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Dietary aluminum may trigger IBS
Aluminum ingested in small amounts causes visceral hypersensitivity in rats, suggesting that dietary levels of aluminum may trigger irritable bowel syndrome (IBS) in humans, according to a study published in Cellular and Molecular Gastroenterology and Hepatology.
Rats given oral aluminum exhibited dose-dependent visceral pain along with activation of proteinase-activated receptor-2 (PAR2) and mast cell degranulation, a combination of events that mirror clinical signs and molecular mechanisms of IBS in humans, reported lead author, Nicolas Esquerre, PhD, of Lille Inflammation Research International Center at Université Lille in France, and his colleagues. The study contributes to ongoing research surrounding causes and mechanisms of IBS, which may vary among patients because of disease subsets. These findings suggest that some patients with IBS may benefit from dietary aluminum restriction or chelation therapy.
“[T]he question of the initial trigger [of IBS] still remains unresolved,” the investigators wrote. “A more precise link between food and IBS has been demonstrated for gluten and other wheat proteins, lactose, and nickel, highlighting particular subsets of IBS patients now diagnosed as nonceliac gluten/wheat sensitivity, lactose intolerance, and nickel-allergic contact mucositis,” they added. “Here, we evaluated the effect of aluminum, a common contaminant of food and water, on abdominal pain.”
Aluminum may enter the diet as a food additive, or it may contaminate foods grown in aluminum-rich soil. Other sources of oral exposure include packaging and kitchenware. A previous study showed that most Americans ingest 0.01-1.4 mg/kg of aluminum daily, and 5% ingest 1.58 mg/kg daily (i.e., 95 mg per day for a 60-kg person).
Based on these statistics, rats in the present study received oral aluminum citrate (AlCi) corresponding with three doses of aluminum: 0.5 mg/kg, 1.5 mg/kg, or 3.0 mg/kg. Treatment continued for 30 days, with colorectal distension (CRD) measured on days 2, 4, 8, 15, and 30.
Results showed a dose-dependent relationship between aluminum ingestion and visceral hypersensitivity. Within 2 days, rats receiving 3.0 mg/kg of aluminum exhibited a significantly lower pain threshold, and within 8 days, rats receiving 0.5 mg/kg and 1.5 mg/kg also showed increased visceral hypersensitivity.
After 1 month of treatment, rats receiving 1.5 mg/kg per day demonstrated a 30% increase in pain compared with control animals. In the same group, visceral hypersensitivity began to wane 7 days after cessation of treatment; 4 more weeks were needed to return to baseline. When treatment was restarted, visceral hypersensitivity occurred within 2 days, compared with 8 days upon initial administration. These findings are particularly relevant to some people, as the 1.5-mg/kg dose corresponds with the daily amount of aluminum ingested by 5% of Americans. Similar patterns of response and sensitization were observed in rats ingesting 0.5 mg/kg and 3.0 mg/kg. Female rats were more sensitive to aluminum than were male rats, a sex pattern that mimics human IBS.
Further testing showed that rats treated with zinc citrate (ZnCi) did not exhibit changes to pain threshold, thereby excluding citrate as an aggravating factor. Rat models of noninflammatory and inflammatory colonic hypersensitivity (butyrate enema or intrathecal injection of 25%-50% ethanol in combination with 2,4,6-trinitrobenzenesulfonic acid, respectively) had visceral hypersensitivity similar to that of rats in the 1.5-mg/kg AlCi group.
Testing of colonic tissue from AlCi-treated rats did not reveal inflammatory changes according to a variety of qualifiers, including histology, myeloperoxidase activity, mRNA expression of several inflammatory cytokines, or infiltration of eosinophils or macrophages. Noninflammatory effects of aluminum, however, were found. For instance, treated rats had lower serotonin levels in enteroendocrine cells.
“Enteroendocrine cells are specialized epithelial cells that respond to luminal stimuli by releasing various biologically active compounds,” the investigators wrote. “They regulate several physiological and homeostatic functions of the gastrointestinal tract, such as postprandial secretion, motility, immune responses, and sensory functions. A reduced number of enteroendocrine cells has been observed in the duodenum, ileum, and colon of some patients with IBS.”
In addition to changes in enteroendocrine cells, AlCi-treated rats had greater colonic mast cell degranulation and histamine with upregulation of histidine decarboxylase transcripts, suggesting that aluminum activated mast cells.
To determine the role of mast cell activation in visceral hypersensitivity, rats were given AlCi with cromoglycate, an inhibitor of mast cell degranulation. This treatment reduced mast cell degranulation and visceral pain threshold, compared with AlCi-treated rats not receiving cromoglycate, suggesting that mast cell degranulation is a primary driver of visceral hypersensitivity. This observation was confirmed by a mast cell–deficient mouse strain (Kit W-sh/W-sh), that had a normal number of mast cells incapable of degranulation. Treating the mast cell–deficient mice with AlCi did not induce visceral hypersensitivity, thereby confirming the role of mast cell degranulation.
Along with mast cell degranulation, AlCi treatment led to PAR2 activation. Investigators explored the significance of this finding with PAR2 knockout mice. When treated with AlCi, PAR2 knockout mice showed no increase in visceral hypersensitivity, suggesting that hypersensitivity is dependent on PAR2 activation. Further testing revealed that mast cell–deficient mice (Kit W-sh/W-sh) did not have PAR2 upregulation either, connecting a sequence in which aluminum triggers mast cell degranulation, mast cell degranulation drives PAR2 upregulation, and PAR2 upregulation causes visceral hypersensitivity. The latter two events in this chain – mast cell degranulation and PAR2 upregulation – mirror molecular mechanisms of IBS in humans.
“We speculate that aluminum activates mast cells to release mediators that can increase excitability of nociceptive afferences contributing to the visceral pain phenotype,” the investigators wrote. “Taken together, our results linked aluminum to several mechanisms implicated in IBS pathophysiology, highlighting a possible role for aluminum as a triggering factor in IBS development.”
The investigators suggested that these findings could influence preventive or therapeutic strategies: “Aluminum might be the first identified dietary risk factor for IBS, implying that measures to limit aluminum dietary consumption or to chelate aluminum may represent novel pathways of prevention and treatment of IBS in some susceptible patients,” they wrote.
The study was funded by the European Fund for Regional Economic Development; the Hauts de France Region, Ministère de l’Enseignement Supérieur et de la Recherche (CPER IRENI); and Digestscience (European Research Foundation on Intestinal Diseases and Nutrition).
SOURCE: Esquerre N et al. Cell Mol Gastroenterol Hepatol. 2019 Sep 20. doi: 10.1016/j.jcmgh.2018.09.012.
Irritable bowel syndrome is a chronic functional gastrointestinal disorder, characterized by relapsing/remitting diarrhea, constipation, and visceral pain. IBS afflicts 10%-25% of the population in developed countries.
Despite histologically normal intestinal biopsy specimens, biological signatures of IBS include alterations in intestinal gene expression, increased gut permeability, and changes in gut microbiota composition. Thus, although the cause or causes of IBS are not defined, these and other data highlight the enormous breadth of factors that might play a role in this disorder. Similar alterations also are associated with inflammatory bowel disease (IBD), although the magnitude of changes is typically greater in IBD. Nevertheless, these data suggest that IBS and IBD may share triggers and pathogenetic mechanisms. That prevalence of both IBS and IBD have shown marked increases in incidence, roughly paralleling the modernization of society that accelerated in the mid-20th century, raises the possibility that environmental factors associated with human activity may be a driver of both diseases. Recent findings suggest that aluminum may be one such trigger. While humans have always been exposed to aluminum, the most abundant metal on earth, industrialization has increased the magnitude of exposure owing to the use of aluminum salts as stabilizers in processed foods and the concentration of ground water aluminum in agricultural products. Mimicking estimated average human ingestion of aluminum via administering it orally to rats increases their perception of visceral pain. These results suggest a possible role for increased exposure to aluminum in driving the post–mid-20th-century increased incidence of IBS. Unfortunately, only broad societal estimates of aluminum exposure are available, and aluminum levels are difficult to measure in individuals, making it difficult to epidemiologically investigate the role of aluminum in promoting GI disease in humans. Hence, I submit that levels of aluminum ingestion by humans should be more closely monitored and the potential of aluminum to promote GI disease carefully scrutinized.
Andrew Ted Gewirtz, PhD, distinguished university center professor, Georgia State University’s Institute for Biomedical Sciences’ Center for Inflammation, Immunity and Infection, Atlanta.
Irritable bowel syndrome is a chronic functional gastrointestinal disorder, characterized by relapsing/remitting diarrhea, constipation, and visceral pain. IBS afflicts 10%-25% of the population in developed countries.
Despite histologically normal intestinal biopsy specimens, biological signatures of IBS include alterations in intestinal gene expression, increased gut permeability, and changes in gut microbiota composition. Thus, although the cause or causes of IBS are not defined, these and other data highlight the enormous breadth of factors that might play a role in this disorder. Similar alterations also are associated with inflammatory bowel disease (IBD), although the magnitude of changes is typically greater in IBD. Nevertheless, these data suggest that IBS and IBD may share triggers and pathogenetic mechanisms. That prevalence of both IBS and IBD have shown marked increases in incidence, roughly paralleling the modernization of society that accelerated in the mid-20th century, raises the possibility that environmental factors associated with human activity may be a driver of both diseases. Recent findings suggest that aluminum may be one such trigger. While humans have always been exposed to aluminum, the most abundant metal on earth, industrialization has increased the magnitude of exposure owing to the use of aluminum salts as stabilizers in processed foods and the concentration of ground water aluminum in agricultural products. Mimicking estimated average human ingestion of aluminum via administering it orally to rats increases their perception of visceral pain. These results suggest a possible role for increased exposure to aluminum in driving the post–mid-20th-century increased incidence of IBS. Unfortunately, only broad societal estimates of aluminum exposure are available, and aluminum levels are difficult to measure in individuals, making it difficult to epidemiologically investigate the role of aluminum in promoting GI disease in humans. Hence, I submit that levels of aluminum ingestion by humans should be more closely monitored and the potential of aluminum to promote GI disease carefully scrutinized.
Andrew Ted Gewirtz, PhD, distinguished university center professor, Georgia State University’s Institute for Biomedical Sciences’ Center for Inflammation, Immunity and Infection, Atlanta.
Irritable bowel syndrome is a chronic functional gastrointestinal disorder, characterized by relapsing/remitting diarrhea, constipation, and visceral pain. IBS afflicts 10%-25% of the population in developed countries.
Despite histologically normal intestinal biopsy specimens, biological signatures of IBS include alterations in intestinal gene expression, increased gut permeability, and changes in gut microbiota composition. Thus, although the cause or causes of IBS are not defined, these and other data highlight the enormous breadth of factors that might play a role in this disorder. Similar alterations also are associated with inflammatory bowel disease (IBD), although the magnitude of changes is typically greater in IBD. Nevertheless, these data suggest that IBS and IBD may share triggers and pathogenetic mechanisms. That prevalence of both IBS and IBD have shown marked increases in incidence, roughly paralleling the modernization of society that accelerated in the mid-20th century, raises the possibility that environmental factors associated with human activity may be a driver of both diseases. Recent findings suggest that aluminum may be one such trigger. While humans have always been exposed to aluminum, the most abundant metal on earth, industrialization has increased the magnitude of exposure owing to the use of aluminum salts as stabilizers in processed foods and the concentration of ground water aluminum in agricultural products. Mimicking estimated average human ingestion of aluminum via administering it orally to rats increases their perception of visceral pain. These results suggest a possible role for increased exposure to aluminum in driving the post–mid-20th-century increased incidence of IBS. Unfortunately, only broad societal estimates of aluminum exposure are available, and aluminum levels are difficult to measure in individuals, making it difficult to epidemiologically investigate the role of aluminum in promoting GI disease in humans. Hence, I submit that levels of aluminum ingestion by humans should be more closely monitored and the potential of aluminum to promote GI disease carefully scrutinized.
Andrew Ted Gewirtz, PhD, distinguished university center professor, Georgia State University’s Institute for Biomedical Sciences’ Center for Inflammation, Immunity and Infection, Atlanta.
Aluminum ingested in small amounts causes visceral hypersensitivity in rats, suggesting that dietary levels of aluminum may trigger irritable bowel syndrome (IBS) in humans, according to a study published in Cellular and Molecular Gastroenterology and Hepatology.
Rats given oral aluminum exhibited dose-dependent visceral pain along with activation of proteinase-activated receptor-2 (PAR2) and mast cell degranulation, a combination of events that mirror clinical signs and molecular mechanisms of IBS in humans, reported lead author, Nicolas Esquerre, PhD, of Lille Inflammation Research International Center at Université Lille in France, and his colleagues. The study contributes to ongoing research surrounding causes and mechanisms of IBS, which may vary among patients because of disease subsets. These findings suggest that some patients with IBS may benefit from dietary aluminum restriction or chelation therapy.
“[T]he question of the initial trigger [of IBS] still remains unresolved,” the investigators wrote. “A more precise link between food and IBS has been demonstrated for gluten and other wheat proteins, lactose, and nickel, highlighting particular subsets of IBS patients now diagnosed as nonceliac gluten/wheat sensitivity, lactose intolerance, and nickel-allergic contact mucositis,” they added. “Here, we evaluated the effect of aluminum, a common contaminant of food and water, on abdominal pain.”
Aluminum may enter the diet as a food additive, or it may contaminate foods grown in aluminum-rich soil. Other sources of oral exposure include packaging and kitchenware. A previous study showed that most Americans ingest 0.01-1.4 mg/kg of aluminum daily, and 5% ingest 1.58 mg/kg daily (i.e., 95 mg per day for a 60-kg person).
