5% after 90 days.

I suspect that much of this reduction in prescribing of ACE inhibitors/ARBs will have been in response to an acute dip in estimated glomerular filtration rate (eGFR) or hyperkalemia, which has been a perennial challenge with RAAS inhibitor use in primary care. Ongoing education in primary care is required to manage hyperkalemia and reductions in eGFR after RAAS inhibitor initiation to prevent premature cessation of these foundational therapies. 

On a positive note, there was no acute dip in eGFR after prescribing semaglutide in DKD. This observation will be reassuring for primary care and hopefully prevent unnecessary cessation of therapy.

Also reassuring was the lack of difference in diabetic retinopathy adverse events between the semaglutide and placebo groups. These events raised concerns about semaglutide following the SUSTAIN-6 CVOT study and have affected attitudes in primary care. But the rapidity and magnitude of improvement in glycemic control with semaglutide was believed to be the underlying issue, rather than semaglutide itself. A similar phenomenon has been observed with insulin. The ongoing FOCUS study is exploring the long-term effects of semaglutide on diabetic retinopathy in patients with type 2 diabetes. This study will hopefully provide a definite answer to this issue.

Another useful message from the FLOW study for primary care is the utility of semaglutide for glucose-lowering in the context of CKD. A1c was 0.81% lower in the semaglutide group compared with the placebo group in participants with eGFRs as low as 25 mL/min/1.73 m². It is well established that SGLT2 inhibitors have negligible glucose-lowering effects once eGFR drops below 45 mL/min/1.73 m². Indeed, my usual practice in CKD, if additional glucose-lowering is required once renal protection has been established with an SGLT2 inhibitor, was to add a GLP-1 receptor agonist. It is reassuring to have my clinical practice ratified by the FLOW study.

Semaglutide also helpfully provides an alternative therapeutic option for patients who do not tolerate SGLT2 inhibitors because of, for example, recurrent mycotic genital infections or polyuria, or for those in whom SGLT2 inhibitors are contraindicated, such as patients who have experienced an unprovoked episode of diabetic ketoacidosis. Many of these patients still require cardiovascular and kidney protection, so the FLOW study gives me a viable evidence-based alternative.

As a class, semaglutide and GLP-1 receptor agonists are, of course, not without side effects. Gastrointestinal side effects are the most common, and this finding was echoed in the FLOW study. Gastrointestinal disorders led to permanent treatment discontinuation in 4.5% of the semaglutide group compared with 1.1% of the placebo group. The overall safety profile of semaglutide was favorable, however. 

Gastrointestinal side effects can be particularly concerning in the context of CKD because of the possibility of clinical dehydration and acute kidney injury with persistent vomiting or diarrhea. Patient education is particularly important when using GLP-1 receptor agonists in this group of individuals. Reassuringly, there was no imbalance in dehydration and acute kidney injury between trial arms in the FLOW study. 

Notably, past studies have suggested that patients with CKD are more likely to experience gastrointestinal side effects with GLP-1 receptor agonists; in these patients, the usual mantra of GLP-1 receptor agonist prescribing is particularly important: Start low, go slow.

Finally, medication adherence is a challenge with multiple pillars of GDMT: These evidence-based disease-modifying therapies work only if our patients take them regularly. My senior partner had a lovely turn of phrase when reviewing patients with multiple long-term conditions; he would always start the consultation by asking individuals which medications they were not taking regularly. 

Overall, the FLOW study confirms semaglutide’s position as a new therapeutic pillar for DKD. This treatment will help address the residual renal risk for patients with DKD despite optimal use of GDMT. However, education and support will be required in primary care to prevent worsening therapeutic inertia.
 

Kevin Fernando, general practitioner partner, North Berwick Health Centre, North Berwick, UK, has disclosed the following relevant financial relationships: Received speaker fees from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Dexcom; Daiichi Sankyo; Lilly; Menarini; Novartis; Novo Nordisk; Roche Diagnostics; Embecta; Roche Diabetes Care. Received honoraria for participation in advisory boards from: Amarin; Amgen; AstraZeneca; Bayer; Boehringer Ingelheim; Lilly; Menarini; Novartis; Roche Diabetes Care; Roche Diagnostics; Sanofi. Received funding for conference registration and subsistence from: Menarini; Daiichi Sankyo.

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

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

“Here’s my records.”

I hear that a lot, usually in the context of a patient handing me a flash drive or (less commonly) trying to plug it into my computer. (I have the USB ports turned toward me to keep that from happening.)

Uh, no.

I love flash drives. They definitely make data transfer easy, compared with the CDs, ZIPs, JAZZ, floppies, paper, and punch cards of past years (I should also, as a childhood TRS-80 user, include cassette tapes).

At this point an encrypted flash drive is pretty much the entire briefcase I carry back and forth to work each day.

But there is no patient I trust enough to plug in one they handed me.

I’m sure most, if not all, are well meaning. But look at how many large corporations have been damaged by someone slipping in a flash drive with a malicious program somewhere in their network. Once in, it’s almost impossible to get out, and can spread quickly.

Even if the patient is benign, I have no idea who formatted the gadget, or put the records on. It could be a relative, or friend, with other motives. It could even be a random flash drive and they don’t even know what else is on it.

My desktop is my chart system. I have to protect the data of all my patients, so I exercise caution about what emails I open and what I plug into it. Even the person offering me the flash drive wants the info guarded.

So I don’t, as a rule, plug in anything a patient hands me. All it takes is one malicious file to compromise it all. Yeah, I pay for software to watch for that sort of thing, but you still can’t be too careful.

This is where paper still shines. It’s readable and it’s transportable (at least for small things like an MRI report and lab results). I can scan it into a PDF without risking any damage to my computer. And it definitely shouldn’t be plugged into a USB drive unless you’re trying to start a fire.

Of course, paper isn’t secure, either. If you have it piled up everywhere it’s pretty easy for an unsupervised person to walk off with it. That actually happened to a doctor I shared space with 20 years ago, albeit unintentionally. A patient had brought in a bunch of his records in a folder and set them down on the counter. When he left he grabbed another patient’s chart by mistake and didn’t realize it until the next day. Fortunately he returned them promptly, and there were no issues. But it had the potential to be worse.

Today my charts on roughly 20,000 patients can all fit on a gadget the size of my thumb instead of a multi-room shelving system and storage closet. That’s pretty cool, actually. But it also opens other vulnerabilities.

It ticks some patients off that I won’t plug in their flash drives, but I don’t care. Most of them understand when I explain it, because it’s to protect them, too.

The odds are that they don’t mean any harm, but I can’t take that chance.

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Over the last few decades the patient encounter has changed dramatically. Most recently fueled by the COVID pandemic, face-to-face events between patients and providers have become less frequent. The shift began years before with the slow acceptance of telemedicine by third-party payers.

As more practices have opened portals, the encounters between providers and patients via the internet have become more common, but received mixed reviews, often leaving both providers and patients with more questions than answers. Even more recently, the explosive arrival of generative artificial intelligence (AI) has promised, some might say threatened, to add a whole new complexity and uncertainty to patient encounters regardless of the venue or platform.

Still, among the growing collection of options, I think it is fair to say that a live face-to-face encounter remains the gold standard in the opinions of both patients and providers. Patients may have become increasingly critical and vocal when they feel their provider appears rushed or is over focused on the desktop computer screen. However, given all of the options, I suspect that for the moment patients feel a face-to-face meeting continues to offer them the best chance of being heard and their concerns answered.

Even when the image on the video screen is sharp and the intelligibility of the audio feed is crystal clear, I bet most providers feel they can learn more about the patient during a live face-to-face encounter than a Zoom-style encounter.

Nonetheless, there are hints that face-to-face visits maybe losing their place in the pantheon of patient-provider encounters. A recent study from England found that there were a significant number of patients who were more forthcoming in reporting their preferences for social care-related quality of life when they were surveyed by internet rather than face-to-face. It is unclear what was behind this observation, however it may be that patients were embarrassed and viewed these questions about their social neediness as too sensitive to share face-to-face.

