Incidence of late-onset disease for group B streptococcus is higher than early-onset disease for infants under 90 days old in the United States, according to a multistate study of invasive group B streptococcal disease published in JAMA Pediatrics.

Janice Haney Carr/CDC

Using data from the Active Bacterial Core surveillance (ABCs) program, Srinivas Acharya Nanduri, MD, MPH, at the Centers for Disease Control and Prevention, and colleagues performed an analysis of early-onset disease (EOD) and late-onset disease (LOD) cases of group B Streptococcus (GBS) in infants from 10 different states between 2006 and 2015, and whether mothers of infants with EOD received intrapartum antibiotic prophylaxis (IAP). EOD was defined as between 0 and 6 days old, while LOD occurred between 7 days and 89 days old.

They found 1,277 cases of EOD and 1,387 cases of LOD in total, with a decrease in incidence of EOD from 0.37 per 1,000 live births in 2006 to 0.23 per 1,000 live births in 2015 (P less than .001); LOD incidence remained stable at a mean 0.31 per 1,000 live births during the same time period.

In 2015, the national burden for EOD and LOD was estimated at 840 and 1,265 cases, respectively. Mothers of infants with EOD did not have indications for and did not receive IAP in 617 cases (48%) and did not receive IAP despite indications in 278 (22%) cases.

“While the current culture-based screening strategy has been highly successful in reducing EOD burden, our data show that almost half of remaining infants with EOD were born to mothers with no indication for receiving IAP,” Dr. Nanduri and colleagues wrote.

Because there currently is no effective prevention strategy against LOS GBS, the investigators wrote that a maternal vaccine against the most common serotypes “holds promise to prevent a substantial portion of this remaining burden,” and noted several GBS candidate vaccines were in advanced stages of development.

The researchers also looked at GBS serotype data in 1,743 patients from seven different centers. The most commonly found serotype isolates of 887 EOD cases were Ia (242 cases, 27%) and III (242 cases, 27%) overall. Serotype III was most common for LOD cases (481 cases, 56%) and increased in incidence from 0.12 per 1,000 live births to 0.20 per 1,000 live births during the study period (P less than .001), while serotype IV was responsible for 53 cases (6%) of both EOD and LOD.

Dr. Nanduri and associates wrote that over 99% of the serotyped EOD (881 cases) and serotyped LOD (853 cases) cases were caused by serotypes Ia, Ib, II, III, IV, and V. With regard to antimicrobial resistance, there were no cases of beta-lactam resistance, but there was constitutive clindamycin resistance in 359 isolate test results (21%).

The researchers noted that they were limited in the study by 1 year of whole-genome sequencing data, the ABCs capturing only 10% of live birth data in the United States, and conclusions on EOD prevention restricted to data from labor and delivery records.

This study was funded in part by the CDC. Paula S. Vagnone received grants from the CDC, while William S. Schaffner, MD, received grants from the CDC and personal fees from Pfizer, Merck, SutroVax, Shionogi, Dynavax, and Seqirus outside of the study. The other authors reported no relevant disclosures.

SOURCE: Nanduri SA et al. JAMA Pediatr. 2019 Jan 14. doi: 10.1001/jamapediatrics.2018.4826.

 

Incidence of late-onset disease for group B streptococcus is higher than early-onset disease for infants under 90 days old in the United States, according to a multistate study of invasive group B streptococcal disease published in JAMA Pediatrics.

Janice Haney Carr/CDC

Using data from the Active Bacterial Core surveillance (ABCs) program, Srinivas Acharya Nanduri, MD, MPH, at the Centers for Disease Control and Prevention, and colleagues performed an analysis of early-onset disease (EOD) and late-onset disease (LOD) cases of group B Streptococcus (GBS) in infants from 10 different states between 2006 and 2015, and whether mothers of infants with EOD received intrapartum antibiotic prophylaxis (IAP). EOD was defined as between 0 and 6 days old, while LOD occurred between 7 days and 89 days old.

They found 1,277 cases of EOD and 1,387 cases of LOD in total, with a decrease in incidence of EOD from 0.37 per 1,000 live births in 2006 to 0.23 per 1,000 live births in 2015 (P less than .001); LOD incidence remained stable at a mean 0.31 per 1,000 live births during the same time period.

In 2015, the national burden for EOD and LOD was estimated at 840 and 1,265 cases, respectively. Mothers of infants with EOD did not have indications for and did not receive IAP in 617 cases (48%) and did not receive IAP despite indications in 278 (22%) cases.

