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VIDEO: Advances in noninvasive fat reduction include permanent effects
WAILEA, HAWAII – In the past few years, there have been “exciting” advances in noninvasive techniques to permanently remove fat, according to Suzanne Kilmer, MD, of the department of dermatology, University of California, Davis.
There are devices now available to reduce fat “in a permanent way that’s not injurious, it’s not uncomfortable – patients love it,” Dr. Kilmer said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
Currently, the three noninvasive modalities she considers most effective for reducing fat are cryolipolysis, the 1,060-nm laser, and focused pulsed ultrasound. In the interview, she discussed the ways these treatments work and their safety.
With all three, “the fat that goes away stays away,” said Dr. Kilmer, who is director of the Laser and Skin Surgery Center of Northern California, Sacramento. Treatment results in release of fat, which is “cleared like it is as if you ate a cheeseburger,” she added. Interestingly, she said, trials that have looked at whether the fat reduction is accompanied by weight loss have found that, in most cases, the patient’s weight remains stable.
Dr. Kilmer’s disclosures included serving as a consultant and/or researcher for Allergan, Cutera, Cynosure, Cytrellis, Kythera, Lumenis, Merz, Miramar, Sebacia, Sienna Labs, Solta, Zeltiq, and Zift.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WAILEA, HAWAII – In the past few years, there have been “exciting” advances in noninvasive techniques to permanently remove fat, according to Suzanne Kilmer, MD, of the department of dermatology, University of California, Davis.
There are devices now available to reduce fat “in a permanent way that’s not injurious, it’s not uncomfortable – patients love it,” Dr. Kilmer said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
Currently, the three noninvasive modalities she considers most effective for reducing fat are cryolipolysis, the 1,060-nm laser, and focused pulsed ultrasound. In the interview, she discussed the ways these treatments work and their safety.
With all three, “the fat that goes away stays away,” said Dr. Kilmer, who is director of the Laser and Skin Surgery Center of Northern California, Sacramento. Treatment results in release of fat, which is “cleared like it is as if you ate a cheeseburger,” she added. Interestingly, she said, trials that have looked at whether the fat reduction is accompanied by weight loss have found that, in most cases, the patient’s weight remains stable.
Dr. Kilmer’s disclosures included serving as a consultant and/or researcher for Allergan, Cutera, Cynosure, Cytrellis, Kythera, Lumenis, Merz, Miramar, Sebacia, Sienna Labs, Solta, Zeltiq, and Zift.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WAILEA, HAWAII – In the past few years, there have been “exciting” advances in noninvasive techniques to permanently remove fat, according to Suzanne Kilmer, MD, of the department of dermatology, University of California, Davis.
There are devices now available to reduce fat “in a permanent way that’s not injurious, it’s not uncomfortable – patients love it,” Dr. Kilmer said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
Currently, the three noninvasive modalities she considers most effective for reducing fat are cryolipolysis, the 1,060-nm laser, and focused pulsed ultrasound. In the interview, she discussed the ways these treatments work and their safety.
With all three, “the fat that goes away stays away,” said Dr. Kilmer, who is director of the Laser and Skin Surgery Center of Northern California, Sacramento. Treatment results in release of fat, which is “cleared like it is as if you ate a cheeseburger,” she added. Interestingly, she said, trials that have looked at whether the fat reduction is accompanied by weight loss have found that, in most cases, the patient’s weight remains stable.
Dr. Kilmer’s disclosures included serving as a consultant and/or researcher for Allergan, Cutera, Cynosure, Cytrellis, Kythera, Lumenis, Merz, Miramar, Sebacia, Sienna Labs, Solta, Zeltiq, and Zift.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Second-generation antipsychotics effective for stuttering
LAS VEGAS – There currently is no Food and Drug Administration–approved medication for the symptomatic treatment of stuttering, but current evidence suggests that second-generation antipsychotics risperidone, olanzapine, and asenapine are beneficial, according to Gerald A. Maguire, MD.
At an annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Maguire, who is a stutterer himself, said current clinical trials in adults with childhood onset fluency disorder support the dopamine hypothesis of stuttering, where abnormal elevated cerebral dopaminergic activity is implicated.
Older studies found haloperidol to be effective for the treatment of stuttering, but long-term patient outlook is poor because of side effects such as sedation and sexual dysfunction. In a study led by Dr. Maguire, risperidone at a dose of 0.5-2 mg daily for 6 weeks was shown to decrease the percentage of syllables stuttered, time stuttered as a percentage of total time speaking, and overall stuttering severity, compared with placebo (J Clin Psychopharmacol. 2000;20[4]:479-82). A more recent study he also led found that olanzapine at a dose of 2.5-5 mg daily for 90 days showed a significant reduction in symptoms as measured by multiple tools, including the Stuttering Severity Instrument–Third Edition, the Clinical Global Impression scale, and the subject-rated self-assessment of stuttering scale (Ann Clin Psychiatry. 2004;16[2]:63-7).
Dr. Maguire, also associate dean of graduate medical education at the University of California, Riverside medical school, added that findings from several case reports suggest that asenapine and aripiprazole also are effective for managing stuttering symptoms. “Further studies of these drugs are warranted given better side-effect profiles as compared to other second-generation antipsychotics,” he said. There are ongoing investigations of other medications for the treatment of stuttering, including ecopipam, a D-1 dopamine receptor antagonist. An open-label study of ecopipam in adults who stutter is currently under way.
Dr. Maguire disclosed that he has received grant or research support from Intracellular, the Stanley Foundation, and Sunovion. He also is a consultant for Lundbeck, Otsuka, Sunovion, Takeda, and is a member of the speakers’ bureau or has received honoraria from Acadia, Lundbeck, Otsuka, Sunovion, Takeda, and Vanda.
LAS VEGAS – There currently is no Food and Drug Administration–approved medication for the symptomatic treatment of stuttering, but current evidence suggests that second-generation antipsychotics risperidone, olanzapine, and asenapine are beneficial, according to Gerald A. Maguire, MD.
At an annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Maguire, who is a stutterer himself, said current clinical trials in adults with childhood onset fluency disorder support the dopamine hypothesis of stuttering, where abnormal elevated cerebral dopaminergic activity is implicated.
Older studies found haloperidol to be effective for the treatment of stuttering, but long-term patient outlook is poor because of side effects such as sedation and sexual dysfunction. In a study led by Dr. Maguire, risperidone at a dose of 0.5-2 mg daily for 6 weeks was shown to decrease the percentage of syllables stuttered, time stuttered as a percentage of total time speaking, and overall stuttering severity, compared with placebo (J Clin Psychopharmacol. 2000;20[4]:479-82). A more recent study he also led found that olanzapine at a dose of 2.5-5 mg daily for 90 days showed a significant reduction in symptoms as measured by multiple tools, including the Stuttering Severity Instrument–Third Edition, the Clinical Global Impression scale, and the subject-rated self-assessment of stuttering scale (Ann Clin Psychiatry. 2004;16[2]:63-7).
Dr. Maguire, also associate dean of graduate medical education at the University of California, Riverside medical school, added that findings from several case reports suggest that asenapine and aripiprazole also are effective for managing stuttering symptoms. “Further studies of these drugs are warranted given better side-effect profiles as compared to other second-generation antipsychotics,” he said. There are ongoing investigations of other medications for the treatment of stuttering, including ecopipam, a D-1 dopamine receptor antagonist. An open-label study of ecopipam in adults who stutter is currently under way.
Dr. Maguire disclosed that he has received grant or research support from Intracellular, the Stanley Foundation, and Sunovion. He also is a consultant for Lundbeck, Otsuka, Sunovion, Takeda, and is a member of the speakers’ bureau or has received honoraria from Acadia, Lundbeck, Otsuka, Sunovion, Takeda, and Vanda.
LAS VEGAS – There currently is no Food and Drug Administration–approved medication for the symptomatic treatment of stuttering, but current evidence suggests that second-generation antipsychotics risperidone, olanzapine, and asenapine are beneficial, according to Gerald A. Maguire, MD.
At an annual psychopharmacology update held by the Nevada Psychiatric Association, Dr. Maguire, who is a stutterer himself, said current clinical trials in adults with childhood onset fluency disorder support the dopamine hypothesis of stuttering, where abnormal elevated cerebral dopaminergic activity is implicated.
Older studies found haloperidol to be effective for the treatment of stuttering, but long-term patient outlook is poor because of side effects such as sedation and sexual dysfunction. In a study led by Dr. Maguire, risperidone at a dose of 0.5-2 mg daily for 6 weeks was shown to decrease the percentage of syllables stuttered, time stuttered as a percentage of total time speaking, and overall stuttering severity, compared with placebo (J Clin Psychopharmacol. 2000;20[4]:479-82). A more recent study he also led found that olanzapine at a dose of 2.5-5 mg daily for 90 days showed a significant reduction in symptoms as measured by multiple tools, including the Stuttering Severity Instrument–Third Edition, the Clinical Global Impression scale, and the subject-rated self-assessment of stuttering scale (Ann Clin Psychiatry. 2004;16[2]:63-7).
Dr. Maguire, also associate dean of graduate medical education at the University of California, Riverside medical school, added that findings from several case reports suggest that asenapine and aripiprazole also are effective for managing stuttering symptoms. “Further studies of these drugs are warranted given better side-effect profiles as compared to other second-generation antipsychotics,” he said. There are ongoing investigations of other medications for the treatment of stuttering, including ecopipam, a D-1 dopamine receptor antagonist. An open-label study of ecopipam in adults who stutter is currently under way.
Dr. Maguire disclosed that he has received grant or research support from Intracellular, the Stanley Foundation, and Sunovion. He also is a consultant for Lundbeck, Otsuka, Sunovion, Takeda, and is a member of the speakers’ bureau or has received honoraria from Acadia, Lundbeck, Otsuka, Sunovion, Takeda, and Vanda.
AT THE NPA PSYCHOPHARMACOLOGY UPDATE
VIDEO: Infectious enteritis quadrupled short-term risk of IBS
More than 10% of patients developed irritable bowel syndrome (IBS) within a year after infectious enteritis, which gave them a more than fourfold greater risk than that of controls, according to a systematic review and meta-analysis of 45 studies.
