While often linked to deleterious outcomes in certain disease states, the hepatocyte-produced inflammatory marker C-reactive protein (CRP) may be a checkpoint that protects against acetaminophen-induced acute liver injury, according to research findings.

Based on the study findings, researchers believe long-term suppression of CRP function or expression may increase an individual’s susceptibility to acetaminophen-induced liver injury. In contrast, CRP “could be exploited as a promising therapeutic approach to treat hepatotoxicity caused by drug overdose” wrote study authors Hai-Yun Li, MD, of the Xi’an Jiaotong University in Shaanxi, China, and colleagues in Cellular and Molecular Gastroenterology and Hepatology.

According to Dr. Li and colleagues, a major cause of acute liver failure is acetaminophen-induced liver injury, but despite this risk, very few treatment options for this condition exist. The only approved treatment for this complication is N-acetyl cysteine (NAC).

Although CRP represents a marker for inflammation following tissue injury, a study from 2020 and one from 2018 suggest the protein regulates complement activation and may modulate responses of immune cells. The authors of the current study noted that few studies have explored what roles complement activation and modulated immune cell responses via CRP play in acetaminophen-induced acute liver injury.

To further elucidate the role of CRP in this setting, Dr. Li and researchers assessed the mechanisms of CRP action both in vitro as well as in CRP mice with Fcy receptor 2B knockout. The researchers suggested CRP may modulate immune cell responses via these receptors. Additionally, the investigators assessed CRP action in mice with C3 knockout, given previous studies suggesting C3 knockout may alleviate acetaminophen-induced liver injury in mice. The researchers also investigated hepatic expression of CRP mutants that were defective in complement interaction. Finally, the researchers sought to understand the therapeutic potential of the inflammatory marker by performing intraperitoneal administration of human CRP at 2 or 6 hours after induction of acetaminophen-induced acute liver injury in wild-type mice.

Injection of 300 mg/kg acetaminophen over 24 hours led to overt liver injury in wild-type mice, which was characterized by increased levels of circulating alanine transaminase and aspartate transaminase as well as massive necrosis of hepatocytes. The researchers noted that these manifestations were exacerbated significantly in the CRP knockout mice.

The intravenous administration of human CRP in the mice with the drug-induced liver injury rescued defects caused by mouse CRP knockout. Additionally, human CRP administration alleviated acetaminophen-induced acute liver injury in the wild-type mice. The researchers wrote that these findings demonstrate that endogenous and human CRP “are both protective,” at least in mouse models of acetaminophen-induced liver injury.

In a second experiment, the researchers examined the mechanisms involved in CRP protection in early phases of drug-induced liver injury. Based on the experiment, the researchers found that the knockout of an inhibitory Fcy receptor mediating the anti-inflammatory activities of CRP demonstrated only “marginal effects” on the protection of the protein in acetaminophen-induced liver injury. Overall, the investigators suggested that the inflammatory marker does not likely act via the cellular Fcy receptor 2B to inhibit early phases of acetaminophen-induced hepatocyte injury. Rather, the investigators explained that CRP may act via factor H, which is recruited by CRP in regulating complement activation, to inhibit overactivation of complement on injured hepatocytes. Ultimately, the researchers explained, this results in suppression of the late phase amplification of inflammation that is mediated by neutrophils’ C3a-dependent actions.

Finally, the researchers found that intraperitoneal administration of human CRP at 2.5 mg/kg in wild-type mice at 2 hours following induction of acetaminophen-induced liver injury led to “markedly reduced liver injury,” with an efficacy that was similar to that of 500 mg/kg N-acetylcysteine, the only available treatment approved for acetaminophen-induced liver injury.

The researchers noted that N-acetylcysteine is only effective during the early phases of the acetaminophen-induced liver injury and loses effectiveness at 6 hours following injury. In contrast, human CRP in this study was still highly effective at this time point. “Given that people can tolerate high levels of circulating CRP, the administration of this protein might be a promising option to treat [acetaminophen-induced liver injury] with minimal side effects,” the researchers wrote.

The study was funded by the National Natural Science Foundation of China. The researchers reported no conflicts of interest with any pharmaceutical companies.

This article was updated on Sep. 20, 2022.

While often linked to deleterious outcomes in certain disease states, the hepatocyte-produced inflammatory marker C-reactive protein (CRP) may be a checkpoint that protects against acetaminophen-induced acute liver injury, according to research findings.

Based on the study findings, researchers believe long-term suppression of CRP function or expression may increase an individual’s susceptibility to acetaminophen-induced liver injury. In contrast, CRP “could be exploited as a promising therapeutic approach to treat hepatotoxicity caused by drug overdose” wrote study authors Hai-Yun Li, MD, of the Xi’an Jiaotong University in Shaanxi, China, and colleagues in Cellular and Molecular Gastroenterology and Hepatology.

According to Dr. Li and colleagues, a major cause of acute liver failure is acetaminophen-induced liver injury, but despite this risk, very few treatment options for this condition exist. The only approved treatment for this complication is N-acetyl cysteine (NAC).

Although CRP represents a marker for inflammation following tissue injury, a study from 2020 and one from 2018 suggest the protein regulates complement activation and may modulate responses of immune cells. The authors of the current study noted that few studies have explored what roles complement activation and modulated immune cell responses via CRP play in acetaminophen-induced acute liver injury.