“While the current culture-based screening strategy has been highly successful in reducing EOD burden, our data show that almost half of remaining infants with EOD were born to mothers with no indication for receiving IAP,” Dr. Nanduri and colleagues wrote.

Because there currently is no effective prevention strategy against LOS GBS, the investigators wrote that a maternal vaccine against the most common serotypes “holds promise to prevent a substantial portion of this remaining burden,” and noted several GBS candidate vaccines were in advanced stages of development.

The researchers also looked at GBS serotype data in 1,743 patients from seven different centers. The most commonly found serotype isolates of 887 EOD cases were Ia (242 cases, 27%) and III (242 cases, 27%) overall. Serotype III was most common for LOD cases (481 cases, 56%) and increased in incidence from 0.12 per 1,000 live births to 0.20 per 1,000 live births during the study period (P less than .001), while serotype IV was responsible for 53 cases (6%) of both EOD and LOD.

Dr. Nanduri and associates wrote that over 99% of the serotyped EOD (881 cases) and serotyped LOD (853 cases) cases were caused by serotypes Ia, Ib, II, III, IV, and V. With regard to antimicrobial resistance, there were no cases of beta-lactam resistance, but there was constitutive clindamycin resistance in 359 isolate test results (21%).

The researchers noted that they were limited in the study by 1 year of whole-genome sequencing data, the ABCs capturing only 10% of live birth data in the United States, and conclusions on EOD prevention restricted to data from labor and delivery records.

This study was funded in part by the CDC. Paula S. Vagnone received grants from the CDC, while William S. Schaffner, MD, received grants from the CDC and personal fees from Pfizer, Merck, SutroVax, Shionogi, Dynavax, and Seqirus outside of the study. The other authors reported no relevant disclosures.

SOURCE: Nanduri SA et al. JAMA Pediatr. 2019 Jan 14. doi: 10.1001/jamapediatrics.2018.4826.

 

Incidence of late-onset disease for group B streptococcus is higher than early-onset disease for infants under 90 days old in the United States, according to a multistate study of invasive group B streptococcal disease published in JAMA Pediatrics.

Janice Haney Carr/CDC

Using data from the Active Bacterial Core surveillance (ABCs) program, Srinivas Acharya Nanduri, MD, MPH, at the Centers for Disease Control and Prevention, and colleagues performed an analysis of early-onset disease (EOD) and late-onset disease (LOD) cases of group B Streptococcus (GBS) in infants from 10 different states between 2006 and 2015, and whether mothers of infants with EOD received intrapartum antibiotic prophylaxis (IAP). EOD was defined as between 0 and 6 days old, while LOD occurred between 7 days and 89 days old.

They found 1,277 cases of EOD and 1,387 cases of LOD in total, with a decrease in incidence of EOD from 0.37 per 1,000 live births in 2006 to 0.23 per 1,000 live births in 2015 (P less than .001); LOD incidence remained stable at a mean 0.31 per 1,000 live births during the same time period.

In 2015, the national burden for EOD and LOD was estimated at 840 and 1,265 cases, respectively. Mothers of infants with EOD did not have indications for and did not receive IAP in 617 cases (48%) and did not receive IAP despite indications in 278 (22%) cases.

“While the current culture-based screening strategy has been highly successful in reducing EOD burden, our data show that almost half of remaining infants with EOD were born to mothers with no indication for receiving IAP,” Dr. Nanduri and colleagues wrote.

Because there currently is no effective prevention strategy against LOS GBS, the investigators wrote that a maternal vaccine against the most common serotypes “holds promise to prevent a substantial portion of this remaining burden,” and noted several GBS candidate vaccines were in advanced stages of development.

The researchers also looked at GBS serotype data in 1,743 patients from seven different centers. The most commonly found serotype isolates of 887 EOD cases were Ia (242 cases, 27%) and III (242 cases, 27%) overall. Serotype III was most common for LOD cases (481 cases, 56%) and increased in incidence from 0.12 per 1,000 live births to 0.20 per 1,000 live births during the study period (P less than .001), while serotype IV was responsible for 53 cases (6%) of both EOD and LOD.

Dr. Nanduri and associates wrote that over 99% of the serotyped EOD (881 cases) and serotyped LOD (853 cases) cases were caused by serotypes Ia, Ib, II, III, IV, and V. With regard to antimicrobial resistance, there were no cases of beta-lactam resistance, but there was constitutive clindamycin resistance in 359 isolate test results (21%).