Based on these statistics, rats in the present study received oral aluminum citrate (AlCi) corresponding with three doses of aluminum: 0.5 mg/kg, 1.5 mg/kg, or 3.0 mg/kg. Treatment continued for 30 days, with colorectal distension (CRD) measured on days 2, 4, 8, 15, and 30.
Results showed a dose-dependent relationship between aluminum ingestion and visceral hypersensitivity. Within 2 days, rats receiving 3.0 mg/kg of aluminum exhibited a significantly lower pain threshold, and within 8 days, rats receiving 0.5 mg/kg and 1.5 mg/kg also showed increased visceral hypersensitivity.
After 1 month of treatment, rats receiving 1.5 mg/kg per day demonstrated a 30% increase in pain compared with control animals. In the same group, visceral hypersensitivity began to wane 7 days after cessation of treatment; 4 more weeks were needed to return to baseline. When treatment was restarted, visceral hypersensitivity occurred within 2 days, compared with 8 days upon initial administration. These findings are particularly relevant to some people, as the 1.5-mg/kg dose corresponds with the daily amount of aluminum ingested by 5% of Americans. Similar patterns of response and sensitization were observed in rats ingesting 0.5 mg/kg and 3.0 mg/kg. Female rats were more sensitive to aluminum than were male rats, a sex pattern that mimics human IBS.
Further testing showed that rats treated with zinc citrate (ZnCi) did not exhibit changes to pain threshold, thereby excluding citrate as an aggravating factor. Rat models of noninflammatory and inflammatory colonic hypersensitivity (butyrate enema or intrathecal injection of 25%-50% ethanol in combination with 2,4,6-trinitrobenzenesulfonic acid, respectively) had visceral hypersensitivity similar to that of rats in the 1.5-mg/kg AlCi group.
Testing of colonic tissue from AlCi-treated rats did not reveal inflammatory changes according to a variety of qualifiers, including histology, myeloperoxidase activity, mRNA expression of several inflammatory cytokines, or infiltration of eosinophils or macrophages. Noninflammatory effects of aluminum, however, were found. For instance, treated rats had lower serotonin levels in enteroendocrine cells.
“Enteroendocrine cells are specialized epithelial cells that respond to luminal stimuli by releasing various biologically active compounds,” the investigators wrote. “They regulate several physiological and homeostatic functions of the gastrointestinal tract, such as postprandial secretion, motility, immune responses, and sensory functions. A reduced number of enteroendocrine cells has been observed in the duodenum, ileum, and colon of some patients with IBS.”
In addition to changes in enteroendocrine cells, AlCi-treated rats had greater colonic mast cell degranulation and histamine with upregulation of histidine decarboxylase transcripts, suggesting that aluminum activated mast cells.
To determine the role of mast cell activation in visceral hypersensitivity, rats were given AlCi with cromoglycate, an inhibitor of mast cell degranulation. This treatment reduced mast cell degranulation and visceral pain threshold, compared with AlCi-treated rats not receiving cromoglycate, suggesting that mast cell degranulation is a primary driver of visceral hypersensitivity. This observation was confirmed by a mast cell–deficient mouse strain (Kit W-sh/W-sh), that had a normal number of mast cells incapable of degranulation. Treating the mast cell–deficient mice with AlCi did not induce visceral hypersensitivity, thereby confirming the role of mast cell degranulation.
Along with mast cell degranulation, AlCi treatment led to PAR2 activation. Investigators explored the significance of this finding with PAR2 knockout mice. When treated with AlCi, PAR2 knockout mice showed no increase in visceral hypersensitivity, suggesting that hypersensitivity is dependent on PAR2 activation. Further testing revealed that mast cell–deficient mice (Kit W-sh/W-sh) did not have PAR2 upregulation either, connecting a sequence in which aluminum triggers mast cell degranulation, mast cell degranulation drives PAR2 upregulation, and PAR2 upregulation causes visceral hypersensitivity. The latter two events in this chain – mast cell degranulation and PAR2 upregulation – mirror molecular mechanisms of IBS in humans.
“We speculate that aluminum activates mast cells to release mediators that can increase excitability of nociceptive afferences contributing to the visceral pain phenotype,” the investigators wrote. “Taken together, our results linked aluminum to several mechanisms implicated in IBS pathophysiology, highlighting a possible role for aluminum as a triggering factor in IBS development.”
The investigators suggested that these findings could influence preventive or therapeutic strategies: “Aluminum might be the first identified dietary risk factor for IBS, implying that measures to limit aluminum dietary consumption or to chelate aluminum may represent novel pathways of prevention and treatment of IBS in some susceptible patients,” they wrote.
The study was funded by the European Fund for Regional Economic Development; the Hauts de France Region, Ministère de l’Enseignement Supérieur et de la Recherche (CPER IRENI); and Digestscience (European Research Foundation on Intestinal Diseases and Nutrition).
SOURCE: Esquerre N et al. Cell Mol Gastroenterol Hepatol. 2019 Sep 20. doi: 10.1016/j.jcmgh.2018.09.012.
Aluminum ingested in small amounts causes visceral hypersensitivity in rats, suggesting that dietary levels of aluminum may trigger irritable bowel syndrome (IBS) in humans, according to a study published in Cellular and Molecular Gastroenterology and Hepatology.
Rats given oral aluminum exhibited dose-dependent visceral pain along with activation of proteinase-activated receptor-2 (PAR2) and mast cell degranulation, a combination of events that mirror clinical signs and molecular mechanisms of IBS in humans, reported lead author, Nicolas Esquerre, PhD, of Lille Inflammation Research International Center at Université Lille in France, and his colleagues. The study contributes to ongoing research surrounding causes and mechanisms of IBS, which may vary among patients because of disease subsets. These findings suggest that some patients with IBS may benefit from dietary aluminum restriction or chelation therapy.
“[T]he question of the initial trigger [of IBS] still remains unresolved,” the investigators wrote. “A more precise link between food and IBS has been demonstrated for gluten and other wheat proteins, lactose, and nickel, highlighting particular subsets of IBS patients now diagnosed as nonceliac gluten/wheat sensitivity, lactose intolerance, and nickel-allergic contact mucositis,” they added. “Here, we evaluated the effect of aluminum, a common contaminant of food and water, on abdominal pain.”
Aluminum may enter the diet as a food additive, or it may contaminate foods grown in aluminum-rich soil. Other sources of oral exposure include packaging and kitchenware. A previous study showed that most Americans ingest 0.01-1.4 mg/kg of aluminum daily, and 5% ingest 1.58 mg/kg daily (i.e., 95 mg per day for a 60-kg person).
Based on these statistics, rats in the present study received oral aluminum citrate (AlCi) corresponding with three doses of aluminum: 0.5 mg/kg, 1.5 mg/kg, or 3.0 mg/kg. Treatment continued for 30 days, with colorectal distension (CRD) measured on days 2, 4, 8, 15, and 30.
Results showed a dose-dependent relationship between aluminum ingestion and visceral hypersensitivity. Within 2 days, rats receiving 3.0 mg/kg of aluminum exhibited a significantly lower pain threshold, and within 8 days, rats receiving 0.5 mg/kg and 1.5 mg/kg also showed increased visceral hypersensitivity.
After 1 month of treatment, rats receiving 1.5 mg/kg per day demonstrated a 30% increase in pain compared with control animals. In the same group, visceral hypersensitivity began to wane 7 days after cessation of treatment; 4 more weeks were needed to return to baseline. When treatment was restarted, visceral hypersensitivity occurred within 2 days, compared with 8 days upon initial administration. These findings are particularly relevant to some people, as the 1.5-mg/kg dose corresponds with the daily amount of aluminum ingested by 5% of Americans. Similar patterns of response and sensitization were observed in rats ingesting 0.5 mg/kg and 3.0 mg/kg. Female rats were more sensitive to aluminum than were male rats, a sex pattern that mimics human IBS.
Further testing showed that rats treated with zinc citrate (ZnCi) did not exhibit changes to pain threshold, thereby excluding citrate as an aggravating factor. Rat models of noninflammatory and inflammatory colonic hypersensitivity (butyrate enema or intrathecal injection of 25%-50% ethanol in combination with 2,4,6-trinitrobenzenesulfonic acid, respectively) had visceral hypersensitivity similar to that of rats in the 1.5-mg/kg AlCi group.
Testing of colonic tissue from AlCi-treated rats did not reveal inflammatory changes according to a variety of qualifiers, including histology, myeloperoxidase activity, mRNA expression of several inflammatory cytokines, or infiltration of eosinophils or macrophages. Noninflammatory effects of aluminum, however, were found. For instance, treated rats had lower serotonin levels in enteroendocrine cells.
“Enteroendocrine cells are specialized epithelial cells that respond to luminal stimuli by releasing various biologically active compounds,” the investigators wrote. “They regulate several physiological and homeostatic functions of the gastrointestinal tract, such as postprandial secretion, motility, immune responses, and sensory functions. A reduced number of enteroendocrine cells has been observed in the duodenum, ileum, and colon of some patients with IBS.”
In addition to changes in enteroendocrine cells, AlCi-treated rats had greater colonic mast cell degranulation and histamine with upregulation of histidine decarboxylase transcripts, suggesting that aluminum activated mast cells.
To determine the role of mast cell activation in visceral hypersensitivity, rats were given AlCi with cromoglycate, an inhibitor of mast cell degranulation. This treatment reduced mast cell degranulation and visceral pain threshold, compared with AlCi-treated rats not receiving cromoglycate, suggesting that mast cell degranulation is a primary driver of visceral hypersensitivity. This observation was confirmed by a mast cell–deficient mouse strain (Kit W-sh/W-sh), that had a normal number of mast cells incapable of degranulation. Treating the mast cell–deficient mice with AlCi did not induce visceral hypersensitivity, thereby confirming the role of mast cell degranulation.
Along with mast cell degranulation, AlCi treatment led to PAR2 activation. Investigators explored the significance of this finding with PAR2 knockout mice. When treated with AlCi, PAR2 knockout mice showed no increase in visceral hypersensitivity, suggesting that hypersensitivity is dependent on PAR2 activation. Further testing revealed that mast cell–deficient mice (Kit W-sh/W-sh) did not have PAR2 upregulation either, connecting a sequence in which aluminum triggers mast cell degranulation, mast cell degranulation drives PAR2 upregulation, and PAR2 upregulation causes visceral hypersensitivity. The latter two events in this chain – mast cell degranulation and PAR2 upregulation – mirror molecular mechanisms of IBS in humans.
“We speculate that aluminum activates mast cells to release mediators that can increase excitability of nociceptive afferences contributing to the visceral pain phenotype,” the investigators wrote. “Taken together, our results linked aluminum to several mechanisms implicated in IBS pathophysiology, highlighting a possible role for aluminum as a triggering factor in IBS development.”
The investigators suggested that these findings could influence preventive or therapeutic strategies: “Aluminum might be the first identified dietary risk factor for IBS, implying that measures to limit aluminum dietary consumption or to chelate aluminum may represent novel pathways of prevention and treatment of IBS in some susceptible patients,” they wrote.
The study was funded by the European Fund for Regional Economic Development; the Hauts de France Region, Ministère de l’Enseignement Supérieur et de la Recherche (CPER IRENI); and Digestscience (European Research Foundation on Intestinal Diseases and Nutrition).
SOURCE: Esquerre N et al. Cell Mol Gastroenterol Hepatol. 2019 Sep 20. doi: 10.1016/j.jcmgh.2018.09.012.
FROM CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
Key clinical point: Aluminum ingestion triggers visceral hypersensitivity in rats, suggesting that dietary levels of aluminum may contribute to development of irritable bowel syndrome in humans.
Major finding: In rodents, 1 month of oral aluminum administration led to a 30% increase in pain during colorectal distension, compared with control subjects.
Study details: A rodent study including noninflammatory and inflammatory IBS rat models, mast cell–deficient mice, and PAR2 knockout mice.
Disclosures: The study was funded by the European Fund for Regional Economic Development; the Hauts de France Region, Ministère de l’Enseignement Supérieur et de la Recherche (CPER IRENI); and Digestscience (European Research Foundation on Intestinal Diseases and Nutrition).
Source: Esquerre N et al. Cell Mol Gastroenterol Hepatol. 2019 Sep 20. doi: 10.1016/j.jcmgh.2018.09.012.
Anti-TNFs slow SIJ damage in early axial spondyloarthritis
Long-term anti–tumor necrosis factor therapy seemed to slow progression of sacroiliac joint damage in early axial spondyloarthritis in a German study of 42 patients.
They were all part of the ESTHER trial, which found that in early axial spondyloarthritis (axSpA), active inflammatory lesions on MRI improved significantly more with etanercept (Enbrel) than with sulfasalazine-treated patients (Ann Rheum Dis. 2011 Apr 1;70[4]:590-6).
In the new work, published in the Arthritis & Rheumatology, investigators reviewed 42 ESTHER subjects who were on etanercept for up to 6 years and who also had baseline and at least one bilateral sacroiliac joint (SIJ) x-ray at 2-, 4-, or 6-year follow-up. Two blinded readers scored the x-rays, and a sacroiliitis sum score was assigned to each subject. The sum score ranged from 0, meaning no signs of sacroiliitis, to 8, meaning total ankylosis of both SIJs.
The mean progression in sacroiliitis sum score was 0.13 points from baseline to 2 years; followed by a regression of –0.27 points during years 2-4, and –0.09 points from years 4-6. There was no comparator group of untreated patients, but the authors noted that previous work would suggest a slight, but detectable, progression in joint damage over that time.
Elevated C-reactive protein and the presence of osteitis on MRI, meanwhile, were independently associated with progression.
