Click here to access the August 2016 Digital Edition. 

Table of Contents

• One More Comment on Expanding the Scope of Practice for VA Advanced Practice Nurses
• A Motivational Interviewing Training Program for Tobacco Cessation Counseling in Primary Care
• Impact of a Drop-in Group Medical Appointment on Tobacco Quit Rates
• The Impact of Elder Abuse on a Growing Senior Veteran Population
• An Unusual Infection of Breast Tissue
• Characteristics of High-Functioning Collaborations Between Primary Care and Podiatry in VHA PACTs
• Integrating Palliative Care in COPD Treatment
• Development and Implementation of a Geriatric Walking Clinic

Click here to access the August 2016 Digital Edition. 

Table of Contents

• One More Comment on Expanding the Scope of Practice for VA Advanced Practice Nurses
• A Motivational Interviewing Training Program for Tobacco Cessation Counseling in Primary Care
• Impact of a Drop-in Group Medical Appointment on Tobacco Quit Rates
• The Impact of Elder Abuse on a Growing Senior Veteran Population
• An Unusual Infection of Breast Tissue
• Characteristics of High-Functioning Collaborations Between Primary Care and Podiatry in VHA PACTs
• Integrating Palliative Care in COPD Treatment
• Development and Implementation of a Geriatric Walking Clinic

Click here to access the August 2016 Digital Edition. 

Table of Contents

• One More Comment on Expanding the Scope of Practice for VA Advanced Practice Nurses
• A Motivational Interviewing Training Program for Tobacco Cessation Counseling in Primary Care
• Impact of a Drop-in Group Medical Appointment on Tobacco Quit Rates
• The Impact of Elder Abuse on a Growing Senior Veteran Population
• An Unusual Infection of Breast Tissue
• Characteristics of High-Functioning Collaborations Between Primary Care and Podiatry in VHA PACTs
• Integrating Palliative Care in COPD Treatment
• Development and Implementation of a Geriatric Walking Clinic

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Click here to read the full story.

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Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

SOURCE: AMERICAN GASTROENTEROLOGICAL ASSOCIATION

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

SOURCE: AMERICAN GASTROENTEROLOGICAL ASSOCIATION

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

SOURCE: AMERICAN GASTROENTEROLOGICAL ASSOCIATION

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

Americans from the Punjab region of India had the highest prevalence of celiac disease in a national cross-sectional study of duodenal mucosal biopsies according to a study reported in the August issue of Clinical Gastroenterology and Hepatology.

In contrast, persons of South Asian, East Asian, and Hispanic descent are significantly less likely to receive a biopsy-based diagnosis of celiac disease than were other Americans, Anna Krigel, MD, at Columbia University, New York, reported with her associates. The prevalence of celiac disease among Jewish and Middle Eastern individuals resembled that of other Americans and did not differ by sex, the researchers added. “These findings may have clinical relevance to gastroenterologists across the United States and may aid in their diagnostic practices.”

Dr. Krigel and her associates analyzed a national laboratory pathology registry of 454,885 patients who underwent esophagogastroduodenoscopy with duodenal biopsy between January 2008 and April 2015. Mucosal biopsy specimens were analyzed at three laboratories by histopathologists who had completed fellowships in gastrointestinal pathology. Patients were categorized based on their first and last names as North Indian, South Indian, East Asian, Hispanic, Middle Eastern, Jewish, or as “other Americans,” using a published algorithm. The researchers further validated this algorithm by adjusting it against a list of individuals of known ethnicities until its specificity reached 95%. Two-thirds of patients in the cohort were female, and the median age was 53 years (Clin Gastroenterol Hepatol. 2016 May 31. doi: 10.1016/j.cgh.2016.04.032).

Overall, 7,928 patients (1.7%) had duodenal villous atrophy indicative of disease, including 2% of North Indians, 1.8% of Jewish individuals, 1.8% of other Americans, 1.5% of Middle Easterners, 1.1% of Hispanics, and 0.15% of East Asians, said the investigators. Thus, Jewish persons and Middle Eastern persons had a prevalence of celiac disease similar to that of other Americans. Prevalence also was similar among Ashkenazi and Sephardic Jews. In contrast, none of the 177 South Indians in the study were diagnosed with celiac disease, and both East Asians and Hispanics were significantly less likely to be receive a diagnosis than other Americans, with odds ratios of 0.08 (95% confidence interval, 0.04-0.17) and 0.58 (0.52-0.64), respectively, and P values less than .0001.

Importantly, celiac disease was significantly more common among patients from the Punjab region of India (3.1%) than among other North Indians (1.5%; P = .02). Past studies of celiac disease in India reported similar prevalences of compatible human leukocyte antigen (HLA) haplotypes as in Western countries, without notable regional trends within India, the researchers noted. Substantial regional variations in wheat consumption in India are more likely to explain their findings and patterns of case reports in past studies, they added.

Because the registry lacked serology data, patients diagnosed with celiac disease could have actually had tropical sprue or sprue-like enteropathy due to olmesartan, the researchers acknowledged. “In particular, multiple studies have shown that tropical sprue is still the most common cause of malabsorption syndrome in India, whereas celiac disease is emerging as a more important cause of malabsorption than previously thought,” they said. “However, such cases of tropical sprue and sprue-like enteropathy due to olmesartan are far less common than celiac disease in the United States.” The study also did not account for patients whose celiac disease only was diagnosed by serology and clinical symptoms, and the algorithm probably assigned some individuals who were Hispanic to other ethnicities, because only 7% of the cohort was classified as Hispanic, compared with about 16% of Americans in the 2010 U.S. Census, they noted. But ethnic misclassification was unlikely to have differed by celiac disease status, they said.

The National Institutes of Health partially supported the work. The authors had no disclosures.