There is ample evidence of situations in which the internet can provide a level of anonymity that emboldens the user to say things that are cruel and hurtful, using words they might be afraid to voice in a live setting. This license to act in an uncivil manner is behind much of the harm generated by chat rooms and other social media sites. While in these cases the ability to hide behind the video screen is a negative, this study from England suggests that we should be looking for more opportunities to use this emboldening feature with certain individuals and populations who may be intimidated during a face-to-face encounter. It is likely a hybrid approach may be the most beneficial strategy tailored to the individual patient.

One advantage of a face-to-face visit is that each participant can read the body language of the other. This, of course, can be a disadvantage for the provider who has failed to master the art of disguising his “I’m running behind” stress level, when he should be replacing it with an “I’m ready to listen” posture.

Portals have opened up a whole other can of worms, particularly when the provider has failed to clearly delineate what sort of questions are appropriate for an online forum, not informed the patient who will be providing the answer, and a rough idea of when this will happen. It may take several trips up the learning curve for patients and providers to develop a style of writing that make optimal use of the portal format and make it fit the needs of the practice and the patients.

Regardless of what kind of visit platform we are talking about, a lot hinges on the providers choice of words. I recently reviewed some of the work of Jeffrey D. Robinson, PhD, a professor of communication at the Portland State University, Portland, Oregon. He offers the example of the difference between “some” and “any.” When the patient was asked “Is there something else you would like to address today” almost 80% of the patient’s unmet questions were addressed. However, when the question was “Is there anything else ...” very few of the patient’s unmet questions were addressed. Dr. Robinson has also found that when the question is posed early in the visit rather than at the end, it improves the chances of having the patient’s unmet concerns addressed.

I suspect that the face-to-face patient encounter will survive, but it will continue to lose its market share as other platforms emerge. We can be sure there will be change. We need look no further than generative AI to look for the next step. A well-crafted question could help the patient and the provider choose the most appropriate patient encounter format given the patient’s demographic, chief complaint, and prior history, and match this with the provider’s background and strengths.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

MILAN — Specific combinations of hormonal and biochemical factors were associated with different clinical characteristics and treatment outcomes of alcohol use disorder (AUD) between men and women.

“These hormones and proteins are known to have an influence on behavior, and indeed we see an association between different levels of these compounds and different behavioral aspects of [AUD], although we can’t for sure say that one directly causes another,” said lead researcher Victor M. Karpyak, MD, PhD, professor of psychiatry at the Mayo Clinic, in a release.

The findings were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress.
 

Sex Hormone Signatures

Previous research has highlighted differences in symptoms including cravings, withdrawal, consumption patterns, depression, and anxiety between men and women with AUD, said Dr. Karpyak. Differences in hormones and biochemicals have also been observed between individuals with and without AUD.

However, specific biochemical and hormonal “signatures” associated with male and female responses to treatment have thus far not been explored, he told this news organization.

The study included 400 treatment-seeking individuals (132 women and 268 men; mean age, 41.8 years; 93% White) who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for AUD and were enrolled in a clinical trial of acamprosate.

Baseline assessment included psychiatric comorbidities and substance use with the Psychiatric Research Interview for Substance and Mental Disorders, alcohol consumption pattern over the past 90 days by Timeline Follow-Back calendar, recent craving on the Penn Alcohol Craving Scale (PACS), situations at the risk of drinking on the Inventory of Drug-Taking Situation, recent depression severity on the Patient Health Questionnaire 9 (PHQ-9), and recent anxiety severity on the Generalized Anxiety Disorder 7 scale.

Plasma sex-related hormone and protein measurements were taken at baseline — after detoxification but before treatment. These included total testosterone, estradiol, estrone, progesterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), sex hormone–binding globulin (SHBG), and albumin.

“The important thing is that these measurements were taken during sobriety,” said Dr. Karpyak. Study participants were already in residential treatment programs, and the average time since their last drink was approximately 3 weeks. Relapse was defined as any alcohol consumption during the first 3 months.
 

What Works for Men May Not Work for Women

Results showed that men with symptoms of depression and a higher craving for alcohol, as shown on baseline PHQ-9 and PACS scores, had lower baseline levels of testosterone, estrone, estradiol, and SHBG than those without these symptoms (P = .0102 and P = .0014, respectively).

In addition, a combination of higher progesterone and lower albumin was associated with a lower risk for relapse during the first 3 months (odds ratio [OR], 0.518; P = .0079).

In women, a combination of lower estrone and estradiol and higher FSH and LH levels was associated with higher maximum number of drinks per day (P = .035).

In addition, women who were more likely to relapse during the first 3 months of treatment had higher baseline levels of testosterone, SHBG, and albumin than those at lower relapse risk (OR, 4.536; P = .0057).

Dr. Karpyak noted that these “hormone signatures” were associative and not predictive.

What this means, he said, “is that if you are treating a man and a woman for alcoholism, you are dealing with different biochemical and psychological starting points. This implies that what works for a man may not work for a woman, and vice versa.”
 

Toward Gender Equity

The findings may eventually lead to a way to predict treatment responses in patients with AUD, Dr. Karpyak added, but cautioned that despite statistical significance, these are preliminary findings.

Before these results can be integrated into clinical practice, they need to be replicated. Dr. Karpyak emphasized the need for follow-up research that builds on these findings, using them as preliminary data to determine whether prediction holds real significance.

“Given that many of these differences are related to sex hormones, we particularly want to see how the dramatic hormonal change women experience during the menstrual cycle and at menopause may affect the biochemistry of alcoholism and guide treatment efforts,” he said.

In a statement, Erika Comasco, PhD, associate professor in molecular psychiatry, Uppsala University, Sweden, said the research “is an important step forward to gender equity in medicine.”

“The findings provide an important first insight into the relationship between sex hormones and alcohol use disorder treatment,” she explained. “While sex differences in the way the disorder manifests itself are known, these results suggest that sex hormones may modulate treatment response, potentially supporting sex-specific pharmacological intervention.”

Dr. Comasco shares Dr. Karpyak’s view that hormonal fluctuations linked to the menstrual cycle may influence alcohol misuse and believes more research is needed to explore their impact on treatment and relapse outcomes in female patients.

This study was funded by the National Institute on Alcohol Abuse and Alcoholism (National Institutes of Health) and the Samuel C. Johnson Genomics of Addiction Program at Mayo Clinic. Dr. Karpyak and Dr. Comasco reported no relevant disclosures.
 

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

MILAN — Specific combinations of hormonal and biochemical factors were associated with different clinical characteristics and treatment outcomes of alcohol use disorder (AUD) between men and women.

“These hormones and proteins are known to have an influence on behavior, and indeed we see an association between different levels of these compounds and different behavioral aspects of [AUD], although we can’t for sure say that one directly causes another,” said lead researcher Victor M. Karpyak, MD, PhD, professor of psychiatry at the Mayo Clinic, in a release.

The findings were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress.
 

Sex Hormone Signatures

Previous research has highlighted differences in symptoms including cravings, withdrawal, consumption patterns, depression, and anxiety between men and women with AUD, said Dr. Karpyak. Differences in hormones and biochemicals have also been observed between individuals with and without AUD.

However, specific biochemical and hormonal “signatures” associated with male and female responses to treatment have thus far not been explored, he told this news organization.

The study included 400 treatment-seeking individuals (132 women and 268 men; mean age, 41.8 years; 93% White) who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for AUD and were enrolled in a clinical trial of acamprosate.

Baseline assessment included psychiatric comorbidities and substance use with the Psychiatric Research Interview for Substance and Mental Disorders, alcohol consumption pattern over the past 90 days by Timeline Follow-Back calendar, recent craving on the Penn Alcohol Craving Scale (PACS), situations at the risk of drinking on the Inventory of Drug-Taking Situation, recent depression severity on the Patient Health Questionnaire 9 (PHQ-9), and recent anxiety severity on the Generalized Anxiety Disorder 7 scale.