The researchers noted that they were limited in the study by 1 year of whole-genome sequencing data, the ABCs capturing only 10% of live birth data in the United States, and conclusions on EOD prevention restricted to data from labor and delivery records.

This study was funded in part by the CDC. Paula S. Vagnone received grants from the CDC, while William S. Schaffner, MD, received grants from the CDC and personal fees from Pfizer, Merck, SutroVax, Shionogi, Dynavax, and Seqirus outside of the study. The other authors reported no relevant disclosures.

SOURCE: Nanduri SA et al. JAMA Pediatr. 2019 Jan 14. doi: 10.1001/jamapediatrics.2018.4826.

Background: Per Chest guidelines, VTE prophylaxis is recommended for hospitalized patients at increased risk for VTE but is not recommended for low-risk patients. Risk stratification can be guided by the Padua Prediction Score to categorize patients.

Study design: Multicenter observational study.

Setting: A total of 52 U.S. hospitals (Michigan Hospital Medicine Safety Consortium database).

Synopsis: Patients admitted during Jan. 1, 2015–Dec. 21, 2016, to 52 non–intensive care medical units for 2 or more days were analyzed and stratified as high or low risk for VTE using the Padua Prediction Score. Excessive VTE prophylaxis was defined as low-risk patients prescribed pharmacologic or mechanical prophylaxis, high-risk patients receiving therapy despite a contraindication to prophylaxis, or any patient who received both mechanical and pharmacologic therapy. Underuse of VTE prophylaxis included high-risk patients who did not receive pharmacologic or mechanical prophylaxis. Of the 44,775 patients included in the study, 32,549 were low risk, and 77.9% (25,369 patients) received excessive VTE prophylaxis. Overtreatment also was present in high-risk patients with and without a contraindication to VTE prophylaxis (26.9% and 32.3%, respectively). Underuse of VTE prophylaxis occurred in 2,693 high-risk patients (22%).

Bottom line: Patients who are at low risk for VTE by Padua Prediction Score often are prescribed pharmacologic or mechanical prophylaxis that may be unnecessary. Overuse of VTE prophylaxis was more common than is underuse.

Citation: Grant PJ et al. Use of venous thromboembolism prophylaxis in hospitalized patients. JAMA Intern Med. 2018 Aug 1;178(8):1122-4. Published online May 21, 2018.

Dr. Marr is assistant professor of medicine and an academic hospitalist, University of Utah, Salt Lake City.

Background: Per Chest guidelines, VTE prophylaxis is recommended for hospitalized patients at increased risk for VTE but is not recommended for low-risk patients. Risk stratification can be guided by the Padua Prediction Score to categorize patients.

Study design: Multicenter observational study.

Setting: A total of 52 U.S. hospitals (Michigan Hospital Medicine Safety Consortium database).

Synopsis: Patients admitted during Jan. 1, 2015–Dec. 21, 2016, to 52 non–intensive care medical units for 2 or more days were analyzed and stratified as high or low risk for VTE using the Padua Prediction Score. Excessive VTE prophylaxis was defined as low-risk patients prescribed pharmacologic or mechanical prophylaxis, high-risk patients receiving therapy despite a contraindication to prophylaxis, or any patient who received both mechanical and pharmacologic therapy. Underuse of VTE prophylaxis included high-risk patients who did not receive pharmacologic or mechanical prophylaxis. Of the 44,775 patients included in the study, 32,549 were low risk, and 77.9% (25,369 patients) received excessive VTE prophylaxis. Overtreatment also was present in high-risk patients with and without a contraindication to VTE prophylaxis (26.9% and 32.3%, respectively). Underuse of VTE prophylaxis occurred in 2,693 high-risk patients (22%).

Bottom line: Patients who are at low risk for VTE by Padua Prediction Score often are prescribed pharmacologic or mechanical prophylaxis that may be unnecessary. Overuse of VTE prophylaxis was more common than is underuse.

Citation: Grant PJ et al. Use of venous thromboembolism prophylaxis in hospitalized patients. JAMA Intern Med. 2018 Aug 1;178(8):1122-4. Published online May 21, 2018.

Dr. Marr is assistant professor of medicine and an academic hospitalist, University of Utah, Salt Lake City.

Background: Per Chest guidelines, VTE prophylaxis is recommended for hospitalized patients at increased risk for VTE but is not recommended for low-risk patients. Risk stratification can be guided by the Padua Prediction Score to categorize patients.

Study design: Multicenter observational study.

Setting: A total of 52 U.S. hospitals (Michigan Hospital Medicine Safety Consortium database).

