Serotonin syndrome (SS) is diagnosed by the clinical triad of dysautonomia (fever, mydriasis, diaphoresis, tachycardia), neuromuscular signs (ataxia, hyperreflexia, tremor, myoclonus), and altered mental status (seizures, delirium). Two validated criteria groups are accepted, the Hunter criteria and the Sternbach criteria. These criteria require a menu-like approach of clinical manifestations of the above signs with known addition or increase of a serotonergic medication and the absence of other possible causes, such as neuroleptics.

In 2006, the FDA issued a clinical warning titled “Potentially Life-Threatening Serotonin Syndrome With Combined Use of SSRIs or SNRIs and Triptan Medications.” Subsequently, Randolph W. Evans, MD, and others conducted a close evaluation of the cases used by the FDA as the basis for their warning. They noted that none of the initial cases met Hunter criteria, only 10 of 29 met Sternbach criteria, and a second set of 11 patients also were questionable in terms of the diagnosis of serotonin toxicity. Serotonin (5-HT) toxicity is mediated by excessive activity of 5-HT_2A receptors, and triptans have no action at those receptors, only having activity at 5-HT_1B, _1D, and _1F receptors.

In 2010, the American Headache Society (AHS) published a position paper on this drug-drug interaction. In it, they stated, “with only Class IV evidence available in the literature and available through the FDA registration of adverse events, …the currently available evidence does not support limiting the use of triptans with SSRIs or SNRIs, or the use of triptan monotherapy, due to concerns for serotonin syndrome (Level U).”

Confirming the lack of evidence for an interaction, Dr. Yulia Orlova from the Graham Headache Center in Boston reported from the Partners Healthcare System Research Patient Data Registry on about 48,000 patients prescribed triptans, of whom about 19,000 were also co-prescribed SSRI or SNRI antidepressants. None of the cases met Hunter and Sternbach criteria and one patient who manifested serotonin toxicity had signs that preceded triptan use.  A previous trial of a cohort of 240,268 patients receiving pharmacy benefits reported that the frequency of co-prescription of triptans with SSRIs was about 20%. With the size of these reports, the absence of documented cases fulfilling both sets of criteria, and the lack of receptor plausibility as a cause for serotonin toxicity from triptans, the likelihood of the syndrome from triptan use is low, and the warning inappropriate. The co-occurrence of depression, anxiety, and migraine often makes co-prescription of triptans and antidepressants necessary, and the concern for co-prescription excessive.

—Stewart J. Tepper, MD
Professor of Neurology
Geisel School of Medicine at Dartmouth

Serotonin syndrome (SS) is diagnosed by the clinical triad of dysautonomia (fever, mydriasis, diaphoresis, tachycardia), neuromuscular signs (ataxia, hyperreflexia, tremor, myoclonus), and altered mental status (seizures, delirium). Two validated criteria groups are accepted, the Hunter criteria and the Sternbach criteria. These criteria require a menu-like approach of clinical manifestations of the above signs with known addition or increase of a serotonergic medication and the absence of other possible causes, such as neuroleptics.

In 2006, the FDA issued a clinical warning titled “Potentially Life-Threatening Serotonin Syndrome With Combined Use of SSRIs or SNRIs and Triptan Medications.” Subsequently, Randolph W. Evans, MD, and others conducted a close evaluation of the cases used by the FDA as the basis for their warning. They noted that none of the initial cases met Hunter criteria, only 10 of 29 met Sternbach criteria, and a second set of 11 patients also were questionable in terms of the diagnosis of serotonin toxicity. Serotonin (5-HT) toxicity is mediated by excessive activity of 5-HT_2A receptors, and triptans have no action at those receptors, only having activity at 5-HT_1B, _1D, and _1F receptors.

In 2010, the American Headache Society (AHS) published a position paper on this drug-drug interaction. In it, they stated, “with only Class IV evidence available in the literature and available through the FDA registration of adverse events, …the currently available evidence does not support limiting the use of triptans with SSRIs or SNRIs, or the use of triptan monotherapy, due to concerns for serotonin syndrome (Level U).”

Confirming the lack of evidence for an interaction, Dr. Yulia Orlova from the Graham Headache Center in Boston reported from the Partners Healthcare System Research Patient Data Registry on about 48,000 patients prescribed triptans, of whom about 19,000 were also co-prescribed SSRI or SNRI antidepressants. None of the cases met Hunter and Sternbach criteria and one patient who manifested serotonin toxicity had signs that preceded triptan use.  A previous trial of a cohort of 240,268 patients receiving pharmacy benefits reported that the frequency of co-prescription of triptans with SSRIs was about 20%. With the size of these reports, the absence of documented cases fulfilling both sets of criteria, and the lack of receptor plausibility as a cause for serotonin toxicity from triptans, the likelihood of the syndrome from triptan use is low, and the warning inappropriate. The co-occurrence of depression, anxiety, and migraine often makes co-prescription of triptans and antidepressants necessary, and the concern for co-prescription excessive.

—Stewart J. Tepper, MD
Professor of Neurology
Geisel School of Medicine at Dartmouth

Serotonin syndrome (SS) is diagnosed by the clinical triad of dysautonomia (fever, mydriasis, diaphoresis, tachycardia), neuromuscular signs (ataxia, hyperreflexia, tremor, myoclonus), and altered mental status (seizures, delirium). Two validated criteria groups are accepted, the Hunter criteria and the Sternbach criteria. These criteria require a menu-like approach of clinical manifestations of the above signs with known addition or increase of a serotonergic medication and the absence of other possible causes, such as neuroleptics.

In 2006, the FDA issued a clinical warning titled “Potentially Life-Threatening Serotonin Syndrome With Combined Use of SSRIs or SNRIs and Triptan Medications.” Subsequently, Randolph W. Evans, MD, and others conducted a close evaluation of the cases used by the FDA as the basis for their warning. They noted that none of the initial cases met Hunter criteria, only 10 of 29 met Sternbach criteria, and a second set of 11 patients also were questionable in terms of the diagnosis of serotonin toxicity. Serotonin (5-HT) toxicity is mediated by excessive activity of 5-HT_2A receptors, and triptans have no action at those receptors, only having activity at 5-HT_1B, _1D, and _1F receptors.

In 2010, the American Headache Society (AHS) published a position paper on this drug-drug interaction. In it, they stated, “with only Class IV evidence available in the literature and available through the FDA registration of adverse events, …the currently available evidence does not support limiting the use of triptans with SSRIs or SNRIs, or the use of triptan monotherapy, due to concerns for serotonin syndrome (Level U).”

Confirming the lack of evidence for an interaction, Dr. Yulia Orlova from the Graham Headache Center in Boston reported from the Partners Healthcare System Research Patient Data Registry on about 48,000 patients prescribed triptans, of whom about 19,000 were also co-prescribed SSRI or SNRI antidepressants. None of the cases met Hunter and Sternbach criteria and one patient who manifested serotonin toxicity had signs that preceded triptan use.  A previous trial of a cohort of 240,268 patients receiving pharmacy benefits reported that the frequency of co-prescription of triptans with SSRIs was about 20%. With the size of these reports, the absence of documented cases fulfilling both sets of criteria, and the lack of receptor plausibility as a cause for serotonin toxicity from triptans, the likelihood of the syndrome from triptan use is low, and the warning inappropriate. The co-occurrence of depression, anxiety, and migraine often makes co-prescription of triptans and antidepressants necessary, and the concern for co-prescription excessive.

—Stewart J. Tepper, MD
Professor of Neurology
Geisel School of Medicine at Dartmouth

LOS ANGELES – The benefits of mechanical thrombectomy observed in the DAWN trial for patients with acute ischemic stroke and a mismatch between core imaging and clinical presentation out to 24 hours appear to apply regardless of whether their eligibility is determined by CT perfusion or diffusion-weighted magnetic resonance imaging, according to a subanalysis of the trial data.

Diffusion-weighted magnetic resonance imaging (DW-MRI) is considered the gold standard, but it is not as widely available as CT perfusion (CTP) and previous studies have shown that MR is associated with longer times between stroke onset and treatment randomization. “Though MR was originally preferred in DAWN, it was pretty clear that CT perfusion was going to need to be employed in the trial as well,” Cathy Sila, MD, said during her presentation of the results of the subanalysis at the International Stroke Conference 2018, sponsored by the American Heart Association.

The research sought to determine if the two imaging methods perform similarly. CTP is more readily available, but it has some issues. In patients with severe heart failure, a severe proximal stenosis, or a contralateral severe stenosis, the technique may struggle to accurately image the core infarct, which has led some to wonder if the outcomes would be as good using CTP as selection criteria. “In our institution, we’ve had this conversation very frequently,” said Dr. Sila, who is a vascular neurologist and the director of the University Hospitals Systems stroke program in Cleveland.

To be eligible for DAWN, the core infarct had to correspond to at least a 30% decrease in regional blood flow in the CTP map, or an apparent diffusion coefficient of less than 620 on DW-MRI.

The researchers included all 206 patients in the DAWN study (N Engl J Med. 2018;378:11-21), separating them into DW-MRI or CTP groups based on which imaging method was used to randomize them during the trial. There were no statistically significant differences in any of the baseline characteristics between the two imaging groups.

The 26 sites participating in DAWN had clear differences in their preferences for imaging techniques; 19 exclusively used CTP, 4 used only DW-MRI, and 3 sites used a combination of both imaging methods.

