Two conservative interventions are effective for treating acute and subacute spine pain, new research suggests.

Results from the SPINE CARE randomized controlled trial showed that 6-8 weeks of an individualized postural therapy (IPT) or a multidisciplinary biopsychosocial intervention known as ICE (identify, coordinate, and enhance) that includes physical therapy were associated with small but statistically significant reductions in pain-related disability at 3 months compared with usual care.

In addition, spine-related health care spending did not differ significantly between ICE and usual care. However, IPT significantly increased spending compared with usual care.

“We found that, compared to usual primary care, both interventions reduced pain-related disability at 3 months and that these changes were sustained and clinically meaningful at 12 months – long after the interventions were over,” lead author Niteesh K. Choudhry, MD, PhD, Brigham and Women’s Hospital and Harvard Medical School, Boston, told this news organization.

The findings were published online in JAMA.
 

Common complaint

Spine pain is defined as pain that occurs in the neck or back, the investigators noted. It “accounted for more health spending than any other health condition in the U.S. in 2016,” they added.

“Spine pain is an exceptionally common reason for patients to visit their primary care providers,” Dr. Choudhry said.

The SPINE CARE trial enrolled 2,971 adults (60% were women; mean age was 51 years) with back or neck pain that had lasted less than 12 weeks. All were randomly allocated to usual care (no intervention, n = 992) or to the ICE (n = 829) or IPT (n = 1150) interventions.

The ICE care model stratifies patients on the basis of their risk of progression from acute to chronic pain and addresses biopsychosocial contributors to pain. Low-risk patients received one physical therapy (PT) visit and one coaching call, while higher-risk patients received three PT visits, three coaching calls, and one e-consultation.

The IPT intervention, which was delivered in 8 weekly sessions, focuses on postural realignment. IPT also emphasizes self-efficacy and self-management, including daily exercises to improve postural control, coordination, and muscle balance.

Results at 3 months showed that both the ICE and IPT groups improved significantly more in Oswestry Disability Index (ODI) scores than in the usual care group (ICE, 31.2 to 15.4; IPT, 29.3 to 15.4; usual care, 28.9 to 19.5).

At 3 months, the absolute difference in ODI score vs. usual care was −5.8 for ICE (95% confidence interval [CI], −7.7 to −3.9; P < .001) and −4.3 for IPT (95% CI, −5.9 to −2.6; P < .001) for IPT.

Both interventions reduced resource utilization, such as diagnostic imaging, procedures, and specialist visits, Dr. Choudhry reported. “Because of this, both reduced spending unrelated to the interventions themselves,” he added.

When the intervention costs were included, ICE resulted in lower costs overall than those of usual care ($139 less), while overall spending for IPT was higher than for usual care (by $941).

“We tested the interventions in a way that was integrated into primary care, so implementing them in other practice settings should be quite straightforward,” Dr. Choudhry said.

He noted that the ICE model does not currently exist as a complete program – but its components, such as physical therapy or specialist e-consults, do. “And we think that our results justify exploring how to set this up more broadly,” he said.

Dr. Choudhry added that IPT was tested using a specific provider (Egoscue), “which has locations in a variety of places in the U.S. and internationally, and so should also be straightforward to integrate into routine practice.”

However, other important factors, such as insurance coverage, will need to be explored in the future, he said.
 

Confirmatory evidence?

In an accompanying editorial, Erin Krebs, MD, Minneapolis VA Health Care System, and colleagues, noted that past systematic reviews have concluded that exercise therapies are “generally effective” for chronic back and neck pain, which is usually defined as pain lasting more than 12 weeks, but not for acute pain, defined as pain lasting less than 4-6 weeks.

“The present trial contributes evidence for effectiveness of exercise therapy among patients with a current episode of less than 12 weeks, meaning not yet chronic, but not necessarily acute,” the editorialists wrote.

“Clinicians should more often recommend structured exercise programs for subacute back or neck pain, especially when the pain is recurrent,” they added.

The study was funded by unrestricted philanthropic gifts to Stanford (Calif.) University. Dr. Choudhry received grants from Stanford University during the conduct of the study.

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

Two conservative interventions are effective for treating acute and subacute spine pain, new research suggests.

Results from the SPINE CARE randomized controlled trial showed that 6-8 weeks of an individualized postural therapy (IPT) or a multidisciplinary biopsychosocial intervention known as ICE (identify, coordinate, and enhance) that includes physical therapy were associated with small but statistically significant reductions in pain-related disability at 3 months compared with usual care.

In addition, spine-related health care spending did not differ significantly between ICE and usual care. However, IPT significantly increased spending compared with usual care.

“We found that, compared to usual primary care, both interventions reduced pain-related disability at 3 months and that these changes were sustained and clinically meaningful at 12 months – long after the interventions were over,” lead author Niteesh K. Choudhry, MD, PhD, Brigham and Women’s Hospital and Harvard Medical School, Boston, told this news organization.

The findings were published online in JAMA.
 

Common complaint

Spine pain is defined as pain that occurs in the neck or back, the investigators noted. It “accounted for more health spending than any other health condition in the U.S. in 2016,” they added.

“Spine pain is an exceptionally common reason for patients to visit their primary care providers,” Dr. Choudhry said.

The SPINE CARE trial enrolled 2,971 adults (60% were women; mean age was 51 years) with back or neck pain that had lasted less than 12 weeks. All were randomly allocated to usual care (no intervention, n = 992) or to the ICE (n = 829) or IPT (n = 1150) interventions.

The ICE care model stratifies patients on the basis of their risk of progression from acute to chronic pain and addresses biopsychosocial contributors to pain. Low-risk patients received one physical therapy (PT) visit and one coaching call, while higher-risk patients received three PT visits, three coaching calls, and one e-consultation.

The IPT intervention, which was delivered in 8 weekly sessions, focuses on postural realignment. IPT also emphasizes self-efficacy and self-management, including daily exercises to improve postural control, coordination, and muscle balance.

Results at 3 months showed that both the ICE and IPT groups improved significantly more in Oswestry Disability Index (ODI) scores than in the usual care group (ICE, 31.2 to 15.4; IPT, 29.3 to 15.4; usual care, 28.9 to 19.5).

At 3 months, the absolute difference in ODI score vs. usual care was −5.8 for ICE (95% confidence interval [CI], −7.7 to −3.9; P < .001) and −4.3 for IPT (95% CI, −5.9 to −2.6; P < .001) for IPT.

Both interventions reduced resource utilization, such as diagnostic imaging, procedures, and specialist visits, Dr. Choudhry reported. “Because of this, both reduced spending unrelated to the interventions themselves,” he added.

When the intervention costs were included, ICE resulted in lower costs overall than those of usual care ($139 less), while overall spending for IPT was higher than for usual care (by $941).

“We tested the interventions in a way that was integrated into primary care, so implementing them in other practice settings should be quite straightforward,” Dr. Choudhry said.

He noted that the ICE model does not currently exist as a complete program – but its components, such as physical therapy or specialist e-consults, do. “And we think that our results justify exploring how to set this up more broadly,” he said.

Dr. Choudhry added that IPT was tested using a specific provider (Egoscue), “which has locations in a variety of places in the U.S. and internationally, and so should also be straightforward to integrate into routine practice.”

