Bags and vials of blood

Photo by Daniel Gay

Researchers have discovered a bloodborne virus, known as human pegivirus 2 (HPgV-2), in patients with hepatitis C virus (HCV).

The team identified 8 complete strains of HPgV-2 and noted that the virus was only found in patients who tested positive for HCV RNA. However, it’s not clear if HPgV-2 causes hepatitis.

Charles Chiu, MD, PhD, of the University of California San Francisco, and his colleagues described their discovery of HPgV-2 in PLOS Pathogens.

The team identified the virus by sequencing plasma from an HCV-infected patient with multiple bloodborne exposures who died from sepsis of unknown etiology.

They said HPgV-2 is “highly divergent,” sharing less than 32% amino acid identity with its nearest relatives, rodent and bat pegiviruses.

After their initial discovery, the researchers screened an additional 2440 plasma samples and found 11 HPgV-2 RNA-positive samples.

All 12 HPgV-2 RNA-positive cases were found in patients who tested positive for HCV RNA, including 2 patients who were also infected with HIV.

The researchers performed longitudinal sampling in 2 patients and found that active HPgV-2 infection can persist in blood for at least 7 weeks, despite the presence of virus-specific antibodies.

The team also identified 1 patient with HPgV-2 and HCV RNA who was seronegative for both viruses. They said this suggests a high likelihood of simultaneous acquisition of HCV and HPgV-2 infection from an acute co-transmission event.

“Based on our findings, our team used the genetic makeup of the virus to develop both a molecular test for detecting it in the bloodstream and an antibody test for determining an immune response to the virus,” said John Hackett Jr, PhD, of Abbott Laboratories, Inc. in Abbott Park, Illinois.

“Our next step is to explore whether this new virus can cause disease, and if so, work with blood banks to continue to help safeguard the world’s blood supply against these types of new viruses. Research such as this is ultimately focused on unlocking new technologies that hold the potential for significant improvements to the practice of healthcare.”

Bags and vials of blood

Photo by Daniel Gay

Researchers have discovered a bloodborne virus, known as human pegivirus 2 (HPgV-2), in patients with hepatitis C virus (HCV).

The team identified 8 complete strains of HPgV-2 and noted that the virus was only found in patients who tested positive for HCV RNA. However, it’s not clear if HPgV-2 causes hepatitis.

Charles Chiu, MD, PhD, of the University of California San Francisco, and his colleagues described their discovery of HPgV-2 in PLOS Pathogens.

The team identified the virus by sequencing plasma from an HCV-infected patient with multiple bloodborne exposures who died from sepsis of unknown etiology.

They said HPgV-2 is “highly divergent,” sharing less than 32% amino acid identity with its nearest relatives, rodent and bat pegiviruses.

After their initial discovery, the researchers screened an additional 2440 plasma samples and found 11 HPgV-2 RNA-positive samples.

All 12 HPgV-2 RNA-positive cases were found in patients who tested positive for HCV RNA, including 2 patients who were also infected with HIV.

The researchers performed longitudinal sampling in 2 patients and found that active HPgV-2 infection can persist in blood for at least 7 weeks, despite the presence of virus-specific antibodies.

The team also identified 1 patient with HPgV-2 and HCV RNA who was seronegative for both viruses. They said this suggests a high likelihood of simultaneous acquisition of HCV and HPgV-2 infection from an acute co-transmission event.

“Based on our findings, our team used the genetic makeup of the virus to develop both a molecular test for detecting it in the bloodstream and an antibody test for determining an immune response to the virus,” said John Hackett Jr, PhD, of Abbott Laboratories, Inc. in Abbott Park, Illinois.

“Our next step is to explore whether this new virus can cause disease, and if so, work with blood banks to continue to help safeguard the world’s blood supply against these types of new viruses. Research such as this is ultimately focused on unlocking new technologies that hold the potential for significant improvements to the practice of healthcare.”

Bags and vials of blood

Photo by Daniel Gay

Researchers have discovered a bloodborne virus, known as human pegivirus 2 (HPgV-2), in patients with hepatitis C virus (HCV).

The team identified 8 complete strains of HPgV-2 and noted that the virus was only found in patients who tested positive for HCV RNA. However, it’s not clear if HPgV-2 causes hepatitis.

Charles Chiu, MD, PhD, of the University of California San Francisco, and his colleagues described their discovery of HPgV-2 in PLOS Pathogens.

The team identified the virus by sequencing plasma from an HCV-infected patient with multiple bloodborne exposures who died from sepsis of unknown etiology.

They said HPgV-2 is “highly divergent,” sharing less than 32% amino acid identity with its nearest relatives, rodent and bat pegiviruses.

After their initial discovery, the researchers screened an additional 2440 plasma samples and found 11 HPgV-2 RNA-positive samples.

All 12 HPgV-2 RNA-positive cases were found in patients who tested positive for HCV RNA, including 2 patients who were also infected with HIV.

The researchers performed longitudinal sampling in 2 patients and found that active HPgV-2 infection can persist in blood for at least 7 weeks, despite the presence of virus-specific antibodies.

The team also identified 1 patient with HPgV-2 and HCV RNA who was seronegative for both viruses. They said this suggests a high likelihood of simultaneous acquisition of HCV and HPgV-2 infection from an acute co-transmission event.

“Based on our findings, our team used the genetic makeup of the virus to develop both a molecular test for detecting it in the bloodstream and an antibody test for determining an immune response to the virus,” said John Hackett Jr, PhD, of Abbott Laboratories, Inc. in Abbott Park, Illinois.

“Our next step is to explore whether this new virus can cause disease, and if so, work with blood banks to continue to help safeguard the world’s blood supply against these types of new viruses. Research such as this is ultimately focused on unlocking new technologies that hold the potential for significant improvements to the practice of healthcare.”

Click here to access the 2016 Directory of VA and DoD Facilities Digital Edition

Table of Contents

• Letter From the Publisher
• Explanatory Notes and Abbreviation Key
• Veterans Integrated Service Network (VISN) Guide / MyVA Regions Guide
• Department of Veterans Affairs Health Care Facilities
• TRICARE Region Guide
• Department of Defense Health Care Facilities

Click here to access the 2016 Directory of VA and DoD Facilities Digital Edition

Table of Contents

• Letter From the Publisher
• Explanatory Notes and Abbreviation Key
• Veterans Integrated Service Network (VISN) Guide / MyVA Regions Guide
• Department of Veterans Affairs Health Care Facilities
• TRICARE Region Guide
• Department of Defense Health Care Facilities

Click here to access the 2016 Directory of VA and DoD Facilities Digital Edition

Table of Contents

• Letter From the Publisher
• Explanatory Notes and Abbreviation Key
• Veterans Integrated Service Network (VISN) Guide / MyVA Regions Guide
• Department of Veterans Affairs Health Care Facilities
• TRICARE Region Guide
• Department of Defense Health Care Facilities

Patients with hepatitis C virus (HCV) infection face a significantly increased risk of cardiovascular death, subclinical carotid thickening and atherosclerosis, and cerebrocardiovascular events, especially when they also have diabetes and hypertension, according to a systematic review and meta-analysis of 22 studies published in the January issue of Gastroenterology.

“To our knowledge, our meta-analysis clearly highlights, for the first time, that HCV infection increases the risk of cardiovascular disease-related mortality,” wrote Dr. Salvatore Petta and his associates at the University of Palermo, Italy. “We [also] found a twofold higher risk of subclinical carotid plaques among HCV-infected individuals compared to uninfected controls, without significant heterogeneity among studies, as well as an increased risk of carotid thickening. We observed a slightly significant increase in cerebrocardiovascular events among HCV-infected patients, despite the high heterogeneity among studies that was mostly related to the prevalence of diabetes mellitus and hypertension.”

Jezperklauzen/ThinkStock.com

A number of observational studies have reported cardiovascular outcomes in HCV-infected patients, but results have been “ambiguous,” Dr. Petta and his colleagues said. For their meta-analysis, they searched PubMed, Medline, EMBASE, the Cochrane Library, and reference lists of articles to identify studies published through July 2015 that either compared cardiovascular disease between HCV-infected and uninfected patients, or evaluated the prevalence of HCV infection among patients with cardiovascular disease. This literature search identified 12 case-control studies and 10 cohort studies. Outcome measures included carotid atherosclerosis (nine studies), intima media thickness (eight studies), coronary artery disease (seven studies), stroke (six studies), and cardiovascular mortality (three studies) (Gastroenterology. 2015 Sep 18. doi: 10.1053/j.gastro.2015.09.00).In the pooled analysis, the odds of cardiovascular death were 65% higher in HCV-infected patients, compared with uninfected individuals (95% confidence interval for this increase, 1.07%-2.56%). Compared with controls, HCV-infected patients also were at higher risk of carotid plaques (odds ratio, 2.27; 95% CI, 1.76-2.94), especially when they were smokers (P = .02). HCV infection also significantly increased the odds of carotid artery intima-media thickening (OR, 1.20; 95% CI, 1.03-1.40), and cerebrocardiovascular events (OR, 1.30; 95% CI, 1.10-1.55). However, subgroup analyses showed that HCV infection only increased the likelihood of cerebrocardiovascular events in populations with a more than 10% prevalence of diabetes or a more than 20% prevalence of hypertension (OR, 1.71; P less than .001 for both subgroup analyses).

