MDedge Rheumatology

Key clinical point: This real-world study confirmed the efficacy and safety of the interleukin (IL)-23 inhibitors guselkumab and risankizumab in patients with psoriatic arthritis (PsA).

Major finding: Mean Disease Activity Index for PsA (DAPSA) score was 43.6 at baseline and reduced significantly at 4 (36.8), 16 (23.6), and 24 (20.5) weeks of treatment (all P < .001). At 24 weeks, 29.2% and 16.7% of patients reported low disease activity and remission, respectively. None of the patients discontinued treatment due to safety concerns.

Study details: Findings are from a single-center retrospective study including 59 patients with moderate-to-severe plaque psoriasis who received guselkumab or risankizumab, of which 24 patients had concomitant PsA.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Vaiopoulos AG et al. Real-world data show high efficacy of IL23 inhibitors guselkumab and risankizumab in psoriatic arthritis and difficult-to-treat areas. Int J Dermatol. 2023;62:1404-1413 (Sep 25). doi: 10.1111/ijd.16849

Key clinical point: This real-world study confirmed the efficacy and safety of the interleukin (IL)-23 inhibitors guselkumab and risankizumab in patients with psoriatic arthritis (PsA).

Major finding: Mean Disease Activity Index for PsA (DAPSA) score was 43.6 at baseline and reduced significantly at 4 (36.8), 16 (23.6), and 24 (20.5) weeks of treatment (all P < .001). At 24 weeks, 29.2% and 16.7% of patients reported low disease activity and remission, respectively. None of the patients discontinued treatment due to safety concerns.

Study details: Findings are from a single-center retrospective study including 59 patients with moderate-to-severe plaque psoriasis who received guselkumab or risankizumab, of which 24 patients had concomitant PsA.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Vaiopoulos AG et al. Real-world data show high efficacy of IL23 inhibitors guselkumab and risankizumab in psoriatic arthritis and difficult-to-treat areas. Int J Dermatol. 2023;62:1404-1413 (Sep 25). doi: 10.1111/ijd.16849

Key clinical point: This real-world study confirmed the efficacy and safety of the interleukin (IL)-23 inhibitors guselkumab and risankizumab in patients with psoriatic arthritis (PsA).

Major finding: Mean Disease Activity Index for PsA (DAPSA) score was 43.6 at baseline and reduced significantly at 4 (36.8), 16 (23.6), and 24 (20.5) weeks of treatment (all P < .001). At 24 weeks, 29.2% and 16.7% of patients reported low disease activity and remission, respectively. None of the patients discontinued treatment due to safety concerns.

Study details: Findings are from a single-center retrospective study including 59 patients with moderate-to-severe plaque psoriasis who received guselkumab or risankizumab, of which 24 patients had concomitant PsA.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Vaiopoulos AG et al. Real-world data show high efficacy of IL23 inhibitors guselkumab and risankizumab in psoriatic arthritis and difficult-to-treat areas. Int J Dermatol. 2023;62:1404-1413 (Sep 25). doi: 10.1111/ijd.16849

Key clinical point: Intestinal permeability as well as fecal and plasma metabolomic profiles significantly affected the clinical response to fecal microbial transplantation (FMT) or sham transplantation in patients having peripheral moderate-to-high psoriatic arthritis (PsA) despite receiving methotrexate for ≥3 months.

Major finding: Lactulose-to-mannitol ratio was higher at week 26 (0.027 vs 0.012; P = .013), indicating greater small intestinal permeability; moreover, fecal (P < .0001) and plasma (P = .005) metabolomic profiles differed in patients who needed vs did not need treatment intensification after undergoing an FMT or sham transplantation.

Study details: This exploratory study of the FLORA trial included 31 patients who had peripheral moderate-to-high PsA despite ≥3 months of methotrexate treatment and were randomly assigned to undergo either gastroscopic-guided single-donor FMT (n = 15) or sham transplantation (n = 16).

Disclosures: This study was supported by Sygeforsikringen “danmark” and other sources. Three authors declared receiving financial support, grants, or lectureship awards from various sources.

Source: Kragsnaes MS et al. Small intestinal permeability and metabolomic profiles in feces and plasma associate with clinical response in patients with active psoriatic arthritis participating in a fecal microbiota transplantation trial: Exploratory findings from the FLORA trial. ACR Open Rheumatol. 2023 (Sep 22). doi: 10.1002/acr2.11604

Key clinical point: Intestinal permeability as well as fecal and plasma metabolomic profiles significantly affected the clinical response to fecal microbial transplantation (FMT) or sham transplantation in patients having peripheral moderate-to-high psoriatic arthritis (PsA) despite receiving methotrexate for ≥3 months.

Major finding: Lactulose-to-mannitol ratio was higher at week 26 (0.027 vs 0.012; P = .013), indicating greater small intestinal permeability; moreover, fecal (P < .0001) and plasma (P = .005) metabolomic profiles differed in patients who needed vs did not need treatment intensification after undergoing an FMT or sham transplantation.

Study details: This exploratory study of the FLORA trial included 31 patients who had peripheral moderate-to-high PsA despite ≥3 months of methotrexate treatment and were randomly assigned to undergo either gastroscopic-guided single-donor FMT (n = 15) or sham transplantation (n = 16).

Disclosures: This study was supported by Sygeforsikringen “danmark” and other sources. Three authors declared receiving financial support, grants, or lectureship awards from various sources.

Source: Kragsnaes MS et al. Small intestinal permeability and metabolomic profiles in feces and plasma associate with clinical response in patients with active psoriatic arthritis participating in a fecal microbiota transplantation trial: Exploratory findings from the FLORA trial. ACR Open Rheumatol. 2023 (Sep 22). doi: 10.1002/acr2.11604

Key clinical point: Intestinal permeability as well as fecal and plasma metabolomic profiles significantly affected the clinical response to fecal microbial transplantation (FMT) or sham transplantation in patients having peripheral moderate-to-high psoriatic arthritis (PsA) despite receiving methotrexate for ≥3 months.

Major finding: Lactulose-to-mannitol ratio was higher at week 26 (0.027 vs 0.012; P = .013), indicating greater small intestinal permeability; moreover, fecal (P < .0001) and plasma (P = .005) metabolomic profiles differed in patients who needed vs did not need treatment intensification after undergoing an FMT or sham transplantation.

Study details: This exploratory study of the FLORA trial included 31 patients who had peripheral moderate-to-high PsA despite ≥3 months of methotrexate treatment and were randomly assigned to undergo either gastroscopic-guided single-donor FMT (n = 15) or sham transplantation (n = 16).

Disclosures: This study was supported by Sygeforsikringen “danmark” and other sources. Three authors declared receiving financial support, grants, or lectureship awards from various sources.

Source: Kragsnaes MS et al. Small intestinal permeability and metabolomic profiles in feces and plasma associate with clinical response in patients with active psoriatic arthritis participating in a fecal microbiota transplantation trial: Exploratory findings from the FLORA trial. ACR Open Rheumatol. 2023 (Sep 22). doi: 10.1002/acr2.11604

Key clinical point: In patients with psoriatic arthritis (PsA), year-long treatment with interleukin-17 inhibitors (IL-17i) and IL-23(p19) inhibitors (IL23-[19]i), led to comparable drug survival and clinical response outcomes as tumor necrosis factor inhibitor (TNFi) treatment.

Major finding: At 12 months, the drug withdrawal rates for IL-17i (hazard ratio [HR] 1.36; 95% CI 0.59-3.14) and IL23-(19)i (HR 0.56; 95% CI 0.10-3.24) were comparable with those for TNFi. Moreover, the proportion of patients who achieved ≥50% improvement in the American College of Rheumatology scores was similar across the IL-17i, IL-23(19)i, and TNFi groups (19%, 29%, and 19%, respectively).

Study details: Findings are from a target trial emulation study including 109 patients with PsA who presented with peripheral manifestations and initiated either TNFi (n = 75), IL-7i (n = 26), or IL-23(19)i (n = 8).

Disclosures: This study was supported by the Danish Rheumatism Association and other sources. Some authors declared serving as speakers or consultants for or receiving research grants, fees, or other support from various sources.

Source: Stisen ZR et al. Tolerability and comparative effectiveness of TNF-, IL-17-, and IL-23(p19) inhibitors in psoriatic arthritis: A target trial emulation study. Rheumatology (Oxford). 2023 (Sep 15). doi: 10.1093/rheumatology/kead488

Key clinical point: In patients with psoriatic arthritis (PsA), year-long treatment with interleukin-17 inhibitors (IL-17i) and IL-23(p19) inhibitors (IL23-[19]i), led to comparable drug survival and clinical response outcomes as tumor necrosis factor inhibitor (TNFi) treatment.

Major finding: At 12 months, the drug withdrawal rates for IL-17i (hazard ratio [HR] 1.36; 95% CI 0.59-3.14) and IL23-(19)i (HR 0.56; 95% CI 0.10-3.24) were comparable with those for TNFi. Moreover, the proportion of patients who achieved ≥50% improvement in the American College of Rheumatology scores was similar across the IL-17i, IL-23(19)i, and TNFi groups (19%, 29%, and 19%, respectively).

Study details: Findings are from a target trial emulation study including 109 patients with PsA who presented with peripheral manifestations and initiated either TNFi (n = 75), IL-7i (n = 26), or IL-23(19)i (n = 8).

Disclosures: This study was supported by the Danish Rheumatism Association and other sources. Some authors declared serving as speakers or consultants for or receiving research grants, fees, or other support from various sources.

Source: Stisen ZR et al. Tolerability and comparative effectiveness of TNF-, IL-17-, and IL-23(p19) inhibitors in psoriatic arthritis: A target trial emulation study. Rheumatology (Oxford). 2023 (Sep 15). doi: 10.1093/rheumatology/kead488

Key clinical point: In patients with psoriatic arthritis (PsA), year-long treatment with interleukin-17 inhibitors (IL-17i) and IL-23(p19) inhibitors (IL23-[19]i), led to comparable drug survival and clinical response outcomes as tumor necrosis factor inhibitor (TNFi) treatment.

Major finding: At 12 months, the drug withdrawal rates for IL-17i (hazard ratio [HR] 1.36; 95% CI 0.59-3.14) and IL23-(19)i (HR 0.56; 95% CI 0.10-3.24) were comparable with those for TNFi. Moreover, the proportion of patients who achieved ≥50% improvement in the American College of Rheumatology scores was similar across the IL-17i, IL-23(19)i, and TNFi groups (19%, 29%, and 19%, respectively).

Study details: Findings are from a target trial emulation study including 109 patients with PsA who presented with peripheral manifestations and initiated either TNFi (n = 75), IL-7i (n = 26), or IL-23(19)i (n = 8).

Disclosures: This study was supported by the Danish Rheumatism Association and other sources. Some authors declared serving as speakers or consultants for or receiving research grants, fees, or other support from various sources.

Source: Stisen ZR et al. Tolerability and comparative effectiveness of TNF-, IL-17-, and IL-23(p19) inhibitors in psoriatic arthritis: A target trial emulation study. Rheumatology (Oxford). 2023 (Sep 15). doi: 10.1093/rheumatology/kead488

Key clinical point: Bimekizumab led to sustained improvements in clinical response up to week 52 and had a consistent safety profile in patients with active psoriatic arthritis (PsA) who were naive to biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: At week 16, 43.9% of patients receiving bimekizumab achieved ≥50% improvement in the American College of Rheumatology scores (ACR50), with the response being maintained until week 52 (54.5%). Among patients who switched from placebo to bimekizumab at week 16, a similar proportion (53.0%) achieved ACR50 at week 52. No new safety signals were observed.

Study details: Findings are from the phase 3 BE OPTIMAL study including 852 bDMARD-naive patients with active PsA who were randomly assigned to receive bimekizumab, adalimumab, or placebo.

Disclosures: This study was sponsored by UCB Pharma. Four authors declared being employees and shareholders of UCB Pharma. The other authors declared ties with several sources, including UCB Pharma.

Source: Ritchlin CT et al. Bimekizumab treatment in biologic DMARD-naïve patients with active psoriatic arthritis: 52-week efficacy and safety results from the phase III, randomised, placebo-controlled, active reference BE OPTIMAL study. Ann Rheum Dis. 2023;82:1404-1414 (Sep 11). doi: 10.1136/ard-2023-224431

Key clinical point: Bimekizumab led to sustained improvements in clinical response up to week 52 and had a consistent safety profile in patients with active psoriatic arthritis (PsA) who were naive to biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: At week 16, 43.9% of patients receiving bimekizumab achieved ≥50% improvement in the American College of Rheumatology scores (ACR50), with the response being maintained until week 52 (54.5%). Among patients who switched from placebo to bimekizumab at week 16, a similar proportion (53.0%) achieved ACR50 at week 52. No new safety signals were observed.