Plasma sex-related hormone and protein measurements were taken at baseline — after detoxification but before treatment. These included total testosterone, estradiol, estrone, progesterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), sex hormone–binding globulin (SHBG), and albumin.

“The important thing is that these measurements were taken during sobriety,” said Dr. Karpyak. Study participants were already in residential treatment programs, and the average time since their last drink was approximately 3 weeks. Relapse was defined as any alcohol consumption during the first 3 months.
 

What Works for Men May Not Work for Women

Results showed that men with symptoms of depression and a higher craving for alcohol, as shown on baseline PHQ-9 and PACS scores, had lower baseline levels of testosterone, estrone, estradiol, and SHBG than those without these symptoms (P = .0102 and P = .0014, respectively).

In addition, a combination of higher progesterone and lower albumin was associated with a lower risk for relapse during the first 3 months (odds ratio [OR], 0.518; P = .0079).

In women, a combination of lower estrone and estradiol and higher FSH and LH levels was associated with higher maximum number of drinks per day (P = .035).

In addition, women who were more likely to relapse during the first 3 months of treatment had higher baseline levels of testosterone, SHBG, and albumin than those at lower relapse risk (OR, 4.536; P = .0057).

Dr. Karpyak noted that these “hormone signatures” were associative and not predictive.

What this means, he said, “is that if you are treating a man and a woman for alcoholism, you are dealing with different biochemical and psychological starting points. This implies that what works for a man may not work for a woman, and vice versa.”
 

Toward Gender Equity

The findings may eventually lead to a way to predict treatment responses in patients with AUD, Dr. Karpyak added, but cautioned that despite statistical significance, these are preliminary findings.

Before these results can be integrated into clinical practice, they need to be replicated. Dr. Karpyak emphasized the need for follow-up research that builds on these findings, using them as preliminary data to determine whether prediction holds real significance.

“Given that many of these differences are related to sex hormones, we particularly want to see how the dramatic hormonal change women experience during the menstrual cycle and at menopause may affect the biochemistry of alcoholism and guide treatment efforts,” he said.

In a statement, Erika Comasco, PhD, associate professor in molecular psychiatry, Uppsala University, Sweden, said the research “is an important step forward to gender equity in medicine.”

“The findings provide an important first insight into the relationship between sex hormones and alcohol use disorder treatment,” she explained. “While sex differences in the way the disorder manifests itself are known, these results suggest that sex hormones may modulate treatment response, potentially supporting sex-specific pharmacological intervention.”

Dr. Comasco shares Dr. Karpyak’s view that hormonal fluctuations linked to the menstrual cycle may influence alcohol misuse and believes more research is needed to explore their impact on treatment and relapse outcomes in female patients.

This study was funded by the National Institute on Alcohol Abuse and Alcoholism (National Institutes of Health) and the Samuel C. Johnson Genomics of Addiction Program at Mayo Clinic. Dr. Karpyak and Dr. Comasco reported no relevant disclosures.
 

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

MILAN — Specific combinations of hormonal and biochemical factors were associated with different clinical characteristics and treatment outcomes of alcohol use disorder (AUD) between men and women.

“These hormones and proteins are known to have an influence on behavior, and indeed we see an association between different levels of these compounds and different behavioral aspects of [AUD], although we can’t for sure say that one directly causes another,” said lead researcher Victor M. Karpyak, MD, PhD, professor of psychiatry at the Mayo Clinic, in a release.

The findings were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress.
 

Sex Hormone Signatures

Previous research has highlighted differences in symptoms including cravings, withdrawal, consumption patterns, depression, and anxiety between men and women with AUD, said Dr. Karpyak. Differences in hormones and biochemicals have also been observed between individuals with and without AUD.

However, specific biochemical and hormonal “signatures” associated with male and female responses to treatment have thus far not been explored, he told this news organization.

The study included 400 treatment-seeking individuals (132 women and 268 men; mean age, 41.8 years; 93% White) who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for AUD and were enrolled in a clinical trial of acamprosate.

Baseline assessment included psychiatric comorbidities and substance use with the Psychiatric Research Interview for Substance and Mental Disorders, alcohol consumption pattern over the past 90 days by Timeline Follow-Back calendar, recent craving on the Penn Alcohol Craving Scale (PACS), situations at the risk of drinking on the Inventory of Drug-Taking Situation, recent depression severity on the Patient Health Questionnaire 9 (PHQ-9), and recent anxiety severity on the Generalized Anxiety Disorder 7 scale.

Plasma sex-related hormone and protein measurements were taken at baseline — after detoxification but before treatment. These included total testosterone, estradiol, estrone, progesterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), sex hormone–binding globulin (SHBG), and albumin.

“The important thing is that these measurements were taken during sobriety,” said Dr. Karpyak. Study participants were already in residential treatment programs, and the average time since their last drink was approximately 3 weeks. Relapse was defined as any alcohol consumption during the first 3 months.
 

What Works for Men May Not Work for Women

Results showed that men with symptoms of depression and a higher craving for alcohol, as shown on baseline PHQ-9 and PACS scores, had lower baseline levels of testosterone, estrone, estradiol, and SHBG than those without these symptoms (P = .0102 and P = .0014, respectively).

In addition, a combination of higher progesterone and lower albumin was associated with a lower risk for relapse during the first 3 months (odds ratio [OR], 0.518; P = .0079).

In women, a combination of lower estrone and estradiol and higher FSH and LH levels was associated with higher maximum number of drinks per day (P = .035).

In addition, women who were more likely to relapse during the first 3 months of treatment had higher baseline levels of testosterone, SHBG, and albumin than those at lower relapse risk (OR, 4.536; P = .0057).

Dr. Karpyak noted that these “hormone signatures” were associative and not predictive.

What this means, he said, “is that if you are treating a man and a woman for alcoholism, you are dealing with different biochemical and psychological starting points. This implies that what works for a man may not work for a woman, and vice versa.”
 

Toward Gender Equity

The findings may eventually lead to a way to predict treatment responses in patients with AUD, Dr. Karpyak added, but cautioned that despite statistical significance, these are preliminary findings.

Before these results can be integrated into clinical practice, they need to be replicated. Dr. Karpyak emphasized the need for follow-up research that builds on these findings, using them as preliminary data to determine whether prediction holds real significance.

“Given that many of these differences are related to sex hormones, we particularly want to see how the dramatic hormonal change women experience during the menstrual cycle and at menopause may affect the biochemistry of alcoholism and guide treatment efforts,” he said.

In a statement, Erika Comasco, PhD, associate professor in molecular psychiatry, Uppsala University, Sweden, said the research “is an important step forward to gender equity in medicine.”

“The findings provide an important first insight into the relationship between sex hormones and alcohol use disorder treatment,” she explained. “While sex differences in the way the disorder manifests itself are known, these results suggest that sex hormones may modulate treatment response, potentially supporting sex-specific pharmacological intervention.”

Dr. Comasco shares Dr. Karpyak’s view that hormonal fluctuations linked to the menstrual cycle may influence alcohol misuse and believes more research is needed to explore their impact on treatment and relapse outcomes in female patients.

This study was funded by the National Institute on Alcohol Abuse and Alcoholism (National Institutes of Health) and the Samuel C. Johnson Genomics of Addiction Program at Mayo Clinic. Dr. Karpyak and Dr. Comasco reported no relevant disclosures.
 

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

Ferritin is the parameter most often used in primary care to diagnose iron deficiency. The cutoff value of ferritin can affect the number of cases diagnosed, however. A study published in JAMA Network Open  investigated how different cutoff values affect the diagnosis of iron deficiency.

The study, which included 255,351 adult primary care patients in Switzerland, showed that ferritin cutoff values of 15, 30, and 45 ng/mL were associated with incidences of iron deficiency diagnoses of 10.9, 29.9, and 48.3 cases per 1000 patient-years, respectively. In other words, as the cutoff value increases, the frequency of diagnosis also increases.