“This is the first study to analyze the long-term (up to 6 years) progression of radiographic sacroiliitis in patients with axSpA treated with an anti-TNF agent, in this case with etanercept. Our results suggest that long-term treatment with a potent anti-inflammatory drug like a TNF inhibitor may influence the evolution of the disease by decelerating the radiographic progression of SIJ [damage] in patients with” early axSpA, wrote the investigators, led by Valeria Rios Rodriguez, MD, of the Charité Universitätsmedizin, Berlin.
Progression from nonradiographic to radiographic axSpA occurred only in the first 2 years of treatment, among 5 of 27 patients, while 2 of 15 patients who started with radiographic disease regressed to nonradiographic axSpA, yielding a net progression of 7.1%.
Although that’s higher than what’s been reported in previous studies, it might be related to greater inflammation in the SIJ at baseline in ESTHER, since active osteitis on MRI was an inclusion criteria. Also, “treatment with a TNF inhibitor ... might have triggered a faster bone repair visible on x-rays as a progression of structural damage,” the investigators said.
The results seem “congruent with the retardation of the spine progression seen in [ankylosing spondylitis] patients treated long-term with TNF inhibitors. ... Long-term treatment with TNF inhibitors could reduce ... new bone formation by preventing the development of new inflammatory lesions resulting in structural damage” of the SIJ, they said, which, in turn, “might have an impact on the functional status and spinal mobility in patients with axSpA, independently of structural damage of the spine.”
Two-thirds of the trial participants were men; the mean age was 34 years, and mean duration of symptoms 3.1 years at baseline. No information was reported on adverse events.
The work was funded by Pfizer, a marketer of etanercept. Some of the investigators disclosed consulting and other payments from the company, as well as other companies involved in marketing and/or development of drugs for axSpA. One investigator was an employee of Pfizer.
SOURCE: Rios Rodriguez V et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40786
Long-term anti–tumor necrosis factor therapy seemed to slow progression of sacroiliac joint damage in early axial spondyloarthritis in a German study of 42 patients.
They were all part of the ESTHER trial, which found that in early axial spondyloarthritis (axSpA), active inflammatory lesions on MRI improved significantly more with etanercept (Enbrel) than with sulfasalazine-treated patients (Ann Rheum Dis. 2011 Apr 1;70[4]:590-6).
In the new work, published in the Arthritis & Rheumatology, investigators reviewed 42 ESTHER subjects who were on etanercept for up to 6 years and who also had baseline and at least one bilateral sacroiliac joint (SIJ) x-ray at 2-, 4-, or 6-year follow-up. Two blinded readers scored the x-rays, and a sacroiliitis sum score was assigned to each subject. The sum score ranged from 0, meaning no signs of sacroiliitis, to 8, meaning total ankylosis of both SIJs.
The mean progression in sacroiliitis sum score was 0.13 points from baseline to 2 years; followed by a regression of –0.27 points during years 2-4, and –0.09 points from years 4-6. There was no comparator group of untreated patients, but the authors noted that previous work would suggest a slight, but detectable, progression in joint damage over that time.
Elevated C-reactive protein and the presence of osteitis on MRI, meanwhile, were independently associated with progression.
“This is the first study to analyze the long-term (up to 6 years) progression of radiographic sacroiliitis in patients with axSpA treated with an anti-TNF agent, in this case with etanercept. Our results suggest that long-term treatment with a potent anti-inflammatory drug like a TNF inhibitor may influence the evolution of the disease by decelerating the radiographic progression of SIJ [damage] in patients with” early axSpA, wrote the investigators, led by Valeria Rios Rodriguez, MD, of the Charité Universitätsmedizin, Berlin.
Progression from nonradiographic to radiographic axSpA occurred only in the first 2 years of treatment, among 5 of 27 patients, while 2 of 15 patients who started with radiographic disease regressed to nonradiographic axSpA, yielding a net progression of 7.1%.
Although that’s higher than what’s been reported in previous studies, it might be related to greater inflammation in the SIJ at baseline in ESTHER, since active osteitis on MRI was an inclusion criteria. Also, “treatment with a TNF inhibitor ... might have triggered a faster bone repair visible on x-rays as a progression of structural damage,” the investigators said.
The results seem “congruent with the retardation of the spine progression seen in [ankylosing spondylitis] patients treated long-term with TNF inhibitors. ... Long-term treatment with TNF inhibitors could reduce ... new bone formation by preventing the development of new inflammatory lesions resulting in structural damage” of the SIJ, they said, which, in turn, “might have an impact on the functional status and spinal mobility in patients with axSpA, independently of structural damage of the spine.”
Two-thirds of the trial participants were men; the mean age was 34 years, and mean duration of symptoms 3.1 years at baseline. No information was reported on adverse events.
The work was funded by Pfizer, a marketer of etanercept. Some of the investigators disclosed consulting and other payments from the company, as well as other companies involved in marketing and/or development of drugs for axSpA. One investigator was an employee of Pfizer.
SOURCE: Rios Rodriguez V et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40786
Long-term anti–tumor necrosis factor therapy seemed to slow progression of sacroiliac joint damage in early axial spondyloarthritis in a German study of 42 patients.
They were all part of the ESTHER trial, which found that in early axial spondyloarthritis (axSpA), active inflammatory lesions on MRI improved significantly more with etanercept (Enbrel) than with sulfasalazine-treated patients (Ann Rheum Dis. 2011 Apr 1;70[4]:590-6).
In the new work, published in the Arthritis & Rheumatology, investigators reviewed 42 ESTHER subjects who were on etanercept for up to 6 years and who also had baseline and at least one bilateral sacroiliac joint (SIJ) x-ray at 2-, 4-, or 6-year follow-up. Two blinded readers scored the x-rays, and a sacroiliitis sum score was assigned to each subject. The sum score ranged from 0, meaning no signs of sacroiliitis, to 8, meaning total ankylosis of both SIJs.
The mean progression in sacroiliitis sum score was 0.13 points from baseline to 2 years; followed by a regression of –0.27 points during years 2-4, and –0.09 points from years 4-6. There was no comparator group of untreated patients, but the authors noted that previous work would suggest a slight, but detectable, progression in joint damage over that time.
Elevated C-reactive protein and the presence of osteitis on MRI, meanwhile, were independently associated with progression.
“This is the first study to analyze the long-term (up to 6 years) progression of radiographic sacroiliitis in patients with axSpA treated with an anti-TNF agent, in this case with etanercept. Our results suggest that long-term treatment with a potent anti-inflammatory drug like a TNF inhibitor may influence the evolution of the disease by decelerating the radiographic progression of SIJ [damage] in patients with” early axSpA, wrote the investigators, led by Valeria Rios Rodriguez, MD, of the Charité Universitätsmedizin, Berlin.
Progression from nonradiographic to radiographic axSpA occurred only in the first 2 years of treatment, among 5 of 27 patients, while 2 of 15 patients who started with radiographic disease regressed to nonradiographic axSpA, yielding a net progression of 7.1%.
Although that’s higher than what’s been reported in previous studies, it might be related to greater inflammation in the SIJ at baseline in ESTHER, since active osteitis on MRI was an inclusion criteria. Also, “treatment with a TNF inhibitor ... might have triggered a faster bone repair visible on x-rays as a progression of structural damage,” the investigators said.
The results seem “congruent with the retardation of the spine progression seen in [ankylosing spondylitis] patients treated long-term with TNF inhibitors. ... Long-term treatment with TNF inhibitors could reduce ... new bone formation by preventing the development of new inflammatory lesions resulting in structural damage” of the SIJ, they said, which, in turn, “might have an impact on the functional status and spinal mobility in patients with axSpA, independently of structural damage of the spine.”
Two-thirds of the trial participants were men; the mean age was 34 years, and mean duration of symptoms 3.1 years at baseline. No information was reported on adverse events.
The work was funded by Pfizer, a marketer of etanercept. Some of the investigators disclosed consulting and other payments from the company, as well as other companies involved in marketing and/or development of drugs for axSpA. One investigator was an employee of Pfizer.
SOURCE: Rios Rodriguez V et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40786
FROM ARTHRITIS & RHEUMATOLOGY
Key clinical point:
Major finding: The mean progression in sacroiliitis sum score was 0.13 points from baseline to 2 years; followed by a regression of –0.27 points during years 2-4, and –0.09 points from years 4-6.
Study details: Review of 42 patients with early disease.
Disclosures: The work was funded by Pfizer, a marketer of etanercept. Some of the investigators disclosed consulting and other payments from the company, as well as other companies involved in marketing and/or development of drugs for axSpA. One investigator was an employee of Pfizer.
Source: Rios Rodriguez V et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40786
Clinical trial: AVATaR studies pulmonary complications following robotic surgery
A trial is underway to assess the incidence of postoperative pulmonary complications in patients undergoing and to study current practices of mechanical ventilation and the potential link between ventilatory parameters and postoperative pulmonary complications.
The Assessment of Ventilatory Management During General Anesthesia for Robotic Surgery (AVATaR) trial is an international observational, prospective study involving more than a dozen institutions in the United States and elsewhere, with the goal of eventually recruiting 40-50 institutions worldwide. Enrollment of consecutive patients undergoing mechanical ventilation for robotic surgery is ongoing. Exclusions are pregnant patients and those procedures not carried out in the OR.
A predefined composite of pulmonary complications was the primary outcome measured. These predefined complications are recorded regularly from medical chart until the first 5 postoperative days, discharge from hospital, or death, whatever comes first.
For full details and recruitment information on the AVATaR study (NCT02989415), go to clinicaltrials.gov.
A trial is underway to assess the incidence of postoperative pulmonary complications in patients undergoing and to study current practices of mechanical ventilation and the potential link between ventilatory parameters and postoperative pulmonary complications.
The Assessment of Ventilatory Management During General Anesthesia for Robotic Surgery (AVATaR) trial is an international observational, prospective study involving more than a dozen institutions in the United States and elsewhere, with the goal of eventually recruiting 40-50 institutions worldwide. Enrollment of consecutive patients undergoing mechanical ventilation for robotic surgery is ongoing. Exclusions are pregnant patients and those procedures not carried out in the OR.
A predefined composite of pulmonary complications was the primary outcome measured. These predefined complications are recorded regularly from medical chart until the first 5 postoperative days, discharge from hospital, or death, whatever comes first.
For full details and recruitment information on the AVATaR study (NCT02989415), go to clinicaltrials.gov.
A trial is underway to assess the incidence of postoperative pulmonary complications in patients undergoing and to study current practices of mechanical ventilation and the potential link between ventilatory parameters and postoperative pulmonary complications.
The Assessment of Ventilatory Management During General Anesthesia for Robotic Surgery (AVATaR) trial is an international observational, prospective study involving more than a dozen institutions in the United States and elsewhere, with the goal of eventually recruiting 40-50 institutions worldwide. Enrollment of consecutive patients undergoing mechanical ventilation for robotic surgery is ongoing. Exclusions are pregnant patients and those procedures not carried out in the OR.
A predefined composite of pulmonary complications was the primary outcome measured. These predefined complications are recorded regularly from medical chart until the first 5 postoperative days, discharge from hospital, or death, whatever comes first.
For full details and recruitment information on the AVATaR study (NCT02989415), go to clinicaltrials.gov.
HDL-P subfractions may be prognostic in heart failure
In heart failure, derangements in HDL cholesterol particle (HDL-P) subfractions have prognostic implications beyond those of conventional cardiovascular risk factors, according to investigators who analyzed plasma samples from more than 6,500 patients.
The study revealed derangements that were shared and more severe in heart failure with reduced ejection fraction (HFrEF) as compared to heart failure with preserved ejection fraction (HFpEF), according to the researchers, who said their study is the largest to date of HDL-P subfractions in heart failure.
Both total HDL-P and small HDL-P had a strong inverse association with adverse outcomes, consistent with the conclusions of previous studies, they said in a report on their study in the Journal of the American College of Cardiology.
“Altogether, our findings support total and small HDL-P as important markers of residual risk in both HFrEF and HFpEF,” said the investigators, led by Wynn G. Hunter, MD, of Duke University, Durham, N.C.
Dr. Hunter and colleagues used the CATHGEN (Catheterization Genetics) biorepository to identify plasma samples obtained at catheterization for 782 patients with HFrEF, 1,004 with HFpEF, and 4,742 with no heart failure.
Lipoprotein profiling of the samples revealed that mean HDL-P size was greater in HFrEF than in HFpEF, and in both of those cases, mean HDL-P size was greater than in patients with no heart failure (P less than .0001), investigators reported.
Concentrations of small HDL-P and total HDL-P were by contrast lower in HFrEF versus HFpEF, and again, the values for both HFrEF and HFpEF were lower than in patients without heart failure (P less than .0001), they added.
Small HDL-P and total HDL-P had an inverse association with time to adverse events and all-cause mortality for both the HFrEF and HFpEF groups, according to investigators, who said those links remained robust even after multivariate adjustment for 14 cardiovascular risk factors, including diabetes, LDL particle, and GlycA, a marker of inflammation.
For example, small HDL-P and total HDL-P were inversely associated with all-cause mortality risk, with adjusted hazard ratios of 0.69-0.79 (P less than .0001), they reported. Similarly, a greater mean HDL-P size was associated with increased risk of all-cause mortality, yielding adjusted hazard ratios of 1.23-1.46 (P less than .0001).
Further studies are needed to clarify the role of HDL-P in the pathophysiology of heart failure, and to identify treatments that might increase total and small HDL-P in heart failure patients, Dr. Hunter and coauthors concluded.
