“Why did the other doctor say that?”

I get that question here and there, and it’s always irritating. How should I know?

Generally it’s referring to something they say their family doctor told them: A scan that showed normal pressure hydrocephalus or multiple sclerosis, but when I actually get the neuroradiologist’s report it was normal. Sometimes it’s an alleged side effect from a drug for which I can find nothing in the literature or something that requires urgent surgery in spite of all objective evidence to the contrary.

These appointments are always frustrating. The patient is upset that what they’ve been told (or at least think they’ve been told) is incorrect. They’ve spent a few weeks doing medical research on Google for a condition they don’t have. They’re angry at me for shooting them down. They’re angry at the person who referred them for not being right. They’re angry that they wasted their time coming to me.

And then they ask me why the other doctor said that. I wasn’t there. I don’t know. Medicine is a less-than-perfect science. Maybe they were looking at the wrong report. Maybe they’d gotten an incorrect “wet read” by phone. (How many doctors today even know where the term came from?) Maybe they were having a bad day, were overwhelmed, and misread something.

There’s also the possibility that the other doctor didn’t say it at all. Many people will only hear what they want to hear. Or they’ve already decided what they have and are claiming “the other doctor” told them just to give credence to it, even if it’s not true.

Such visits often end on an ugly note. The patient doesn’t want to be billed because I didn’t say what they wanted me to say. Or pay a copay. Or just get up and leave.

I try, very hard, to be polite when this happens. I don’t know what really went on at the other office – if what’s claimed even happened at all. Even if the patient is telling the truth, all doctors, like all people, make mistakes. It’s not like they were trying to be wrong or deceptive. I don’t fault my colleagues if they make an error, and hope they feel the same way about me.

But it’s still frustrating when it occurs. In many cases I’m left dictating a polite note back to the referring physician, explaining what happened. I chalk it up to a communication error, or experience, or even just a difficult patient. I never really know for sure.

I don’t think any of us are here to willfully deceive patients. We want to do our best for them. It’s frustrating when something happens to lead them to believe otherwise.

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

“Why did the other doctor say that?”

I get that question here and there, and it’s always irritating. How should I know?

Generally it’s referring to something they say their family doctor told them: A scan that showed normal pressure hydrocephalus or multiple sclerosis, but when I actually get the neuroradiologist’s report it was normal. Sometimes it’s an alleged side effect from a drug for which I can find nothing in the literature or something that requires urgent surgery in spite of all objective evidence to the contrary.

These appointments are always frustrating. The patient is upset that what they’ve been told (or at least think they’ve been told) is incorrect. They’ve spent a few weeks doing medical research on Google for a condition they don’t have. They’re angry at me for shooting them down. They’re angry at the person who referred them for not being right. They’re angry that they wasted their time coming to me.

And then they ask me why the other doctor said that. I wasn’t there. I don’t know. Medicine is a less-than-perfect science. Maybe they were looking at the wrong report. Maybe they’d gotten an incorrect “wet read” by phone. (How many doctors today even know where the term came from?) Maybe they were having a bad day, were overwhelmed, and misread something.

There’s also the possibility that the other doctor didn’t say it at all. Many people will only hear what they want to hear. Or they’ve already decided what they have and are claiming “the other doctor” told them just to give credence to it, even if it’s not true.

Such visits often end on an ugly note. The patient doesn’t want to be billed because I didn’t say what they wanted me to say. Or pay a copay. Or just get up and leave.

I try, very hard, to be polite when this happens. I don’t know what really went on at the other office – if what’s claimed even happened at all. Even if the patient is telling the truth, all doctors, like all people, make mistakes. It’s not like they were trying to be wrong or deceptive. I don’t fault my colleagues if they make an error, and hope they feel the same way about me.

But it’s still frustrating when it occurs. In many cases I’m left dictating a polite note back to the referring physician, explaining what happened. I chalk it up to a communication error, or experience, or even just a difficult patient. I never really know for sure.

I don’t think any of us are here to willfully deceive patients. We want to do our best for them. It’s frustrating when something happens to lead them to believe otherwise.

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

“Why did the other doctor say that?”

I get that question here and there, and it’s always irritating. How should I know?

Generally it’s referring to something they say their family doctor told them: A scan that showed normal pressure hydrocephalus or multiple sclerosis, but when I actually get the neuroradiologist’s report it was normal. Sometimes it’s an alleged side effect from a drug for which I can find nothing in the literature or something that requires urgent surgery in spite of all objective evidence to the contrary.

These appointments are always frustrating. The patient is upset that what they’ve been told (or at least think they’ve been told) is incorrect. They’ve spent a few weeks doing medical research on Google for a condition they don’t have. They’re angry at me for shooting them down. They’re angry at the person who referred them for not being right. They’re angry that they wasted their time coming to me.

And then they ask me why the other doctor said that. I wasn’t there. I don’t know. Medicine is a less-than-perfect science. Maybe they were looking at the wrong report. Maybe they’d gotten an incorrect “wet read” by phone. (How many doctors today even know where the term came from?) Maybe they were having a bad day, were overwhelmed, and misread something.

There’s also the possibility that the other doctor didn’t say it at all. Many people will only hear what they want to hear. Or they’ve already decided what they have and are claiming “the other doctor” told them just to give credence to it, even if it’s not true.

Such visits often end on an ugly note. The patient doesn’t want to be billed because I didn’t say what they wanted me to say. Or pay a copay. Or just get up and leave.

I try, very hard, to be polite when this happens. I don’t know what really went on at the other office – if what’s claimed even happened at all. Even if the patient is telling the truth, all doctors, like all people, make mistakes. It’s not like they were trying to be wrong or deceptive. I don’t fault my colleagues if they make an error, and hope they feel the same way about me.

But it’s still frustrating when it occurs. In many cases I’m left dictating a polite note back to the referring physician, explaining what happened. I chalk it up to a communication error, or experience, or even just a difficult patient. I never really know for sure.

I don’t think any of us are here to willfully deceive patients. We want to do our best for them. It’s frustrating when something happens to lead them to believe otherwise.

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

Dairy intake may increase risk of Parkinson’s disease in men, according to investigators. Men of European ancestry with a genetic marker predicting dairy consumption had significantly greater risk of Parkinson’s disease than individuals without the marker, suggesting a causal relationship between dairy intake and Parkinson’s disease, lead author Cloé Domenighetti, MSc, a PhD student at UVSQ, Université Paris Sud, and colleagues reported.

“Previous studies highlighted dairy intake as a risk factor of Parkinson’s disease,” the investigators wrote in Movement Disorders. “A meta-analysis of prospective studies reported a 40% increased Parkinson’s disease risk in participants with the highest intake. It is unclear whether the association is causal or explained by confounding or reverse causation, given the long prodromal phase of Parkinson’s disease.”
 

A Mendelian randomization study

The investigators evaluated this link by comparing 9,823 cases of Parkinson’s disease with 8,376 controls, all individuals of European ancestry from the Courage-Parkinson’s disease consortium, comprising 23 studies. Data were analyzed by two-sample Mendelian randomization, a technique that uses genotype to predict behavior, thereby replacing conventional methods of capturing behavior, such as questionnaires. In this case, the investigators screened all participants for rs4988235, a single-nucleotide polymorphism (SNP) upstream of the lactase gene that is well documented to predict dairy intake among individuals of European ancestry.

“Mendelian randomization uses genetic variants associated with exposures as instrumental variables to estimate causal relationships between exposures and outcomes,” the investigators wrote. “Mendelian randomization analyses are less likely to be biased by confounding or reverse causation than observational studies if a set of assumptions are met.”

The approach uncovered a significant association between rs4988235 and Parkinson’s disease, with a 70% increase in disease risk per one serving of dairy per day (odds ratio, 1.70; 95% confidence interval, 1.12-2.60; P = .013). Further analysis revealed that this finding was driven by men, who had a 2.5-fold increased risk of Parkinson’s disease per one serving per day (OR, 2.50; 95% CI, 1.37-4.56; P = .003) versus women, among whom there was no significant association (OR, 1.04; 95% CI, 0.56-1.92; P = .91). No significant associations were observed among individuals grouped by age or Parkinson’s disease duration.