“It is a study to take into account, especially because of the number of patients it includes, and it can guide primary care clinical practice. As expected, as the cutoff point increases with respect to ferritin values, the incidence percentages of both iron deficiency and iron-deficiency anemia also increase,” Miguel Turégano-Yedro, MD, a family physician at the Casar de Cáceres Health Center in Spain, and coordinator of the Hematology Working Group of the Spanish Society of Primary Care Physicians, told this news organization. Ferritin is the most sensitive parameter for diagnosing iron deficiency and iron-deficiency anemia, he added. “When it is necessary to supplement a patient with iron, other parameters are taken into account, such as hemoglobin, to see if there is anemia.”
 

Ferritin Level

The ferritin level associated with iron deficiency in primary care is usually 15 ng/mL, said Dr. Turégano-Yedro. “If we assess patients with a ferritin level of 15 or less than 15, then we know that many cases will be symptomatic (with fatigue, tiredness, or lack of appetite) and, therefore, will need iron treatment. But if the ferritin cutoff value is increased to 30 ng/mL or 45 ng/mL, the incidence will be higher, although in many cases they will be asymptomatic and iron supplementation will not be necessary.”

He also pointed out that he does not consider it necessary to raise the cutoff to 45 ng/mL; however, “establishing the cutoff at 30 ng/mL, in a certain population at risk of iron deficiency or iron-deficiency anemia, may be interesting, for example in women of childbearing age, women with very heavy menstruation, children, frail elderly, people with gastrointestinal bleeding, or those who engage in physical exercise.”

Iron deficiency must be distinguished from anemia. “If the ferritin is below 15 ng/mL, there is iron deficiency, which may or may not be accompanied by symptoms, although usually most patients will have symptoms. Normally, to diagnose a patient with iron-deficiency anemia, on the one hand, they must have low hemoglobin, which indicates anemia, and on the other hand, low ferritin, which indicates iron deficiency.” Taking these parameters into account, the study does have a weakness. “It is striking that a percentage of patients in the study requested ferritin analysis without including hemoglobin, when hemoglobin is part of the basic analysis performed in Spain,” said Dr. Turégano-Yedro.
 

When to Supplement

The study highlights the incidence of nonanemic iron deficiency diagnoses associated with the choice of ferritin cutoff value. However, as Dr. Turégano-Yedro explained, the percentage of patients who have iron deficiency but do not have anemia is not very relevant. “In the case of family physicians in Spain, it is not usually taken into account, because if a patient has iron deficiency with or without anemia and is symptomatic, they should be given iron supplements.”

What if they do not have a deficiency but do have anemia? “In principle, iron supplementation is not necessary, because that anemia may be due to chronic disorders or it may be hemolytic anemia, so the case should be studied,” Dr. Turégano-Yedro concluded.

This story was translated from Univadis Spain, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Ferritin is the parameter most often used in primary care to diagnose iron deficiency. The cutoff value of ferritin can affect the number of cases diagnosed, however. A study published in JAMA Network Open  investigated how different cutoff values affect the diagnosis of iron deficiency.

The study, which included 255,351 adult primary care patients in Switzerland, showed that ferritin cutoff values of 15, 30, and 45 ng/mL were associated with incidences of iron deficiency diagnoses of 10.9, 29.9, and 48.3 cases per 1000 patient-years, respectively. In other words, as the cutoff value increases, the frequency of diagnosis also increases.

“It is a study to take into account, especially because of the number of patients it includes, and it can guide primary care clinical practice. As expected, as the cutoff point increases with respect to ferritin values, the incidence percentages of both iron deficiency and iron-deficiency anemia also increase,” Miguel Turégano-Yedro, MD, a family physician at the Casar de Cáceres Health Center in Spain, and coordinator of the Hematology Working Group of the Spanish Society of Primary Care Physicians, told this news organization. Ferritin is the most sensitive parameter for diagnosing iron deficiency and iron-deficiency anemia, he added. “When it is necessary to supplement a patient with iron, other parameters are taken into account, such as hemoglobin, to see if there is anemia.”
 

Ferritin Level

The ferritin level associated with iron deficiency in primary care is usually 15 ng/mL, said Dr. Turégano-Yedro. “If we assess patients with a ferritin level of 15 or less than 15, then we know that many cases will be symptomatic (with fatigue, tiredness, or lack of appetite) and, therefore, will need iron treatment. But if the ferritin cutoff value is increased to 30 ng/mL or 45 ng/mL, the incidence will be higher, although in many cases they will be asymptomatic and iron supplementation will not be necessary.”

He also pointed out that he does not consider it necessary to raise the cutoff to 45 ng/mL; however, “establishing the cutoff at 30 ng/mL, in a certain population at risk of iron deficiency or iron-deficiency anemia, may be interesting, for example in women of childbearing age, women with very heavy menstruation, children, frail elderly, people with gastrointestinal bleeding, or those who engage in physical exercise.”

Iron deficiency must be distinguished from anemia. “If the ferritin is below 15 ng/mL, there is iron deficiency, which may or may not be accompanied by symptoms, although usually most patients will have symptoms. Normally, to diagnose a patient with iron-deficiency anemia, on the one hand, they must have low hemoglobin, which indicates anemia, and on the other hand, low ferritin, which indicates iron deficiency.” Taking these parameters into account, the study does have a weakness. “It is striking that a percentage of patients in the study requested ferritin analysis without including hemoglobin, when hemoglobin is part of the basic analysis performed in Spain,” said Dr. Turégano-Yedro.
 

When to Supplement

The study highlights the incidence of nonanemic iron deficiency diagnoses associated with the choice of ferritin cutoff value. However, as Dr. Turégano-Yedro explained, the percentage of patients who have iron deficiency but do not have anemia is not very relevant. “In the case of family physicians in Spain, it is not usually taken into account, because if a patient has iron deficiency with or without anemia and is symptomatic, they should be given iron supplements.”

What if they do not have a deficiency but do have anemia? “In principle, iron supplementation is not necessary, because that anemia may be due to chronic disorders or it may be hemolytic anemia, so the case should be studied,” Dr. Turégano-Yedro concluded.

This story was translated from Univadis Spain, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Ferritin is the parameter most often used in primary care to diagnose iron deficiency. The cutoff value of ferritin can affect the number of cases diagnosed, however. A study published in JAMA Network Open  investigated how different cutoff values affect the diagnosis of iron deficiency.

The study, which included 255,351 adult primary care patients in Switzerland, showed that ferritin cutoff values of 15, 30, and 45 ng/mL were associated with incidences of iron deficiency diagnoses of 10.9, 29.9, and 48.3 cases per 1000 patient-years, respectively. In other words, as the cutoff value increases, the frequency of diagnosis also increases.

“It is a study to take into account, especially because of the number of patients it includes, and it can guide primary care clinical practice. As expected, as the cutoff point increases with respect to ferritin values, the incidence percentages of both iron deficiency and iron-deficiency anemia also increase,” Miguel Turégano-Yedro, MD, a family physician at the Casar de Cáceres Health Center in Spain, and coordinator of the Hematology Working Group of the Spanish Society of Primary Care Physicians, told this news organization. Ferritin is the most sensitive parameter for diagnosing iron deficiency and iron-deficiency anemia, he added. “When it is necessary to supplement a patient with iron, other parameters are taken into account, such as hemoglobin, to see if there is anemia.”
 

Ferritin Level

The ferritin level associated with iron deficiency in primary care is usually 15 ng/mL, said Dr. Turégano-Yedro. “If we assess patients with a ferritin level of 15 or less than 15, then we know that many cases will be symptomatic (with fatigue, tiredness, or lack of appetite) and, therefore, will need iron treatment. But if the ferritin cutoff value is increased to 30 ng/mL or 45 ng/mL, the incidence will be higher, although in many cases they will be asymptomatic and iron supplementation will not be necessary.”