To further elucidate the role of CRP in this setting, Dr. Li and researchers assessed the mechanisms of CRP action both in vitro as well as in CRP mice with Fcy receptor 2B knockout. The researchers suggested CRP may modulate immune cell responses via these receptors. Additionally, the investigators assessed CRP action in mice with C3 knockout, given previous studies suggesting C3 knockout may alleviate acetaminophen-induced liver injury in mice. The researchers also investigated hepatic expression of CRP mutants that were defective in complement interaction. Finally, the researchers sought to understand the therapeutic potential of the inflammatory marker by performing intraperitoneal administration of human CRP at 2 or 6 hours after induction of acetaminophen-induced acute liver injury in wild-type mice.

Injection of 300 mg/kg acetaminophen over 24 hours led to overt liver injury in wild-type mice, which was characterized by increased levels of circulating alanine transaminase and aspartate transaminase as well as massive necrosis of hepatocytes. The researchers noted that these manifestations were exacerbated significantly in the CRP knockout mice.

The intravenous administration of human CRP in the mice with the drug-induced liver injury rescued defects caused by mouse CRP knockout. Additionally, human CRP administration alleviated acetaminophen-induced acute liver injury in the wild-type mice. The researchers wrote that these findings demonstrate that endogenous and human CRP “are both protective,” at least in mouse models of acetaminophen-induced liver injury.

In a second experiment, the researchers examined the mechanisms involved in CRP protection in early phases of drug-induced liver injury. Based on the experiment, the researchers found that the knockout of an inhibitory Fcy receptor mediating the anti-inflammatory activities of CRP demonstrated only “marginal effects” on the protection of the protein in acetaminophen-induced liver injury. Overall, the investigators suggested that the inflammatory marker does not likely act via the cellular Fcy receptor 2B to inhibit early phases of acetaminophen-induced hepatocyte injury. Rather, the investigators explained that CRP may act via factor H, which is recruited by CRP in regulating complement activation, to inhibit overactivation of complement on injured hepatocytes. Ultimately, the researchers explained, this results in suppression of the late phase amplification of inflammation that is mediated by neutrophils’ C3a-dependent actions.

Finally, the researchers found that intraperitoneal administration of human CRP at 2.5 mg/kg in wild-type mice at 2 hours following induction of acetaminophen-induced liver injury led to “markedly reduced liver injury,” with an efficacy that was similar to that of 500 mg/kg N-acetylcysteine, the only available treatment approved for acetaminophen-induced liver injury.

The researchers noted that N-acetylcysteine is only effective during the early phases of the acetaminophen-induced liver injury and loses effectiveness at 6 hours following injury. In contrast, human CRP in this study was still highly effective at this time point. “Given that people can tolerate high levels of circulating CRP, the administration of this protein might be a promising option to treat [acetaminophen-induced liver injury] with minimal side effects,” the researchers wrote.

The study was funded by the National Natural Science Foundation of China. The researchers reported no conflicts of interest with any pharmaceutical companies.

This article was updated on Sep. 20, 2022.

While often linked to deleterious outcomes in certain disease states, the hepatocyte-produced inflammatory marker C-reactive protein (CRP) may be a checkpoint that protects against acetaminophen-induced acute liver injury, according to research findings.

Based on the study findings, researchers believe long-term suppression of CRP function or expression may increase an individual’s susceptibility to acetaminophen-induced liver injury. In contrast, CRP “could be exploited as a promising therapeutic approach to treat hepatotoxicity caused by drug overdose” wrote study authors Hai-Yun Li, MD, of the Xi’an Jiaotong University in Shaanxi, China, and colleagues in Cellular and Molecular Gastroenterology and Hepatology.

According to Dr. Li and colleagues, a major cause of acute liver failure is acetaminophen-induced liver injury, but despite this risk, very few treatment options for this condition exist. The only approved treatment for this complication is N-acetyl cysteine (NAC).

Although CRP represents a marker for inflammation following tissue injury, a study from 2020 and one from 2018 suggest the protein regulates complement activation and may modulate responses of immune cells. The authors of the current study noted that few studies have explored what roles complement activation and modulated immune cell responses via CRP play in acetaminophen-induced acute liver injury.

To further elucidate the role of CRP in this setting, Dr. Li and researchers assessed the mechanisms of CRP action both in vitro as well as in CRP mice with Fcy receptor 2B knockout. The researchers suggested CRP may modulate immune cell responses via these receptors. Additionally, the investigators assessed CRP action in mice with C3 knockout, given previous studies suggesting C3 knockout may alleviate acetaminophen-induced liver injury in mice. The researchers also investigated hepatic expression of CRP mutants that were defective in complement interaction. Finally, the researchers sought to understand the therapeutic potential of the inflammatory marker by performing intraperitoneal administration of human CRP at 2 or 6 hours after induction of acetaminophen-induced acute liver injury in wild-type mice.

Injection of 300 mg/kg acetaminophen over 24 hours led to overt liver injury in wild-type mice, which was characterized by increased levels of circulating alanine transaminase and aspartate transaminase as well as massive necrosis of hepatocytes. The researchers noted that these manifestations were exacerbated significantly in the CRP knockout mice.

The intravenous administration of human CRP in the mice with the drug-induced liver injury rescued defects caused by mouse CRP knockout. Additionally, human CRP administration alleviated acetaminophen-induced acute liver injury in the wild-type mice. The researchers wrote that these findings demonstrate that endogenous and human CRP “are both protective,” at least in mouse models of acetaminophen-induced liver injury.