“Our findings suggest that dairy intake increases Parkinson’s disease risk,” the investigators concluded. “Therefore, diets with limited milk intake (e.g., Mediterranean diet) may be beneficial with respect to Parkinson’s disease.”
 

Further evidence supporting a link between diet and Parkinson’s disease

According to Silke Appel-Cresswell, MD, Marg Meikle Professor for Parkinson’s Research at the University of British Columbia, Vancouver, the findings align with previous prospective cohort studies demonstrating an increased risk of Parkinson’s disease with greater consumption of dairy.

“What the current study adds,” Dr. Appel-Cresswell said, “is a complementary approach to assess the association where the risk of reverse causation and of confounding are minimized. Like in some of the previous studies, the authors find sex differences with an increased risk for men but not women.”

Dr. Appel-Cresswell noted that an increasing body of evidence supports a link between diet and Parkinson’s disease, including a study of her own published last year, which showed later onset of Parkinson’s disease among individuals with a Mediterranean-style diet.

“We are accumulating evidence for a role of diet (or more broadly, the food exposome) for the risk to develop Parkinson’s disease,” Dr. Appel-Cresswell said, noting that “key pieces are still missing, including mechanisms underlying associations, clinical trials in individuals with established Parkinson’s disease and – eventually – preventive interventions. This research is urgently needed and analyses will need to take sex differences and a large range of potential other factors into account.”
 

A ‘modest’ contributing factor?

Vikas Kotagal, MD, associate professor of neurology at the University of Michigan, Ann Arbor, offered a perspective on the study methodology, and suggested that a causal link between dairy intake and Parkinson’s disease, if present, is likely minimal.

“Limitations to the study include the fact that participants weren’t actually asked or tested for how much dairy they truly consumed,” Dr. Kotagal said*. “Their dairy intake was estimated based on their genetic background – there are certainly many assumptions baked into this analytic approach which may or may not be true. It is also worth noting the fact that this causal association was seen in men and not women, suggesting that even if dairy intake was truly causal, it is likely to be a modest contributing factor and not a significant cause of Parkinson’s disease in the broader population in general.”

Still, Dr. Kotagal agreed with Dr. Appel-Cresswell that underlying mechanisms need further investigation.

“The biggest takeaway here is to heighten the urgency for researchers and funders to explore whether factors that might cluster with dairy intake – including pesticide exposure in milk or even the make-up of bacterial populations in different peoples’ intestines – might deserve closer scrutiny as a missing link connecting dairy consumption to increased Parkinson’s disease risk,” Dr. Kotagal said.
 

Dietary advice

Considering all available evidence, Dr. Appel-Cresswell offered some dietary advice with benefits that may extend beyond prevention of Parkinson’s disease.

“From a clinical point of view, I suggest to limit dairy intake to a moderate amount,” she said. “Mediterranean diets so far have the best supporting evidence for a lower Parkinson’s disease risk, although data is lacking for benefits in established Parkinson’s disease. Given the low risk of the Mediterranean diet and the established benefits for a host of other medical conditions, this is generally a safe and delicious recommendation whether one is living with Parkinson’s or not.”

The study was supported by the European Union Joint Program for Neurodegenerative Disease Research, the National Centre of Excellence in Research on Parkinson’s Disease, the National Institutes of Health, and others. The investigators disclosed additional relationships with Astellas Pharma, Sanofi, Pfizer, and others. Dr. Kotagal and Dr. Appel-Cresswell reported no relevant conflicts of interest.

*Correction, 2/10/22: An earlier version of this article misstated Dr. Kotagal's name in certain instances, including a photo caption.

Dairy intake may increase risk of Parkinson’s disease in men, according to investigators. Men of European ancestry with a genetic marker predicting dairy consumption had significantly greater risk of Parkinson’s disease than individuals without the marker, suggesting a causal relationship between dairy intake and Parkinson’s disease, lead author Cloé Domenighetti, MSc, a PhD student at UVSQ, Université Paris Sud, and colleagues reported.

“Previous studies highlighted dairy intake as a risk factor of Parkinson’s disease,” the investigators wrote in Movement Disorders. “A meta-analysis of prospective studies reported a 40% increased Parkinson’s disease risk in participants with the highest intake. It is unclear whether the association is causal or explained by confounding or reverse causation, given the long prodromal phase of Parkinson’s disease.”
 

A Mendelian randomization study

The investigators evaluated this link by comparing 9,823 cases of Parkinson’s disease with 8,376 controls, all individuals of European ancestry from the Courage-Parkinson’s disease consortium, comprising 23 studies. Data were analyzed by two-sample Mendelian randomization, a technique that uses genotype to predict behavior, thereby replacing conventional methods of capturing behavior, such as questionnaires. In this case, the investigators screened all participants for rs4988235, a single-nucleotide polymorphism (SNP) upstream of the lactase gene that is well documented to predict dairy intake among individuals of European ancestry.

“Mendelian randomization uses genetic variants associated with exposures as instrumental variables to estimate causal relationships between exposures and outcomes,” the investigators wrote. “Mendelian randomization analyses are less likely to be biased by confounding or reverse causation than observational studies if a set of assumptions are met.”

The approach uncovered a significant association between rs4988235 and Parkinson’s disease, with a 70% increase in disease risk per one serving of dairy per day (odds ratio, 1.70; 95% confidence interval, 1.12-2.60; P = .013). Further analysis revealed that this finding was driven by men, who had a 2.5-fold increased risk of Parkinson’s disease per one serving per day (OR, 2.50; 95% CI, 1.37-4.56; P = .003) versus women, among whom there was no significant association (OR, 1.04; 95% CI, 0.56-1.92; P = .91). No significant associations were observed among individuals grouped by age or Parkinson’s disease duration.

“Our findings suggest that dairy intake increases Parkinson’s disease risk,” the investigators concluded. “Therefore, diets with limited milk intake (e.g., Mediterranean diet) may be beneficial with respect to Parkinson’s disease.”
 

Further evidence supporting a link between diet and Parkinson’s disease

According to Silke Appel-Cresswell, MD, Marg Meikle Professor for Parkinson’s Research at the University of British Columbia, Vancouver, the findings align with previous prospective cohort studies demonstrating an increased risk of Parkinson’s disease with greater consumption of dairy.

“What the current study adds,” Dr. Appel-Cresswell said, “is a complementary approach to assess the association where the risk of reverse causation and of confounding are minimized. Like in some of the previous studies, the authors find sex differences with an increased risk for men but not women.”

Dr. Appel-Cresswell noted that an increasing body of evidence supports a link between diet and Parkinson’s disease, including a study of her own published last year, which showed later onset of Parkinson’s disease among individuals with a Mediterranean-style diet.

“We are accumulating evidence for a role of diet (or more broadly, the food exposome) for the risk to develop Parkinson’s disease,” Dr. Appel-Cresswell said, noting that “key pieces are still missing, including mechanisms underlying associations, clinical trials in individuals with established Parkinson’s disease and – eventually – preventive interventions. This research is urgently needed and analyses will need to take sex differences and a large range of potential other factors into account.”
 

A ‘modest’ contributing factor?

Vikas Kotagal, MD, associate professor of neurology at the University of Michigan, Ann Arbor, offered a perspective on the study methodology, and suggested that a causal link between dairy intake and Parkinson’s disease, if present, is likely minimal.

“Limitations to the study include the fact that participants weren’t actually asked or tested for how much dairy they truly consumed,” Dr. Kotagal said*. “Their dairy intake was estimated based on their genetic background – there are certainly many assumptions baked into this analytic approach which may or may not be true. It is also worth noting the fact that this causal association was seen in men and not women, suggesting that even if dairy intake was truly causal, it is likely to be a modest contributing factor and not a significant cause of Parkinson’s disease in the broader population in general.”