However, other important factors, such as insurance coverage, will need to be explored in the future, he said.
 

Confirmatory evidence?

In an accompanying editorial, Erin Krebs, MD, Minneapolis VA Health Care System, and colleagues, noted that past systematic reviews have concluded that exercise therapies are “generally effective” for chronic back and neck pain, which is usually defined as pain lasting more than 12 weeks, but not for acute pain, defined as pain lasting less than 4-6 weeks.

“The present trial contributes evidence for effectiveness of exercise therapy among patients with a current episode of less than 12 weeks, meaning not yet chronic, but not necessarily acute,” the editorialists wrote.

“Clinicians should more often recommend structured exercise programs for subacute back or neck pain, especially when the pain is recurrent,” they added.

The study was funded by unrestricted philanthropic gifts to Stanford (Calif.) University. Dr. Choudhry received grants from Stanford University during the conduct of the study.

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

Two conservative interventions are effective for treating acute and subacute spine pain, new research suggests.

Results from the SPINE CARE randomized controlled trial showed that 6-8 weeks of an individualized postural therapy (IPT) or a multidisciplinary biopsychosocial intervention known as ICE (identify, coordinate, and enhance) that includes physical therapy were associated with small but statistically significant reductions in pain-related disability at 3 months compared with usual care.

In addition, spine-related health care spending did not differ significantly between ICE and usual care. However, IPT significantly increased spending compared with usual care.

“We found that, compared to usual primary care, both interventions reduced pain-related disability at 3 months and that these changes were sustained and clinically meaningful at 12 months – long after the interventions were over,” lead author Niteesh K. Choudhry, MD, PhD, Brigham and Women’s Hospital and Harvard Medical School, Boston, told this news organization.

The findings were published online in JAMA.
 

Common complaint

Spine pain is defined as pain that occurs in the neck or back, the investigators noted. It “accounted for more health spending than any other health condition in the U.S. in 2016,” they added.

“Spine pain is an exceptionally common reason for patients to visit their primary care providers,” Dr. Choudhry said.

The SPINE CARE trial enrolled 2,971 adults (60% were women; mean age was 51 years) with back or neck pain that had lasted less than 12 weeks. All were randomly allocated to usual care (no intervention, n = 992) or to the ICE (n = 829) or IPT (n = 1150) interventions.

The ICE care model stratifies patients on the basis of their risk of progression from acute to chronic pain and addresses biopsychosocial contributors to pain. Low-risk patients received one physical therapy (PT) visit and one coaching call, while higher-risk patients received three PT visits, three coaching calls, and one e-consultation.

The IPT intervention, which was delivered in 8 weekly sessions, focuses on postural realignment. IPT also emphasizes self-efficacy and self-management, including daily exercises to improve postural control, coordination, and muscle balance.

Results at 3 months showed that both the ICE and IPT groups improved significantly more in Oswestry Disability Index (ODI) scores than in the usual care group (ICE, 31.2 to 15.4; IPT, 29.3 to 15.4; usual care, 28.9 to 19.5).

At 3 months, the absolute difference in ODI score vs. usual care was −5.8 for ICE (95% confidence interval [CI], −7.7 to −3.9; P < .001) and −4.3 for IPT (95% CI, −5.9 to −2.6; P < .001) for IPT.

Both interventions reduced resource utilization, such as diagnostic imaging, procedures, and specialist visits, Dr. Choudhry reported. “Because of this, both reduced spending unrelated to the interventions themselves,” he added.

When the intervention costs were included, ICE resulted in lower costs overall than those of usual care ($139 less), while overall spending for IPT was higher than for usual care (by $941).

“We tested the interventions in a way that was integrated into primary care, so implementing them in other practice settings should be quite straightforward,” Dr. Choudhry said.

He noted that the ICE model does not currently exist as a complete program – but its components, such as physical therapy or specialist e-consults, do. “And we think that our results justify exploring how to set this up more broadly,” he said.

Dr. Choudhry added that IPT was tested using a specific provider (Egoscue), “which has locations in a variety of places in the U.S. and internationally, and so should also be straightforward to integrate into routine practice.”

However, other important factors, such as insurance coverage, will need to be explored in the future, he said.
 

Confirmatory evidence?

In an accompanying editorial, Erin Krebs, MD, Minneapolis VA Health Care System, and colleagues, noted that past systematic reviews have concluded that exercise therapies are “generally effective” for chronic back and neck pain, which is usually defined as pain lasting more than 12 weeks, but not for acute pain, defined as pain lasting less than 4-6 weeks.

“The present trial contributes evidence for effectiveness of exercise therapy among patients with a current episode of less than 12 weeks, meaning not yet chronic, but not necessarily acute,” the editorialists wrote.

“Clinicians should more often recommend structured exercise programs for subacute back or neck pain, especially when the pain is recurrent,” they added.

The study was funded by unrestricted philanthropic gifts to Stanford (Calif.) University. Dr. Choudhry received grants from Stanford University during the conduct of the study.

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

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

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

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

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

A recent study found that people with obesity have lower blood levels of vitamin D than people of healthy weight. This association of obesity with low vitamin D levels has led to much speculation on whether low vitamin D levels cause obesity or whether obesity causes low vitamin D levels. The interest in this topic is piqued by the possibility that if vitamin D deficiency causes obesity, perhaps treatment could be as simple as providing vitamin D supplementation to enhance weight loss.

What is known about vitamin D’s role in the body?

It’s well known that vitamin D is essential for bone health as well as balancing the minerals calcium and phosphorus, but what is its role in weight management? Approximately 80%-90% of vitamin D in the body is from the skin synthesis of cholecalciferol through ultraviolet B radiation from sun exposure. The normal range of 25-hydroxy vitamin D is measured as nanograms per milliliter (ng/mL). Most experts recommend a level between 20 and 40 ng/mL, but this has been a controversial topic of never-ending debate in the medical literature.

Vitamin D levels and obesity

A strong link exists between low vitamin D levels (serum 25[OH] vitamin D) and obesity. This has been noted for many years without identifying the underlying reasons beyond the sequestering of vitamin D in adipose tissue, although I’ll discuss other possibilities.

The inverse correlation between vitamin D and obesity has been seen in other diseases, such as cardiovascular disease, hypertension, prediabetes, and insulin resistance, as well as in sarcopenia and aging. Most studies emphasized the correlation between increasing adiposity with vitamin D deficiency in all ethnic and age groups. The causes and potential direct consequences of the vitamin D deficiency state in obesity are not well understood.
 

Vitamin D and adipose tissue

It’s been proposed that low vitamin D status in obesity might be due to increased vitamin D clearance from serum and enhanced storage of vitamin D by adipose tissue.

In adipose tissue, vitamin D exerts a variety of effects on inflammation, innate immunity, metabolism, and differentiation and apoptosis in many cell types. There is a stronger association between 25(OH)D and visceral fat as compared to subcutaneous adipose tissue, which suggests an influence of inflammation and components of the metabolic syndrome on vitamin D metabolism.