Because the studies of cerebrocardiovascular events were heterogeneous, the researchers also stratified them by study design and by the average age of patients. Pooled odds ratios for the link between HCV infection and cerebrocardiovascular events remained significant at 1.21 for the cohort studies, 2.01 for the case-control studies, 2.46 among patients who averaged more than 50 years of age, and 1.35 among younger patients.

The Egger test for publication bias showed that the literature search was unlikely to have overlooked studies in terms of any of the outcome measures, the investigators noted. “From a clinical standpoint, the results of our meta-analysis suggest that HCV infection increases cardiovascular risk, particularly for individuals who already have cardiovascular risk factors, such as diabetes and hypertension,” they concluded. “Although effective and safe oral antiviral regimens are available, more information is needed to confirm whether anti-HCV medications will decrease cardiovascular risk, as suggested in some studies.”

The researchers reported having no funding sources or conflicts of interest.

Source: American Gastroenterological Association

Patients with hepatitis C virus (HCV) infection face a significantly increased risk of cardiovascular death, subclinical carotid thickening and atherosclerosis, and cerebrocardiovascular events, especially when they also have diabetes and hypertension, according to a systematic review and meta-analysis of 22 studies published in the January issue of Gastroenterology.

“To our knowledge, our meta-analysis clearly highlights, for the first time, that HCV infection increases the risk of cardiovascular disease-related mortality,” wrote Dr. Salvatore Petta and his associates at the University of Palermo, Italy. “We [also] found a twofold higher risk of subclinical carotid plaques among HCV-infected individuals compared to uninfected controls, without significant heterogeneity among studies, as well as an increased risk of carotid thickening. We observed a slightly significant increase in cerebrocardiovascular events among HCV-infected patients, despite the high heterogeneity among studies that was mostly related to the prevalence of diabetes mellitus and hypertension.”

Jezperklauzen/ThinkStock.com

A number of observational studies have reported cardiovascular outcomes in HCV-infected patients, but results have been “ambiguous,” Dr. Petta and his colleagues said. For their meta-analysis, they searched PubMed, Medline, EMBASE, the Cochrane Library, and reference lists of articles to identify studies published through July 2015 that either compared cardiovascular disease between HCV-infected and uninfected patients, or evaluated the prevalence of HCV infection among patients with cardiovascular disease. This literature search identified 12 case-control studies and 10 cohort studies. Outcome measures included carotid atherosclerosis (nine studies), intima media thickness (eight studies), coronary artery disease (seven studies), stroke (six studies), and cardiovascular mortality (three studies) (Gastroenterology. 2015 Sep 18. doi: 10.1053/j.gastro.2015.09.00).In the pooled analysis, the odds of cardiovascular death were 65% higher in HCV-infected patients, compared with uninfected individuals (95% confidence interval for this increase, 1.07%-2.56%). Compared with controls, HCV-infected patients also were at higher risk of carotid plaques (odds ratio, 2.27; 95% CI, 1.76-2.94), especially when they were smokers (P = .02). HCV infection also significantly increased the odds of carotid artery intima-media thickening (OR, 1.20; 95% CI, 1.03-1.40), and cerebrocardiovascular events (OR, 1.30; 95% CI, 1.10-1.55). However, subgroup analyses showed that HCV infection only increased the likelihood of cerebrocardiovascular events in populations with a more than 10% prevalence of diabetes or a more than 20% prevalence of hypertension (OR, 1.71; P less than .001 for both subgroup analyses).

Because the studies of cerebrocardiovascular events were heterogeneous, the researchers also stratified them by study design and by the average age of patients. Pooled odds ratios for the link between HCV infection and cerebrocardiovascular events remained significant at 1.21 for the cohort studies, 2.01 for the case-control studies, 2.46 among patients who averaged more than 50 years of age, and 1.35 among younger patients.

The Egger test for publication bias showed that the literature search was unlikely to have overlooked studies in terms of any of the outcome measures, the investigators noted. “From a clinical standpoint, the results of our meta-analysis suggest that HCV infection increases cardiovascular risk, particularly for individuals who already have cardiovascular risk factors, such as diabetes and hypertension,” they concluded. “Although effective and safe oral antiviral regimens are available, more information is needed to confirm whether anti-HCV medications will decrease cardiovascular risk, as suggested in some studies.”

The researchers reported having no funding sources or conflicts of interest.

Source: American Gastroenterological Association

Patients with hepatitis C virus (HCV) infection face a significantly increased risk of cardiovascular death, subclinical carotid thickening and atherosclerosis, and cerebrocardiovascular events, especially when they also have diabetes and hypertension, according to a systematic review and meta-analysis of 22 studies published in the January issue of Gastroenterology.

“To our knowledge, our meta-analysis clearly highlights, for the first time, that HCV infection increases the risk of cardiovascular disease-related mortality,” wrote Dr. Salvatore Petta and his associates at the University of Palermo, Italy. “We [also] found a twofold higher risk of subclinical carotid plaques among HCV-infected individuals compared to uninfected controls, without significant heterogeneity among studies, as well as an increased risk of carotid thickening. We observed a slightly significant increase in cerebrocardiovascular events among HCV-infected patients, despite the high heterogeneity among studies that was mostly related to the prevalence of diabetes mellitus and hypertension.”

Jezperklauzen/ThinkStock.com

A number of observational studies have reported cardiovascular outcomes in HCV-infected patients, but results have been “ambiguous,” Dr. Petta and his colleagues said. For their meta-analysis, they searched PubMed, Medline, EMBASE, the Cochrane Library, and reference lists of articles to identify studies published through July 2015 that either compared cardiovascular disease between HCV-infected and uninfected patients, or evaluated the prevalence of HCV infection among patients with cardiovascular disease. This literature search identified 12 case-control studies and 10 cohort studies. Outcome measures included carotid atherosclerosis (nine studies), intima media thickness (eight studies), coronary artery disease (seven studies), stroke (six studies), and cardiovascular mortality (three studies) (Gastroenterology. 2015 Sep 18. doi: 10.1053/j.gastro.2015.09.00).In the pooled analysis, the odds of cardiovascular death were 65% higher in HCV-infected patients, compared with uninfected individuals (95% confidence interval for this increase, 1.07%-2.56%). Compared with controls, HCV-infected patients also were at higher risk of carotid plaques (odds ratio, 2.27; 95% CI, 1.76-2.94), especially when they were smokers (P = .02). HCV infection also significantly increased the odds of carotid artery intima-media thickening (OR, 1.20; 95% CI, 1.03-1.40), and cerebrocardiovascular events (OR, 1.30; 95% CI, 1.10-1.55). However, subgroup analyses showed that HCV infection only increased the likelihood of cerebrocardiovascular events in populations with a more than 10% prevalence of diabetes or a more than 20% prevalence of hypertension (OR, 1.71; P less than .001 for both subgroup analyses).

Because the studies of cerebrocardiovascular events were heterogeneous, the researchers also stratified them by study design and by the average age of patients. Pooled odds ratios for the link between HCV infection and cerebrocardiovascular events remained significant at 1.21 for the cohort studies, 2.01 for the case-control studies, 2.46 among patients who averaged more than 50 years of age, and 1.35 among younger patients.

The Egger test for publication bias showed that the literature search was unlikely to have overlooked studies in terms of any of the outcome measures, the investigators noted. “From a clinical standpoint, the results of our meta-analysis suggest that HCV infection increases cardiovascular risk, particularly for individuals who already have cardiovascular risk factors, such as diabetes and hypertension,” they concluded. “Although effective and safe oral antiviral regimens are available, more information is needed to confirm whether anti-HCV medications will decrease cardiovascular risk, as suggested in some studies.”

The researchers reported having no funding sources or conflicts of interest.

Source: American Gastroenterological Association

About 13% of U.S. veterans with hepatocellular carcinoma had no evidence of preexisting cirrhosis, according to a report published in the January issue of Clinical Gastroenterology and Hepatology.

“The main risk factors for this entity were nonalcoholic fatty liver disease [NAFLD] or metabolic syndrome” – not hepatitis C virus infection [HCV], HBV [hepatitis B virus] infection, or alcohol abuse, said Dr. Sahil Mittal of the Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston. Screening all patients with NAFLD for hepatocellular carcinoma [HCC] is impractical, so studies should seek “actionable risk factors” or biomarkers that reliably identify NAFLD patients who are at particular risk of HCC, wrote Dr. Mittal and his coinvestigators.