There were no statistically significant differences between the two groups in any of the measured clinical outcomes, including neurologic deterioration in hospital (22.8% with CTP vs. 15.7% with DW-MRII, P = .286), symptomatic intracranial hemorrhage (4.1% with CTP vs. 4.8% with DW-MRI, P = 1.000), or death related to stroke (19.5% with CTP vs. 13.3% with DW-MRI, P = .263). Outcomes at 90 days proved to be similar between CTP and DW-MRI for achieving functional independence (29.3% vs. 34.9%, respectively; P = .445) and utility-weighted modified Rankin Scale scores (4.2 vs. 4.9, respectively; P = .172).

Multivariate analyses showed that 90-day functional independence was predicted by thrombectomy treatment, age, blood glucose level, baseline National Institutes of Health Stroke Scale score, and core lab ASPECTS (Alberta Stroke Program Early CT Score), but not the method of imaging.

“The efficacy and safety of mechanical thrombectomy for patients meeting those clinical mismatch criteria at 6-24 hours were comparable whether the small core infarcts were measured by diffusion imaging or cerebral blood flow imaging. I believe that future clinical trials aiming to extend the eligibility outside of this prespecified population should include both imaging modalities to determine whether these results are generalizable,” Dr. Sila said.

The DAWN study was funded by Stryker Neurovascular. Dr. Sila has reported receiving honoraria from Medtronic.

SOURCE: Sila C et al. ISC 2018, abstract LB11.

LOS ANGELES – The benefits of mechanical thrombectomy observed in the DAWN trial for patients with acute ischemic stroke and a mismatch between core imaging and clinical presentation out to 24 hours appear to apply regardless of whether their eligibility is determined by CT perfusion or diffusion-weighted magnetic resonance imaging, according to a subanalysis of the trial data.

Diffusion-weighted magnetic resonance imaging (DW-MRI) is considered the gold standard, but it is not as widely available as CT perfusion (CTP) and previous studies have shown that MR is associated with longer times between stroke onset and treatment randomization. “Though MR was originally preferred in DAWN, it was pretty clear that CT perfusion was going to need to be employed in the trial as well,” Cathy Sila, MD, said during her presentation of the results of the subanalysis at the International Stroke Conference 2018, sponsored by the American Heart Association.

The research sought to determine if the two imaging methods perform similarly. CTP is more readily available, but it has some issues. In patients with severe heart failure, a severe proximal stenosis, or a contralateral severe stenosis, the technique may struggle to accurately image the core infarct, which has led some to wonder if the outcomes would be as good using CTP as selection criteria. “In our institution, we’ve had this conversation very frequently,” said Dr. Sila, who is a vascular neurologist and the director of the University Hospitals Systems stroke program in Cleveland.

To be eligible for DAWN, the core infarct had to correspond to at least a 30% decrease in regional blood flow in the CTP map, or an apparent diffusion coefficient of less than 620 on DW-MRI.

The researchers included all 206 patients in the DAWN study (N Engl J Med. 2018;378:11-21), separating them into DW-MRI or CTP groups based on which imaging method was used to randomize them during the trial. There were no statistically significant differences in any of the baseline characteristics between the two imaging groups.

The 26 sites participating in DAWN had clear differences in their preferences for imaging techniques; 19 exclusively used CTP, 4 used only DW-MRI, and 3 sites used a combination of both imaging methods.

There were no statistically significant differences between the two groups in any of the measured clinical outcomes, including neurologic deterioration in hospital (22.8% with CTP vs. 15.7% with DW-MRII, P = .286), symptomatic intracranial hemorrhage (4.1% with CTP vs. 4.8% with DW-MRI, P = 1.000), or death related to stroke (19.5% with CTP vs. 13.3% with DW-MRI, P = .263). Outcomes at 90 days proved to be similar between CTP and DW-MRI for achieving functional independence (29.3% vs. 34.9%, respectively; P = .445) and utility-weighted modified Rankin Scale scores (4.2 vs. 4.9, respectively; P = .172).

Multivariate analyses showed that 90-day functional independence was predicted by thrombectomy treatment, age, blood glucose level, baseline National Institutes of Health Stroke Scale score, and core lab ASPECTS (Alberta Stroke Program Early CT Score), but not the method of imaging.

“The efficacy and safety of mechanical thrombectomy for patients meeting those clinical mismatch criteria at 6-24 hours were comparable whether the small core infarcts were measured by diffusion imaging or cerebral blood flow imaging. I believe that future clinical trials aiming to extend the eligibility outside of this prespecified population should include both imaging modalities to determine whether these results are generalizable,” Dr. Sila said.

The DAWN study was funded by Stryker Neurovascular. Dr. Sila has reported receiving honoraria from Medtronic.

SOURCE: Sila C et al. ISC 2018, abstract LB11.

LOS ANGELES – The benefits of mechanical thrombectomy observed in the DAWN trial for patients with acute ischemic stroke and a mismatch between core imaging and clinical presentation out to 24 hours appear to apply regardless of whether their eligibility is determined by CT perfusion or diffusion-weighted magnetic resonance imaging, according to a subanalysis of the trial data.

Diffusion-weighted magnetic resonance imaging (DW-MRI) is considered the gold standard, but it is not as widely available as CT perfusion (CTP) and previous studies have shown that MR is associated with longer times between stroke onset and treatment randomization. “Though MR was originally preferred in DAWN, it was pretty clear that CT perfusion was going to need to be employed in the trial as well,” Cathy Sila, MD, said during her presentation of the results of the subanalysis at the International Stroke Conference 2018, sponsored by the American Heart Association.

The research sought to determine if the two imaging methods perform similarly. CTP is more readily available, but it has some issues. In patients with severe heart failure, a severe proximal stenosis, or a contralateral severe stenosis, the technique may struggle to accurately image the core infarct, which has led some to wonder if the outcomes would be as good using CTP as selection criteria. “In our institution, we’ve had this conversation very frequently,” said Dr. Sila, who is a vascular neurologist and the director of the University Hospitals Systems stroke program in Cleveland.

To be eligible for DAWN, the core infarct had to correspond to at least a 30% decrease in regional blood flow in the CTP map, or an apparent diffusion coefficient of less than 620 on DW-MRI.

The researchers included all 206 patients in the DAWN study (N Engl J Med. 2018;378:11-21), separating them into DW-MRI or CTP groups based on which imaging method was used to randomize them during the trial. There were no statistically significant differences in any of the baseline characteristics between the two imaging groups.

The 26 sites participating in DAWN had clear differences in their preferences for imaging techniques; 19 exclusively used CTP, 4 used only DW-MRI, and 3 sites used a combination of both imaging methods.

There were no statistically significant differences between the two groups in any of the measured clinical outcomes, including neurologic deterioration in hospital (22.8% with CTP vs. 15.7% with DW-MRII, P = .286), symptomatic intracranial hemorrhage (4.1% with CTP vs. 4.8% with DW-MRI, P = 1.000), or death related to stroke (19.5% with CTP vs. 13.3% with DW-MRI, P = .263). Outcomes at 90 days proved to be similar between CTP and DW-MRI for achieving functional independence (29.3% vs. 34.9%, respectively; P = .445) and utility-weighted modified Rankin Scale scores (4.2 vs. 4.9, respectively; P = .172).

Multivariate analyses showed that 90-day functional independence was predicted by thrombectomy treatment, age, blood glucose level, baseline National Institutes of Health Stroke Scale score, and core lab ASPECTS (Alberta Stroke Program Early CT Score), but not the method of imaging.

“The efficacy and safety of mechanical thrombectomy for patients meeting those clinical mismatch criteria at 6-24 hours were comparable whether the small core infarcts were measured by diffusion imaging or cerebral blood flow imaging. I believe that future clinical trials aiming to extend the eligibility outside of this prespecified population should include both imaging modalities to determine whether these results are generalizable,” Dr. Sila said.

The DAWN study was funded by Stryker Neurovascular. Dr. Sila has reported receiving honoraria from Medtronic.

SOURCE: Sila C et al. ISC 2018, abstract LB11.

Emicizumab looks like it’s headed toward approval in Europe for the prevention and reduction of bleeding episodes in patients with hemophilia A with factor VIII inhibitors.

The European Medicines Agency’s Committee for Medicinal Products for Human Use recommended granting marketing authorization to the drug in January 2018, according to a statement. The recommendation will now be considered by the European Commission.

Crystal/Wikimedia Commons/Creative Commons Attribution 2.0

Emicizumab, which is marketed in the United States as Hemlibra, was approved by the Food and Drug Administration for adult and pediatric patients with hemophilia A with Factor VIII inhibitors in November. It is the first monoclonal antibody to be recommended for use in patients with hemophilia A with inhibitors, says the statement.

[email protected]

Emicizumab looks like it’s headed toward approval in Europe for the prevention and reduction of bleeding episodes in patients with hemophilia A with factor VIII inhibitors.

The European Medicines Agency’s Committee for Medicinal Products for Human Use recommended granting marketing authorization to the drug in January 2018, according to a statement. The recommendation will now be considered by the European Commission.

Crystal/Wikimedia Commons/Creative Commons Attribution 2.0

Emicizumab, which is marketed in the United States as Hemlibra, was approved by the Food and Drug Administration for adult and pediatric patients with hemophilia A with Factor VIII inhibitors in November. It is the first monoclonal antibody to be recommended for use in patients with hemophilia A with inhibitors, says the statement.

[email protected]

Emicizumab looks like it’s headed toward approval in Europe for the prevention and reduction of bleeding episodes in patients with hemophilia A with factor VIII inhibitors.

The European Medicines Agency’s Committee for Medicinal Products for Human Use recommended granting marketing authorization to the drug in January 2018, according to a statement. The recommendation will now be considered by the European Commission.