Study details: Findings are from the phase 3 BE OPTIMAL study including 852 bDMARD-naive patients with active PsA who were randomly assigned to receive bimekizumab, adalimumab, or placebo.

Disclosures: This study was sponsored by UCB Pharma. Four authors declared being employees and shareholders of UCB Pharma. The other authors declared ties with several sources, including UCB Pharma.

Source: Ritchlin CT et al. Bimekizumab treatment in biologic DMARD-naïve patients with active psoriatic arthritis: 52-week efficacy and safety results from the phase III, randomised, placebo-controlled, active reference BE OPTIMAL study. Ann Rheum Dis. 2023;82:1404-1414 (Sep 11). doi: 10.1136/ard-2023-224431

Key clinical point: Bimekizumab led to sustained improvements in clinical response up to week 52 and had a consistent safety profile in patients with active psoriatic arthritis (PsA) who were naive to biologic disease-modifying antirheumatic drugs (bDMARD).

Major finding: At week 16, 43.9% of patients receiving bimekizumab achieved ≥50% improvement in the American College of Rheumatology scores (ACR50), with the response being maintained until week 52 (54.5%). Among patients who switched from placebo to bimekizumab at week 16, a similar proportion (53.0%) achieved ACR50 at week 52. No new safety signals were observed.

Study details: Findings are from the phase 3 BE OPTIMAL study including 852 bDMARD-naive patients with active PsA who were randomly assigned to receive bimekizumab, adalimumab, or placebo.

Disclosures: This study was sponsored by UCB Pharma. Four authors declared being employees and shareholders of UCB Pharma. The other authors declared ties with several sources, including UCB Pharma.

Source: Ritchlin CT et al. Bimekizumab treatment in biologic DMARD-naïve patients with active psoriatic arthritis: 52-week efficacy and safety results from the phase III, randomised, placebo-controlled, active reference BE OPTIMAL study. Ann Rheum Dis. 2023;82:1404-1414 (Sep 11). doi: 10.1136/ard-2023-224431

VANCOUVER – With treatment with a bisphosphonate following sequential use of teriparatide (Forteo) and denosumab (Prolia) for premenopausal women with idiopathic osteoporosis, bone mineral density (BMD) was maintained over the first year following denosumab cessation, according to results from a small, nonrandomized extension of a phase 2 study.

Bisphosphonates are recommended for patients after they have completed a course of denosumab because cessation of the bone resorption blocker is known to increase bone turnover markers, decrease BMD, and raise the risk of vertebral fractures. Although there is evidence to support this treatment sequence for postmenopausal women, there was no evidence regarding premenopausal women with idiopathic osteoporosis, said Adi Cohen, MD, who presented the results of the study at the annual meeting of the American Society for Bone and Mineral Research.

In the extension study, neither length of treatment with denosumab nor transition to menopause affected BMD results. Weekly doses of alendronate (ALN) better suppressed C-terminal telopeptide (CTX) than did zoledronic acid (ZOL) and led to better maintenance of BMD than did a single dose of ZOL. The researchers suggested that single-dose ZOL may not prevent bone loss for an entire year.

It is too early to call the results practice changing, said Dr. Cohen, professor of medicine and endocrinology at Columbia University Irving Medical Center, New York, but she noted, “It’s important just to provide information about how sequences of osteoporosis medications might be used in a rare but certainly understudied group of premenopausal women with osteoporosis who need treatment, and these data hopefully will help make some treatment decisions.”

In the early 2000s, researchers initially believed that premenopausal women with low BMD had experienced some kind of temporary event and that they would likely improve on their own over time. “I think we now recognize that whatever it is that causes this is an ongoing issue and that this is a problem they’re going to have to deal with for the rest of their lives. This is something that they have to stay on top of,” said coauthor Elizabeth Shane, MD, who is a professor of medicine at CUIMC.

However, there are no practice guidelines for the management of osteoporosis in premenopausal women, according to Dr. Shane. She noted that there is controversy as to whether to treat women with low bone density who do not have a history of fractures. “I think that there’s pretty much agreement that anybody who has a lot of fractures has an early-onset form of osteoporosis. The controversy is what to do about the person who just has a low bone density and hasn’t yet fractured and what is the utility of trying to treat them at that point and perhaps prevent a fracture. I don’t think we have enough data to address that,” Dr. Shane said.

Still, the research has provided some clarity in her own practice. “I think if somebody would come to my office who had very low bone density, I would probably treat them. If they have fractures, I would definitely treat them. I think that our work has provided a framework for people to approach that,” she said.

The study was an extension of a sequential treatment approach that began with 2 years of teriparatide (20 mcg daily) followed by an extension study of 2–3 years of treatment with denosumab (60 mg every 6 months). Seven months after the last dose of denosumab, patients underwent 1 year of treatment with ALN (70 mg weekly; n = 18) or a single dose of ZOL (5 mg IV; n = 6), according to patient choice.

The original phase 2 study started with 41 women. At 24 months, teriparatide treatment led to BMD increases of 13% in the lumbar spine (LS), 5% in the total hip (TH), and 5% in the femoral neck (FN). There was a 2% decline in BMD in the forearm (distal radius [DR]). A group of 32 of the women participated in an extension study and took denosumab for 12 months. Of those patients, 29 continued to take it for another 12 months. At 12 months, BMD increased 5% in the LS, 3% in the TH, 3% in the FN, and 1% in the DR (P < .05 for all). At 24 months, BMD rose by 22%, 10%, and 10% at the first three of those locations. BMD in the DR remained stable, compared with the baseline after taking teriparatide.

The bisphosphonate phase of the extension study included 24 women (mean age, 43 years). The mean body mass index of the patients was 23.0 kg/m². The patients had experienced a mean of 3.0 fractures in adulthood, and 38% of patients had a history of vertebral fracture.

Over 12 months of follow-up, the researchers found no statistically significant difference in BMD in the LS, TH, or FN, compared with bisphosphonate extension baseline. There was also no statistically significant change in serum CTX. There was evidence that, among patients with higher rates of bone turnover, there were higher rates of LS and FN bone loss during bisphosphonate treatment.

Among patients taking ZOL, at 12 months there was a statistically significant rise in CTX levels, but not among patients taking ALN. There were no new vertebral fractures among any participants during the bisphosphonate extension period.

The results represent critical data for an understudied population, according to Yumie Rhee, MD, PhD, who was comoderator of the session in which the study was presented. “They are showing that by using a bisphosphonate [patients] have this just slight decrease, but within error, so it’s maintaining the BMD, at least. I think it’s very important. It will be fascinating to see next year’s follow-up,” said Dr. Rhee, a professor of endocrinology at Yonsei University College of Medicine in Seoul, South Korea. “The problem with premenopausal osteoporosis is that we don’t have good evidence. Even though this study is very small, we’re just following that data, all of us.”

Comoderator Maria Zanchetta, MD, a professor of osteology at the Institute of Diagnostics and Metabolic Research, Universidad del Salvador, Buenos Aires, agreed. “We know what to do when we stop denosumab in postmenopausal women. We didn’t have any work about what to do when we stopped in premenopausal women. You can think that probably it’s going to be the same, but this is the first time you have the evidence that if you give bisphosphonate, you will maintain BMD.”

Limitations to the study include its small size and the lack of a placebo-treated control group. In addition, the bisphosphonate extension was not randomized.

The studies were funded by the U.S. Food and Drug Administration and Amgen. Dr. Cohen and Dr. Shane received research funding from Amgen. Dr. Rhee and Dr. Zanchetta have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

VANCOUVER – With treatment with a bisphosphonate following sequential use of teriparatide (Forteo) and denosumab (Prolia) for premenopausal women with idiopathic osteoporosis, bone mineral density (BMD) was maintained over the first year following denosumab cessation, according to results from a small, nonrandomized extension of a phase 2 study.

Bisphosphonates are recommended for patients after they have completed a course of denosumab because cessation of the bone resorption blocker is known to increase bone turnover markers, decrease BMD, and raise the risk of vertebral fractures. Although there is evidence to support this treatment sequence for postmenopausal women, there was no evidence regarding premenopausal women with idiopathic osteoporosis, said Adi Cohen, MD, who presented the results of the study at the annual meeting of the American Society for Bone and Mineral Research.

In the extension study, neither length of treatment with denosumab nor transition to menopause affected BMD results. Weekly doses of alendronate (ALN) better suppressed C-terminal telopeptide (CTX) than did zoledronic acid (ZOL) and led to better maintenance of BMD than did a single dose of ZOL. The researchers suggested that single-dose ZOL may not prevent bone loss for an entire year.

It is too early to call the results practice changing, said Dr. Cohen, professor of medicine and endocrinology at Columbia University Irving Medical Center, New York, but she noted, “It’s important just to provide information about how sequences of osteoporosis medications might be used in a rare but certainly understudied group of premenopausal women with osteoporosis who need treatment, and these data hopefully will help make some treatment decisions.”

In the early 2000s, researchers initially believed that premenopausal women with low BMD had experienced some kind of temporary event and that they would likely improve on their own over time. “I think we now recognize that whatever it is that causes this is an ongoing issue and that this is a problem they’re going to have to deal with for the rest of their lives. This is something that they have to stay on top of,” said coauthor Elizabeth Shane, MD, who is a professor of medicine at CUIMC.

However, there are no practice guidelines for the management of osteoporosis in premenopausal women, according to Dr. Shane. She noted that there is controversy as to whether to treat women with low bone density who do not have a history of fractures. “I think that there’s pretty much agreement that anybody who has a lot of fractures has an early-onset form of osteoporosis. The controversy is what to do about the person who just has a low bone density and hasn’t yet fractured and what is the utility of trying to treat them at that point and perhaps prevent a fracture. I don’t think we have enough data to address that,” Dr. Shane said.

Still, the research has provided some clarity in her own practice. “I think if somebody would come to my office who had very low bone density, I would probably treat them. If they have fractures, I would definitely treat them. I think that our work has provided a framework for people to approach that,” she said.

The study was an extension of a sequential treatment approach that began with 2 years of teriparatide (20 mcg daily) followed by an extension study of 2–3 years of treatment with denosumab (60 mg every 6 months). Seven months after the last dose of denosumab, patients underwent 1 year of treatment with ALN (70 mg weekly; n = 18) or a single dose of ZOL (5 mg IV; n = 6), according to patient choice.

The original phase 2 study started with 41 women. At 24 months, teriparatide treatment led to BMD increases of 13% in the lumbar spine (LS), 5% in the total hip (TH), and 5% in the femoral neck (FN). There was a 2% decline in BMD in the forearm (distal radius [DR]). A group of 32 of the women participated in an extension study and took denosumab for 12 months. Of those patients, 29 continued to take it for another 12 months. At 12 months, BMD increased 5% in the LS, 3% in the TH, 3% in the FN, and 1% in the DR (P < .05 for all). At 24 months, BMD rose by 22%, 10%, and 10% at the first three of those locations. BMD in the DR remained stable, compared with the baseline after taking teriparatide.

The bisphosphonate phase of the extension study included 24 women (mean age, 43 years). The mean body mass index of the patients was 23.0 kg/m². The patients had experienced a mean of 3.0 fractures in adulthood, and 38% of patients had a history of vertebral fracture.

Over 12 months of follow-up, the researchers found no statistically significant difference in BMD in the LS, TH, or FN, compared with bisphosphonate extension baseline. There was also no statistically significant change in serum CTX. There was evidence that, among patients with higher rates of bone turnover, there were higher rates of LS and FN bone loss during bisphosphonate treatment.

Among patients taking ZOL, at 12 months there was a statistically significant rise in CTX levels, but not among patients taking ALN. There were no new vertebral fractures among any participants during the bisphosphonate extension period.

The results represent critical data for an understudied population, according to Yumie Rhee, MD, PhD, who was comoderator of the session in which the study was presented. “They are showing that by using a bisphosphonate [patients] have this just slight decrease, but within error, so it’s maintaining the BMD, at least. I think it’s very important. It will be fascinating to see next year’s follow-up,” said Dr. Rhee, a professor of endocrinology at Yonsei University College of Medicine in Seoul, South Korea. “The problem with premenopausal osteoporosis is that we don’t have good evidence. Even though this study is very small, we’re just following that data, all of us.”

Comoderator Maria Zanchetta, MD, a professor of osteology at the Institute of Diagnostics and Metabolic Research, Universidad del Salvador, Buenos Aires, agreed. “We know what to do when we stop denosumab in postmenopausal women. We didn’t have any work about what to do when we stopped in premenopausal women. You can think that probably it’s going to be the same, but this is the first time you have the evidence that if you give bisphosphonate, you will maintain BMD.”