In a second experiment, the researchers examined the mechanisms involved in CRP protection in early phases of drug-induced liver injury. Based on the experiment, the researchers found that the knockout of an inhibitory Fcy receptor mediating the anti-inflammatory activities of CRP demonstrated only “marginal effects” on the protection of the protein in acetaminophen-induced liver injury. Overall, the investigators suggested that the inflammatory marker does not likely act via the cellular Fcy receptor 2B to inhibit early phases of acetaminophen-induced hepatocyte injury. Rather, the investigators explained that CRP may act via factor H, which is recruited by CRP in regulating complement activation, to inhibit overactivation of complement on injured hepatocytes. Ultimately, the researchers explained, this results in suppression of the late phase amplification of inflammation that is mediated by neutrophils’ C3a-dependent actions.

Finally, the researchers found that intraperitoneal administration of human CRP at 2.5 mg/kg in wild-type mice at 2 hours following induction of acetaminophen-induced liver injury led to “markedly reduced liver injury,” with an efficacy that was similar to that of 500 mg/kg N-acetylcysteine, the only available treatment approved for acetaminophen-induced liver injury.

The researchers noted that N-acetylcysteine is only effective during the early phases of the acetaminophen-induced liver injury and loses effectiveness at 6 hours following injury. In contrast, human CRP in this study was still highly effective at this time point. “Given that people can tolerate high levels of circulating CRP, the administration of this protein might be a promising option to treat [acetaminophen-induced liver injury] with minimal side effects,” the researchers wrote.

The study was funded by the National Natural Science Foundation of China. The researchers reported no conflicts of interest with any pharmaceutical companies.

This article was updated on Sep. 20, 2022.

In this quiz to Dermatology News, test your current knowledge of Generalized Pustular Psoriasis. Join Abby S. Van Voorhees, MD, as she shares insights on GPP and understanding the disorder. 

Learn More

PC-US-123740 December 2021

In this quiz to Dermatology News, test your current knowledge of Generalized Pustular Psoriasis. Join Abby S. Van Voorhees, MD, as she shares insights on GPP and understanding the disorder. 

Learn More

PC-US-123740 December 2021

In this quiz to Dermatology News, test your current knowledge of Generalized Pustular Psoriasis. Join Abby S. Van Voorhees, MD, as she shares insights on GPP and understanding the disorder. 

Learn More

PC-US-123740 December 2021

The COVID-19 pandemic highlighted a major gap in our institutional infrastructure in medicine – specifically, the absence of established policies and programs to support clinician wellbeing and organizational resilience.

In a 2020 report, the National Academy of Medicine advocated for “fixing the workplace,” rather than “fixing the worker,” as a more sustainable mechanism to advance physician wellbeing and foster organizational resilience. According to the report, “A resilient organization, or one that has matched job demands with job resources for its workers and that has created a culture of connection, transparency, and improvement, is better positioned to achieve organizational objectives during ordinary times and also to weather challenges during times of crisis” (Sinsky CA et al. “Organizational Evidence-Based and Promising Practices for Improving Clinician Well-Being.” National Academy of Medicine. Nov. 2, 2020.

The report highlights six domains of evidence-based practices to support organizational resilience and improve clinician well-being: organizational commitment, workforce assessment (such as measurement of physician wellbeing and burnout); leadership (including shared accountability, distributed leadership, and the emerging role of a chief wellness officer), policy (such as eliminating and/or re-envisioning policies and practices that interfere with clinicians’ ability to provide high-quality patient care), (5) efficiency (such as minimizing administrative tasks to allow clinicians to focus on patient care), and (6) support (such as providing resources and/or policies to support work-life balance, fostering a culture of connection at work). While many organizations (including both academic and community practices) already have begun to invest in this transformation, I urge you to think creatively about whether there is more your practice can do at an organizational level to support and sustain clinician wellbeing and prevent burnout.

In this month’s issue of GIHN, we highlight AGA’s new Clinical Practice Guideline on Coagulation in Cirrhosis, as well as results from a study confirming the benefits of coffee for liver health (welcome news to the caffeine-lovers among us!). We also report on a novel text-based patient-education intervention that aims to connect patients newly diagnosed with colorectal cancer to valuable resources and support.

Thank you for your dedicated readership – we look forward to continuing to bring you engaging, clinically-relevant content in 2022!

Megan A. Adams, MD, JD, MSc
Editor in Chief

The COVID-19 pandemic highlighted a major gap in our institutional infrastructure in medicine – specifically, the absence of established policies and programs to support clinician wellbeing and organizational resilience.

In a 2020 report, the National Academy of Medicine advocated for “fixing the workplace,” rather than “fixing the worker,” as a more sustainable mechanism to advance physician wellbeing and foster organizational resilience. According to the report, “A resilient organization, or one that has matched job demands with job resources for its workers and that has created a culture of connection, transparency, and improvement, is better positioned to achieve organizational objectives during ordinary times and also to weather challenges during times of crisis” (Sinsky CA et al. “Organizational Evidence-Based and Promising Practices for Improving Clinician Well-Being.” National Academy of Medicine. Nov. 2, 2020.

The report highlights six domains of evidence-based practices to support organizational resilience and improve clinician well-being: organizational commitment, workforce assessment (such as measurement of physician wellbeing and burnout); leadership (including shared accountability, distributed leadership, and the emerging role of a chief wellness officer), policy (such as eliminating and/or re-envisioning policies and practices that interfere with clinicians’ ability to provide high-quality patient care), (5) efficiency (such as minimizing administrative tasks to allow clinicians to focus on patient care), and (6) support (such as providing resources and/or policies to support work-life balance, fostering a culture of connection at work). While many organizations (including both academic and community practices) already have begun to invest in this transformation, I urge you to think creatively about whether there is more your practice can do at an organizational level to support and sustain clinician wellbeing and prevent burnout.