Courtesy of Wikimedia / Nephron / Creative Commons License

Researchers have debated whether chronic HCV infection or alcohol abuse can lead to HCC in the absence of cirrhosis, while at least one study has shown that NAFLD can predispose patients to this disease entity (Arch Pathol Lab Med. 2008;132:1761-6).

But few studies have systematically examined risk factors for HCC without cirrhosis in the general population, the investigators said. Therefore, they randomly selected 1,500 patients from the U.S. Veterans Affairs system who were diagnosed with HCC between 2005 and 2010 on the basis of histopathology or established imaging criteria (Hepatology 2005;42:1208-36).

They reviewed complete medical records for these patients, and classified those who did not have cirrhosis according to the quality of supporting histology, laboratory, and imaging data (Clin Gastroenterol Hepatol. 2015. doi: 0.1016/j.cgh.2015.07.019).

In all, 3% of the cohort had level 1 (“highest-quality”) evidence for not having cirrhosis, while another 10% had level 2 evidence for no cirrhosis, the investigators said. “Compared with HCC in the presence of cirrhosis, these patients were more likely to have metabolic syndrome or NAFLD or no identifiable risk factor, and less likely to have alcohol abuse or HCV infection,” they added. Only two-thirds of NAFLD patients with HCC had cirrhosis, compared with 91% of patients with chronic HCV infection, 92% of HCV-infected patients, and 88% of patients with an alcohol use disorder. Notably, the odds of HCC in the absence of cirrhosis were more than five times higher when patients had NAFLD (odds ratio [OR], 5.4; 95% confidence interval [CI], 3.4-8.5) or metabolic syndrome (OR, 5.0; 95% CI, 3.1-7.8) compared with HCV infection.

Patients with cirrhosis often go unscreened for HCC even though they are at greatest risk of this cancer. Therefore, trying to screen all patients with NAFLD for HCC would be “logistically impractical,” particularly when the absolute risk of HCC in noncirrhotic patients is unknown and no one has examined the best ways to screen this population, the investigators said. Instead, clinicians could prioritize screening and treating NAFLD patients for diabetes mellitus and obesity, both of which are associated with HCC. “There is evidence to suggest that metformin reduces the risk of HCC among diabetics,” they added. “Studies of these and other risk factors of HCC among NAFLD patients with and without cirrhosis are needed.”

Most patients in the study were male, potentially limiting the generalizability of the findings, the researchers noted.

The National Cancer Institute, the Houston Veterans Affairs Health Services Research and Development Center of Excellence, the Michael E. DeBakey Veterans Affairs Medical Center, and the Dan Duncan Cancer Center funded the study. The researchers had no disclosures.

About 13% of U.S. veterans with hepatocellular carcinoma had no evidence of preexisting cirrhosis, according to a report published in the January issue of Clinical Gastroenterology and Hepatology.

“The main risk factors for this entity were nonalcoholic fatty liver disease [NAFLD] or metabolic syndrome” – not hepatitis C virus infection [HCV], HBV [hepatitis B virus] infection, or alcohol abuse, said Dr. Sahil Mittal of the Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston. Screening all patients with NAFLD for hepatocellular carcinoma [HCC] is impractical, so studies should seek “actionable risk factors” or biomarkers that reliably identify NAFLD patients who are at particular risk of HCC, wrote Dr. Mittal and his coinvestigators.

Courtesy of Wikimedia / Nephron / Creative Commons License

Researchers have debated whether chronic HCV infection or alcohol abuse can lead to HCC in the absence of cirrhosis, while at least one study has shown that NAFLD can predispose patients to this disease entity (Arch Pathol Lab Med. 2008;132:1761-6).

But few studies have systematically examined risk factors for HCC without cirrhosis in the general population, the investigators said. Therefore, they randomly selected 1,500 patients from the U.S. Veterans Affairs system who were diagnosed with HCC between 2005 and 2010 on the basis of histopathology or established imaging criteria (Hepatology 2005;42:1208-36).

They reviewed complete medical records for these patients, and classified those who did not have cirrhosis according to the quality of supporting histology, laboratory, and imaging data (Clin Gastroenterol Hepatol. 2015. doi: 0.1016/j.cgh.2015.07.019).

In all, 3% of the cohort had level 1 (“highest-quality”) evidence for not having cirrhosis, while another 10% had level 2 evidence for no cirrhosis, the investigators said. “Compared with HCC in the presence of cirrhosis, these patients were more likely to have metabolic syndrome or NAFLD or no identifiable risk factor, and less likely to have alcohol abuse or HCV infection,” they added. Only two-thirds of NAFLD patients with HCC had cirrhosis, compared with 91% of patients with chronic HCV infection, 92% of HCV-infected patients, and 88% of patients with an alcohol use disorder. Notably, the odds of HCC in the absence of cirrhosis were more than five times higher when patients had NAFLD (odds ratio [OR], 5.4; 95% confidence interval [CI], 3.4-8.5) or metabolic syndrome (OR, 5.0; 95% CI, 3.1-7.8) compared with HCV infection.

Patients with cirrhosis often go unscreened for HCC even though they are at greatest risk of this cancer. Therefore, trying to screen all patients with NAFLD for HCC would be “logistically impractical,” particularly when the absolute risk of HCC in noncirrhotic patients is unknown and no one has examined the best ways to screen this population, the investigators said. Instead, clinicians could prioritize screening and treating NAFLD patients for diabetes mellitus and obesity, both of which are associated with HCC. “There is evidence to suggest that metformin reduces the risk of HCC among diabetics,” they added. “Studies of these and other risk factors of HCC among NAFLD patients with and without cirrhosis are needed.”

Most patients in the study were male, potentially limiting the generalizability of the findings, the researchers noted.

The National Cancer Institute, the Houston Veterans Affairs Health Services Research and Development Center of Excellence, the Michael E. DeBakey Veterans Affairs Medical Center, and the Dan Duncan Cancer Center funded the study. The researchers had no disclosures.

About 13% of U.S. veterans with hepatocellular carcinoma had no evidence of preexisting cirrhosis, according to a report published in the January issue of Clinical Gastroenterology and Hepatology.

“The main risk factors for this entity were nonalcoholic fatty liver disease [NAFLD] or metabolic syndrome” – not hepatitis C virus infection [HCV], HBV [hepatitis B virus] infection, or alcohol abuse, said Dr. Sahil Mittal of the Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston. Screening all patients with NAFLD for hepatocellular carcinoma [HCC] is impractical, so studies should seek “actionable risk factors” or biomarkers that reliably identify NAFLD patients who are at particular risk of HCC, wrote Dr. Mittal and his coinvestigators.

Courtesy of Wikimedia / Nephron / Creative Commons License

Researchers have debated whether chronic HCV infection or alcohol abuse can lead to HCC in the absence of cirrhosis, while at least one study has shown that NAFLD can predispose patients to this disease entity (Arch Pathol Lab Med. 2008;132:1761-6).

But few studies have systematically examined risk factors for HCC without cirrhosis in the general population, the investigators said. Therefore, they randomly selected 1,500 patients from the U.S. Veterans Affairs system who were diagnosed with HCC between 2005 and 2010 on the basis of histopathology or established imaging criteria (Hepatology 2005;42:1208-36).

They reviewed complete medical records for these patients, and classified those who did not have cirrhosis according to the quality of supporting histology, laboratory, and imaging data (Clin Gastroenterol Hepatol. 2015. doi: 0.1016/j.cgh.2015.07.019).

In all, 3% of the cohort had level 1 (“highest-quality”) evidence for not having cirrhosis, while another 10% had level 2 evidence for no cirrhosis, the investigators said. “Compared with HCC in the presence of cirrhosis, these patients were more likely to have metabolic syndrome or NAFLD or no identifiable risk factor, and less likely to have alcohol abuse or HCV infection,” they added. Only two-thirds of NAFLD patients with HCC had cirrhosis, compared with 91% of patients with chronic HCV infection, 92% of HCV-infected patients, and 88% of patients with an alcohol use disorder. Notably, the odds of HCC in the absence of cirrhosis were more than five times higher when patients had NAFLD (odds ratio [OR], 5.4; 95% confidence interval [CI], 3.4-8.5) or metabolic syndrome (OR, 5.0; 95% CI, 3.1-7.8) compared with HCV infection.

Patients with cirrhosis often go unscreened for HCC even though they are at greatest risk of this cancer. Therefore, trying to screen all patients with NAFLD for HCC would be “logistically impractical,” particularly when the absolute risk of HCC in noncirrhotic patients is unknown and no one has examined the best ways to screen this population, the investigators said. Instead, clinicians could prioritize screening and treating NAFLD patients for diabetes mellitus and obesity, both of which are associated with HCC. “There is evidence to suggest that metformin reduces the risk of HCC among diabetics,” they added. “Studies of these and other risk factors of HCC among NAFLD patients with and without cirrhosis are needed.”