Americans from the Punjab region of India had the highest prevalence of celiac disease in a national cross-sectional study of duodenal mucosal biopsies according to a study reported in the August issue of Clinical Gastroenterology and Hepatology.

In contrast, persons of South Asian, East Asian, and Hispanic descent are significantly less likely to receive a biopsy-based diagnosis of celiac disease than were other Americans, Anna Krigel, MD, at Columbia University, New York, reported with her associates. The prevalence of celiac disease among Jewish and Middle Eastern individuals resembled that of other Americans and did not differ by sex, the researchers added. “These findings may have clinical relevance to gastroenterologists across the United States and may aid in their diagnostic practices.”

Dr. Krigel and her associates analyzed a national laboratory pathology registry of 454,885 patients who underwent esophagogastroduodenoscopy with duodenal biopsy between January 2008 and April 2015. Mucosal biopsy specimens were analyzed at three laboratories by histopathologists who had completed fellowships in gastrointestinal pathology. Patients were categorized based on their first and last names as North Indian, South Indian, East Asian, Hispanic, Middle Eastern, Jewish, or as “other Americans,” using a published algorithm. The researchers further validated this algorithm by adjusting it against a list of individuals of known ethnicities until its specificity reached 95%. Two-thirds of patients in the cohort were female, and the median age was 53 years (Clin Gastroenterol Hepatol. 2016 May 31. doi: 10.1016/j.cgh.2016.04.032).

Overall, 7,928 patients (1.7%) had duodenal villous atrophy indicative of disease, including 2% of North Indians, 1.8% of Jewish individuals, 1.8% of other Americans, 1.5% of Middle Easterners, 1.1% of Hispanics, and 0.15% of East Asians, said the investigators. Thus, Jewish persons and Middle Eastern persons had a prevalence of celiac disease similar to that of other Americans. Prevalence also was similar among Ashkenazi and Sephardic Jews. In contrast, none of the 177 South Indians in the study were diagnosed with celiac disease, and both East Asians and Hispanics were significantly less likely to be receive a diagnosis than other Americans, with odds ratios of 0.08 (95% confidence interval, 0.04-0.17) and 0.58 (0.52-0.64), respectively, and P values less than .0001.

Importantly, celiac disease was significantly more common among patients from the Punjab region of India (3.1%) than among other North Indians (1.5%; P = .02). Past studies of celiac disease in India reported similar prevalences of compatible human leukocyte antigen (HLA) haplotypes as in Western countries, without notable regional trends within India, the researchers noted. Substantial regional variations in wheat consumption in India are more likely to explain their findings and patterns of case reports in past studies, they added.

Because the registry lacked serology data, patients diagnosed with celiac disease could have actually had tropical sprue or sprue-like enteropathy due to olmesartan, the researchers acknowledged. “In particular, multiple studies have shown that tropical sprue is still the most common cause of malabsorption syndrome in India, whereas celiac disease is emerging as a more important cause of malabsorption than previously thought,” they said. “However, such cases of tropical sprue and sprue-like enteropathy due to olmesartan are far less common than celiac disease in the United States.” The study also did not account for patients whose celiac disease only was diagnosed by serology and clinical symptoms, and the algorithm probably assigned some individuals who were Hispanic to other ethnicities, because only 7% of the cohort was classified as Hispanic, compared with about 16% of Americans in the 2010 U.S. Census, they noted. But ethnic misclassification was unlikely to have differed by celiac disease status, they said.

The National Institutes of Health partially supported the work. The authors had no disclosures.

Americans from the Punjab region of India had the highest prevalence of celiac disease in a national cross-sectional study of duodenal mucosal biopsies according to a study reported in the August issue of Clinical Gastroenterology and Hepatology.

In contrast, persons of South Asian, East Asian, and Hispanic descent are significantly less likely to receive a biopsy-based diagnosis of celiac disease than were other Americans, Anna Krigel, MD, at Columbia University, New York, reported with her associates. The prevalence of celiac disease among Jewish and Middle Eastern individuals resembled that of other Americans and did not differ by sex, the researchers added. “These findings may have clinical relevance to gastroenterologists across the United States and may aid in their diagnostic practices.”

Dr. Krigel and her associates analyzed a national laboratory pathology registry of 454,885 patients who underwent esophagogastroduodenoscopy with duodenal biopsy between January 2008 and April 2015. Mucosal biopsy specimens were analyzed at three laboratories by histopathologists who had completed fellowships in gastrointestinal pathology. Patients were categorized based on their first and last names as North Indian, South Indian, East Asian, Hispanic, Middle Eastern, Jewish, or as “other Americans,” using a published algorithm. The researchers further validated this algorithm by adjusting it against a list of individuals of known ethnicities until its specificity reached 95%. Two-thirds of patients in the cohort were female, and the median age was 53 years (Clin Gastroenterol Hepatol. 2016 May 31. doi: 10.1016/j.cgh.2016.04.032).

Overall, 7,928 patients (1.7%) had duodenal villous atrophy indicative of disease, including 2% of North Indians, 1.8% of Jewish individuals, 1.8% of other Americans, 1.5% of Middle Easterners, 1.1% of Hispanics, and 0.15% of East Asians, said the investigators. Thus, Jewish persons and Middle Eastern persons had a prevalence of celiac disease similar to that of other Americans. Prevalence also was similar among Ashkenazi and Sephardic Jews. In contrast, none of the 177 South Indians in the study were diagnosed with celiac disease, and both East Asians and Hispanics were significantly less likely to be receive a diagnosis than other Americans, with odds ratios of 0.08 (95% confidence interval, 0.04-0.17) and 0.58 (0.52-0.64), respectively, and P values less than .0001.