Dr. Hunter reported no disclosures related to the study. Coauthors provided disclosures related to Amgen, Ostuka, Roche Diagnostics, Novartis, Trevena, Singulex, Medtronic, AstraZeneca, Bristol-Myers Squibb, Janssen, Portola, Boston Scientific, Gilead, GlaxoSmithKline, Merck, Alnylam, Ikaria Pharmaceuticals, Pfizer, Philips, LipoScience, and Pfizer, among others.
SOURCE: Hunter WG et al. J Am Coll Cardiol. 2019 Jan 22;73(2):177-86.
Although the study by Dr. Hunter and colleagues confirms the role of HDL cholesterol and HDL-P subfractions in heart failure, the immediate clinical implications of their findings are uncertain.
However, clinical use as a biomarker remains a “distant vision,” in part because a useful biomarker must be proven to provide an incremental benefit in terms of reducing disease-associated morbidity or mortality.
Even so, the present study could begin to inform future therapeutic studies looking at increasing specific HDL-P subfractions, rather than increasing HDL cholesterol across the board.
“Perhaps, this study will possibly serve to spur investigation into therapies designed to reduce derangements of [HDL cholesterol] metabolism and primarily target HDL-P as a regulator molecule, a promise that may keep the HDL story alive into the near future of scientific excursion.”
These comments were taken from an accompanying editorial by Hector O. Ventura, MD, and Carl J. Lavie, MD, of the University of Queensland Ochsner Clinical School, Brisbane, Australia, and New Orleans; and Mandeep R. Mehra, MD, of the Center of Advanced Heart Disease, Harvard University, Boston (J Am Coll Cardiol 2019 Jan 22;73[2]:187-9). Dr. Mehra reported that he is a consultant for Abbott, Medtronic, nupulseCV, Portola, Bayer, and FineHeart.
Although the study by Dr. Hunter and colleagues confirms the role of HDL cholesterol and HDL-P subfractions in heart failure, the immediate clinical implications of their findings are uncertain.
However, clinical use as a biomarker remains a “distant vision,” in part because a useful biomarker must be proven to provide an incremental benefit in terms of reducing disease-associated morbidity or mortality.
Even so, the present study could begin to inform future therapeutic studies looking at increasing specific HDL-P subfractions, rather than increasing HDL cholesterol across the board.
“Perhaps, this study will possibly serve to spur investigation into therapies designed to reduce derangements of [HDL cholesterol] metabolism and primarily target HDL-P as a regulator molecule, a promise that may keep the HDL story alive into the near future of scientific excursion.”
These comments were taken from an accompanying editorial by Hector O. Ventura, MD, and Carl J. Lavie, MD, of the University of Queensland Ochsner Clinical School, Brisbane, Australia, and New Orleans; and Mandeep R. Mehra, MD, of the Center of Advanced Heart Disease, Harvard University, Boston (J Am Coll Cardiol 2019 Jan 22;73[2]:187-9). Dr. Mehra reported that he is a consultant for Abbott, Medtronic, nupulseCV, Portola, Bayer, and FineHeart.
Although the study by Dr. Hunter and colleagues confirms the role of HDL cholesterol and HDL-P subfractions in heart failure, the immediate clinical implications of their findings are uncertain.
However, clinical use as a biomarker remains a “distant vision,” in part because a useful biomarker must be proven to provide an incremental benefit in terms of reducing disease-associated morbidity or mortality.
Even so, the present study could begin to inform future therapeutic studies looking at increasing specific HDL-P subfractions, rather than increasing HDL cholesterol across the board.
“Perhaps, this study will possibly serve to spur investigation into therapies designed to reduce derangements of [HDL cholesterol] metabolism and primarily target HDL-P as a regulator molecule, a promise that may keep the HDL story alive into the near future of scientific excursion.”
These comments were taken from an accompanying editorial by Hector O. Ventura, MD, and Carl J. Lavie, MD, of the University of Queensland Ochsner Clinical School, Brisbane, Australia, and New Orleans; and Mandeep R. Mehra, MD, of the Center of Advanced Heart Disease, Harvard University, Boston (J Am Coll Cardiol 2019 Jan 22;73[2]:187-9). Dr. Mehra reported that he is a consultant for Abbott, Medtronic, nupulseCV, Portola, Bayer, and FineHeart.
In heart failure, derangements in HDL cholesterol particle (HDL-P) subfractions have prognostic implications beyond those of conventional cardiovascular risk factors, according to investigators who analyzed plasma samples from more than 6,500 patients.
The study revealed derangements that were shared and more severe in heart failure with reduced ejection fraction (HFrEF) as compared to heart failure with preserved ejection fraction (HFpEF), according to the researchers, who said their study is the largest to date of HDL-P subfractions in heart failure.
Both total HDL-P and small HDL-P had a strong inverse association with adverse outcomes, consistent with the conclusions of previous studies, they said in a report on their study in the Journal of the American College of Cardiology.
“Altogether, our findings support total and small HDL-P as important markers of residual risk in both HFrEF and HFpEF,” said the investigators, led by Wynn G. Hunter, MD, of Duke University, Durham, N.C.
Dr. Hunter and colleagues used the CATHGEN (Catheterization Genetics) biorepository to identify plasma samples obtained at catheterization for 782 patients with HFrEF, 1,004 with HFpEF, and 4,742 with no heart failure.
Lipoprotein profiling of the samples revealed that mean HDL-P size was greater in HFrEF than in HFpEF, and in both of those cases, mean HDL-P size was greater than in patients with no heart failure (P less than .0001), investigators reported.
Concentrations of small HDL-P and total HDL-P were by contrast lower in HFrEF versus HFpEF, and again, the values for both HFrEF and HFpEF were lower than in patients without heart failure (P less than .0001), they added.
Small HDL-P and total HDL-P had an inverse association with time to adverse events and all-cause mortality for both the HFrEF and HFpEF groups, according to investigators, who said those links remained robust even after multivariate adjustment for 14 cardiovascular risk factors, including diabetes, LDL particle, and GlycA, a marker of inflammation.
For example, small HDL-P and total HDL-P were inversely associated with all-cause mortality risk, with adjusted hazard ratios of 0.69-0.79 (P less than .0001), they reported. Similarly, a greater mean HDL-P size was associated with increased risk of all-cause mortality, yielding adjusted hazard ratios of 1.23-1.46 (P less than .0001).
Further studies are needed to clarify the role of HDL-P in the pathophysiology of heart failure, and to identify treatments that might increase total and small HDL-P in heart failure patients, Dr. Hunter and coauthors concluded.
Dr. Hunter reported no disclosures related to the study. Coauthors provided disclosures related to Amgen, Ostuka, Roche Diagnostics, Novartis, Trevena, Singulex, Medtronic, AstraZeneca, Bristol-Myers Squibb, Janssen, Portola, Boston Scientific, Gilead, GlaxoSmithKline, Merck, Alnylam, Ikaria Pharmaceuticals, Pfizer, Philips, LipoScience, and Pfizer, among others.
SOURCE: Hunter WG et al. J Am Coll Cardiol. 2019 Jan 22;73(2):177-86.
In heart failure, derangements in HDL cholesterol particle (HDL-P) subfractions have prognostic implications beyond those of conventional cardiovascular risk factors, according to investigators who analyzed plasma samples from more than 6,500 patients.
The study revealed derangements that were shared and more severe in heart failure with reduced ejection fraction (HFrEF) as compared to heart failure with preserved ejection fraction (HFpEF), according to the researchers, who said their study is the largest to date of HDL-P subfractions in heart failure.
Both total HDL-P and small HDL-P had a strong inverse association with adverse outcomes, consistent with the conclusions of previous studies, they said in a report on their study in the Journal of the American College of Cardiology.
“Altogether, our findings support total and small HDL-P as important markers of residual risk in both HFrEF and HFpEF,” said the investigators, led by Wynn G. Hunter, MD, of Duke University, Durham, N.C.
Dr. Hunter and colleagues used the CATHGEN (Catheterization Genetics) biorepository to identify plasma samples obtained at catheterization for 782 patients with HFrEF, 1,004 with HFpEF, and 4,742 with no heart failure.
Lipoprotein profiling of the samples revealed that mean HDL-P size was greater in HFrEF than in HFpEF, and in both of those cases, mean HDL-P size was greater than in patients with no heart failure (P less than .0001), investigators reported.
Concentrations of small HDL-P and total HDL-P were by contrast lower in HFrEF versus HFpEF, and again, the values for both HFrEF and HFpEF were lower than in patients without heart failure (P less than .0001), they added.
Small HDL-P and total HDL-P had an inverse association with time to adverse events and all-cause mortality for both the HFrEF and HFpEF groups, according to investigators, who said those links remained robust even after multivariate adjustment for 14 cardiovascular risk factors, including diabetes, LDL particle, and GlycA, a marker of inflammation.
For example, small HDL-P and total HDL-P were inversely associated with all-cause mortality risk, with adjusted hazard ratios of 0.69-0.79 (P less than .0001), they reported. Similarly, a greater mean HDL-P size was associated with increased risk of all-cause mortality, yielding adjusted hazard ratios of 1.23-1.46 (P less than .0001).
Further studies are needed to clarify the role of HDL-P in the pathophysiology of heart failure, and to identify treatments that might increase total and small HDL-P in heart failure patients, Dr. Hunter and coauthors concluded.
Dr. Hunter reported no disclosures related to the study. Coauthors provided disclosures related to Amgen, Ostuka, Roche Diagnostics, Novartis, Trevena, Singulex, Medtronic, AstraZeneca, Bristol-Myers Squibb, Janssen, Portola, Boston Scientific, Gilead, GlaxoSmithKline, Merck, Alnylam, Ikaria Pharmaceuticals, Pfizer, Philips, LipoScience, and Pfizer, among others.
SOURCE: Hunter WG et al. J Am Coll Cardiol. 2019 Jan 22;73(2):177-86.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Key clinical point: Derangements in HDL particle (HDL-P) subfractions may have prognostic implications in patients with heart failure with reduced or preserved ejection fraction.
Major finding: (P less than .0001).
Study details: Study based on lipid profiling of more than 6,500 plasma samples obtained at catheterization.
Disclosures: Study authors provided disclosures related to Amgen, Ostuka, Roche Diagnostics, Novartis, Medtronic, and others.
Source: Hunter WG et al. J Am Coll Cardiol. 2019 Jan 22;73(2):177-86.
Too much, too little sleep linked to atherosclerosis
in healthy middle-aged men and women in a Spanish investigation of bank employees.
“Overall, our findings support the potential role of healthy sleeping in protecting against atherosclerosis. Thus, recommending a good sleep hygiene” – 7-8 hours a night – “should be part of the lifestyle modifications provided in our daily clinical practice,” said investigators led by Fernando Domínguez, MD, PhD, of Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid. The report is in the Journal of the American College of Cardiology.
Studies have linked sleep problems to increased cardiovascular risk before, but the investigations tended to focus on patients with obstructive sleep apnea (OSA) and other problems, and often relied on patient self-report. The investors wanted to see if the relationship held in healthy adults, using an objective measure.
The participants – all with no known cardiovascular disease – wore Acti Trainers accelerometers (Actigraph, Pensacola, Fla.) around their waists for 7 days to record sleep duration and quality. Subjects also had their plaque burdens assessed by 3-dimensional vascular ultrasound (VUS) at their carotid and femoral arteries bilaterally. Cardiac CT was used to assess coronary artery calcification as a surrogate for coronary artery atherosclerosis.
The 3,974 participants had a mean age of 46 years, and a third were women; they had a low prevalence of both hypertension and diabetes. OSA patients were excluded from the study. Overall, 27% had very short sleep duration (VSSD), less than 6 hours a night; 38% had short sleep duration (SSD), 31% slept from 7 to 8 hours per night, and served as the reference group for healthy sleep habits; and 4% had long sleep duration (LSD), greater than 8 hours.
After adjustment for a wide range of cardiovascular risk factors, including body mass index, hypertension, and smoking, VSSD was independently associated with a higher atherosclerotic burden, compared to the reference group (odds ratio, 1.27; 95% confidence interval, 1.06-1.52; P = 0.008). Participants in the highest quintile of sleep fragmentation were more likely to have plaques at multiple sites (OR, 1.34; 95% CI, 1.09-1.64; P = 0.006). The Framingham risk score at both 10 and 30 years was significantly higher in participants with VSSD or SSD, and in the highest quintiles of sleep fragmentation.
LSD was also associated with a higher plaque burden, which reached statistical significance in women. “Too-long sleep duration may not be healthy either ... Recommendations should be restricted to 7 to 8 hours,” the investigators said.
Sleep duration and quality were not associated with inflammation markers or coronary artery calcification. The investigators noted that CT for coronary artery calcification might not be as sensitive as VUS for picking up subclinical atherosclerosis.
Short sleepers tended to have higher intakes of alcohol and caffeine than did those in the 7- to 8-hour group.
The work was funded by CNIC and Banco Santander, among others. Dr. Domínguez had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.
SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.
This study extends the published reports on sleep duration and vascular disease to an early middle-aged cohort by using an objective measure of sleep duration and sensitive measures of atherosclerosis in multiple vascular territories.
Ultimately, studies of sleep extension are needed to determine whether modification of sleep behaviors will improve vascular health outcomes. The potentially enormous impact of sleep deprivation and disruption on population health, reinforced by the present study, is ample justification for such trials, which are needed to place sleep with confidence alongside diet and exercise as a key pillar of a healthy lifestyle.
However, both hypertension and diabetes were more common in the group sleeping fewer than 6 hours per night, but neither blood pressure nor glucose metabolism was assessed with sufficiently comprehensive measures to explore these factors as potential effect mediators.
More importantly, the causes of short sleep duration and sleep fragmentation in this cohort are unknown. It is unclear to what extent short sleep duration in this cohort reflects voluntary behaviors that limit time available for sleep versus insomnia. Insomnia is itself associated with increased risk of vascular disease.