Most patients in the study were male, potentially limiting the generalizability of the findings, the researchers noted.

The National Cancer Institute, the Houston Veterans Affairs Health Services Research and Development Center of Excellence, the Michael E. DeBakey Veterans Affairs Medical Center, and the Dan Duncan Cancer Center funded the study. The researchers had no disclosures.

Neural progenitor cells from the proximal colons of patients with Hirschsprung disease divided and formed neurons and glia in their own distal aganglionic colon tissue, according to a study published in the January issue of Cellular and Molecular Gastroenterology and Hepatology.

The approach could lead to “a promising therapeutic strategy” for Hirschsprung disease, because autologous transplantation of nerve progenitor cells would prevent immune rejection, said Dr. Benjamin Rollo of Murdoch Children’s Research Institute in Victoria, Australia, and his associates. But they cautioned against reading too much into their findings, “as there are distributional hurdles to surmount” before cell therapy can be used alone or in combination with surgery.

Hirschsprung disease is a congenital disorder in which embryonic neural crest cells fail to form the distal part of the enteric nervous system. The resulting lack of bowel motility leads to severe constipation and potentially fatal megacolon. Treatment involves surgically resecting the aganglionic distal bowel and anastomosing the normal proximal bowel to the anorectum, but this approach itself can cause constipation as well as fecal soiling, the investigators noted (Cell Molec Gastroenterol Hepatol. 2015 Oct. 22 [doi: 10.1016/j.jcmgh.2015.09.007]).

For the study, they harvested tissue from the proximal (neuronal) and distal (aneuronal) margins of resection of the colons of 31 infants and children with Hirschsprung disease. They cultured cells from the myenteric plexus of the proximal colon, and separated out nerve cells by using flow cytometry for the p75 neural crest marker. To test whether these nerve cells could colonize aganglionic colon, they co-cultured them with aneural avian embryo gut and with patients’ own aneuronal colon muscle. In addition, they co-cultured embryonic mouse enteric nernous system cells with human aneuronal colon muscle. They used quantitative reverse transcriptase PCR and several other standard laboratory techniques to detect cellular markers and mitosis.

Ganglia from the patients’ proximal colons expressed the neural crest markers p75, SOX10, and HNK1, as well as several neuronal, neurite, and glial markers, the researchers reported. The proximal colon specimens also contained ENS progenitor cells, which were SOX10-positive but lacked neuronal or glial markers. The progenitor cells comprised less than 5% of all cells from the proximal colon, but proliferated fourfold more after supplementation with CHIR-99021, a selective inhibitor of glycogen synthase kinase 3. They successfully colonized avian aneural embryonic gut and autologous postnatal aneuronal colon tissue, and the latter also was colonized successfully by mouse enteric neural crest cells.

The study “fulfilled three key requirements” for transplantation – harvesting enteric nervous system cells from the proximal colons of patients with Hirschsprung disease; confirming that postnatal aneuronal colon tissue could support an enteric nervous system; and showing that enteric nervous system–derived cells could colonize both embryonic gut and autologous postnatal colon tissue, said the researchers. More work is needed to sufficiently expand embryonic neural crest stem or progenitor cells and transplant them over a large area of colon, although supplementation with growth factors and use of elastic polymer substrates might help, they added.

The National Health and Medical Research Council, Murdoch Children’s Research Institute, Graham Burke and Yvonne Spencer, the Federation of Chinese Associations, Fonds du Service de chirurgie pédiatrique et de Perfectionnement du CHUV, Fondation SICPA, and Société Académique Vaudoise funded the study. The researchers disclosed no conflicts of interest.

Neural progenitor cells from the proximal colons of patients with Hirschsprung disease divided and formed neurons and glia in their own distal aganglionic colon tissue, according to a study published in the January issue of Cellular and Molecular Gastroenterology and Hepatology.

The approach could lead to “a promising therapeutic strategy” for Hirschsprung disease, because autologous transplantation of nerve progenitor cells would prevent immune rejection, said Dr. Benjamin Rollo of Murdoch Children’s Research Institute in Victoria, Australia, and his associates. But they cautioned against reading too much into their findings, “as there are distributional hurdles to surmount” before cell therapy can be used alone or in combination with surgery.

Hirschsprung disease is a congenital disorder in which embryonic neural crest cells fail to form the distal part of the enteric nervous system. The resulting lack of bowel motility leads to severe constipation and potentially fatal megacolon. Treatment involves surgically resecting the aganglionic distal bowel and anastomosing the normal proximal bowel to the anorectum, but this approach itself can cause constipation as well as fecal soiling, the investigators noted (Cell Molec Gastroenterol Hepatol. 2015 Oct. 22 [doi: 10.1016/j.jcmgh.2015.09.007]).

For the study, they harvested tissue from the proximal (neuronal) and distal (aneuronal) margins of resection of the colons of 31 infants and children with Hirschsprung disease. They cultured cells from the myenteric plexus of the proximal colon, and separated out nerve cells by using flow cytometry for the p75 neural crest marker. To test whether these nerve cells could colonize aganglionic colon, they co-cultured them with aneural avian embryo gut and with patients’ own aneuronal colon muscle. In addition, they co-cultured embryonic mouse enteric nernous system cells with human aneuronal colon muscle. They used quantitative reverse transcriptase PCR and several other standard laboratory techniques to detect cellular markers and mitosis.

Ganglia from the patients’ proximal colons expressed the neural crest markers p75, SOX10, and HNK1, as well as several neuronal, neurite, and glial markers, the researchers reported. The proximal colon specimens also contained ENS progenitor cells, which were SOX10-positive but lacked neuronal or glial markers. The progenitor cells comprised less than 5% of all cells from the proximal colon, but proliferated fourfold more after supplementation with CHIR-99021, a selective inhibitor of glycogen synthase kinase 3. They successfully colonized avian aneural embryonic gut and autologous postnatal aneuronal colon tissue, and the latter also was colonized successfully by mouse enteric neural crest cells.

The study “fulfilled three key requirements” for transplantation – harvesting enteric nervous system cells from the proximal colons of patients with Hirschsprung disease; confirming that postnatal aneuronal colon tissue could support an enteric nervous system; and showing that enteric nervous system–derived cells could colonize both embryonic gut and autologous postnatal colon tissue, said the researchers. More work is needed to sufficiently expand embryonic neural crest stem or progenitor cells and transplant them over a large area of colon, although supplementation with growth factors and use of elastic polymer substrates might help, they added.

The National Health and Medical Research Council, Murdoch Children’s Research Institute, Graham Burke and Yvonne Spencer, the Federation of Chinese Associations, Fonds du Service de chirurgie pédiatrique et de Perfectionnement du CHUV, Fondation SICPA, and Société Académique Vaudoise funded the study. The researchers disclosed no conflicts of interest.

Neural progenitor cells from the proximal colons of patients with Hirschsprung disease divided and formed neurons and glia in their own distal aganglionic colon tissue, according to a study published in the January issue of Cellular and Molecular Gastroenterology and Hepatology.

The approach could lead to “a promising therapeutic strategy” for Hirschsprung disease, because autologous transplantation of nerve progenitor cells would prevent immune rejection, said Dr. Benjamin Rollo of Murdoch Children’s Research Institute in Victoria, Australia, and his associates. But they cautioned against reading too much into their findings, “as there are distributional hurdles to surmount” before cell therapy can be used alone or in combination with surgery.

Hirschsprung disease is a congenital disorder in which embryonic neural crest cells fail to form the distal part of the enteric nervous system. The resulting lack of bowel motility leads to severe constipation and potentially fatal megacolon. Treatment involves surgically resecting the aganglionic distal bowel and anastomosing the normal proximal bowel to the anorectum, but this approach itself can cause constipation as well as fecal soiling, the investigators noted (Cell Molec Gastroenterol Hepatol. 2015 Oct. 22 [doi: 10.1016/j.jcmgh.2015.09.007]).

For the study, they harvested tissue from the proximal (neuronal) and distal (aneuronal) margins of resection of the colons of 31 infants and children with Hirschsprung disease. They cultured cells from the myenteric plexus of the proximal colon, and separated out nerve cells by using flow cytometry for the p75 neural crest marker. To test whether these nerve cells could colonize aganglionic colon, they co-cultured them with aneural avian embryo gut and with patients’ own aneuronal colon muscle. In addition, they co-cultured embryonic mouse enteric nernous system cells with human aneuronal colon muscle. They used quantitative reverse transcriptase PCR and several other standard laboratory techniques to detect cellular markers and mitosis.