Still, Dr. Kotagal agreed with Dr. Appel-Cresswell that underlying mechanisms need further investigation.

“The biggest takeaway here is to heighten the urgency for researchers and funders to explore whether factors that might cluster with dairy intake – including pesticide exposure in milk or even the make-up of bacterial populations in different peoples’ intestines – might deserve closer scrutiny as a missing link connecting dairy consumption to increased Parkinson’s disease risk,” Dr. Kotagal said.
 

Dietary advice

Considering all available evidence, Dr. Appel-Cresswell offered some dietary advice with benefits that may extend beyond prevention of Parkinson’s disease.

“From a clinical point of view, I suggest to limit dairy intake to a moderate amount,” she said. “Mediterranean diets so far have the best supporting evidence for a lower Parkinson’s disease risk, although data is lacking for benefits in established Parkinson’s disease. Given the low risk of the Mediterranean diet and the established benefits for a host of other medical conditions, this is generally a safe and delicious recommendation whether one is living with Parkinson’s or not.”

The study was supported by the European Union Joint Program for Neurodegenerative Disease Research, the National Centre of Excellence in Research on Parkinson’s Disease, the National Institutes of Health, and others. The investigators disclosed additional relationships with Astellas Pharma, Sanofi, Pfizer, and others. Dr. Kotagal and Dr. Appel-Cresswell reported no relevant conflicts of interest.

*Correction, 2/10/22: An earlier version of this article misstated Dr. Kotagal's name in certain instances, including a photo caption.

Dairy intake may increase risk of Parkinson’s disease in men, according to investigators. Men of European ancestry with a genetic marker predicting dairy consumption had significantly greater risk of Parkinson’s disease than individuals without the marker, suggesting a causal relationship between dairy intake and Parkinson’s disease, lead author Cloé Domenighetti, MSc, a PhD student at UVSQ, Université Paris Sud, and colleagues reported.

“Previous studies highlighted dairy intake as a risk factor of Parkinson’s disease,” the investigators wrote in Movement Disorders. “A meta-analysis of prospective studies reported a 40% increased Parkinson’s disease risk in participants with the highest intake. It is unclear whether the association is causal or explained by confounding or reverse causation, given the long prodromal phase of Parkinson’s disease.”
 

A Mendelian randomization study

The investigators evaluated this link by comparing 9,823 cases of Parkinson’s disease with 8,376 controls, all individuals of European ancestry from the Courage-Parkinson’s disease consortium, comprising 23 studies. Data were analyzed by two-sample Mendelian randomization, a technique that uses genotype to predict behavior, thereby replacing conventional methods of capturing behavior, such as questionnaires. In this case, the investigators screened all participants for rs4988235, a single-nucleotide polymorphism (SNP) upstream of the lactase gene that is well documented to predict dairy intake among individuals of European ancestry.

“Mendelian randomization uses genetic variants associated with exposures as instrumental variables to estimate causal relationships between exposures and outcomes,” the investigators wrote. “Mendelian randomization analyses are less likely to be biased by confounding or reverse causation than observational studies if a set of assumptions are met.”

The approach uncovered a significant association between rs4988235 and Parkinson’s disease, with a 70% increase in disease risk per one serving of dairy per day (odds ratio, 1.70; 95% confidence interval, 1.12-2.60; P = .013). Further analysis revealed that this finding was driven by men, who had a 2.5-fold increased risk of Parkinson’s disease per one serving per day (OR, 2.50; 95% CI, 1.37-4.56; P = .003) versus women, among whom there was no significant association (OR, 1.04; 95% CI, 0.56-1.92; P = .91). No significant associations were observed among individuals grouped by age or Parkinson’s disease duration.

“Our findings suggest that dairy intake increases Parkinson’s disease risk,” the investigators concluded. “Therefore, diets with limited milk intake (e.g., Mediterranean diet) may be beneficial with respect to Parkinson’s disease.”
 

Further evidence supporting a link between diet and Parkinson’s disease

According to Silke Appel-Cresswell, MD, Marg Meikle Professor for Parkinson’s Research at the University of British Columbia, Vancouver, the findings align with previous prospective cohort studies demonstrating an increased risk of Parkinson’s disease with greater consumption of dairy.

“What the current study adds,” Dr. Appel-Cresswell said, “is a complementary approach to assess the association where the risk of reverse causation and of confounding are minimized. Like in some of the previous studies, the authors find sex differences with an increased risk for men but not women.”

Dr. Appel-Cresswell noted that an increasing body of evidence supports a link between diet and Parkinson’s disease, including a study of her own published last year, which showed later onset of Parkinson’s disease among individuals with a Mediterranean-style diet.

“We are accumulating evidence for a role of diet (or more broadly, the food exposome) for the risk to develop Parkinson’s disease,” Dr. Appel-Cresswell said, noting that “key pieces are still missing, including mechanisms underlying associations, clinical trials in individuals with established Parkinson’s disease and – eventually – preventive interventions. This research is urgently needed and analyses will need to take sex differences and a large range of potential other factors into account.”
 

A ‘modest’ contributing factor?

Vikas Kotagal, MD, associate professor of neurology at the University of Michigan, Ann Arbor, offered a perspective on the study methodology, and suggested that a causal link between dairy intake and Parkinson’s disease, if present, is likely minimal.

“Limitations to the study include the fact that participants weren’t actually asked or tested for how much dairy they truly consumed,” Dr. Kotagal said*. “Their dairy intake was estimated based on their genetic background – there are certainly many assumptions baked into this analytic approach which may or may not be true. It is also worth noting the fact that this causal association was seen in men and not women, suggesting that even if dairy intake was truly causal, it is likely to be a modest contributing factor and not a significant cause of Parkinson’s disease in the broader population in general.”

Still, Dr. Kotagal agreed with Dr. Appel-Cresswell that underlying mechanisms need further investigation.

“The biggest takeaway here is to heighten the urgency for researchers and funders to explore whether factors that might cluster with dairy intake – including pesticide exposure in milk or even the make-up of bacterial populations in different peoples’ intestines – might deserve closer scrutiny as a missing link connecting dairy consumption to increased Parkinson’s disease risk,” Dr. Kotagal said.
 

Dietary advice

Considering all available evidence, Dr. Appel-Cresswell offered some dietary advice with benefits that may extend beyond prevention of Parkinson’s disease.

“From a clinical point of view, I suggest to limit dairy intake to a moderate amount,” she said. “Mediterranean diets so far have the best supporting evidence for a lower Parkinson’s disease risk, although data is lacking for benefits in established Parkinson’s disease. Given the low risk of the Mediterranean diet and the established benefits for a host of other medical conditions, this is generally a safe and delicious recommendation whether one is living with Parkinson’s or not.”

The study was supported by the European Union Joint Program for Neurodegenerative Disease Research, the National Centre of Excellence in Research on Parkinson’s Disease, the National Institutes of Health, and others. The investigators disclosed additional relationships with Astellas Pharma, Sanofi, Pfizer, and others. Dr. Kotagal and Dr. Appel-Cresswell reported no relevant conflicts of interest.

*Correction, 2/10/22: An earlier version of this article misstated Dr. Kotagal's name in certain instances, including a photo caption.

Violence against women remains a global dilemma in need of attention. Physical violence in particular, is the most prevalent type of violence across all genders, races, and nationalities.

The Centers for Disease Control and Prevention says more than 43 million women and 38 million men report experiencing psychological aggression by an intimate partner in their lifetime. Meanwhile, 11 million women and 5 million men report enduring sexual or physical violence and intimate partner violence (IPV), and/or stalking by an intimate partner during their lifetimes, according to the CDC.1

COVID pandemic’s influence

Isolation tied to the COVID-19 pandemic has been linked to increased IPV. A study conducted by researchers at the University of California, Davis, suggested that extra stress experienced during the COVID-19 pandemic caused by income loss, and the inability to pay for housing and food exacerbated the prevalence of IPV early during the pandemic.⁶

That study, where researchers collected in surveys of nearly 400 adults in the beginning in April 2020 for 10 weeks, showed that more services and communication are needed so that frontline health care and food bank workers, for example, in addition to social workers, doctors, and therapists, can spot the signs and ask clients questions about potential IPV. They could then link survivors to pertinent assistance and resources.