Synopsis: Patients admitted during Jan. 1, 2015–Dec. 21, 2016, to 52 non–intensive care medical units for 2 or more days were analyzed and stratified as high or low risk for VTE using the Padua Prediction Score. Excessive VTE prophylaxis was defined as low-risk patients prescribed pharmacologic or mechanical prophylaxis, high-risk patients receiving therapy despite a contraindication to prophylaxis, or any patient who received both mechanical and pharmacologic therapy. Underuse of VTE prophylaxis included high-risk patients who did not receive pharmacologic or mechanical prophylaxis. Of the 44,775 patients included in the study, 32,549 were low risk, and 77.9% (25,369 patients) received excessive VTE prophylaxis. Overtreatment also was present in high-risk patients with and without a contraindication to VTE prophylaxis (26.9% and 32.3%, respectively). Underuse of VTE prophylaxis occurred in 2,693 high-risk patients (22%).

Bottom line: Patients who are at low risk for VTE by Padua Prediction Score often are prescribed pharmacologic or mechanical prophylaxis that may be unnecessary. Overuse of VTE prophylaxis was more common than is underuse.

Citation: Grant PJ et al. Use of venous thromboembolism prophylaxis in hospitalized patients. JAMA Intern Med. 2018 Aug 1;178(8):1122-4. Published online May 21, 2018.

Dr. Marr is assistant professor of medicine and an academic hospitalist, University of Utah, Salt Lake City.

 

My recent column on proper telephone technique for front office employees triggered some interesting commentary. “What about the calls we take?” someone asked. “The phone etiquette among most professionals leaves a lot to be desired.”

alvarez/Getty Images

How true! Haven’t we all answered a call from another physician, only to hear, “Please hold for Dr. ___________”?

Let’s begin with that, since it’s one of my major pet peeves: Long tradition, and common courtesy, dictate that the person initiating a call be on the line when the recipient picks up the receiver. So don’t ask an assistant to dial calls for you. Is it really that much bother to do it yourself? A peer should never answer and then be expected to wait while your employee tracks you down. It is impolite, and implies that you consider your time much more valuable than his or hers.

Speaking of common courtesy: Always give callers your undivided attention; they can tell if you are distracted. If it’s not a good time for you, say so honestly, at the outset. “Listen, I can give you a couple of minutes, but I’m right in the middle of office hours ...” That’s much more polite than abruptly cutting someone off, mid-conversation. If the caller needs more time, offer to call back.

By the same token, if you are the caller, be sure to ask, “Is this a good time for you?” Then, be aware of how long you keep the other person on the line. We all have a finite amount of time, and not everyone knows how to end a phone conversation gracefully. Respect others’ time and get to your point quickly.

When you reach an answering machine or voice mail, talk clearly and distinctly. Few things are more frustrating than a mumbled message that no one can decipher. I always repeat my name and phone number for clarity’s sake. And please don’t leave a callback number that no one answers, or that automatically rejects all unidentified callers.

Mobile phones have become so ubiquitous, it is hard to believe that they were relatively scarce only 15 years ago. A distinct set of faux pas has evolved around them; for example, few things are less professional than a loud, indiscreet, annoying, or profane ring tone. Your recorded voice mail message needs to sound professional too – especially if patients will be hearing it.

It should be obvious that cell phones be turned off in theaters and during meetings, but many still remain on. Vibrate mode doesn’t count; anyone close by will still hear it, and you’ll be tempted to answer it. If you get a call during a movie or show, or at a meeting, and you absolutely have to answer it, quietly excuse yourself, and don’t take the call until you are alone. If you miss the call, you can always call the person back.

Answering phone calls in a restaurant is my wife’s biggest pet peeve. She says it is rude and inappropriate, and she’s right – yet it is now, arguably, the most common etiquette mistake. Never take calls (or worse, answer texts or emails) while seated at the table – which leads to another issue: Don’t put your phone on the table! You can hear it just fine from your purse or pocket; and putting it on the table implies to your companions that you are looking for something – anything – more interesting than their company. If you must take a call or read a message, excuse yourself and go to a private area.

In fact, you shouldn’t answer any nonemergent calls or texts when you are with others; it makes your friends and colleagues feel unimportant and ignored. The people you are with should always take precedence over your phone, unless it is a medical emergency or otherwise extremely urgent. On those rare occasions when it is, be polite: “Do you mind if I take this call? It’s important.” Then, once again, excuse yourself to answer privately.