He also pointed out that he does not consider it necessary to raise the cutoff to 45 ng/mL; however, “establishing the cutoff at 30 ng/mL, in a certain population at risk of iron deficiency or iron-deficiency anemia, may be interesting, for example in women of childbearing age, women with very heavy menstruation, children, frail elderly, people with gastrointestinal bleeding, or those who engage in physical exercise.”

Iron deficiency must be distinguished from anemia. “If the ferritin is below 15 ng/mL, there is iron deficiency, which may or may not be accompanied by symptoms, although usually most patients will have symptoms. Normally, to diagnose a patient with iron-deficiency anemia, on the one hand, they must have low hemoglobin, which indicates anemia, and on the other hand, low ferritin, which indicates iron deficiency.” Taking these parameters into account, the study does have a weakness. “It is striking that a percentage of patients in the study requested ferritin analysis without including hemoglobin, when hemoglobin is part of the basic analysis performed in Spain,” said Dr. Turégano-Yedro.
 

When to Supplement

The study highlights the incidence of nonanemic iron deficiency diagnoses associated with the choice of ferritin cutoff value. However, as Dr. Turégano-Yedro explained, the percentage of patients who have iron deficiency but do not have anemia is not very relevant. “In the case of family physicians in Spain, it is not usually taken into account, because if a patient has iron deficiency with or without anemia and is symptomatic, they should be given iron supplements.”

What if they do not have a deficiency but do have anemia? “In principle, iron supplementation is not necessary, because that anemia may be due to chronic disorders or it may be hemolytic anemia, so the case should be studied,” Dr. Turégano-Yedro concluded.

This story was translated from Univadis Spain, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

A noninvasive eye test could help people with Sjögren disease — a disorder that can go undiagnosed for years — get relief sooner, suggested a pilot study published in Therapeutic Advances in Musculoskeletal Disease.

Researchers led by Jing Wu, Department of Ophthalmology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and colleagues used infrared imaging to detect atrophy of the oil-producing meibomian glands, which lubricate the eyelids and eyes, in 56 patients with suspected Sjögren disease. The test can be administered by an eye care practitioner using a Keratograph 5M machine. Patients also underwent salivary gland biopsies to detect Sjögren disease.

A total of 34 patients diagnosed with primary Sjögren disease had more significant atrophy and shortening of the meibomian glands in their upper eyelids than 22 patients with other types of dry eye who served as control patients. The accuracy of temporal and total meibomian gland dysfunction dropout rates in the upper eyelids to predict primary Sjögren disease classification was good, with an area under the curve of 0.94 and 0.91, respectively.

“Sjögren’s-related dry eye is definitely inflammatory,” said Esen Akpek, MD, director of the Ocular Surface Disease and Dry Eye Clinic at Johns Hopkins Medicine, Baltimore, who was not involved with the study. “It starts as inflammation, and then the inflammation spreads to the meibomian glands, to the conjunctiva, cornea, and there will be other findings, like corneal ulcers, corneal melts, cyclitis, retinitis, optic neuritis, uveitis, all these inflammatory diseases of the eye could happen with Sjögren’s.”

With other types of dry eye, such as blepharitis or even meibomian gland dysfunction without Sjögren disease, inflammation is usually confined to the ocular surface, Akpek said. As a result, symptoms tend to be less severe and progressive.

The results of this small study need validation in a larger cohort, said Steven Carsons, MD, chief of the Division of Rheumatology at NYU Langone Hospital–Long Island, who was not involved with the study. In general, however, noninvasive alternatives to today’s tests for Sjögren disease could be useful for patients and physicians.

“The definitive diagnosis is a minor salivary glandular biopsy, which is invasive and isn’t really appealing to a lot of patients,” Dr. Carsons said. This test can also be difficult to access if patients don’t live near a medical center that specializes in Sjögren disease, he said.

“I think it’s everybody’s goal to have a noninvasive test be able, at some point, to replace biopsy,” Dr. Carsons said.

Then there are blood tests. “The other more objective test, the SSA antibodies, are not very specific for Sjögren’s syndrome,” he said. “They’re fairly sensitive, but can also be seen in other autoimmune conditions, particularly lupus.”

With existing tools, however, optometrists and ophthalmologists can do more to diagnose Sjögren disease early, Dr. Akpek said.

“The issue with Sjögren’s is not that there are no earlier diagnostic aids or anything like that,” Dr. Akpek said.

Lissamine green, a dye that stains degraded cells on the eye’s surface, can reveal clues in young adult patients before other signs. “In my opinion, the earliest clinical finding that indicates presence of the disease is lissamine green staining of conjunctiva,” Akpek said.

Meibomian gland imaging would detect the disease at a later point. “By the time you get meibomian gland dysfunction, there has been longer-standing inflammation,” she said.

Two challenges hold back diagnoses, she said. One is that many practitioners mistakenly believe Sjögren disease is just a nuisance even though it can threaten vision through ocular complications and have more far-reaching effects, too.

“There are a lot of extraglandular systemic manifestations of Sjögren’s that cause morbidity in these patients,” Dr. Akpek said. For example, Sjögren disease is associated with lymphoma and other malignancies, interstitial nephritis, autoimmune hepatitis, and interstitial lung disease with fibrosis.

The second challenge, she said, is that many ophthalmologists and optometrists assume rheumatologists will make the Sjögren disease diagnosis first and then refer patients to them. But eye doctors are well positioned to spot the first signs — if they look for them.

“When you complain of dry eye, unless the doctor puts certain dyes and takes a look at the surface with the dye staining, they can’t see that you are dry,” Dr. Akpek said.

Unfortunately, these tests are underutilized. “I’m sorry to say, dry eye testing, like clinical testing, is not very commonly done,” she said. “Dry eye is managed according to patient symptoms. A lot of the time, Sjögren’s patients have such severe dry eye that they don’t complain of dryness anymore because their corneas become numb.”

Another way to prevent diagnostic delay is to collaborate, communicate, and carefully review patient records shared by other specialists.

“Particularly because of the wide involvement of different organ systems, such as the eyes, the mouth with dental problems, and then systemic features, including joints, it really does need the cooperation of ophthalmologists, dental specialists, and rheumatologists — immunologists sometimes — to come together and make this diagnosis,” Dr. Carsons said.

The study was supported by grants from the National Natural Science Foundation of China. The authors had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

A noninvasive eye test could help people with Sjögren disease — a disorder that can go undiagnosed for years — get relief sooner, suggested a pilot study published in Therapeutic Advances in Musculoskeletal Disease.

Researchers led by Jing Wu, Department of Ophthalmology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and colleagues used infrared imaging to detect atrophy of the oil-producing meibomian glands, which lubricate the eyelids and eyes, in 56 patients with suspected Sjögren disease. The test can be administered by an eye care practitioner using a Keratograph 5M machine. Patients also underwent salivary gland biopsies to detect Sjögren disease.

A total of 34 patients diagnosed with primary Sjögren disease had more significant atrophy and shortening of the meibomian glands in their upper eyelids than 22 patients with other types of dry eye who served as control patients. The accuracy of temporal and total meibomian gland dysfunction dropout rates in the upper eyelids to predict primary Sjögren disease classification was good, with an area under the curve of 0.94 and 0.91, respectively.

“Sjögren’s-related dry eye is definitely inflammatory,” said Esen Akpek, MD, director of the Ocular Surface Disease and Dry Eye Clinic at Johns Hopkins Medicine, Baltimore, who was not involved with the study. “It starts as inflammation, and then the inflammation spreads to the meibomian glands, to the conjunctiva, cornea, and there will be other findings, like corneal ulcers, corneal melts, cyclitis, retinitis, optic neuritis, uveitis, all these inflammatory diseases of the eye could happen with Sjögren’s.”

With other types of dry eye, such as blepharitis or even meibomian gland dysfunction without Sjögren disease, inflammation is usually confined to the ocular surface, Akpek said. As a result, symptoms tend to be less severe and progressive.