Limitations to the study include its small size and the lack of a placebo-treated control group. In addition, the bisphosphonate extension was not randomized.

The studies were funded by the U.S. Food and Drug Administration and Amgen. Dr. Cohen and Dr. Shane received research funding from Amgen. Dr. Rhee and Dr. Zanchetta have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

VANCOUVER – With treatment with a bisphosphonate following sequential use of teriparatide (Forteo) and denosumab (Prolia) for premenopausal women with idiopathic osteoporosis, bone mineral density (BMD) was maintained over the first year following denosumab cessation, according to results from a small, nonrandomized extension of a phase 2 study.

Bisphosphonates are recommended for patients after they have completed a course of denosumab because cessation of the bone resorption blocker is known to increase bone turnover markers, decrease BMD, and raise the risk of vertebral fractures. Although there is evidence to support this treatment sequence for postmenopausal women, there was no evidence regarding premenopausal women with idiopathic osteoporosis, said Adi Cohen, MD, who presented the results of the study at the annual meeting of the American Society for Bone and Mineral Research.

In the extension study, neither length of treatment with denosumab nor transition to menopause affected BMD results. Weekly doses of alendronate (ALN) better suppressed C-terminal telopeptide (CTX) than did zoledronic acid (ZOL) and led to better maintenance of BMD than did a single dose of ZOL. The researchers suggested that single-dose ZOL may not prevent bone loss for an entire year.

It is too early to call the results practice changing, said Dr. Cohen, professor of medicine and endocrinology at Columbia University Irving Medical Center, New York, but she noted, “It’s important just to provide information about how sequences of osteoporosis medications might be used in a rare but certainly understudied group of premenopausal women with osteoporosis who need treatment, and these data hopefully will help make some treatment decisions.”

In the early 2000s, researchers initially believed that premenopausal women with low BMD had experienced some kind of temporary event and that they would likely improve on their own over time. “I think we now recognize that whatever it is that causes this is an ongoing issue and that this is a problem they’re going to have to deal with for the rest of their lives. This is something that they have to stay on top of,” said coauthor Elizabeth Shane, MD, who is a professor of medicine at CUIMC.

However, there are no practice guidelines for the management of osteoporosis in premenopausal women, according to Dr. Shane. She noted that there is controversy as to whether to treat women with low bone density who do not have a history of fractures. “I think that there’s pretty much agreement that anybody who has a lot of fractures has an early-onset form of osteoporosis. The controversy is what to do about the person who just has a low bone density and hasn’t yet fractured and what is the utility of trying to treat them at that point and perhaps prevent a fracture. I don’t think we have enough data to address that,” Dr. Shane said.

Still, the research has provided some clarity in her own practice. “I think if somebody would come to my office who had very low bone density, I would probably treat them. If they have fractures, I would definitely treat them. I think that our work has provided a framework for people to approach that,” she said.

The study was an extension of a sequential treatment approach that began with 2 years of teriparatide (20 mcg daily) followed by an extension study of 2–3 years of treatment with denosumab (60 mg every 6 months). Seven months after the last dose of denosumab, patients underwent 1 year of treatment with ALN (70 mg weekly; n = 18) or a single dose of ZOL (5 mg IV; n = 6), according to patient choice.

The original phase 2 study started with 41 women. At 24 months, teriparatide treatment led to BMD increases of 13% in the lumbar spine (LS), 5% in the total hip (TH), and 5% in the femoral neck (FN). There was a 2% decline in BMD in the forearm (distal radius [DR]). A group of 32 of the women participated in an extension study and took denosumab for 12 months. Of those patients, 29 continued to take it for another 12 months. At 12 months, BMD increased 5% in the LS, 3% in the TH, 3% in the FN, and 1% in the DR (P < .05 for all). At 24 months, BMD rose by 22%, 10%, and 10% at the first three of those locations. BMD in the DR remained stable, compared with the baseline after taking teriparatide.

The bisphosphonate phase of the extension study included 24 women (mean age, 43 years). The mean body mass index of the patients was 23.0 kg/m². The patients had experienced a mean of 3.0 fractures in adulthood, and 38% of patients had a history of vertebral fracture.

Over 12 months of follow-up, the researchers found no statistically significant difference in BMD in the LS, TH, or FN, compared with bisphosphonate extension baseline. There was also no statistically significant change in serum CTX. There was evidence that, among patients with higher rates of bone turnover, there were higher rates of LS and FN bone loss during bisphosphonate treatment.

Among patients taking ZOL, at 12 months there was a statistically significant rise in CTX levels, but not among patients taking ALN. There were no new vertebral fractures among any participants during the bisphosphonate extension period.

The results represent critical data for an understudied population, according to Yumie Rhee, MD, PhD, who was comoderator of the session in which the study was presented. “They are showing that by using a bisphosphonate [patients] have this just slight decrease, but within error, so it’s maintaining the BMD, at least. I think it’s very important. It will be fascinating to see next year’s follow-up,” said Dr. Rhee, a professor of endocrinology at Yonsei University College of Medicine in Seoul, South Korea. “The problem with premenopausal osteoporosis is that we don’t have good evidence. Even though this study is very small, we’re just following that data, all of us.”

Comoderator Maria Zanchetta, MD, a professor of osteology at the Institute of Diagnostics and Metabolic Research, Universidad del Salvador, Buenos Aires, agreed. “We know what to do when we stop denosumab in postmenopausal women. We didn’t have any work about what to do when we stopped in premenopausal women. You can think that probably it’s going to be the same, but this is the first time you have the evidence that if you give bisphosphonate, you will maintain BMD.”

Limitations to the study include its small size and the lack of a placebo-treated control group. In addition, the bisphosphonate extension was not randomized.

The studies were funded by the U.S. Food and Drug Administration and Amgen. Dr. Cohen and Dr. Shane received research funding from Amgen. Dr. Rhee and Dr. Zanchetta have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Researchers have identified two genes that may contribute to Raynaud’s phenomenon, a condition where blood vessels in the extremities constrict and limit blood flow.

Raynaud’s is a relatively common condition, affecting 2%-5% of the general population. Though Raynaud’s can be an annoyance for some, it can also cause severe pain and can require medication.

Barb Elkin/iStock/Getty Images Plus

These newly identified genes will hopefully lead to new therapeutic options, said Maik Pietzner, PhD, chair in health data modeling at Queen Mary University of London’s Precision Healthcare University Research Institute (PHURI) and group leader in the Computational Medicine Group at the Berlin Institute of Health at Charité – Universitätsmedizin Berlin, Germany.

Berlin Institute of Health at Charité - Universitätsmedizin Berlin

Dr. Pietzner led the research along with Claudia Langenberg, MD, PhD, director of PHURI.

The study was published in Nature Communications.


 

Largest genomic study of Raynaud’s to date

The researchers looked through electronic medical records from the UK Biobank, a large-scale database that contains genetic and health information on half a million participants. They identified more than 5,100 individuals with Raynaud’s, of which 68% had primary Raynaud’s. These participants were compared with more than 439,000 controls who did not have Raynaud’s.

In a secondary analysis, the team also used health records from the Queen Mary University of London Genes & Health Study, which contains health information on individuals of South Asian ancestry.

The researchers identified two genes that are likely involved with Raynaud’s. The first, ADRA2A, encodes for the alpha-2A adrenergic receptor that can cause vasoconstriction of small blood vessels in response to stress hormones. Researchers have long suspected that this type of receptor could be involved with Raynaud’s, but there was debate over which receptor subtype was responsible.

“Our finding of alpha-2A receptors is quite interesting because the focus has always been on alpha-2C receptors,” said Dr. Pietzner. “It’s only a letter, but it’s a massive difference in terms of biology and physiology,” he said, and could be why therapies targeting 2C receptors have been ineffective.

The second strongest association was for the transcription factor IRX1. Less is known about this gene, but the data we do have suggest that it is involved with regulating the dilation of blood vessels, Dr. Pietzner noted.

“There might be balance between the ADRA2A finding being responsible for constriction and the IRX1 finding indirectly linked to the dilation of those vessels following constrictions. Having both may explain why these prolonged episodes of vasoconstriction lead to a loss of oxygen to the tissues,” so they turn white and then blue, he said.

Because the Biobank cohort was European-centric, Dr. Pietzner and colleagues also identified 400 cases of Raynaud’s in British individuals of Bangladeshi and Pakistani ancestry and were able to replicate the association between IRX1 and Raynaud’s. Data on ADRA2A were unavailable.

The genes identified are associated with primary Raynaud’s. Secondary Raynaud’s is a rarer type of the condition that occurs along with autoimmune disorders, such as scleroderma, and is generally more severe.

It’s long been suspected that Raynaud’s had some genetic component, because half of patients with Raynaud’s have another family member with the same condition, said Laura Hummers, MD, who codirects the John Hopkins Scleroderma Center in Baltimore. She was not involved with the study.

Johns Hopkins University

This is “the largest study of this kind that’s been done,” she said, and the first to show a potential mechanism behind this genetic association.

The main gene finding, ADRA2A, “points to a receptor on the cells that regulate the tone of these blood vessels,” she continued. “It suggests maybe there’s too many of these receptors or they’re overly sensitive; something about them is different that makes patients more susceptible to these cold triggers. Knowing that is potentially really important, because it could give you a direct way to intervene, if true.”
 

New therapeutic avenues

The first-line treatment for primary Raynaud’s is behavioral interventions, such as maintaining body and extremity warmth and avoiding certain vasoconstricting drugs, said Kimberly Lakin, MD, a rheumatologist at the Hospital for Special Surgery in New York, who not involved in the research. These drugs could include over-the-counter decongestants and certain medications for attention-deficit/hyperactivity disorder.

Hospital for Special Surgery

If these behavioral interventions are not enough, clinicians most commonly prescribe calcium channel blockers. These medications are vasodilators but can be a concern for people with normal or already low blood pressure, Dr. Lakin said. They can also cause symptoms such as headache, leg swelling, constipation, and other gastrointestinal symptoms.

Other medications, such as fluoxetine, may also be considered as a later-line therapy, “but the effectiveness is fairly limited in Raynaud’s,” she said. “Certainly, other medication options that would be helpful and driven by the mechanisms of Raynaud’s would add to our ability to help patients.”

As it turns out, one of the genes identified in the study, ADRA2A, “is actually one of the most commonly targeted genes by drugs,” said Dr. Pietzner. Because the findings suggest that ADRA2A is overexpressed in Raynaud, a selective inhibitor like the antidepressant mirtazapine could be a promising candidate to repurpose for treating Raynaud’s, he said.
 

Limitations to electronic medical record analyses

Both Dr. Hummers and Dr. Lakin noted that research using diagnostic codes from medical records to identify cases has some limitations. The study may have included patients misdiagnosed with Raynaud’s when perhaps they had another condition. Patients with milder Raynaud’s who have not sought medical attention for the condition would not be represented in the study, Dr. Lakin said.

The UK Biobank includes individuals of mostly European descent, so an analysis confirming these findings in a more diverse population would be helpful, she said.

However, both Dr. Lakin and Dr. Hummers agreed that the study contributes to the understanding of the mechanisms behind Raynaud’s. Although the two identified genes were tied to primary Raynaud’s, the study’s findings could potentially apply to secondary Raynaud’s as well, Dr. Hummers said.

“Anything we learn about primary Raynaud’s may have implication for Raynaud’s more broadly,” she noted.

Dr. Hummers and Dr. Lakin disclosed no relevant financial relationships. Dr. Pietzner has received partnership funding for the MRC Clinical Pharmacology Training Scheme (cofunded by MRC and Roche, UCB, Eli Lilly, and Novartis) and a PhD studentship jointly funded by the UK Engineering and Physical Sciences Research Council and AstraZeneca. Dr. Pietzner also has unrestricted educational grant support for the UK Pharmacogenetics and Stratified Medicine Network from Bristol-Myers Squibb.

A version of this article appeared on Medscape.com.

Researchers have identified two genes that may contribute to Raynaud’s phenomenon, a condition where blood vessels in the extremities constrict and limit blood flow.

Raynaud’s is a relatively common condition, affecting 2%-5% of the general population. Though Raynaud’s can be an annoyance for some, it can also cause severe pain and can require medication.

Barb Elkin/iStock/Getty Images Plus

These newly identified genes will hopefully lead to new therapeutic options, said Maik Pietzner, PhD, chair in health data modeling at Queen Mary University of London’s Precision Healthcare University Research Institute (PHURI) and group leader in the Computational Medicine Group at the Berlin Institute of Health at Charité – Universitätsmedizin Berlin, Germany.

Berlin Institute of Health at Charité - Universitätsmedizin Berlin

Dr. Pietzner led the research along with Claudia Langenberg, MD, PhD, director of PHURI.