Importantly, celiac disease was significantly more common among patients from the Punjab region of India (3.1%) than among other North Indians (1.5%; P = .02). Past studies of celiac disease in India reported similar prevalences of compatible human leukocyte antigen (HLA) haplotypes as in Western countries, without notable regional trends within India, the researchers noted. Substantial regional variations in wheat consumption in India are more likely to explain their findings and patterns of case reports in past studies, they added.

Because the registry lacked serology data, patients diagnosed with celiac disease could have actually had tropical sprue or sprue-like enteropathy due to olmesartan, the researchers acknowledged. “In particular, multiple studies have shown that tropical sprue is still the most common cause of malabsorption syndrome in India, whereas celiac disease is emerging as a more important cause of malabsorption than previously thought,” they said. “However, such cases of tropical sprue and sprue-like enteropathy due to olmesartan are far less common than celiac disease in the United States.” The study also did not account for patients whose celiac disease only was diagnosed by serology and clinical symptoms, and the algorithm probably assigned some individuals who were Hispanic to other ethnicities, because only 7% of the cohort was classified as Hispanic, compared with about 16% of Americans in the 2010 U.S. Census, they noted. But ethnic misclassification was unlikely to have differed by celiac disease status, they said.

The National Institutes of Health partially supported the work. The authors had no disclosures.

Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

Resuming low-dose aspirin after an initial lower gastrointestinal bleed significantly increased the chances of recurrence but protected against serious cardiovascular events, based on a single-center retrospective study published in the August issue of Gastroenterology.

In contrast, “we did not find concomitant use of anticoagulants, antiplatelets, and steroids as a predictor of recurrent lower GI bleeding,” said Dr. Francis Chan of the Prince of Wales Hospital in Hong Kong and his associates. “This may be due to the low percentage of concomitant drug use in both groups. Multicenter studies with a large number of patients will be required to identify additional risk factors for recurrent lower GI bleeding with aspirin use.”

Low-dose aspirin has long been known to help prevent coronary artery and cerebrovascular disease, and more recently has been found to potentially reduce the risk of several types of cancer, the researchers noted. Aspirin is well known to increase the risk of upper GI bleeding, but some studies have also linked it to lower GI bleeding. However, “patients with underlying cardiovascular diseases often require lifelong aspirin,” they added. The risks and benefits of stopping or remaining on aspirin after an initial lower GI bleed are unclear (Gastroenterology 2016 Apr 26. doi: 10.1053/j.gastro.2016.04.013).

Accordingly, the researchers retrospectively studied 295 patients who had an initial aspirin-associated lower GI bleed, defined as 325 mg aspirin a day within a week of bleeding onset. All patients had melena or hematochezia documented by an attending physician and had no endoscopic evidence of upper GI bleeding.

For patients who continued using aspirin at least half the time, the 5-year cumulative incidence of recurrent lower GI bleeding was 19% (95% confidence interval [CI], 13%-25%) – more than double the rate among patients who used aspirin 20% or less of the time (5-year cumulative incidence, 7%; 95% CI, 3%-13%; P = .01). However, the 5-year cumulative incidence of serious cardiovascular events among nonusers was 37% (95% CI, 27%-46%), while the rate among aspirin users was 23% (95% CI, 17%-30%; P = .02). Mortality from noncardiovascular causes was also higher among nonusers (27%) than users (8%; P less than .001), probably because nonusers of aspirin tended to be older than users, but perhaps also because aspirin had a “nonvascular protective effect,” the researchers said.

A multivariate analysis confirmed these findings, linking lower GI bleeding to aspirin but not to use of steroids, anticoagulants, or antiplatelet drugs, or to age, sex, alcohol consumption, smoking, comorbidities, or cardiovascular risks. Indeed, continued aspirin use nearly tripled the chances of a recurrent lower GI bleed (hazard ratio, 2.76; 95% CI, 1.3-6.0; P = .01), but cut the risk of serious cardiovascular events by about 40% (HR, 0.59; 95% CI, 0.4-0.9; P = .02).

Deciding whether to resume aspirin after a severe lower GI bleed “presents a management dilemma for physicians, patients, and their families, particularly in the absence of risk-mitigating therapies and a lack of data on the risks and benefits of resuming aspirin,” the investigators emphasized. Their findings highlight the importance of weighing the cardiovascular benefits of aspirin against GI toxicity, they said. “Since there is substantial risk of recurrent bleeding, physicians should critically evaluate individual patients’ cardiovascular risk before resuming aspirin therapy. Our findings also suggest a need for a composite endpoint to evaluate clinically significant events throughout the GI tract in patients receiving antiplatelet drugs.”

The Chinese University of Hong Kong funded the study. Dr. Chan reported financial ties to Pfizer, Eisai, Takeda, Otsuka, and Astrazeneca.

A single, 100-mg rectal dose of indomethacin cut the odds of moderate to severe pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP) by 85% in a single-center retrospective study of more than 4,000 patients reported in the August issue of Gastroenterology.

The effect extended to low-risk patients and those with malignant biliary obstruction, who make up the majority of ERCP patients in community practice, said Nikhil R. Thiruvengadam, MD, and his associates at the University of Pennsylvania. “Usage of rectal indomethacin in current clinical practice is low, as most endoscopists outside of referral centers perform ERCP for indications that are considered low-risk for PEP [post-ERCP pancreatitis], and until now, there were no data to support a benefit of rectal NSAIDs in this population,” they wrote in Gastroenterology. Their “real-world analysis” clearly shows the benefits of rectal indomethacin in low-risk patients and supports its increased use after ERCP, they added.