Ganglia from the patients’ proximal colons expressed the neural crest markers p75, SOX10, and HNK1, as well as several neuronal, neurite, and glial markers, the researchers reported. The proximal colon specimens also contained ENS progenitor cells, which were SOX10-positive but lacked neuronal or glial markers. The progenitor cells comprised less than 5% of all cells from the proximal colon, but proliferated fourfold more after supplementation with CHIR-99021, a selective inhibitor of glycogen synthase kinase 3. They successfully colonized avian aneural embryonic gut and autologous postnatal aneuronal colon tissue, and the latter also was colonized successfully by mouse enteric neural crest cells.

The study “fulfilled three key requirements” for transplantation – harvesting enteric nervous system cells from the proximal colons of patients with Hirschsprung disease; confirming that postnatal aneuronal colon tissue could support an enteric nervous system; and showing that enteric nervous system–derived cells could colonize both embryonic gut and autologous postnatal colon tissue, said the researchers. More work is needed to sufficiently expand embryonic neural crest stem or progenitor cells and transplant them over a large area of colon, although supplementation with growth factors and use of elastic polymer substrates might help, they added.

The National Health and Medical Research Council, Murdoch Children’s Research Institute, Graham Burke and Yvonne Spencer, the Federation of Chinese Associations, Fonds du Service de chirurgie pédiatrique et de Perfectionnement du CHUV, Fondation SICPA, and Société Académique Vaudoise funded the study. The researchers disclosed no conflicts of interest.

About half of patients with symptomatic esophageal eosinophilia achieved complete clinical and histologic remission on proton pump inhibitors (PPIs), according to a systematic review and meta-analysis of 33 studies.

“Our results support the concept of PPIs as first-line therapy in both children and adults,” Dr. Alfredo Lucendo of the Servicio de Salud de Castillo–La Mancha, Hospital General de Tomelloso, Albacete, Spain, and his associates wrote in the January issue of Clinical Gastroenterology and Hepatology. “Other effective alternatives, such as dietary or topical steroid therapy, likely might be set aside as second-line treatment, owing to long-term safety concerns (topical steroid therapy) and impairment of quality of life and nutritional inadequacy (dietary interventions).”

©Magnus Manske/Wikimedia Commons/CC SA 3.0

The study also confirmed that esophageal pH monitoring does not accurately predict therapeutic response to PPI therapy. “The performance of this test before histologic reevaluation on PPI therapy should be discouraged,” according to the researchers (Clin Gastroenterol Hepatol. 2015. [doi:10.1016/j.cgh.2015.07.041]). Eosinophilic esophagitis was first described as a distinct disorder about 20 years ago, but only recently was understood to be the most common cause of chronic esophageal symptoms among children and young adults. Some cases are now known to respond to PPI therapy, but reported remission rates have varied depending on study design and patient population, the investigators said. In addition, no one had systematically reviewed studies of PPI-responsive esophageal eosinophilia for quality or to determine the optimal type of PPI, dose, or treatment duration.

Therefore, the investigators searched MEDLINE, EMBASE, SCOPUS, and abstracts from the annual meetings of the American Gastroenterological Association, the American College of Gastroenterology, and United European Gastroenterology, identifying 33 studies of 619 patients with symptomatic esophageal eosinophilia. Eleven of the studies were prospective, of which only two were randomized controlled trials. The researchers defined a histologic response as less than 15 eosinophils per high-powered frame after PPI therapy. “Missing data regarding PPI therapy were common and prevented us from drawing conclusions on the most effective PPI drug and doses,” they said. In addition, most studies lacked structured or objective survey tools or other measures of clinical improvement, making it impossible to rule out self-adapted coping strategies as a main cause of improvement over time.

With those caveats in mind, about 61% of patients in the pooled analysis had a clinical response to PPI therapy (95% confidence interval, 48%-72%), and half achieved clinical and histologic remission (95% CI, 42%-59%), the investigators reported. Therapy was somewhat more effective when administered twice a day instead of once daily, when clinicians used esophageal pH monitoring, and when studies were prospective instead of retrospective, but the differences were not significant. Nor did therapeutic response significantly differ based on the age of patients, type of report, or quality of the study.

The overall findings “should be interpreted with caution because of poor-quality evidence, heterogeneity, and publication bias,” the researchers said. Prospective studies are needed to examine the best PPI, dose, and dosing interval to use in an initial trial in the clinic; to clarify long-term effects and dosing strategies; to assess the ability of PPIs to reverse fibrotic esophageal remodeling; and to examine the effects of the CYP2C19 genotype on clinical and histologic response, they added. “More quality evidence on pediatric PPI-responsive eosinophilic esophagitis is needed urgently,” they emphasized.

The authors reported no funding sources and had no disclosures.

About half of patients with symptomatic esophageal eosinophilia achieved complete clinical and histologic remission on proton pump inhibitors (PPIs), according to a systematic review and meta-analysis of 33 studies.

“Our results support the concept of PPIs as first-line therapy in both children and adults,” Dr. Alfredo Lucendo of the Servicio de Salud de Castillo–La Mancha, Hospital General de Tomelloso, Albacete, Spain, and his associates wrote in the January issue of Clinical Gastroenterology and Hepatology. “Other effective alternatives, such as dietary or topical steroid therapy, likely might be set aside as second-line treatment, owing to long-term safety concerns (topical steroid therapy) and impairment of quality of life and nutritional inadequacy (dietary interventions).”

©Magnus Manske/Wikimedia Commons/CC SA 3.0

The study also confirmed that esophageal pH monitoring does not accurately predict therapeutic response to PPI therapy. “The performance of this test before histologic reevaluation on PPI therapy should be discouraged,” according to the researchers (Clin Gastroenterol Hepatol. 2015. [doi:10.1016/j.cgh.2015.07.041]). Eosinophilic esophagitis was first described as a distinct disorder about 20 years ago, but only recently was understood to be the most common cause of chronic esophageal symptoms among children and young adults. Some cases are now known to respond to PPI therapy, but reported remission rates have varied depending on study design and patient population, the investigators said. In addition, no one had systematically reviewed studies of PPI-responsive esophageal eosinophilia for quality or to determine the optimal type of PPI, dose, or treatment duration.

Therefore, the investigators searched MEDLINE, EMBASE, SCOPUS, and abstracts from the annual meetings of the American Gastroenterological Association, the American College of Gastroenterology, and United European Gastroenterology, identifying 33 studies of 619 patients with symptomatic esophageal eosinophilia. Eleven of the studies were prospective, of which only two were randomized controlled trials. The researchers defined a histologic response as less than 15 eosinophils per high-powered frame after PPI therapy. “Missing data regarding PPI therapy were common and prevented us from drawing conclusions on the most effective PPI drug and doses,” they said. In addition, most studies lacked structured or objective survey tools or other measures of clinical improvement, making it impossible to rule out self-adapted coping strategies as a main cause of improvement over time.

With those caveats in mind, about 61% of patients in the pooled analysis had a clinical response to PPI therapy (95% confidence interval, 48%-72%), and half achieved clinical and histologic remission (95% CI, 42%-59%), the investigators reported. Therapy was somewhat more effective when administered twice a day instead of once daily, when clinicians used esophageal pH monitoring, and when studies were prospective instead of retrospective, but the differences were not significant. Nor did therapeutic response significantly differ based on the age of patients, type of report, or quality of the study.

The overall findings “should be interpreted with caution because of poor-quality evidence, heterogeneity, and publication bias,” the researchers said. Prospective studies are needed to examine the best PPI, dose, and dosing interval to use in an initial trial in the clinic; to clarify long-term effects and dosing strategies; to assess the ability of PPIs to reverse fibrotic esophageal remodeling; and to examine the effects of the CYP2C19 genotype on clinical and histologic response, they added. “More quality evidence on pediatric PPI-responsive eosinophilic esophagitis is needed urgently,” they emphasized.

The authors reported no funding sources and had no disclosures.

About half of patients with symptomatic esophageal eosinophilia achieved complete clinical and histologic remission on proton pump inhibitors (PPIs), according to a systematic review and meta-analysis of 33 studies.

“Our results support the concept of PPIs as first-line therapy in both children and adults,” Dr. Alfredo Lucendo of the Servicio de Salud de Castillo–La Mancha, Hospital General de Tomelloso, Albacete, Spain, and his associates wrote in the January issue of Clinical Gastroenterology and Hepatology. “Other effective alternatives, such as dietary or topical steroid therapy, likely might be set aside as second-line treatment, owing to long-term safety concerns (topical steroid therapy) and impairment of quality of life and nutritional inadequacy (dietary interventions).”