The study was published in Nature Communications.


 

Largest genomic study of Raynaud’s to date

The researchers looked through electronic medical records from the UK Biobank, a large-scale database that contains genetic and health information on half a million participants. They identified more than 5,100 individuals with Raynaud’s, of which 68% had primary Raynaud’s. These participants were compared with more than 439,000 controls who did not have Raynaud’s.

In a secondary analysis, the team also used health records from the Queen Mary University of London Genes & Health Study, which contains health information on individuals of South Asian ancestry.

The researchers identified two genes that are likely involved with Raynaud’s. The first, ADRA2A, encodes for the alpha-2A adrenergic receptor that can cause vasoconstriction of small blood vessels in response to stress hormones. Researchers have long suspected that this type of receptor could be involved with Raynaud’s, but there was debate over which receptor subtype was responsible.

“Our finding of alpha-2A receptors is quite interesting because the focus has always been on alpha-2C receptors,” said Dr. Pietzner. “It’s only a letter, but it’s a massive difference in terms of biology and physiology,” he said, and could be why therapies targeting 2C receptors have been ineffective.

The second strongest association was for the transcription factor IRX1. Less is known about this gene, but the data we do have suggest that it is involved with regulating the dilation of blood vessels, Dr. Pietzner noted.

“There might be balance between the ADRA2A finding being responsible for constriction and the IRX1 finding indirectly linked to the dilation of those vessels following constrictions. Having both may explain why these prolonged episodes of vasoconstriction lead to a loss of oxygen to the tissues,” so they turn white and then blue, he said.

Because the Biobank cohort was European-centric, Dr. Pietzner and colleagues also identified 400 cases of Raynaud’s in British individuals of Bangladeshi and Pakistani ancestry and were able to replicate the association between IRX1 and Raynaud’s. Data on ADRA2A were unavailable.

The genes identified are associated with primary Raynaud’s. Secondary Raynaud’s is a rarer type of the condition that occurs along with autoimmune disorders, such as scleroderma, and is generally more severe.

It’s long been suspected that Raynaud’s had some genetic component, because half of patients with Raynaud’s have another family member with the same condition, said Laura Hummers, MD, who codirects the John Hopkins Scleroderma Center in Baltimore. She was not involved with the study.

Johns Hopkins University

This is “the largest study of this kind that’s been done,” she said, and the first to show a potential mechanism behind this genetic association.

The main gene finding, ADRA2A, “points to a receptor on the cells that regulate the tone of these blood vessels,” she continued. “It suggests maybe there’s too many of these receptors or they’re overly sensitive; something about them is different that makes patients more susceptible to these cold triggers. Knowing that is potentially really important, because it could give you a direct way to intervene, if true.”
 

New therapeutic avenues

The first-line treatment for primary Raynaud’s is behavioral interventions, such as maintaining body and extremity warmth and avoiding certain vasoconstricting drugs, said Kimberly Lakin, MD, a rheumatologist at the Hospital for Special Surgery in New York, who not involved in the research. These drugs could include over-the-counter decongestants and certain medications for attention-deficit/hyperactivity disorder.

Hospital for Special Surgery

If these behavioral interventions are not enough, clinicians most commonly prescribe calcium channel blockers. These medications are vasodilators but can be a concern for people with normal or already low blood pressure, Dr. Lakin said. They can also cause symptoms such as headache, leg swelling, constipation, and other gastrointestinal symptoms.

Other medications, such as fluoxetine, may also be considered as a later-line therapy, “but the effectiveness is fairly limited in Raynaud’s,” she said. “Certainly, other medication options that would be helpful and driven by the mechanisms of Raynaud’s would add to our ability to help patients.”

As it turns out, one of the genes identified in the study, ADRA2A, “is actually one of the most commonly targeted genes by drugs,” said Dr. Pietzner. Because the findings suggest that ADRA2A is overexpressed in Raynaud, a selective inhibitor like the antidepressant mirtazapine could be a promising candidate to repurpose for treating Raynaud’s, he said.
 

Limitations to electronic medical record analyses

Both Dr. Hummers and Dr. Lakin noted that research using diagnostic codes from medical records to identify cases has some limitations. The study may have included patients misdiagnosed with Raynaud’s when perhaps they had another condition. Patients with milder Raynaud’s who have not sought medical attention for the condition would not be represented in the study, Dr. Lakin said.

The UK Biobank includes individuals of mostly European descent, so an analysis confirming these findings in a more diverse population would be helpful, she said.

However, both Dr. Lakin and Dr. Hummers agreed that the study contributes to the understanding of the mechanisms behind Raynaud’s. Although the two identified genes were tied to primary Raynaud’s, the study’s findings could potentially apply to secondary Raynaud’s as well, Dr. Hummers said.

“Anything we learn about primary Raynaud’s may have implication for Raynaud’s more broadly,” she noted.

Dr. Hummers and Dr. Lakin disclosed no relevant financial relationships. Dr. Pietzner has received partnership funding for the MRC Clinical Pharmacology Training Scheme (cofunded by MRC and Roche, UCB, Eli Lilly, and Novartis) and a PhD studentship jointly funded by the UK Engineering and Physical Sciences Research Council and AstraZeneca. Dr. Pietzner also has unrestricted educational grant support for the UK Pharmacogenetics and Stratified Medicine Network from Bristol-Myers Squibb.

A version of this article appeared on Medscape.com.

Researchers have identified two genes that may contribute to Raynaud’s phenomenon, a condition where blood vessels in the extremities constrict and limit blood flow.

Raynaud’s is a relatively common condition, affecting 2%-5% of the general population. Though Raynaud’s can be an annoyance for some, it can also cause severe pain and can require medication.

Barb Elkin/iStock/Getty Images Plus

These newly identified genes will hopefully lead to new therapeutic options, said Maik Pietzner, PhD, chair in health data modeling at Queen Mary University of London’s Precision Healthcare University Research Institute (PHURI) and group leader in the Computational Medicine Group at the Berlin Institute of Health at Charité – Universitätsmedizin Berlin, Germany.

Berlin Institute of Health at Charité - Universitätsmedizin Berlin

Dr. Pietzner led the research along with Claudia Langenberg, MD, PhD, director of PHURI.

The study was published in Nature Communications.


 

Largest genomic study of Raynaud’s to date

The researchers looked through electronic medical records from the UK Biobank, a large-scale database that contains genetic and health information on half a million participants. They identified more than 5,100 individuals with Raynaud’s, of which 68% had primary Raynaud’s. These participants were compared with more than 439,000 controls who did not have Raynaud’s.

In a secondary analysis, the team also used health records from the Queen Mary University of London Genes & Health Study, which contains health information on individuals of South Asian ancestry.

The researchers identified two genes that are likely involved with Raynaud’s. The first, ADRA2A, encodes for the alpha-2A adrenergic receptor that can cause vasoconstriction of small blood vessels in response to stress hormones. Researchers have long suspected that this type of receptor could be involved with Raynaud’s, but there was debate over which receptor subtype was responsible.

“Our finding of alpha-2A receptors is quite interesting because the focus has always been on alpha-2C receptors,” said Dr. Pietzner. “It’s only a letter, but it’s a massive difference in terms of biology and physiology,” he said, and could be why therapies targeting 2C receptors have been ineffective.

The second strongest association was for the transcription factor IRX1. Less is known about this gene, but the data we do have suggest that it is involved with regulating the dilation of blood vessels, Dr. Pietzner noted.

“There might be balance between the ADRA2A finding being responsible for constriction and the IRX1 finding indirectly linked to the dilation of those vessels following constrictions. Having both may explain why these prolonged episodes of vasoconstriction lead to a loss of oxygen to the tissues,” so they turn white and then blue, he said.

Because the Biobank cohort was European-centric, Dr. Pietzner and colleagues also identified 400 cases of Raynaud’s in British individuals of Bangladeshi and Pakistani ancestry and were able to replicate the association between IRX1 and Raynaud’s. Data on ADRA2A were unavailable.

The genes identified are associated with primary Raynaud’s. Secondary Raynaud’s is a rarer type of the condition that occurs along with autoimmune disorders, such as scleroderma, and is generally more severe.

It’s long been suspected that Raynaud’s had some genetic component, because half of patients with Raynaud’s have another family member with the same condition, said Laura Hummers, MD, who codirects the John Hopkins Scleroderma Center in Baltimore. She was not involved with the study.

Johns Hopkins University

This is “the largest study of this kind that’s been done,” she said, and the first to show a potential mechanism behind this genetic association.

The main gene finding, ADRA2A, “points to a receptor on the cells that regulate the tone of these blood vessels,” she continued. “It suggests maybe there’s too many of these receptors or they’re overly sensitive; something about them is different that makes patients more susceptible to these cold triggers. Knowing that is potentially really important, because it could give you a direct way to intervene, if true.”
 

New therapeutic avenues

The first-line treatment for primary Raynaud’s is behavioral interventions, such as maintaining body and extremity warmth and avoiding certain vasoconstricting drugs, said Kimberly Lakin, MD, a rheumatologist at the Hospital for Special Surgery in New York, who not involved in the research. These drugs could include over-the-counter decongestants and certain medications for attention-deficit/hyperactivity disorder.

Hospital for Special Surgery

If these behavioral interventions are not enough, clinicians most commonly prescribe calcium channel blockers. These medications are vasodilators but can be a concern for people with normal or already low blood pressure, Dr. Lakin said. They can also cause symptoms such as headache, leg swelling, constipation, and other gastrointestinal symptoms.

Other medications, such as fluoxetine, may also be considered as a later-line therapy, “but the effectiveness is fairly limited in Raynaud’s,” she said. “Certainly, other medication options that would be helpful and driven by the mechanisms of Raynaud’s would add to our ability to help patients.”

As it turns out, one of the genes identified in the study, ADRA2A, “is actually one of the most commonly targeted genes by drugs,” said Dr. Pietzner. Because the findings suggest that ADRA2A is overexpressed in Raynaud, a selective inhibitor like the antidepressant mirtazapine could be a promising candidate to repurpose for treating Raynaud’s, he said.
 

Limitations to electronic medical record analyses

Both Dr. Hummers and Dr. Lakin noted that research using diagnostic codes from medical records to identify cases has some limitations. The study may have included patients misdiagnosed with Raynaud’s when perhaps they had another condition. Patients with milder Raynaud’s who have not sought medical attention for the condition would not be represented in the study, Dr. Lakin said.

The UK Biobank includes individuals of mostly European descent, so an analysis confirming these findings in a more diverse population would be helpful, she said.

However, both Dr. Lakin and Dr. Hummers agreed that the study contributes to the understanding of the mechanisms behind Raynaud’s. Although the two identified genes were tied to primary Raynaud’s, the study’s findings could potentially apply to secondary Raynaud’s as well, Dr. Hummers said.

“Anything we learn about primary Raynaud’s may have implication for Raynaud’s more broadly,” she noted.

Dr. Hummers and Dr. Lakin disclosed no relevant financial relationships. Dr. Pietzner has received partnership funding for the MRC Clinical Pharmacology Training Scheme (cofunded by MRC and Roche, UCB, Eli Lilly, and Novartis) and a PhD studentship jointly funded by the UK Engineering and Physical Sciences Research Council and AstraZeneca. Dr. Pietzner also has unrestricted educational grant support for the UK Pharmacogenetics and Stratified Medicine Network from Bristol-Myers Squibb.

A version of this article appeared on Medscape.com.

VANCOUVER – In patients with type 2 diabetes, sodium-glucose cotransporter 2 (SGLT2) inhibitors as an adjunct to metformin were not associated with an increase in fracture risk, according to a new real-world study.

There have been some reports of an increase in fracture risk associated with SGLT2 inhibitors, and it was observed in the phase 3 CANVAS trial of canagliflozin (Invokana), which led to a Food and Drug Administration warning of fracture risks associated with canagliflozin use. Some ensuing studies did not show an increased risk, but these studies were generally less than a year in duration and may have missed longer-term risk, according to Veerle van Hulten, MSc.

“Fracture risk is something that takes a long time to develop, so we wanted to have a longer follow-up. We looked into the CPRD [Clinical Practice Research Datalink], which is a beautiful database containing real-world data from primary care practices,” said Ms. van Hulten, a PhD student at Maastricht (the Netherlands) University, who presented the study at the annual meeting of the American Society for Bone and Mineral Research.

Ms. van Hulten and colleagues compared SGLT2 inhibitors with dipeptidyl peptidase–4 (DPP-4) inhibitors because the latter are used in similar populations and have been shown to have no effect on fracture risk.