In this month’s issue of GIHN, we highlight AGA’s new Clinical Practice Guideline on Coagulation in Cirrhosis, as well as results from a study confirming the benefits of coffee for liver health (welcome news to the caffeine-lovers among us!). We also report on a novel text-based patient-education intervention that aims to connect patients newly diagnosed with colorectal cancer to valuable resources and support.

Thank you for your dedicated readership – we look forward to continuing to bring you engaging, clinically-relevant content in 2022!

Megan A. Adams, MD, JD, MSc
Editor in Chief

The COVID-19 pandemic highlighted a major gap in our institutional infrastructure in medicine – specifically, the absence of established policies and programs to support clinician wellbeing and organizational resilience.

In a 2020 report, the National Academy of Medicine advocated for “fixing the workplace,” rather than “fixing the worker,” as a more sustainable mechanism to advance physician wellbeing and foster organizational resilience. According to the report, “A resilient organization, or one that has matched job demands with job resources for its workers and that has created a culture of connection, transparency, and improvement, is better positioned to achieve organizational objectives during ordinary times and also to weather challenges during times of crisis” (Sinsky CA et al. “Organizational Evidence-Based and Promising Practices for Improving Clinician Well-Being.” National Academy of Medicine. Nov. 2, 2020.

The report highlights six domains of evidence-based practices to support organizational resilience and improve clinician well-being: organizational commitment, workforce assessment (such as measurement of physician wellbeing and burnout); leadership (including shared accountability, distributed leadership, and the emerging role of a chief wellness officer), policy (such as eliminating and/or re-envisioning policies and practices that interfere with clinicians’ ability to provide high-quality patient care), (5) efficiency (such as minimizing administrative tasks to allow clinicians to focus on patient care), and (6) support (such as providing resources and/or policies to support work-life balance, fostering a culture of connection at work). While many organizations (including both academic and community practices) already have begun to invest in this transformation, I urge you to think creatively about whether there is more your practice can do at an organizational level to support and sustain clinician wellbeing and prevent burnout.

In this month’s issue of GIHN, we highlight AGA’s new Clinical Practice Guideline on Coagulation in Cirrhosis, as well as results from a study confirming the benefits of coffee for liver health (welcome news to the caffeine-lovers among us!). We also report on a novel text-based patient-education intervention that aims to connect patients newly diagnosed with colorectal cancer to valuable resources and support.

Thank you for your dedicated readership – we look forward to continuing to bring you engaging, clinically-relevant content in 2022!

Megan A. Adams, MD, JD, MSc
Editor in Chief

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community (https://community.gastro.org) to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. Here’s a preview of a recent popular clinical discussion:  

Robert Herman, MD, wrote in “Rectal lesion”:

A 42-year-old healthy female was seen by me for symptoms of non-ulcer dyspepsia that was unresponsive to H2 Blockers and for assessment for screening colonoscopy. Her father had developed colon cancer at the age of 50. She denied changes in bowel habits, pattern, rectal bleeding, or melena. An EGD revealed a medium sized hiatal hernia and LA Grade B esophagitis that responded well to an OTC PPI qd.

A colonoscopy was performed and revealed a 4-cm anterior rectal “bulge” just above the hemorrhoidal plexus, appearing somewhat firm and mobile on probing the lesion with a closed biopsy forceps, and a 1 cm sessile IC valve adenomatous polyp.

And then the endoscopic medical assistant made a comment that changed everything. Read the full case discussion: https://community.gastro.org/posts/25568.
 

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community (https://community.gastro.org) to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. Here’s a preview of a recent popular clinical discussion:  

Robert Herman, MD, wrote in “Rectal lesion”:

A 42-year-old healthy female was seen by me for symptoms of non-ulcer dyspepsia that was unresponsive to H2 Blockers and for assessment for screening colonoscopy. Her father had developed colon cancer at the age of 50. She denied changes in bowel habits, pattern, rectal bleeding, or melena. An EGD revealed a medium sized hiatal hernia and LA Grade B esophagitis that responded well to an OTC PPI qd.

A colonoscopy was performed and revealed a 4-cm anterior rectal “bulge” just above the hemorrhoidal plexus, appearing somewhat firm and mobile on probing the lesion with a closed biopsy forceps, and a 1 cm sessile IC valve adenomatous polyp.

And then the endoscopic medical assistant made a comment that changed everything. Read the full case discussion: https://community.gastro.org/posts/25568.
 

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community (https://community.gastro.org) to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. Here’s a preview of a recent popular clinical discussion:  

Robert Herman, MD, wrote in “Rectal lesion”:

A 42-year-old healthy female was seen by me for symptoms of non-ulcer dyspepsia that was unresponsive to H2 Blockers and for assessment for screening colonoscopy. Her father had developed colon cancer at the age of 50. She denied changes in bowel habits, pattern, rectal bleeding, or melena. An EGD revealed a medium sized hiatal hernia and LA Grade B esophagitis that responded well to an OTC PPI qd.

A colonoscopy was performed and revealed a 4-cm anterior rectal “bulge” just above the hemorrhoidal plexus, appearing somewhat firm and mobile on probing the lesion with a closed biopsy forceps, and a 1 cm sessile IC valve adenomatous polyp.