©Magnus Manske/Wikimedia Commons/CC SA 3.0

The study also confirmed that esophageal pH monitoring does not accurately predict therapeutic response to PPI therapy. “The performance of this test before histologic reevaluation on PPI therapy should be discouraged,” according to the researchers (Clin Gastroenterol Hepatol. 2015. [doi:10.1016/j.cgh.2015.07.041]). Eosinophilic esophagitis was first described as a distinct disorder about 20 years ago, but only recently was understood to be the most common cause of chronic esophageal symptoms among children and young adults. Some cases are now known to respond to PPI therapy, but reported remission rates have varied depending on study design and patient population, the investigators said. In addition, no one had systematically reviewed studies of PPI-responsive esophageal eosinophilia for quality or to determine the optimal type of PPI, dose, or treatment duration.

Therefore, the investigators searched MEDLINE, EMBASE, SCOPUS, and abstracts from the annual meetings of the American Gastroenterological Association, the American College of Gastroenterology, and United European Gastroenterology, identifying 33 studies of 619 patients with symptomatic esophageal eosinophilia. Eleven of the studies were prospective, of which only two were randomized controlled trials. The researchers defined a histologic response as less than 15 eosinophils per high-powered frame after PPI therapy. “Missing data regarding PPI therapy were common and prevented us from drawing conclusions on the most effective PPI drug and doses,” they said. In addition, most studies lacked structured or objective survey tools or other measures of clinical improvement, making it impossible to rule out self-adapted coping strategies as a main cause of improvement over time.

With those caveats in mind, about 61% of patients in the pooled analysis had a clinical response to PPI therapy (95% confidence interval, 48%-72%), and half achieved clinical and histologic remission (95% CI, 42%-59%), the investigators reported. Therapy was somewhat more effective when administered twice a day instead of once daily, when clinicians used esophageal pH monitoring, and when studies were prospective instead of retrospective, but the differences were not significant. Nor did therapeutic response significantly differ based on the age of patients, type of report, or quality of the study.

The overall findings “should be interpreted with caution because of poor-quality evidence, heterogeneity, and publication bias,” the researchers said. Prospective studies are needed to examine the best PPI, dose, and dosing interval to use in an initial trial in the clinic; to clarify long-term effects and dosing strategies; to assess the ability of PPIs to reverse fibrotic esophageal remodeling; and to examine the effects of the CYP2C19 genotype on clinical and histologic response, they added. “More quality evidence on pediatric PPI-responsive eosinophilic esophagitis is needed urgently,” they emphasized.

The authors reported no funding sources and had no disclosures.

Facilities that performed outpatient colonoscopies varied significantly in terms of subsequent unplanned hospital visits, even after patient-level risk factors were adjusted for, according to a Medicare claims analysis reported in the January issue of Gastroenterology.

This first-in-kind quality measure will help “make transparent the full range of adverse events requiring hospital care that patients experience post-[colonoscopy], inform patient choice, create incentives for improved care, and assist providers’ quality improvement efforts, wrote Dr. Isuru Ranasinghe of Yale–New Haven (Conn.) Hospital and his associates. Preventing unplanned hospitals visits after colonoscopy could also help improve patient outcomes and cut health care costs, they added.

© HUNG KUO CHUN/Thinkstock

More than 90% of colonoscopies occur in outpatient settings, where it is difficult to follow-up and track serious adverse events such as colonic perforation or gastrointestinal bleeding. Furthermore, there are no publicly available quality reports of providers or facilities that perform outpatient colonoscopies. To help fill that gap, the researchers tracked unplanned hospital visits within 7 days after colonoscopy as part of an outpatient quality initiative by the Centers for Medicare & Medicaid Services. The analysis included 20% of Medicare outpatient colonoscopy claims in 2010, which amounted to 331,880 colonoscopies performed at 8,140 facilities (Gastroenterology 2015 [doi: 10.1053/j.gastro.2015.09.009]).

In 2010, there were 16.3 unplanned hospital visits for every 1,000 Medicare claims for outpatient colonoscopies, which equated to 27,000 such visits nationwide, the investigators said. Patients who were older than 85 years were significantly more likely to have an unplanned hospital visit than were patients aged 65-69 years (odds ratio, 1.87; 95% confidence interval, 1.54-2.28). The other most significant predictors included having an electrolyte or acid/base imbalance (OR, 1.43) or a psychiatric disorder (OR, 1.34). After adjusting for these factors, unplanned admission rates varied significantly among facilities in all four states with available data, including New York, California, Florida, and Nebraska, the researchers said.

These findings might not apply to patients who are too young to be enrolled in Medicare, which “is important, as most colonoscopies are performed among patients aged less than 65 years, although older patients are more likely to suffer adverse events,” Dr. Ranasinghe and his associates noted. The study also did not assess deaths, the one-third of GI bleeding events that occur more than a week after colonoscopy, or the various factors that might affect quality of care, such as type of anesthesia, polypectomy technique, and access to follow-up care. “The goal of the measure is to reveal the opportunity for improvement, and to prompt facilities to examine their practices in depth to identify ways to lower hospital visit rates to the level achieved by the best providers,” the researchers emphasized.

The work was supported by the Centers for Medicare & Medicaid Services, the National Health and Medical Research Council, the National Heart Foundation of Australia, the National Institute on Aging, the American Federation for Aging Research. Dr. Ranasinghe and nine coinvestigators reported working under contract with CMS to develop and maintain performance measures. Three coinvestigators reported financial relationships with AbbVie, qMed, Pentax, Olympus, Myriad Genetics, UnitedHealth, Medtronic, and Johnson & Johnson.

Source: American Gastroenterological Association

Facilities that performed outpatient colonoscopies varied significantly in terms of subsequent unplanned hospital visits, even after patient-level risk factors were adjusted for, according to a Medicare claims analysis reported in the January issue of Gastroenterology.

This first-in-kind quality measure will help “make transparent the full range of adverse events requiring hospital care that patients experience post-[colonoscopy], inform patient choice, create incentives for improved care, and assist providers’ quality improvement efforts, wrote Dr. Isuru Ranasinghe of Yale–New Haven (Conn.) Hospital and his associates. Preventing unplanned hospitals visits after colonoscopy could also help improve patient outcomes and cut health care costs, they added.

© HUNG KUO CHUN/Thinkstock

More than 90% of colonoscopies occur in outpatient settings, where it is difficult to follow-up and track serious adverse events such as colonic perforation or gastrointestinal bleeding. Furthermore, there are no publicly available quality reports of providers or facilities that perform outpatient colonoscopies. To help fill that gap, the researchers tracked unplanned hospital visits within 7 days after colonoscopy as part of an outpatient quality initiative by the Centers for Medicare & Medicaid Services. The analysis included 20% of Medicare outpatient colonoscopy claims in 2010, which amounted to 331,880 colonoscopies performed at 8,140 facilities (Gastroenterology 2015 [doi: 10.1053/j.gastro.2015.09.009]).

In 2010, there were 16.3 unplanned hospital visits for every 1,000 Medicare claims for outpatient colonoscopies, which equated to 27,000 such visits nationwide, the investigators said. Patients who were older than 85 years were significantly more likely to have an unplanned hospital visit than were patients aged 65-69 years (odds ratio, 1.87; 95% confidence interval, 1.54-2.28). The other most significant predictors included having an electrolyte or acid/base imbalance (OR, 1.43) or a psychiatric disorder (OR, 1.34). After adjusting for these factors, unplanned admission rates varied significantly among facilities in all four states with available data, including New York, California, Florida, and Nebraska, the researchers said.

These findings might not apply to patients who are too young to be enrolled in Medicare, which “is important, as most colonoscopies are performed among patients aged less than 65 years, although older patients are more likely to suffer adverse events,” Dr. Ranasinghe and his associates noted. The study also did not assess deaths, the one-third of GI bleeding events that occur more than a week after colonoscopy, or the various factors that might affect quality of care, such as type of anesthesia, polypectomy technique, and access to follow-up care. “The goal of the measure is to reveal the opportunity for improvement, and to prompt facilities to examine their practices in depth to identify ways to lower hospital visit rates to the level achieved by the best providers,” the researchers emphasized.

The work was supported by the Centers for Medicare & Medicaid Services, the National Health and Medical Research Council, the National Heart Foundation of Australia, the National Institute on Aging, the American Federation for Aging Research. Dr. Ranasinghe and nine coinvestigators reported working under contract with CMS to develop and maintain performance measures. Three coinvestigators reported financial relationships with AbbVie, qMed, Pentax, Olympus, Myriad Genetics, UnitedHealth, Medtronic, and Johnson & Johnson.

Source: American Gastroenterological Association

Facilities that performed outpatient colonoscopies varied significantly in terms of subsequent unplanned hospital visits, even after patient-level risk factors were adjusted for, according to a Medicare claims analysis reported in the January issue of Gastroenterology.