Pancreatitis, the most common complication of ERCP, affected 2%-9% of patients in prior studies and costs about $200 million in the United States annually, the investigators noted. Pancreatic duct stents help prevent post-ERCP pancreatitis, but require experience to place and have their own complications that limit their use in low-risk patients. Past studies of rectal indomethacin after ERCP reported mixed results and mainly focused on high-risk patients, leaving questions about whether to routinely use this NSAID after ERCP, said the researchers (Gastroenterology. 2016 May 20. doi: 10.1053/j.gastro.2016.04.048). Their study included 4,017 patients who underwent ERCP at the University of Pennsylvania between 2009 and 2015. From 2012 onward, nearly all patients received 100 mg rectal indomethacin immediately after the duodenoscope was withdrawn. This indomethacin group included 2,007 patients, while 2,010 patients in the study did not receive rectal indomethacin. In all, 95 (4.73%) untreated patients developed post-ERCP pancreatitis, compared with only 40 (1.99%) patients who received indomethacin, for a 65% reduction in the odds of post-ERCP pancreatitis (odds ratio, 0.35; 95% confidence interval, 0.24-0.51; P less than .001). Rectal indomethacin also led to an 83% drop in the odds of moderate to severe post-ERCP pancreatitis (OR, 0.17; 95% CI, 0.09-0.32; P less than .001) and showed very similar protective effects for patients with malignant obstruction (OR, 0.35; 95% CI, 0.17-0.75; P less than .001] and 0.20; 95% CI, 0.07-0.63; P less than 0.001, respectively).

Rectal indomethacin was particularly beneficial for patients with malignant obstruction and pancreatic adenocarcinoma, the investigators noted. Such patients had post-ERCP rates of 2.31% when they received rectal indomethacin and 7.53% otherwise (P less than .001). They also had a nearly sevenfold lower rate of moderate to severe post-ERCP pancreatitis when they received rectal indomethacin (P = .001).

Treatment did not affect the chances of perforation and did not cause anaphylaxis, but was tied to a slightly higher rate of postprocedural gastrointestinal bleeding among sphincterotomy patients (0.65% with treatment versus 0.45% without; P = .52). However, sphincterotomy patients were much less likely to develop pancreatitis when they received rectal indomethacin than when they did not (0% and 9.58% of patients, respectively; P = .003).

“The majority of ERCPs were performed by experienced endoscopists at a tertiary care center, which may have limited the effects of variable procedural skills on the risk of PEP,” the researchers said. “Therefore, generalizability of our findings to other populations may be limited. However, it should be noted that the overall PEP rate in both the unexposed and indomethacin groups was fairly low and similar to large community-based estimates, suggesting that our overall patient population was of similar overall risk.” The study was not powered to assess the combined effects of rectal indomethacin and pancreatic duct stents, they noted.

The investigators reported no funding sources and had no disclosures.

A single, 100-mg rectal dose of indomethacin cut the odds of moderate to severe pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP) by 85% in a single-center retrospective study of more than 4,000 patients reported in the August issue of Gastroenterology.

The effect extended to low-risk patients and those with malignant biliary obstruction, who make up the majority of ERCP patients in community practice, said Nikhil R. Thiruvengadam, MD, and his associates at the University of Pennsylvania. “Usage of rectal indomethacin in current clinical practice is low, as most endoscopists outside of referral centers perform ERCP for indications that are considered low-risk for PEP [post-ERCP pancreatitis], and until now, there were no data to support a benefit of rectal NSAIDs in this population,” they wrote in Gastroenterology. Their “real-world analysis” clearly shows the benefits of rectal indomethacin in low-risk patients and supports its increased use after ERCP, they added.

Pancreatitis, the most common complication of ERCP, affected 2%-9% of patients in prior studies and costs about $200 million in the United States annually, the investigators noted. Pancreatic duct stents help prevent post-ERCP pancreatitis, but require experience to place and have their own complications that limit their use in low-risk patients. Past studies of rectal indomethacin after ERCP reported mixed results and mainly focused on high-risk patients, leaving questions about whether to routinely use this NSAID after ERCP, said the researchers (Gastroenterology. 2016 May 20. doi: 10.1053/j.gastro.2016.04.048). Their study included 4,017 patients who underwent ERCP at the University of Pennsylvania between 2009 and 2015. From 2012 onward, nearly all patients received 100 mg rectal indomethacin immediately after the duodenoscope was withdrawn. This indomethacin group included 2,007 patients, while 2,010 patients in the study did not receive rectal indomethacin. In all, 95 (4.73%) untreated patients developed post-ERCP pancreatitis, compared with only 40 (1.99%) patients who received indomethacin, for a 65% reduction in the odds of post-ERCP pancreatitis (odds ratio, 0.35; 95% confidence interval, 0.24-0.51; P less than .001). Rectal indomethacin also led to an 83% drop in the odds of moderate to severe post-ERCP pancreatitis (OR, 0.17; 95% CI, 0.09-0.32; P less than .001) and showed very similar protective effects for patients with malignant obstruction (OR, 0.35; 95% CI, 0.17-0.75; P less than .001] and 0.20; 95% CI, 0.07-0.63; P less than 0.001, respectively).

Rectal indomethacin was particularly beneficial for patients with malignant obstruction and pancreatic adenocarcinoma, the investigators noted. Such patients had post-ERCP rates of 2.31% when they received rectal indomethacin and 7.53% otherwise (P less than .001). They also had a nearly sevenfold lower rate of moderate to severe post-ERCP pancreatitis when they received rectal indomethacin (P = .001).

Treatment did not affect the chances of perforation and did not cause anaphylaxis, but was tied to a slightly higher rate of postprocedural gastrointestinal bleeding among sphincterotomy patients (0.65% with treatment versus 0.45% without; P = .52). However, sphincterotomy patients were much less likely to develop pancreatitis when they received rectal indomethacin than when they did not (0% and 9.58% of patients, respectively; P = .003).