Deepak Bhatt , MD, professor of cardiovascular medicine, and Daniel Gottlieb , MD, an associate professor of medicine at Harvard Medical School, Boston, made these comments in an accompanying editorial ( J Am Coll Cardiol. 2019 Jan 14;73[2]:145-7 ). Dr. Gottlieb is also the director of the Boston Veterans Affairs Sleep Disorders Center. Dr. Bhatt reported research funding and income from a number of companies, including Abbott, Boehringer Ingelheim, and Medtronic.
This study extends the published reports on sleep duration and vascular disease to an early middle-aged cohort by using an objective measure of sleep duration and sensitive measures of atherosclerosis in multiple vascular territories.
Ultimately, studies of sleep extension are needed to determine whether modification of sleep behaviors will improve vascular health outcomes. The potentially enormous impact of sleep deprivation and disruption on population health, reinforced by the present study, is ample justification for such trials, which are needed to place sleep with confidence alongside diet and exercise as a key pillar of a healthy lifestyle.
However, both hypertension and diabetes were more common in the group sleeping fewer than 6 hours per night, but neither blood pressure nor glucose metabolism was assessed with sufficiently comprehensive measures to explore these factors as potential effect mediators.
More importantly, the causes of short sleep duration and sleep fragmentation in this cohort are unknown. It is unclear to what extent short sleep duration in this cohort reflects voluntary behaviors that limit time available for sleep versus insomnia. Insomnia is itself associated with increased risk of vascular disease.
Deepak Bhatt , MD, professor of cardiovascular medicine, and Daniel Gottlieb , MD, an associate professor of medicine at Harvard Medical School, Boston, made these comments in an accompanying editorial ( J Am Coll Cardiol. 2019 Jan 14;73[2]:145-7 ). Dr. Gottlieb is also the director of the Boston Veterans Affairs Sleep Disorders Center. Dr. Bhatt reported research funding and income from a number of companies, including Abbott, Boehringer Ingelheim, and Medtronic.
This study extends the published reports on sleep duration and vascular disease to an early middle-aged cohort by using an objective measure of sleep duration and sensitive measures of atherosclerosis in multiple vascular territories.
Ultimately, studies of sleep extension are needed to determine whether modification of sleep behaviors will improve vascular health outcomes. The potentially enormous impact of sleep deprivation and disruption on population health, reinforced by the present study, is ample justification for such trials, which are needed to place sleep with confidence alongside diet and exercise as a key pillar of a healthy lifestyle.
However, both hypertension and diabetes were more common in the group sleeping fewer than 6 hours per night, but neither blood pressure nor glucose metabolism was assessed with sufficiently comprehensive measures to explore these factors as potential effect mediators.
More importantly, the causes of short sleep duration and sleep fragmentation in this cohort are unknown. It is unclear to what extent short sleep duration in this cohort reflects voluntary behaviors that limit time available for sleep versus insomnia. Insomnia is itself associated with increased risk of vascular disease.
Deepak Bhatt , MD, professor of cardiovascular medicine, and Daniel Gottlieb , MD, an associate professor of medicine at Harvard Medical School, Boston, made these comments in an accompanying editorial ( J Am Coll Cardiol. 2019 Jan 14;73[2]:145-7 ). Dr. Gottlieb is also the director of the Boston Veterans Affairs Sleep Disorders Center. Dr. Bhatt reported research funding and income from a number of companies, including Abbott, Boehringer Ingelheim, and Medtronic.
in healthy middle-aged men and women in a Spanish investigation of bank employees.
“Overall, our findings support the potential role of healthy sleeping in protecting against atherosclerosis. Thus, recommending a good sleep hygiene” – 7-8 hours a night – “should be part of the lifestyle modifications provided in our daily clinical practice,” said investigators led by Fernando Domínguez, MD, PhD, of Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid. The report is in the Journal of the American College of Cardiology.
Studies have linked sleep problems to increased cardiovascular risk before, but the investigations tended to focus on patients with obstructive sleep apnea (OSA) and other problems, and often relied on patient self-report. The investors wanted to see if the relationship held in healthy adults, using an objective measure.
The participants – all with no known cardiovascular disease – wore Acti Trainers accelerometers (Actigraph, Pensacola, Fla.) around their waists for 7 days to record sleep duration and quality. Subjects also had their plaque burdens assessed by 3-dimensional vascular ultrasound (VUS) at their carotid and femoral arteries bilaterally. Cardiac CT was used to assess coronary artery calcification as a surrogate for coronary artery atherosclerosis.
The 3,974 participants had a mean age of 46 years, and a third were women; they had a low prevalence of both hypertension and diabetes. OSA patients were excluded from the study. Overall, 27% had very short sleep duration (VSSD), less than 6 hours a night; 38% had short sleep duration (SSD), 31% slept from 7 to 8 hours per night, and served as the reference group for healthy sleep habits; and 4% had long sleep duration (LSD), greater than 8 hours.
After adjustment for a wide range of cardiovascular risk factors, including body mass index, hypertension, and smoking, VSSD was independently associated with a higher atherosclerotic burden, compared to the reference group (odds ratio, 1.27; 95% confidence interval, 1.06-1.52; P = 0.008). Participants in the highest quintile of sleep fragmentation were more likely to have plaques at multiple sites (OR, 1.34; 95% CI, 1.09-1.64; P = 0.006). The Framingham risk score at both 10 and 30 years was significantly higher in participants with VSSD or SSD, and in the highest quintiles of sleep fragmentation.
LSD was also associated with a higher plaque burden, which reached statistical significance in women. “Too-long sleep duration may not be healthy either ... Recommendations should be restricted to 7 to 8 hours,” the investigators said.
Sleep duration and quality were not associated with inflammation markers or coronary artery calcification. The investigators noted that CT for coronary artery calcification might not be as sensitive as VUS for picking up subclinical atherosclerosis.
Short sleepers tended to have higher intakes of alcohol and caffeine than did those in the 7- to 8-hour group.
The work was funded by CNIC and Banco Santander, among others. Dr. Domínguez had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.
SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.
in healthy middle-aged men and women in a Spanish investigation of bank employees.
“Overall, our findings support the potential role of healthy sleeping in protecting against atherosclerosis. Thus, recommending a good sleep hygiene” – 7-8 hours a night – “should be part of the lifestyle modifications provided in our daily clinical practice,” said investigators led by Fernando Domínguez, MD, PhD, of Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid. The report is in the Journal of the American College of Cardiology.
Studies have linked sleep problems to increased cardiovascular risk before, but the investigations tended to focus on patients with obstructive sleep apnea (OSA) and other problems, and often relied on patient self-report. The investors wanted to see if the relationship held in healthy adults, using an objective measure.
The participants – all with no known cardiovascular disease – wore Acti Trainers accelerometers (Actigraph, Pensacola, Fla.) around their waists for 7 days to record sleep duration and quality. Subjects also had their plaque burdens assessed by 3-dimensional vascular ultrasound (VUS) at their carotid and femoral arteries bilaterally. Cardiac CT was used to assess coronary artery calcification as a surrogate for coronary artery atherosclerosis.
The 3,974 participants had a mean age of 46 years, and a third were women; they had a low prevalence of both hypertension and diabetes. OSA patients were excluded from the study. Overall, 27% had very short sleep duration (VSSD), less than 6 hours a night; 38% had short sleep duration (SSD), 31% slept from 7 to 8 hours per night, and served as the reference group for healthy sleep habits; and 4% had long sleep duration (LSD), greater than 8 hours.
After adjustment for a wide range of cardiovascular risk factors, including body mass index, hypertension, and smoking, VSSD was independently associated with a higher atherosclerotic burden, compared to the reference group (odds ratio, 1.27; 95% confidence interval, 1.06-1.52; P = 0.008). Participants in the highest quintile of sleep fragmentation were more likely to have plaques at multiple sites (OR, 1.34; 95% CI, 1.09-1.64; P = 0.006). The Framingham risk score at both 10 and 30 years was significantly higher in participants with VSSD or SSD, and in the highest quintiles of sleep fragmentation.
LSD was also associated with a higher plaque burden, which reached statistical significance in women. “Too-long sleep duration may not be healthy either ... Recommendations should be restricted to 7 to 8 hours,” the investigators said.
Sleep duration and quality were not associated with inflammation markers or coronary artery calcification. The investigators noted that CT for coronary artery calcification might not be as sensitive as VUS for picking up subclinical atherosclerosis.
Short sleepers tended to have higher intakes of alcohol and caffeine than did those in the 7- to 8-hour group.
The work was funded by CNIC and Banco Santander, among others. Dr. Domínguez had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.
SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Key clinical point: Even among healthy men and women, both too much and too little sleep are associated with atherosclerosis.
Major finding: Sleeping less than 6 hours a night was independently associated with a higher noncardiac atherosclerotic burden (OR ,1.27; 95% CI, 1.06-1.52; P = .008)
Study details: Spanish study of 3,974 bank employees.
Disclosures: The work was funded by CNIC and Banco Santander, among others. The study lead had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.
Source: Domínguez F et al. J Am Coll Cardiol. 2019;73:134-44.
No drop in gout prevalence, but no increase either
according to data from an ongoing, nationally representative survey.
Findings from the National Health and Nutrition Examination Survey (NHANES) also show that only about one-third of gout patients were using urate-lowering therapies, Michael Chen-Xu, MBChB, MPH, of the Harvard T.H. Chan School of Public Health, Boston, and his associates wrote in Arthritis & Rheumatology.
“The prevalence of gout and hyperuricemia in the United States more than doubled between the 1960s and the 1990s and continued to increase steadily afterwards,” they wrote. By 2007-2008, the earliest 2-year NHANES cycle in the study, gout prevalence among adults stood at 3.9%, but after a slight dip and a rise it was 3.9% again in 2015-2016, the last cycle in the study, the investigators reported.
The prevalence of hyperuricemia – defined as a serum urate level of more than 7.0 mg/dL in males and more than 5.7 mg/dL in females – did drop from 21.4% in 2007-2008 to 20.1% in 2015-16, but the change was not significant, Dr. Chen-Xu and his associates said.
Overall use of urate-lowering therapy (ULT) among patients with gout was 32.8% over the study period, with use showing a nonsignificant increase from 33.0% in 2007-2008 to 35.5% in 2013-2014, with a dip down to 29.4% in 2011-2012. (Data on ULT use were not available for the 2015-2016 NHANES cycle.) Current ULT use among male gout patients was 35.5% in 2013-2014 and 15.5% among women, and nearly all ULT use (95.3%) consisted of allopurinol, they said.
“Although we did not find a significant change in the trends of gout or hyperuricemia prevalence from 2007 to 2016,” Dr. Chen-Xu and his associates wrote, “10 years may not be long enough to detect what might actually be a significant trend(s) over a longer period.”
The study was supported by Ironwood and Horizon. Dr. Chen-Xu had no conflicts to disclose. One of his associates has served on advisory boards for Takeda, Ironwood, Horizon, Kowa, and Selecta. Another has served on advisory boards for Pfizer, Horizon, SOBI, and Ironwood and as a study site investigator for Takeda.
SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.
according to data from an ongoing, nationally representative survey.
Findings from the National Health and Nutrition Examination Survey (NHANES) also show that only about one-third of gout patients were using urate-lowering therapies, Michael Chen-Xu, MBChB, MPH, of the Harvard T.H. Chan School of Public Health, Boston, and his associates wrote in Arthritis & Rheumatology.
“The prevalence of gout and hyperuricemia in the United States more than doubled between the 1960s and the 1990s and continued to increase steadily afterwards,” they wrote. By 2007-2008, the earliest 2-year NHANES cycle in the study, gout prevalence among adults stood at 3.9%, but after a slight dip and a rise it was 3.9% again in 2015-2016, the last cycle in the study, the investigators reported.
The prevalence of hyperuricemia – defined as a serum urate level of more than 7.0 mg/dL in males and more than 5.7 mg/dL in females – did drop from 21.4% in 2007-2008 to 20.1% in 2015-16, but the change was not significant, Dr. Chen-Xu and his associates said.
Overall use of urate-lowering therapy (ULT) among patients with gout was 32.8% over the study period, with use showing a nonsignificant increase from 33.0% in 2007-2008 to 35.5% in 2013-2014, with a dip down to 29.4% in 2011-2012. (Data on ULT use were not available for the 2015-2016 NHANES cycle.) Current ULT use among male gout patients was 35.5% in 2013-2014 and 15.5% among women, and nearly all ULT use (95.3%) consisted of allopurinol, they said.
“Although we did not find a significant change in the trends of gout or hyperuricemia prevalence from 2007 to 2016,” Dr. Chen-Xu and his associates wrote, “10 years may not be long enough to detect what might actually be a significant trend(s) over a longer period.”
The study was supported by Ironwood and Horizon. Dr. Chen-Xu had no conflicts to disclose. One of his associates has served on advisory boards for Takeda, Ironwood, Horizon, Kowa, and Selecta. Another has served on advisory boards for Pfizer, Horizon, SOBI, and Ironwood and as a study site investigator for Takeda.
SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.
according to data from an ongoing, nationally representative survey.
Findings from the National Health and Nutrition Examination Survey (NHANES) also show that only about one-third of gout patients were using urate-lowering therapies, Michael Chen-Xu, MBChB, MPH, of the Harvard T.H. Chan School of Public Health, Boston, and his associates wrote in Arthritis & Rheumatology.