Furthermore, multiple factors probably have played a pivotal role in increasing the prevalence of IPV during the COVID-19 pandemic. For instance, disruption to usual health and social services as well as diminished access to support systems, such as shelters, and charity helplines negatively affected the reporting of domestic violence.

Long before the pandemic, over the past decade, international and national bodies have played a crucial role in terms of improving the awareness and response to domestic violence.^7,8 In addition, several policies have been introduced in countries around the globe emphasizing the need to inquire routinely about domestic violence. Nevertheless, mental health services often fail to adequately address domestic violence in clinical encounters. A systematic review of domestic violence assessment screening performed in a variety of health care settings found that evidence was insufficient to conclude that routine inquiry improved morbidity and mortality among victims of IPV.⁹ So the question becomes: How can we get our patients to tell us about these experiences so we can intervene?
 

Gender differences in perpetuating IPV

Several studies have found that abuse can result in various mental illnesses, such as depression, PTSD, anxiety, and suicidal ideation. Again, men have a disproportionately higher rate of perpetrating IPV, compared with women. This theory has been a source of debate in the academic community for years, but recent research has confirmed that women do perpetuate violence against their partners to some extent.^10,11

Some members of the LGBTQ+ community also report experiencing violence from partners, so as clinicians, we also need to raise our awareness about the existence of violence among same-sex couples. In fact, a team of Italian researchers report more than 50% of gay men and almost 75% of lesbian women reported that they had been psychologically abused by a partner.¹² More research into this area is needed.
 

Our role as health care professionals

The U.S. Preventive Services Task Force advises that all clinic visits include regular IPV screening.¹³ But these screenings are all too rare. In fact, a meta-analysis of 19 trials of more than 1,600 participants showed only 9%-40% of doctors routinely test for IPV.¹⁴ That research clearly shows how important it is for all clinicians to execute IPV screening. However, numerous challenges toward screening exist, including personal discomfort, limited time during appointments, insufficient resources, and inadequate training.

One ongoing debate revolves around which clinician should screen for IPV. Should the psychiatrist carry out this role – or perhaps the primary care physician, nurse, or social worker? These issues become even more fraught when clinicians worry about offending the patient – especially if the clinician is a male.¹⁵

The bottom line is that physicians should inquire about intimate partner violence, because research indicates that women are more likely to reveal abuse when prompted. In addition, during physician appointments, they can use the physician-patient therapeutic connection to conduct a domestic violence evaluation, give resources to victims, and provide ongoing care. Patients who exhibit treatment resistance, persistent pain, depression, sleeplessness, and headaches should prompt psychiatrists to conduct additional investigations into the likelihood of intimate partner violence and domestic abuse.

W also should be attentive when counseling patients about domestic violence when suggesting life-changing events such as pregnancy, employment loss, separation, or divorce. Similar to the recommendations of the USPSTF that all women and men should be screened for IPV, it is suggested that physicians be conscious of facilitating a conversation and not being overtly judgmental while observing body cues. Using the statements such as “we have been hearing a lot of violence in our community lately” could be a segue to introduce the subject.

Asking the question of whether you are being hit rather than being abused has allowed more women to open up more about domestic violence. While physicians are aware that most victims might recant and often go back to their abusers, victims need to be counseled that the abuse might intensify and lead to death.

For women who perpetuate IPV and survivors of IPV, safety is the priority. Physicians should provide safety options and be the facilitators. Studies have shown that fewer victims get the referral to the supporting agencies when IPV is indicated, which puts their safety at risk. In women who commit IPV, clinicians should assess the role of the individual in an IPV disclosure. There are various treatment modalities, whether the violence is performed through self-defense, bidirectionally, or because of aggression.

With the advancement of technology, web-based training on how to ask for IPV, documentation, acknowledgment, and structured referral increase physicians’ confidence when faced with an IPV disclosure than none.¹⁶ Treatment modalities should include medication reconciliation and cognitive-behavioral therapy – focusing on emotion regulation.

Using instruments such as the danger assessment tool can help physicians intervene early, reducing the risk of domestic violence and IPV recurrence instead of using clinical assessment alone.¹⁷ Physicians should convey empathy, validate victims, and help, especially when abuse is reported.

Also, it is important to evaluate survivors’ safety. Counseling can help people rebuild their self-esteem. Structured referrals for psychiatric help and support services are needed to help survivors on the long road to recovery.

Training all physicians, regardless of specialty, is essential to improve prompt IPV identification and bring awareness to resources available to survivors when IPV is disclosed. Although we described an association between IPV victims becoming possible perpetrators of IPV, more long-term studies are required to show the various processes that influence IPV perpetration rates, especially by survivors.

We would also like international and national regulatory bodies to increase the awareness of IPV and adequately address IPV with special emphasis on how mental health services should assess, identify, and respond to services for people who are survivors and perpetrators of IPV.

Dr. Kumari, Dr. Otite, Dr. Afzal, Dr. Alcera, and Dr. Doumas are affiliated with Hackensack Meridian Health at Ocean Medical Center, Brick, N.J. They have no conflicts of interest.

References

1. Centers for Disease Control and Prevention. Preventing intimate partner violence. 2020 Oct 9.

2. Yu R et al. PLOS Med. 16(12):e1002995. doi: 10.1371/journal.pmed.1002995.

3. Oram S et al. Epidemiol Psychiatr Sci. 2014 Dec;23(4):361-76.

4. Munro OE and Sellbom M. Pers Ment Health. 2020 Mar 11. doi: 10.1002/pmh.1480.

5. Sahraian A et al. Asian J Psychiatry. 2020 Jun. doi: 10.1016/j.ajp.2020.102062.

6. Nikos-Rose K. “COVID-19 Isolation Linked to Increased Domestic Violence, Researchers Suggest.” 2021 Feb 24. University of California, Davis.

7. World Health Organization. “Responding to intimate partner violence and sexual violence against women.” WHO clinical policy guidelines. 2013.

8. National Institute for Health and Care Excellence. “Domestic violence and abuse: Multi-agency working.” PH50. 2014 Feb 26.

9. Feder GS et al. Arch Intern Med. 2006;166(1):22-37.

10. Gondolf EW. Violence Against Women. 2014 Dec;20(12)1539-46.

11. Hamberger LK and Larsen SE. J Fam Violence. 2015;30(6):699-717.

12. Rollè L et al. Front Psychol. 21 Aug 2018. doi: 10.3389/fpsyg.2018.01506.

13. Paterno MT and Draughon JE. J Midwif Women Health. 2016;61(31):370-5.

14. Kalra N et al. Cochrane Database Syst Rev. 2021 May 31;5(5)CD012423.

15. Larsen SE and Hamberger LK. J Fam Viol. 2015;30:1007-30.

16. Kalra N et al. Cochrane Database Syst Rev. 2017 Feb;2017(2):CD012423.

17. Campbell JC et al. J Interpers Violence. 2009;24(4):653-74.

Violence against women remains a global dilemma in need of attention. Physical violence in particular, is the most prevalent type of violence across all genders, races, and nationalities.