The results of this small study need validation in a larger cohort, said Steven Carsons, MD, chief of the Division of Rheumatology at NYU Langone Hospital–Long Island, who was not involved with the study. In general, however, noninvasive alternatives to today’s tests for Sjögren disease could be useful for patients and physicians.

“The definitive diagnosis is a minor salivary glandular biopsy, which is invasive and isn’t really appealing to a lot of patients,” Dr. Carsons said. This test can also be difficult to access if patients don’t live near a medical center that specializes in Sjögren disease, he said.

“I think it’s everybody’s goal to have a noninvasive test be able, at some point, to replace biopsy,” Dr. Carsons said.

Then there are blood tests. “The other more objective test, the SSA antibodies, are not very specific for Sjögren’s syndrome,” he said. “They’re fairly sensitive, but can also be seen in other autoimmune conditions, particularly lupus.”

With existing tools, however, optometrists and ophthalmologists can do more to diagnose Sjögren disease early, Dr. Akpek said.

“The issue with Sjögren’s is not that there are no earlier diagnostic aids or anything like that,” Dr. Akpek said.

Lissamine green, a dye that stains degraded cells on the eye’s surface, can reveal clues in young adult patients before other signs. “In my opinion, the earliest clinical finding that indicates presence of the disease is lissamine green staining of conjunctiva,” Akpek said.

Meibomian gland imaging would detect the disease at a later point. “By the time you get meibomian gland dysfunction, there has been longer-standing inflammation,” she said.

Two challenges hold back diagnoses, she said. One is that many practitioners mistakenly believe Sjögren disease is just a nuisance even though it can threaten vision through ocular complications and have more far-reaching effects, too.

“There are a lot of extraglandular systemic manifestations of Sjögren’s that cause morbidity in these patients,” Dr. Akpek said. For example, Sjögren disease is associated with lymphoma and other malignancies, interstitial nephritis, autoimmune hepatitis, and interstitial lung disease with fibrosis.

The second challenge, she said, is that many ophthalmologists and optometrists assume rheumatologists will make the Sjögren disease diagnosis first and then refer patients to them. But eye doctors are well positioned to spot the first signs — if they look for them.

“When you complain of dry eye, unless the doctor puts certain dyes and takes a look at the surface with the dye staining, they can’t see that you are dry,” Dr. Akpek said.

Unfortunately, these tests are underutilized. “I’m sorry to say, dry eye testing, like clinical testing, is not very commonly done,” she said. “Dry eye is managed according to patient symptoms. A lot of the time, Sjögren’s patients have such severe dry eye that they don’t complain of dryness anymore because their corneas become numb.”

Another way to prevent diagnostic delay is to collaborate, communicate, and carefully review patient records shared by other specialists.

“Particularly because of the wide involvement of different organ systems, such as the eyes, the mouth with dental problems, and then systemic features, including joints, it really does need the cooperation of ophthalmologists, dental specialists, and rheumatologists — immunologists sometimes — to come together and make this diagnosis,” Dr. Carsons said.

The study was supported by grants from the National Natural Science Foundation of China. The authors had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

A noninvasive eye test could help people with Sjögren disease — a disorder that can go undiagnosed for years — get relief sooner, suggested a pilot study published in Therapeutic Advances in Musculoskeletal Disease.

Researchers led by Jing Wu, Department of Ophthalmology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and colleagues used infrared imaging to detect atrophy of the oil-producing meibomian glands, which lubricate the eyelids and eyes, in 56 patients with suspected Sjögren disease. The test can be administered by an eye care practitioner using a Keratograph 5M machine. Patients also underwent salivary gland biopsies to detect Sjögren disease.

A total of 34 patients diagnosed with primary Sjögren disease had more significant atrophy and shortening of the meibomian glands in their upper eyelids than 22 patients with other types of dry eye who served as control patients. The accuracy of temporal and total meibomian gland dysfunction dropout rates in the upper eyelids to predict primary Sjögren disease classification was good, with an area under the curve of 0.94 and 0.91, respectively.

“Sjögren’s-related dry eye is definitely inflammatory,” said Esen Akpek, MD, director of the Ocular Surface Disease and Dry Eye Clinic at Johns Hopkins Medicine, Baltimore, who was not involved with the study. “It starts as inflammation, and then the inflammation spreads to the meibomian glands, to the conjunctiva, cornea, and there will be other findings, like corneal ulcers, corneal melts, cyclitis, retinitis, optic neuritis, uveitis, all these inflammatory diseases of the eye could happen with Sjögren’s.”

With other types of dry eye, such as blepharitis or even meibomian gland dysfunction without Sjögren disease, inflammation is usually confined to the ocular surface, Akpek said. As a result, symptoms tend to be less severe and progressive.

The results of this small study need validation in a larger cohort, said Steven Carsons, MD, chief of the Division of Rheumatology at NYU Langone Hospital–Long Island, who was not involved with the study. In general, however, noninvasive alternatives to today’s tests for Sjögren disease could be useful for patients and physicians.

“The definitive diagnosis is a minor salivary glandular biopsy, which is invasive and isn’t really appealing to a lot of patients,” Dr. Carsons said. This test can also be difficult to access if patients don’t live near a medical center that specializes in Sjögren disease, he said.

“I think it’s everybody’s goal to have a noninvasive test be able, at some point, to replace biopsy,” Dr. Carsons said.

Then there are blood tests. “The other more objective test, the SSA antibodies, are not very specific for Sjögren’s syndrome,” he said. “They’re fairly sensitive, but can also be seen in other autoimmune conditions, particularly lupus.”

With existing tools, however, optometrists and ophthalmologists can do more to diagnose Sjögren disease early, Dr. Akpek said.

“The issue with Sjögren’s is not that there are no earlier diagnostic aids or anything like that,” Dr. Akpek said.

Lissamine green, a dye that stains degraded cells on the eye’s surface, can reveal clues in young adult patients before other signs. “In my opinion, the earliest clinical finding that indicates presence of the disease is lissamine green staining of conjunctiva,” Akpek said.

Meibomian gland imaging would detect the disease at a later point. “By the time you get meibomian gland dysfunction, there has been longer-standing inflammation,” she said.

Two challenges hold back diagnoses, she said. One is that many practitioners mistakenly believe Sjögren disease is just a nuisance even though it can threaten vision through ocular complications and have more far-reaching effects, too.

“There are a lot of extraglandular systemic manifestations of Sjögren’s that cause morbidity in these patients,” Dr. Akpek said. For example, Sjögren disease is associated with lymphoma and other malignancies, interstitial nephritis, autoimmune hepatitis, and interstitial lung disease with fibrosis.

The second challenge, she said, is that many ophthalmologists and optometrists assume rheumatologists will make the Sjögren disease diagnosis first and then refer patients to them. But eye doctors are well positioned to spot the first signs — if they look for them.

“When you complain of dry eye, unless the doctor puts certain dyes and takes a look at the surface with the dye staining, they can’t see that you are dry,” Dr. Akpek said.

Unfortunately, these tests are underutilized. “I’m sorry to say, dry eye testing, like clinical testing, is not very commonly done,” she said. “Dry eye is managed according to patient symptoms. A lot of the time, Sjögren’s patients have such severe dry eye that they don’t complain of dryness anymore because their corneas become numb.”

Another way to prevent diagnostic delay is to collaborate, communicate, and carefully review patient records shared by other specialists.

“Particularly because of the wide involvement of different organ systems, such as the eyes, the mouth with dental problems, and then systemic features, including joints, it really does need the cooperation of ophthalmologists, dental specialists, and rheumatologists — immunologists sometimes — to come together and make this diagnosis,” Dr. Carsons said.

The study was supported by grants from the National Natural Science Foundation of China. The authors had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Short-term mortality, hospitalizations, and cardiovascular disease (CVD) events are not significantly different between patients diagnosed with chronic kidney disease (CKD) during routine medical care and those through screening, in a study that found older age, being male, and having a diagnosis of heart failure are associated with an increased risk for mortality in patients with CKD.