Because vitamin D has anti-inflammatory properties, it’s possible that low vitamin D status contributes to adipose tissue inflammation, a key link between obesity and its associated metabolic complications in obesity. A higher storage of vitamin D in adipose tissue, if accompanied by a parallel increase in the local synthesis of 1,25(OH)2D3 and action, may conceivably modulate adipocyte function as well as the activity of adipose tissue macrophages and hence the level of adipose tissue inflammation. In addition, it seems likely that 1,25(OH)2D3 also regulates the function of macrophages and other immune cell populations within adipose tissue.

It’s well known that vitamin D is stored in body fat, leading to the assumption that this was important in the evolution of vertebrates, including humans, who lived at latitudes where vitamin D could not be made in the winter and vitamin D stores had to be mobilized to maintain vitamin D sufficiency.
 

What is vitamin D’s role in obesity?

The main question that has eluded an answer so far is this one: Is vitamin D deficiency only a coincidental finding in obesity due to sequestration of the vitamin in fat, or does it have a role in the development of obesity and its complications, such as cardiovascular disease, type 2 diabetes, and hypertension?

Low vitamin D usually leads to impaired calcium absorption in the intestine and a lower calcium level, and eventually enhanced bone turnover and impaired bone mineral density (BMD).

However, it is known that in obesity there is greater BMD than in those who are lean. This leads to the conclusion that because there is a lack of vitamin D deficiency effects on bone in those with obesity, there is not really a vitamin D deficiency, and it may be that the sequestration in adipose tissue leads to a permanent supply that can maintain bone health.

An alternative explanation is that there is greater skeletal loading in obesity, and elevations in hormones such as estrogen and leptin could compensate for the vitamin D deficiency, leading to greater BMD in obesity.

Several other potential mechanisms besides sequestration of vitamin D in adipose tissue have been identified for low vitamin D and obesity. These include impaired hepatic 25-hydroxylation in nonalcoholic fatty liver disease, less sunlight exposure due to lower mobility and different clothing habits in people with obesity vs. their lean counterparts, and adverse dietary habits. For example, people with higher BMIs spend less time exercising outdoors and are more sedentary in general than their lean counterparts. Therefore, they are less likely to get sun exposure because of a decrease in time spent outdoors. Those with higher BMIs also tend to cover their bodies, showing less skin when outdoors than their leaner counterparts, and thus there is likely to be less conversion to vitamin D via skin and sun exposure in people with obesity.

Some studies suggest that an increased level of parathyroid hormone due to vitamin D deficiency promotes lipogenesis because of greater calcium influx in adipocytes. Another hypothesis is that the active form of vitamin D, 1,25(OH) D, inhibits adipogenesis through actions modulated by vitamin D receptors. These studies are promising, but prospective randomized trials are needed to determine whether vitamin D supplementation is a treatment option in preventing obesity. So far, vitamin D supplementation shows inconsistent results.

To conclude, there is a high prevalence of vitamin D deficiency in obesity, most likely because of dilution and sequestration in greater volumes of fat, blood muscle, and liver in obesity. Low vitamin D levels can’t be ruled out as a cause of obesity because of the research showing some interesting findings in vitamin D receptors in adipose tissue. Vitamin D deficiency in obesity doesn’t seem to affect bone mass but could have deleterious effects on other organ systems.

Weight loss improves obesity and complications, including the risk for cardiovascular disease and type 2 diabetes as well as vitamin D deficiency.
 

What do the guidelines say?

Treatment of vitamin D deficiency requires higher doses in obesity to achieve the same serum concentration compared with lean persons. Maintenance doses should not differ between those with obesity and lean persons.

The association of vitamin D and obesity remains elusive. Studies need to focus on vitamin D, vitamin D receptors, and actions of vitamin D in adipose tissue to investigate this relationship further.

In the meantime, media attention remains focused on the potential treatment and prevention of obesity with the mighty, all-purpose vitamin D, even though there is scant evidence.

Dr. Apovian is codirector at the Center for Weight Management and Wellness at Brigham and Women’s Hospital and professor of medicine in the division of endocrinology, diabetes and hypertension at Harvard University, Boston. She disclosed conflicts of interest with Abbott, Allergan, Altimmune, Bariatrix Nutrition, Cowen and Company, Curavit, Rhythm Pharma, Jazz, Nutrisystem, Roman, Novo Nordisk, EnteroMedics, Gelesis Srl, Zafgen, Xeno, L-Nutra, Tivity, and Real Appeal.

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

Lupin Pharmaceuticals is recalling four lots of quinapril tablets because of unacceptable levels of the nitrosamine impurity, N-nitroso-quinapril, a potential carcinogen.

Nitrosamines “may increase the risk of cancer if people are exposed to them above acceptable levels over long periods of time,” the company says in a recall notice posted on the Food and Drug Administration website.

Lupin says it “has received no reports of illness that appear to relate to this issue.”

Quinapril is an ACE inhibitor used to treat hypertension. Lupin stopped marketing quinapril tablets in September 2022.

The recalled product – quinapril tablets USP 20 mg and 40 mg – are packaged in 90-count bottles and were distributed nationwide to U.S. wholesalers, drug chains, mail order pharmacies, and supermarkets between March 15, 2021, and Sept. 1, 2022.

Lupin is notifying customers to immediately stop distribution of the recalled product and is arranging for the affected product lots to be returned to the company.

The company is advising patients to continue taking their medication and to contact their pharmacist, physician, or healthcare professional for advice regarding an alternative treatment.

Questions regarding this recall should be directed to Inmar Rx Solutions at (877) 538-8445 Monday to Friday between 9:00 a.m. to 5:00 p.m. EST.

Patients and physicians are also advised to report any adverse events or side effects related to the affected products to MedWatch, the FDA’s Safety Information and Adverse Event Reporting program.

Pfizer recalled several lots of quinapril owing to the presence of the same impurity in March 2022and again in April.

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

Lupin Pharmaceuticals is recalling four lots of quinapril tablets because of unacceptable levels of the nitrosamine impurity, N-nitroso-quinapril, a potential carcinogen.

Nitrosamines “may increase the risk of cancer if people are exposed to them above acceptable levels over long periods of time,” the company says in a recall notice posted on the Food and Drug Administration website.

Lupin says it “has received no reports of illness that appear to relate to this issue.”

Quinapril is an ACE inhibitor used to treat hypertension. Lupin stopped marketing quinapril tablets in September 2022.

The recalled product – quinapril tablets USP 20 mg and 40 mg – are packaged in 90-count bottles and were distributed nationwide to U.S. wholesalers, drug chains, mail order pharmacies, and supermarkets between March 15, 2021, and Sept. 1, 2022.

Lupin is notifying customers to immediately stop distribution of the recalled product and is arranging for the affected product lots to be returned to the company.

The company is advising patients to continue taking their medication and to contact their pharmacist, physician, or healthcare professional for advice regarding an alternative treatment.

Questions regarding this recall should be directed to Inmar Rx Solutions at (877) 538-8445 Monday to Friday between 9:00 a.m. to 5:00 p.m. EST.

Patients and physicians are also advised to report any adverse events or side effects related to the affected products to MedWatch, the FDA’s Safety Information and Adverse Event Reporting program.