“What we found is that SGLT2 inhibitors are not associated with an increased fracture risk. Even with a duration of use of over 811 days, we did not observe an increased hazard ratio for fractures when compared DPP-4 inhibitor users,” Ms. van Hulten said.

SGLT2 inhibitors reduce blood sugar by increasing elimination of sugar in the urine. They also increase phosphate, reduce calcium, and increase parathyroid hormone, which could in turn negatively affect bone turnover, according to Ms. van Hulten.

In the new study, conducted between January 2013 and June 2020, the researchers used propensity score matching to compare adult patients, including 13,807 who were prescribed SGLT2 inhibitors and 28,524 who were prescribed DPP-4 inhibitors for the first time. They matched patients based on demographics, comorbidities, comedication, and lifestyle factors.

There was no association between SGLT2 inhibitor use and overall fracture risk or major osteoporotic, hip, vertebral, humerus, radius, or ulna fractures. There was no difference in risk for any duration of use, even with the longest duration of use of 811 days (adjusted hazard ratio, 1.0). There were no differences among specific SGLT2 inhibitors, including canagliflozin (aHR, 1.12; 95% confidence interval, 0.73-1.72). Analyses by sex and age also revealed no statistically significant differences between the two drug classes.

During the Q&A session after the presentation, Sarah Berry, MD, MPH, an associate professor of medicine at Harvard Medical School and a clinical researcher at the Marcus Institute for Aging Research, both in Boston, noted the trend toward an increase in fracture risk in the first 90 days. “It looked like there was something going on in the first 90 days, and then after that the results were much closer to the null. I would put out maybe another potential mechanism whereby the SGLT2 inhibitors might cause fracture, and that’s falls. They cause polyuria, and any drug you give that causes women to rush to the bathroom may well cause fractures, particularly in the short term,” Dr. Berry said.

Ms. van Hulten agreed, and also brought up that the drugs can cause osmotic diuresis. That can lead to hypovolemia, the symptoms of which include weakness, fatigue, and dizziness. “And increased falls, of course, increases fracture risk. We do not expect anything to happen to bone metabolism in the first 90 days. I think we can agree that there would be more time needed to alter the bone enough to increase fracture risk, so we expect that this trend toward an increased risk might be attributable to that increased fall risk that might occur with SGLT2 inhibitor use,” she said.

It’s possible that such a mechanism explains increased fracture risk seen in some earlier short-term studies, she added.

Overall, Ms. van Hulten said that the results should provide some confidence in SGLT2 inhibitors, though more work needs to be done. “I think we provide reassurance that SGLT2 inhibitors are safe to use. However, we still only have a median follow-up of 1.6 years. It’s not as long as we maybe would like, but it’s the best we can do with the data available, since the SGLT2 inhibitors have only been used since 2013. So maybe it’s best to prescribe it and keep [fall risk] in mind and look into the effects later on again, but it seems to be safe to use.”

The study received funding from the Novo Nordisk Foundation. Ms. van Hulten and Dr. Berry reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

VANCOUVER – In patients with type 2 diabetes, sodium-glucose cotransporter 2 (SGLT2) inhibitors as an adjunct to metformin were not associated with an increase in fracture risk, according to a new real-world study.

There have been some reports of an increase in fracture risk associated with SGLT2 inhibitors, and it was observed in the phase 3 CANVAS trial of canagliflozin (Invokana), which led to a Food and Drug Administration warning of fracture risks associated with canagliflozin use. Some ensuing studies did not show an increased risk, but these studies were generally less than a year in duration and may have missed longer-term risk, according to Veerle van Hulten, MSc.

“Fracture risk is something that takes a long time to develop, so we wanted to have a longer follow-up. We looked into the CPRD [Clinical Practice Research Datalink], which is a beautiful database containing real-world data from primary care practices,” said Ms. van Hulten, a PhD student at Maastricht (the Netherlands) University, who presented the study at the annual meeting of the American Society for Bone and Mineral Research.

Ms. van Hulten and colleagues compared SGLT2 inhibitors with dipeptidyl peptidase–4 (DPP-4) inhibitors because the latter are used in similar populations and have been shown to have no effect on fracture risk.

“What we found is that SGLT2 inhibitors are not associated with an increased fracture risk. Even with a duration of use of over 811 days, we did not observe an increased hazard ratio for fractures when compared DPP-4 inhibitor users,” Ms. van Hulten said.

SGLT2 inhibitors reduce blood sugar by increasing elimination of sugar in the urine. They also increase phosphate, reduce calcium, and increase parathyroid hormone, which could in turn negatively affect bone turnover, according to Ms. van Hulten.

In the new study, conducted between January 2013 and June 2020, the researchers used propensity score matching to compare adult patients, including 13,807 who were prescribed SGLT2 inhibitors and 28,524 who were prescribed DPP-4 inhibitors for the first time. They matched patients based on demographics, comorbidities, comedication, and lifestyle factors.

There was no association between SGLT2 inhibitor use and overall fracture risk or major osteoporotic, hip, vertebral, humerus, radius, or ulna fractures. There was no difference in risk for any duration of use, even with the longest duration of use of 811 days (adjusted hazard ratio, 1.0). There were no differences among specific SGLT2 inhibitors, including canagliflozin (aHR, 1.12; 95% confidence interval, 0.73-1.72). Analyses by sex and age also revealed no statistically significant differences between the two drug classes.

During the Q&A session after the presentation, Sarah Berry, MD, MPH, an associate professor of medicine at Harvard Medical School and a clinical researcher at the Marcus Institute for Aging Research, both in Boston, noted the trend toward an increase in fracture risk in the first 90 days. “It looked like there was something going on in the first 90 days, and then after that the results were much closer to the null. I would put out maybe another potential mechanism whereby the SGLT2 inhibitors might cause fracture, and that’s falls. They cause polyuria, and any drug you give that causes women to rush to the bathroom may well cause fractures, particularly in the short term,” Dr. Berry said.

Ms. van Hulten agreed, and also brought up that the drugs can cause osmotic diuresis. That can lead to hypovolemia, the symptoms of which include weakness, fatigue, and dizziness. “And increased falls, of course, increases fracture risk. We do not expect anything to happen to bone metabolism in the first 90 days. I think we can agree that there would be more time needed to alter the bone enough to increase fracture risk, so we expect that this trend toward an increased risk might be attributable to that increased fall risk that might occur with SGLT2 inhibitor use,” she said.

It’s possible that such a mechanism explains increased fracture risk seen in some earlier short-term studies, she added.

Overall, Ms. van Hulten said that the results should provide some confidence in SGLT2 inhibitors, though more work needs to be done. “I think we provide reassurance that SGLT2 inhibitors are safe to use. However, we still only have a median follow-up of 1.6 years. It’s not as long as we maybe would like, but it’s the best we can do with the data available, since the SGLT2 inhibitors have only been used since 2013. So maybe it’s best to prescribe it and keep [fall risk] in mind and look into the effects later on again, but it seems to be safe to use.”

The study received funding from the Novo Nordisk Foundation. Ms. van Hulten and Dr. Berry reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

VANCOUVER – In patients with type 2 diabetes, sodium-glucose cotransporter 2 (SGLT2) inhibitors as an adjunct to metformin were not associated with an increase in fracture risk, according to a new real-world study.

There have been some reports of an increase in fracture risk associated with SGLT2 inhibitors, and it was observed in the phase 3 CANVAS trial of canagliflozin (Invokana), which led to a Food and Drug Administration warning of fracture risks associated with canagliflozin use. Some ensuing studies did not show an increased risk, but these studies were generally less than a year in duration and may have missed longer-term risk, according to Veerle van Hulten, MSc.

“Fracture risk is something that takes a long time to develop, so we wanted to have a longer follow-up. We looked into the CPRD [Clinical Practice Research Datalink], which is a beautiful database containing real-world data from primary care practices,” said Ms. van Hulten, a PhD student at Maastricht (the Netherlands) University, who presented the study at the annual meeting of the American Society for Bone and Mineral Research.

Ms. van Hulten and colleagues compared SGLT2 inhibitors with dipeptidyl peptidase–4 (DPP-4) inhibitors because the latter are used in similar populations and have been shown to have no effect on fracture risk.

“What we found is that SGLT2 inhibitors are not associated with an increased fracture risk. Even with a duration of use of over 811 days, we did not observe an increased hazard ratio for fractures when compared DPP-4 inhibitor users,” Ms. van Hulten said.

SGLT2 inhibitors reduce blood sugar by increasing elimination of sugar in the urine. They also increase phosphate, reduce calcium, and increase parathyroid hormone, which could in turn negatively affect bone turnover, according to Ms. van Hulten.

In the new study, conducted between January 2013 and June 2020, the researchers used propensity score matching to compare adult patients, including 13,807 who were prescribed SGLT2 inhibitors and 28,524 who were prescribed DPP-4 inhibitors for the first time. They matched patients based on demographics, comorbidities, comedication, and lifestyle factors.

There was no association between SGLT2 inhibitor use and overall fracture risk or major osteoporotic, hip, vertebral, humerus, radius, or ulna fractures. There was no difference in risk for any duration of use, even with the longest duration of use of 811 days (adjusted hazard ratio, 1.0). There were no differences among specific SGLT2 inhibitors, including canagliflozin (aHR, 1.12; 95% confidence interval, 0.73-1.72). Analyses by sex and age also revealed no statistically significant differences between the two drug classes.

During the Q&A session after the presentation, Sarah Berry, MD, MPH, an associate professor of medicine at Harvard Medical School and a clinical researcher at the Marcus Institute for Aging Research, both in Boston, noted the trend toward an increase in fracture risk in the first 90 days. “It looked like there was something going on in the first 90 days, and then after that the results were much closer to the null. I would put out maybe another potential mechanism whereby the SGLT2 inhibitors might cause fracture, and that’s falls. They cause polyuria, and any drug you give that causes women to rush to the bathroom may well cause fractures, particularly in the short term,” Dr. Berry said.

Ms. van Hulten agreed, and also brought up that the drugs can cause osmotic diuresis. That can lead to hypovolemia, the symptoms of which include weakness, fatigue, and dizziness. “And increased falls, of course, increases fracture risk. We do not expect anything to happen to bone metabolism in the first 90 days. I think we can agree that there would be more time needed to alter the bone enough to increase fracture risk, so we expect that this trend toward an increased risk might be attributable to that increased fall risk that might occur with SGLT2 inhibitor use,” she said.

It’s possible that such a mechanism explains increased fracture risk seen in some earlier short-term studies, she added.

Overall, Ms. van Hulten said that the results should provide some confidence in SGLT2 inhibitors, though more work needs to be done. “I think we provide reassurance that SGLT2 inhibitors are safe to use. However, we still only have a median follow-up of 1.6 years. It’s not as long as we maybe would like, but it’s the best we can do with the data available, since the SGLT2 inhibitors have only been used since 2013. So maybe it’s best to prescribe it and keep [fall risk] in mind and look into the effects later on again, but it seems to be safe to use.”

The study received funding from the Novo Nordisk Foundation. Ms. van Hulten and Dr. Berry reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

The strike by health care workers at Kaiser Permanente may not involve physicians (yet). But as more doctors in the United States are finding themselves working as salaried employees, physicians can – and probably will – become a powerful force for change in a health care system that has shown itself to be increasingly hostile to employee concerns over issues involving patient care, wages and benefits, safety, and well-being.

Salaried employment has its challenges. Physician-employees may have less autonomy and voice in decision-making that affects patients. They may splinter into fragmented work groups; feel isolated; and have different imperatives based on who they are, what they want, and where they work. They may feel more removed from their patients and struggle to build strong relationships, with their employers in the way.

Yet important opportunities exist for doctors when embracing their employee side. These opportunities can help them and other health care workers fight effectively for their interests and those of patients in a corporatized health care system. Examples of these interests include adequate compensation, wellness, job security, patient and worker safety, health care quality, reasonable workloads and schedules, and fair treatment by employers, including the need to exhibit a strong collective voice in organizational decision-making.

Some believe that physician-employees must be unionized to maximize their rights and power as employees. Many expect physician unionization to take hold more fully over time. Medical residents, the doctors of tomorrow, are already considering unionization in greater numbers. Some are also doing it in the same employment setting alongside other health professionals, such as nurses.

Having studied doctors and their employment situations for years, I am convinced that whether through unionization or another approach, physicians must also change how they think about control; train and learn alongside other health care workers who share similar interests; and elevate at an early career stage their knowledge of the business side of health care.
 

Adopt a more pragmatic definition of autonomy

Doctors must embrace an updated definition of autonomy – one that matches their status as highly paid labor.

When I have spoken to physicians in my research about what autonomy means to them, many seem unable to reconceptualize it from a vague and absolute form of their profession’s strategic control over their economic fates and technical skills toward an individualized control that is situation-specific, one centered on winning the daily fights about workplace bread-and-butter issues such as those mentioned above.