One final thought: Don’t walk around wearing one of those wireless Bluetooth earpieces on your ear, as if the Governor might call at any moment. Everyone around you has to guess whether you’re addressing them or some unseen caller; and frankly – with all respect – it looks ridiculous. And pretentious.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

 

My recent column on proper telephone technique for front office employees triggered some interesting commentary. “What about the calls we take?” someone asked. “The phone etiquette among most professionals leaves a lot to be desired.”

alvarez/Getty Images

How true! Haven’t we all answered a call from another physician, only to hear, “Please hold for Dr. ___________”?

Let’s begin with that, since it’s one of my major pet peeves: Long tradition, and common courtesy, dictate that the person initiating a call be on the line when the recipient picks up the receiver. So don’t ask an assistant to dial calls for you. Is it really that much bother to do it yourself? A peer should never answer and then be expected to wait while your employee tracks you down. It is impolite, and implies that you consider your time much more valuable than his or hers.

Speaking of common courtesy: Always give callers your undivided attention; they can tell if you are distracted. If it’s not a good time for you, say so honestly, at the outset. “Listen, I can give you a couple of minutes, but I’m right in the middle of office hours ...” That’s much more polite than abruptly cutting someone off, mid-conversation. If the caller needs more time, offer to call back.

By the same token, if you are the caller, be sure to ask, “Is this a good time for you?” Then, be aware of how long you keep the other person on the line. We all have a finite amount of time, and not everyone knows how to end a phone conversation gracefully. Respect others’ time and get to your point quickly.

When you reach an answering machine or voice mail, talk clearly and distinctly. Few things are more frustrating than a mumbled message that no one can decipher. I always repeat my name and phone number for clarity’s sake. And please don’t leave a callback number that no one answers, or that automatically rejects all unidentified callers.

Mobile phones have become so ubiquitous, it is hard to believe that they were relatively scarce only 15 years ago. A distinct set of faux pas has evolved around them; for example, few things are less professional than a loud, indiscreet, annoying, or profane ring tone. Your recorded voice mail message needs to sound professional too – especially if patients will be hearing it.

It should be obvious that cell phones be turned off in theaters and during meetings, but many still remain on. Vibrate mode doesn’t count; anyone close by will still hear it, and you’ll be tempted to answer it. If you get a call during a movie or show, or at a meeting, and you absolutely have to answer it, quietly excuse yourself, and don’t take the call until you are alone. If you miss the call, you can always call the person back.

Answering phone calls in a restaurant is my wife’s biggest pet peeve. She says it is rude and inappropriate, and she’s right – yet it is now, arguably, the most common etiquette mistake. Never take calls (or worse, answer texts or emails) while seated at the table – which leads to another issue: Don’t put your phone on the table! You can hear it just fine from your purse or pocket; and putting it on the table implies to your companions that you are looking for something – anything – more interesting than their company. If you must take a call or read a message, excuse yourself and go to a private area.

In fact, you shouldn’t answer any nonemergent calls or texts when you are with others; it makes your friends and colleagues feel unimportant and ignored. The people you are with should always take precedence over your phone, unless it is a medical emergency or otherwise extremely urgent. On those rare occasions when it is, be polite: “Do you mind if I take this call? It’s important.” Then, once again, excuse yourself to answer privately.

One final thought: Don’t walk around wearing one of those wireless Bluetooth earpieces on your ear, as if the Governor might call at any moment. Everyone around you has to guess whether you’re addressing them or some unseen caller; and frankly – with all respect – it looks ridiculous. And pretentious.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

 

My recent column on proper telephone technique for front office employees triggered some interesting commentary. “What about the calls we take?” someone asked. “The phone etiquette among most professionals leaves a lot to be desired.”

alvarez/Getty Images

How true! Haven’t we all answered a call from another physician, only to hear, “Please hold for Dr. ___________”?

Let’s begin with that, since it’s one of my major pet peeves: Long tradition, and common courtesy, dictate that the person initiating a call be on the line when the recipient picks up the receiver. So don’t ask an assistant to dial calls for you. Is it really that much bother to do it yourself? A peer should never answer and then be expected to wait while your employee tracks you down. It is impolite, and implies that you consider your time much more valuable than his or hers.

Speaking of common courtesy: Always give callers your undivided attention; they can tell if you are distracted. If it’s not a good time for you, say so honestly, at the outset. “Listen, I can give you a couple of minutes, but I’m right in the middle of office hours ...” That’s much more polite than abruptly cutting someone off, mid-conversation. If the caller needs more time, offer to call back.