Pfizer recalled several lots of quinapril owing to the presence of the same impurity in March 2022and again in April.

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

Lupin Pharmaceuticals is recalling four lots of quinapril tablets because of unacceptable levels of the nitrosamine impurity, N-nitroso-quinapril, a potential carcinogen.

Nitrosamines “may increase the risk of cancer if people are exposed to them above acceptable levels over long periods of time,” the company says in a recall notice posted on the Food and Drug Administration website.

Lupin says it “has received no reports of illness that appear to relate to this issue.”

Quinapril is an ACE inhibitor used to treat hypertension. Lupin stopped marketing quinapril tablets in September 2022.

The recalled product – quinapril tablets USP 20 mg and 40 mg – are packaged in 90-count bottles and were distributed nationwide to U.S. wholesalers, drug chains, mail order pharmacies, and supermarkets between March 15, 2021, and Sept. 1, 2022.

Lupin is notifying customers to immediately stop distribution of the recalled product and is arranging for the affected product lots to be returned to the company.

The company is advising patients to continue taking their medication and to contact their pharmacist, physician, or healthcare professional for advice regarding an alternative treatment.

Questions regarding this recall should be directed to Inmar Rx Solutions at (877) 538-8445 Monday to Friday between 9:00 a.m. to 5:00 p.m. EST.

Patients and physicians are also advised to report any adverse events or side effects related to the affected products to MedWatch, the FDA’s Safety Information and Adverse Event Reporting program.

Pfizer recalled several lots of quinapril owing to the presence of the same impurity in March 2022and again in April.

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

SAN DIEGO – In the clinical experience of Jeremy B. Green, MD, men typically require a higher dose of facial neuromodulators for nonsurgical wrinkle reduction compared with women because of anatomical differences.

“Men generally have larger facial muscle mass,” Dr. Green, a dermatologist in Coral Gables, Fla., said at the annual Masters of Aesthetics Symposium. “We need a higher dose to treat them, or they will not be happy. In general, I try to increase the dose by about 50% for my male patients.”

Two early trials of dose adjustments support this practice, he said. In one, 80 men were randomized to receive a total dose of either 20, 40, 60, or 80 U of botulinum toxin type A (Botox) in the glabellar area. The researchers found that the 40, 60, and 80 U doses of botulinum toxin type A were consistently more effective in reducing glabellar lines than the 20 U dose.

In a subsequent study, researchers administered botulinum toxin type A (Dysport) 0.5 to 0.7 mL for men (60, 70, or 80 units), based on procerus/corrugator muscle mass. Efficacy was assessed by a blinded evaluator and patient self-evaluation at several time points up to 150 days post treatment. The median duration of effect was 109 days vs. 0 days for placebo in the blinded evaluator evaluation and 107 days vs. 0 for placebo in the patient self-evaluation.

Most injection algorithms for treating the glabella rely on a 5- or 7-point injection technique, but in 2021, researchers led by Sebastian Cotofana, MD, PhD, of the department of clinical anatomy at Mayo Clinic, Rochester, Minn., reported results from a study of the efficacy and safety of a refined 3-point injection technique targeting horizontal and vertical lines to prevent brow ptosis.

“Prior to this study Sebastian asked me, ‘Why do you guys always inject the body of the muscle?’ ” Dr. Green said. “‘If you inject the origin of the muscle on bone, you could more effectively wipe out the entire muscle’s movement. You’re going to get a better result at a lower dose, so let’s study this.’”

The injection technique involves targeting the midline level of the connecting line between left and right medial canthal ligaments with a 90-degree injection angle with bone contact, as well as the medial and inferior margin of eyebrows with a 45-degree injection angle in relation to midline with frontal bone contact. These three points are located inferior to the traditional (on-label) glabellar frown line injections used to treat the frontalis and the brow depressors.

The researchers used the 5-point glabellar line severity scale to evaluate the time of effect onset and the injection-related outcome 120 days after the treatment in 27 men and 78 women. They found that the onset of the neuromodulator effect occurred in an average of 3.5 days, and no adverse events such as eyebrow ptosis, upper eyelid ptosis, medial eyebrow ptosis, and lateral frontalis hyperactivity occurred during the study period.

“If you inject the origin of these muscles, you can get a brow lift with this technique by avoiding frontalis altogether,” Dr. Green said. “The caveat is, it’s so great at lifting the brows that if you treat the forehead, you may create a midline horizontal ‘shelf’ like I’ve never seen before, where the eyebrows elevate into an immobile superior frontalis.”

To avoid this when treating the forehead as well, he’s learned to split the dose of neuromodulator. “If I was injecting 5 units in the procerus before, I’ll do 2.5 units on nasal bone at the insertion of the muscle and then 2.5 units higher up in the traditional midline procerus injection site,” Dr. Green said.

“Same with the corrugators,” he continued. “Then, remember to inject more superficially in the lateral part, the tail of the corrugators, because the tail of the corrugators is inserting into the undersurface of the dermis. That’s why you see that skin puckering in the lateral brows when people frown. You’re pretty safe to chase that laterally if the brow’s already flat as in men, but I caution you [not] to do that in women, because you may flatten the brow.”

Dr. Green said that he is aware of two cases of lid ptosis from the 3-point technique, one of which happened to him.

“When you’re on the bone with your thumb you can feel that liquid traveling along the bone,” he said. “It can travel all the way to the midline pupil where the levator palpebrae superioris muscle is. I now don’t come in contact with bone with my corrugator origin injections, but rather float the needle a couple of millimeters off bone (in muscle) to hopefully prevent that from happening. Alternatively, some people will compress the brow along frontal bone lateral to that corrugator injection site while they’re injecting to prevent backflow of the neuromodulator.”

Dr. Green reported having received research funding and/or consulting fees from many device and pharmaceutical companies.

SAN DIEGO – In the clinical experience of Jeremy B. Green, MD, men typically require a higher dose of facial neuromodulators for nonsurgical wrinkle reduction compared with women because of anatomical differences.

“Men generally have larger facial muscle mass,” Dr. Green, a dermatologist in Coral Gables, Fla., said at the annual Masters of Aesthetics Symposium. “We need a higher dose to treat them, or they will not be happy. In general, I try to increase the dose by about 50% for my male patients.”

Two early trials of dose adjustments support this practice, he said. In one, 80 men were randomized to receive a total dose of either 20, 40, 60, or 80 U of botulinum toxin type A (Botox) in the glabellar area. The researchers found that the 40, 60, and 80 U doses of botulinum toxin type A were consistently more effective in reducing glabellar lines than the 20 U dose.

In a subsequent study, researchers administered botulinum toxin type A (Dysport) 0.5 to 0.7 mL for men (60, 70, or 80 units), based on procerus/corrugator muscle mass. Efficacy was assessed by a blinded evaluator and patient self-evaluation at several time points up to 150 days post treatment. The median duration of effect was 109 days vs. 0 days for placebo in the blinded evaluator evaluation and 107 days vs. 0 for placebo in the patient self-evaluation.

Most injection algorithms for treating the glabella rely on a 5- or 7-point injection technique, but in 2021, researchers led by Sebastian Cotofana, MD, PhD, of the department of clinical anatomy at Mayo Clinic, Rochester, Minn., reported results from a study of the efficacy and safety of a refined 3-point injection technique targeting horizontal and vertical lines to prevent brow ptosis.