This first-in-kind quality measure will help “make transparent the full range of adverse events requiring hospital care that patients experience post-[colonoscopy], inform patient choice, create incentives for improved care, and assist providers’ quality improvement efforts, wrote Dr. Isuru Ranasinghe of Yale–New Haven (Conn.) Hospital and his associates. Preventing unplanned hospitals visits after colonoscopy could also help improve patient outcomes and cut health care costs, they added.

© HUNG KUO CHUN/Thinkstock

More than 90% of colonoscopies occur in outpatient settings, where it is difficult to follow-up and track serious adverse events such as colonic perforation or gastrointestinal bleeding. Furthermore, there are no publicly available quality reports of providers or facilities that perform outpatient colonoscopies. To help fill that gap, the researchers tracked unplanned hospital visits within 7 days after colonoscopy as part of an outpatient quality initiative by the Centers for Medicare & Medicaid Services. The analysis included 20% of Medicare outpatient colonoscopy claims in 2010, which amounted to 331,880 colonoscopies performed at 8,140 facilities (Gastroenterology 2015 [doi: 10.1053/j.gastro.2015.09.009]).

In 2010, there were 16.3 unplanned hospital visits for every 1,000 Medicare claims for outpatient colonoscopies, which equated to 27,000 such visits nationwide, the investigators said. Patients who were older than 85 years were significantly more likely to have an unplanned hospital visit than were patients aged 65-69 years (odds ratio, 1.87; 95% confidence interval, 1.54-2.28). The other most significant predictors included having an electrolyte or acid/base imbalance (OR, 1.43) or a psychiatric disorder (OR, 1.34). After adjusting for these factors, unplanned admission rates varied significantly among facilities in all four states with available data, including New York, California, Florida, and Nebraska, the researchers said.

These findings might not apply to patients who are too young to be enrolled in Medicare, which “is important, as most colonoscopies are performed among patients aged less than 65 years, although older patients are more likely to suffer adverse events,” Dr. Ranasinghe and his associates noted. The study also did not assess deaths, the one-third of GI bleeding events that occur more than a week after colonoscopy, or the various factors that might affect quality of care, such as type of anesthesia, polypectomy technique, and access to follow-up care. “The goal of the measure is to reveal the opportunity for improvement, and to prompt facilities to examine their practices in depth to identify ways to lower hospital visit rates to the level achieved by the best providers,” the researchers emphasized.

The work was supported by the Centers for Medicare & Medicaid Services, the National Health and Medical Research Council, the National Heart Foundation of Australia, the National Institute on Aging, the American Federation for Aging Research. Dr. Ranasinghe and nine coinvestigators reported working under contract with CMS to develop and maintain performance measures. Three coinvestigators reported financial relationships with AbbVie, qMed, Pentax, Olympus, Myriad Genetics, UnitedHealth, Medtronic, and Johnson & Johnson.

Source: American Gastroenterological Association

Allergic Reaction Versus Anaphylaxis

A 34-year-old woman presented to ED with complaints of an allergic reaction, the onset of which began approximately 1 hour prior. The patient did not know what might have caused her symptoms. She complained of hives and itching all over; she denied difficulty swallowing, wheezing, and shortness of breath. Her medical history was unremarkable. She was on no medications, and she denied any alcohol or tobacco use. She had no known medication or food allergies.

Physical examination revealed a woman in mild discomfort, secondary to generalized itching. Her vital signs, including pulse oximetry, were normal. There was no swelling of the face, lips, or oropharynx. The lungs were clear to auscultation bilaterally. The heart and abdominal examinations were normal. Examination of the skin revealed diffuse urticaria without petechiae or purpura.

The emergency physician (EP) ordered 125 mg of methylprednisolone sodium succinate and 25 mg of diphenhydramine intravenously (IV). After approximately 1 hour, the hives and itching decreased and the patient felt improved. She was diagnosed with an allergic reaction and discharged home with a prescription for diphenhydramine and a methylprednisolone dose pack.

The following day, the patient collapsed at home and emergency medical services was called. Unfortunately, the patient could not be resuscitated and was pronounced dead at the scene. An autopsy revealed the patient had died from anaphylaxis and laryngeal edema, with an extremely elevated tryptase level of 200 ng/mL (normal, <11.5 ng/mL).

The patient’s family sued the EP for failure to diagnose and treat anaphylaxis, failure to treat with epinephrine, and failure to admit the patient to the hospital. The defense claimed the patient did not present with anaphylaxis, but rather simply a worsening of the hives and angioedema, and that the treatment provided was appropriate. The jury found in favor of the defendants.

Discussion

It does not appear the patient presented with anaphylaxis on the first visit, but may have had it on the second visit. In 2004, the National Institutes of Allergy and Infectious Disease (NIAID) panel and the Food Allergy and Anaphylaxis Network (FAAN) developed criteria for the diagnosis of anaphylaxis.¹ According to the criteria, anaphylaxis is likely when any one of the following three criteria are present: (1) acute onset of symptoms involving the skin or mucosa (eg, pruritus, hives, angioedema), and either respiratory compromise (eg, dyspnea, wheezing, stridor, hypoxia) or hypotension/end-organ dysfunction (eg, syncope, incontinence); (2) two or more symptoms (eg, respiratory compromise, hypotension/end-organ dysfunction, persistent gastrointestinal [GI] symptoms such as vomiting, diarrhea, or crampy abdominal pain) that occur rapidly after exposure involving the skin or mucosa; or (3) hypotension from a known allergen to the patient. The accuracy of these criteria has been retrospectively evaluated in an ED study, and found to have a 97% sensitivity and an 82% specificity.² The negative predictive value was good at 98%, but the positive predictive value was only 69%.²

When a patient presents with minimal or subtle symptoms, anaphylaxis can be a very difficult diagnosis to make in the ED early on in the process. While no EP will miss the diagnosis in a patient with hives, hypotension, and wheezing, it can be easy to miss when the predominant symptoms are GI, such as nausea, vomiting, or diarrhea. In addition, the differential diagnosis for the presentation of anaphylaxis in the ED can be extremely broad and include vasovagal reaction, asthma attack, myocardial infarction, gastroenteritis, panic attack, or airway obstruction.

Due to the nature of emergency medicine, EPs must consider multiple etiologies before determining an evaluation and management plan. While recognizing there are limitations to the NIAID/FAAN criteria, EPs should be aware of them. We are very good at treating these types of symptoms with antihistamines and steroids; however, we frequently fail to give epinephrine when indicated. It is important to remember that epinephrine is the first-line treatment for anaphylaxis—not corticosteroids or antihistamines.³

Reasons for not administering epinephrine are multiple. First, as discussed above, if the diagnosis of anaphylaxis is not considered, the EP is not going to administer the drug of choice. Secondly, EPs have been taught to have a healthy respect for epinephrine and its effects, especially in older patients. Due to this cautious approach, epinephrine is frequently not given to patients with mild symptoms or to those who present early in the course of disease.

Emergency physicians have experience giving epinephrine subcutaneously, but not nearly as much with the intramuscular (IM) route. This is important, because an IM injection in the anterolateral thigh is the recommended location for the treatment of anaphylaxis. The dose should be weight based (0.01 mg/kg) to a maximum of 0.5 mg. This dose can be given every 5 to 15 minutes as necessary to control symptoms.³ The dosing is important to remember, since many EDs stock only autoinjectable epinephrine devices for use in anaphylaxis. These autoinjectors only contain 0.3 mg of epinephrine, so some patients may be underdosed if used.

In the management of allergic reactions and anaphylaxis, EPs frequently administer antihistamines and corticosteroids. While there is no direct evidence to support their use in the management of anaphylaxis, theoretical benefits do exist.³ This, combined with the excellent medication safety profile and lack of serious side effects, make these two medication classes appropriate for use in the ED.

Allergic Reaction Versus Anaphylaxis

A 34-year-old woman presented to ED with complaints of an allergic reaction, the onset of which began approximately 1 hour prior. The patient did not know what might have caused her symptoms. She complained of hives and itching all over; she denied difficulty swallowing, wheezing, and shortness of breath. Her medical history was unremarkable. She was on no medications, and she denied any alcohol or tobacco use. She had no known medication or food allergies.

Physical examination revealed a woman in mild discomfort, secondary to generalized itching. Her vital signs, including pulse oximetry, were normal. There was no swelling of the face, lips, or oropharynx. The lungs were clear to auscultation bilaterally. The heart and abdominal examinations were normal. Examination of the skin revealed diffuse urticaria without petechiae or purpura.

The emergency physician (EP) ordered 125 mg of methylprednisolone sodium succinate and 25 mg of diphenhydramine intravenously (IV). After approximately 1 hour, the hives and itching decreased and the patient felt improved. She was diagnosed with an allergic reaction and discharged home with a prescription for diphenhydramine and a methylprednisolone dose pack.