Crystal/Wikimedia Commons/Creative Commons Attribution 2.0

Emicizumab, which is marketed in the United States as Hemlibra, was approved by the Food and Drug Administration for adult and pediatric patients with hemophilia A with Factor VIII inhibitors in November. It is the first monoclonal antibody to be recommended for use in patients with hemophilia A with inhibitors, says the statement.

[email protected]

Body mass index accounts for a 43.7% discordance in fibrosis findings between magnetic resonance elastography (MRE) and transient elastography (TE), according to a study from the University of California, San Diego.

“This study demonstrates that BMI is a significant factor of discordancy between MRE and TE for the stage of significant fibrosis (2-4 vs. 0-1),” wrote Cyrielle Caussy, MD, and her colleagues (Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037). “Furthermore, this study showed that the grade of obesity is also a significant predictor of discordancy between MRE and TE because the discordance rate between MRE and TE increases with the increase in BMI.”

Dr. Caussy of the University of California, San Diego, and her colleagues had noted that MRE and TE had discordant findings in obese patients. To ascertain under what conditions TE and MRE produce the same readings, Dr. Caussy and her associates conducted a cross-sectional study of two cohorts with nonalcoholic fatty liver disease (NAFLD) who underwent contemporaneous MRE, TE, and liver biopsy. TE utilized both M and XL probes during imaging. The training cohort involved 119 adult patients undergoing NAFLD testing from October 2011 through January 2017. The validation cohort, consisting of 75 adults with NAFLD undergoing liver imaging from March 2010 through May 2013, was formed to validate the findings of the training cohort.

The study revealed that BMI was a significant predictor of the difference between MRE and TE results and made it difficult to assess the stage of liver fibrosis (2-4 vs. 0-1). After adjustment for age and sex, BMI accounted for a 5-unit increase of 1.694 (95% confidence interval, 1.145-2.507; P = .008). This was not a static relationship, and as BMI increased, so did the discordance between MRE and TE (P = .0309). Interestingly, the discordance rate was significantly higher in participants with BMIs greater than 35 kg/m², compared with participants with BMIs below 35 (63.0% vs. 38.0%; P = .022), the investigators reported. In severely obese adults with liver disease caused mainly by NAFLD, the accuracy of MRE was higher than TE for diagnosing significant fibrosis and advanced fibrosis.

While the study revealed valuable information, it had both strengths and limitations. A strength of the study was the use of two cohorts, specifically the validation cohort. The use of the liver biopsy as a reference, which is the standard for assessing fibrosis, was also a strength of the study. A limitation was that the study was conducted at specialized, tertiary care centers using advanced imaging techniques that may not be available at other clinics. Additionally, the cohorts included a small number of patients with advanced fibrosis.

“The integration of the BMI in the screening strategy for the noninvasive detection of liver fibrosis in NAFLD should be considered, and this parameter would help to determine when MRE is not needed in future guidelines” wrote Dr. Caussy and her associates. “Further cost-effectiveness studies are necessary to evaluate the clinical utility of MRE, TE, and/or liver biopsy to develop optimal screening strategies for diagnosing NAFLD-associated fibrosis.”

Jun Chen, MD, Meng Yin, MD, and Richard L. Ehman, MD, all have intellectual property rights and financial interests in elastography technology. Dr. Ehman also serves as an noncompensated CEO of Resoundant. Claude B. Sirlin, MD, has served as a consultant to Bayer and GE Healthcare. All other authors did not disclose any conflicts.

[email protected]

SOURCE: Caussy C et al. Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037.

Body mass index accounts for a 43.7% discordance in fibrosis findings between magnetic resonance elastography (MRE) and transient elastography (TE), according to a study from the University of California, San Diego.

“This study demonstrates that BMI is a significant factor of discordancy between MRE and TE for the stage of significant fibrosis (2-4 vs. 0-1),” wrote Cyrielle Caussy, MD, and her colleagues (Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037). “Furthermore, this study showed that the grade of obesity is also a significant predictor of discordancy between MRE and TE because the discordance rate between MRE and TE increases with the increase in BMI.”

Dr. Caussy of the University of California, San Diego, and her colleagues had noted that MRE and TE had discordant findings in obese patients. To ascertain under what conditions TE and MRE produce the same readings, Dr. Caussy and her associates conducted a cross-sectional study of two cohorts with nonalcoholic fatty liver disease (NAFLD) who underwent contemporaneous MRE, TE, and liver biopsy. TE utilized both M and XL probes during imaging. The training cohort involved 119 adult patients undergoing NAFLD testing from October 2011 through January 2017. The validation cohort, consisting of 75 adults with NAFLD undergoing liver imaging from March 2010 through May 2013, was formed to validate the findings of the training cohort.

The study revealed that BMI was a significant predictor of the difference between MRE and TE results and made it difficult to assess the stage of liver fibrosis (2-4 vs. 0-1). After adjustment for age and sex, BMI accounted for a 5-unit increase of 1.694 (95% confidence interval, 1.145-2.507; P = .008). This was not a static relationship, and as BMI increased, so did the discordance between MRE and TE (P = .0309). Interestingly, the discordance rate was significantly higher in participants with BMIs greater than 35 kg/m², compared with participants with BMIs below 35 (63.0% vs. 38.0%; P = .022), the investigators reported. In severely obese adults with liver disease caused mainly by NAFLD, the accuracy of MRE was higher than TE for diagnosing significant fibrosis and advanced fibrosis.

While the study revealed valuable information, it had both strengths and limitations. A strength of the study was the use of two cohorts, specifically the validation cohort. The use of the liver biopsy as a reference, which is the standard for assessing fibrosis, was also a strength of the study. A limitation was that the study was conducted at specialized, tertiary care centers using advanced imaging techniques that may not be available at other clinics. Additionally, the cohorts included a small number of patients with advanced fibrosis.

“The integration of the BMI in the screening strategy for the noninvasive detection of liver fibrosis in NAFLD should be considered, and this parameter would help to determine when MRE is not needed in future guidelines” wrote Dr. Caussy and her associates. “Further cost-effectiveness studies are necessary to evaluate the clinical utility of MRE, TE, and/or liver biopsy to develop optimal screening strategies for diagnosing NAFLD-associated fibrosis.”

Jun Chen, MD, Meng Yin, MD, and Richard L. Ehman, MD, all have intellectual property rights and financial interests in elastography technology. Dr. Ehman also serves as an noncompensated CEO of Resoundant. Claude B. Sirlin, MD, has served as a consultant to Bayer and GE Healthcare. All other authors did not disclose any conflicts.

[email protected]

SOURCE: Caussy C et al. Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037.

Body mass index accounts for a 43.7% discordance in fibrosis findings between magnetic resonance elastography (MRE) and transient elastography (TE), according to a study from the University of California, San Diego.

“This study demonstrates that BMI is a significant factor of discordancy between MRE and TE for the stage of significant fibrosis (2-4 vs. 0-1),” wrote Cyrielle Caussy, MD, and her colleagues (Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037). “Furthermore, this study showed that the grade of obesity is also a significant predictor of discordancy between MRE and TE because the discordance rate between MRE and TE increases with the increase in BMI.”

Dr. Caussy of the University of California, San Diego, and her colleagues had noted that MRE and TE had discordant findings in obese patients. To ascertain under what conditions TE and MRE produce the same readings, Dr. Caussy and her associates conducted a cross-sectional study of two cohorts with nonalcoholic fatty liver disease (NAFLD) who underwent contemporaneous MRE, TE, and liver biopsy. TE utilized both M and XL probes during imaging. The training cohort involved 119 adult patients undergoing NAFLD testing from October 2011 through January 2017. The validation cohort, consisting of 75 adults with NAFLD undergoing liver imaging from March 2010 through May 2013, was formed to validate the findings of the training cohort.

The study revealed that BMI was a significant predictor of the difference between MRE and TE results and made it difficult to assess the stage of liver fibrosis (2-4 vs. 0-1). After adjustment for age and sex, BMI accounted for a 5-unit increase of 1.694 (95% confidence interval, 1.145-2.507; P = .008). This was not a static relationship, and as BMI increased, so did the discordance between MRE and TE (P = .0309). Interestingly, the discordance rate was significantly higher in participants with BMIs greater than 35 kg/m², compared with participants with BMIs below 35 (63.0% vs. 38.0%; P = .022), the investigators reported. In severely obese adults with liver disease caused mainly by NAFLD, the accuracy of MRE was higher than TE for diagnosing significant fibrosis and advanced fibrosis.

While the study revealed valuable information, it had both strengths and limitations. A strength of the study was the use of two cohorts, specifically the validation cohort. The use of the liver biopsy as a reference, which is the standard for assessing fibrosis, was also a strength of the study. A limitation was that the study was conducted at specialized, tertiary care centers using advanced imaging techniques that may not be available at other clinics. Additionally, the cohorts included a small number of patients with advanced fibrosis.

“The integration of the BMI in the screening strategy for the noninvasive detection of liver fibrosis in NAFLD should be considered, and this parameter would help to determine when MRE is not needed in future guidelines” wrote Dr. Caussy and her associates. “Further cost-effectiveness studies are necessary to evaluate the clinical utility of MRE, TE, and/or liver biopsy to develop optimal screening strategies for diagnosing NAFLD-associated fibrosis.”

Jun Chen, MD, Meng Yin, MD, and Richard L. Ehman, MD, all have intellectual property rights and financial interests in elastography technology. Dr. Ehman also serves as an noncompensated CEO of Resoundant. Claude B. Sirlin, MD, has served as a consultant to Bayer and GE Healthcare. All other authors did not disclose any conflicts.