“Prior to this study Sebastian asked me, ‘Why do you guys always inject the body of the muscle?’ ” Dr. Green said. “‘If you inject the origin of the muscle on bone, you could more effectively wipe out the entire muscle’s movement. You’re going to get a better result at a lower dose, so let’s study this.’”

The injection technique involves targeting the midline level of the connecting line between left and right medial canthal ligaments with a 90-degree injection angle with bone contact, as well as the medial and inferior margin of eyebrows with a 45-degree injection angle in relation to midline with frontal bone contact. These three points are located inferior to the traditional (on-label) glabellar frown line injections used to treat the frontalis and the brow depressors.

The researchers used the 5-point glabellar line severity scale to evaluate the time of effect onset and the injection-related outcome 120 days after the treatment in 27 men and 78 women. They found that the onset of the neuromodulator effect occurred in an average of 3.5 days, and no adverse events such as eyebrow ptosis, upper eyelid ptosis, medial eyebrow ptosis, and lateral frontalis hyperactivity occurred during the study period.

“If you inject the origin of these muscles, you can get a brow lift with this technique by avoiding frontalis altogether,” Dr. Green said. “The caveat is, it’s so great at lifting the brows that if you treat the forehead, you may create a midline horizontal ‘shelf’ like I’ve never seen before, where the eyebrows elevate into an immobile superior frontalis.”

To avoid this when treating the forehead as well, he’s learned to split the dose of neuromodulator. “If I was injecting 5 units in the procerus before, I’ll do 2.5 units on nasal bone at the insertion of the muscle and then 2.5 units higher up in the traditional midline procerus injection site,” Dr. Green said.

“Same with the corrugators,” he continued. “Then, remember to inject more superficially in the lateral part, the tail of the corrugators, because the tail of the corrugators is inserting into the undersurface of the dermis. That’s why you see that skin puckering in the lateral brows when people frown. You’re pretty safe to chase that laterally if the brow’s already flat as in men, but I caution you [not] to do that in women, because you may flatten the brow.”

Dr. Green said that he is aware of two cases of lid ptosis from the 3-point technique, one of which happened to him.

“When you’re on the bone with your thumb you can feel that liquid traveling along the bone,” he said. “It can travel all the way to the midline pupil where the levator palpebrae superioris muscle is. I now don’t come in contact with bone with my corrugator origin injections, but rather float the needle a couple of millimeters off bone (in muscle) to hopefully prevent that from happening. Alternatively, some people will compress the brow along frontal bone lateral to that corrugator injection site while they’re injecting to prevent backflow of the neuromodulator.”

Dr. Green reported having received research funding and/or consulting fees from many device and pharmaceutical companies.

SAN DIEGO – In the clinical experience of Jeremy B. Green, MD, men typically require a higher dose of facial neuromodulators for nonsurgical wrinkle reduction compared with women because of anatomical differences.

“Men generally have larger facial muscle mass,” Dr. Green, a dermatologist in Coral Gables, Fla., said at the annual Masters of Aesthetics Symposium. “We need a higher dose to treat them, or they will not be happy. In general, I try to increase the dose by about 50% for my male patients.”

Two early trials of dose adjustments support this practice, he said. In one, 80 men were randomized to receive a total dose of either 20, 40, 60, or 80 U of botulinum toxin type A (Botox) in the glabellar area. The researchers found that the 40, 60, and 80 U doses of botulinum toxin type A were consistently more effective in reducing glabellar lines than the 20 U dose.

In a subsequent study, researchers administered botulinum toxin type A (Dysport) 0.5 to 0.7 mL for men (60, 70, or 80 units), based on procerus/corrugator muscle mass. Efficacy was assessed by a blinded evaluator and patient self-evaluation at several time points up to 150 days post treatment. The median duration of effect was 109 days vs. 0 days for placebo in the blinded evaluator evaluation and 107 days vs. 0 for placebo in the patient self-evaluation.

Most injection algorithms for treating the glabella rely on a 5- or 7-point injection technique, but in 2021, researchers led by Sebastian Cotofana, MD, PhD, of the department of clinical anatomy at Mayo Clinic, Rochester, Minn., reported results from a study of the efficacy and safety of a refined 3-point injection technique targeting horizontal and vertical lines to prevent brow ptosis.

“Prior to this study Sebastian asked me, ‘Why do you guys always inject the body of the muscle?’ ” Dr. Green said. “‘If you inject the origin of the muscle on bone, you could more effectively wipe out the entire muscle’s movement. You’re going to get a better result at a lower dose, so let’s study this.’”

The injection technique involves targeting the midline level of the connecting line between left and right medial canthal ligaments with a 90-degree injection angle with bone contact, as well as the medial and inferior margin of eyebrows with a 45-degree injection angle in relation to midline with frontal bone contact. These three points are located inferior to the traditional (on-label) glabellar frown line injections used to treat the frontalis and the brow depressors.

The researchers used the 5-point glabellar line severity scale to evaluate the time of effect onset and the injection-related outcome 120 days after the treatment in 27 men and 78 women. They found that the onset of the neuromodulator effect occurred in an average of 3.5 days, and no adverse events such as eyebrow ptosis, upper eyelid ptosis, medial eyebrow ptosis, and lateral frontalis hyperactivity occurred during the study period.

“If you inject the origin of these muscles, you can get a brow lift with this technique by avoiding frontalis altogether,” Dr. Green said. “The caveat is, it’s so great at lifting the brows that if you treat the forehead, you may create a midline horizontal ‘shelf’ like I’ve never seen before, where the eyebrows elevate into an immobile superior frontalis.”

To avoid this when treating the forehead as well, he’s learned to split the dose of neuromodulator. “If I was injecting 5 units in the procerus before, I’ll do 2.5 units on nasal bone at the insertion of the muscle and then 2.5 units higher up in the traditional midline procerus injection site,” Dr. Green said.

“Same with the corrugators,” he continued. “Then, remember to inject more superficially in the lateral part, the tail of the corrugators, because the tail of the corrugators is inserting into the undersurface of the dermis. That’s why you see that skin puckering in the lateral brows when people frown. You’re pretty safe to chase that laterally if the brow’s already flat as in men, but I caution you [not] to do that in women, because you may flatten the brow.”

Dr. Green said that he is aware of two cases of lid ptosis from the 3-point technique, one of which happened to him.

“When you’re on the bone with your thumb you can feel that liquid traveling along the bone,” he said. “It can travel all the way to the midline pupil where the levator palpebrae superioris muscle is. I now don’t come in contact with bone with my corrugator origin injections, but rather float the needle a couple of millimeters off bone (in muscle) to hopefully prevent that from happening. Alternatively, some people will compress the brow along frontal bone lateral to that corrugator injection site while they’re injecting to prevent backflow of the neuromodulator.”

Dr. Green reported having received research funding and/or consulting fees from many device and pharmaceutical companies.

A gastroenterologist affiliated with the Cleveland Clinic was recently arrested and charged with multiple felonies.