“The prevalence of gout and hyperuricemia in the United States more than doubled between the 1960s and the 1990s and continued to increase steadily afterwards,” they wrote. By 2007-2008, the earliest 2-year NHANES cycle in the study, gout prevalence among adults stood at 3.9%, but after a slight dip and a rise it was 3.9% again in 2015-2016, the last cycle in the study, the investigators reported.
The prevalence of hyperuricemia – defined as a serum urate level of more than 7.0 mg/dL in males and more than 5.7 mg/dL in females – did drop from 21.4% in 2007-2008 to 20.1% in 2015-16, but the change was not significant, Dr. Chen-Xu and his associates said.
Overall use of urate-lowering therapy (ULT) among patients with gout was 32.8% over the study period, with use showing a nonsignificant increase from 33.0% in 2007-2008 to 35.5% in 2013-2014, with a dip down to 29.4% in 2011-2012. (Data on ULT use were not available for the 2015-2016 NHANES cycle.) Current ULT use among male gout patients was 35.5% in 2013-2014 and 15.5% among women, and nearly all ULT use (95.3%) consisted of allopurinol, they said.
“Although we did not find a significant change in the trends of gout or hyperuricemia prevalence from 2007 to 2016,” Dr. Chen-Xu and his associates wrote, “10 years may not be long enough to detect what might actually be a significant trend(s) over a longer period.”
The study was supported by Ironwood and Horizon. Dr. Chen-Xu had no conflicts to disclose. One of his associates has served on advisory boards for Takeda, Ironwood, Horizon, Kowa, and Selecta. Another has served on advisory boards for Pfizer, Horizon, SOBI, and Ironwood and as a study site investigator for Takeda.
SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.
FROM ARTHRITIS & RHEUMATOLOGY
Baselga moves to industry; MD Anderson mourns
Jose Baselga, MD, PhD, the former chief medical officer at Memorial Sloan Kettering Cancer Center in New York, made headlines recently by accepting a position with the drugmaker AstraZeneca.
Dr. Baselga had stepped down from his position at Memorial Sloan Kettering in September 2018 after a ProPublica investigation revealed that he had failed to disclose industry funding in dozens of instances when publishing in top medical journals. In his new role, Dr. Baselga, who acknowledged the missing disclosures but said they were unintentional, will head up the research and development unit for oncology, AstraZeneca said in a press release.
The American Society of Clinical Oncology (ASCO) has elected new leadership. Lori J. Pierce, MD, a radiation oncologist and leader in breast cancer research, is the newly elected president-elect. She will serve in that role beginning June 2019 and will end her 1-year term as president of ASCO in June 2020. Dr. Pierce is a professor and vice provost for academic and faculty affairs at the University of Michigan, Ann Arbor, and the director of the Michigan Radiation Oncology Quality Consortium.
Three physicians were also elected to the ASCO board of directors. Michael A. Thompson, MD, PhD, of Advocate Aurora Health in Milwaukee, was elected to the community oncologist seat. Elizabeth A. Mittendorf, MD, PhD, of Brigham and Women’s Hospital and the Dana-Farber Cancer Institute in Boston, was elected to the surgical oncologist seat. Ethan Basch, MD, of the University of North Carolina, was elected to the undesignated specialty seat. They will all begin 4-year terms on the board of directors starting in June 2019.
A radiation oncologist is moving up the ranks at the Centers for Medicare & Medicaid Services. Anand Shah, MD, has been named senior medical advisor for innovation at the Center for Medicare & Medicaid Innovation (CMMI), part of CMS. He had previously served as the CMMI’s chief medical officer. Dr. Shah is getting congratulations from ASCO and the American Society of Radiation Oncology (ASTRO), both of whom have a lot to say about CMMI policies such as attempts to revive the Competitive Acquisition Program for Part B drugs and alternative payment models for oncology.
Julian Schink, MD, has been appointed chief medical officer at Cancer Treatment Centers of America (CTCA). Dr. Schink, a gynecologic oncologist, joined CTCA in 2017 as chief of gynecologic oncology. Before that, he had worked at the University of Wisconsin–Madison and the Northwestern University, Chicago.
In sad news, John Mendelsohn, MD, the president emeritus of the University of Texas MD Anderson Cancer Center, died on Jan. 7 at the age of 82 years. He had been diagnosed with glioblastoma 15 months earlier. Before working in medical leadership, Dr. Mendelsohn had worked with his colleagues at the University of California, San Diego, on research to block epidermal growth factor receptors. That work led to the development of the drug cetuximab, which was approved by the Food and Drug Administration to treat advanced colorectal cancer and later head and neck cancer.
The MD Anderson community also mourned the passing of Waun Ki Hong, MD, a physician-scientist who led the institution’s division of cancer medicine during 2001-2014. He died at age 76 years. Dr. Hong, who was also a past president of the American Association for Cancer Research, was well known for advancing the fields of targeted therapy and chemoprevention.
Movers in Medicine highlights career moves and personal achievements by hematologists and oncologists. Did you switch jobs, take on a new role, climb a mountain? Tell us all about it at [email protected], and you could be featured in Movers in Medicine.
Jose Baselga, MD, PhD, the former chief medical officer at Memorial Sloan Kettering Cancer Center in New York, made headlines recently by accepting a position with the drugmaker AstraZeneca.
Dr. Baselga had stepped down from his position at Memorial Sloan Kettering in September 2018 after a ProPublica investigation revealed that he had failed to disclose industry funding in dozens of instances when publishing in top medical journals. In his new role, Dr. Baselga, who acknowledged the missing disclosures but said they were unintentional, will head up the research and development unit for oncology, AstraZeneca said in a press release.
The American Society of Clinical Oncology (ASCO) has elected new leadership. Lori J. Pierce, MD, a radiation oncologist and leader in breast cancer research, is the newly elected president-elect. She will serve in that role beginning June 2019 and will end her 1-year term as president of ASCO in June 2020. Dr. Pierce is a professor and vice provost for academic and faculty affairs at the University of Michigan, Ann Arbor, and the director of the Michigan Radiation Oncology Quality Consortium.
Three physicians were also elected to the ASCO board of directors. Michael A. Thompson, MD, PhD, of Advocate Aurora Health in Milwaukee, was elected to the community oncologist seat. Elizabeth A. Mittendorf, MD, PhD, of Brigham and Women’s Hospital and the Dana-Farber Cancer Institute in Boston, was elected to the surgical oncologist seat. Ethan Basch, MD, of the University of North Carolina, was elected to the undesignated specialty seat. They will all begin 4-year terms on the board of directors starting in June 2019.
A radiation oncologist is moving up the ranks at the Centers for Medicare & Medicaid Services. Anand Shah, MD, has been named senior medical advisor for innovation at the Center for Medicare & Medicaid Innovation (CMMI), part of CMS. He had previously served as the CMMI’s chief medical officer. Dr. Shah is getting congratulations from ASCO and the American Society of Radiation Oncology (ASTRO), both of whom have a lot to say about CMMI policies such as attempts to revive the Competitive Acquisition Program for Part B drugs and alternative payment models for oncology.
Julian Schink, MD, has been appointed chief medical officer at Cancer Treatment Centers of America (CTCA). Dr. Schink, a gynecologic oncologist, joined CTCA in 2017 as chief of gynecologic oncology. Before that, he had worked at the University of Wisconsin–Madison and the Northwestern University, Chicago.
In sad news, John Mendelsohn, MD, the president emeritus of the University of Texas MD Anderson Cancer Center, died on Jan. 7 at the age of 82 years. He had been diagnosed with glioblastoma 15 months earlier. Before working in medical leadership, Dr. Mendelsohn had worked with his colleagues at the University of California, San Diego, on research to block epidermal growth factor receptors. That work led to the development of the drug cetuximab, which was approved by the Food and Drug Administration to treat advanced colorectal cancer and later head and neck cancer.
The MD Anderson community also mourned the passing of Waun Ki Hong, MD, a physician-scientist who led the institution’s division of cancer medicine during 2001-2014. He died at age 76 years. Dr. Hong, who was also a past president of the American Association for Cancer Research, was well known for advancing the fields of targeted therapy and chemoprevention.
Movers in Medicine highlights career moves and personal achievements by hematologists and oncologists. Did you switch jobs, take on a new role, climb a mountain? Tell us all about it at [email protected], and you could be featured in Movers in Medicine.
Jose Baselga, MD, PhD, the former chief medical officer at Memorial Sloan Kettering Cancer Center in New York, made headlines recently by accepting a position with the drugmaker AstraZeneca.
Dr. Baselga had stepped down from his position at Memorial Sloan Kettering in September 2018 after a ProPublica investigation revealed that he had failed to disclose industry funding in dozens of instances when publishing in top medical journals. In his new role, Dr. Baselga, who acknowledged the missing disclosures but said they were unintentional, will head up the research and development unit for oncology, AstraZeneca said in a press release.
The American Society of Clinical Oncology (ASCO) has elected new leadership. Lori J. Pierce, MD, a radiation oncologist and leader in breast cancer research, is the newly elected president-elect. She will serve in that role beginning June 2019 and will end her 1-year term as president of ASCO in June 2020. Dr. Pierce is a professor and vice provost for academic and faculty affairs at the University of Michigan, Ann Arbor, and the director of the Michigan Radiation Oncology Quality Consortium.
Three physicians were also elected to the ASCO board of directors. Michael A. Thompson, MD, PhD, of Advocate Aurora Health in Milwaukee, was elected to the community oncologist seat. Elizabeth A. Mittendorf, MD, PhD, of Brigham and Women’s Hospital and the Dana-Farber Cancer Institute in Boston, was elected to the surgical oncologist seat. Ethan Basch, MD, of the University of North Carolina, was elected to the undesignated specialty seat. They will all begin 4-year terms on the board of directors starting in June 2019.
A radiation oncologist is moving up the ranks at the Centers for Medicare & Medicaid Services. Anand Shah, MD, has been named senior medical advisor for innovation at the Center for Medicare & Medicaid Innovation (CMMI), part of CMS. He had previously served as the CMMI’s chief medical officer. Dr. Shah is getting congratulations from ASCO and the American Society of Radiation Oncology (ASTRO), both of whom have a lot to say about CMMI policies such as attempts to revive the Competitive Acquisition Program for Part B drugs and alternative payment models for oncology.
Julian Schink, MD, has been appointed chief medical officer at Cancer Treatment Centers of America (CTCA). Dr. Schink, a gynecologic oncologist, joined CTCA in 2017 as chief of gynecologic oncology. Before that, he had worked at the University of Wisconsin–Madison and the Northwestern University, Chicago.
In sad news, John Mendelsohn, MD, the president emeritus of the University of Texas MD Anderson Cancer Center, died on Jan. 7 at the age of 82 years. He had been diagnosed with glioblastoma 15 months earlier. Before working in medical leadership, Dr. Mendelsohn had worked with his colleagues at the University of California, San Diego, on research to block epidermal growth factor receptors. That work led to the development of the drug cetuximab, which was approved by the Food and Drug Administration to treat advanced colorectal cancer and later head and neck cancer.
The MD Anderson community also mourned the passing of Waun Ki Hong, MD, a physician-scientist who led the institution’s division of cancer medicine during 2001-2014. He died at age 76 years. Dr. Hong, who was also a past president of the American Association for Cancer Research, was well known for advancing the fields of targeted therapy and chemoprevention.
Movers in Medicine highlights career moves and personal achievements by hematologists and oncologists. Did you switch jobs, take on a new role, climb a mountain? Tell us all about it at [email protected], and you could be featured in Movers in Medicine.
Platinum-etoposide, taxanes best for small cell transformed EGFR-mutant lung cancer
Epidermal growth factor receptor (EGFR)–mutant non–small cell lung tumors transformed to small cell disease an average of 17.8 months after diagnosis, and this shift often involved Rb1, TP53, and PIK3CA mutations, according to the findings of a multicenter retrospective study of 67 patients.
After transformation, platinum-etoposide, paclitaxel, and nab-paclitaxel each yielded clinical response rates of 71%, while patients did not respond to programmed death-1 or programmed death-ligand 1 checkpoint inhibition, reported Nicolas Marcoux, MD, of Massachusetts General Hospital in Boston and his associates. “Indeed, none of the 17 patients [who received a checkpoint inhibitor] even seemed to derive clinical benefit from these therapies, as the longest time to progression was only 9 weeks,” the researchers wrote in the Journal of Clinical Oncology.
Interestingly, docetaxel produced no responses among six treated patients. Transformation often led to central nervous system metastases and patients survived a median of 10.7 months after transformation (95% confidence interval, 8.0-13.7 months).
Repeat biopsies showed that 3%-10% of EGFR-mutant non–small cell lung cancers transformed to small cell lung cancers. However, the subsequent clinical course has not been well characterized. Patients in this study were treated at eight cancer centers, had a history of EGFR-mutant small cell lung cancer, and most (87%) had non–small cell histology at diagnosis and received at least one EGFR tyrosine kinase inhibitor. The other nine patients had de novo small cell lung cancer or mixed histology.
All 59 patients with tissue genotyping at first evidence of small cell lung cancer retained their founder EGFR mutations, Dr. Marcoux and his associates reported. Among 19 patients with a history of EGFR T790M positivity, 15 patients were T790 wild-type at transformation. “Other recurrent mutations included TP53, Rb1, and PIK3CA,” they wrote.
The study supports the first-line use of platinum-etoposide for EGFR-mutant lung cancers that transform to small cell lung cancer, the researchers concluded. “Conversely, these tumors do not respond well to checkpoint inhibitors and the use of these therapies outside of a clinical trial should currently be discouraged.”
Funders included the National Institutes of Health, LungStrong, Targeting a Cure for Lung Cancer, Be a Piece of the Solution, the Susanne E. Coyne Memorial Fund, and a STOP Cancer Carrie Scott Grant. Dr. Marcoux disclosed honoraria from Bristol-Myers Squibb.