The Centers for Disease Control and Prevention says more than 43 million women and 38 million men report experiencing psychological aggression by an intimate partner in their lifetime. Meanwhile, 11 million women and 5 million men report enduring sexual or physical violence and intimate partner violence (IPV), and/or stalking by an intimate partner during their lifetimes, according to the CDC.1

COVID pandemic’s influence

Isolation tied to the COVID-19 pandemic has been linked to increased IPV. A study conducted by researchers at the University of California, Davis, suggested that extra stress experienced during the COVID-19 pandemic caused by income loss, and the inability to pay for housing and food exacerbated the prevalence of IPV early during the pandemic.⁶

That study, where researchers collected in surveys of nearly 400 adults in the beginning in April 2020 for 10 weeks, showed that more services and communication are needed so that frontline health care and food bank workers, for example, in addition to social workers, doctors, and therapists, can spot the signs and ask clients questions about potential IPV. They could then link survivors to pertinent assistance and resources.

Furthermore, multiple factors probably have played a pivotal role in increasing the prevalence of IPV during the COVID-19 pandemic. For instance, disruption to usual health and social services as well as diminished access to support systems, such as shelters, and charity helplines negatively affected the reporting of domestic violence.

Long before the pandemic, over the past decade, international and national bodies have played a crucial role in terms of improving the awareness and response to domestic violence.^7,8 In addition, several policies have been introduced in countries around the globe emphasizing the need to inquire routinely about domestic violence. Nevertheless, mental health services often fail to adequately address domestic violence in clinical encounters. A systematic review of domestic violence assessment screening performed in a variety of health care settings found that evidence was insufficient to conclude that routine inquiry improved morbidity and mortality among victims of IPV.⁹ So the question becomes: How can we get our patients to tell us about these experiences so we can intervene?
 

Gender differences in perpetuating IPV

Several studies have found that abuse can result in various mental illnesses, such as depression, PTSD, anxiety, and suicidal ideation. Again, men have a disproportionately higher rate of perpetrating IPV, compared with women. This theory has been a source of debate in the academic community for years, but recent research has confirmed that women do perpetuate violence against their partners to some extent.^10,11

Some members of the LGBTQ+ community also report experiencing violence from partners, so as clinicians, we also need to raise our awareness about the existence of violence among same-sex couples. In fact, a team of Italian researchers report more than 50% of gay men and almost 75% of lesbian women reported that they had been psychologically abused by a partner.¹² More research into this area is needed.
 

Our role as health care professionals

The U.S. Preventive Services Task Force advises that all clinic visits include regular IPV screening.¹³ But these screenings are all too rare. In fact, a meta-analysis of 19 trials of more than 1,600 participants showed only 9%-40% of doctors routinely test for IPV.¹⁴ That research clearly shows how important it is for all clinicians to execute IPV screening. However, numerous challenges toward screening exist, including personal discomfort, limited time during appointments, insufficient resources, and inadequate training.

One ongoing debate revolves around which clinician should screen for IPV. Should the psychiatrist carry out this role – or perhaps the primary care physician, nurse, or social worker? These issues become even more fraught when clinicians worry about offending the patient – especially if the clinician is a male.¹⁵

The bottom line is that physicians should inquire about intimate partner violence, because research indicates that women are more likely to reveal abuse when prompted. In addition, during physician appointments, they can use the physician-patient therapeutic connection to conduct a domestic violence evaluation, give resources to victims, and provide ongoing care. Patients who exhibit treatment resistance, persistent pain, depression, sleeplessness, and headaches should prompt psychiatrists to conduct additional investigations into the likelihood of intimate partner violence and domestic abuse.

W also should be attentive when counseling patients about domestic violence when suggesting life-changing events such as pregnancy, employment loss, separation, or divorce. Similar to the recommendations of the USPSTF that all women and men should be screened for IPV, it is suggested that physicians be conscious of facilitating a conversation and not being overtly judgmental while observing body cues. Using the statements such as “we have been hearing a lot of violence in our community lately” could be a segue to introduce the subject.

Asking the question of whether you are being hit rather than being abused has allowed more women to open up more about domestic violence. While physicians are aware that most victims might recant and often go back to their abusers, victims need to be counseled that the abuse might intensify and lead to death.

For women who perpetuate IPV and survivors of IPV, safety is the priority. Physicians should provide safety options and be the facilitators. Studies have shown that fewer victims get the referral to the supporting agencies when IPV is indicated, which puts their safety at risk. In women who commit IPV, clinicians should assess the role of the individual in an IPV disclosure. There are various treatment modalities, whether the violence is performed through self-defense, bidirectionally, or because of aggression.

With the advancement of technology, web-based training on how to ask for IPV, documentation, acknowledgment, and structured referral increase physicians’ confidence when faced with an IPV disclosure than none.¹⁶ Treatment modalities should include medication reconciliation and cognitive-behavioral therapy – focusing on emotion regulation.

Using instruments such as the danger assessment tool can help physicians intervene early, reducing the risk of domestic violence and IPV recurrence instead of using clinical assessment alone.¹⁷ Physicians should convey empathy, validate victims, and help, especially when abuse is reported.

Also, it is important to evaluate survivors’ safety. Counseling can help people rebuild their self-esteem. Structured referrals for psychiatric help and support services are needed to help survivors on the long road to recovery.

Training all physicians, regardless of specialty, is essential to improve prompt IPV identification and bring awareness to resources available to survivors when IPV is disclosed. Although we described an association between IPV victims becoming possible perpetrators of IPV, more long-term studies are required to show the various processes that influence IPV perpetration rates, especially by survivors.

We would also like international and national regulatory bodies to increase the awareness of IPV and adequately address IPV with special emphasis on how mental health services should assess, identify, and respond to services for people who are survivors and perpetrators of IPV.

Dr. Kumari, Dr. Otite, Dr. Afzal, Dr. Alcera, and Dr. Doumas are affiliated with Hackensack Meridian Health at Ocean Medical Center, Brick, N.J. They have no conflicts of interest.

References

1. Centers for Disease Control and Prevention. Preventing intimate partner violence. 2020 Oct 9.

2. Yu R et al. PLOS Med. 16(12):e1002995. doi: 10.1371/journal.pmed.1002995.

3. Oram S et al. Epidemiol Psychiatr Sci. 2014 Dec;23(4):361-76.

4. Munro OE and Sellbom M. Pers Ment Health. 2020 Mar 11. doi: 10.1002/pmh.1480.

5. Sahraian A et al. Asian J Psychiatry. 2020 Jun. doi: 10.1016/j.ajp.2020.102062.

6. Nikos-Rose K. “COVID-19 Isolation Linked to Increased Domestic Violence, Researchers Suggest.” 2021 Feb 24. University of California, Davis.

7. World Health Organization. “Responding to intimate partner violence and sexual violence against women.” WHO clinical policy guidelines. 2013.

8. National Institute for Health and Care Excellence. “Domestic violence and abuse: Multi-agency working.” PH50. 2014 Feb 26.

9. Feder GS et al. Arch Intern Med. 2006;166(1):22-37.

10. Gondolf EW. Violence Against Women. 2014 Dec;20(12)1539-46.

11. Hamberger LK and Larsen SE. J Fam Violence. 2015;30(6):699-717.

12. Rollè L et al. Front Psychol. 21 Aug 2018. doi: 10.3389/fpsyg.2018.01506.

13. Paterno MT and Draughon JE. J Midwif Women Health. 2016;61(31):370-5.

14. Kalra N et al. Cochrane Database Syst Rev. 2021 May 31;5(5)CD012423.

15. Larsen SE and Hamberger LK. J Fam Viol. 2015;30:1007-30.

16. Kalra N et al. Cochrane Database Syst Rev. 2017 Feb;2017(2):CD012423.

17. Campbell JC et al. J Interpers Violence. 2009;24(4):653-74.

Violence against women remains a global dilemma in need of attention. Physical violence in particular, is the most prevalent type of violence across all genders, races, and nationalities.