According to Cleveland Municipal Court records, Omar Massoud, MD, PhD, of Westlake, Ohio, has been charged with three counts of kidnapping, all first-degree felonies, and three counts of gross sexual imposition, all third-degree felonies.

The assaults are alleged to have happened during liver examinations on March 25, Nov. 11, and Nov. 28, 2022 at Cleveland Clinic’s main campus located at 9500 Euclid Avenue.

No further details were provided.

Dr. Massoud is the former chief of hepatology at the Cleveland Clinic.

In a statement, the Cleveland Clinic said it “immediately reported the accusations to the appropriate law enforcement agencies and are fully cooperating with the investigations.”

“Following a thorough internal investigation,” Dr. Massoud was fired, the Cleveland Clinic said.

“Cleveland Clinic is strongly committed to protecting the rights and safety of our patients, visitors, and caregivers from any type of inappropriate behavior. We care deeply about patient safety and any form of misconduct is not tolerated,” the statement said.

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

A gastroenterologist affiliated with the Cleveland Clinic was recently arrested and charged with multiple felonies.

According to Cleveland Municipal Court records, Omar Massoud, MD, PhD, of Westlake, Ohio, has been charged with three counts of kidnapping, all first-degree felonies, and three counts of gross sexual imposition, all third-degree felonies.

The assaults are alleged to have happened during liver examinations on March 25, Nov. 11, and Nov. 28, 2022 at Cleveland Clinic’s main campus located at 9500 Euclid Avenue.

No further details were provided.

Dr. Massoud is the former chief of hepatology at the Cleveland Clinic.

In a statement, the Cleveland Clinic said it “immediately reported the accusations to the appropriate law enforcement agencies and are fully cooperating with the investigations.”

“Following a thorough internal investigation,” Dr. Massoud was fired, the Cleveland Clinic said.

“Cleveland Clinic is strongly committed to protecting the rights and safety of our patients, visitors, and caregivers from any type of inappropriate behavior. We care deeply about patient safety and any form of misconduct is not tolerated,” the statement said.

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

A gastroenterologist affiliated with the Cleveland Clinic was recently arrested and charged with multiple felonies.

According to Cleveland Municipal Court records, Omar Massoud, MD, PhD, of Westlake, Ohio, has been charged with three counts of kidnapping, all first-degree felonies, and three counts of gross sexual imposition, all third-degree felonies.

The assaults are alleged to have happened during liver examinations on March 25, Nov. 11, and Nov. 28, 2022 at Cleveland Clinic’s main campus located at 9500 Euclid Avenue.

No further details were provided.

Dr. Massoud is the former chief of hepatology at the Cleveland Clinic.

In a statement, the Cleveland Clinic said it “immediately reported the accusations to the appropriate law enforcement agencies and are fully cooperating with the investigations.”

“Following a thorough internal investigation,” Dr. Massoud was fired, the Cleveland Clinic said.

“Cleveland Clinic is strongly committed to protecting the rights and safety of our patients, visitors, and caregivers from any type of inappropriate behavior. We care deeply about patient safety and any form of misconduct is not tolerated,” the statement said.

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

Kiwifruit can increase the frequency of bowel movements for people with constipation, according to researchers in New Zealand.

“In addition to improved measures of constipation status, there was a significant improvement in stool consistency, reduction in constipation, indigestion/reflux, and abdominal pain resulting in an improved overall level of GI comfort,” write Richard Gearry, MD, PhD, of the University of Otago, New Zealand, and colleagues.

Dr. Gearry and colleagues describe their international multicenter controlled trial of kiwifruit as a constipation treatment in the American Journal of Gastroenterology.

Although constipation is common, previous researchers have reported a high rate of dissatisfaction with pharmaceutical treatments.

Fiber found in kiwifruit cell walls swells and holds water, which can soften stools and increase stool frequency. Other components of kiwifruit, such as raphides, may alter mucin production, leading to improved laxation.

Several previous studies have suggested that regular consumption of fresh, green kiwifruit may be effective as a treatment for constipation. However, these studies have typically been small with nonstandardized endpoints, Dr. Gearry and colleagues note. In their article, they did not comment on studies of other fresh fruits or vegetables as constipation treatments.

The researchers set out to test the benefits of the fruit in a more rigorous trial. They recruited adults in New Zealand, Italy, and Japan who had either functional constipation or constipation-predominant irritable bowel syndrome (IBS-C), as well as healthy people as controls. The primary difference between functional constipation and IBS-C is that people with IBS-C experience abdominal pain along with constipation, they write.

Between June 12, 2014, and June 17, 2017, 184 participants were enrolled. Participants included 136 women and 48 men, a proportion consistent with the gender prevalence of constipation. The mean age was 30.5 years in Japan, 36.9 years in Italy, and 44.8 years in New Zealand, and the mean body mass index was 20.6 in Japan, 23.0 in Italy, and 25.4 in New Zealand.

For 2 weeks following recruitment, the participants became accustomed to recording their bowel movements with respect to frequency, completeness, spontaneity, stool form, laxative use, and degree of straining.

Participants were then randomly assigned to consume either two ripe green kiwifruit (Actinidia chinensis var. deliciosa “Hayward”) without the skins, or 7.5 g of psyllium per day for 4 weeks. Psyllium is considered a first-line treatment for both the constipation conditions with which participants were diagnosed. The fiber content of psyllium is similar to that of kiwifruit.

After 4 weeks, treatments were stopped for 4 weeks as a washout period, after which patients were switched to the other treatment for another 4 weeks.

The researchers provided them with two bisacodyl (5-g suppositories) as a pharmacologic rescue therapy.

Overall, 169 participants completed the study, and compliance with diary completion was more than 80%.

At the end of the 4-week treatment periods, the people with functional constipation who ate kiwifruit demonstrated an average increase of 1.53 bowel movements per week, a statistically significant increase (P < .0001). Those with IBS-C demonstrated an increase of 1.73 (P = .0001). Both groups reported significantly improved gastrointestinal comfort on the gastrointestinal symptom rating scale.

The frequency of bowel movements in the healthy participants did not increase.

Among those participants who took psyllium, only those with IBS-C experienced a statistically significant increase in the frequency of their bowel movements or a decrease in their gastrointestinal symptoms. Their bowel movements increased by an average of 1.87 per week (P = .0051).

The participants who ate kiwifruit reported softening of stool consistency, reduction in straining, and improvement in quality of life compared with baseline, and these improvements in straining and stool consistency were better than was reported by those who took psyllium.

“Taken in conjunction with previous clinical trials of green kiwifruit and the emerging physiological data from functional studies, consumption of two green kiwifruit can be safely recommended as an effective treatment for constipation in those with functional gastrointestinal disorders that will also provide improvements in symptoms of GI comfort,” the researchers conclude.

Two of the researchers were employed by Zespri International, a cooperative of kiwifruit growers, which partially funded the study and approved its design. The New Zealand study center trial was jointly funded by a grant from the New Zealand government.

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

Kiwifruit can increase the frequency of bowel movements for people with constipation, according to researchers in New Zealand.

“In addition to improved measures of constipation status, there was a significant improvement in stool consistency, reduction in constipation, indigestion/reflux, and abdominal pain resulting in an improved overall level of GI comfort,” write Richard Gearry, MD, PhD, of the University of Otago, New Zealand, and colleagues.