But a more pragmatic definition of autonomy could get doctors focused on influencing important issues of the patient-care day and enhance their negotiating power with employers. It would allow physicians to break out of what often seems a paralysis of inaction – waiting for employers, insurers, or the government to reinstate the profession’s idealized version of control by handing it back the keys to the health care system through major regulatory, structural, and reimbursement-related changes. This fantasy is unlikely to become reality.

Physician-employees I’ve talked to over the years understand their everyday challenges. But when it comes to engaging in localized and sustained action to overcome them, they often perform less well, leading to feelings of helplessness and burnout. Valuing tactical control over their jobs and work setting will yield smaller but more impactful wins as employees intent on making their everyday work lives better.
 

Train alongside other health care professionals

Physicians must accept that how they are trained no longer prepares them for the employee world into which most are dropped. For instance, unless doctors are trained collaboratively alongside other health care professionals – such as nurses – they are less likely to identify closely with these colleagues once in practice. There is strength in numbers, so this mutual identification empowers both groups of employees. Yet, medical education remains largely the same: training young medical students in isolation for the first couple of years, then placing them into clerkships and residencies where true interprofessional care opportunities remain stunted and secondary to the “physician as captain of the team” mantra.

Unfortunately, the “hidden curriculum” of medicine helps convince medical students and residents early in their careers that they are the unquestioned leaders in patient care settings. This hierarchy encourages some doctors to keep their psychological distance from other members of the health care team and to resist sharing power, concerns, or insights with less skilled health care workers. This socialization harms the ability of physicians to act in a unified fashion alongside these other workers. Having physicians learn and train alongside other health professionals yields positive benefits for collective advocacy, including a shared sense of purpose, positive views on collaboration with others in the health setting, and greater development of bonds with nonphysician coworkers.
 

Integrate business with medical training in real time

Medical students and residents generally lack exposure to the everyday business realities of the U.S. health care system. This gap hinders their ability to understand the employee world and push for the types of changes and work conditions that benefit all health care workers. Formal business and management training should be a required part of every U.S. medical school and residency curriculum from day one. If you see it at all in medical schools now, it is mostly by accident, or given separate treatment in the form of standalone MBA or MPH degrees that rarely integrate organically and in real time with actual medical training. Not every doctor needs an MBA or MPH degree. However, all of them require a stronger contextual understanding of how the medicine they wish to practice is shaped by the economic and fiscal circumstances surrounding it – circumstances they do not control.

This is another reason why young doctors are unhappy and burned out. They cannot push for specific changes or properly critique the pros and cons of how their work is structured because they have not been made aware, in real time as they learn clinical practice, how their jobs are shaped by realities such as insurance coverage and reimbursement, the fragmentation of the care delivery system, their employer’s financial health , and the socioeconomic circumstances of their patients. They aren’t given the methods and tools related to process and quality improvement, budgeting, negotiation, risk management, leadership, and talent management that might help them navigate these undermining forces. They also get little advance exposure in their training to important workplace “soft” skills in such areas as how to work in teams, networking, communication and listening, empathy, and problem-solving – all necessary foci for bringing them closer to other health care workers and advocating alongside them effectively with health care employers.

Now is the time for physicians to embrace their identity as employees. Doing so is in their own best interest as professionals. It will help others in the health care workforce as well as patients. Moreover, it provides a needed counterbalance to the powerful corporate ethos now ascendant in U.S. health care.

Timothy Hoff, PhD, is a professor of management and healthcare systems at Northeastern University, Boston, and an associate fellow at the University of Oxford, England. He disclosed no relevant conflicts of interest.

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

The strike by health care workers at Kaiser Permanente may not involve physicians (yet). But as more doctors in the United States are finding themselves working as salaried employees, physicians can – and probably will – become a powerful force for change in a health care system that has shown itself to be increasingly hostile to employee concerns over issues involving patient care, wages and benefits, safety, and well-being.

Salaried employment has its challenges. Physician-employees may have less autonomy and voice in decision-making that affects patients. They may splinter into fragmented work groups; feel isolated; and have different imperatives based on who they are, what they want, and where they work. They may feel more removed from their patients and struggle to build strong relationships, with their employers in the way.

Yet important opportunities exist for doctors when embracing their employee side. These opportunities can help them and other health care workers fight effectively for their interests and those of patients in a corporatized health care system. Examples of these interests include adequate compensation, wellness, job security, patient and worker safety, health care quality, reasonable workloads and schedules, and fair treatment by employers, including the need to exhibit a strong collective voice in organizational decision-making.

Some believe that physician-employees must be unionized to maximize their rights and power as employees. Many expect physician unionization to take hold more fully over time. Medical residents, the doctors of tomorrow, are already considering unionization in greater numbers. Some are also doing it in the same employment setting alongside other health professionals, such as nurses.

Having studied doctors and their employment situations for years, I am convinced that whether through unionization or another approach, physicians must also change how they think about control; train and learn alongside other health care workers who share similar interests; and elevate at an early career stage their knowledge of the business side of health care.
 

Adopt a more pragmatic definition of autonomy

Doctors must embrace an updated definition of autonomy – one that matches their status as highly paid labor.

When I have spoken to physicians in my research about what autonomy means to them, many seem unable to reconceptualize it from a vague and absolute form of their profession’s strategic control over their economic fates and technical skills toward an individualized control that is situation-specific, one centered on winning the daily fights about workplace bread-and-butter issues such as those mentioned above.

But a more pragmatic definition of autonomy could get doctors focused on influencing important issues of the patient-care day and enhance their negotiating power with employers. It would allow physicians to break out of what often seems a paralysis of inaction – waiting for employers, insurers, or the government to reinstate the profession’s idealized version of control by handing it back the keys to the health care system through major regulatory, structural, and reimbursement-related changes. This fantasy is unlikely to become reality.

Physician-employees I’ve talked to over the years understand their everyday challenges. But when it comes to engaging in localized and sustained action to overcome them, they often perform less well, leading to feelings of helplessness and burnout. Valuing tactical control over their jobs and work setting will yield smaller but more impactful wins as employees intent on making their everyday work lives better.
 

Train alongside other health care professionals

Physicians must accept that how they are trained no longer prepares them for the employee world into which most are dropped. For instance, unless doctors are trained collaboratively alongside other health care professionals – such as nurses – they are less likely to identify closely with these colleagues once in practice. There is strength in numbers, so this mutual identification empowers both groups of employees. Yet, medical education remains largely the same: training young medical students in isolation for the first couple of years, then placing them into clerkships and residencies where true interprofessional care opportunities remain stunted and secondary to the “physician as captain of the team” mantra.

Unfortunately, the “hidden curriculum” of medicine helps convince medical students and residents early in their careers that they are the unquestioned leaders in patient care settings. This hierarchy encourages some doctors to keep their psychological distance from other members of the health care team and to resist sharing power, concerns, or insights with less skilled health care workers. This socialization harms the ability of physicians to act in a unified fashion alongside these other workers. Having physicians learn and train alongside other health professionals yields positive benefits for collective advocacy, including a shared sense of purpose, positive views on collaboration with others in the health setting, and greater development of bonds with nonphysician coworkers.
 

Integrate business with medical training in real time

Medical students and residents generally lack exposure to the everyday business realities of the U.S. health care system. This gap hinders their ability to understand the employee world and push for the types of changes and work conditions that benefit all health care workers. Formal business and management training should be a required part of every U.S. medical school and residency curriculum from day one. If you see it at all in medical schools now, it is mostly by accident, or given separate treatment in the form of standalone MBA or MPH degrees that rarely integrate organically and in real time with actual medical training. Not every doctor needs an MBA or MPH degree. However, all of them require a stronger contextual understanding of how the medicine they wish to practice is shaped by the economic and fiscal circumstances surrounding it – circumstances they do not control.

This is another reason why young doctors are unhappy and burned out. They cannot push for specific changes or properly critique the pros and cons of how their work is structured because they have not been made aware, in real time as they learn clinical practice, how their jobs are shaped by realities such as insurance coverage and reimbursement, the fragmentation of the care delivery system, their employer’s financial health , and the socioeconomic circumstances of their patients. They aren’t given the methods and tools related to process and quality improvement, budgeting, negotiation, risk management, leadership, and talent management that might help them navigate these undermining forces. They also get little advance exposure in their training to important workplace “soft” skills in such areas as how to work in teams, networking, communication and listening, empathy, and problem-solving – all necessary foci for bringing them closer to other health care workers and advocating alongside them effectively with health care employers.

Now is the time for physicians to embrace their identity as employees. Doing so is in their own best interest as professionals. It will help others in the health care workforce as well as patients. Moreover, it provides a needed counterbalance to the powerful corporate ethos now ascendant in U.S. health care.

Timothy Hoff, PhD, is a professor of management and healthcare systems at Northeastern University, Boston, and an associate fellow at the University of Oxford, England. He disclosed no relevant conflicts of interest.

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

The strike by health care workers at Kaiser Permanente may not involve physicians (yet). But as more doctors in the United States are finding themselves working as salaried employees, physicians can – and probably will – become a powerful force for change in a health care system that has shown itself to be increasingly hostile to employee concerns over issues involving patient care, wages and benefits, safety, and well-being.

Salaried employment has its challenges. Physician-employees may have less autonomy and voice in decision-making that affects patients. They may splinter into fragmented work groups; feel isolated; and have different imperatives based on who they are, what they want, and where they work. They may feel more removed from their patients and struggle to build strong relationships, with their employers in the way.

Yet important opportunities exist for doctors when embracing their employee side. These opportunities can help them and other health care workers fight effectively for their interests and those of patients in a corporatized health care system. Examples of these interests include adequate compensation, wellness, job security, patient and worker safety, health care quality, reasonable workloads and schedules, and fair treatment by employers, including the need to exhibit a strong collective voice in organizational decision-making.

Some believe that physician-employees must be unionized to maximize their rights and power as employees. Many expect physician unionization to take hold more fully over time. Medical residents, the doctors of tomorrow, are already considering unionization in greater numbers. Some are also doing it in the same employment setting alongside other health professionals, such as nurses.

Having studied doctors and their employment situations for years, I am convinced that whether through unionization or another approach, physicians must also change how they think about control; train and learn alongside other health care workers who share similar interests; and elevate at an early career stage their knowledge of the business side of health care.
 

Adopt a more pragmatic definition of autonomy

Doctors must embrace an updated definition of autonomy – one that matches their status as highly paid labor.

When I have spoken to physicians in my research about what autonomy means to them, many seem unable to reconceptualize it from a vague and absolute form of their profession’s strategic control over their economic fates and technical skills toward an individualized control that is situation-specific, one centered on winning the daily fights about workplace bread-and-butter issues such as those mentioned above.

But a more pragmatic definition of autonomy could get doctors focused on influencing important issues of the patient-care day and enhance their negotiating power with employers. It would allow physicians to break out of what often seems a paralysis of inaction – waiting for employers, insurers, or the government to reinstate the profession’s idealized version of control by handing it back the keys to the health care system through major regulatory, structural, and reimbursement-related changes. This fantasy is unlikely to become reality.

Physician-employees I’ve talked to over the years understand their everyday challenges. But when it comes to engaging in localized and sustained action to overcome them, they often perform less well, leading to feelings of helplessness and burnout. Valuing tactical control over their jobs and work setting will yield smaller but more impactful wins as employees intent on making their everyday work lives better.
 

Train alongside other health care professionals

Physicians must accept that how they are trained no longer prepares them for the employee world into which most are dropped. For instance, unless doctors are trained collaboratively alongside other health care professionals – such as nurses – they are less likely to identify closely with these colleagues once in practice. There is strength in numbers, so this mutual identification empowers both groups of employees. Yet, medical education remains largely the same: training young medical students in isolation for the first couple of years, then placing them into clerkships and residencies where true interprofessional care opportunities remain stunted and secondary to the “physician as captain of the team” mantra.

Unfortunately, the “hidden curriculum” of medicine helps convince medical students and residents early in their careers that they are the unquestioned leaders in patient care settings. This hierarchy encourages some doctors to keep their psychological distance from other members of the health care team and to resist sharing power, concerns, or insights with less skilled health care workers. This socialization harms the ability of physicians to act in a unified fashion alongside these other workers. Having physicians learn and train alongside other health professionals yields positive benefits for collective advocacy, including a shared sense of purpose, positive views on collaboration with others in the health setting, and greater development of bonds with nonphysician coworkers.
 