“Protozoal and bacterial enteritis confer the greatest overall risk, although the magnitude of increased risk diminishes with time since exposure,” Fabiane B. Klem, MD, and Akhilesh Wadhwa, MD, of Mayo Clinic in Rochester, Minn., and their associates wrote in the April issue of Gastroenterology. Other significant risk factors for postinfectious IBS (PI-IBS) included female sex, clinically severe infections, antibiotic therapy, and comorbid psychological distress, they said.
Postinfectious IBS can last at least a decade after resolution of campylobacteriosis, shigellosis, salmonellosis, giardiasis, and norovirus infections, even when patients have no other risk factors for IBS, the researchers noted. To update and expand the most recent meta-analysis of this topic (Aliment Pharmacol Ther. 2007;26:535-44), the investigators searched Ovid Medline, EMBASE, Web of Science, and Cochrane Database of Systematic Reviews for studies published from 2006 through Aug. 31, 2015. This search yielded 45 studies, including 30 studies comparing infected patients with controls, who were usually matched by age, sex, and geographic location (Gastroenterology. 2017 Jan 6. doi: 10.1053/j.gastro.2016.12.039).
In all, 10.1% of patients with infectious enteritis developed IBS in the next 12 months (95% confidence interval, 7.2-14.1) – a 4.2-fold increase in risk, compared with that of controls (risk ratio, 4.2; 95% CI, 3.2-5.7). This risk subsequently dropped, but remained significantly elevated (RR, 2.3; 95% CI, 1.8-3.0), compared with controls. “Of patients with enteritis caused by protozoa or parasites, 41.9% developed IBS; of patients with enteritis caused by bacterial infection, 13.8% developed IBS,” the researchers emphasized. Patients with these infections remained at elevated risk of PI-IBS even after 1 year. Viral enteritis also significantly increased the risk of PI-IBS, but risk dropped to baseline levels after a year.
Among 10 pooled studies of IBS subtypes, 46% of patients had mixed IBS, 39% had diarrhea-predominant IBS, and 15% had constipation-predominant IBS. Female sex doubled the odds of PI-IBS (odds ratio, 2.2; 95% CI, 1.6-3.1) in 11 pooled studies. Significant clinical risk factors for PI-IBS included diarrhea lasting more than 7 days (eight studies; OR, 2.6; 95% CI, 1.5-4.6), bloody stool (four studies; OR, 1.9; 95% CI, 1.1-3.0), and antibiotic therapy during infectious enteritis (seven studies; OR, 1.7; 95% CI, 1.2-2.4).
Multiple reports linked PI-IBS to clinical psychological distress at the time of infectious enteritis. Specific risk factors included depression based on the Hospitalization Anxiety and Depression Scale (five studies; OR, 1.5; 95% CI, 1.2-1.9), anxiety based on the Hospital Anxiety and Depression Scale (four studies; OR, 2.0; 95% CI, 1.3-2.9), somatization (four studies; OR, 4.1; 95% CI, 2.7-6.0), and neuroticism (two studies; OR, 3.3; 95% CI, 1.6-6.6). Isolated studies also implicated hypochondriasis, extroversion, negative illness beliefs, stress, sleep disturbance, and adverse life events in the preceding year, the researchers said.
They found no evidence of publication bias, but noted a substantial amount of heterogeneity among studies. Also, some studies did not report multivariate analyses, so individual odds ratios might reflect “a conglomeration of factors,” they said.
The National Institutes of Health and the American Gastroenterological Association funded the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
The phenomenon of IBS developing after a bout of gastroenteritis (postinfectious [PI]–IBS) was first reported in 1950 and subsequently elaborated by studies from Oxford (Q J Med. 1962;123:307-22), Sheffield (Gut. 1999;44:400-6), and Nottingham (BMJ 1997;314:779-82; Gut. 2000;47:804-11). It has proven to be a fertile area for research, which is the basis for this excellent meta-analysis.
The authors identified 45 studies, 29 in the last decade including a total of 21,421 participants with exposure to gastroenteritis. The pooled prevalence for PI-IBS was 11.5% (95% CI, 8.2%-15.8%) but with considerable heterogeneity, which the authors attempted to explain by a number of subgroup analyses. The authors report that protozoal infection seems to have a higher rate of PI-IBS than bacterial or viral infection, though some caution is warranted, since these figures rely on reports from just one outbreak of giardiasis in Bergen, Norway (Scand J Gastroenterol. 2012;47:956-61). However, if true, this might suggest that a different immune response could be responsible, a feature which others have suggested might predispose particular individuals to PI-IBS (Gut. 2016;65[8]1279-88).
The meta-analysis confirms the consistent increased risk in female patients (odds ratio, 1.69), anxiety (OR, 1.97), and somatization (greatest RR, 4.05), all common risks for the development of IBS but not specific to PI-IBS. Initial disease severity indicators, including bloody stool and more than 7 days of initial illness, which might indicate the severity of underlying damage to the gut, were shown to be significant risk factors. Animal studies of acute infection, particularly parasitic infestation, indicate that significant changes can be seen in both nerve and muscle, but routine histology in PI-IBS patients is normal. Infection produces a striking increase in gut permeability (Gut 2000;47:804-11), a feature of IBS whose molecular basis has been demonstrated by a series of elegant studies (Gut. 2017 Jan 12 [Epub ahead of print]; Gut. 2015;64:1379-88) demonstrating altered tight junctions and immune activation in IBS with diarrhea. The authors found treatment with antibiotics increased the risk of PI-IBS but whether this is attributable to confounding by indication is unclear.
This meta-analysis indicates that PI-IBS also potentially is the most common cause of IBS, given that both the Centers for Disease Control and Prevention in the United States and community surveys in the United Kingdom (BMJ. 1999;318:1046-50) indicate that gastroenteritis affects around 1 in 5 of the population each year. If the incidence of PI-IBS is around 10%, modeling suggests PI-IBS could account for the majority of new cases (J Neurogastroenterol Motil. 2012;18:200-4).
Dr. Robin Spiller is professor of gastroenterology, NIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham Digestive Diseases Centre, University of Nottingham, England. He has no relevant conflicts of interest.
The phenomenon of IBS developing after a bout of gastroenteritis (postinfectious [PI]–IBS) was first reported in 1950 and subsequently elaborated by studies from Oxford (Q J Med. 1962;123:307-22), Sheffield (Gut. 1999;44:400-6), and Nottingham (BMJ 1997;314:779-82; Gut. 2000;47:804-11). It has proven to be a fertile area for research, which is the basis for this excellent meta-analysis.
The authors identified 45 studies, 29 in the last decade including a total of 21,421 participants with exposure to gastroenteritis. The pooled prevalence for PI-IBS was 11.5% (95% CI, 8.2%-15.8%) but with considerable heterogeneity, which the authors attempted to explain by a number of subgroup analyses. The authors report that protozoal infection seems to have a higher rate of PI-IBS than bacterial or viral infection, though some caution is warranted, since these figures rely on reports from just one outbreak of giardiasis in Bergen, Norway (Scand J Gastroenterol. 2012;47:956-61). However, if true, this might suggest that a different immune response could be responsible, a feature which others have suggested might predispose particular individuals to PI-IBS (Gut. 2016;65[8]1279-88).
The meta-analysis confirms the consistent increased risk in female patients (odds ratio, 1.69), anxiety (OR, 1.97), and somatization (greatest RR, 4.05), all common risks for the development of IBS but not specific to PI-IBS. Initial disease severity indicators, including bloody stool and more than 7 days of initial illness, which might indicate the severity of underlying damage to the gut, were shown to be significant risk factors. Animal studies of acute infection, particularly parasitic infestation, indicate that significant changes can be seen in both nerve and muscle, but routine histology in PI-IBS patients is normal. Infection produces a striking increase in gut permeability (Gut 2000;47:804-11), a feature of IBS whose molecular basis has been demonstrated by a series of elegant studies (Gut. 2017 Jan 12 [Epub ahead of print]; Gut. 2015;64:1379-88) demonstrating altered tight junctions and immune activation in IBS with diarrhea. The authors found treatment with antibiotics increased the risk of PI-IBS but whether this is attributable to confounding by indication is unclear.
This meta-analysis indicates that PI-IBS also potentially is the most common cause of IBS, given that both the Centers for Disease Control and Prevention in the United States and community surveys in the United Kingdom (BMJ. 1999;318:1046-50) indicate that gastroenteritis affects around 1 in 5 of the population each year. If the incidence of PI-IBS is around 10%, modeling suggests PI-IBS could account for the majority of new cases (J Neurogastroenterol Motil. 2012;18:200-4).
Dr. Robin Spiller is professor of gastroenterology, NIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham Digestive Diseases Centre, University of Nottingham, England. He has no relevant conflicts of interest.
The phenomenon of IBS developing after a bout of gastroenteritis (postinfectious [PI]–IBS) was first reported in 1950 and subsequently elaborated by studies from Oxford (Q J Med. 1962;123:307-22), Sheffield (Gut. 1999;44:400-6), and Nottingham (BMJ 1997;314:779-82; Gut. 2000;47:804-11). It has proven to be a fertile area for research, which is the basis for this excellent meta-analysis.
The authors identified 45 studies, 29 in the last decade including a total of 21,421 participants with exposure to gastroenteritis. The pooled prevalence for PI-IBS was 11.5% (95% CI, 8.2%-15.8%) but with considerable heterogeneity, which the authors attempted to explain by a number of subgroup analyses. The authors report that protozoal infection seems to have a higher rate of PI-IBS than bacterial or viral infection, though some caution is warranted, since these figures rely on reports from just one outbreak of giardiasis in Bergen, Norway (Scand J Gastroenterol. 2012;47:956-61). However, if true, this might suggest that a different immune response could be responsible, a feature which others have suggested might predispose particular individuals to PI-IBS (Gut. 2016;65[8]1279-88).
The meta-analysis confirms the consistent increased risk in female patients (odds ratio, 1.69), anxiety (OR, 1.97), and somatization (greatest RR, 4.05), all common risks for the development of IBS but not specific to PI-IBS. Initial disease severity indicators, including bloody stool and more than 7 days of initial illness, which might indicate the severity of underlying damage to the gut, were shown to be significant risk factors. Animal studies of acute infection, particularly parasitic infestation, indicate that significant changes can be seen in both nerve and muscle, but routine histology in PI-IBS patients is normal. Infection produces a striking increase in gut permeability (Gut 2000;47:804-11), a feature of IBS whose molecular basis has been demonstrated by a series of elegant studies (Gut. 2017 Jan 12 [Epub ahead of print]; Gut. 2015;64:1379-88) demonstrating altered tight junctions and immune activation in IBS with diarrhea. The authors found treatment with antibiotics increased the risk of PI-IBS but whether this is attributable to confounding by indication is unclear.