And then the endoscopic medical assistant made a comment that changed everything. Read the full case discussion: https://community.gastro.org/posts/25568.
 

Key clinical point: Vitamin D status was inversely associated with severe sarcopenia, impaired physical performance, and decreased skeletal muscle mass in females with rheumatoid arthritis (RA), highlighting the need to investigate vitamin D supplementation as a therapeutic strategy for sarcopenic patients with RA.

Major finding: Low 25-hydroxyvitamin D (25[OH])D status (16.0 ng/mL or lower) was significantly associated with a high prevalence of severe sarcopenia (adjusted odds ratio [aOR], 6.00; P = .0006) in females with RA. Low physical performance (aOR, 2.65; P = .0043) and skeletal muscle mass (aOR, 2.54; P = .027) were the major components of sarcopenia linked with a low serum 25(OH)D level.

Study details: This was a cross-sectional study involving 156 female outpatients with RA.

Disclosures: This study was funded by AMED and Daiichi Sankyo Co. Ltd. Several authors reported receiving research grants and speaker’s fees from various sources including Daiichi Sankyo. Some of the authors including the lead author declared no conflict of interests.

Source: Minamino H et al. Sci Rep. 2021 Oct 14. doi: 10.1038/s41598-021-99894-6.

Key clinical point: Vitamin D status was inversely associated with severe sarcopenia, impaired physical performance, and decreased skeletal muscle mass in females with rheumatoid arthritis (RA), highlighting the need to investigate vitamin D supplementation as a therapeutic strategy for sarcopenic patients with RA.

Major finding: Low 25-hydroxyvitamin D (25[OH])D status (16.0 ng/mL or lower) was significantly associated with a high prevalence of severe sarcopenia (adjusted odds ratio [aOR], 6.00; P = .0006) in females with RA. Low physical performance (aOR, 2.65; P = .0043) and skeletal muscle mass (aOR, 2.54; P = .027) were the major components of sarcopenia linked with a low serum 25(OH)D level.

Study details: This was a cross-sectional study involving 156 female outpatients with RA.

Disclosures: This study was funded by AMED and Daiichi Sankyo Co. Ltd. Several authors reported receiving research grants and speaker’s fees from various sources including Daiichi Sankyo. Some of the authors including the lead author declared no conflict of interests.

Source: Minamino H et al. Sci Rep. 2021 Oct 14. doi: 10.1038/s41598-021-99894-6.

Key clinical point: Vitamin D status was inversely associated with severe sarcopenia, impaired physical performance, and decreased skeletal muscle mass in females with rheumatoid arthritis (RA), highlighting the need to investigate vitamin D supplementation as a therapeutic strategy for sarcopenic patients with RA.

Major finding: Low 25-hydroxyvitamin D (25[OH])D status (16.0 ng/mL or lower) was significantly associated with a high prevalence of severe sarcopenia (adjusted odds ratio [aOR], 6.00; P = .0006) in females with RA. Low physical performance (aOR, 2.65; P = .0043) and skeletal muscle mass (aOR, 2.54; P = .027) were the major components of sarcopenia linked with a low serum 25(OH)D level.

Study details: This was a cross-sectional study involving 156 female outpatients with RA.

Disclosures: This study was funded by AMED and Daiichi Sankyo Co. Ltd. Several authors reported receiving research grants and speaker’s fees from various sources including Daiichi Sankyo. Some of the authors including the lead author declared no conflict of interests.

Source: Minamino H et al. Sci Rep. 2021 Oct 14. doi: 10.1038/s41598-021-99894-6.

Key clinical point: The anti-inflammatory diet did not enhance health-related quality of life in patients with rheumatoid arthritis (RA) compared with a control diet. However, physical functioning improved significantly, particularly in patients who did not alter antirheumatic medication.

Major finding: The Health Assessment Questionnaire was not significantly different between the intervention and control diet periods (P = .503); however, the physical functioning improved significantly during intervention diet vs. control diet period (mean, 5.791; 95% CI, 1.576-10.005), particularly in patients without pharmacological treatment changes (mean, 7.898; P = .036).

Study details: Findings are from the ADIRA trial, a controlled crossover trial including 50 patients with RA who were randomly assigned to either an intervention diet including foods with suggested anti-inflammatory properties and promising effects on RA symptoms (n=24) or control diet (usual Swedish diet; n=26) for 10 weeks before switching to the other diet.

Disclosures: This study received grants from the Swedish government, Swedish Research Council for Health, Working Life and Welfare, and others. No conflict of interests was reported.

Source: Turesson Wadell A et al. PLoS One. 2021 Oct 14. doi: 10.1371/journal.pone.0258716.

Key clinical point: The anti-inflammatory diet did not enhance health-related quality of life in patients with rheumatoid arthritis (RA) compared with a control diet. However, physical functioning improved significantly, particularly in patients who did not alter antirheumatic medication.

Major finding: The Health Assessment Questionnaire was not significantly different between the intervention and control diet periods (P = .503); however, the physical functioning improved significantly during intervention diet vs. control diet period (mean, 5.791; 95% CI, 1.576-10.005), particularly in patients without pharmacological treatment changes (mean, 7.898; P = .036).

Study details: Findings are from the ADIRA trial, a controlled crossover trial including 50 patients with RA who were randomly assigned to either an intervention diet including foods with suggested anti-inflammatory properties and promising effects on RA symptoms (n=24) or control diet (usual Swedish diet; n=26) for 10 weeks before switching to the other diet.