METHODOLOGY:

• Researchers conducted a prospective cohort study involving 892 primary care patients aged 60 years or older with CKD from the Oxford Renal Cohort Study in England.
• Participants were categorized into those with existing CKD (n = 257; median age, 75 years), screen-detected CKD (n = 185; median age, roughly 73 years), or temporary reduction in kidney function (n = 450; median age, roughly 73 years).
• The primary outcome was a composite of all-cause mortality, hospitalization, CVD, or end-stage kidney disease.
• The secondary outcomes were the individual components of the composite primary outcome and factors associated with mortality in those with CKD.

TAKEAWAY:

• The composite outcomes were not significantly different between patients with preexisting CKD and kidney disease identified during screening (adjusted hazard ratio [aHR], 0.94; 95% CI, 0.67-1.33).
• Risks for death, hospitalization, CVD, or end-stage kidney disease were not significantly different between the two groups.
• Older age (aHR per year, 1.10; 95% CI, 1.06-1.15), male sex (aHR, 2.31; 95% CI, 1.26-4.24), and heart failure (aHR, 5.18; 95% CI, 2.45-10.97) were associated with higher risks for death.
• No cases of end-stage kidney disease were reported during the study period.

IN PRACTICE:

“Our findings show that the risk of short-term mortality, hospitalization, and CVD is comparable in people diagnosed through screening to those diagnosed routinely in primary care. This suggests that screening older people for CKD may be of value to increase detection and enable disease-modifying treatment to be initiated at an earlier stage,” the study authors wrote.

SOURCE:

The study was led by Anna K. Forbes, MBChB, and José M. Ordóñez-Mena, PhD, of the Nuffield Department of Primary Care Health Sciences at the University of Oxford, England. It was published online in BJGP Open.

LIMITATIONS:

The study had a relatively short follow-up period and a cohort primarily consisting of individuals with early-stage CKD, which may have limited the identification of end-stage cases of the condition. The study population predominantly consisted of White individuals, affecting the generalizability of the results to more diverse populations. Misclassification bias may have occurred due to changes in the kidney function over time.

DISCLOSURES:

The data linkage provided by NHS Digital was supported by funding from the NIHR School of Primary Care Research. Some authors were partly supported by the NIHR Oxford Biomedical Research Centre and NIHR Oxford Thames Valley Applied Research Collaborative. One author reported receiving financial support for attending a conference, while another received consulting fees from various pharmaceutical companies. Another author reported receiving a grant from the Wellcome Trust and payment while working as a presenter for NB Medical and is an unpaid trustee of some charities.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Short-term mortality, hospitalizations, and cardiovascular disease (CVD) events are not significantly different between patients diagnosed with chronic kidney disease (CKD) during routine medical care and those through screening, in a study that found older age, being male, and having a diagnosis of heart failure are associated with an increased risk for mortality in patients with CKD.

METHODOLOGY:

• Researchers conducted a prospective cohort study involving 892 primary care patients aged 60 years or older with CKD from the Oxford Renal Cohort Study in England.
• Participants were categorized into those with existing CKD (n = 257; median age, 75 years), screen-detected CKD (n = 185; median age, roughly 73 years), or temporary reduction in kidney function (n = 450; median age, roughly 73 years).
• The primary outcome was a composite of all-cause mortality, hospitalization, CVD, or end-stage kidney disease.
• The secondary outcomes were the individual components of the composite primary outcome and factors associated with mortality in those with CKD.

TAKEAWAY:

• The composite outcomes were not significantly different between patients with preexisting CKD and kidney disease identified during screening (adjusted hazard ratio [aHR], 0.94; 95% CI, 0.67-1.33).
• Risks for death, hospitalization, CVD, or end-stage kidney disease were not significantly different between the two groups.
• Older age (aHR per year, 1.10; 95% CI, 1.06-1.15), male sex (aHR, 2.31; 95% CI, 1.26-4.24), and heart failure (aHR, 5.18; 95% CI, 2.45-10.97) were associated with higher risks for death.
• No cases of end-stage kidney disease were reported during the study period.

IN PRACTICE:

“Our findings show that the risk of short-term mortality, hospitalization, and CVD is comparable in people diagnosed through screening to those diagnosed routinely in primary care. This suggests that screening older people for CKD may be of value to increase detection and enable disease-modifying treatment to be initiated at an earlier stage,” the study authors wrote.

SOURCE:

The study was led by Anna K. Forbes, MBChB, and José M. Ordóñez-Mena, PhD, of the Nuffield Department of Primary Care Health Sciences at the University of Oxford, England. It was published online in BJGP Open.

LIMITATIONS:

The study had a relatively short follow-up period and a cohort primarily consisting of individuals with early-stage CKD, which may have limited the identification of end-stage cases of the condition. The study population predominantly consisted of White individuals, affecting the generalizability of the results to more diverse populations. Misclassification bias may have occurred due to changes in the kidney function over time.

DISCLOSURES:

The data linkage provided by NHS Digital was supported by funding from the NIHR School of Primary Care Research. Some authors were partly supported by the NIHR Oxford Biomedical Research Centre and NIHR Oxford Thames Valley Applied Research Collaborative. One author reported receiving financial support for attending a conference, while another received consulting fees from various pharmaceutical companies. Another author reported receiving a grant from the Wellcome Trust and payment while working as a presenter for NB Medical and is an unpaid trustee of some charities.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Short-term mortality, hospitalizations, and cardiovascular disease (CVD) events are not significantly different between patients diagnosed with chronic kidney disease (CKD) during routine medical care and those through screening, in a study that found older age, being male, and having a diagnosis of heart failure are associated with an increased risk for mortality in patients with CKD.

METHODOLOGY:

• Researchers conducted a prospective cohort study involving 892 primary care patients aged 60 years or older with CKD from the Oxford Renal Cohort Study in England.
• Participants were categorized into those with existing CKD (n = 257; median age, 75 years), screen-detected CKD (n = 185; median age, roughly 73 years), or temporary reduction in kidney function (n = 450; median age, roughly 73 years).
• The primary outcome was a composite of all-cause mortality, hospitalization, CVD, or end-stage kidney disease.
• The secondary outcomes were the individual components of the composite primary outcome and factors associated with mortality in those with CKD.

TAKEAWAY:

• The composite outcomes were not significantly different between patients with preexisting CKD and kidney disease identified during screening (adjusted hazard ratio [aHR], 0.94; 95% CI, 0.67-1.33).
• Risks for death, hospitalization, CVD, or end-stage kidney disease were not significantly different between the two groups.
• Older age (aHR per year, 1.10; 95% CI, 1.06-1.15), male sex (aHR, 2.31; 95% CI, 1.26-4.24), and heart failure (aHR, 5.18; 95% CI, 2.45-10.97) were associated with higher risks for death.
• No cases of end-stage kidney disease were reported during the study period.

IN PRACTICE:

“Our findings show that the risk of short-term mortality, hospitalization, and CVD is comparable in people diagnosed through screening to those diagnosed routinely in primary care. This suggests that screening older people for CKD may be of value to increase detection and enable disease-modifying treatment to be initiated at an earlier stage,” the study authors wrote.

SOURCE:

The study was led by Anna K. Forbes, MBChB, and José M. Ordóñez-Mena, PhD, of the Nuffield Department of Primary Care Health Sciences at the University of Oxford, England. It was published online in BJGP Open.

LIMITATIONS:

The study had a relatively short follow-up period and a cohort primarily consisting of individuals with early-stage CKD, which may have limited the identification of end-stage cases of the condition. The study population predominantly consisted of White individuals, affecting the generalizability of the results to more diverse populations. Misclassification bias may have occurred due to changes in the kidney function over time.