This meta-analysis indicates that PI-IBS also potentially is the most common cause of IBS, given that both the Centers for Disease Control and Prevention in the United States and community surveys in the United Kingdom (BMJ. 1999;318:1046-50) indicate that gastroenteritis affects around 1 in 5 of the population each year. If the incidence of PI-IBS is around 10%, modeling suggests PI-IBS could account for the majority of new cases (J Neurogastroenterol Motil. 2012;18:200-4).
Dr. Robin Spiller is professor of gastroenterology, NIHR Nottingham Digestive Diseases Biomedical Research Unit, Nottingham Digestive Diseases Centre, University of Nottingham, England. He has no relevant conflicts of interest.
More than 10% of patients developed irritable bowel syndrome (IBS) within a year after infectious enteritis, which gave them a more than fourfold greater risk than that of controls, according to a systematic review and meta-analysis of 45 studies.
“Protozoal and bacterial enteritis confer the greatest overall risk, although the magnitude of increased risk diminishes with time since exposure,” Fabiane B. Klem, MD, and Akhilesh Wadhwa, MD, of Mayo Clinic in Rochester, Minn., and their associates wrote in the April issue of Gastroenterology. Other significant risk factors for postinfectious IBS (PI-IBS) included female sex, clinically severe infections, antibiotic therapy, and comorbid psychological distress, they said.
Postinfectious IBS can last at least a decade after resolution of campylobacteriosis, shigellosis, salmonellosis, giardiasis, and norovirus infections, even when patients have no other risk factors for IBS, the researchers noted. To update and expand the most recent meta-analysis of this topic (Aliment Pharmacol Ther. 2007;26:535-44), the investigators searched Ovid Medline, EMBASE, Web of Science, and Cochrane Database of Systematic Reviews for studies published from 2006 through Aug. 31, 2015. This search yielded 45 studies, including 30 studies comparing infected patients with controls, who were usually matched by age, sex, and geographic location (Gastroenterology. 2017 Jan 6. doi: 10.1053/j.gastro.2016.12.039).
In all, 10.1% of patients with infectious enteritis developed IBS in the next 12 months (95% confidence interval, 7.2-14.1) – a 4.2-fold increase in risk, compared with that of controls (risk ratio, 4.2; 95% CI, 3.2-5.7). This risk subsequently dropped, but remained significantly elevated (RR, 2.3; 95% CI, 1.8-3.0), compared with controls. “Of patients with enteritis caused by protozoa or parasites, 41.9% developed IBS; of patients with enteritis caused by bacterial infection, 13.8% developed IBS,” the researchers emphasized. Patients with these infections remained at elevated risk of PI-IBS even after 1 year. Viral enteritis also significantly increased the risk of PI-IBS, but risk dropped to baseline levels after a year.
Among 10 pooled studies of IBS subtypes, 46% of patients had mixed IBS, 39% had diarrhea-predominant IBS, and 15% had constipation-predominant IBS. Female sex doubled the odds of PI-IBS (odds ratio, 2.2; 95% CI, 1.6-3.1) in 11 pooled studies. Significant clinical risk factors for PI-IBS included diarrhea lasting more than 7 days (eight studies; OR, 2.6; 95% CI, 1.5-4.6), bloody stool (four studies; OR, 1.9; 95% CI, 1.1-3.0), and antibiotic therapy during infectious enteritis (seven studies; OR, 1.7; 95% CI, 1.2-2.4).
Multiple reports linked PI-IBS to clinical psychological distress at the time of infectious enteritis. Specific risk factors included depression based on the Hospitalization Anxiety and Depression Scale (five studies; OR, 1.5; 95% CI, 1.2-1.9), anxiety based on the Hospital Anxiety and Depression Scale (four studies; OR, 2.0; 95% CI, 1.3-2.9), somatization (four studies; OR, 4.1; 95% CI, 2.7-6.0), and neuroticism (two studies; OR, 3.3; 95% CI, 1.6-6.6). Isolated studies also implicated hypochondriasis, extroversion, negative illness beliefs, stress, sleep disturbance, and adverse life events in the preceding year, the researchers said.
They found no evidence of publication bias, but noted a substantial amount of heterogeneity among studies. Also, some studies did not report multivariate analyses, so individual odds ratios might reflect “a conglomeration of factors,” they said.
The National Institutes of Health and the American Gastroenterological Association funded the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
More than 10% of patients developed irritable bowel syndrome (IBS) within a year after infectious enteritis, which gave them a more than fourfold greater risk than that of controls, according to a systematic review and meta-analysis of 45 studies.
“Protozoal and bacterial enteritis confer the greatest overall risk, although the magnitude of increased risk diminishes with time since exposure,” Fabiane B. Klem, MD, and Akhilesh Wadhwa, MD, of Mayo Clinic in Rochester, Minn., and their associates wrote in the April issue of Gastroenterology. Other significant risk factors for postinfectious IBS (PI-IBS) included female sex, clinically severe infections, antibiotic therapy, and comorbid psychological distress, they said.
Postinfectious IBS can last at least a decade after resolution of campylobacteriosis, shigellosis, salmonellosis, giardiasis, and norovirus infections, even when patients have no other risk factors for IBS, the researchers noted. To update and expand the most recent meta-analysis of this topic (Aliment Pharmacol Ther. 2007;26:535-44), the investigators searched Ovid Medline, EMBASE, Web of Science, and Cochrane Database of Systematic Reviews for studies published from 2006 through Aug. 31, 2015. This search yielded 45 studies, including 30 studies comparing infected patients with controls, who were usually matched by age, sex, and geographic location (Gastroenterology. 2017 Jan 6. doi: 10.1053/j.gastro.2016.12.039).
In all, 10.1% of patients with infectious enteritis developed IBS in the next 12 months (95% confidence interval, 7.2-14.1) – a 4.2-fold increase in risk, compared with that of controls (risk ratio, 4.2; 95% CI, 3.2-5.7). This risk subsequently dropped, but remained significantly elevated (RR, 2.3; 95% CI, 1.8-3.0), compared with controls. “Of patients with enteritis caused by protozoa or parasites, 41.9% developed IBS; of patients with enteritis caused by bacterial infection, 13.8% developed IBS,” the researchers emphasized. Patients with these infections remained at elevated risk of PI-IBS even after 1 year. Viral enteritis also significantly increased the risk of PI-IBS, but risk dropped to baseline levels after a year.
Among 10 pooled studies of IBS subtypes, 46% of patients had mixed IBS, 39% had diarrhea-predominant IBS, and 15% had constipation-predominant IBS. Female sex doubled the odds of PI-IBS (odds ratio, 2.2; 95% CI, 1.6-3.1) in 11 pooled studies. Significant clinical risk factors for PI-IBS included diarrhea lasting more than 7 days (eight studies; OR, 2.6; 95% CI, 1.5-4.6), bloody stool (four studies; OR, 1.9; 95% CI, 1.1-3.0), and antibiotic therapy during infectious enteritis (seven studies; OR, 1.7; 95% CI, 1.2-2.4).
Multiple reports linked PI-IBS to clinical psychological distress at the time of infectious enteritis. Specific risk factors included depression based on the Hospitalization Anxiety and Depression Scale (five studies; OR, 1.5; 95% CI, 1.2-1.9), anxiety based on the Hospital Anxiety and Depression Scale (four studies; OR, 2.0; 95% CI, 1.3-2.9), somatization (four studies; OR, 4.1; 95% CI, 2.7-6.0), and neuroticism (two studies; OR, 3.3; 95% CI, 1.6-6.6). Isolated studies also implicated hypochondriasis, extroversion, negative illness beliefs, stress, sleep disturbance, and adverse life events in the preceding year, the researchers said.
They found no evidence of publication bias, but noted a substantial amount of heterogeneity among studies. Also, some studies did not report multivariate analyses, so individual odds ratios might reflect “a conglomeration of factors,” they said.
The National Institutes of Health and the American Gastroenterological Association funded the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
FROM GASTROENTEROLOGY
Key clinical point.
Major finding: A total of 10.1% of patients with infectious enteritis developed IBS in the next 12 months, a 4.2-fold increase in risk, compared with that of controls.
Data source: A systematic review and meta-analysis of 45 studies.
Disclosures: The National Institutes of Health and the American Gastroenterological Association funded the work. The investigators reported having no conflicts of interest.
Familial hypercholesterolemia: Look for it!
SNOWMASS, COLO. – Familial hypercholesterolemia (FH), the most common genetic cause of premature atherosclerotic cardiovascular disease, affects an estimated 1 in 250 Americans. It doesn’t help that physicians are doing a terrible job of finding and treating them, Robert A. Vogel, MD, said at the Annual Cardiovascular Conference at Snowmass.
Indeed, it’s estimated that U.S. physicians diagnose fewer than 1% of affected individuals, as compared with a world’s-best 71% rate in the Netherlands, 43% in Norway, 13% in Sweden, and 12% in the United Kingdom (Eur Heart J. 2013 Dec 1;34[45]:3478-90a).
“You all have patients with FH in your practices. You have the parents, who already have atherosclerotic cardiovascular disease, but the kids need to be identified as well. Nothing is as gratifying as preventing disease in someone who would suffer a stroke or MI in the future,” the cardiologist continued.
FH is present in 7.5% of men and fully 11.1% of women with coronary heart disease (CHD), according to an analysis of more than 7,000 CHD patients in the EUROASPIRE IV study (Atherosclerosis. 2015 Jul;241[1]:169-75). Swiss investigators have shown, in a prospective study of 4,534 patients with acute coronary syndrome, that those who have FH are at significantly greater 1-year risk of recurrent fatal and nonfatal coronary events (Circulation. 2016 Sep 6;134[10]:698-709).
“You’re going to do worse after an MI if you have FH. These are very-high-risk folks. We need to find them because treatment is effective,” Dr. Vogel emphasized.