SOURCE: Marcoux N et al. J Clin Oncol. 2018 Dec 14. doi: 10.1200/JCO.18.01585.
Epidermal growth factor receptor (EGFR)–mutant non–small cell lung tumors transformed to small cell disease an average of 17.8 months after diagnosis, and this shift often involved Rb1, TP53, and PIK3CA mutations, according to the findings of a multicenter retrospective study of 67 patients.
After transformation, platinum-etoposide, paclitaxel, and nab-paclitaxel each yielded clinical response rates of 71%, while patients did not respond to programmed death-1 or programmed death-ligand 1 checkpoint inhibition, reported Nicolas Marcoux, MD, of Massachusetts General Hospital in Boston and his associates. “Indeed, none of the 17 patients [who received a checkpoint inhibitor] even seemed to derive clinical benefit from these therapies, as the longest time to progression was only 9 weeks,” the researchers wrote in the Journal of Clinical Oncology.
Interestingly, docetaxel produced no responses among six treated patients. Transformation often led to central nervous system metastases and patients survived a median of 10.7 months after transformation (95% confidence interval, 8.0-13.7 months).
Repeat biopsies showed that 3%-10% of EGFR-mutant non–small cell lung cancers transformed to small cell lung cancers. However, the subsequent clinical course has not been well characterized. Patients in this study were treated at eight cancer centers, had a history of EGFR-mutant small cell lung cancer, and most (87%) had non–small cell histology at diagnosis and received at least one EGFR tyrosine kinase inhibitor. The other nine patients had de novo small cell lung cancer or mixed histology.
All 59 patients with tissue genotyping at first evidence of small cell lung cancer retained their founder EGFR mutations, Dr. Marcoux and his associates reported. Among 19 patients with a history of EGFR T790M positivity, 15 patients were T790 wild-type at transformation. “Other recurrent mutations included TP53, Rb1, and PIK3CA,” they wrote.
The study supports the first-line use of platinum-etoposide for EGFR-mutant lung cancers that transform to small cell lung cancer, the researchers concluded. “Conversely, these tumors do not respond well to checkpoint inhibitors and the use of these therapies outside of a clinical trial should currently be discouraged.”
Funders included the National Institutes of Health, LungStrong, Targeting a Cure for Lung Cancer, Be a Piece of the Solution, the Susanne E. Coyne Memorial Fund, and a STOP Cancer Carrie Scott Grant. Dr. Marcoux disclosed honoraria from Bristol-Myers Squibb.
SOURCE: Marcoux N et al. J Clin Oncol. 2018 Dec 14. doi: 10.1200/JCO.18.01585.
Epidermal growth factor receptor (EGFR)–mutant non–small cell lung tumors transformed to small cell disease an average of 17.8 months after diagnosis, and this shift often involved Rb1, TP53, and PIK3CA mutations, according to the findings of a multicenter retrospective study of 67 patients.
After transformation, platinum-etoposide, paclitaxel, and nab-paclitaxel each yielded clinical response rates of 71%, while patients did not respond to programmed death-1 or programmed death-ligand 1 checkpoint inhibition, reported Nicolas Marcoux, MD, of Massachusetts General Hospital in Boston and his associates. “Indeed, none of the 17 patients [who received a checkpoint inhibitor] even seemed to derive clinical benefit from these therapies, as the longest time to progression was only 9 weeks,” the researchers wrote in the Journal of Clinical Oncology.
Interestingly, docetaxel produced no responses among six treated patients. Transformation often led to central nervous system metastases and patients survived a median of 10.7 months after transformation (95% confidence interval, 8.0-13.7 months).
Repeat biopsies showed that 3%-10% of EGFR-mutant non–small cell lung cancers transformed to small cell lung cancers. However, the subsequent clinical course has not been well characterized. Patients in this study were treated at eight cancer centers, had a history of EGFR-mutant small cell lung cancer, and most (87%) had non–small cell histology at diagnosis and received at least one EGFR tyrosine kinase inhibitor. The other nine patients had de novo small cell lung cancer or mixed histology.
All 59 patients with tissue genotyping at first evidence of small cell lung cancer retained their founder EGFR mutations, Dr. Marcoux and his associates reported. Among 19 patients with a history of EGFR T790M positivity, 15 patients were T790 wild-type at transformation. “Other recurrent mutations included TP53, Rb1, and PIK3CA,” they wrote.
The study supports the first-line use of platinum-etoposide for EGFR-mutant lung cancers that transform to small cell lung cancer, the researchers concluded. “Conversely, these tumors do not respond well to checkpoint inhibitors and the use of these therapies outside of a clinical trial should currently be discouraged.”
Funders included the National Institutes of Health, LungStrong, Targeting a Cure for Lung Cancer, Be a Piece of the Solution, the Susanne E. Coyne Memorial Fund, and a STOP Cancer Carrie Scott Grant. Dr. Marcoux disclosed honoraria from Bristol-Myers Squibb.
SOURCE: Marcoux N et al. J Clin Oncol. 2018 Dec 14. doi: 10.1200/JCO.18.01585.
FROM THE JOURNAL OF CLINICAL ONCOLOGY
Key clinical point: Platinum-etoposide and taxane therapies elicited high response rates after transformation of EGFR-mutant non–small cell lung cancer.
Major finding: Median time to transformation was 17.8 months (95% CI, 14.3-26.2 months). Both platinum-etoposide and taxane therapies produced high response rates (71% each), but patients did not respond to checkpoint inhibitor therapy.
Data source: Multicenter retrospective study of 67 patients with EGFR-mutant small cell lung cancer.
Disclosures: Funders included the National Institutes of Health, LungStrong, Targeting a Cure for Lung Cancer, Be a Piece of the Solution, the Susanne E. Coyne Memorial Fund, and a STOP Cancer Carrie Scott Grant. Dr. Marcoux disclosed honoraria from Bristol-Myers Squibb.
Source: Marcoux N et al. J Clin Oncol. 2018 Dec 14. doi: 10.1200/JCO.18.01585.
Looking into the future and making history
Emergence of population health management
For the first time ever, on March 7, 2019, tens of thousands of hospitalists across the United States and around the world will celebrate their day, National Hospitalist Day.
On this day, we will honor the hard work and dedication of hospitalists in the care of millions of hospitalized patients. With more than 62,000 hospitalists across the United States, hospital medicine has been the fastest growing medical specialty and among the largest of all specialties in medicine. Hospitalists now lead clinical care in over 75% of U.S. hospitals, caring for patients in their communities. We educate the future providers of health care by serving as teachers and mentors. We push the boundaries of science in hospital care through innovative research that defines the evidence-based practices for our field. Hospitalists, proudly celebrate all that we have accomplished together on March 7, and moving forward, every first Thursday in March annually.
The Society for Hospital Medicine’s celebration of National Hospitalist Day will include spotlights on hospitalists, a social medical campaign, downloadable customizable posters, and much more. Stay tuned for details!
Attend the only meeting designed just for you
Be among the thousands of hospitalists who will celebrate hospital medicine in person at Hospital Medicine 2019 (HM19), March 24-27 in National Harbor, Md.
While at HM19, check out more than 20 educational tracks, including clinical updates, diagnostic reasoning, and health policy. New this year are two mini tracks: “Between the Guidelines” and “Clinical Mastery”. Between the Guidelines explores how we can address some of the most challenging cases we encounter in hospital medicine, where clear guidelines don’t exist. Clinical Mastery is designed to enhance our bedside diagnostic skills, from ECGs to ultrasounds.
Get ready to vote in HM19’s “The Great Debate” – pairing two talented clinicians who will debate opposing sides of challenging clinical decisions that we encounter on the front lines of health care delivery. Attendees have the opportunity to hear the two sides and then vote on who they believe has the right approach. There are six precourses planned for HM19, with a new offering in Palliative Care and Pain Management. This year, the annual conference also features additional sessions for our NP/PA attendees. They include specific workshops as well as a track that includes 4 didactic sessions. Lastly, HM19 will offer CME, MOC, AOS, AAFP, and Pharmacology credits to address the needs of our attendees.
Looking into the future
While hospitalists are a vital part of U.S. health care, our delivery systems are in transition with greater focus on value-based care. To ensure hospital medicine continues to thrive in today’s dynamic scene, SHM’s Board of Directors held a strategic meeting in October 2018 to focus on the role of hospitalists and hospital medicine in population health management.
There are many hospitalists across the nation who are currently involved in population health management. These range from medical directors to vice presidents of accountable care organizations, population health management, or value-based care. Hospitalists are seeking communities focused on population health management to share best practices and learn from each other. To address this, SHM’s Advocacy and Public Policy HMX community has served as a meeting point to discuss issues related to value-based care. To join the discussion, visit the community by logging in at hospitalmedicine.org/hmx. Furthermore, at HM19, hospitalists will have the opportunity to meet face to face regarding these issues in the Advocacy Special Interest Forum.
Key points: Population health management
- Source of truth
SHM has served as the source of reliable and trusted information about hospital medicine. We will continue to develop content and resources specific to population health management on our website so hospitalists can easily access this information. To increase our awareness about population health management, presenters at HM19 will integrate a slide about the implications of population health management on their clinical topic. These slides will illustrate the clinical and nonclinical services that are necessary to enhance the patient’s quality of care and life. In addition to best practice care, these slides will highlight topics like the role of style modification and prevention, risk stratification, chronic disease management, and care coordination throughout the continuum of care.
- Advocating for us
In addition to providing a home for hospitalists to collaborate regarding population health management, SHM will advance this agenda from a regulatory perspective. The Public Policy and Performance Measurement & Reporting Committees are actively evaluating and leading the transition from value to volume. SHM is also working with potential key partners and organizations in the areas of primary care, skilled nursing facilities, and accountable care organizations that will help improve the effectiveness of delivering population health management.
- Creating expertise
SHM will lead best practice development for tools and skills that are necessary for hospitalists to lead population health management. Telemedicine is an increasingly critical tool as we help manage our patients in other facilities, inpatient or skilled nursing facilities, as well as at home. SHM has developed a white paper about telemedicine in hospital medicine that highlights modalities, offerings, implementation of programs, and work flows necessary for success. You can find it under “Resources” at hospitalmedicine.org/telemedicine.
SHM will continue to actively develop tools that appropriately address the challenges we’re facing. From National Hospitalist Day to population health management, this is an exciting time in hospital medicine – I hope to see you at HM19 to celebrate our specialty and our bright future.
Dr. Afsar is president of the Society of Hospital Medicine, and chief ambulatory officer and chief medical officer for accountable care organizations at UC Irvine Health.
Emergence of population health management
Emergence of population health management
For the first time ever, on March 7, 2019, tens of thousands of hospitalists across the United States and around the world will celebrate their day, National Hospitalist Day.
On this day, we will honor the hard work and dedication of hospitalists in the care of millions of hospitalized patients. With more than 62,000 hospitalists across the United States, hospital medicine has been the fastest growing medical specialty and among the largest of all specialties in medicine. Hospitalists now lead clinical care in over 75% of U.S. hospitals, caring for patients in their communities. We educate the future providers of health care by serving as teachers and mentors. We push the boundaries of science in hospital care through innovative research that defines the evidence-based practices for our field. Hospitalists, proudly celebrate all that we have accomplished together on March 7, and moving forward, every first Thursday in March annually.
The Society for Hospital Medicine’s celebration of National Hospitalist Day will include spotlights on hospitalists, a social medical campaign, downloadable customizable posters, and much more. Stay tuned for details!
Attend the only meeting designed just for you
Be among the thousands of hospitalists who will celebrate hospital medicine in person at Hospital Medicine 2019 (HM19), March 24-27 in National Harbor, Md.
While at HM19, check out more than 20 educational tracks, including clinical updates, diagnostic reasoning, and health policy. New this year are two mini tracks: “Between the Guidelines” and “Clinical Mastery”. Between the Guidelines explores how we can address some of the most challenging cases we encounter in hospital medicine, where clear guidelines don’t exist. Clinical Mastery is designed to enhance our bedside diagnostic skills, from ECGs to ultrasounds.
Get ready to vote in HM19’s “The Great Debate” – pairing two talented clinicians who will debate opposing sides of challenging clinical decisions that we encounter on the front lines of health care delivery. Attendees have the opportunity to hear the two sides and then vote on who they believe has the right approach. There are six precourses planned for HM19, with a new offering in Palliative Care and Pain Management. This year, the annual conference also features additional sessions for our NP/PA attendees. They include specific workshops as well as a track that includes 4 didactic sessions. Lastly, HM19 will offer CME, MOC, AOS, AAFP, and Pharmacology credits to address the needs of our attendees.
Looking into the future
While hospitalists are a vital part of U.S. health care, our delivery systems are in transition with greater focus on value-based care. To ensure hospital medicine continues to thrive in today’s dynamic scene, SHM’s Board of Directors held a strategic meeting in October 2018 to focus on the role of hospitalists and hospital medicine in population health management.
There are many hospitalists across the nation who are currently involved in population health management. These range from medical directors to vice presidents of accountable care organizations, population health management, or value-based care. Hospitalists are seeking communities focused on population health management to share best practices and learn from each other. To address this, SHM’s Advocacy and Public Policy HMX community has served as a meeting point to discuss issues related to value-based care. To join the discussion, visit the community by logging in at hospitalmedicine.org/hmx. Furthermore, at HM19, hospitalists will have the opportunity to meet face to face regarding these issues in the Advocacy Special Interest Forum.