“The majority of ERCPs were performed by experienced endoscopists at a tertiary care center, which may have limited the effects of variable procedural skills on the risk of PEP,” the researchers said. “Therefore, generalizability of our findings to other populations may be limited. However, it should be noted that the overall PEP rate in both the unexposed and indomethacin groups was fairly low and similar to large community-based estimates, suggesting that our overall patient population was of similar overall risk.” The study was not powered to assess the combined effects of rectal indomethacin and pancreatic duct stents, they noted.

The investigators reported no funding sources and had no disclosures.

A single, 100-mg rectal dose of indomethacin cut the odds of moderate to severe pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP) by 85% in a single-center retrospective study of more than 4,000 patients reported in the August issue of Gastroenterology.

The effect extended to low-risk patients and those with malignant biliary obstruction, who make up the majority of ERCP patients in community practice, said Nikhil R. Thiruvengadam, MD, and his associates at the University of Pennsylvania. “Usage of rectal indomethacin in current clinical practice is low, as most endoscopists outside of referral centers perform ERCP for indications that are considered low-risk for PEP [post-ERCP pancreatitis], and until now, there were no data to support a benefit of rectal NSAIDs in this population,” they wrote in Gastroenterology. Their “real-world analysis” clearly shows the benefits of rectal indomethacin in low-risk patients and supports its increased use after ERCP, they added.

Pancreatitis, the most common complication of ERCP, affected 2%-9% of patients in prior studies and costs about $200 million in the United States annually, the investigators noted. Pancreatic duct stents help prevent post-ERCP pancreatitis, but require experience to place and have their own complications that limit their use in low-risk patients. Past studies of rectal indomethacin after ERCP reported mixed results and mainly focused on high-risk patients, leaving questions about whether to routinely use this NSAID after ERCP, said the researchers (Gastroenterology. 2016 May 20. doi: 10.1053/j.gastro.2016.04.048). Their study included 4,017 patients who underwent ERCP at the University of Pennsylvania between 2009 and 2015. From 2012 onward, nearly all patients received 100 mg rectal indomethacin immediately after the duodenoscope was withdrawn. This indomethacin group included 2,007 patients, while 2,010 patients in the study did not receive rectal indomethacin. In all, 95 (4.73%) untreated patients developed post-ERCP pancreatitis, compared with only 40 (1.99%) patients who received indomethacin, for a 65% reduction in the odds of post-ERCP pancreatitis (odds ratio, 0.35; 95% confidence interval, 0.24-0.51; P less than .001). Rectal indomethacin also led to an 83% drop in the odds of moderate to severe post-ERCP pancreatitis (OR, 0.17; 95% CI, 0.09-0.32; P less than .001) and showed very similar protective effects for patients with malignant obstruction (OR, 0.35; 95% CI, 0.17-0.75; P less than .001] and 0.20; 95% CI, 0.07-0.63; P less than 0.001, respectively).

Rectal indomethacin was particularly beneficial for patients with malignant obstruction and pancreatic adenocarcinoma, the investigators noted. Such patients had post-ERCP rates of 2.31% when they received rectal indomethacin and 7.53% otherwise (P less than .001). They also had a nearly sevenfold lower rate of moderate to severe post-ERCP pancreatitis when they received rectal indomethacin (P = .001).

Treatment did not affect the chances of perforation and did not cause anaphylaxis, but was tied to a slightly higher rate of postprocedural gastrointestinal bleeding among sphincterotomy patients (0.65% with treatment versus 0.45% without; P = .52). However, sphincterotomy patients were much less likely to develop pancreatitis when they received rectal indomethacin than when they did not (0% and 9.58% of patients, respectively; P = .003).

“The majority of ERCPs were performed by experienced endoscopists at a tertiary care center, which may have limited the effects of variable procedural skills on the risk of PEP,” the researchers said. “Therefore, generalizability of our findings to other populations may be limited. However, it should be noted that the overall PEP rate in both the unexposed and indomethacin groups was fairly low and similar to large community-based estimates, suggesting that our overall patient population was of similar overall risk.” The study was not powered to assess the combined effects of rectal indomethacin and pancreatic duct stents, they noted.

The investigators reported no funding sources and had no disclosures.

To the Editor: I read the excellent overview article on measles by Drs. Kumar and Sabella.¹ However, there are additional important clinical points regarding measles diagnosis that deserve further comment. Prior to definitive diagnosis, measles is a clinical diagnosis. Properly, much attention is given to the rash, but there are important clinical clues besides the rash that are helpful diagnostically.

Some clinical findings are more characteristic of a disease than others, eg, eye findings in measles, and clinicians should specifically look for them. Other findings not characteristic but consistent with the diagnosis are less helpful, eg, measles with diarrhea.² Measles is a systemic infection with several extradermatologic manifestations. Characteristically, measles involves the respiratory tract, manifested by runny nose, dry cough, or shortness of breath, ie, measles pneumonia.²

Gastrointestinal involvement may be manifested as nausea, vomiting, diarrhea, or abdominal pain. Abdominal pain, when located in the right lower quadrant, may mimic acute appendicitis, ie, pseudoappendicitis. In patients undergoing appendectomy, pathologically the appendix is normal but contains multinucleated giant cells (Warthin-Finkeldey cells). Measles pseudoappendicitis can be perplexing because it presents before the rash. Even without appendiceal involvement (pseudoappendicitis), Warthin-Finkeldey cells are also present in the nasal mucosa. If nasal swab cytology shows Warthin-Finkeldey cells, an early diagnosis of measles may be made days before IgM measles antibodies are reported.³

Other often-overlooked important clues are eye findings, eg, watery eyes, lower lid edema, conjunctival suffusion, and keratitis. No other disease in the differential diagnosis of measles presents with watery eyes with bilateral lower lid edema and conjunctival suffusion. Headache, mental confusion or oral ulcers may suggest alternate diagnoses. Typically, nonspecific laboratory abnormalities include leukopenia and thrombocytopenia, and importantly, the erythrocyte sedimentation rate is not elevated (Table 1).^4,5

In measles, much is made of Koplik spots, which are found early on dark red buccal mucosa (vs Fordyce spots).¹ However, if these are missed or not present, clinicians can use other characteristic findings to make a presumptive diagnosis of measles.