Three different sets of diagnostic criteria are available for FH: the Dutch Lipid Clinic Network diagnostic criteria, the Simon Broome criteria, and most recently, the American Heart Association criteria (Circulation. 2015 Dec 1;132[22]:2167-92).
There are common themes among the three sets of diagnostic criteria: Think FH when you encounter an LDL cholesterol level greater than 190 mg/dL in a patient not on statin therapy or more than 130 mg/dL on statin therapy, a personal or family history of premature atherosclerotic cardiovascular disease, or a patient with the characteristic findings of FH on physical examination.
These characteristic physical findings are xanthelasmas, corneal arcus, tuberous xanthomas, and Achilles tendon xanthomas, which Dr. Vogel called “the sine qua non of FH.”
The importance of tendon xanthomas as a manifestation of FH is vividly illustrated in the Dutch diagnostic criteria. Under the Dutch points-based scheme, various numbers of points are given for LDL level; a personal or family history of premature CAD, peripheral vascular disease, or stroke; positive physical findings; and a genetic test positive for a functional mutation in the LDL receptor gene. “Definite FH” requires a total of more than eight points, and a finding of tendon xanthomas alone provides six of them.
Tendon xanthomas are not only a key diagnostic feature, they are also important prognostically. They indicate that a patient is going to do relatively worse, independent of LDL level or LDL receptor gene mutation status (Arterioscler Thromb Vasc Biol. 2005 Sep;25[9]:1960-5).
A genetic test isn’t needed most of the time to diagnose FH, but it’s nevertheless helpful because it provides specific information about the patient’s LDL receptor status. A patient with a receptor-negative mutation in the LDL receptor gene is going to be much less responsive to maximum-intensity statin therapy than if defective LDL receptors are present.
Another test well worth ordering in a patient with FH is a lipoprotein(a) measurement. As shown in the prospective SAFEHEART trial (Spanish Familial Hypercholesterolemia Cohort Study), lipoprotein(a) is an independent predictor of cardiovascular disease in both men and women with FH. The risk is highest in those with lipoprotein(a) above 50 mg/dL – a normal level is below 30 mg/dL – who carry a null mutation in the LDL receptor gene (J Am Coll Cardiol. 2014 May 20;63[19]:1982-9).
Dr. Vogel reported serving as U.S. national coordinator for the ongoing ODYSSEY trial of the PCSK9 inhibitor alirocumab for cardiovascular risk reduction.
SNOWMASS, COLO. – Familial hypercholesterolemia (FH), the most common genetic cause of premature atherosclerotic cardiovascular disease, affects an estimated 1 in 250 Americans. It doesn’t help that physicians are doing a terrible job of finding and treating them, Robert A. Vogel, MD, said at the Annual Cardiovascular Conference at Snowmass.
Indeed, it’s estimated that U.S. physicians diagnose fewer than 1% of affected individuals, as compared with a world’s-best 71% rate in the Netherlands, 43% in Norway, 13% in Sweden, and 12% in the United Kingdom (Eur Heart J. 2013 Dec 1;34[45]:3478-90a).
“You all have patients with FH in your practices. You have the parents, who already have atherosclerotic cardiovascular disease, but the kids need to be identified as well. Nothing is as gratifying as preventing disease in someone who would suffer a stroke or MI in the future,” the cardiologist continued.
FH is present in 7.5% of men and fully 11.1% of women with coronary heart disease (CHD), according to an analysis of more than 7,000 CHD patients in the EUROASPIRE IV study (Atherosclerosis. 2015 Jul;241[1]:169-75). Swiss investigators have shown, in a prospective study of 4,534 patients with acute coronary syndrome, that those who have FH are at significantly greater 1-year risk of recurrent fatal and nonfatal coronary events (Circulation. 2016 Sep 6;134[10]:698-709).
“You’re going to do worse after an MI if you have FH. These are very-high-risk folks. We need to find them because treatment is effective,” Dr. Vogel emphasized.
Three different sets of diagnostic criteria are available for FH: the Dutch Lipid Clinic Network diagnostic criteria, the Simon Broome criteria, and most recently, the American Heart Association criteria (Circulation. 2015 Dec 1;132[22]:2167-92).
There are common themes among the three sets of diagnostic criteria: Think FH when you encounter an LDL cholesterol level greater than 190 mg/dL in a patient not on statin therapy or more than 130 mg/dL on statin therapy, a personal or family history of premature atherosclerotic cardiovascular disease, or a patient with the characteristic findings of FH on physical examination.
These characteristic physical findings are xanthelasmas, corneal arcus, tuberous xanthomas, and Achilles tendon xanthomas, which Dr. Vogel called “the sine qua non of FH.”
The importance of tendon xanthomas as a manifestation of FH is vividly illustrated in the Dutch diagnostic criteria. Under the Dutch points-based scheme, various numbers of points are given for LDL level; a personal or family history of premature CAD, peripheral vascular disease, or stroke; positive physical findings; and a genetic test positive for a functional mutation in the LDL receptor gene. “Definite FH” requires a total of more than eight points, and a finding of tendon xanthomas alone provides six of them.
Tendon xanthomas are not only a key diagnostic feature, they are also important prognostically. They indicate that a patient is going to do relatively worse, independent of LDL level or LDL receptor gene mutation status (Arterioscler Thromb Vasc Biol. 2005 Sep;25[9]:1960-5).
A genetic test isn’t needed most of the time to diagnose FH, but it’s nevertheless helpful because it provides specific information about the patient’s LDL receptor status. A patient with a receptor-negative mutation in the LDL receptor gene is going to be much less responsive to maximum-intensity statin therapy than if defective LDL receptors are present.
Another test well worth ordering in a patient with FH is a lipoprotein(a) measurement. As shown in the prospective SAFEHEART trial (Spanish Familial Hypercholesterolemia Cohort Study), lipoprotein(a) is an independent predictor of cardiovascular disease in both men and women with FH. The risk is highest in those with lipoprotein(a) above 50 mg/dL – a normal level is below 30 mg/dL – who carry a null mutation in the LDL receptor gene (J Am Coll Cardiol. 2014 May 20;63[19]:1982-9).
Dr. Vogel reported serving as U.S. national coordinator for the ongoing ODYSSEY trial of the PCSK9 inhibitor alirocumab for cardiovascular risk reduction.
SNOWMASS, COLO. – Familial hypercholesterolemia (FH), the most common genetic cause of premature atherosclerotic cardiovascular disease, affects an estimated 1 in 250 Americans. It doesn’t help that physicians are doing a terrible job of finding and treating them, Robert A. Vogel, MD, said at the Annual Cardiovascular Conference at Snowmass.
Indeed, it’s estimated that U.S. physicians diagnose fewer than 1% of affected individuals, as compared with a world’s-best 71% rate in the Netherlands, 43% in Norway, 13% in Sweden, and 12% in the United Kingdom (Eur Heart J. 2013 Dec 1;34[45]:3478-90a).
“You all have patients with FH in your practices. You have the parents, who already have atherosclerotic cardiovascular disease, but the kids need to be identified as well. Nothing is as gratifying as preventing disease in someone who would suffer a stroke or MI in the future,” the cardiologist continued.
FH is present in 7.5% of men and fully 11.1% of women with coronary heart disease (CHD), according to an analysis of more than 7,000 CHD patients in the EUROASPIRE IV study (Atherosclerosis. 2015 Jul;241[1]:169-75). Swiss investigators have shown, in a prospective study of 4,534 patients with acute coronary syndrome, that those who have FH are at significantly greater 1-year risk of recurrent fatal and nonfatal coronary events (Circulation. 2016 Sep 6;134[10]:698-709).
“You’re going to do worse after an MI if you have FH. These are very-high-risk folks. We need to find them because treatment is effective,” Dr. Vogel emphasized.
Three different sets of diagnostic criteria are available for FH: the Dutch Lipid Clinic Network diagnostic criteria, the Simon Broome criteria, and most recently, the American Heart Association criteria (Circulation. 2015 Dec 1;132[22]:2167-92).
There are common themes among the three sets of diagnostic criteria: Think FH when you encounter an LDL cholesterol level greater than 190 mg/dL in a patient not on statin therapy or more than 130 mg/dL on statin therapy, a personal or family history of premature atherosclerotic cardiovascular disease, or a patient with the characteristic findings of FH on physical examination.
These characteristic physical findings are xanthelasmas, corneal arcus, tuberous xanthomas, and Achilles tendon xanthomas, which Dr. Vogel called “the sine qua non of FH.”
The importance of tendon xanthomas as a manifestation of FH is vividly illustrated in the Dutch diagnostic criteria. Under the Dutch points-based scheme, various numbers of points are given for LDL level; a personal or family history of premature CAD, peripheral vascular disease, or stroke; positive physical findings; and a genetic test positive for a functional mutation in the LDL receptor gene. “Definite FH” requires a total of more than eight points, and a finding of tendon xanthomas alone provides six of them.
Tendon xanthomas are not only a key diagnostic feature, they are also important prognostically. They indicate that a patient is going to do relatively worse, independent of LDL level or LDL receptor gene mutation status (Arterioscler Thromb Vasc Biol. 2005 Sep;25[9]:1960-5).
A genetic test isn’t needed most of the time to diagnose FH, but it’s nevertheless helpful because it provides specific information about the patient’s LDL receptor status. A patient with a receptor-negative mutation in the LDL receptor gene is going to be much less responsive to maximum-intensity statin therapy than if defective LDL receptors are present.
Another test well worth ordering in a patient with FH is a lipoprotein(a) measurement. As shown in the prospective SAFEHEART trial (Spanish Familial Hypercholesterolemia Cohort Study), lipoprotein(a) is an independent predictor of cardiovascular disease in both men and women with FH. The risk is highest in those with lipoprotein(a) above 50 mg/dL – a normal level is below 30 mg/dL – who carry a null mutation in the LDL receptor gene (J Am Coll Cardiol. 2014 May 20;63[19]:1982-9).
Dr. Vogel reported serving as U.S. national coordinator for the ongoing ODYSSEY trial of the PCSK9 inhibitor alirocumab for cardiovascular risk reduction.
EXPERT ANALYSIS FROM THE CARDIOVASCULAR CONFERENCE AT SNOWMASS
Early delivery by morbidly obese moms improves outcomes
LAS VEGAS – Delivery at 38 weeks’ gestation is linked with improved perinatal survival among singleton infants born to morbidly obese mothers in a retrospective review of more than 2 million U.S. births.