The following day, the patient collapsed at home and emergency medical services was called. Unfortunately, the patient could not be resuscitated and was pronounced dead at the scene. An autopsy revealed the patient had died from anaphylaxis and laryngeal edema, with an extremely elevated tryptase level of 200 ng/mL (normal, <11.5 ng/mL).

The patient’s family sued the EP for failure to diagnose and treat anaphylaxis, failure to treat with epinephrine, and failure to admit the patient to the hospital. The defense claimed the patient did not present with anaphylaxis, but rather simply a worsening of the hives and angioedema, and that the treatment provided was appropriate. The jury found in favor of the defendants.

Discussion

It does not appear the patient presented with anaphylaxis on the first visit, but may have had it on the second visit. In 2004, the National Institutes of Allergy and Infectious Disease (NIAID) panel and the Food Allergy and Anaphylaxis Network (FAAN) developed criteria for the diagnosis of anaphylaxis.¹ According to the criteria, anaphylaxis is likely when any one of the following three criteria are present: (1) acute onset of symptoms involving the skin or mucosa (eg, pruritus, hives, angioedema), and either respiratory compromise (eg, dyspnea, wheezing, stridor, hypoxia) or hypotension/end-organ dysfunction (eg, syncope, incontinence); (2) two or more symptoms (eg, respiratory compromise, hypotension/end-organ dysfunction, persistent gastrointestinal [GI] symptoms such as vomiting, diarrhea, or crampy abdominal pain) that occur rapidly after exposure involving the skin or mucosa; or (3) hypotension from a known allergen to the patient. The accuracy of these criteria has been retrospectively evaluated in an ED study, and found to have a 97% sensitivity and an 82% specificity.² The negative predictive value was good at 98%, but the positive predictive value was only 69%.²

When a patient presents with minimal or subtle symptoms, anaphylaxis can be a very difficult diagnosis to make in the ED early on in the process. While no EP will miss the diagnosis in a patient with hives, hypotension, and wheezing, it can be easy to miss when the predominant symptoms are GI, such as nausea, vomiting, or diarrhea. In addition, the differential diagnosis for the presentation of anaphylaxis in the ED can be extremely broad and include vasovagal reaction, asthma attack, myocardial infarction, gastroenteritis, panic attack, or airway obstruction.

Due to the nature of emergency medicine, EPs must consider multiple etiologies before determining an evaluation and management plan. While recognizing there are limitations to the NIAID/FAAN criteria, EPs should be aware of them. We are very good at treating these types of symptoms with antihistamines and steroids; however, we frequently fail to give epinephrine when indicated. It is important to remember that epinephrine is the first-line treatment for anaphylaxis—not corticosteroids or antihistamines.³

Reasons for not administering epinephrine are multiple. First, as discussed above, if the diagnosis of anaphylaxis is not considered, the EP is not going to administer the drug of choice. Secondly, EPs have been taught to have a healthy respect for epinephrine and its effects, especially in older patients. Due to this cautious approach, epinephrine is frequently not given to patients with mild symptoms or to those who present early in the course of disease.

Emergency physicians have experience giving epinephrine subcutaneously, but not nearly as much with the intramuscular (IM) route. This is important, because an IM injection in the anterolateral thigh is the recommended location for the treatment of anaphylaxis. The dose should be weight based (0.01 mg/kg) to a maximum of 0.5 mg. This dose can be given every 5 to 15 minutes as necessary to control symptoms.³ The dosing is important to remember, since many EDs stock only autoinjectable epinephrine devices for use in anaphylaxis. These autoinjectors only contain 0.3 mg of epinephrine, so some patients may be underdosed if used.

In the management of allergic reactions and anaphylaxis, EPs frequently administer antihistamines and corticosteroids. While there is no direct evidence to support their use in the management of anaphylaxis, theoretical benefits do exist.³ This, combined with the excellent medication safety profile and lack of serious side effects, make these two medication classes appropriate for use in the ED.

Allergic Reaction Versus Anaphylaxis

A 34-year-old woman presented to ED with complaints of an allergic reaction, the onset of which began approximately 1 hour prior. The patient did not know what might have caused her symptoms. She complained of hives and itching all over; she denied difficulty swallowing, wheezing, and shortness of breath. Her medical history was unremarkable. She was on no medications, and she denied any alcohol or tobacco use. She had no known medication or food allergies.

Physical examination revealed a woman in mild discomfort, secondary to generalized itching. Her vital signs, including pulse oximetry, were normal. There was no swelling of the face, lips, or oropharynx. The lungs were clear to auscultation bilaterally. The heart and abdominal examinations were normal. Examination of the skin revealed diffuse urticaria without petechiae or purpura.

The emergency physician (EP) ordered 125 mg of methylprednisolone sodium succinate and 25 mg of diphenhydramine intravenously (IV). After approximately 1 hour, the hives and itching decreased and the patient felt improved. She was diagnosed with an allergic reaction and discharged home with a prescription for diphenhydramine and a methylprednisolone dose pack.

The following day, the patient collapsed at home and emergency medical services was called. Unfortunately, the patient could not be resuscitated and was pronounced dead at the scene. An autopsy revealed the patient had died from anaphylaxis and laryngeal edema, with an extremely elevated tryptase level of 200 ng/mL (normal, <11.5 ng/mL).

The patient’s family sued the EP for failure to diagnose and treat anaphylaxis, failure to treat with epinephrine, and failure to admit the patient to the hospital. The defense claimed the patient did not present with anaphylaxis, but rather simply a worsening of the hives and angioedema, and that the treatment provided was appropriate. The jury found in favor of the defendants.

Discussion

It does not appear the patient presented with anaphylaxis on the first visit, but may have had it on the second visit. In 2004, the National Institutes of Allergy and Infectious Disease (NIAID) panel and the Food Allergy and Anaphylaxis Network (FAAN) developed criteria for the diagnosis of anaphylaxis.¹ According to the criteria, anaphylaxis is likely when any one of the following three criteria are present: (1) acute onset of symptoms involving the skin or mucosa (eg, pruritus, hives, angioedema), and either respiratory compromise (eg, dyspnea, wheezing, stridor, hypoxia) or hypotension/end-organ dysfunction (eg, syncope, incontinence); (2) two or more symptoms (eg, respiratory compromise, hypotension/end-organ dysfunction, persistent gastrointestinal [GI] symptoms such as vomiting, diarrhea, or crampy abdominal pain) that occur rapidly after exposure involving the skin or mucosa; or (3) hypotension from a known allergen to the patient. The accuracy of these criteria has been retrospectively evaluated in an ED study, and found to have a 97% sensitivity and an 82% specificity.² The negative predictive value was good at 98%, but the positive predictive value was only 69%.²

When a patient presents with minimal or subtle symptoms, anaphylaxis can be a very difficult diagnosis to make in the ED early on in the process. While no EP will miss the diagnosis in a patient with hives, hypotension, and wheezing, it can be easy to miss when the predominant symptoms are GI, such as nausea, vomiting, or diarrhea. In addition, the differential diagnosis for the presentation of anaphylaxis in the ED can be extremely broad and include vasovagal reaction, asthma attack, myocardial infarction, gastroenteritis, panic attack, or airway obstruction.

Due to the nature of emergency medicine, EPs must consider multiple etiologies before determining an evaluation and management plan. While recognizing there are limitations to the NIAID/FAAN criteria, EPs should be aware of them. We are very good at treating these types of symptoms with antihistamines and steroids; however, we frequently fail to give epinephrine when indicated. It is important to remember that epinephrine is the first-line treatment for anaphylaxis—not corticosteroids or antihistamines.³

Reasons for not administering epinephrine are multiple. First, as discussed above, if the diagnosis of anaphylaxis is not considered, the EP is not going to administer the drug of choice. Secondly, EPs have been taught to have a healthy respect for epinephrine and its effects, especially in older patients. Due to this cautious approach, epinephrine is frequently not given to patients with mild symptoms or to those who present early in the course of disease.

Emergency physicians have experience giving epinephrine subcutaneously, but not nearly as much with the intramuscular (IM) route. This is important, because an IM injection in the anterolateral thigh is the recommended location for the treatment of anaphylaxis. The dose should be weight based (0.01 mg/kg) to a maximum of 0.5 mg. This dose can be given every 5 to 15 minutes as necessary to control symptoms.³ The dosing is important to remember, since many EDs stock only autoinjectable epinephrine devices for use in anaphylaxis. These autoinjectors only contain 0.3 mg of epinephrine, so some patients may be underdosed if used.

In the management of allergic reactions and anaphylaxis, EPs frequently administer antihistamines and corticosteroids. While there is no direct evidence to support their use in the management of anaphylaxis, theoretical benefits do exist.³ This, combined with the excellent medication safety profile and lack of serious side effects, make these two medication classes appropriate for use in the ED.

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