Disclosures: This study received grants from the Swedish government, Swedish Research Council for Health, Working Life and Welfare, and others. No conflict of interests was reported.

Source: Turesson Wadell A et al. PLoS One. 2021 Oct 14. doi: 10.1371/journal.pone.0258716.

Key clinical point: The anti-inflammatory diet did not enhance health-related quality of life in patients with rheumatoid arthritis (RA) compared with a control diet. However, physical functioning improved significantly, particularly in patients who did not alter antirheumatic medication.

Major finding: The Health Assessment Questionnaire was not significantly different between the intervention and control diet periods (P = .503); however, the physical functioning improved significantly during intervention diet vs. control diet period (mean, 5.791; 95% CI, 1.576-10.005), particularly in patients without pharmacological treatment changes (mean, 7.898; P = .036).

Study details: Findings are from the ADIRA trial, a controlled crossover trial including 50 patients with RA who were randomly assigned to either an intervention diet including foods with suggested anti-inflammatory properties and promising effects on RA symptoms (n=24) or control diet (usual Swedish diet; n=26) for 10 weeks before switching to the other diet.

Disclosures: This study received grants from the Swedish government, Swedish Research Council for Health, Working Life and Welfare, and others. No conflict of interests was reported.

Source: Turesson Wadell A et al. PLoS One. 2021 Oct 14. doi: 10.1371/journal.pone.0258716.

Key clinical point: Sinusitis, pharyngitis, and acute respiratory burden all raised the likelihood of developing rheumatoid arthritis (RA).

Major finding: Acute sinusitis (odds ratio [OR], 1.61; 95% CI, 1.05-2.45), chronic sinusitis (OR, 2.16; 95% CI, 1.39-3.35), asthma (OR, 1.39; 95% CI, 1.03-1.87), and burden of acute respiratory tract disease during the preindex exposure period (OR, 1.30 per 10 codes; 95% CI, 1.08-1.55) were associated with an elevated risk for RA. Acute pharyngitis was associated with seronegative RA (OR, 1.68; 95% CI, 1.02-2.74), whereas chronic rhinitis/pharyngitis was associated with seropositive RA (OR, 2.46; 95% CI, 1.01-5.99).

Study details: This was a case-control study involving 741 patients with RA matched with 2,223 healthy controls.

Disclosures: The National Institute of Arthritis and Musculoskeletal and Skin Diseases and Rheumatology Research Foundation funded this research. No conflict of interests was reported.

Source: Kronzer VL et al. J Rheumatol. 2021 Oct 15. doi: 10.3899/jrheum.210580.

Key clinical point: Sinusitis, pharyngitis, and acute respiratory burden all raised the likelihood of developing rheumatoid arthritis (RA).

Major finding: Acute sinusitis (odds ratio [OR], 1.61; 95% CI, 1.05-2.45), chronic sinusitis (OR, 2.16; 95% CI, 1.39-3.35), asthma (OR, 1.39; 95% CI, 1.03-1.87), and burden of acute respiratory tract disease during the preindex exposure period (OR, 1.30 per 10 codes; 95% CI, 1.08-1.55) were associated with an elevated risk for RA. Acute pharyngitis was associated with seronegative RA (OR, 1.68; 95% CI, 1.02-2.74), whereas chronic rhinitis/pharyngitis was associated with seropositive RA (OR, 2.46; 95% CI, 1.01-5.99).

Study details: This was a case-control study involving 741 patients with RA matched with 2,223 healthy controls.

Disclosures: The National Institute of Arthritis and Musculoskeletal and Skin Diseases and Rheumatology Research Foundation funded this research. No conflict of interests was reported.

Source: Kronzer VL et al. J Rheumatol. 2021 Oct 15. doi: 10.3899/jrheum.210580.

Key clinical point: Sinusitis, pharyngitis, and acute respiratory burden all raised the likelihood of developing rheumatoid arthritis (RA).

Major finding: Acute sinusitis (odds ratio [OR], 1.61; 95% CI, 1.05-2.45), chronic sinusitis (OR, 2.16; 95% CI, 1.39-3.35), asthma (OR, 1.39; 95% CI, 1.03-1.87), and burden of acute respiratory tract disease during the preindex exposure period (OR, 1.30 per 10 codes; 95% CI, 1.08-1.55) were associated with an elevated risk for RA. Acute pharyngitis was associated with seronegative RA (OR, 1.68; 95% CI, 1.02-2.74), whereas chronic rhinitis/pharyngitis was associated with seropositive RA (OR, 2.46; 95% CI, 1.01-5.99).

Study details: This was a case-control study involving 741 patients with RA matched with 2,223 healthy controls.

Disclosures: The National Institute of Arthritis and Musculoskeletal and Skin Diseases and Rheumatology Research Foundation funded this research. No conflict of interests was reported.

Source: Kronzer VL et al. J Rheumatol. 2021 Oct 15. doi: 10.3899/jrheum.210580.

Key clinical point: Filgotinib 200 mg (FIL200) and 100 mg (FIL100) showed similar safety/tolerability in patients with moderate-to-severe rheumatoid arthritis (RA) with over a median of 1.6 years and maximum of 5.6 years of exposure, with FIL200 showing a lower infection rate in the long term.