“If reasonable, consider delivery at 38 weeks in morbidly obese mothers” delivering singleton pregnancies, Ruofan Yao, MD, said at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.
When mothers have diabetes, hypertension, or cholestasis, they receive frequent prenatal testing and fetal growth measurements, and delivery is typically at 37, 38, or 39 weeks. “This is what we also need to think about for morbidly obese mothers,” Dr. Yao said.
“Because of increased fetal growth in morbidly obese mothers there is probably earlier placental insufficiency,” he said in an interview.
The upshot is that, once a morbidly obese mother reaches 38 weeks’ gestation, induced labor should be considered, according to Dr. Yao. Induction could start immediately if the mother’s cervix is ripe, or clinicians could first take steps to hasten cervical ripening.
Induction can be especially slow in morbidly obese women, who are generally less sensitive to oxytocin and can require multiple induction strategies.
While Dr. Yao considered the evidence he reported persuasive enough to recommend this strategy, he cautioned that, ideally, the benefits of an early-delivery approach should be confirmed in a prospective, randomized trial.
The study used delivery records maintained by the state of Texas for 2006-2011. Of the more than 2.4 million births recorded during the period, Dr. Yao excluded multiple deliveries, births at less than 34 weeks’ or more than 42 weeks’ gestation, deliveries from underweight mothers (less than 18.5 kg/m2), and fetal anomalies. This left 2,181,530 births, of which 52% were by normal weight mothers (18.5-24 kg/m2), 26% by overweight mothers (25-29 kg/m2), 18% by obese mothers (30-39 kg/m2), and 4% by morbidly obese mothers (40 kg/m2 or greater). The women averaged 27 years old, 4% had preeclampsia, and 4% had pregestational diabetes.
The researchers then calculated perinatal mortality rates relative to gestational age at birth for women in each body mass index stratum. The calculations showed no significant impact of gestational age among late-term deliveries by normal weight, overweight, and obese mothers, but, among morbidly obese mothers, early deliveries made a difference and were significantly linked with reduced perinatal mortality.
Every 400 deliveries, approximately, induced at 38 weeks among morbidly obese mothers resulted in one less perinatal death, Dr. Yao reported. This relationship held even when the researchers excluded mothers with preeclampsia or pregestational diabetes (about 8% of the study group).
Dr. Yao had no disclosures.
[email protected]
On Twitter @mitchelzoler
LAS VEGAS – Delivery at 38 weeks’ gestation is linked with improved perinatal survival among singleton infants born to morbidly obese mothers in a retrospective review of more than 2 million U.S. births.
“If reasonable, consider delivery at 38 weeks in morbidly obese mothers” delivering singleton pregnancies, Ruofan Yao, MD, said at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.
When mothers have diabetes, hypertension, or cholestasis, they receive frequent prenatal testing and fetal growth measurements, and delivery is typically at 37, 38, or 39 weeks. “This is what we also need to think about for morbidly obese mothers,” Dr. Yao said.
“Because of increased fetal growth in morbidly obese mothers there is probably earlier placental insufficiency,” he said in an interview.
The upshot is that, once a morbidly obese mother reaches 38 weeks’ gestation, induced labor should be considered, according to Dr. Yao. Induction could start immediately if the mother’s cervix is ripe, or clinicians could first take steps to hasten cervical ripening.
Induction can be especially slow in morbidly obese women, who are generally less sensitive to oxytocin and can require multiple induction strategies.
While Dr. Yao considered the evidence he reported persuasive enough to recommend this strategy, he cautioned that, ideally, the benefits of an early-delivery approach should be confirmed in a prospective, randomized trial.
The study used delivery records maintained by the state of Texas for 2006-2011. Of the more than 2.4 million births recorded during the period, Dr. Yao excluded multiple deliveries, births at less than 34 weeks’ or more than 42 weeks’ gestation, deliveries from underweight mothers (less than 18.5 kg/m2), and fetal anomalies. This left 2,181,530 births, of which 52% were by normal weight mothers (18.5-24 kg/m2), 26% by overweight mothers (25-29 kg/m2), 18% by obese mothers (30-39 kg/m2), and 4% by morbidly obese mothers (40 kg/m2 or greater). The women averaged 27 years old, 4% had preeclampsia, and 4% had pregestational diabetes.
The researchers then calculated perinatal mortality rates relative to gestational age at birth for women in each body mass index stratum. The calculations showed no significant impact of gestational age among late-term deliveries by normal weight, overweight, and obese mothers, but, among morbidly obese mothers, early deliveries made a difference and were significantly linked with reduced perinatal mortality.
Every 400 deliveries, approximately, induced at 38 weeks among morbidly obese mothers resulted in one less perinatal death, Dr. Yao reported. This relationship held even when the researchers excluded mothers with preeclampsia or pregestational diabetes (about 8% of the study group).
Dr. Yao had no disclosures.
[email protected]
On Twitter @mitchelzoler
LAS VEGAS – Delivery at 38 weeks’ gestation is linked with improved perinatal survival among singleton infants born to morbidly obese mothers in a retrospective review of more than 2 million U.S. births.
“If reasonable, consider delivery at 38 weeks in morbidly obese mothers” delivering singleton pregnancies, Ruofan Yao, MD, said at the annual Pregnancy Meeting sponsored by the Society for Maternal-Fetal Medicine.
When mothers have diabetes, hypertension, or cholestasis, they receive frequent prenatal testing and fetal growth measurements, and delivery is typically at 37, 38, or 39 weeks. “This is what we also need to think about for morbidly obese mothers,” Dr. Yao said.
“Because of increased fetal growth in morbidly obese mothers there is probably earlier placental insufficiency,” he said in an interview.
The upshot is that, once a morbidly obese mother reaches 38 weeks’ gestation, induced labor should be considered, according to Dr. Yao. Induction could start immediately if the mother’s cervix is ripe, or clinicians could first take steps to hasten cervical ripening.
Induction can be especially slow in morbidly obese women, who are generally less sensitive to oxytocin and can require multiple induction strategies.
While Dr. Yao considered the evidence he reported persuasive enough to recommend this strategy, he cautioned that, ideally, the benefits of an early-delivery approach should be confirmed in a prospective, randomized trial.
The study used delivery records maintained by the state of Texas for 2006-2011. Of the more than 2.4 million births recorded during the period, Dr. Yao excluded multiple deliveries, births at less than 34 weeks’ or more than 42 weeks’ gestation, deliveries from underweight mothers (less than 18.5 kg/m2), and fetal anomalies. This left 2,181,530 births, of which 52% were by normal weight mothers (18.5-24 kg/m2), 26% by overweight mothers (25-29 kg/m2), 18% by obese mothers (30-39 kg/m2), and 4% by morbidly obese mothers (40 kg/m2 or greater). The women averaged 27 years old, 4% had preeclampsia, and 4% had pregestational diabetes.
The researchers then calculated perinatal mortality rates relative to gestational age at birth for women in each body mass index stratum. The calculations showed no significant impact of gestational age among late-term deliveries by normal weight, overweight, and obese mothers, but, among morbidly obese mothers, early deliveries made a difference and were significantly linked with reduced perinatal mortality.
Every 400 deliveries, approximately, induced at 38 weeks among morbidly obese mothers resulted in one less perinatal death, Dr. Yao reported. This relationship held even when the researchers excluded mothers with preeclampsia or pregestational diabetes (about 8% of the study group).
Dr. Yao had no disclosures.
[email protected]
On Twitter @mitchelzoler
AT THE PREGNANCY MEETING
Key clinical point:
Major finding: Every 400 deliveries at 38 weeks is linked with one fewer perinatal death, compared with full-term deliveries.
Data source: Review of 2,181,530 Texas births during 2006-2011.
Disclosures: Dr. Yao had no disclosures.
VIDEO: Molecular testing helps pinpoint ambiguous lesions
WAILEA, HAWAII – In a video interview, Pedram Gerami, MD, professor of dermatology, pathology, and pediatrics, Northwestern University, Chicago, discusses the use of molecular testing for melanoma and suspicious lesions.
Molecular tests are available for various components of diagnosis and prognosis of melanoma, and one of the most popular scenarios for their use is to confirm a diagnosis if a lesion is biopsied and the histopathologist “feels that the diagnosis is ambiguous by standard pathology methods,” Dr. Gerami said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
On average, between 1% and 5% of cases of suspicious lesions may need molecular testing to confirm the diagnosis, he noted. Of the available options for molecular testing, FISH (fluorescence in situ hybridization) testing is the most validated in the setting of ambiguous histology, he said.
Dr. Gerami disclosed serving as a consultant and researcher for Castle Biosciences, Myriad Genetics, and DermTech.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WAILEA, HAWAII – In a video interview, Pedram Gerami, MD, professor of dermatology, pathology, and pediatrics, Northwestern University, Chicago, discusses the use of molecular testing for melanoma and suspicious lesions.
Molecular tests are available for various components of diagnosis and prognosis of melanoma, and one of the most popular scenarios for their use is to confirm a diagnosis if a lesion is biopsied and the histopathologist “feels that the diagnosis is ambiguous by standard pathology methods,” Dr. Gerami said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
On average, between 1% and 5% of cases of suspicious lesions may need molecular testing to confirm the diagnosis, he noted. Of the available options for molecular testing, FISH (fluorescence in situ hybridization) testing is the most validated in the setting of ambiguous histology, he said.
Dr. Gerami disclosed serving as a consultant and researcher for Castle Biosciences, Myriad Genetics, and DermTech.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WAILEA, HAWAII – In a video interview, Pedram Gerami, MD, professor of dermatology, pathology, and pediatrics, Northwestern University, Chicago, discusses the use of molecular testing for melanoma and suspicious lesions.
Molecular tests are available for various components of diagnosis and prognosis of melanoma, and one of the most popular scenarios for their use is to confirm a diagnosis if a lesion is biopsied and the histopathologist “feels that the diagnosis is ambiguous by standard pathology methods,” Dr. Gerami said in a video interview at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
On average, between 1% and 5% of cases of suspicious lesions may need molecular testing to confirm the diagnosis, he noted. Of the available options for molecular testing, FISH (fluorescence in situ hybridization) testing is the most validated in the setting of ambiguous histology, he said.