To the Editor: I read the excellent overview article on measles by Drs. Kumar and Sabella.¹ However, there are additional important clinical points regarding measles diagnosis that deserve further comment. Prior to definitive diagnosis, measles is a clinical diagnosis. Properly, much attention is given to the rash, but there are important clinical clues besides the rash that are helpful diagnostically.

Some clinical findings are more characteristic of a disease than others, eg, eye findings in measles, and clinicians should specifically look for them. Other findings not characteristic but consistent with the diagnosis are less helpful, eg, measles with diarrhea.² Measles is a systemic infection with several extradermatologic manifestations. Characteristically, measles involves the respiratory tract, manifested by runny nose, dry cough, or shortness of breath, ie, measles pneumonia.²

Gastrointestinal involvement may be manifested as nausea, vomiting, diarrhea, or abdominal pain. Abdominal pain, when located in the right lower quadrant, may mimic acute appendicitis, ie, pseudoappendicitis. In patients undergoing appendectomy, pathologically the appendix is normal but contains multinucleated giant cells (Warthin-Finkeldey cells). Measles pseudoappendicitis can be perplexing because it presents before the rash. Even without appendiceal involvement (pseudoappendicitis), Warthin-Finkeldey cells are also present in the nasal mucosa. If nasal swab cytology shows Warthin-Finkeldey cells, an early diagnosis of measles may be made days before IgM measles antibodies are reported.³

Other often-overlooked important clues are eye findings, eg, watery eyes, lower lid edema, conjunctival suffusion, and keratitis. No other disease in the differential diagnosis of measles presents with watery eyes with bilateral lower lid edema and conjunctival suffusion. Headache, mental confusion or oral ulcers may suggest alternate diagnoses. Typically, nonspecific laboratory abnormalities include leukopenia and thrombocytopenia, and importantly, the erythrocyte sedimentation rate is not elevated (Table 1).^4,5

In measles, much is made of Koplik spots, which are found early on dark red buccal mucosa (vs Fordyce spots).¹ However, if these are missed or not present, clinicians can use other characteristic findings to make a presumptive diagnosis of measles.

To the Editor: I read the excellent overview article on measles by Drs. Kumar and Sabella.¹ However, there are additional important clinical points regarding measles diagnosis that deserve further comment. Prior to definitive diagnosis, measles is a clinical diagnosis. Properly, much attention is given to the rash, but there are important clinical clues besides the rash that are helpful diagnostically.

Some clinical findings are more characteristic of a disease than others, eg, eye findings in measles, and clinicians should specifically look for them. Other findings not characteristic but consistent with the diagnosis are less helpful, eg, measles with diarrhea.² Measles is a systemic infection with several extradermatologic manifestations. Characteristically, measles involves the respiratory tract, manifested by runny nose, dry cough, or shortness of breath, ie, measles pneumonia.²

Gastrointestinal involvement may be manifested as nausea, vomiting, diarrhea, or abdominal pain. Abdominal pain, when located in the right lower quadrant, may mimic acute appendicitis, ie, pseudoappendicitis. In patients undergoing appendectomy, pathologically the appendix is normal but contains multinucleated giant cells (Warthin-Finkeldey cells). Measles pseudoappendicitis can be perplexing because it presents before the rash. Even without appendiceal involvement (pseudoappendicitis), Warthin-Finkeldey cells are also present in the nasal mucosa. If nasal swab cytology shows Warthin-Finkeldey cells, an early diagnosis of measles may be made days before IgM measles antibodies are reported.³

Other often-overlooked important clues are eye findings, eg, watery eyes, lower lid edema, conjunctival suffusion, and keratitis. No other disease in the differential diagnosis of measles presents with watery eyes with bilateral lower lid edema and conjunctival suffusion. Headache, mental confusion or oral ulcers may suggest alternate diagnoses. Typically, nonspecific laboratory abnormalities include leukopenia and thrombocytopenia, and importantly, the erythrocyte sedimentation rate is not elevated (Table 1).^4,5

In measles, much is made of Koplik spots, which are found early on dark red buccal mucosa (vs Fordyce spots).¹ However, if these are missed or not present, clinicians can use other characteristic findings to make a presumptive diagnosis of measles.

In Reply: We thank Dr. Cunha for his comments and appreciate the opportunity to emphasize important points that he highlights.

We agree that measles is a systemic illness with important extradermatologic manifestations that are critical to the diagnosis, and that the nondermatologic manifestations often precede the rash and serve to distinguish measles from other systemic illnesses. As discussed in our review, the respiratory prodrome of cough, coryza, and conjunctivitis is very distinctive and serves as an important clue to the diagnosis. Likewise, we acknowledge the importance of gastrointestinal findings in measles and note appendicitis as an important complication that is well described. Although Koplik spots are pathognomonic, we do stress that these often are not present at the time of presentation.

Finally, we agree that measles is a clinical diagnosis, and that the clinical manifestations beyond the dermatologic manifestations noted in our review and highlighted by Dr. Cunha are extremely helpful to the clinician in considering the diagnosis.

In Reply: We thank Dr. Cunha for his comments and appreciate the opportunity to emphasize important points that he highlights.

We agree that measles is a systemic illness with important extradermatologic manifestations that are critical to the diagnosis, and that the nondermatologic manifestations often precede the rash and serve to distinguish measles from other systemic illnesses. As discussed in our review, the respiratory prodrome of cough, coryza, and conjunctivitis is very distinctive and serves as an important clue to the diagnosis. Likewise, we acknowledge the importance of gastrointestinal findings in measles and note appendicitis as an important complication that is well described. Although Koplik spots are pathognomonic, we do stress that these often are not present at the time of presentation.