[email protected]

SOURCE: Caussy C et al. Clin Gastrolenterol Hepatol. 2018 Jan 15. doi: 10.1016/j.cgh.2017.10.037.

Neurologists should recommend twice-weekly exercise to patients diagnosed with mild cognitive impairment (MCI) as part of an overall approach to management, according to a practice guideline update from the American Academy of Neurology (AAN). The Level B recommendation is based on six-month studies that suggest that such exercise possibly improves cognition. The update was published online ahead of print December 27, 2017, in Neurology.

“Regular physical exercise has long been shown to have heart health benefits, and now we can say exercise also may help improve memory for people with MCI,” said Ronald Petersen, MD, PhD, Director of the Alzheimer’s Disease Research Center at the Mayo Clinic in Rochester, Minnesota, and lead author of the update. “What is good for your heart can be good for your brain.”

Document Updates 2001 Practice Parameter

The current practice guideline update revises the AAN’s 2001 practice parameter that provided recommendations for the diagnosis and treatment of MCI. Dr. Petersen and colleagues based the update on a systematic review of articles about MCI prevalence, prognosis, and treatment. They classified evidence according to AAN criteria and based recommendations on modified Delphi consensus.

The authors found that the prevalence of MCI is 6.7% for people between ages 60 and 64, 8.4% for people between ages 65 and 69, 10.1% for people between ages 70 and 74, 14.8% for people between ages 75 and 79, and 25.2% for people between ages 80 and 84. Approximately 15% of people with MCI who are older than 65 develop dementia during two years of follow-up.

No Evidence for Pharmacologic Treatment

Evidence does not support a symptomatic cognitive benefit in MCI for any pharmacologic or dietary agents, according to the authors. The FDA has not approved any medication for treating MCI. If clinicians offer cholinesterase inhibitors to their patients with MCI, they must first discuss the fact that the treatment is off label and not backed by empirical evidence, according to the update. Gastrointestinal symptoms and cardiac concerns are common side effects of cholinesterase inhibitors.

Assessment for MCI is appropriate for patients who complain of impaired memory or cognition, as well as those who present for a Medicare Annual Wellness Visit, according to the update. Clinicians should evaluate patients with MCI for risk factors that are potentially modifiable. Patients with MCI also should undergo serial assessments over time so that clinicians can monitor them for changes in cognitive status.

—Erik Greb

Suggested Reading

Langa KM, Levine DA. The diagnosis and management of mild cognitive impairment: a clinical review. JAMA. 2014;312(23):2551-2561.

Petersen RC, Lopez O, Armstrong MJ, et al. Practice guideline update summary: Mild cognitive impairment: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2017 Dec 27 [Epub ahead of print].

Vega JN, Newhouse PA. Mild cognitive impairment: diagnosis, longitudinal course, and emerging treatments. Curr Psychiatry Rep. 2014;16(10):490.

Neurologists should recommend twice-weekly exercise to patients diagnosed with mild cognitive impairment (MCI) as part of an overall approach to management, according to a practice guideline update from the American Academy of Neurology (AAN). The Level B recommendation is based on six-month studies that suggest that such exercise possibly improves cognition. The update was published online ahead of print December 27, 2017, in Neurology.

“Regular physical exercise has long been shown to have heart health benefits, and now we can say exercise also may help improve memory for people with MCI,” said Ronald Petersen, MD, PhD, Director of the Alzheimer’s Disease Research Center at the Mayo Clinic in Rochester, Minnesota, and lead author of the update. “What is good for your heart can be good for your brain.”

Document Updates 2001 Practice Parameter

The current practice guideline update revises the AAN’s 2001 practice parameter that provided recommendations for the diagnosis and treatment of MCI. Dr. Petersen and colleagues based the update on a systematic review of articles about MCI prevalence, prognosis, and treatment. They classified evidence according to AAN criteria and based recommendations on modified Delphi consensus.

The authors found that the prevalence of MCI is 6.7% for people between ages 60 and 64, 8.4% for people between ages 65 and 69, 10.1% for people between ages 70 and 74, 14.8% for people between ages 75 and 79, and 25.2% for people between ages 80 and 84. Approximately 15% of people with MCI who are older than 65 develop dementia during two years of follow-up.

No Evidence for Pharmacologic Treatment

Evidence does not support a symptomatic cognitive benefit in MCI for any pharmacologic or dietary agents, according to the authors. The FDA has not approved any medication for treating MCI. If clinicians offer cholinesterase inhibitors to their patients with MCI, they must first discuss the fact that the treatment is off label and not backed by empirical evidence, according to the update. Gastrointestinal symptoms and cardiac concerns are common side effects of cholinesterase inhibitors.

Assessment for MCI is appropriate for patients who complain of impaired memory or cognition, as well as those who present for a Medicare Annual Wellness Visit, according to the update. Clinicians should evaluate patients with MCI for risk factors that are potentially modifiable. Patients with MCI also should undergo serial assessments over time so that clinicians can monitor them for changes in cognitive status.

—Erik Greb

Suggested Reading

Langa KM, Levine DA. The diagnosis and management of mild cognitive impairment: a clinical review. JAMA. 2014;312(23):2551-2561.

Petersen RC, Lopez O, Armstrong MJ, et al. Practice guideline update summary: Mild cognitive impairment: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2017 Dec 27 [Epub ahead of print].

Vega JN, Newhouse PA. Mild cognitive impairment: diagnosis, longitudinal course, and emerging treatments. Curr Psychiatry Rep. 2014;16(10):490.

Neurologists should recommend twice-weekly exercise to patients diagnosed with mild cognitive impairment (MCI) as part of an overall approach to management, according to a practice guideline update from the American Academy of Neurology (AAN). The Level B recommendation is based on six-month studies that suggest that such exercise possibly improves cognition. The update was published online ahead of print December 27, 2017, in Neurology.

“Regular physical exercise has long been shown to have heart health benefits, and now we can say exercise also may help improve memory for people with MCI,” said Ronald Petersen, MD, PhD, Director of the Alzheimer’s Disease Research Center at the Mayo Clinic in Rochester, Minnesota, and lead author of the update. “What is good for your heart can be good for your brain.”

Document Updates 2001 Practice Parameter

The current practice guideline update revises the AAN’s 2001 practice parameter that provided recommendations for the diagnosis and treatment of MCI. Dr. Petersen and colleagues based the update on a systematic review of articles about MCI prevalence, prognosis, and treatment. They classified evidence according to AAN criteria and based recommendations on modified Delphi consensus.

The authors found that the prevalence of MCI is 6.7% for people between ages 60 and 64, 8.4% for people between ages 65 and 69, 10.1% for people between ages 70 and 74, 14.8% for people between ages 75 and 79, and 25.2% for people between ages 80 and 84. Approximately 15% of people with MCI who are older than 65 develop dementia during two years of follow-up.

No Evidence for Pharmacologic Treatment

Evidence does not support a symptomatic cognitive benefit in MCI for any pharmacologic or dietary agents, according to the authors. The FDA has not approved any medication for treating MCI. If clinicians offer cholinesterase inhibitors to their patients with MCI, they must first discuss the fact that the treatment is off label and not backed by empirical evidence, according to the update. Gastrointestinal symptoms and cardiac concerns are common side effects of cholinesterase inhibitors.

Assessment for MCI is appropriate for patients who complain of impaired memory or cognition, as well as those who present for a Medicare Annual Wellness Visit, according to the update. Clinicians should evaluate patients with MCI for risk factors that are potentially modifiable. Patients with MCI also should undergo serial assessments over time so that clinicians can monitor them for changes in cognitive status.

—Erik Greb

Suggested Reading

Langa KM, Levine DA. The diagnosis and management of mild cognitive impairment: a clinical review. JAMA. 2014;312(23):2551-2561.

Petersen RC, Lopez O, Armstrong MJ, et al. Practice guideline update summary: Mild cognitive impairment: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2017 Dec 27 [Epub ahead of print].

Vega JN, Newhouse PA. Mild cognitive impairment: diagnosis, longitudinal course, and emerging treatments. Curr Psychiatry Rep. 2014;16(10):490.

SNOWMASS, COLO. – By 2020, 75% of all isolated aortic valve replacements will be done as endovascular procedures, Michael J. Mack, MD, predicted at the Annual Cardiovascular Conference at Snowmass.

That’s assuming, hypothetically, that two ongoing randomized trials – PARTNER 3 and EVOLUT R – comparing TAVR (transcatheter aortic valve replacement) and SAVR (surgical aortic valve replacement) in low-surgical-risk patients have positive results. If so, TAVR will be proven noninferior to SAVR, as has already been convincingly shown in randomized trials conducted in high- and intermediate-surgical-risk patients.

Bruce Jancin/Frontline Medical News

• Younger patients. Many younger, low-surgical-risk patients will be concerned about TAVR valves’ durability and the current higher pacemaker rate.

“We have some idea of what durability is in the surgical population. What we usually quote is 12-15 years. There has been no major signal of early valve deterioration in TAVR, but there aren’t yet a significant number of patients alive for more than 5 years. Be that as it may, no significant concerns yet, but the other shoe hasn’t dropped,” the cardiothoracic surgeon observed.

Both PARTNER 3 and the EVOLUT R low-risk trial will follow participants annually for 10 years, eventually providing a robust, combined 2,000-patient database to assess comparative device durability.

The 30-day rates of permanent pacemaker implantation in TAVR recipients without a preexisting pacemaker is in the 12%-16% range with the newer-generation Evolut R and Sapien 3 valves. The indication is often new-onset left bundle branch block or complete heart block.