The Centers for Disease Control and Prevention says more than 43 million women and 38 million men report experiencing psychological aggression by an intimate partner in their lifetime. Meanwhile, 11 million women and 5 million men report enduring sexual or physical violence and intimate partner violence (IPV), and/or stalking by an intimate partner during their lifetimes, according to the CDC.1

COVID pandemic’s influence

Isolation tied to the COVID-19 pandemic has been linked to increased IPV. A study conducted by researchers at the University of California, Davis, suggested that extra stress experienced during the COVID-19 pandemic caused by income loss, and the inability to pay for housing and food exacerbated the prevalence of IPV early during the pandemic.⁶

That study, where researchers collected in surveys of nearly 400 adults in the beginning in April 2020 for 10 weeks, showed that more services and communication are needed so that frontline health care and food bank workers, for example, in addition to social workers, doctors, and therapists, can spot the signs and ask clients questions about potential IPV. They could then link survivors to pertinent assistance and resources.

Furthermore, multiple factors probably have played a pivotal role in increasing the prevalence of IPV during the COVID-19 pandemic. For instance, disruption to usual health and social services as well as diminished access to support systems, such as shelters, and charity helplines negatively affected the reporting of domestic violence.

Long before the pandemic, over the past decade, international and national bodies have played a crucial role in terms of improving the awareness and response to domestic violence.^7,8 In addition, several policies have been introduced in countries around the globe emphasizing the need to inquire routinely about domestic violence. Nevertheless, mental health services often fail to adequately address domestic violence in clinical encounters. A systematic review of domestic violence assessment screening performed in a variety of health care settings found that evidence was insufficient to conclude that routine inquiry improved morbidity and mortality among victims of IPV.⁹ So the question becomes: How can we get our patients to tell us about these experiences so we can intervene?
 

Gender differences in perpetuating IPV

Several studies have found that abuse can result in various mental illnesses, such as depression, PTSD, anxiety, and suicidal ideation. Again, men have a disproportionately higher rate of perpetrating IPV, compared with women. This theory has been a source of debate in the academic community for years, but recent research has confirmed that women do perpetuate violence against their partners to some extent.^10,11

Some members of the LGBTQ+ community also report experiencing violence from partners, so as clinicians, we also need to raise our awareness about the existence of violence among same-sex couples. In fact, a team of Italian researchers report more than 50% of gay men and almost 75% of lesbian women reported that they had been psychologically abused by a partner.¹² More research into this area is needed.
 

Our role as health care professionals

The U.S. Preventive Services Task Force advises that all clinic visits include regular IPV screening.¹³ But these screenings are all too rare. In fact, a meta-analysis of 19 trials of more than 1,600 participants showed only 9%-40% of doctors routinely test for IPV.¹⁴ That research clearly shows how important it is for all clinicians to execute IPV screening. However, numerous challenges toward screening exist, including personal discomfort, limited time during appointments, insufficient resources, and inadequate training.

One ongoing debate revolves around which clinician should screen for IPV. Should the psychiatrist carry out this role – or perhaps the primary care physician, nurse, or social worker? These issues become even more fraught when clinicians worry about offending the patient – especially if the clinician is a male.¹⁵

The bottom line is that physicians should inquire about intimate partner violence, because research indicates that women are more likely to reveal abuse when prompted. In addition, during physician appointments, they can use the physician-patient therapeutic connection to conduct a domestic violence evaluation, give resources to victims, and provide ongoing care. Patients who exhibit treatment resistance, persistent pain, depression, sleeplessness, and headaches should prompt psychiatrists to conduct additional investigations into the likelihood of intimate partner violence and domestic abuse.

W also should be attentive when counseling patients about domestic violence when suggesting life-changing events such as pregnancy, employment loss, separation, or divorce. Similar to the recommendations of the USPSTF that all women and men should be screened for IPV, it is suggested that physicians be conscious of facilitating a conversation and not being overtly judgmental while observing body cues. Using the statements such as “we have been hearing a lot of violence in our community lately” could be a segue to introduce the subject.

Asking the question of whether you are being hit rather than being abused has allowed more women to open up more about domestic violence. While physicians are aware that most victims might recant and often go back to their abusers, victims need to be counseled that the abuse might intensify and lead to death.

For women who perpetuate IPV and survivors of IPV, safety is the priority. Physicians should provide safety options and be the facilitators. Studies have shown that fewer victims get the referral to the supporting agencies when IPV is indicated, which puts their safety at risk. In women who commit IPV, clinicians should assess the role of the individual in an IPV disclosure. There are various treatment modalities, whether the violence is performed through self-defense, bidirectionally, or because of aggression.

With the advancement of technology, web-based training on how to ask for IPV, documentation, acknowledgment, and structured referral increase physicians’ confidence when faced with an IPV disclosure than none.¹⁶ Treatment modalities should include medication reconciliation and cognitive-behavioral therapy – focusing on emotion regulation.

Using instruments such as the danger assessment tool can help physicians intervene early, reducing the risk of domestic violence and IPV recurrence instead of using clinical assessment alone.¹⁷ Physicians should convey empathy, validate victims, and help, especially when abuse is reported.

Also, it is important to evaluate survivors’ safety. Counseling can help people rebuild their self-esteem. Structured referrals for psychiatric help and support services are needed to help survivors on the long road to recovery.

Training all physicians, regardless of specialty, is essential to improve prompt IPV identification and bring awareness to resources available to survivors when IPV is disclosed. Although we described an association between IPV victims becoming possible perpetrators of IPV, more long-term studies are required to show the various processes that influence IPV perpetration rates, especially by survivors.

We would also like international and national regulatory bodies to increase the awareness of IPV and adequately address IPV with special emphasis on how mental health services should assess, identify, and respond to services for people who are survivors and perpetrators of IPV.

Dr. Kumari, Dr. Otite, Dr. Afzal, Dr. Alcera, and Dr. Doumas are affiliated with Hackensack Meridian Health at Ocean Medical Center, Brick, N.J. They have no conflicts of interest.

References

1. Centers for Disease Control and Prevention. Preventing intimate partner violence. 2020 Oct 9.

2. Yu R et al. PLOS Med. 16(12):e1002995. doi: 10.1371/journal.pmed.1002995.

3. Oram S et al. Epidemiol Psychiatr Sci. 2014 Dec;23(4):361-76.

4. Munro OE and Sellbom M. Pers Ment Health. 2020 Mar 11. doi: 10.1002/pmh.1480.

5. Sahraian A et al. Asian J Psychiatry. 2020 Jun. doi: 10.1016/j.ajp.2020.102062.

6. Nikos-Rose K. “COVID-19 Isolation Linked to Increased Domestic Violence, Researchers Suggest.” 2021 Feb 24. University of California, Davis.

7. World Health Organization. “Responding to intimate partner violence and sexual violence against women.” WHO clinical policy guidelines. 2013.

8. National Institute for Health and Care Excellence. “Domestic violence and abuse: Multi-agency working.” PH50. 2014 Feb 26.

9. Feder GS et al. Arch Intern Med. 2006;166(1):22-37.

10. Gondolf EW. Violence Against Women. 2014 Dec;20(12)1539-46.

11. Hamberger LK and Larsen SE. J Fam Violence. 2015;30(6):699-717.

12. Rollè L et al. Front Psychol. 21 Aug 2018. doi: 10.3389/fpsyg.2018.01506.

13. Paterno MT and Draughon JE. J Midwif Women Health. 2016;61(31):370-5.

14. Kalra N et al. Cochrane Database Syst Rev. 2021 May 31;5(5)CD012423.

15. Larsen SE and Hamberger LK. J Fam Viol. 2015;30:1007-30.

16. Kalra N et al. Cochrane Database Syst Rev. 2017 Feb;2017(2):CD012423.

17. Campbell JC et al. J Interpers Violence. 2009;24(4):653-74.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: Upadacitinib alone or in combination with methotrexate inhibits structural joint damage progression over a year in patients with rheumatoid arthritis (RA).

Major finding: The mean change in modified total Sharp score (mTSS) at 1 year for 15 mg upadacitinib and 30 mg upadacitinib vs. methotrexate was 0.03 and 0.14 vs. 1.00 (all P < .001). In methotrexate-inadequate responders (IR), mean change in mTSS with 15 mg upadacitinib vs. placebo (both with background methotrexate) was 0.28 vs. 1.73 (P < .001).