Integrate business with medical training in real time

Medical students and residents generally lack exposure to the everyday business realities of the U.S. health care system. This gap hinders their ability to understand the employee world and push for the types of changes and work conditions that benefit all health care workers. Formal business and management training should be a required part of every U.S. medical school and residency curriculum from day one. If you see it at all in medical schools now, it is mostly by accident, or given separate treatment in the form of standalone MBA or MPH degrees that rarely integrate organically and in real time with actual medical training. Not every doctor needs an MBA or MPH degree. However, all of them require a stronger contextual understanding of how the medicine they wish to practice is shaped by the economic and fiscal circumstances surrounding it – circumstances they do not control.

This is another reason why young doctors are unhappy and burned out. They cannot push for specific changes or properly critique the pros and cons of how their work is structured because they have not been made aware, in real time as they learn clinical practice, how their jobs are shaped by realities such as insurance coverage and reimbursement, the fragmentation of the care delivery system, their employer’s financial health , and the socioeconomic circumstances of their patients. They aren’t given the methods and tools related to process and quality improvement, budgeting, negotiation, risk management, leadership, and talent management that might help them navigate these undermining forces. They also get little advance exposure in their training to important workplace “soft” skills in such areas as how to work in teams, networking, communication and listening, empathy, and problem-solving – all necessary foci for bringing them closer to other health care workers and advocating alongside them effectively with health care employers.

Now is the time for physicians to embrace their identity as employees. Doing so is in their own best interest as professionals. It will help others in the health care workforce as well as patients. Moreover, it provides a needed counterbalance to the powerful corporate ethos now ascendant in U.S. health care.

Timothy Hoff, PhD, is a professor of management and healthcare systems at Northeastern University, Boston, and an associate fellow at the University of Oxford, England. He disclosed no relevant conflicts of interest.

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

The Food and Drug Administration has approved bimekizumab-bkzx (Bimzelx) for the treatment of moderate to severe plaque psoriasis in adults, the manufacturer announced in a press release.

The indication is for adults who are candidates for systemic therapy or phototherapy.

With this approval, bimekizumab becomes the only interleukin (IL)-17A and IL-17F inhibitor approved for the treatment of these patients. Psoriasis affects more than 7.5 million U.S. adults, according to the National Psoriasis Foundation.

“We have been eagerly awaiting bimekizumab,” Mark Lebwohl, MD, bimekizumab investigator and dean for clinical therapeutics at the Icahn School of Medicine at Mount Sinai, New York City, said in the press release.

Dr. Lebwohl states that bimekizumab “achieved superior levels of skin clearance at week 16 compared to placebo and three existing biologics for psoriasis, with responses being rapid and lasting up to a year. Long-term data have also shown that the majority of patients maintained high levels of clinical response through three years.”

The most common adverse reactions (occurring in at least 1% of patients) are upper respiratory infections, oral candidiasis, headache, tinea infections, gastroenteritis, herpes simplex infections, acne, folliculitis, other Candida infections, fatigue, and injection site reactions, according to the company, UCB.
 

Available in about 1 month in U.S.

Bimekizumab can be administered by a health care provider or it can be self-injected by a patient after training. It is available as a single-dose prefilled autoinjector and a single-dose prefilled syringe and will be available in the United States in about 1 month.

The recommended dosage of bimekizumab for patients with psoriasis is 320 mg (two subcutaneous injections of 160 mg each) at baseline, then on weeks 4, 8, 12, and 16, then every 8 weeks thereafter. For patients weighing at least 120 kg (about 265 lb), a dosage of 320 mg every 4 weeks after week 16 may be considered, the company states.

Three phase 3 trials

Approval was based on three phase 3 multicenter, randomized, placebo and/or active comparator-controlled trials: bimekizumab versus placebo and ustekinumab (BE VIVID); versus placebo (BE READY); and versus adalimumab (BE SURE).

“All studies met their co-primary endpoints and all ranked secondary endpoints,” the company reports. Secondary endpoints included the Psoriasis Area and Severity Index (PASI) 75 at week 4 and PASI 100 (complete skin clearance) at week 16.

Highlights from the trials include the following results, according to UCB:

• Clear or almost clear skin: More than 8 out of 10 patients achieved a 90% or greater reduction from baseline in the PASI 90 and an Investigator’s Global Assessment score of 0/1 at week 16.
• Complete skin clearance: About 60% of patients achieved PASI 100 at week 16.
• Time to response: More than 70% of patients achieved PASI 75 at week 4 following one 320-mg dose.

Safety information

The safety information includes the statement that bimekizumab may increase the risk for suicidal ideation and behavior, though a causal association has not been established. Prescribers should advise patients, caregivers, and families “to monitor for emergence or worsening of depression, suicidal ideation, or other mood changes,” according to the prescribing information.

Bimekizumab is being studied for other conditions, including hidradenitis suppurativa. In the European Union, it was approved for the treatment of psoriasis in 2021 and for the treatment of psoriatic arthritis and ankylosing spondylitis in June 2023.

Dr. Lebwohl is an investigator for UCB. He has not accepted any consulting payments from UCB.

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

The Food and Drug Administration has approved bimekizumab-bkzx (Bimzelx) for the treatment of moderate to severe plaque psoriasis in adults, the manufacturer announced in a press release.

The indication is for adults who are candidates for systemic therapy or phototherapy.

With this approval, bimekizumab becomes the only interleukin (IL)-17A and IL-17F inhibitor approved for the treatment of these patients. Psoriasis affects more than 7.5 million U.S. adults, according to the National Psoriasis Foundation.

“We have been eagerly awaiting bimekizumab,” Mark Lebwohl, MD, bimekizumab investigator and dean for clinical therapeutics at the Icahn School of Medicine at Mount Sinai, New York City, said in the press release.

Dr. Lebwohl states that bimekizumab “achieved superior levels of skin clearance at week 16 compared to placebo and three existing biologics for psoriasis, with responses being rapid and lasting up to a year. Long-term data have also shown that the majority of patients maintained high levels of clinical response through three years.”

The most common adverse reactions (occurring in at least 1% of patients) are upper respiratory infections, oral candidiasis, headache, tinea infections, gastroenteritis, herpes simplex infections, acne, folliculitis, other Candida infections, fatigue, and injection site reactions, according to the company, UCB.
 

Available in about 1 month in U.S.

Bimekizumab can be administered by a health care provider or it can be self-injected by a patient after training. It is available as a single-dose prefilled autoinjector and a single-dose prefilled syringe and will be available in the United States in about 1 month.

The recommended dosage of bimekizumab for patients with psoriasis is 320 mg (two subcutaneous injections of 160 mg each) at baseline, then on weeks 4, 8, 12, and 16, then every 8 weeks thereafter. For patients weighing at least 120 kg (about 265 lb), a dosage of 320 mg every 4 weeks after week 16 may be considered, the company states.

Three phase 3 trials

Approval was based on three phase 3 multicenter, randomized, placebo and/or active comparator-controlled trials: bimekizumab versus placebo and ustekinumab (BE VIVID); versus placebo (BE READY); and versus adalimumab (BE SURE).

“All studies met their co-primary endpoints and all ranked secondary endpoints,” the company reports. Secondary endpoints included the Psoriasis Area and Severity Index (PASI) 75 at week 4 and PASI 100 (complete skin clearance) at week 16.

Highlights from the trials include the following results, according to UCB:

• Clear or almost clear skin: More than 8 out of 10 patients achieved a 90% or greater reduction from baseline in the PASI 90 and an Investigator’s Global Assessment score of 0/1 at week 16.
• Complete skin clearance: About 60% of patients achieved PASI 100 at week 16.
• Time to response: More than 70% of patients achieved PASI 75 at week 4 following one 320-mg dose.

Safety information

The safety information includes the statement that bimekizumab may increase the risk for suicidal ideation and behavior, though a causal association has not been established. Prescribers should advise patients, caregivers, and families “to monitor for emergence or worsening of depression, suicidal ideation, or other mood changes,” according to the prescribing information.

Bimekizumab is being studied for other conditions, including hidradenitis suppurativa. In the European Union, it was approved for the treatment of psoriasis in 2021 and for the treatment of psoriatic arthritis and ankylosing spondylitis in June 2023.

Dr. Lebwohl is an investigator for UCB. He has not accepted any consulting payments from UCB.

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

The Food and Drug Administration has approved bimekizumab-bkzx (Bimzelx) for the treatment of moderate to severe plaque psoriasis in adults, the manufacturer announced in a press release.

The indication is for adults who are candidates for systemic therapy or phototherapy.

With this approval, bimekizumab becomes the only interleukin (IL)-17A and IL-17F inhibitor approved for the treatment of these patients. Psoriasis affects more than 7.5 million U.S. adults, according to the National Psoriasis Foundation.

“We have been eagerly awaiting bimekizumab,” Mark Lebwohl, MD, bimekizumab investigator and dean for clinical therapeutics at the Icahn School of Medicine at Mount Sinai, New York City, said in the press release.

Dr. Lebwohl states that bimekizumab “achieved superior levels of skin clearance at week 16 compared to placebo and three existing biologics for psoriasis, with responses being rapid and lasting up to a year. Long-term data have also shown that the majority of patients maintained high levels of clinical response through three years.”

The most common adverse reactions (occurring in at least 1% of patients) are upper respiratory infections, oral candidiasis, headache, tinea infections, gastroenteritis, herpes simplex infections, acne, folliculitis, other Candida infections, fatigue, and injection site reactions, according to the company, UCB.
 

Available in about 1 month in U.S.

Bimekizumab can be administered by a health care provider or it can be self-injected by a patient after training. It is available as a single-dose prefilled autoinjector and a single-dose prefilled syringe and will be available in the United States in about 1 month.

The recommended dosage of bimekizumab for patients with psoriasis is 320 mg (two subcutaneous injections of 160 mg each) at baseline, then on weeks 4, 8, 12, and 16, then every 8 weeks thereafter. For patients weighing at least 120 kg (about 265 lb), a dosage of 320 mg every 4 weeks after week 16 may be considered, the company states.

Three phase 3 trials

Approval was based on three phase 3 multicenter, randomized, placebo and/or active comparator-controlled trials: bimekizumab versus placebo and ustekinumab (BE VIVID); versus placebo (BE READY); and versus adalimumab (BE SURE).

“All studies met their co-primary endpoints and all ranked secondary endpoints,” the company reports. Secondary endpoints included the Psoriasis Area and Severity Index (PASI) 75 at week 4 and PASI 100 (complete skin clearance) at week 16.

Highlights from the trials include the following results, according to UCB:

• Clear or almost clear skin: More than 8 out of 10 patients achieved a 90% or greater reduction from baseline in the PASI 90 and an Investigator’s Global Assessment score of 0/1 at week 16.
• Complete skin clearance: About 60% of patients achieved PASI 100 at week 16.
• Time to response: More than 70% of patients achieved PASI 75 at week 4 following one 320-mg dose.

Safety information

The safety information includes the statement that bimekizumab may increase the risk for suicidal ideation and behavior, though a causal association has not been established. Prescribers should advise patients, caregivers, and families “to monitor for emergence or worsening of depression, suicidal ideation, or other mood changes,” according to the prescribing information.

Bimekizumab is being studied for other conditions, including hidradenitis suppurativa. In the European Union, it was approved for the treatment of psoriasis in 2021 and for the treatment of psoriatic arthritis and ankylosing spondylitis in June 2023.

Dr. Lebwohl is an investigator for UCB. He has not accepted any consulting payments from UCB.

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

In the year since generative artificial intelligence (AI) software first began to emerge for use, the staggering pace and breadth of development has condensed years of growth and change into months and weeks. Among the settings where these tools may find the greatest straight-line relevance is private medical practice.

Last month’s column on the basics of AI sparked some interesting questions regarding the various generative algorithms and their usefulness to us in medicine. A multitude of generative AI products with potential medical applications are now available, with new ones appearing almost weekly. (As always, I have no financial interest in any product or service mentioned in this column.)

Last month, I discussed ChatGPT, the best-known AI algorithm, and some of its applications in clinical practice, such as generating website, video, and blog content. ChatGPT can also provide rapid and concise answers to general medical questions, like a search engine – but with more natural language processing and contextual understanding. Additionally, the algorithm can draft generic medical documents, including templates for after-visit summaries, postprocedure instructions, referrals, prior authorization appeal letters, and educational handouts.

Another useful feature of ChatGPT is its ability to provide accurate and conversational language translations, thus serving as an interpreter during clinic visits in situations where a human translator is not available. It also has potential uses in clinical research by finding resources, formulating hypotheses, drafting study protocols, and collecting large amounts of data in short periods of time. Other possibilities include survey administration, clinical trial recruitment, and automatic medication monitoring.