“I don’t think the increased pacemaker incidence is a huge problem now, but with the younger population I think it’s going to be more of an issue,” according to Dr. Mack. “It’s one thing to need a pacemaker if you’re 80-85 years old, but it’s totally different in somebody who’s 55 or 65 that has 30-35 years to live. Pacemaker leads are not benign in that population.”

“On the other hand, there is a thought that younger patients have less intrinsic conduction system disease. It may be that they are less prone to needing a new pacemaker afterward,” he added.

TAVR valve leaflet thrombosis is a concern. While a change in transvalvular gradient on echocardiography provides a signal for this complication, the actual diagnosis of valve thrombosis requires four-dimensional CT. Much better data on the true incidence and clinical ramifications of valve thrombosis in both TAVR and SAVR are coming. For example, the PARTNER 3 and EVOLUT R LR trials will each include 400-patient substudies with four-dimensional CT aimed at answering questions about valve thrombosis. The GALILEO trial, involving 1,520 TAVR patients, is designed to determine whether low-dose rivaroxaban prevents valve thrombosis and periprocedural embolization. Results of this randomized trial are due in about a year. Similarly, the 1,509-patient randomized ATLANTIS trial is looking at the effects of apixaban versus warfarin versus dual or single antiplatelet therapy.

If long-term anticoagulation in TAVR patients is found to be beneficial, that may steer some patients toward SAVR, especially if they are physically active or at high bleeding risk.

• Aortic stenosis patients with a high Syntax score and multivessel coronary artery disease. This group is best served by concomitant SAVR and coronary artery bypass grafting surgery.
• Patients with low or intermediate surgical risk with multivalve disease. “We know that patients with moderate to severe mitral regurgitation and/or moderate to severe tricuspid regurgitation do not do well after TAVR,” the surgeon said.
• Rheumatic valve disease patients.
• Patients who present at a site that offers SAVR only. “There are about 1,150 cardiac surgery programs in the United States and about 560 TAVR programs. There is concern that patients who don’t come in to a center that offers TAVR will not be offered TAVR as an option. I think there’s probably some truth to that,” Dr. Mack said.
• Patients going to sites without a well-functioning collaborative heart team. “In institutions where surgeons and cardiologists don’t get along, turf is much more of an issue, and surgeons are going to hold on to those patients more closely,” he observed.
• Patient’s with certain preferences. “All other things being equal, the patient is always going to choose the less invasive option. However, we do see some patients – I think it’s about 1 out of 10 – who express a preference to stay with the tried and true surgery,” according to Dr. Mack.

He reported receiving research grants from Abbott Vascular, Edwards Lifesciences, and Medtronic.

[email protected]

SNOWMASS, COLO. – By 2020, 75% of all isolated aortic valve replacements will be done as endovascular procedures, Michael J. Mack, MD, predicted at the Annual Cardiovascular Conference at Snowmass.

That’s assuming, hypothetically, that two ongoing randomized trials – PARTNER 3 and EVOLUT R – comparing TAVR (transcatheter aortic valve replacement) and SAVR (surgical aortic valve replacement) in low-surgical-risk patients have positive results. If so, TAVR will be proven noninferior to SAVR, as has already been convincingly shown in randomized trials conducted in high- and intermediate-surgical-risk patients.

Bruce Jancin/Frontline Medical News

• Younger patients. Many younger, low-surgical-risk patients will be concerned about TAVR valves’ durability and the current higher pacemaker rate.

“We have some idea of what durability is in the surgical population. What we usually quote is 12-15 years. There has been no major signal of early valve deterioration in TAVR, but there aren’t yet a significant number of patients alive for more than 5 years. Be that as it may, no significant concerns yet, but the other shoe hasn’t dropped,” the cardiothoracic surgeon observed.

Both PARTNER 3 and the EVOLUT R low-risk trial will follow participants annually for 10 years, eventually providing a robust, combined 2,000-patient database to assess comparative device durability.

The 30-day rates of permanent pacemaker implantation in TAVR recipients without a preexisting pacemaker is in the 12%-16% range with the newer-generation Evolut R and Sapien 3 valves. The indication is often new-onset left bundle branch block or complete heart block.

“I don’t think the increased pacemaker incidence is a huge problem now, but with the younger population I think it’s going to be more of an issue,” according to Dr. Mack. “It’s one thing to need a pacemaker if you’re 80-85 years old, but it’s totally different in somebody who’s 55 or 65 that has 30-35 years to live. Pacemaker leads are not benign in that population.”

“On the other hand, there is a thought that younger patients have less intrinsic conduction system disease. It may be that they are less prone to needing a new pacemaker afterward,” he added.

TAVR valve leaflet thrombosis is a concern. While a change in transvalvular gradient on echocardiography provides a signal for this complication, the actual diagnosis of valve thrombosis requires four-dimensional CT. Much better data on the true incidence and clinical ramifications of valve thrombosis in both TAVR and SAVR are coming. For example, the PARTNER 3 and EVOLUT R LR trials will each include 400-patient substudies with four-dimensional CT aimed at answering questions about valve thrombosis. The GALILEO trial, involving 1,520 TAVR patients, is designed to determine whether low-dose rivaroxaban prevents valve thrombosis and periprocedural embolization. Results of this randomized trial are due in about a year. Similarly, the 1,509-patient randomized ATLANTIS trial is looking at the effects of apixaban versus warfarin versus dual or single antiplatelet therapy.

If long-term anticoagulation in TAVR patients is found to be beneficial, that may steer some patients toward SAVR, especially if they are physically active or at high bleeding risk.

• Aortic stenosis patients with a high Syntax score and multivessel coronary artery disease. This group is best served by concomitant SAVR and coronary artery bypass grafting surgery.
• Patients with low or intermediate surgical risk with multivalve disease. “We know that patients with moderate to severe mitral regurgitation and/or moderate to severe tricuspid regurgitation do not do well after TAVR,” the surgeon said.
• Rheumatic valve disease patients.
• Patients who present at a site that offers SAVR only. “There are about 1,150 cardiac surgery programs in the United States and about 560 TAVR programs. There is concern that patients who don’t come in to a center that offers TAVR will not be offered TAVR as an option. I think there’s probably some truth to that,” Dr. Mack said.
• Patients going to sites without a well-functioning collaborative heart team. “In institutions where surgeons and cardiologists don’t get along, turf is much more of an issue, and surgeons are going to hold on to those patients more closely,” he observed.
• Patient’s with certain preferences. “All other things being equal, the patient is always going to choose the less invasive option. However, we do see some patients – I think it’s about 1 out of 10 – who express a preference to stay with the tried and true surgery,” according to Dr. Mack.

He reported receiving research grants from Abbott Vascular, Edwards Lifesciences, and Medtronic.

[email protected]

SNOWMASS, COLO. – By 2020, 75% of all isolated aortic valve replacements will be done as endovascular procedures, Michael J. Mack, MD, predicted at the Annual Cardiovascular Conference at Snowmass.

That’s assuming, hypothetically, that two ongoing randomized trials – PARTNER 3 and EVOLUT R – comparing TAVR (transcatheter aortic valve replacement) and SAVR (surgical aortic valve replacement) in low-surgical-risk patients have positive results. If so, TAVR will be proven noninferior to SAVR, as has already been convincingly shown in randomized trials conducted in high- and intermediate-surgical-risk patients.

Bruce Jancin/Frontline Medical News

• Younger patients. Many younger, low-surgical-risk patients will be concerned about TAVR valves’ durability and the current higher pacemaker rate.

“We have some idea of what durability is in the surgical population. What we usually quote is 12-15 years. There has been no major signal of early valve deterioration in TAVR, but there aren’t yet a significant number of patients alive for more than 5 years. Be that as it may, no significant concerns yet, but the other shoe hasn’t dropped,” the cardiothoracic surgeon observed.

Both PARTNER 3 and the EVOLUT R low-risk trial will follow participants annually for 10 years, eventually providing a robust, combined 2,000-patient database to assess comparative device durability.

The 30-day rates of permanent pacemaker implantation in TAVR recipients without a preexisting pacemaker is in the 12%-16% range with the newer-generation Evolut R and Sapien 3 valves. The indication is often new-onset left bundle branch block or complete heart block.

“I don’t think the increased pacemaker incidence is a huge problem now, but with the younger population I think it’s going to be more of an issue,” according to Dr. Mack. “It’s one thing to need a pacemaker if you’re 80-85 years old, but it’s totally different in somebody who’s 55 or 65 that has 30-35 years to live. Pacemaker leads are not benign in that population.”

“On the other hand, there is a thought that younger patients have less intrinsic conduction system disease. It may be that they are less prone to needing a new pacemaker afterward,” he added.

TAVR valve leaflet thrombosis is a concern. While a change in transvalvular gradient on echocardiography provides a signal for this complication, the actual diagnosis of valve thrombosis requires four-dimensional CT. Much better data on the true incidence and clinical ramifications of valve thrombosis in both TAVR and SAVR are coming. For example, the PARTNER 3 and EVOLUT R LR trials will each include 400-patient substudies with four-dimensional CT aimed at answering questions about valve thrombosis. The GALILEO trial, involving 1,520 TAVR patients, is designed to determine whether low-dose rivaroxaban prevents valve thrombosis and periprocedural embolization. Results of this randomized trial are due in about a year. Similarly, the 1,509-patient randomized ATLANTIS trial is looking at the effects of apixaban versus warfarin versus dual or single antiplatelet therapy.