Major finding: Treatment-emergent adverse events (TEAEs) were similar between FIL200 (exposure-adjusted incidence rate [EAIR], 195.4 per 100 patient-years of exposure [100 PYE]), FIL100 (176.3 per 100 PYE), and placebo (175.9 per 100 PYE) during the 12-week period. During long-term exposure, EAIR for grade ≥3 TEAEs were 6.4 and 7.6 per 100 PYE for FIL200 and FIL100, respectively, but serious infectious AEs were lower with FIL200 vs. FIL100 (EAIR, 1.6 vs. 3.1 per 100 PYE).

Study details: Data come from integrated analysis of 7 clinical trials including patients with moderate-to-severe RA who received ≥1 dose of FIL200, FIL100, or placebo.

Disclosures: This study was funded by Gilead Sciences, Inc. Some investigators including the lead author reported receiving grants, honoraria, consultancy/speaker’s fees, and being an employee of or shareholder of various sources including Gilead Sciences.

Source: Winthrop KL et al. Ann Rheum Dis. 2021 Nov 5. doi: 10.1136/annrheumdis-2021-221051.

Key clinical point: Filgotinib 200 mg (FIL200) and 100 mg (FIL100) showed similar safety/tolerability in patients with moderate-to-severe rheumatoid arthritis (RA) with over a median of 1.6 years and maximum of 5.6 years of exposure, with FIL200 showing a lower infection rate in the long term.

Major finding: Treatment-emergent adverse events (TEAEs) were similar between FIL200 (exposure-adjusted incidence rate [EAIR], 195.4 per 100 patient-years of exposure [100 PYE]), FIL100 (176.3 per 100 PYE), and placebo (175.9 per 100 PYE) during the 12-week period. During long-term exposure, EAIR for grade ≥3 TEAEs were 6.4 and 7.6 per 100 PYE for FIL200 and FIL100, respectively, but serious infectious AEs were lower with FIL200 vs. FIL100 (EAIR, 1.6 vs. 3.1 per 100 PYE).

Study details: Data come from integrated analysis of 7 clinical trials including patients with moderate-to-severe RA who received ≥1 dose of FIL200, FIL100, or placebo.

Disclosures: This study was funded by Gilead Sciences, Inc. Some investigators including the lead author reported receiving grants, honoraria, consultancy/speaker’s fees, and being an employee of or shareholder of various sources including Gilead Sciences.

Source: Winthrop KL et al. Ann Rheum Dis. 2021 Nov 5. doi: 10.1136/annrheumdis-2021-221051.

Key clinical point: Filgotinib 200 mg (FIL200) and 100 mg (FIL100) showed similar safety/tolerability in patients with moderate-to-severe rheumatoid arthritis (RA) with over a median of 1.6 years and maximum of 5.6 years of exposure, with FIL200 showing a lower infection rate in the long term.

Major finding: Treatment-emergent adverse events (TEAEs) were similar between FIL200 (exposure-adjusted incidence rate [EAIR], 195.4 per 100 patient-years of exposure [100 PYE]), FIL100 (176.3 per 100 PYE), and placebo (175.9 per 100 PYE) during the 12-week period. During long-term exposure, EAIR for grade ≥3 TEAEs were 6.4 and 7.6 per 100 PYE for FIL200 and FIL100, respectively, but serious infectious AEs were lower with FIL200 vs. FIL100 (EAIR, 1.6 vs. 3.1 per 100 PYE).

Study details: Data come from integrated analysis of 7 clinical trials including patients with moderate-to-severe RA who received ≥1 dose of FIL200, FIL100, or placebo.

Disclosures: This study was funded by Gilead Sciences, Inc. Some investigators including the lead author reported receiving grants, honoraria, consultancy/speaker’s fees, and being an employee of or shareholder of various sources including Gilead Sciences.

Source: Winthrop KL et al. Ann Rheum Dis. 2021 Nov 5. doi: 10.1136/annrheumdis-2021-221051.

Key clinical point: Obesity, anxiety, depression, and illness perception at baseline were associated with treatment outcomes, pain, and fatigue in patients with rheumatoid arthritis (RA).

Major finding: At 12 months, obesity vs. normal weight was associated with a lower likelihood of remission (adjusted odds ratio [aOR], 0.33; P=.005). Obesity and illness perception were significantly associated with pain (aOR, 8.16; P = .002 and aOR, 0.62; P < .001, respectively) and fatigue (aOR, 5.66; P = .049 and aOR, 0.51; P = .001, respectively) with patients with severe vs. no anxiety having higher pain (aOR, 9.60; P = .010) and those with severe (aOR, 17.07; P < .001) and moderate (aOR, 10.13; P = .001) depression having higher fatigue.

Study details: This secondary analysis of the TITRATE trial included 335 patients with RA treated with intensive management (n=168) or standard care (n=167).

Disclosures: This study was funded by the National Institute for Health Research. E Nikiphorou received speaker fees and served on advisory boards for various sources. Other authors declared no competing interest.

Source: Lee SY et al. Arthritis Res Ther. 2021 Nov 4. doi: 10.1186/s13075-021-02653-1.

Key clinical point: Obesity, anxiety, depression, and illness perception at baseline were associated with treatment outcomes, pain, and fatigue in patients with rheumatoid arthritis (RA).

Major finding: At 12 months, obesity vs. normal weight was associated with a lower likelihood of remission (adjusted odds ratio [aOR], 0.33; P=.005). Obesity and illness perception were significantly associated with pain (aOR, 8.16; P = .002 and aOR, 0.62; P < .001, respectively) and fatigue (aOR, 5.66; P = .049 and aOR, 0.51; P = .001, respectively) with patients with severe vs. no anxiety having higher pain (aOR, 9.60; P = .010) and those with severe (aOR, 17.07; P < .001) and moderate (aOR, 10.13; P = .001) depression having higher fatigue.