Dr. Gearry and colleagues describe their international multicenter controlled trial of kiwifruit as a constipation treatment in the American Journal of Gastroenterology.

Although constipation is common, previous researchers have reported a high rate of dissatisfaction with pharmaceutical treatments.

Fiber found in kiwifruit cell walls swells and holds water, which can soften stools and increase stool frequency. Other components of kiwifruit, such as raphides, may alter mucin production, leading to improved laxation.

Several previous studies have suggested that regular consumption of fresh, green kiwifruit may be effective as a treatment for constipation. However, these studies have typically been small with nonstandardized endpoints, Dr. Gearry and colleagues note. In their article, they did not comment on studies of other fresh fruits or vegetables as constipation treatments.

The researchers set out to test the benefits of the fruit in a more rigorous trial. They recruited adults in New Zealand, Italy, and Japan who had either functional constipation or constipation-predominant irritable bowel syndrome (IBS-C), as well as healthy people as controls. The primary difference between functional constipation and IBS-C is that people with IBS-C experience abdominal pain along with constipation, they write.

Between June 12, 2014, and June 17, 2017, 184 participants were enrolled. Participants included 136 women and 48 men, a proportion consistent with the gender prevalence of constipation. The mean age was 30.5 years in Japan, 36.9 years in Italy, and 44.8 years in New Zealand, and the mean body mass index was 20.6 in Japan, 23.0 in Italy, and 25.4 in New Zealand.

For 2 weeks following recruitment, the participants became accustomed to recording their bowel movements with respect to frequency, completeness, spontaneity, stool form, laxative use, and degree of straining.

Participants were then randomly assigned to consume either two ripe green kiwifruit (Actinidia chinensis var. deliciosa “Hayward”) without the skins, or 7.5 g of psyllium per day for 4 weeks. Psyllium is considered a first-line treatment for both the constipation conditions with which participants were diagnosed. The fiber content of psyllium is similar to that of kiwifruit.

After 4 weeks, treatments were stopped for 4 weeks as a washout period, after which patients were switched to the other treatment for another 4 weeks.

The researchers provided them with two bisacodyl (5-g suppositories) as a pharmacologic rescue therapy.

Overall, 169 participants completed the study, and compliance with diary completion was more than 80%.

At the end of the 4-week treatment periods, the people with functional constipation who ate kiwifruit demonstrated an average increase of 1.53 bowel movements per week, a statistically significant increase (P < .0001). Those with IBS-C demonstrated an increase of 1.73 (P = .0001). Both groups reported significantly improved gastrointestinal comfort on the gastrointestinal symptom rating scale.

The frequency of bowel movements in the healthy participants did not increase.

Among those participants who took psyllium, only those with IBS-C experienced a statistically significant increase in the frequency of their bowel movements or a decrease in their gastrointestinal symptoms. Their bowel movements increased by an average of 1.87 per week (P = .0051).

The participants who ate kiwifruit reported softening of stool consistency, reduction in straining, and improvement in quality of life compared with baseline, and these improvements in straining and stool consistency were better than was reported by those who took psyllium.

“Taken in conjunction with previous clinical trials of green kiwifruit and the emerging physiological data from functional studies, consumption of two green kiwifruit can be safely recommended as an effective treatment for constipation in those with functional gastrointestinal disorders that will also provide improvements in symptoms of GI comfort,” the researchers conclude.

Two of the researchers were employed by Zespri International, a cooperative of kiwifruit growers, which partially funded the study and approved its design. The New Zealand study center trial was jointly funded by a grant from the New Zealand government.

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

Kiwifruit can increase the frequency of bowel movements for people with constipation, according to researchers in New Zealand.

“In addition to improved measures of constipation status, there was a significant improvement in stool consistency, reduction in constipation, indigestion/reflux, and abdominal pain resulting in an improved overall level of GI comfort,” write Richard Gearry, MD, PhD, of the University of Otago, New Zealand, and colleagues.

Dr. Gearry and colleagues describe their international multicenter controlled trial of kiwifruit as a constipation treatment in the American Journal of Gastroenterology.

Although constipation is common, previous researchers have reported a high rate of dissatisfaction with pharmaceutical treatments.

Fiber found in kiwifruit cell walls swells and holds water, which can soften stools and increase stool frequency. Other components of kiwifruit, such as raphides, may alter mucin production, leading to improved laxation.

Several previous studies have suggested that regular consumption of fresh, green kiwifruit may be effective as a treatment for constipation. However, these studies have typically been small with nonstandardized endpoints, Dr. Gearry and colleagues note. In their article, they did not comment on studies of other fresh fruits or vegetables as constipation treatments.

The researchers set out to test the benefits of the fruit in a more rigorous trial. They recruited adults in New Zealand, Italy, and Japan who had either functional constipation or constipation-predominant irritable bowel syndrome (IBS-C), as well as healthy people as controls. The primary difference between functional constipation and IBS-C is that people with IBS-C experience abdominal pain along with constipation, they write.

Between June 12, 2014, and June 17, 2017, 184 participants were enrolled. Participants included 136 women and 48 men, a proportion consistent with the gender prevalence of constipation. The mean age was 30.5 years in Japan, 36.9 years in Italy, and 44.8 years in New Zealand, and the mean body mass index was 20.6 in Japan, 23.0 in Italy, and 25.4 in New Zealand.

For 2 weeks following recruitment, the participants became accustomed to recording their bowel movements with respect to frequency, completeness, spontaneity, stool form, laxative use, and degree of straining.

Participants were then randomly assigned to consume either two ripe green kiwifruit (Actinidia chinensis var. deliciosa “Hayward”) without the skins, or 7.5 g of psyllium per day for 4 weeks. Psyllium is considered a first-line treatment for both the constipation conditions with which participants were diagnosed. The fiber content of psyllium is similar to that of kiwifruit.

After 4 weeks, treatments were stopped for 4 weeks as a washout period, after which patients were switched to the other treatment for another 4 weeks.

The researchers provided them with two bisacodyl (5-g suppositories) as a pharmacologic rescue therapy.

Overall, 169 participants completed the study, and compliance with diary completion was more than 80%.

At the end of the 4-week treatment periods, the people with functional constipation who ate kiwifruit demonstrated an average increase of 1.53 bowel movements per week, a statistically significant increase (P < .0001). Those with IBS-C demonstrated an increase of 1.73 (P = .0001). Both groups reported significantly improved gastrointestinal comfort on the gastrointestinal symptom rating scale.

The frequency of bowel movements in the healthy participants did not increase.

Among those participants who took psyllium, only those with IBS-C experienced a statistically significant increase in the frequency of their bowel movements or a decrease in their gastrointestinal symptoms. Their bowel movements increased by an average of 1.87 per week (P = .0051).

The participants who ate kiwifruit reported softening of stool consistency, reduction in straining, and improvement in quality of life compared with baseline, and these improvements in straining and stool consistency were better than was reported by those who took psyllium.