Finally, we agree that measles is a clinical diagnosis, and that the clinical manifestations beyond the dermatologic manifestations noted in our review and highlighted by Dr. Cunha are extremely helpful to the clinician in considering the diagnosis.

In Reply: We thank Dr. Cunha for his comments and appreciate the opportunity to emphasize important points that he highlights.

We agree that measles is a systemic illness with important extradermatologic manifestations that are critical to the diagnosis, and that the nondermatologic manifestations often precede the rash and serve to distinguish measles from other systemic illnesses. As discussed in our review, the respiratory prodrome of cough, coryza, and conjunctivitis is very distinctive and serves as an important clue to the diagnosis. Likewise, we acknowledge the importance of gastrointestinal findings in measles and note appendicitis as an important complication that is well described. Although Koplik spots are pathognomonic, we do stress that these often are not present at the time of presentation.

Finally, we agree that measles is a clinical diagnosis, and that the clinical manifestations beyond the dermatologic manifestations noted in our review and highlighted by Dr. Cunha are extremely helpful to the clinician in considering the diagnosis.

To the Editor: As a primary care physician who has practiced for 31 years, I have a few concerns about the article “Prescribing opioids in primary care: Safely starting, monitoring, and stopping” by Drs. Daniel Tobin, Rebecca Andrews, and William Becker in your March 2016 issue.

Prescribing narcotics and other controlled medications has become a hot topic with legal implications. Many physicians have lost their license, and some have lost their freedom as well.

The article notes that primary care physicians provide most of the care for chronic pain but implies that we don’t know what we are doing. Although we might not have completed a residency in the management of chronic pain, we were required to attend a graduate medical school and to complete residency programs. We are also required to read the medical literature and keep up with our CME requirements. We too strive to keep up with and practice the latest cutting-edge medicine. And we have experience. After seeing thousands of patients and writing millions of prescriptions, I think I do know something about whether or not a medicine is safe, effective, and cost-effective. I have encountered quite a few patients with pain, and not one of them has overdosed by taking the medications as prescribed.

Most of what is being said and published about pain medication focuses on the epidemic of young people who are getting pain medications (prescription narcotics) and street narcotics (heroin) illegally. Directly, it has nothing to do with conscientious physicians prescribing narcotics for pain, but indirectly, it has to do with all adults in society. We are allowing our young people to be destroyed by drugs and by a lack of proper discipline in our homes that spills over into society. Where are our children getting these drugs, and who is bringing them into our neighborhoods? The practice of medicine is not the primary problem. I am for scientific, conscientious regulations concerning controlled substances. Medicine needs to inform all doctors about the changing laws surrounding the prescribing of controlled substances.

Cigarettes and alcohol are sold on every corner, and places selling marijuana are popping up everywhere. The former two drugs are harming and killing more young people than all the illegal drugs combined, and marijuana is fast approaching number three. I feel we need to stop picking on the medical profession and stop trying to blame it for all the woes that our young people are encountering every day. The reality is that legal and illegal drugs are not going to go away. We need to love our children more and better prepare them while in our homes to deal with the evils in our society.

To the Editor: As a primary care physician who has practiced for 31 years, I have a few concerns about the article “Prescribing opioids in primary care: Safely starting, monitoring, and stopping” by Drs. Daniel Tobin, Rebecca Andrews, and William Becker in your March 2016 issue.

Prescribing narcotics and other controlled medications has become a hot topic with legal implications. Many physicians have lost their license, and some have lost their freedom as well.

The article notes that primary care physicians provide most of the care for chronic pain but implies that we don’t know what we are doing. Although we might not have completed a residency in the management of chronic pain, we were required to attend a graduate medical school and to complete residency programs. We are also required to read the medical literature and keep up with our CME requirements. We too strive to keep up with and practice the latest cutting-edge medicine. And we have experience. After seeing thousands of patients and writing millions of prescriptions, I think I do know something about whether or not a medicine is safe, effective, and cost-effective. I have encountered quite a few patients with pain, and not one of them has overdosed by taking the medications as prescribed.

Most of what is being said and published about pain medication focuses on the epidemic of young people who are getting pain medications (prescription narcotics) and street narcotics (heroin) illegally. Directly, it has nothing to do with conscientious physicians prescribing narcotics for pain, but indirectly, it has to do with all adults in society. We are allowing our young people to be destroyed by drugs and by a lack of proper discipline in our homes that spills over into society. Where are our children getting these drugs, and who is bringing them into our neighborhoods? The practice of medicine is not the primary problem. I am for scientific, conscientious regulations concerning controlled substances. Medicine needs to inform all doctors about the changing laws surrounding the prescribing of controlled substances.

Cigarettes and alcohol are sold on every corner, and places selling marijuana are popping up everywhere. The former two drugs are harming and killing more young people than all the illegal drugs combined, and marijuana is fast approaching number three. I feel we need to stop picking on the medical profession and stop trying to blame it for all the woes that our young people are encountering every day. The reality is that legal and illegal drugs are not going to go away. We need to love our children more and better prepare them while in our homes to deal with the evils in our society.

To the Editor: As a primary care physician who has practiced for 31 years, I have a few concerns about the article “Prescribing opioids in primary care: Safely starting, monitoring, and stopping” by Drs. Daniel Tobin, Rebecca Andrews, and William Becker in your March 2016 issue.

Prescribing narcotics and other controlled medications has become a hot topic with legal implications. Many physicians have lost their license, and some have lost their freedom as well.