If long-term anticoagulation in TAVR patients is found to be beneficial, that may steer some patients toward SAVR, especially if they are physically active or at high bleeding risk.

• Aortic stenosis patients with a high Syntax score and multivessel coronary artery disease. This group is best served by concomitant SAVR and coronary artery bypass grafting surgery.
• Patients with low or intermediate surgical risk with multivalve disease. “We know that patients with moderate to severe mitral regurgitation and/or moderate to severe tricuspid regurgitation do not do well after TAVR,” the surgeon said.
• Rheumatic valve disease patients.
• Patients who present at a site that offers SAVR only. “There are about 1,150 cardiac surgery programs in the United States and about 560 TAVR programs. There is concern that patients who don’t come in to a center that offers TAVR will not be offered TAVR as an option. I think there’s probably some truth to that,” Dr. Mack said.
• Patients going to sites without a well-functioning collaborative heart team. “In institutions where surgeons and cardiologists don’t get along, turf is much more of an issue, and surgeons are going to hold on to those patients more closely,” he observed.
• Patient’s with certain preferences. “All other things being equal, the patient is always going to choose the less invasive option. However, we do see some patients – I think it’s about 1 out of 10 – who express a preference to stay with the tried and true surgery,” according to Dr. Mack.

He reported receiving research grants from Abbott Vascular, Edwards Lifesciences, and Medtronic.

[email protected]

Low serum caffeine and caffeine metabolite levels after an overnight fast may be a sensitive way to detect Parkinson’s disease, according to the results of a case–control study published online ahead of print January 3 in Neurology.

In the study, levels of caffeine and its metabolites were lower in patients with Parkinson’s disease and motor dysfunction, compared with those without motor dysfunction. The investigators detected no differences in serum levels of caffeine metabolites between patients with mild Parkinson’s disease and those with severe Parkinson’s disease, said Motoki Fujimaki, MD, of Juntendo University School of Medicine in Tokyo, and colleagues.

A Single-Center Study

Previous research had shown that people drinking four or more cups of coffee per day had a greater than fivefold reduction in the risk of developing Parkinson’s disease. Mouse models of Parkinson’s disease showed that caffeine and two of its metabolites have a neuroprotective effect. Those results suggested that serum caffeine might be useful as a blood marker for Parkinson’s disease.

To test that idea, Dr. Fujimaki and associates recruited 31 healthy controls (18 women) and 108 patients with Parkinson’s disease but no dementia (50 women). The control group’s mean caffeine intake of 115.81 mg/day was similar to that of patients with Parkinson’s disease (107.50 mg/day).

Serum caffeine levels measured after an overnight fast showed that a cutoff of 33.04 pmol/10 µL identified Parkinson’s disease with an area under the curve (AUC) of 0.78 (sensitivity, 76.9%; specificity, 74.2%). Inclusion of the primary caffeine metabolites theophylline, theobromine, and paraxanthine increased the AUC to 0.87. When the researchers included all 11 measurable metabolites, the AUC increased further to 0.98.

Genetic analyses revealed no significant differences in the frequencies of caffeine metabolism–associated genetic variants between patients and controls.

The study was limited by the fact that it was conducted at a single university hospital, and the patient population did not include many severe cases. The association should also be studied in other Parkinson’s disease patient populations, according to the authors.

Did Treatment Effects Influence the Findings?

A key question that the study raises is what caused the decrease in serum concentration found in patients with Parkinson’s disease, said David G. Munoz, MD, of the Department of Laboratory Medicine and Pathobiology at the University of Toronto, and Shinsuke Fujioka, MD, of the Department of Neurology at Fukuoka University in Japan, in an accompanying editorial. Almost all of the patients were receiving treatment, which could have affected serum levels, they added. The researchers looked for, but did not find, an association between serum caffeine metabolite levels and levodopa equivalent doses.

“The validity of the study depends on whether caffeine metabolism may be affected by treatment,” said Drs. Munoz and Fujioka. “To demonstrate the utility of caffeine metabolites unequivocally, a future study will have to reproduce these results in patients with untreated Parkinson’s disease or subjects at high risk of Parkinson’s disease, such as those with prodromal signs of Parkinson’s disease.”

—Jim Kling

Suggested Reading

Fujimaki M, Saiki S, Li Y, et al. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology. 2018 Jan 3 [Epub ahead of print].

Munoz DG, Fujioka S. Caffeine and Parkinson disease: A possible diagnostic and pathogenic breakthrough. Neurology. 2018 Jan 3 [Epub ahead of print].

Low serum caffeine and caffeine metabolite levels after an overnight fast may be a sensitive way to detect Parkinson’s disease, according to the results of a case–control study published online ahead of print January 3 in Neurology.

In the study, levels of caffeine and its metabolites were lower in patients with Parkinson’s disease and motor dysfunction, compared with those without motor dysfunction. The investigators detected no differences in serum levels of caffeine metabolites between patients with mild Parkinson’s disease and those with severe Parkinson’s disease, said Motoki Fujimaki, MD, of Juntendo University School of Medicine in Tokyo, and colleagues.

A Single-Center Study

Previous research had shown that people drinking four or more cups of coffee per day had a greater than fivefold reduction in the risk of developing Parkinson’s disease. Mouse models of Parkinson’s disease showed that caffeine and two of its metabolites have a neuroprotective effect. Those results suggested that serum caffeine might be useful as a blood marker for Parkinson’s disease.

To test that idea, Dr. Fujimaki and associates recruited 31 healthy controls (18 women) and 108 patients with Parkinson’s disease but no dementia (50 women). The control group’s mean caffeine intake of 115.81 mg/day was similar to that of patients with Parkinson’s disease (107.50 mg/day).

Serum caffeine levels measured after an overnight fast showed that a cutoff of 33.04 pmol/10 µL identified Parkinson’s disease with an area under the curve (AUC) of 0.78 (sensitivity, 76.9%; specificity, 74.2%). Inclusion of the primary caffeine metabolites theophylline, theobromine, and paraxanthine increased the AUC to 0.87. When the researchers included all 11 measurable metabolites, the AUC increased further to 0.98.

Genetic analyses revealed no significant differences in the frequencies of caffeine metabolism–associated genetic variants between patients and controls.

The study was limited by the fact that it was conducted at a single university hospital, and the patient population did not include many severe cases. The association should also be studied in other Parkinson’s disease patient populations, according to the authors.

Did Treatment Effects Influence the Findings?

A key question that the study raises is what caused the decrease in serum concentration found in patients with Parkinson’s disease, said David G. Munoz, MD, of the Department of Laboratory Medicine and Pathobiology at the University of Toronto, and Shinsuke Fujioka, MD, of the Department of Neurology at Fukuoka University in Japan, in an accompanying editorial. Almost all of the patients were receiving treatment, which could have affected serum levels, they added. The researchers looked for, but did not find, an association between serum caffeine metabolite levels and levodopa equivalent doses.

“The validity of the study depends on whether caffeine metabolism may be affected by treatment,” said Drs. Munoz and Fujioka. “To demonstrate the utility of caffeine metabolites unequivocally, a future study will have to reproduce these results in patients with untreated Parkinson’s disease or subjects at high risk of Parkinson’s disease, such as those with prodromal signs of Parkinson’s disease.”

—Jim Kling

Suggested Reading

Fujimaki M, Saiki S, Li Y, et al. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology. 2018 Jan 3 [Epub ahead of print].

Munoz DG, Fujioka S. Caffeine and Parkinson disease: A possible diagnostic and pathogenic breakthrough. Neurology. 2018 Jan 3 [Epub ahead of print].

Low serum caffeine and caffeine metabolite levels after an overnight fast may be a sensitive way to detect Parkinson’s disease, according to the results of a case–control study published online ahead of print January 3 in Neurology.

In the study, levels of caffeine and its metabolites were lower in patients with Parkinson’s disease and motor dysfunction, compared with those without motor dysfunction. The investigators detected no differences in serum levels of caffeine metabolites between patients with mild Parkinson’s disease and those with severe Parkinson’s disease, said Motoki Fujimaki, MD, of Juntendo University School of Medicine in Tokyo, and colleagues.

A Single-Center Study

Previous research had shown that people drinking four or more cups of coffee per day had a greater than fivefold reduction in the risk of developing Parkinson’s disease. Mouse models of Parkinson’s disease showed that caffeine and two of its metabolites have a neuroprotective effect. Those results suggested that serum caffeine might be useful as a blood marker for Parkinson’s disease.

To test that idea, Dr. Fujimaki and associates recruited 31 healthy controls (18 women) and 108 patients with Parkinson’s disease but no dementia (50 women). The control group’s mean caffeine intake of 115.81 mg/day was similar to that of patients with Parkinson’s disease (107.50 mg/day).

Serum caffeine levels measured after an overnight fast showed that a cutoff of 33.04 pmol/10 µL identified Parkinson’s disease with an area under the curve (AUC) of 0.78 (sensitivity, 76.9%; specificity, 74.2%). Inclusion of the primary caffeine metabolites theophylline, theobromine, and paraxanthine increased the AUC to 0.87. When the researchers included all 11 measurable metabolites, the AUC increased further to 0.98.

Genetic analyses revealed no significant differences in the frequencies of caffeine metabolism–associated genetic variants between patients and controls.

The study was limited by the fact that it was conducted at a single university hospital, and the patient population did not include many severe cases. The association should also be studied in other Parkinson’s disease patient populations, according to the authors.

Did Treatment Effects Influence the Findings?