Dr. Gerami disclosed serving as a consultant and researcher for Castle Biosciences, Myriad Genetics, and DermTech.
SDEF and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT SDEF HAWAII DERMATOLOGY SEMINAR
Hydrogel coils improve outcomes in medium-sized intracranial aneurysms
HOUSTON – Hydrogel coils significantly outperformed bare platinum coils in treating patients with medium-sized intracranial aneurysms, reducing the incidence of adverse outcomes by about 9% in an open-label, randomized trial.
Compared against the platinum coils, the self-expandable, hydrophilic coils scored significantly better on a composite endpoint of aneurysm recurrence at 18 months, re-treatment by 18 months, serious morbidity that prevented angiographic follow-up, and death, Christian Taschner, MD, said at the International Stroke Conference sponsored by the America Heart Association.
These are the company’s second-generation products, said Dr. Taschner, a neuroradiologist at University Hospital Freiburg (Germany). The initial hydrogel-coated coils were not well received because they were too stiff, he said in an interview.
The 18-month study comprised 513 patients and was conducted in 15 centers in France and 7 in Germany. Patients with medium-sized aneurysms (4-12 mm) were randomized to coiling with either the hydrogel coils or bare platinum coils and followed for 18 months. The cohort was stratified by rupture status in the analysis.
Angiographic images of the aneurysm were obtained before treatment, immediately after treatment, at 6 months, and at 18 months. All images were reviewed by an independent laboratory that was blinded to the treatment.
In addition to the primary composite outcome, the study assessed secondary endpoints of modified Rankin Scale (mRS) score at 18 months and coil packing density.
The final analysis included 484 patients. They were a mean of 52 years old, and about 70% were women. The aneurysms were ruptured at baseline in about 43% of cases. The mean aneurysm size was 7 mm, and the mean neck size, 3.5 mm. The dome-to-neck ratio was less than 1.5 in about a third of the group. Most lesions (89%) had anterior circulation.
Most patients needed some kind of adjunctive endovascular-assisting device during the procedure. These included balloon remodeling, which was necessary in about 50% of cases to help keep the coils from extruding into the parent vessel, and stents in 22%.
Intraoperative adverse events were uncommon in both groups. They were numerically, but not significantly, less common in the hydrogel group. These included thromboembolism (8 vs. 12), intraoperative rupture (3 vs. 7), parent vessel occlusion (1 vs. 3), and vessel perforation (one in each group). There were no vessel dissections.
By 18 months, 20% of the hydrogel group and 29% of the platinum coil group had experienced the composite primary endpoint. The 9% absolute difference was statistically significant. It was largely driven by the subcomponents of major recurrence (12% vs. 18%) and re-treatment (3% vs. 6%).
An mRS of 3-5 was used as the proxy for patients whose clinical status prevented them from having angiographic follow-up. That endpoint occurred in three patients in the hydrogel group but in none of the platinum coil group. Dr. Taschner said that difference was not statistically significant.
In an analysis that stratified by baseline rupture status and by aneurysm size, the hydrogel coils were largely superior to bare platinum. However, the hydrogel coils were not significantly more effective than the platinum coils for aneurysms 10 mm or larger, Dr. Taschner noted.
There was no significant difference in the secondary endpoint of mRS at 18 months. Most patients (85% vs. 86%) did well, with an mRS of 0. Scores of 1-2 were seen in 9% of each group. An mRS of 3-5 occurred in 3% of the hydrogel group and 1% of the platinum coil group. There were 17 deaths: 7 in the hydrogel group and 10 in the platinum coil group (3% vs. 4%). This was not a significant difference.
Patients whose aneurysms were unruptured at baseline did significantly better than did those with ruptured lesions, although the mRS scores did not vary significantly between treatment groups. Among those with intact lesions, 90% of the hydrogel and 94% of the platinum coil group achieved an mRS of 0, and 2% of each group died. Among those with ruptured lesions at baseline, 78% of the hydrogel group and 75% of the platinum coil group achieved an mRS of 0. Five patients in the hydrogel group and seven in the platinum coil group died.
On the technical outcome of coil volume, hydrogel did somewhat better (0.041 cm3 vs. 0.038 cm3). The mean packing density was significantly higher (39% vs. 31%).
Dr. Taschner said the study provides good support for using the hydrogel coils in medium-sized aneurysms, and that other recent data reaffirm this.
“A recent trial in Canada and the U.S. looked at hydrogel coils in aneurysms 12 mm or larger, with broad necks, and it failed to show a benefit of the hydrogel coils.”
Additionally, a study published in January found that hydrogel coils were no better than platinum coils in 250 patients with large or recurrent aneurysms (AJNR Am J Neuroradiol. 2017 Jan 12. doi: 10.3174/ajnr.A5101).
“I myself would use them in medium-sized aneurysms with an unfavorable dome-to-neck ratio, and in those that have a broad neck. In those instances, I do think that hydrogel coils have their place. I wouldn’t use them in really large aneurysms. I don’t think they are well suited for that. In those cases, I would probably use platinum coils in combination with a flow diverter. That really provides very stable aneurysm occlusion with acceptable complication rates.”
Dr. Taschner said that he received research support from MicroVention during the study.
[email protected]
On Twitter @alz_gal
HOUSTON – Hydrogel coils significantly outperformed bare platinum coils in treating patients with medium-sized intracranial aneurysms, reducing the incidence of adverse outcomes by about 9% in an open-label, randomized trial.
Compared against the platinum coils, the self-expandable, hydrophilic coils scored significantly better on a composite endpoint of aneurysm recurrence at 18 months, re-treatment by 18 months, serious morbidity that prevented angiographic follow-up, and death, Christian Taschner, MD, said at the International Stroke Conference sponsored by the America Heart Association.
These are the company’s second-generation products, said Dr. Taschner, a neuroradiologist at University Hospital Freiburg (Germany). The initial hydrogel-coated coils were not well received because they were too stiff, he said in an interview.
The 18-month study comprised 513 patients and was conducted in 15 centers in France and 7 in Germany. Patients with medium-sized aneurysms (4-12 mm) were randomized to coiling with either the hydrogel coils or bare platinum coils and followed for 18 months. The cohort was stratified by rupture status in the analysis.
Angiographic images of the aneurysm were obtained before treatment, immediately after treatment, at 6 months, and at 18 months. All images were reviewed by an independent laboratory that was blinded to the treatment.
In addition to the primary composite outcome, the study assessed secondary endpoints of modified Rankin Scale (mRS) score at 18 months and coil packing density.
The final analysis included 484 patients. They were a mean of 52 years old, and about 70% were women. The aneurysms were ruptured at baseline in about 43% of cases. The mean aneurysm size was 7 mm, and the mean neck size, 3.5 mm. The dome-to-neck ratio was less than 1.5 in about a third of the group. Most lesions (89%) had anterior circulation.
Most patients needed some kind of adjunctive endovascular-assisting device during the procedure. These included balloon remodeling, which was necessary in about 50% of cases to help keep the coils from extruding into the parent vessel, and stents in 22%.
Intraoperative adverse events were uncommon in both groups. They were numerically, but not significantly, less common in the hydrogel group. These included thromboembolism (8 vs. 12), intraoperative rupture (3 vs. 7), parent vessel occlusion (1 vs. 3), and vessel perforation (one in each group). There were no vessel dissections.
By 18 months, 20% of the hydrogel group and 29% of the platinum coil group had experienced the composite primary endpoint. The 9% absolute difference was statistically significant. It was largely driven by the subcomponents of major recurrence (12% vs. 18%) and re-treatment (3% vs. 6%).
An mRS of 3-5 was used as the proxy for patients whose clinical status prevented them from having angiographic follow-up. That endpoint occurred in three patients in the hydrogel group but in none of the platinum coil group. Dr. Taschner said that difference was not statistically significant.
In an analysis that stratified by baseline rupture status and by aneurysm size, the hydrogel coils were largely superior to bare platinum. However, the hydrogel coils were not significantly more effective than the platinum coils for aneurysms 10 mm or larger, Dr. Taschner noted.
There was no significant difference in the secondary endpoint of mRS at 18 months. Most patients (85% vs. 86%) did well, with an mRS of 0. Scores of 1-2 were seen in 9% of each group. An mRS of 3-5 occurred in 3% of the hydrogel group and 1% of the platinum coil group. There were 17 deaths: 7 in the hydrogel group and 10 in the platinum coil group (3% vs. 4%). This was not a significant difference.
Patients whose aneurysms were unruptured at baseline did significantly better than did those with ruptured lesions, although the mRS scores did not vary significantly between treatment groups. Among those with intact lesions, 90% of the hydrogel and 94% of the platinum coil group achieved an mRS of 0, and 2% of each group died. Among those with ruptured lesions at baseline, 78% of the hydrogel group and 75% of the platinum coil group achieved an mRS of 0. Five patients in the hydrogel group and seven in the platinum coil group died.
On the technical outcome of coil volume, hydrogel did somewhat better (0.041 cm3 vs. 0.038 cm3). The mean packing density was significantly higher (39% vs. 31%).
Dr. Taschner said the study provides good support for using the hydrogel coils in medium-sized aneurysms, and that other recent data reaffirm this.
“A recent trial in Canada and the U.S. looked at hydrogel coils in aneurysms 12 mm or larger, with broad necks, and it failed to show a benefit of the hydrogel coils.”
Additionally, a study published in January found that hydrogel coils were no better than platinum coils in 250 patients with large or recurrent aneurysms (AJNR Am J Neuroradiol. 2017 Jan 12. doi: 10.3174/ajnr.A5101).
“I myself would use them in medium-sized aneurysms with an unfavorable dome-to-neck ratio, and in those that have a broad neck. In those instances, I do think that hydrogel coils have their place. I wouldn’t use them in really large aneurysms. I don’t think they are well suited for that. In those cases, I would probably use platinum coils in combination with a flow diverter. That really provides very stable aneurysm occlusion with acceptable complication rates.”
Dr. Taschner said that he received research support from MicroVention during the study.
[email protected]
On Twitter @alz_gal
HOUSTON – Hydrogel coils significantly outperformed bare platinum coils in treating patients with medium-sized intracranial aneurysms, reducing the incidence of adverse outcomes by about 9% in an open-label, randomized trial.