The article notes that primary care physicians provide most of the care for chronic pain but implies that we don’t know what we are doing. Although we might not have completed a residency in the management of chronic pain, we were required to attend a graduate medical school and to complete residency programs. We are also required to read the medical literature and keep up with our CME requirements. We too strive to keep up with and practice the latest cutting-edge medicine. And we have experience. After seeing thousands of patients and writing millions of prescriptions, I think I do know something about whether or not a medicine is safe, effective, and cost-effective. I have encountered quite a few patients with pain, and not one of them has overdosed by taking the medications as prescribed.

Most of what is being said and published about pain medication focuses on the epidemic of young people who are getting pain medications (prescription narcotics) and street narcotics (heroin) illegally. Directly, it has nothing to do with conscientious physicians prescribing narcotics for pain, but indirectly, it has to do with all adults in society. We are allowing our young people to be destroyed by drugs and by a lack of proper discipline in our homes that spills over into society. Where are our children getting these drugs, and who is bringing them into our neighborhoods? The practice of medicine is not the primary problem. I am for scientific, conscientious regulations concerning controlled substances. Medicine needs to inform all doctors about the changing laws surrounding the prescribing of controlled substances.

Cigarettes and alcohol are sold on every corner, and places selling marijuana are popping up everywhere. The former two drugs are harming and killing more young people than all the illegal drugs combined, and marijuana is fast approaching number three. I feel we need to stop picking on the medical profession and stop trying to blame it for all the woes that our young people are encountering every day. The reality is that legal and illegal drugs are not going to go away. We need to love our children more and better prepare them while in our homes to deal with the evils in our society.

In Reply: We thank Dr. Pettiway for his remarks. The intent of our article was to identify common challenges when prescribing opioids for chronic pain and offer tips to the provider struggling with how to do so safely. We hope these comments will offer additional clarity.

First, as general internists who are essentially “self-trained” in the management of chronic pain, we fully acknowledge the importance of practical experience in learning how to prescribe opioids safely and effectively. Dr. Pettiway is correct that a dedicated physician who keeps up with the medical literature, attends relevant continuing medical education courses, and strives to provide deliberate, rational, and evidence-based care to his or her patients can do so effectively. However, the medical literature suggests that medical school training in the management of chronic pain is sparse; one review found that in 2011 only 5 out of 133 US medical schools required coursework on pain management, and only 13 offered it as an elective.¹ Many primary care providers do feel unprepared to handle this challenge.

Additionally, Dr. Pettiway raises a good question about where misused prescription opioids originate and whether prescribers are responsible. The data show that the majority of misused prescription opioids are obtained from a family member or friend and not directly from a physician.^2,3 However, this supply does generally originate from a prescription. Providers need to educate their patients about the risk for diversion, the need to keep pills safely hidden and locked away, and the importance of safely discarding unused supplies. Responsible prescribers need to anticipate these concerns and educate patients about them.

In summary, we firmly believe that primary care providers are capable of safe, effective, and responsible opioid prescribing and hope that our paper provides additional guidance on how to do so.

In Reply: We thank Dr. Pettiway for his remarks. The intent of our article was to identify common challenges when prescribing opioids for chronic pain and offer tips to the provider struggling with how to do so safely. We hope these comments will offer additional clarity.

First, as general internists who are essentially “self-trained” in the management of chronic pain, we fully acknowledge the importance of practical experience in learning how to prescribe opioids safely and effectively. Dr. Pettiway is correct that a dedicated physician who keeps up with the medical literature, attends relevant continuing medical education courses, and strives to provide deliberate, rational, and evidence-based care to his or her patients can do so effectively. However, the medical literature suggests that medical school training in the management of chronic pain is sparse; one review found that in 2011 only 5 out of 133 US medical schools required coursework on pain management, and only 13 offered it as an elective.¹ Many primary care providers do feel unprepared to handle this challenge.

Additionally, Dr. Pettiway raises a good question about where misused prescription opioids originate and whether prescribers are responsible. The data show that the majority of misused prescription opioids are obtained from a family member or friend and not directly from a physician.^2,3 However, this supply does generally originate from a prescription. Providers need to educate their patients about the risk for diversion, the need to keep pills safely hidden and locked away, and the importance of safely discarding unused supplies. Responsible prescribers need to anticipate these concerns and educate patients about them.

In summary, we firmly believe that primary care providers are capable of safe, effective, and responsible opioid prescribing and hope that our paper provides additional guidance on how to do so.

In Reply: We thank Dr. Pettiway for his remarks. The intent of our article was to identify common challenges when prescribing opioids for chronic pain and offer tips to the provider struggling with how to do so safely. We hope these comments will offer additional clarity.

First, as general internists who are essentially “self-trained” in the management of chronic pain, we fully acknowledge the importance of practical experience in learning how to prescribe opioids safely and effectively. Dr. Pettiway is correct that a dedicated physician who keeps up with the medical literature, attends relevant continuing medical education courses, and strives to provide deliberate, rational, and evidence-based care to his or her patients can do so effectively. However, the medical literature suggests that medical school training in the management of chronic pain is sparse; one review found that in 2011 only 5 out of 133 US medical schools required coursework on pain management, and only 13 offered it as an elective.¹ Many primary care providers do feel unprepared to handle this challenge.

Additionally, Dr. Pettiway raises a good question about where misused prescription opioids originate and whether prescribers are responsible. The data show that the majority of misused prescription opioids are obtained from a family member or friend and not directly from a physician.^2,3 However, this supply does generally originate from a prescription. Providers need to educate their patients about the risk for diversion, the need to keep pills safely hidden and locked away, and the importance of safely discarding unused supplies. Responsible prescribers need to anticipate these concerns and educate patients about them.

In summary, we firmly believe that primary care providers are capable of safe, effective, and responsible opioid prescribing and hope that our paper provides additional guidance on how to do so.