A key question that the study raises is what caused the decrease in serum concentration found in patients with Parkinson’s disease, said David G. Munoz, MD, of the Department of Laboratory Medicine and Pathobiology at the University of Toronto, and Shinsuke Fujioka, MD, of the Department of Neurology at Fukuoka University in Japan, in an accompanying editorial. Almost all of the patients were receiving treatment, which could have affected serum levels, they added. The researchers looked for, but did not find, an association between serum caffeine metabolite levels and levodopa equivalent doses.

“The validity of the study depends on whether caffeine metabolism may be affected by treatment,” said Drs. Munoz and Fujioka. “To demonstrate the utility of caffeine metabolites unequivocally, a future study will have to reproduce these results in patients with untreated Parkinson’s disease or subjects at high risk of Parkinson’s disease, such as those with prodromal signs of Parkinson’s disease.”

—Jim Kling

Suggested Reading

Fujimaki M, Saiki S, Li Y, et al. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology. 2018 Jan 3 [Epub ahead of print].

Munoz DG, Fujioka S. Caffeine and Parkinson disease: A possible diagnostic and pathogenic breakthrough. Neurology. 2018 Jan 3 [Epub ahead of print].

ANAHEIM, CALIF. – Adherence to the American Heart Association’s widely publicized “Life’s Simple 7” program addressing key modifiable cardiovascular health factors substantially reduces the risk of developing peripheral arterial disease, Parveen Garg, MD, said at the American Heart Association scientific sessions.

This is new evidence-supported information. Until this new analysis from the landmark ARIC (Atherosclerosis Risk in Communities) study, the relationship between Life’s Simple 7 and peripheral arterial disease (PAD) hadn’t been studied. It’s a relationship worthy of examination, considering that more than 8 million Americans have PAD, and nearly 40% of them don’t have concomitant coronary or cerebrovascular disease, which raised the question of whether Life’s Simple 7 applied to PAD risk, noted Dr. Garg of the University of Southern California, Los Angeles.

Bruce Jancin/Frontline Medical News

[email protected]

ANAHEIM, CALIF. – Adherence to the American Heart Association’s widely publicized “Life’s Simple 7” program addressing key modifiable cardiovascular health factors substantially reduces the risk of developing peripheral arterial disease, Parveen Garg, MD, said at the American Heart Association scientific sessions.

This is new evidence-supported information. Until this new analysis from the landmark ARIC (Atherosclerosis Risk in Communities) study, the relationship between Life’s Simple 7 and peripheral arterial disease (PAD) hadn’t been studied. It’s a relationship worthy of examination, considering that more than 8 million Americans have PAD, and nearly 40% of them don’t have concomitant coronary or cerebrovascular disease, which raised the question of whether Life’s Simple 7 applied to PAD risk, noted Dr. Garg of the University of Southern California, Los Angeles.

Bruce Jancin/Frontline Medical News

[email protected]

ANAHEIM, CALIF. – Adherence to the American Heart Association’s widely publicized “Life’s Simple 7” program addressing key modifiable cardiovascular health factors substantially reduces the risk of developing peripheral arterial disease, Parveen Garg, MD, said at the American Heart Association scientific sessions.

This is new evidence-supported information. Until this new analysis from the landmark ARIC (Atherosclerosis Risk in Communities) study, the relationship between Life’s Simple 7 and peripheral arterial disease (PAD) hadn’t been studied. It’s a relationship worthy of examination, considering that more than 8 million Americans have PAD, and nearly 40% of them don’t have concomitant coronary or cerebrovascular disease, which raised the question of whether Life’s Simple 7 applied to PAD risk, noted Dr. Garg of the University of Southern California, Los Angeles.

Bruce Jancin/Frontline Medical News

[email protected]

BOSTON—Walking appears to moderate cognitive decline in people with elevated levels of amyloid in the brain, according to a four-year observational study described at the Clinical Trials on Alzheimer’s Disease conference.

Among a group of cognitively normal older adults with beta-amyloid brain plaques, those who walked the most had significantly less decline in memory and thinking than those who walked little, said Dylan Kirn, MPH. Walking did not affect any biomarkers of Alzheimer’s disease, such as brain glucose utilization, amyloid accumulation, or hippocampal volume, but it was associated with significantly better cognitive scores on a composite measure of memory over time.

The Harvard Aging Brain Study

The research is part of the ongoing Harvard Aging Brain Study, which is a longitudinal investigation of cognitively normal elderly individuals that seeks to identify the earliest changes in molecular, functional, and structural imaging markers that signal a transition from normal cognition to progressive cognitive decline and preclinical Alzheimer’s disease. The walking study included 255 subjects with a mean age of 73. Participants were highly educated, with a mean of 16 years’ schooling. About 24% of the population was amyloid-positive on PET imaging. All patients were cognitively normal, with a Clinical Dementia Rating scale score of 0. Activity was measured at baseline with a pedometer, which was worn for seven consecutive days; only people who walked at least 100 steps per day were included in the analysis.

In addition to amyloid PET imaging, subjects underwent an ¹⁸F-fluorodeoxyglucose (FDG) PET scan to assess brain glucose utilization, and MRI to measure hippocampal volume changes and white matter hyperintensities (WMHs). Changes in all of these biomarkers can herald the onset of Alzheimer’s disease.

The study’s primary outcome was the relationship between physical activity, as measured by number of walking steps per day, and changes on the Preclinical Alzheimer’s Cognitive Composite (PACC) test. This relatively new cognitive scale is gaining increasing use in clinical trials. The PACC is a composite of the Digit Symbol Substitution Test score from the Wechsler Adult Intelligence Scale–Revised, the Mini-Mental State Examination, the Total Recall score from the Free and Cued Selective Reminding Test, and the Delayed Recall score on the Logical Memory IIa subtest of the Wechsler Memory Scale. It correlates well with amyloid accumulation in the brain, said Mr. Kirn.

The cohort was followed for as long as six years (median follow-up, four years), and PACC scores were calculated annually. The investigators examined the relationship between walking at baseline and PACC decline during the study period in two multivariate models. One model controlled for age, sex, and years of education, and the second controlled for those variables plus cortical WMHs, bilateral hippocampal volume (HV), and FDG PET in brain regions typically affected by Alzheimer’s disease.

The investigators sorted physical activity into tertiles by the average number of steps per day over the seven-day measuring period. The middle tertile was the mean (ie, 5,616 steps/day), the top tertile was one standard deviation above the mean (ie, 8,482 steps/day), and the bottom tertile was one standard deviation below the mean (ie, 2,751 steps/day). Amyloid-positive patients were further categorized as having high or low brain amyloid load.

No Relationship Between Activity and Biomarkers

The researchers found no significant relationships between any of the biomarkers and any level of physical activity in either of the analyses, said Mr. Kirn. When looking at the time-linked changes in the PACC, however, they found significant differences. Subjects who walked at least the mean number of steps per day were much more likely to maintain a stable cognitive score, while those who walked the fewest steps declined by about a quarter of a point on the PACC. The difference in decline between the high-activity and low-activity subjects was statistically significant, even when the investigators controlled for amyloid burden and other Alzheimer’s disease biomarkers.

The level of physical activity at baseline was a particularly strong predictor of cognitive health among amyloid-positive subjects. Those in the high-activity group maintained a steady score on the PACC. Those in the mean activity group declined slightly, and those in the low activity group showed a sharp decline, losing almost a full point on the PACC by the end of follow-up.

In the amyloid-negative group, the researchers found no association between cognition and activity. PACC scores improved for all groups during the study period, which probably reflects a practice effect, said Mr. Kirn.

“We observed that physical activity was significantly predictive of cognitive decline in high-amyloid participants, but not in low-amyloid participants,” he said. “Individuals with high amyloid and low physical activity at baseline had the steepest decline in cognition over time. But in those with high amyloid and high physical activity at baseline, we did not see a tremendous amount of decline.”

The study suggests that pedometers may help stratify patients for clinical trials or assess cognitive risk in elderly subjects. “Most studies that have looked at physical activity and dementia use a self-reported activity level, so the results have been varied,” said Mr. Kirn. “These findings support consideration of objectively measured physical activity in clinical research, and perhaps in stratification for risk of cognitive decline.”

—Michele G. Sullivan

BOSTON—Walking appears to moderate cognitive decline in people with elevated levels of amyloid in the brain, according to a four-year observational study described at the Clinical Trials on Alzheimer’s Disease conference.

Among a group of cognitively normal older adults with beta-amyloid brain plaques, those who walked the most had significantly less decline in memory and thinking than those who walked little, said Dylan Kirn, MPH. Walking did not affect any biomarkers of Alzheimer’s disease, such as brain glucose utilization, amyloid accumulation, or hippocampal volume, but it was associated with significantly better cognitive scores on a composite measure of memory over time.

The Harvard Aging Brain Study

The research is part of the ongoing Harvard Aging Brain Study, which is a longitudinal investigation of cognitively normal elderly individuals that seeks to identify the earliest changes in molecular, functional, and structural imaging markers that signal a transition from normal cognition to progressive cognitive decline and preclinical Alzheimer’s disease. The walking study included 255 subjects with a mean age of 73. Participants were highly educated, with a mean of 16 years’ schooling. About 24% of the population was amyloid-positive on PET imaging. All patients were cognitively normal, with a Clinical Dementia Rating scale score of 0. Activity was measured at baseline with a pedometer, which was worn for seven consecutive days; only people who walked at least 100 steps per day were included in the analysis.

In addition to amyloid PET imaging, subjects underwent an ¹⁸F-fluorodeoxyglucose (FDG) PET scan to assess brain glucose utilization, and MRI to measure hippocampal volume changes and white matter hyperintensities (WMHs). Changes in all of these biomarkers can herald the onset of Alzheimer’s disease.