Compared against the platinum coils, the self-expandable, hydrophilic coils scored significantly better on a composite endpoint of aneurysm recurrence at 18 months, re-treatment by 18 months, serious morbidity that prevented angiographic follow-up, and death, Christian Taschner, MD, said at the International Stroke Conference sponsored by the America Heart Association.
These are the company’s second-generation products, said Dr. Taschner, a neuroradiologist at University Hospital Freiburg (Germany). The initial hydrogel-coated coils were not well received because they were too stiff, he said in an interview.
The 18-month study comprised 513 patients and was conducted in 15 centers in France and 7 in Germany. Patients with medium-sized aneurysms (4-12 mm) were randomized to coiling with either the hydrogel coils or bare platinum coils and followed for 18 months. The cohort was stratified by rupture status in the analysis.
Angiographic images of the aneurysm were obtained before treatment, immediately after treatment, at 6 months, and at 18 months. All images were reviewed by an independent laboratory that was blinded to the treatment.
In addition to the primary composite outcome, the study assessed secondary endpoints of modified Rankin Scale (mRS) score at 18 months and coil packing density.
The final analysis included 484 patients. They were a mean of 52 years old, and about 70% were women. The aneurysms were ruptured at baseline in about 43% of cases. The mean aneurysm size was 7 mm, and the mean neck size, 3.5 mm. The dome-to-neck ratio was less than 1.5 in about a third of the group. Most lesions (89%) had anterior circulation.
Most patients needed some kind of adjunctive endovascular-assisting device during the procedure. These included balloon remodeling, which was necessary in about 50% of cases to help keep the coils from extruding into the parent vessel, and stents in 22%.
Intraoperative adverse events were uncommon in both groups. They were numerically, but not significantly, less common in the hydrogel group. These included thromboembolism (8 vs. 12), intraoperative rupture (3 vs. 7), parent vessel occlusion (1 vs. 3), and vessel perforation (one in each group). There were no vessel dissections.
By 18 months, 20% of the hydrogel group and 29% of the platinum coil group had experienced the composite primary endpoint. The 9% absolute difference was statistically significant. It was largely driven by the subcomponents of major recurrence (12% vs. 18%) and re-treatment (3% vs. 6%).
An mRS of 3-5 was used as the proxy for patients whose clinical status prevented them from having angiographic follow-up. That endpoint occurred in three patients in the hydrogel group but in none of the platinum coil group. Dr. Taschner said that difference was not statistically significant.
In an analysis that stratified by baseline rupture status and by aneurysm size, the hydrogel coils were largely superior to bare platinum. However, the hydrogel coils were not significantly more effective than the platinum coils for aneurysms 10 mm or larger, Dr. Taschner noted.
There was no significant difference in the secondary endpoint of mRS at 18 months. Most patients (85% vs. 86%) did well, with an mRS of 0. Scores of 1-2 were seen in 9% of each group. An mRS of 3-5 occurred in 3% of the hydrogel group and 1% of the platinum coil group. There were 17 deaths: 7 in the hydrogel group and 10 in the platinum coil group (3% vs. 4%). This was not a significant difference.
Patients whose aneurysms were unruptured at baseline did significantly better than did those with ruptured lesions, although the mRS scores did not vary significantly between treatment groups. Among those with intact lesions, 90% of the hydrogel and 94% of the platinum coil group achieved an mRS of 0, and 2% of each group died. Among those with ruptured lesions at baseline, 78% of the hydrogel group and 75% of the platinum coil group achieved an mRS of 0. Five patients in the hydrogel group and seven in the platinum coil group died.
On the technical outcome of coil volume, hydrogel did somewhat better (0.041 cm3 vs. 0.038 cm3). The mean packing density was significantly higher (39% vs. 31%).
Dr. Taschner said the study provides good support for using the hydrogel coils in medium-sized aneurysms, and that other recent data reaffirm this.
“A recent trial in Canada and the U.S. looked at hydrogel coils in aneurysms 12 mm or larger, with broad necks, and it failed to show a benefit of the hydrogel coils.”
Additionally, a study published in January found that hydrogel coils were no better than platinum coils in 250 patients with large or recurrent aneurysms (AJNR Am J Neuroradiol. 2017 Jan 12. doi: 10.3174/ajnr.A5101).
“I myself would use them in medium-sized aneurysms with an unfavorable dome-to-neck ratio, and in those that have a broad neck. In those instances, I do think that hydrogel coils have their place. I wouldn’t use them in really large aneurysms. I don’t think they are well suited for that. In those cases, I would probably use platinum coils in combination with a flow diverter. That really provides very stable aneurysm occlusion with acceptable complication rates.”
Dr. Taschner said that he received research support from MicroVention during the study.
[email protected]
On Twitter @alz_gal
AT THE INTERNATIONAL STROKE CONFERENCE
Key clinical point:
Major finding: Compared with bare-metal coils, hydrogel coils reduced by 9% the incidence of a composite primary outcome of recurrence, re-treatment, morbidity, and death.
Data source: An 18-month, open-label, randomized study of 513 patients.
Disclosures: MicroVention sponsored the study. Dr. Taschner said that he received research support from the company during the study.
Docs create guideline to aid workup of acute leukemia
Two physician groups have published an evidence-based guideline that addresses the initial workup of acute leukemia.
The guideline includes 27 recommendations intended to aid treating physicians and pathologists involved in the diagnostic and prognostic evaluation of acute leukemia samples, including those from patients with acute lymphoblastic leukemia, acute myeloid leukemia, and acute leukemias of ambiguous lineage.
The guideline, which was developed through a collaboration between the College of American Pathologists (CAP) and the American Society of Hematology (ASH), has been published in the Archives of Pathology and Laboratory Medicine.
The recommendations in the guideline will also be available in a pocket guide and via the ASH Pocket Guides app in March.
“With its multidisciplinary perspective, this guideline reflects contemporary, integrated cancer care, and, therefore, it will also help providers realize efficiencies in test management,” said ASH guideline co-chair James W. Vardiman, MD, of the University of Chicago in Illinois.
To create this guideline, Dr Vardiman and his colleagues sought and reviewed relevant published evidence.
The group set out to answer 6 questions for the initial diagnosis of acute leukemias:
1) What clinical and laboratory information should be available?
2) What samples and specimen types should be evaluated?
3) What tests are required for all patients during the initial evaluation?
4) What tests are required for only a subset of patients?
5) Where should laboratory testing be performed?
6) How should the results be reported?
The authors say the guideline’s 27 recommendations answer these questions, providing a framework for the steps involved in the evaluation of acute leukemia samples.
In particular, the guideline includes steps to coordinate and communicate across clinical teams, specifying information that must be shared—particularly among treating physicians and pathologists—for optimal patient outcomes and to avoid duplicative testing.
“The laboratory testing to diagnose acute leukemia and inform treatment is increasingly complex, making this guideline essential,” said CAP guideline co-chair Daniel A. Arber, MD, of the University of Chicago.
“New gene mutations and protein expressions have been described over the last decade in all types of acute leukemia, and many of them impact diagnosis or inform prognosis.” 
Two physician groups have published an evidence-based guideline that addresses the initial workup of acute leukemia.
The guideline includes 27 recommendations intended to aid treating physicians and pathologists involved in the diagnostic and prognostic evaluation of acute leukemia samples, including those from patients with acute lymphoblastic leukemia, acute myeloid leukemia, and acute leukemias of ambiguous lineage.
The guideline, which was developed through a collaboration between the College of American Pathologists (CAP) and the American Society of Hematology (ASH), has been published in the Archives of Pathology and Laboratory Medicine.
The recommendations in the guideline will also be available in a pocket guide and via the ASH Pocket Guides app in March.
“With its multidisciplinary perspective, this guideline reflects contemporary, integrated cancer care, and, therefore, it will also help providers realize efficiencies in test management,” said ASH guideline co-chair James W. Vardiman, MD, of the University of Chicago in Illinois.
To create this guideline, Dr Vardiman and his colleagues sought and reviewed relevant published evidence.
The group set out to answer 6 questions for the initial diagnosis of acute leukemias:
1) What clinical and laboratory information should be available?
2) What samples and specimen types should be evaluated?
3) What tests are required for all patients during the initial evaluation?
4) What tests are required for only a subset of patients?
5) Where should laboratory testing be performed?
6) How should the results be reported?
The authors say the guideline’s 27 recommendations answer these questions, providing a framework for the steps involved in the evaluation of acute leukemia samples.
In particular, the guideline includes steps to coordinate and communicate across clinical teams, specifying information that must be shared—particularly among treating physicians and pathologists—for optimal patient outcomes and to avoid duplicative testing.
“The laboratory testing to diagnose acute leukemia and inform treatment is increasingly complex, making this guideline essential,” said CAP guideline co-chair Daniel A. Arber, MD, of the University of Chicago.
“New gene mutations and protein expressions have been described over the last decade in all types of acute leukemia, and many of them impact diagnosis or inform prognosis.”
Two physician groups have published an evidence-based guideline that addresses the initial workup of acute leukemia.
The guideline includes 27 recommendations intended to aid treating physicians and pathologists involved in the diagnostic and prognostic evaluation of acute leukemia samples, including those from patients with acute lymphoblastic leukemia, acute myeloid leukemia, and acute leukemias of ambiguous lineage.
The guideline, which was developed through a collaboration between the College of American Pathologists (CAP) and the American Society of Hematology (ASH), has been published in the Archives of Pathology and Laboratory Medicine.
The recommendations in the guideline will also be available in a pocket guide and via the ASH Pocket Guides app in March.
“With its multidisciplinary perspective, this guideline reflects contemporary, integrated cancer care, and, therefore, it will also help providers realize efficiencies in test management,” said ASH guideline co-chair James W. Vardiman, MD, of the University of Chicago in Illinois.
To create this guideline, Dr Vardiman and his colleagues sought and reviewed relevant published evidence.
The group set out to answer 6 questions for the initial diagnosis of acute leukemias:
1) What clinical and laboratory information should be available?
2) What samples and specimen types should be evaluated?
3) What tests are required for all patients during the initial evaluation?
4) What tests are required for only a subset of patients?
5) Where should laboratory testing be performed?
6) How should the results be reported?
The authors say the guideline’s 27 recommendations answer these questions, providing a framework for the steps involved in the evaluation of acute leukemia samples.