DISCLOSURES:

The data linkage provided by NHS Digital was supported by funding from the NIHR School of Primary Care Research. Some authors were partly supported by the NIHR Oxford Biomedical Research Centre and NIHR Oxford Thames Valley Applied Research Collaborative. One author reported receiving financial support for attending a conference, while another received consulting fees from various pharmaceutical companies. Another author reported receiving a grant from the Wellcome Trust and payment while working as a presenter for NB Medical and is an unpaid trustee of some charities.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Diabetes is associated with a lower incidence of uterine fibroids in midlife women receiving diabetes treatment, especially metformin. The association between diabetes and the risk for uterine fibroids may vary based on menopausal status.

METHODOLOGY:

• Previous studies have provided inconsistent evidence regarding associations between the risk for uterine fibroids and markers of cardiometabolic health, such as fasting insulin, fasting glucose, and diabetes.
• Researchers conducted a prospective cohort study to examine the association of fasting levels of cardiometabolic blood biomarkers, diabetes, and diabetes treatment with the incidence of new fibroid diagnoses in midlife women.
• They included participants from the Study of Women’s Health Across the Nation cohort who reported fibroid diagnoses at enrollment and during 13 follow-up visits.
• At all visits, levels of glucose, insulin, and sex hormone–binding globulin (SHBG) were measured in fasting blood samples, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated.
• Discrete-time survival models were used to estimate the hazard ratios (HRs) for the associations of biomarkers and diabetes with fibroid diagnoses, adjusted for demographics and healthcare utilization.

TAKEAWAY:

• Researchers identified 2570 eligible women (median age, 45 years; 45% perimenopausal women), among whom approximately 3% had diabetes at baseline.
• Diabetes was associated with a 28% lower incidence of new fibroid diagnosis (adjusted HR, 0.72).
• This association was particularly strong among participants with treated diabetes, especially those on metformin, who had a 51% lower incidence of self-reported fibroids than those without diabetes. The estimates, however, had wide CIs suggesting uncertainty.
• Time-varying HOMA-IR and SHBG, insulin, and glucose levels were not significantly associated with the new fibroid diagnosis.
• When stratified by menopausal status, higher HOMA-IR and insulin levels were associated with a greater incidence of fibroid diagnosis during premenopause but not during perimenopause.

IN PRACTICE:

“Our findings contribute to preliminary evidence indicating a protective association between diabetes and risk of incident fibroids,” the authors wrote.

SOURCE:

The study was led by Susanna D. Mitro, Division of Research, Kaiser Permanente, Pleasanton, California, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study relied on self-reported fibroid diagnoses, which may result in the misclassification of cases. The sample size of participants with diabetes was small, which resulted in reduced precision and confidence in the findings. The baseline eligibility criteria (midlife participants with an intact uterus and no history of fibroid incidence) may have limited the generalizability of the findings to the wider population at risk for fibroids.

DISCLOSURES:

This study was supported by the National Institutes of Health (NIH), through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women’s Health. One author reported being a consultant and adviser for various pharmaceutical companies. Two other authors reported receiving salary support and royalties from various pharmaceutical companies and organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Diabetes is associated with a lower incidence of uterine fibroids in midlife women receiving diabetes treatment, especially metformin. The association between diabetes and the risk for uterine fibroids may vary based on menopausal status.

METHODOLOGY:

• Previous studies have provided inconsistent evidence regarding associations between the risk for uterine fibroids and markers of cardiometabolic health, such as fasting insulin, fasting glucose, and diabetes.
• Researchers conducted a prospective cohort study to examine the association of fasting levels of cardiometabolic blood biomarkers, diabetes, and diabetes treatment with the incidence of new fibroid diagnoses in midlife women.
• They included participants from the Study of Women’s Health Across the Nation cohort who reported fibroid diagnoses at enrollment and during 13 follow-up visits.
• At all visits, levels of glucose, insulin, and sex hormone–binding globulin (SHBG) were measured in fasting blood samples, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated.
• Discrete-time survival models were used to estimate the hazard ratios (HRs) for the associations of biomarkers and diabetes with fibroid diagnoses, adjusted for demographics and healthcare utilization.

TAKEAWAY:

• Researchers identified 2570 eligible women (median age, 45 years; 45% perimenopausal women), among whom approximately 3% had diabetes at baseline.
• Diabetes was associated with a 28% lower incidence of new fibroid diagnosis (adjusted HR, 0.72).
• This association was particularly strong among participants with treated diabetes, especially those on metformin, who had a 51% lower incidence of self-reported fibroids than those without diabetes. The estimates, however, had wide CIs suggesting uncertainty.
• Time-varying HOMA-IR and SHBG, insulin, and glucose levels were not significantly associated with the new fibroid diagnosis.
• When stratified by menopausal status, higher HOMA-IR and insulin levels were associated with a greater incidence of fibroid diagnosis during premenopause but not during perimenopause.

IN PRACTICE:

“Our findings contribute to preliminary evidence indicating a protective association between diabetes and risk of incident fibroids,” the authors wrote.

SOURCE:

The study was led by Susanna D. Mitro, Division of Research, Kaiser Permanente, Pleasanton, California, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study relied on self-reported fibroid diagnoses, which may result in the misclassification of cases. The sample size of participants with diabetes was small, which resulted in reduced precision and confidence in the findings. The baseline eligibility criteria (midlife participants with an intact uterus and no history of fibroid incidence) may have limited the generalizability of the findings to the wider population at risk for fibroids.

DISCLOSURES:

This study was supported by the National Institutes of Health (NIH), through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women’s Health. One author reported being a consultant and adviser for various pharmaceutical companies. Two other authors reported receiving salary support and royalties from various pharmaceutical companies and organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Diabetes is associated with a lower incidence of uterine fibroids in midlife women receiving diabetes treatment, especially metformin. The association between diabetes and the risk for uterine fibroids may vary based on menopausal status.

METHODOLOGY:

• Previous studies have provided inconsistent evidence regarding associations between the risk for uterine fibroids and markers of cardiometabolic health, such as fasting insulin, fasting glucose, and diabetes.
• Researchers conducted a prospective cohort study to examine the association of fasting levels of cardiometabolic blood biomarkers, diabetes, and diabetes treatment with the incidence of new fibroid diagnoses in midlife women.
• They included participants from the Study of Women’s Health Across the Nation cohort who reported fibroid diagnoses at enrollment and during 13 follow-up visits.
• At all visits, levels of glucose, insulin, and sex hormone–binding globulin (SHBG) were measured in fasting blood samples, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated.
• Discrete-time survival models were used to estimate the hazard ratios (HRs) for the associations of biomarkers and diabetes with fibroid diagnoses, adjusted for demographics and healthcare utilization.

TAKEAWAY:

• Researchers identified 2570 eligible women (median age, 45 years; 45% perimenopausal women), among whom approximately 3% had diabetes at baseline.
• Diabetes was associated with a 28% lower incidence of new fibroid diagnosis (adjusted HR, 0.72).
• This association was particularly strong among participants with treated diabetes, especially those on metformin, who had a 51% lower incidence of self-reported fibroids than those without diabetes. The estimates, however, had wide CIs suggesting uncertainty.
• Time-varying HOMA-IR and SHBG, insulin, and glucose levels were not significantly associated with the new fibroid diagnosis.
• When stratified by menopausal status, higher HOMA-IR and insulin levels were associated with a greater incidence of fibroid diagnosis during premenopause but not during perimenopause.

IN PRACTICE:

“Our findings contribute to preliminary evidence indicating a protective association between diabetes and risk of incident fibroids,” the authors wrote.

SOURCE:

The study was led by Susanna D. Mitro, Division of Research, Kaiser Permanente, Pleasanton, California, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study relied on self-reported fibroid diagnoses, which may result in the misclassification of cases. The sample size of participants with diabetes was small, which resulted in reduced precision and confidence in the findings. The baseline eligibility criteria (midlife participants with an intact uterus and no history of fibroid incidence) may have limited the generalizability of the findings to the wider population at risk for fibroids.

DISCLOSURES:

This study was supported by the National Institutes of Health (NIH), through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women’s Health. One author reported being a consultant and adviser for various pharmaceutical companies. Two other authors reported receiving salary support and royalties from various pharmaceutical companies and organizations.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.