The study’s primary outcome was the relationship between physical activity, as measured by number of walking steps per day, and changes on the Preclinical Alzheimer’s Cognitive Composite (PACC) test. This relatively new cognitive scale is gaining increasing use in clinical trials. The PACC is a composite of the Digit Symbol Substitution Test score from the Wechsler Adult Intelligence Scale–Revised, the Mini-Mental State Examination, the Total Recall score from the Free and Cued Selective Reminding Test, and the Delayed Recall score on the Logical Memory IIa subtest of the Wechsler Memory Scale. It correlates well with amyloid accumulation in the brain, said Mr. Kirn.

The cohort was followed for as long as six years (median follow-up, four years), and PACC scores were calculated annually. The investigators examined the relationship between walking at baseline and PACC decline during the study period in two multivariate models. One model controlled for age, sex, and years of education, and the second controlled for those variables plus cortical WMHs, bilateral hippocampal volume (HV), and FDG PET in brain regions typically affected by Alzheimer’s disease.

The investigators sorted physical activity into tertiles by the average number of steps per day over the seven-day measuring period. The middle tertile was the mean (ie, 5,616 steps/day), the top tertile was one standard deviation above the mean (ie, 8,482 steps/day), and the bottom tertile was one standard deviation below the mean (ie, 2,751 steps/day). Amyloid-positive patients were further categorized as having high or low brain amyloid load.

No Relationship Between Activity and Biomarkers

The researchers found no significant relationships between any of the biomarkers and any level of physical activity in either of the analyses, said Mr. Kirn. When looking at the time-linked changes in the PACC, however, they found significant differences. Subjects who walked at least the mean number of steps per day were much more likely to maintain a stable cognitive score, while those who walked the fewest steps declined by about a quarter of a point on the PACC. The difference in decline between the high-activity and low-activity subjects was statistically significant, even when the investigators controlled for amyloid burden and other Alzheimer’s disease biomarkers.

The level of physical activity at baseline was a particularly strong predictor of cognitive health among amyloid-positive subjects. Those in the high-activity group maintained a steady score on the PACC. Those in the mean activity group declined slightly, and those in the low activity group showed a sharp decline, losing almost a full point on the PACC by the end of follow-up.

In the amyloid-negative group, the researchers found no association between cognition and activity. PACC scores improved for all groups during the study period, which probably reflects a practice effect, said Mr. Kirn.

“We observed that physical activity was significantly predictive of cognitive decline in high-amyloid participants, but not in low-amyloid participants,” he said. “Individuals with high amyloid and low physical activity at baseline had the steepest decline in cognition over time. But in those with high amyloid and high physical activity at baseline, we did not see a tremendous amount of decline.”

The study suggests that pedometers may help stratify patients for clinical trials or assess cognitive risk in elderly subjects. “Most studies that have looked at physical activity and dementia use a self-reported activity level, so the results have been varied,” said Mr. Kirn. “These findings support consideration of objectively measured physical activity in clinical research, and perhaps in stratification for risk of cognitive decline.”

—Michele G. Sullivan

BOSTON—Walking appears to moderate cognitive decline in people with elevated levels of amyloid in the brain, according to a four-year observational study described at the Clinical Trials on Alzheimer’s Disease conference.

Among a group of cognitively normal older adults with beta-amyloid brain plaques, those who walked the most had significantly less decline in memory and thinking than those who walked little, said Dylan Kirn, MPH. Walking did not affect any biomarkers of Alzheimer’s disease, such as brain glucose utilization, amyloid accumulation, or hippocampal volume, but it was associated with significantly better cognitive scores on a composite measure of memory over time.

The Harvard Aging Brain Study

The research is part of the ongoing Harvard Aging Brain Study, which is a longitudinal investigation of cognitively normal elderly individuals that seeks to identify the earliest changes in molecular, functional, and structural imaging markers that signal a transition from normal cognition to progressive cognitive decline and preclinical Alzheimer’s disease. The walking study included 255 subjects with a mean age of 73. Participants were highly educated, with a mean of 16 years’ schooling. About 24% of the population was amyloid-positive on PET imaging. All patients were cognitively normal, with a Clinical Dementia Rating scale score of 0. Activity was measured at baseline with a pedometer, which was worn for seven consecutive days; only people who walked at least 100 steps per day were included in the analysis.

In addition to amyloid PET imaging, subjects underwent an ¹⁸F-fluorodeoxyglucose (FDG) PET scan to assess brain glucose utilization, and MRI to measure hippocampal volume changes and white matter hyperintensities (WMHs). Changes in all of these biomarkers can herald the onset of Alzheimer’s disease.

The study’s primary outcome was the relationship between physical activity, as measured by number of walking steps per day, and changes on the Preclinical Alzheimer’s Cognitive Composite (PACC) test. This relatively new cognitive scale is gaining increasing use in clinical trials. The PACC is a composite of the Digit Symbol Substitution Test score from the Wechsler Adult Intelligence Scale–Revised, the Mini-Mental State Examination, the Total Recall score from the Free and Cued Selective Reminding Test, and the Delayed Recall score on the Logical Memory IIa subtest of the Wechsler Memory Scale. It correlates well with amyloid accumulation in the brain, said Mr. Kirn.

The cohort was followed for as long as six years (median follow-up, four years), and PACC scores were calculated annually. The investigators examined the relationship between walking at baseline and PACC decline during the study period in two multivariate models. One model controlled for age, sex, and years of education, and the second controlled for those variables plus cortical WMHs, bilateral hippocampal volume (HV), and FDG PET in brain regions typically affected by Alzheimer’s disease.

The investigators sorted physical activity into tertiles by the average number of steps per day over the seven-day measuring period. The middle tertile was the mean (ie, 5,616 steps/day), the top tertile was one standard deviation above the mean (ie, 8,482 steps/day), and the bottom tertile was one standard deviation below the mean (ie, 2,751 steps/day). Amyloid-positive patients were further categorized as having high or low brain amyloid load.

No Relationship Between Activity and Biomarkers

The researchers found no significant relationships between any of the biomarkers and any level of physical activity in either of the analyses, said Mr. Kirn. When looking at the time-linked changes in the PACC, however, they found significant differences. Subjects who walked at least the mean number of steps per day were much more likely to maintain a stable cognitive score, while those who walked the fewest steps declined by about a quarter of a point on the PACC. The difference in decline between the high-activity and low-activity subjects was statistically significant, even when the investigators controlled for amyloid burden and other Alzheimer’s disease biomarkers.

The level of physical activity at baseline was a particularly strong predictor of cognitive health among amyloid-positive subjects. Those in the high-activity group maintained a steady score on the PACC. Those in the mean activity group declined slightly, and those in the low activity group showed a sharp decline, losing almost a full point on the PACC by the end of follow-up.

In the amyloid-negative group, the researchers found no association between cognition and activity. PACC scores improved for all groups during the study period, which probably reflects a practice effect, said Mr. Kirn.

“We observed that physical activity was significantly predictive of cognitive decline in high-amyloid participants, but not in low-amyloid participants,” he said. “Individuals with high amyloid and low physical activity at baseline had the steepest decline in cognition over time. But in those with high amyloid and high physical activity at baseline, we did not see a tremendous amount of decline.”

The study suggests that pedometers may help stratify patients for clinical trials or assess cognitive risk in elderly subjects. “Most studies that have looked at physical activity and dementia use a self-reported activity level, so the results have been varied,” said Mr. Kirn. “These findings support consideration of objectively measured physical activity in clinical research, and perhaps in stratification for risk of cognitive decline.”

—Michele G. Sullivan

Adult inpatients with hepatitis C are much more likely to have mental health comorbidities, compared with those who do not have hepatitis C, according to the Agency for Healthcare Research and Quality.

All four comorbidities skewed younger, and the oldest patients (73 years and older) with hepatitis C presented with each condition at about the same rate as the non–hepatitis C population. The proportions of hepatitis C–related inpatient stays with alcohol abuse by age, for example, were 20.5% for 18-51 years, 23.3% for those aged 52-72, and 5.8% for the 73-and-older group, according to data from the National Inpatient Sample, which includes more than 95% of all discharges from community (short-term, nonfederal, nonrehabilitation) hospitals in the United States.

[email protected]

Adult inpatients with hepatitis C are much more likely to have mental health comorbidities, compared with those who do not have hepatitis C, according to the Agency for Healthcare Research and Quality.

All four comorbidities skewed younger, and the oldest patients (73 years and older) with hepatitis C presented with each condition at about the same rate as the non–hepatitis C population. The proportions of hepatitis C–related inpatient stays with alcohol abuse by age, for example, were 20.5% for 18-51 years, 23.3% for those aged 52-72, and 5.8% for the 73-and-older group, according to data from the National Inpatient Sample, which includes more than 95% of all discharges from community (short-term, nonfederal, nonrehabilitation) hospitals in the United States.

[email protected]

Adult inpatients with hepatitis C are much more likely to have mental health comorbidities, compared with those who do not have hepatitis C, according to the Agency for Healthcare Research and Quality.

All four comorbidities skewed younger, and the oldest patients (73 years and older) with hepatitis C presented with each condition at about the same rate as the non–hepatitis C population. The proportions of hepatitis C–related inpatient stays with alcohol abuse by age, for example, were 20.5% for 18-51 years, 23.3% for those aged 52-72, and 5.8% for the 73-and-older group, according to data from the National Inpatient Sample, which includes more than 95% of all discharges from community (short-term, nonfederal, nonrehabilitation) hospitals in the United States.

[email protected]