“Taken in conjunction with previous clinical trials of green kiwifruit and the emerging physiological data from functional studies, consumption of two green kiwifruit can be safely recommended as an effective treatment for constipation in those with functional gastrointestinal disorders that will also provide improvements in symptoms of GI comfort,” the researchers conclude.

Two of the researchers were employed by Zespri International, a cooperative of kiwifruit growers, which partially funded the study and approved its design. The New Zealand study center trial was jointly funded by a grant from the New Zealand government.

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

Among Hispanic/Latinx patients with alopecia areata, the mean age at diagnosis was 33 years, 24% had concomitant atopy, and 18% had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis.

Those are among key findings from a retrospective analysis of Hispanic/Latinx patients at the University of California, Irvine (UCI) by Natasha Mesinkovska, MD, PhD, of UCI’s department of dermatology, and her coauthors. The findings were published online in the Journal of the American Academy of Dermatology.

A recent study examined the epidemiology of alopecia areata (AA) in Black patients, wrote Dr. Mesinkovska and coauthors Celine Phong, a UCI medical student, and Amy J. McMichael, MD, professor of dermatology at Wake Forest University, Winston-Salem, N.C. “A similar unmet need exists to describe the characteristics of AA in Hispanic/Latinx (H/L) patients, the prevalent majority in California,” they added.

Drawing from chart reviews, ICD codes, and documented physical exams, they retrospectively identified 197 Hispanic/Latinx patients diagnosed with AA at UCI between 2015 and 2022, including alopecia totalis and alopecia universalis.

Nearly two-thirds of patients with alopecia were female (63%), and their mean age at diagnosis was 33 years. Most patients (79%) presented with patchy pattern AA, 13% had diffuse pattern AA, and only 12% had eyebrow, eyelash, or beard involvement. The most common comorbidity in patients overall was atopy (24%), including allergic rhinitis (12%), asthma (10%), and/or atopic dermatitis (7%).

The authors found that 18% of patients had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis (9%) and thyroid disease (6%). No patients had celiac disease, myasthenia gravis, or inflammatory bowel disease, but 43% had another dermatologic condition.

In other findings, 22% of patients had vitamin D deficiency, 20% had hyperlipidemia, 18% had obesity, 16% had gastroesophageal reflux disease, and 12% had anemia. At the same time, depression, anxiety, or sleep disorders were identified in 14% of patients.

“Interestingly, the most common autoimmune comorbidity in H/L was rheumatoid arthritis, compared to thyroid disease in Black patients and overall AA patients,” the authors wrote. “This finding may be a reflection of a larger trend, as rheumatoid arthritis in the H/L population has been on the rise.”

The authors acknowledged certain limitations of the study including its small sample size and lack of a control group, and reported having no financial disclosures.

Among Hispanic/Latinx patients with alopecia areata, the mean age at diagnosis was 33 years, 24% had concomitant atopy, and 18% had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis.

Those are among key findings from a retrospective analysis of Hispanic/Latinx patients at the University of California, Irvine (UCI) by Natasha Mesinkovska, MD, PhD, of UCI’s department of dermatology, and her coauthors. The findings were published online in the Journal of the American Academy of Dermatology.

A recent study examined the epidemiology of alopecia areata (AA) in Black patients, wrote Dr. Mesinkovska and coauthors Celine Phong, a UCI medical student, and Amy J. McMichael, MD, professor of dermatology at Wake Forest University, Winston-Salem, N.C. “A similar unmet need exists to describe the characteristics of AA in Hispanic/Latinx (H/L) patients, the prevalent majority in California,” they added.

Drawing from chart reviews, ICD codes, and documented physical exams, they retrospectively identified 197 Hispanic/Latinx patients diagnosed with AA at UCI between 2015 and 2022, including alopecia totalis and alopecia universalis.

Nearly two-thirds of patients with alopecia were female (63%), and their mean age at diagnosis was 33 years. Most patients (79%) presented with patchy pattern AA, 13% had diffuse pattern AA, and only 12% had eyebrow, eyelash, or beard involvement. The most common comorbidity in patients overall was atopy (24%), including allergic rhinitis (12%), asthma (10%), and/or atopic dermatitis (7%).

The authors found that 18% of patients had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis (9%) and thyroid disease (6%). No patients had celiac disease, myasthenia gravis, or inflammatory bowel disease, but 43% had another dermatologic condition.

In other findings, 22% of patients had vitamin D deficiency, 20% had hyperlipidemia, 18% had obesity, 16% had gastroesophageal reflux disease, and 12% had anemia. At the same time, depression, anxiety, or sleep disorders were identified in 14% of patients.

“Interestingly, the most common autoimmune comorbidity in H/L was rheumatoid arthritis, compared to thyroid disease in Black patients and overall AA patients,” the authors wrote. “This finding may be a reflection of a larger trend, as rheumatoid arthritis in the H/L population has been on the rise.”

The authors acknowledged certain limitations of the study including its small sample size and lack of a control group, and reported having no financial disclosures.

Among Hispanic/Latinx patients with alopecia areata, the mean age at diagnosis was 33 years, 24% had concomitant atopy, and 18% had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis.

Those are among key findings from a retrospective analysis of Hispanic/Latinx patients at the University of California, Irvine (UCI) by Natasha Mesinkovska, MD, PhD, of UCI’s department of dermatology, and her coauthors. The findings were published online in the Journal of the American Academy of Dermatology.

A recent study examined the epidemiology of alopecia areata (AA) in Black patients, wrote Dr. Mesinkovska and coauthors Celine Phong, a UCI medical student, and Amy J. McMichael, MD, professor of dermatology at Wake Forest University, Winston-Salem, N.C. “A similar unmet need exists to describe the characteristics of AA in Hispanic/Latinx (H/L) patients, the prevalent majority in California,” they added.

Drawing from chart reviews, ICD codes, and documented physical exams, they retrospectively identified 197 Hispanic/Latinx patients diagnosed with AA at UCI between 2015 and 2022, including alopecia totalis and alopecia universalis.

Nearly two-thirds of patients with alopecia were female (63%), and their mean age at diagnosis was 33 years. Most patients (79%) presented with patchy pattern AA, 13% had diffuse pattern AA, and only 12% had eyebrow, eyelash, or beard involvement. The most common comorbidity in patients overall was atopy (24%), including allergic rhinitis (12%), asthma (10%), and/or atopic dermatitis (7%).

The authors found that 18% of patients had one or more coexisting autoimmune conditions, most commonly rheumatoid arthritis (9%) and thyroid disease (6%). No patients had celiac disease, myasthenia gravis, or inflammatory bowel disease, but 43% had another dermatologic condition.

In other findings, 22% of patients had vitamin D deficiency, 20% had hyperlipidemia, 18% had obesity, 16% had gastroesophageal reflux disease, and 12% had anemia. At the same time, depression, anxiety, or sleep disorders were identified in 14% of patients.

“Interestingly, the most common autoimmune comorbidity in H/L was rheumatoid arthritis, compared to thyroid disease in Black patients and overall AA patients,” the authors wrote. “This finding may be a reflection of a larger trend, as rheumatoid arthritis in the H/L population has been on the rise.”

The authors acknowledged certain limitations of the study including its small sample size and lack of a control group, and reported having no financial disclosures.

The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.