By the same token, if you are the caller, be sure to ask, “Is this a good time for you?” Then, be aware of how long you keep the other person on the line. We all have a finite amount of time, and not everyone knows how to end a phone conversation gracefully. Respect others’ time and get to your point quickly.

When you reach an answering machine or voice mail, talk clearly and distinctly. Few things are more frustrating than a mumbled message that no one can decipher. I always repeat my name and phone number for clarity’s sake. And please don’t leave a callback number that no one answers, or that automatically rejects all unidentified callers.

Mobile phones have become so ubiquitous, it is hard to believe that they were relatively scarce only 15 years ago. A distinct set of faux pas has evolved around them; for example, few things are less professional than a loud, indiscreet, annoying, or profane ring tone. Your recorded voice mail message needs to sound professional too – especially if patients will be hearing it.

It should be obvious that cell phones be turned off in theaters and during meetings, but many still remain on. Vibrate mode doesn’t count; anyone close by will still hear it, and you’ll be tempted to answer it. If you get a call during a movie or show, or at a meeting, and you absolutely have to answer it, quietly excuse yourself, and don’t take the call until you are alone. If you miss the call, you can always call the person back.

Answering phone calls in a restaurant is my wife’s biggest pet peeve. She says it is rude and inappropriate, and she’s right – yet it is now, arguably, the most common etiquette mistake. Never take calls (or worse, answer texts or emails) while seated at the table – which leads to another issue: Don’t put your phone on the table! You can hear it just fine from your purse or pocket; and putting it on the table implies to your companions that you are looking for something – anything – more interesting than their company. If you must take a call or read a message, excuse yourself and go to a private area.

In fact, you shouldn’t answer any nonemergent calls or texts when you are with others; it makes your friends and colleagues feel unimportant and ignored. The people you are with should always take precedence over your phone, unless it is a medical emergency or otherwise extremely urgent. On those rare occasions when it is, be polite: “Do you mind if I take this call? It’s important.” Then, once again, excuse yourself to answer privately.

One final thought: Don’t walk around wearing one of those wireless Bluetooth earpieces on your ear, as if the Governor might call at any moment. Everyone around you has to guess whether you’re addressing them or some unseen caller; and frankly – with all respect – it looks ridiculous. And pretentious.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

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.

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.

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.

aotto@mdedge.com

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.

aotto@mdedge.com

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.

aotto@mdedge.com

SOURCE: Rios Rodriguez V et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40786

A trial is underway to assess the incidence of postoperative pulmonary complications in patients undergoing mechanical ventilation during general anesthesia for robotic surgery 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 mechanical ventilation during general anesthesia for robotic surgery 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 mechanical ventilation during general anesthesia for robotic surgery 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.

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.

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.

 

Too little and too much sleep, along with fragmented sleep, were independently linked with increased subclinical, noncardiac atherosclerotic plaque in healthy middle-aged men and women in a Spanish investigation of bank employees.

Wavebreak Media/Thinkstockphotos

“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.

aotto@mdedge.com

SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.

 

Too little and too much sleep, along with fragmented sleep, were independently linked with increased subclinical, noncardiac atherosclerotic plaque in healthy middle-aged men and women in a Spanish investigation of bank employees.

Wavebreak Media/Thinkstockphotos

“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.

aotto@mdedge.com

SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.

 

Too little and too much sleep, along with fragmented sleep, were independently linked with increased subclinical, noncardiac atherosclerotic plaque in healthy middle-aged men and women in a Spanish investigation of bank employees.

Wavebreak Media/Thinkstockphotos

“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.

aotto@mdedge.com

SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.

After decades of increases, the prevalences of gout and hyperuricemia were steady over the past decade, 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.

rfranki@mdedge.com

SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.

After decades of increases, the prevalences of gout and hyperuricemia were steady over the past decade, 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.

rfranki@mdedge.com

SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.

After decades of increases, the prevalences of gout and hyperuricemia were steady over the past decade, 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.

rfranki@mdedge.com

SOURCE: Chen-Xu M et al. Arthritis Rheumatol. 2019 Jan 7. doi: 10.1002/art.40807.

 

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.

Courtesy 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.

Courtesy MD Anderson Cancer Center

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 hematologynews@mdedge.com, 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.

Courtesy 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.

Courtesy MD Anderson Cancer Center

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 hematologynews@mdedge.com, 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.

Courtesy 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.

Courtesy MD Anderson Cancer Center

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 hematologynews@mdedge.com, and you could be featured in Movers in Medicine.