Study details: This was an analysis of 2 phase 3 trials involving patients with active RA who were either methotrexate-naive (SELECT-EARLY) and were randomly assigned to methotrexate monotherapy, 15 mg upadacitinib, or 30 mg upadacitinib or were methotrexate-IR (SELECT-COMPARE) and were randomly assigned to either 15 mg upadacitinib, 40 mg adalimumab, or placebo, all with background methotrexate.

Disclosures: This study was funded by AbbVie. IH Song, A Friedman, T Shaw, Y Li, S Chen, and JV Enejosa reported being full-time employees or owning stocks/stock options of AbbVie, and others reported receiving research grants and consultancy or speakers fees from various sources including AbbVie.

Source: Peterfy CG et al. Rheumatology (Oxford). 2021;keab861 (Dec 13). Doi:  10.1093/rheumatology/keab861.

Key clinical point: A clinically noteworthy improvement in mental health was observed in patients with rheumatoid arthritis (RA) who were treated with Janus kinase (JAK) inhibitors.

Major finding: The pooled incremental mean reduction in short form-36 mental component score with JAK monotherapy was 4.95 (95% CI 4.41-5.48), which was greater than the minimum clinically important difference value of 2.5, indicating significant improvement in mental health following JAK monotherapy.

Study details: This was a meta-analysis of 19 studies involving 14,323 patients with RA.

Disclosures: This study received no specific funding. The authors did not have any potential conflict of interests.

Source: Shamail GMH et al. Rheumatol Ther. 2021 (Dec 13). Doi: 10.1007/s40744-021-00409-6.

Key clinical point: A clinically noteworthy improvement in mental health was observed in patients with rheumatoid arthritis (RA) who were treated with Janus kinase (JAK) inhibitors.

Major finding: The pooled incremental mean reduction in short form-36 mental component score with JAK monotherapy was 4.95 (95% CI 4.41-5.48), which was greater than the minimum clinically important difference value of 2.5, indicating significant improvement in mental health following JAK monotherapy.

Study details: This was a meta-analysis of 19 studies involving 14,323 patients with RA.

Disclosures: This study received no specific funding. The authors did not have any potential conflict of interests.

Source: Shamail GMH et al. Rheumatol Ther. 2021 (Dec 13). Doi: 10.1007/s40744-021-00409-6.

Key clinical point: A clinically noteworthy improvement in mental health was observed in patients with rheumatoid arthritis (RA) who were treated with Janus kinase (JAK) inhibitors.

Major finding: The pooled incremental mean reduction in short form-36 mental component score with JAK monotherapy was 4.95 (95% CI 4.41-5.48), which was greater than the minimum clinically important difference value of 2.5, indicating significant improvement in mental health following JAK monotherapy.

Study details: This was a meta-analysis of 19 studies involving 14,323 patients with RA.

Disclosures: This study received no specific funding. The authors did not have any potential conflict of interests.

Source: Shamail GMH et al. Rheumatol Ther. 2021 (Dec 13). Doi: 10.1007/s40744-021-00409-6.

Key clinical point: In a cohort of patients with early rheumatoid arthritis (RA), illness perceptions and suboptimal psychosocial well-being were associated with a lower likelihood of sustained remission.

Major finding: Among patients who were had a disease activity score in 28 joints-C-reactive protein remission at week 16, those with a low vs. high psychosocial burden profile showed a significantly longer time to first loss-of-remission (hazard ratio 0.51; P < .001).

Study details: This was a post hoc analysis of the CareRA trial involving 379 patients with early RA who received methotrexate ± additional conventional synthetic disease-modifying antirheumatic drugs or glucocorticoids.

Disclosures: This study was supported in part by a Strategic Basic Research Fellowship grant from Fonds Wetenschappelijk Onderzoek. All the authors declared no conflicts of interest.

Source: Doumen M et al. Arthritis Care Res (Hoboken). 2021 (Dec 20). Doi: 10.1002/acr.24847.

Key clinical point: In a cohort of patients with early rheumatoid arthritis (RA), illness perceptions and suboptimal psychosocial well-being were associated with a lower likelihood of sustained remission.

Major finding: Among patients who were had a disease activity score in 28 joints-C-reactive protein remission at week 16, those with a low vs. high psychosocial burden profile showed a significantly longer time to first loss-of-remission (hazard ratio 0.51; P < .001).

Study details: This was a post hoc analysis of the CareRA trial involving 379 patients with early RA who received methotrexate ± additional conventional synthetic disease-modifying antirheumatic drugs or glucocorticoids.

Disclosures: This study was supported in part by a Strategic Basic Research Fellowship grant from Fonds Wetenschappelijk Onderzoek. All the authors declared no conflicts of interest.

Source: Doumen M et al. Arthritis Care Res (Hoboken). 2021 (Dec 20). Doi: 10.1002/acr.24847.

Key clinical point: In a cohort of patients with early rheumatoid arthritis (RA), illness perceptions and suboptimal psychosocial well-being were associated with a lower likelihood of sustained remission.

Major finding: Among patients who were had a disease activity score in 28 joints-C-reactive protein remission at week 16, those with a low vs. high psychosocial burden profile showed a significantly longer time to first loss-of-remission (hazard ratio 0.51; P < .001).

Study details: This was a post hoc analysis of the CareRA trial involving 379 patients with early RA who received methotrexate ± additional conventional synthetic disease-modifying antirheumatic drugs or glucocorticoids.

Disclosures: This study was supported in part by a Strategic Basic Research Fellowship grant from Fonds Wetenschappelijk Onderzoek. All the authors declared no conflicts of interest.

Source: Doumen M et al. Arthritis Care Res (Hoboken). 2021 (Dec 20). Doi: 10.1002/acr.24847.

Key clinical point: Celecoxib appeared to be relatively safer compared with nonselective nonsteroidal anti-inflammatory drugs (NSAID) or placebo in patients with rheumatoid arthritis (RA), regardless of dose or duration.

Major finding: Celecoxib was associated with a lower risk for all-cause mortality (risk ratio [RR] 0.81; 95% CI 0.66-0.98) and cardiovascular morality (RR 0.75; 95% CI 0.57-0.99) compared with NSAIDs and a similar risk for all-cause mortality (RR 0.92; 95% CI 0.26-3.27) and cardiovascular morality (RR 3.02; 95% CI 0.36-25.27) compared with placebo.

Study details: Findings are from a meta-analysis of 21 randomized clinical studies that compared cardiovascular safety of celecoxib with NSAIDs or placebo in patients with RA or osteoarthritis.

Disclosures: This study was supported by the National Natural Science Foundation project and others. No competing interests were declared.

Source: Cheng BR et al. PLoS One. 2021;16(12):e0261239 (Dec 21). Doi:  10.1371/journal.pone.0261239.

Key clinical point: Celecoxib appeared to be relatively safer compared with nonselective nonsteroidal anti-inflammatory drugs (NSAID) or placebo in patients with rheumatoid arthritis (RA), regardless of dose or duration.

Major finding: Celecoxib was associated with a lower risk for all-cause mortality (risk ratio [RR] 0.81; 95% CI 0.66-0.98) and cardiovascular morality (RR 0.75; 95% CI 0.57-0.99) compared with NSAIDs and a similar risk for all-cause mortality (RR 0.92; 95% CI 0.26-3.27) and cardiovascular morality (RR 3.02; 95% CI 0.36-25.27) compared with placebo.

Study details: Findings are from a meta-analysis of 21 randomized clinical studies that compared cardiovascular safety of celecoxib with NSAIDs or placebo in patients with RA or osteoarthritis.

Disclosures: This study was supported by the National Natural Science Foundation project and others. No competing interests were declared.

Source: Cheng BR et al. PLoS One. 2021;16(12):e0261239 (Dec 21). Doi:  10.1371/journal.pone.0261239.