GPT-4, the latest version of ChatGPT, is reported to have greater problem-solving abilities and an even broader knowledge base. Among its claimed skills are the ability to find the latest literature in a given area, write a discharge summary for a patient following an uncomplicated surgery, and an image analysis feature to identify objects in photos. GPT-4 has been praised as having “the potential to help drive medical innovation, from aiding with patient discharge notes, summarizing recent clinical trials, providing information on ethical guidelines, and much more.”

Bard, an AI “chat bot” introduced by Google earlier this year, intends to leverage Google’s enormous database to compete with ChatGPT in providing answers to medical questions. Bard also hopes to play a pivotal role in expanding telemedicine and remote care via Google’s secure connections and access to patient records and medical history, and “facilitate seamless communication through appointment scheduling, messaging, and sharing medical images,” according to PackT, a website for IT professionals. The company claims that Bard’s integration of AI and machine learning capabilities will serve to elevate health care efficiency and patient outcomes, PackT says, and “the platform’s AI system quickly and accurately analyzes patient records, identifies patterns and trends, and aids medical professionals in developing effective treatment plans.”

Doximity has introduced an AI engine called DocsGPT, an encrypted, HIPAA-compliant writing assistant that, the company says, can draft any form of professional correspondence, including prior authorization letters, insurance appeals, patient support letters, and patient education materials. The service is available at no charge to all U.S. physicians and medical students through their Doximity accounts.

Microsoft has introduced several AI products. BioGPT is a language model specifically designed for health care. Compared with GPT models that are trained on more general text data, BioGPT is purported to have a deeper understanding of the language used in biomedical research and can generate more accurate and relevant outputs for biomedical tasks, such as drug discovery, disease classification, and clinical decision support. Fabric is another health care–specific data and analytics platform the company described in an announcement in May. It can combine data from sources such as electronic health records, images, lab systems, medical devices, and claims systems so hospitals and offices can standardize it and access it in the same place. Microsoft said the new tools will help eliminate the “time-consuming” process of searching through these sources one by one. Microsoft will also offer a new generative AI chatbot called the Azure Health Bot, which can pull information from a health organization’s own internal data as well as reputable external sources such as the Food and Drug Administration and the National Institutes of Health.

Several other AI products are available for clinicians. Tana served as an administrative aid and a clinical helper during the height of the COVID-19 pandemic, answering frequently asked questions, facilitating appointment management, and gathering preliminary medical information prior to teleconsultations. Dougall GPT is another AI chatbot tailored for health care professionals. It provides clinicians with AI-tuned answers to their queries, augmented by links to relevant, up-to-date, authoritative resources. It also assists in drafting patient instructions, consultation summaries, speeches, and professional correspondence. Wang has created Clinical Camel, an open-source health care–focused chatbot that assembles medical data with a combination of user-shared conversations and synthetic conversations derived from curated clinical articles. The Chinese company Baidu has rolled out Ernie as a potential rival to ChatGPT. You get the idea.

Of course, the inherent drawbacks of AI, such as producing false or biased information, perpetuating harmful stereotypes, and presenting information that has since been proven inaccurate or out-of-date, must always be kept in mind. All AI algorithms have been criticized for giving wrong answers, as their datasets are generally culled from information published in 2021 or earlier. Several of them have been shown to fabricate information – a phenomenon labeled “artificial hallucinations” in one article. “The scientific community must be vigilant in verifying the accuracy and reliability of the information provided by AI tools,” wrote the authors of that paper. “Researchers should use AI as an aid rather than a replacement for critical thinking and fact-checking.”

In the year since generative artificial intelligence (AI) software first began to emerge for use, the staggering pace and breadth of development has condensed years of growth and change into months and weeks. Among the settings where these tools may find the greatest straight-line relevance is private medical practice.

Last month’s column on the basics of AI sparked some interesting questions regarding the various generative algorithms and their usefulness to us in medicine. A multitude of generative AI products with potential medical applications are now available, with new ones appearing almost weekly. (As always, I have no financial interest in any product or service mentioned in this column.)

Last month, I discussed ChatGPT, the best-known AI algorithm, and some of its applications in clinical practice, such as generating website, video, and blog content. ChatGPT can also provide rapid and concise answers to general medical questions, like a search engine – but with more natural language processing and contextual understanding. Additionally, the algorithm can draft generic medical documents, including templates for after-visit summaries, postprocedure instructions, referrals, prior authorization appeal letters, and educational handouts.

Another useful feature of ChatGPT is its ability to provide accurate and conversational language translations, thus serving as an interpreter during clinic visits in situations where a human translator is not available. It also has potential uses in clinical research by finding resources, formulating hypotheses, drafting study protocols, and collecting large amounts of data in short periods of time. Other possibilities include survey administration, clinical trial recruitment, and automatic medication monitoring.

GPT-4, the latest version of ChatGPT, is reported to have greater problem-solving abilities and an even broader knowledge base. Among its claimed skills are the ability to find the latest literature in a given area, write a discharge summary for a patient following an uncomplicated surgery, and an image analysis feature to identify objects in photos. GPT-4 has been praised as having “the potential to help drive medical innovation, from aiding with patient discharge notes, summarizing recent clinical trials, providing information on ethical guidelines, and much more.”

Bard, an AI “chat bot” introduced by Google earlier this year, intends to leverage Google’s enormous database to compete with ChatGPT in providing answers to medical questions. Bard also hopes to play a pivotal role in expanding telemedicine and remote care via Google’s secure connections and access to patient records and medical history, and “facilitate seamless communication through appointment scheduling, messaging, and sharing medical images,” according to PackT, a website for IT professionals. The company claims that Bard’s integration of AI and machine learning capabilities will serve to elevate health care efficiency and patient outcomes, PackT says, and “the platform’s AI system quickly and accurately analyzes patient records, identifies patterns and trends, and aids medical professionals in developing effective treatment plans.”

Doximity has introduced an AI engine called DocsGPT, an encrypted, HIPAA-compliant writing assistant that, the company says, can draft any form of professional correspondence, including prior authorization letters, insurance appeals, patient support letters, and patient education materials. The service is available at no charge to all U.S. physicians and medical students through their Doximity accounts.

Microsoft has introduced several AI products. BioGPT is a language model specifically designed for health care. Compared with GPT models that are trained on more general text data, BioGPT is purported to have a deeper understanding of the language used in biomedical research and can generate more accurate and relevant outputs for biomedical tasks, such as drug discovery, disease classification, and clinical decision support. Fabric is another health care–specific data and analytics platform the company described in an announcement in May. It can combine data from sources such as electronic health records, images, lab systems, medical devices, and claims systems so hospitals and offices can standardize it and access it in the same place. Microsoft said the new tools will help eliminate the “time-consuming” process of searching through these sources one by one. Microsoft will also offer a new generative AI chatbot called the Azure Health Bot, which can pull information from a health organization’s own internal data as well as reputable external sources such as the Food and Drug Administration and the National Institutes of Health.

Several other AI products are available for clinicians. Tana served as an administrative aid and a clinical helper during the height of the COVID-19 pandemic, answering frequently asked questions, facilitating appointment management, and gathering preliminary medical information prior to teleconsultations. Dougall GPT is another AI chatbot tailored for health care professionals. It provides clinicians with AI-tuned answers to their queries, augmented by links to relevant, up-to-date, authoritative resources. It also assists in drafting patient instructions, consultation summaries, speeches, and professional correspondence. Wang has created Clinical Camel, an open-source health care–focused chatbot that assembles medical data with a combination of user-shared conversations and synthetic conversations derived from curated clinical articles. The Chinese company Baidu has rolled out Ernie as a potential rival to ChatGPT. You get the idea.

Of course, the inherent drawbacks of AI, such as producing false or biased information, perpetuating harmful stereotypes, and presenting information that has since been proven inaccurate or out-of-date, must always be kept in mind. All AI algorithms have been criticized for giving wrong answers, as their datasets are generally culled from information published in 2021 or earlier. Several of them have been shown to fabricate information – a phenomenon labeled “artificial hallucinations” in one article. “The scientific community must be vigilant in verifying the accuracy and reliability of the information provided by AI tools,” wrote the authors of that paper. “Researchers should use AI as an aid rather than a replacement for critical thinking and fact-checking.”

In the year since generative artificial intelligence (AI) software first began to emerge for use, the staggering pace and breadth of development has condensed years of growth and change into months and weeks. Among the settings where these tools may find the greatest straight-line relevance is private medical practice.

Last month’s column on the basics of AI sparked some interesting questions regarding the various generative algorithms and their usefulness to us in medicine. A multitude of generative AI products with potential medical applications are now available, with new ones appearing almost weekly. (As always, I have no financial interest in any product or service mentioned in this column.)

Last month, I discussed ChatGPT, the best-known AI algorithm, and some of its applications in clinical practice, such as generating website, video, and blog content. ChatGPT can also provide rapid and concise answers to general medical questions, like a search engine – but with more natural language processing and contextual understanding. Additionally, the algorithm can draft generic medical documents, including templates for after-visit summaries, postprocedure instructions, referrals, prior authorization appeal letters, and educational handouts.

Another useful feature of ChatGPT is its ability to provide accurate and conversational language translations, thus serving as an interpreter during clinic visits in situations where a human translator is not available. It also has potential uses in clinical research by finding resources, formulating hypotheses, drafting study protocols, and collecting large amounts of data in short periods of time. Other possibilities include survey administration, clinical trial recruitment, and automatic medication monitoring.

GPT-4, the latest version of ChatGPT, is reported to have greater problem-solving abilities and an even broader knowledge base. Among its claimed skills are the ability to find the latest literature in a given area, write a discharge summary for a patient following an uncomplicated surgery, and an image analysis feature to identify objects in photos. GPT-4 has been praised as having “the potential to help drive medical innovation, from aiding with patient discharge notes, summarizing recent clinical trials, providing information on ethical guidelines, and much more.”

Bard, an AI “chat bot” introduced by Google earlier this year, intends to leverage Google’s enormous database to compete with ChatGPT in providing answers to medical questions. Bard also hopes to play a pivotal role in expanding telemedicine and remote care via Google’s secure connections and access to patient records and medical history, and “facilitate seamless communication through appointment scheduling, messaging, and sharing medical images,” according to PackT, a website for IT professionals. The company claims that Bard’s integration of AI and machine learning capabilities will serve to elevate health care efficiency and patient outcomes, PackT says, and “the platform’s AI system quickly and accurately analyzes patient records, identifies patterns and trends, and aids medical professionals in developing effective treatment plans.”

Doximity has introduced an AI engine called DocsGPT, an encrypted, HIPAA-compliant writing assistant that, the company says, can draft any form of professional correspondence, including prior authorization letters, insurance appeals, patient support letters, and patient education materials. The service is available at no charge to all U.S. physicians and medical students through their Doximity accounts.

Microsoft has introduced several AI products. BioGPT is a language model specifically designed for health care. Compared with GPT models that are trained on more general text data, BioGPT is purported to have a deeper understanding of the language used in biomedical research and can generate more accurate and relevant outputs for biomedical tasks, such as drug discovery, disease classification, and clinical decision support. Fabric is another health care–specific data and analytics platform the company described in an announcement in May. It can combine data from sources such as electronic health records, images, lab systems, medical devices, and claims systems so hospitals and offices can standardize it and access it in the same place. Microsoft said the new tools will help eliminate the “time-consuming” process of searching through these sources one by one. Microsoft will also offer a new generative AI chatbot called the Azure Health Bot, which can pull information from a health organization’s own internal data as well as reputable external sources such as the Food and Drug Administration and the National Institutes of Health.

Several other AI products are available for clinicians. Tana served as an administrative aid and a clinical helper during the height of the COVID-19 pandemic, answering frequently asked questions, facilitating appointment management, and gathering preliminary medical information prior to teleconsultations. Dougall GPT is another AI chatbot tailored for health care professionals. It provides clinicians with AI-tuned answers to their queries, augmented by links to relevant, up-to-date, authoritative resources. It also assists in drafting patient instructions, consultation summaries, speeches, and professional correspondence. Wang has created Clinical Camel, an open-source health care–focused chatbot that assembles medical data with a combination of user-shared conversations and synthetic conversations derived from curated clinical articles. The Chinese company Baidu has rolled out Ernie as a potential rival to ChatGPT. You get the idea.

Of course, the inherent drawbacks of AI, such as producing false or biased information, perpetuating harmful stereotypes, and presenting information that has since been proven inaccurate or out-of-date, must always be kept in mind. All AI algorithms have been criticized for giving wrong answers, as their datasets are generally culled from information published in 2021 or earlier. Several of them have been shown to fabricate information – a phenomenon labeled “artificial hallucinations” in one article. “The scientific community must be vigilant in verifying the accuracy and reliability of the information provided by AI tools,” wrote the authors of that paper. “Researchers should use AI as an aid rather than a replacement for critical thinking and fact-checking.”