Key points: Population health management
- Source of truth
SHM has served as the source of reliable and trusted information about hospital medicine. We will continue to develop content and resources specific to population health management on our website so hospitalists can easily access this information. To increase our awareness about population health management, presenters at HM19 will integrate a slide about the implications of population health management on their clinical topic. These slides will illustrate the clinical and nonclinical services that are necessary to enhance the patient’s quality of care and life. In addition to best practice care, these slides will highlight topics like the role of style modification and prevention, risk stratification, chronic disease management, and care coordination throughout the continuum of care.
- Advocating for us
In addition to providing a home for hospitalists to collaborate regarding population health management, SHM will advance this agenda from a regulatory perspective. The Public Policy and Performance Measurement & Reporting Committees are actively evaluating and leading the transition from value to volume. SHM is also working with potential key partners and organizations in the areas of primary care, skilled nursing facilities, and accountable care organizations that will help improve the effectiveness of delivering population health management.
- Creating expertise
SHM will lead best practice development for tools and skills that are necessary for hospitalists to lead population health management. Telemedicine is an increasingly critical tool as we help manage our patients in other facilities, inpatient or skilled nursing facilities, as well as at home. SHM has developed a white paper about telemedicine in hospital medicine that highlights modalities, offerings, implementation of programs, and work flows necessary for success. You can find it under “Resources” at hospitalmedicine.org/telemedicine.
SHM will continue to actively develop tools that appropriately address the challenges we’re facing. From National Hospitalist Day to population health management, this is an exciting time in hospital medicine – I hope to see you at HM19 to celebrate our specialty and our bright future.
Dr. Afsar is president of the Society of Hospital Medicine, and chief ambulatory officer and chief medical officer for accountable care organizations at UC Irvine Health.
For the first time ever, on March 7, 2019, tens of thousands of hospitalists across the United States and around the world will celebrate their day, National Hospitalist Day.
On this day, we will honor the hard work and dedication of hospitalists in the care of millions of hospitalized patients. With more than 62,000 hospitalists across the United States, hospital medicine has been the fastest growing medical specialty and among the largest of all specialties in medicine. Hospitalists now lead clinical care in over 75% of U.S. hospitals, caring for patients in their communities. We educate the future providers of health care by serving as teachers and mentors. We push the boundaries of science in hospital care through innovative research that defines the evidence-based practices for our field. Hospitalists, proudly celebrate all that we have accomplished together on March 7, and moving forward, every first Thursday in March annually.
The Society for Hospital Medicine’s celebration of National Hospitalist Day will include spotlights on hospitalists, a social medical campaign, downloadable customizable posters, and much more. Stay tuned for details!
Attend the only meeting designed just for you
Be among the thousands of hospitalists who will celebrate hospital medicine in person at Hospital Medicine 2019 (HM19), March 24-27 in National Harbor, Md.
While at HM19, check out more than 20 educational tracks, including clinical updates, diagnostic reasoning, and health policy. New this year are two mini tracks: “Between the Guidelines” and “Clinical Mastery”. Between the Guidelines explores how we can address some of the most challenging cases we encounter in hospital medicine, where clear guidelines don’t exist. Clinical Mastery is designed to enhance our bedside diagnostic skills, from ECGs to ultrasounds.
Get ready to vote in HM19’s “The Great Debate” – pairing two talented clinicians who will debate opposing sides of challenging clinical decisions that we encounter on the front lines of health care delivery. Attendees have the opportunity to hear the two sides and then vote on who they believe has the right approach. There are six precourses planned for HM19, with a new offering in Palliative Care and Pain Management. This year, the annual conference also features additional sessions for our NP/PA attendees. They include specific workshops as well as a track that includes 4 didactic sessions. Lastly, HM19 will offer CME, MOC, AOS, AAFP, and Pharmacology credits to address the needs of our attendees.
Looking into the future
While hospitalists are a vital part of U.S. health care, our delivery systems are in transition with greater focus on value-based care. To ensure hospital medicine continues to thrive in today’s dynamic scene, SHM’s Board of Directors held a strategic meeting in October 2018 to focus on the role of hospitalists and hospital medicine in population health management.
There are many hospitalists across the nation who are currently involved in population health management. These range from medical directors to vice presidents of accountable care organizations, population health management, or value-based care. Hospitalists are seeking communities focused on population health management to share best practices and learn from each other. To address this, SHM’s Advocacy and Public Policy HMX community has served as a meeting point to discuss issues related to value-based care. To join the discussion, visit the community by logging in at hospitalmedicine.org/hmx. Furthermore, at HM19, hospitalists will have the opportunity to meet face to face regarding these issues in the Advocacy Special Interest Forum.
Key points: Population health management
- Source of truth
SHM has served as the source of reliable and trusted information about hospital medicine. We will continue to develop content and resources specific to population health management on our website so hospitalists can easily access this information. To increase our awareness about population health management, presenters at HM19 will integrate a slide about the implications of population health management on their clinical topic. These slides will illustrate the clinical and nonclinical services that are necessary to enhance the patient’s quality of care and life. In addition to best practice care, these slides will highlight topics like the role of style modification and prevention, risk stratification, chronic disease management, and care coordination throughout the continuum of care.
- Advocating for us
In addition to providing a home for hospitalists to collaborate regarding population health management, SHM will advance this agenda from a regulatory perspective. The Public Policy and Performance Measurement & Reporting Committees are actively evaluating and leading the transition from value to volume. SHM is also working with potential key partners and organizations in the areas of primary care, skilled nursing facilities, and accountable care organizations that will help improve the effectiveness of delivering population health management.
- Creating expertise
SHM will lead best practice development for tools and skills that are necessary for hospitalists to lead population health management. Telemedicine is an increasingly critical tool as we help manage our patients in other facilities, inpatient or skilled nursing facilities, as well as at home. SHM has developed a white paper about telemedicine in hospital medicine that highlights modalities, offerings, implementation of programs, and work flows necessary for success. You can find it under “Resources” at hospitalmedicine.org/telemedicine.
SHM will continue to actively develop tools that appropriately address the challenges we’re facing. From National Hospitalist Day to population health management, this is an exciting time in hospital medicine – I hope to see you at HM19 to celebrate our specialty and our bright future.
Dr. Afsar is president of the Society of Hospital Medicine, and chief ambulatory officer and chief medical officer for accountable care organizations at UC Irvine Health.
Back pain persists in one in five patients
according to data from a population-based study of more than 12,000 adults in Canada.
“Given that back pain [BP] is often recurrent, it is important to understand the course of back pain over time as this can provide additional insights on risk factors for nonfavorable outcomes,” wrote Mayilee Canizares, PhD, and her colleagues at the University Health Network’s Krembil Research Institute in Toronto.
In a longitudinal study published in Arthritis Care & Research, the investigators followed 12,782 adults from 1994 to 2011. The study population was a representative sample of the Canadian population via the National Population Health Survey, which collected data every 2 years for a total of nine cycles of data. They included people aged 15 years or older in 1994-1995 who had at least three cycles of data from baseline onward.
Over the 16-year study period, 46% of the participants reported at least one episode of back pain. Of these, 18% were identified as persistent, 28% as developing, 21% as recovering, and 33% as occasional.
“A major finding from this study is the negative impact of persistent BP on a range of health-related outcomes, including health care use, after adjustments for sociodemographic, behavior-related factors, and comorbidities,” the researchers wrote.
They examined several sociodemographic variables, including age, gender, educational level, and household income, as well as behavior-related variables including physical activity, work activity, smoking status, and obesity. The average age of the participants at baseline was 39 years; 51% were female.
Individuals who reported any back pain were more likely than those with no back pain to be overweight or obese, to smoke, to engage in moderate to heavy physical activity each day, and to have chronic conditions, including arthritis, depression, high blood pressure, and migraine.
Overall, individuals with persistent or developing BP had more pain, disability, health care visits, and medication use, compared with those in the recovery and occasional BP groups. However, individuals in the recovery group showed increased use of opioids and antidepressants over time as well, suggesting a need for long-term monitoring of back pain patients.
The trend in general disability was greatest for individuals in the persistent group followed by the developing group, recovery group, and occasional BP group.
The study findings were limited by several factors, including the use of self-reports, potential selection bias, and the inability to differentiate the specific types of back pain, the researchers noted. However, the results support and extend data from previous studies and provide clinical implications for understanding back pain.
The researchers concluded that “the different trajectory patterns potentially represent subgroups in the population that may require different interventions. In light of the trend of marked worsening outcomes, particularly for the persistent and developing groups, studies are needed to determine the nature of these groups.”
The authors reported no relevant financial conflicts.
SOURCE: Canizares M et al. Arthritis Care Res. 2019 Jan 14. doi: 10.1002/acr.23811.
according to data from a population-based study of more than 12,000 adults in Canada.
“Given that back pain [BP] is often recurrent, it is important to understand the course of back pain over time as this can provide additional insights on risk factors for nonfavorable outcomes,” wrote Mayilee Canizares, PhD, and her colleagues at the University Health Network’s Krembil Research Institute in Toronto.
In a longitudinal study published in Arthritis Care & Research, the investigators followed 12,782 adults from 1994 to 2011. The study population was a representative sample of the Canadian population via the National Population Health Survey, which collected data every 2 years for a total of nine cycles of data. They included people aged 15 years or older in 1994-1995 who had at least three cycles of data from baseline onward.
Over the 16-year study period, 46% of the participants reported at least one episode of back pain. Of these, 18% were identified as persistent, 28% as developing, 21% as recovering, and 33% as occasional.
“A major finding from this study is the negative impact of persistent BP on a range of health-related outcomes, including health care use, after adjustments for sociodemographic, behavior-related factors, and comorbidities,” the researchers wrote.
They examined several sociodemographic variables, including age, gender, educational level, and household income, as well as behavior-related variables including physical activity, work activity, smoking status, and obesity. The average age of the participants at baseline was 39 years; 51% were female.
Individuals who reported any back pain were more likely than those with no back pain to be overweight or obese, to smoke, to engage in moderate to heavy physical activity each day, and to have chronic conditions, including arthritis, depression, high blood pressure, and migraine.
Overall, individuals with persistent or developing BP had more pain, disability, health care visits, and medication use, compared with those in the recovery and occasional BP groups. However, individuals in the recovery group showed increased use of opioids and antidepressants over time as well, suggesting a need for long-term monitoring of back pain patients.
The trend in general disability was greatest for individuals in the persistent group followed by the developing group, recovery group, and occasional BP group.
The study findings were limited by several factors, including the use of self-reports, potential selection bias, and the inability to differentiate the specific types of back pain, the researchers noted. However, the results support and extend data from previous studies and provide clinical implications for understanding back pain.
The researchers concluded that “the different trajectory patterns potentially represent subgroups in the population that may require different interventions. In light of the trend of marked worsening outcomes, particularly for the persistent and developing groups, studies are needed to determine the nature of these groups.”
The authors reported no relevant financial conflicts.
SOURCE: Canizares M et al. Arthritis Care Res. 2019 Jan 14. doi: 10.1002/acr.23811.
according to data from a population-based study of more than 12,000 adults in Canada.
“Given that back pain [BP] is often recurrent, it is important to understand the course of back pain over time as this can provide additional insights on risk factors for nonfavorable outcomes,” wrote Mayilee Canizares, PhD, and her colleagues at the University Health Network’s Krembil Research Institute in Toronto.
In a longitudinal study published in Arthritis Care & Research, the investigators followed 12,782 adults from 1994 to 2011. The study population was a representative sample of the Canadian population via the National Population Health Survey, which collected data every 2 years for a total of nine cycles of data. They included people aged 15 years or older in 1994-1995 who had at least three cycles of data from baseline onward.
Over the 16-year study period, 46% of the participants reported at least one episode of back pain. Of these, 18% were identified as persistent, 28% as developing, 21% as recovering, and 33% as occasional.
“A major finding from this study is the negative impact of persistent BP on a range of health-related outcomes, including health care use, after adjustments for sociodemographic, behavior-related factors, and comorbidities,” the researchers wrote.
They examined several sociodemographic variables, including age, gender, educational level, and household income, as well as behavior-related variables including physical activity, work activity, smoking status, and obesity. The average age of the participants at baseline was 39 years; 51% were female.
Individuals who reported any back pain were more likely than those with no back pain to be overweight or obese, to smoke, to engage in moderate to heavy physical activity each day, and to have chronic conditions, including arthritis, depression, high blood pressure, and migraine.
Overall, individuals with persistent or developing BP had more pain, disability, health care visits, and medication use, compared with those in the recovery and occasional BP groups. However, individuals in the recovery group showed increased use of opioids and antidepressants over time as well, suggesting a need for long-term monitoring of back pain patients.
The trend in general disability was greatest for individuals in the persistent group followed by the developing group, recovery group, and occasional BP group.
The study findings were limited by several factors, including the use of self-reports, potential selection bias, and the inability to differentiate the specific types of back pain, the researchers noted. However, the results support and extend data from previous studies and provide clinical implications for understanding back pain.
The researchers concluded that “the different trajectory patterns potentially represent subgroups in the population that may require different interventions. In light of the trend of marked worsening outcomes, particularly for the persistent and developing groups, studies are needed to determine the nature of these groups.”
The authors reported no relevant financial conflicts.
SOURCE: Canizares M et al. Arthritis Care Res. 2019 Jan 14. doi: 10.1002/acr.23811.
FROM ARTHRITIS CARE & RESEARCH
Key clinical point: Back pain is a common health problem, and one in five Canadian adults reported persistent back pain.
Major finding: Approximately half (46%) of Canadian adults reported some type of back pain over a 16-year period.
Study details: The data come from a population-based study of 12,782 adults followed from 1994 to 2011.
Disclosures: The authors reported no relevant financial conflicts.
Source: Canizares M et al. Arthritis Care Res. 2019 Jan 14. doi: 10.1002/acr.23811.