Key clinical point: Celecoxib appeared to be relatively safer compared with nonselective nonsteroidal anti-inflammatory drugs (NSAID) or placebo in patients with rheumatoid arthritis (RA), regardless of dose or duration.

Major finding: Celecoxib was associated with a lower risk for all-cause mortality (risk ratio [RR] 0.81; 95% CI 0.66-0.98) and cardiovascular morality (RR 0.75; 95% CI 0.57-0.99) compared with NSAIDs and a similar risk for all-cause mortality (RR 0.92; 95% CI 0.26-3.27) and cardiovascular morality (RR 3.02; 95% CI 0.36-25.27) compared with placebo.

Study details: Findings are from a meta-analysis of 21 randomized clinical studies that compared cardiovascular safety of celecoxib with NSAIDs or placebo in patients with RA or osteoarthritis.

Disclosures: This study was supported by the National Natural Science Foundation project and others. No competing interests were declared.

Source: Cheng BR et al. PLoS One. 2021;16(12):e0261239 (Dec 21). Doi:  10.1371/journal.pone.0261239.

Key clinical point: Patients with rheumatoid arthritis (RA) experienced robust pain reduction with baricitinib, irrespective of opioid use.

Major finding: Compared with placebo, pain reduction was significantly greater at all time points, starting as early as week 1 (all P < .05) in both opioid users and nonusers receiving 4 mg baricitinib and only in opioid users receiving 2 mg baricitinib. Opioid nonusers receiving 2 mg baricitinib showed greater pain relief than placebo starting at week 4 (P < .05).

Study details: This was a post hoc analysis of 3 randomized controlled trials (RA-BEAM, RA-BUILD, and RA-BEACON) involving patients with RA with an inadequate response to either methotrexate, conventional disease-modifying antirheumatic drugs, or at least 1 tumor necrosis factor inhibitor, who were randomly assigned to either placebo, baricitinib (2 mg/4 mg), or adalimumab (40 mg) in addition to background therapy.

Disclosures: This study was funded by Eli Lilly under license from Incyte Corporation. The authors declared no conflict of interests.

Source: Pope JE et al. ACR Open Rheumatol. 2021 (Dec 16). Doi: 10.1002/acr2.11380.

Key clinical point: Patients with rheumatoid arthritis (RA) experienced robust pain reduction with baricitinib, irrespective of opioid use.

Major finding: Compared with placebo, pain reduction was significantly greater at all time points, starting as early as week 1 (all P < .05) in both opioid users and nonusers receiving 4 mg baricitinib and only in opioid users receiving 2 mg baricitinib. Opioid nonusers receiving 2 mg baricitinib showed greater pain relief than placebo starting at week 4 (P < .05).

Study details: This was a post hoc analysis of 3 randomized controlled trials (RA-BEAM, RA-BUILD, and RA-BEACON) involving patients with RA with an inadequate response to either methotrexate, conventional disease-modifying antirheumatic drugs, or at least 1 tumor necrosis factor inhibitor, who were randomly assigned to either placebo, baricitinib (2 mg/4 mg), or adalimumab (40 mg) in addition to background therapy.

Disclosures: This study was funded by Eli Lilly under license from Incyte Corporation. The authors declared no conflict of interests.

Source: Pope JE et al. ACR Open Rheumatol. 2021 (Dec 16). Doi: 10.1002/acr2.11380.

Key clinical point: Patients with rheumatoid arthritis (RA) experienced robust pain reduction with baricitinib, irrespective of opioid use.

Major finding: Compared with placebo, pain reduction was significantly greater at all time points, starting as early as week 1 (all P < .05) in both opioid users and nonusers receiving 4 mg baricitinib and only in opioid users receiving 2 mg baricitinib. Opioid nonusers receiving 2 mg baricitinib showed greater pain relief than placebo starting at week 4 (P < .05).

Study details: This was a post hoc analysis of 3 randomized controlled trials (RA-BEAM, RA-BUILD, and RA-BEACON) involving patients with RA with an inadequate response to either methotrexate, conventional disease-modifying antirheumatic drugs, or at least 1 tumor necrosis factor inhibitor, who were randomly assigned to either placebo, baricitinib (2 mg/4 mg), or adalimumab (40 mg) in addition to background therapy.

Disclosures: This study was funded by Eli Lilly under license from Incyte Corporation. The authors declared no conflict of interests.

Source: Pope JE et al. ACR Open Rheumatol. 2021 (Dec 16). Doi: 10.1002/acr2.11380.

Key clinical point: Significant improvement in patient-reported outcomes was observed with filgotinib in patients with rheumatoid arthritis (RA) with an insufficient response to methotrexate or biological disease-modifying antirheumatic drugs (DMARD) and those who were methotrexate-naive.

Major finding: Filgotinib at doses of 200 mg or 100 mg in combination with methotrexate/conventional synthetic DMARDs or 200 mg filgotinib monotherapy demonstrated a significant improvement in the health-related quality of life, fatigue, and assessments of disease activity and work impairment vs. comparators (all P < .05).

Study details: This was a post hoc analysis of phase 3 studies including patients with RA with an inadequate response to methotrexate (FINCH 1) or biological DMARDs (FINCH 2) and those who were methotrexate-naive (FINCH 3).

Disclosures: This study was supported by Gilead Sciences, Inc., Foster City, CA. SJ Lee, L Ye, and H Hu reported being employees and shareholders of Gilead Sciences. All the other authors disclosed receiving grants/research support and speaker/consultancy fees from various companies including Gilead Sciences.

Source: Bingham CO III et al. Arthritis Res Ther. 2022;24:11 (Jan 3). Doi: 10.1186/s13075-021-02677-7.

Key clinical point: Significant improvement in patient-reported outcomes was observed with filgotinib in patients with rheumatoid arthritis (RA) with an insufficient response to methotrexate or biological disease-modifying antirheumatic drugs (DMARD) and those who were methotrexate-naive.

Major finding: Filgotinib at doses of 200 mg or 100 mg in combination with methotrexate/conventional synthetic DMARDs or 200 mg filgotinib monotherapy demonstrated a significant improvement in the health-related quality of life, fatigue, and assessments of disease activity and work impairment vs. comparators (all P < .05).

Study details: This was a post hoc analysis of phase 3 studies including patients with RA with an inadequate response to methotrexate (FINCH 1) or biological DMARDs (FINCH 2) and those who were methotrexate-naive (FINCH 3).

Disclosures: This study was supported by Gilead Sciences, Inc., Foster City, CA. SJ Lee, L Ye, and H Hu reported being employees and shareholders of Gilead Sciences. All the other authors disclosed receiving grants/research support and speaker/consultancy fees from various companies including Gilead Sciences.

Source: Bingham CO III et al. Arthritis Res Ther. 2022;24:11 (Jan 3). Doi: 10.1186/s13075-021-02677-7.

Key clinical point: Significant improvement in patient-reported outcomes was observed with filgotinib in patients with rheumatoid arthritis (RA) with an insufficient response to methotrexate or biological disease-modifying antirheumatic drugs (DMARD) and those who were methotrexate-naive.

Major finding: Filgotinib at doses of 200 mg or 100 mg in combination with methotrexate/conventional synthetic DMARDs or 200 mg filgotinib monotherapy demonstrated a significant improvement in the health-related quality of life, fatigue, and assessments of disease activity and work impairment vs. comparators (all P < .05).

Study details: This was a post hoc analysis of phase 3 studies including patients with RA with an inadequate response to methotrexate (FINCH 1) or biological DMARDs (FINCH 2) and those who were methotrexate-naive (FINCH 3).

Disclosures: This study was supported by Gilead Sciences, Inc., Foster City, CA. SJ Lee, L Ye, and H Hu reported being employees and shareholders of Gilead Sciences. All the other authors disclosed receiving grants/research support and speaker/consultancy fees from various companies including Gilead Sciences.

Source: Bingham CO III et al. Arthritis Res Ther. 2022;24:11 (Jan 3). Doi: 10.1186/s13075-021-02677-7.