In particular, the guideline includes steps to coordinate and communicate across clinical teams, specifying information that must be shared—particularly among treating physicians and pathologists—for optimal patient outcomes and to avoid duplicative testing.
“The laboratory testing to diagnose acute leukemia and inform treatment is increasingly complex, making this guideline essential,” said CAP guideline co-chair Daniel A. Arber, MD, of the University of Chicago.
“New gene mutations and protein expressions have been described over the last decade in all types of acute leukemia, and many of them impact diagnosis or inform prognosis.”
First case of artemisinin resistance in Africa
Researchers have identified the first known case of artemisinin-resistant malaria originating in Africa, according to a letter published in NEJM.
Resistant Plasmodium falciparum parasites were detected in a Chinese man who had travelled from Equatorial Guinea to China.
The finding means Africa has joined Southeast Asia in hosting parasites that are partially resistant to the first-line antimalaria drug, artemisinin.
Researchers were able to confirm that the parasites in the current case carried a new mutation in the Kelch13 (K13) gene, the main driver for artemisinin resistance in Asia.
Then, the team set out to determine whether the parasite originated from Africa or Southeast Asia.
“We used whole-genome sequencing and bioinformatics tools we had previously developed—like detectives trying to link the culprit parasite to the crime scene,” explained Arnab Pain, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia.
Sequencing and analysis of P falciparum DNA unveiled its origin by disclosing the single nucleotide polymorphisms that vary according to the geographical source of the strain.
The researchers used the nuclear DNA, as well as the one present in 2 organelles of the parasite—the mitochondrium and the apicoplast.
Both methods independently validated the origin of the parasite as West African, confirming the first case of artemisinin resistance mediated by a K13 gene mutation on the African continent.
“The spread of artemisinin resistance in Africa would be a major setback in the fight against malaria, as ACT [artemisinin-based combination therapy] is the only effective and widely used antimalarial treatment at the moment,” Dr Pain said. “Therefore, it is very important to regularly monitor artemisinin resistance worldwide.”
Researchers have identified the first known case of artemisinin-resistant malaria originating in Africa, according to a letter published in NEJM.
Resistant Plasmodium falciparum parasites were detected in a Chinese man who had travelled from Equatorial Guinea to China.
The finding means Africa has joined Southeast Asia in hosting parasites that are partially resistant to the first-line antimalaria drug, artemisinin.
Researchers were able to confirm that the parasites in the current case carried a new mutation in the Kelch13 (K13) gene, the main driver for artemisinin resistance in Asia.
Then, the team set out to determine whether the parasite originated from Africa or Southeast Asia.
“We used whole-genome sequencing and bioinformatics tools we had previously developed—like detectives trying to link the culprit parasite to the crime scene,” explained Arnab Pain, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia.
Sequencing and analysis of P falciparum DNA unveiled its origin by disclosing the single nucleotide polymorphisms that vary according to the geographical source of the strain.
The researchers used the nuclear DNA, as well as the one present in 2 organelles of the parasite—the mitochondrium and the apicoplast.
Both methods independently validated the origin of the parasite as West African, confirming the first case of artemisinin resistance mediated by a K13 gene mutation on the African continent.
“The spread of artemisinin resistance in Africa would be a major setback in the fight against malaria, as ACT [artemisinin-based combination therapy] is the only effective and widely used antimalarial treatment at the moment,” Dr Pain said. “Therefore, it is very important to regularly monitor artemisinin resistance worldwide.”
Researchers have identified the first known case of artemisinin-resistant malaria originating in Africa, according to a letter published in NEJM.
Resistant Plasmodium falciparum parasites were detected in a Chinese man who had travelled from Equatorial Guinea to China.
The finding means Africa has joined Southeast Asia in hosting parasites that are partially resistant to the first-line antimalaria drug, artemisinin.
Researchers were able to confirm that the parasites in the current case carried a new mutation in the Kelch13 (K13) gene, the main driver for artemisinin resistance in Asia.
Then, the team set out to determine whether the parasite originated from Africa or Southeast Asia.
“We used whole-genome sequencing and bioinformatics tools we had previously developed—like detectives trying to link the culprit parasite to the crime scene,” explained Arnab Pain, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia.
Sequencing and analysis of P falciparum DNA unveiled its origin by disclosing the single nucleotide polymorphisms that vary according to the geographical source of the strain.
The researchers used the nuclear DNA, as well as the one present in 2 organelles of the parasite—the mitochondrium and the apicoplast.
Both methods independently validated the origin of the parasite as West African, confirming the first case of artemisinin resistance mediated by a K13 gene mutation on the African continent.
“The spread of artemisinin resistance in Africa would be a major setback in the fight against malaria, as ACT [artemisinin-based combination therapy] is the only effective and widely used antimalarial treatment at the moment,” Dr Pain said. “Therefore, it is very important to regularly monitor artemisinin resistance worldwide.”
Oncolytic virus can eradicate MM in mice
Myxoma virus (MYXV), a nonhuman oncolytic agent, has demonstrated efficacy in mouse models of multiple myeloma (MM), according to research published in Molecular Therapy—Oncolytics.
MYXV significantly improved overall survival in mice with MM, providing a modest delay in disease progression for about two-thirds of the mice and completely eradicating the disease in a quarter of them.
“[W]e could actually get rid of disease, and it didn’t appear to ever come back,” said study author Eric C. Bartee, PhD, of the Medical University of South Carolina in Charleston.
For the past several years, Dr Bartee has been using MYXV to treat MM in cell culture. He and his colleagues previously showed that MYXV was able to kill human MM cells.
The team found that treatment with MYXV could eradicate MM cells in patient stem cell samples prior to transplant, thereby preventing relapse of MM.
In the current study, Dr Bartee and his colleagues took this one step further by assessing whether treatment with MYXV also has a benefit on disease outside the context of transplantation.
Using a mouse model of MM, the researchers showed that systemic treatment with MYXV reduced tumor burden and led to a modest decrease in disease progression (about 6 days) in 66% of mice.
In 25% of mice, there was complete eradication of disease with no evidence of relapse.
Since MYXV does not replicate in MM cells, the researchers postulated that eradication was caused by the host’s immune system. Investigation of the bone marrow showed that it was unaffected by treatment with MYXV.
This suggested that the immune system remained functional and could combat MM. Indeed, treatment with MYXV led to an increase in CD8+ T cells in the bone marrow, indicating a strong antitumor response.
The researchers noted that, although these results are promising, there are hurdles that must be overcome before this treatment can be brought to the clinic. One hurdle is large-scale production of clinical-grade virus. Another is demonstrating a high response rate.
“I think the major next question is ‘How do you get that response rate from 25% to 50% to 80% to 100%?’” Dr Bartee said. “How do you define the patients in which it works?”
Myxoma virus (MYXV), a nonhuman oncolytic agent, has demonstrated efficacy in mouse models of multiple myeloma (MM), according to research published in Molecular Therapy—Oncolytics.
MYXV significantly improved overall survival in mice with MM, providing a modest delay in disease progression for about two-thirds of the mice and completely eradicating the disease in a quarter of them.
“[W]e could actually get rid of disease, and it didn’t appear to ever come back,” said study author Eric C. Bartee, PhD, of the Medical University of South Carolina in Charleston.
For the past several years, Dr Bartee has been using MYXV to treat MM in cell culture. He and his colleagues previously showed that MYXV was able to kill human MM cells.
The team found that treatment with MYXV could eradicate MM cells in patient stem cell samples prior to transplant, thereby preventing relapse of MM.
In the current study, Dr Bartee and his colleagues took this one step further by assessing whether treatment with MYXV also has a benefit on disease outside the context of transplantation.
Using a mouse model of MM, the researchers showed that systemic treatment with MYXV reduced tumor burden and led to a modest decrease in disease progression (about 6 days) in 66% of mice.
In 25% of mice, there was complete eradication of disease with no evidence of relapse.
Since MYXV does not replicate in MM cells, the researchers postulated that eradication was caused by the host’s immune system. Investigation of the bone marrow showed that it was unaffected by treatment with MYXV.
This suggested that the immune system remained functional and could combat MM. Indeed, treatment with MYXV led to an increase in CD8+ T cells in the bone marrow, indicating a strong antitumor response.
The researchers noted that, although these results are promising, there are hurdles that must be overcome before this treatment can be brought to the clinic. One hurdle is large-scale production of clinical-grade virus. Another is demonstrating a high response rate.
“I think the major next question is ‘How do you get that response rate from 25% to 50% to 80% to 100%?’” Dr Bartee said. “How do you define the patients in which it works?”
Myxoma virus (MYXV), a nonhuman oncolytic agent, has demonstrated efficacy in mouse models of multiple myeloma (MM), according to research published in Molecular Therapy—Oncolytics.
MYXV significantly improved overall survival in mice with MM, providing a modest delay in disease progression for about two-thirds of the mice and completely eradicating the disease in a quarter of them.
“[W]e could actually get rid of disease, and it didn’t appear to ever come back,” said study author Eric C. Bartee, PhD, of the Medical University of South Carolina in Charleston.
For the past several years, Dr Bartee has been using MYXV to treat MM in cell culture. He and his colleagues previously showed that MYXV was able to kill human MM cells.
The team found that treatment with MYXV could eradicate MM cells in patient stem cell samples prior to transplant, thereby preventing relapse of MM.
In the current study, Dr Bartee and his colleagues took this one step further by assessing whether treatment with MYXV also has a benefit on disease outside the context of transplantation.
Using a mouse model of MM, the researchers showed that systemic treatment with MYXV reduced tumor burden and led to a modest decrease in disease progression (about 6 days) in 66% of mice.
In 25% of mice, there was complete eradication of disease with no evidence of relapse.
Since MYXV does not replicate in MM cells, the researchers postulated that eradication was caused by the host’s immune system. Investigation of the bone marrow showed that it was unaffected by treatment with MYXV.
This suggested that the immune system remained functional and could combat MM. Indeed, treatment with MYXV led to an increase in CD8+ T cells in the bone marrow, indicating a strong antitumor response.
The researchers noted that, although these results are promising, there are hurdles that must be overcome before this treatment can be brought to the clinic. One hurdle is large-scale production of clinical-grade virus. Another is demonstrating a high response rate.
“I think the major next question is ‘How do you get that response rate from 25% to 50% to 80% to 100%?’” Dr Bartee said. “How do you define the patients in which it works?”