Study details: This secondary analysis of the TITRATE trial included 335 patients with RA treated with intensive management (n=168) or standard care (n=167).

Disclosures: This study was funded by the National Institute for Health Research. E Nikiphorou received speaker fees and served on advisory boards for various sources. Other authors declared no competing interest.

Source: Lee SY et al. Arthritis Res Ther. 2021 Nov 4. doi: 10.1186/s13075-021-02653-1.

Key clinical point: Obesity, anxiety, depression, and illness perception at baseline were associated with treatment outcomes, pain, and fatigue in patients with rheumatoid arthritis (RA).

Major finding: At 12 months, obesity vs. normal weight was associated with a lower likelihood of remission (adjusted odds ratio [aOR], 0.33; P=.005). Obesity and illness perception were significantly associated with pain (aOR, 8.16; P = .002 and aOR, 0.62; P < .001, respectively) and fatigue (aOR, 5.66; P = .049 and aOR, 0.51; P = .001, respectively) with patients with severe vs. no anxiety having higher pain (aOR, 9.60; P = .010) and those with severe (aOR, 17.07; P < .001) and moderate (aOR, 10.13; P = .001) depression having higher fatigue.

Study details: This secondary analysis of the TITRATE trial included 335 patients with RA treated with intensive management (n=168) or standard care (n=167).

Disclosures: This study was funded by the National Institute for Health Research. E Nikiphorou received speaker fees and served on advisory boards for various sources. Other authors declared no competing interest.

Source: Lee SY et al. Arthritis Res Ther. 2021 Nov 4. doi: 10.1186/s13075-021-02653-1.

Key clinical point: Certolizumab (CTZ) monotherapy seemed as effective as combination therapy with methotrexate (MTX) or leflunomide (LFN) or MTX+LFN in patients with rheumatoid arthritis (RA) who failed previous conventional synthetic disease-modifying antirheumatic drugs (csDMARD) therapy.

Major finding: Overall, 63% of patients were in remission or showed low disease activity (LDA) within 3 months of follow-up, with no difference between groups (P = .080). Most patients maintained response at 12 months, with remission or LDA achieved by 94.4%, 81.8%, 80.5%, and 51.4% of patients receiving CTZ monotherapy, CTZ+MTX, CTZ+LFN, and MTX+LFN, respectively (P = .001).

Study details: This was a retrospective cohort study of 181 patients with RA who were treated for a minimum of 3 months with certolizumab as monotherapy (n=24) or in combination with MTX (n=62), LFN (n=47) or MTX+LFN (n=48).

Disclosures: No information on funding was provided. P Santos-Moreno and A Rojas-Villarrage received fees for conferences, counseling, advisory boards, or travel expenses and research grants from various sources.

Source: Santos-Moreno P et al. Biologics. 2021 Oct 22. doi: 10.2147/BTT.S322860.

Key clinical point: Certolizumab (CTZ) monotherapy seemed as effective as combination therapy with methotrexate (MTX) or leflunomide (LFN) or MTX+LFN in patients with rheumatoid arthritis (RA) who failed previous conventional synthetic disease-modifying antirheumatic drugs (csDMARD) therapy.

Major finding: Overall, 63% of patients were in remission or showed low disease activity (LDA) within 3 months of follow-up, with no difference between groups (P = .080). Most patients maintained response at 12 months, with remission or LDA achieved by 94.4%, 81.8%, 80.5%, and 51.4% of patients receiving CTZ monotherapy, CTZ+MTX, CTZ+LFN, and MTX+LFN, respectively (P = .001).

Study details: This was a retrospective cohort study of 181 patients with RA who were treated for a minimum of 3 months with certolizumab as monotherapy (n=24) or in combination with MTX (n=62), LFN (n=47) or MTX+LFN (n=48).

Disclosures: No information on funding was provided. P Santos-Moreno and A Rojas-Villarrage received fees for conferences, counseling, advisory boards, or travel expenses and research grants from various sources.

Source: Santos-Moreno P et al. Biologics. 2021 Oct 22. doi: 10.2147/BTT.S322860.

Key clinical point: Certolizumab (CTZ) monotherapy seemed as effective as combination therapy with methotrexate (MTX) or leflunomide (LFN) or MTX+LFN in patients with rheumatoid arthritis (RA) who failed previous conventional synthetic disease-modifying antirheumatic drugs (csDMARD) therapy.

Major finding: Overall, 63% of patients were in remission or showed low disease activity (LDA) within 3 months of follow-up, with no difference between groups (P = .080). Most patients maintained response at 12 months, with remission or LDA achieved by 94.4%, 81.8%, 80.5%, and 51.4% of patients receiving CTZ monotherapy, CTZ+MTX, CTZ+LFN, and MTX+LFN, respectively (P = .001).

Study details: This was a retrospective cohort study of 181 patients with RA who were treated for a minimum of 3 months with certolizumab as monotherapy (n=24) or in combination with MTX (n=62), LFN (n=47) or MTX+LFN (n=48).

Disclosures: No information on funding was provided. P Santos-Moreno and A Rojas-Villarrage received fees for conferences, counseling, advisory boards, or travel expenses and research grants from various sources.

Source: Santos-Moreno P et al. Biologics. 2021 Oct 22. doi: 10.2147/BTT.S322860.