Oral cancer has a low 5-year survival rate compared with other major types of cancer, and the rate hasn’t improved much in recent years, say researchers from China Medical University, Asia University, Taichung Veterans General Hospital, and National Yang-Ming University; all in Taichung, Taiwan. That may be due in part to delay in treatment, they say. Their analysis of data of 21,263 patients with oral cavity squamous cell carcinoma (OCSCC) bears out their theory.

Related: Predicting Tongue Cancer Recurrence

About 40% of the patients presented with stage IV disease. More than one-third had tongue cancer. The average time from diagnosis to treatment was 24 days. Most patients (86%) were treated within 30 days of diagnosis; 12% were treated between 31 and 120 days after diagnosis, and 2.7% received treatment 120 days after diagnosis. Surgery was usually the first treatment.

The time interval from diagnosis to treatment (the phrase the researchers prefer to “treatment delay” or “wait time”) was an independent prognostic factor in OCSCC patients. The average interval was 24 days. Those treated within 30 days tended to have a higher survival rate. Treatment after 120 days from diagnosis increased the risk of death by 1.32-fold.

The average follow-up period was 44 months. When the researchers stratified patients according to the time between diagnosis and treatment, they found patients aged ≥ 65 years or who had advanced cancer were more likely to be treated later. Patients treated initially with radiotherapy or chemotherapy were more likely to have a longer mean time interval when compared with those who were treated first with surgery.

Related: Shorter Length of Stay May Not Mean Higher Readmission Rates

The researchers also found that patients treated in private hospitals had a shorter time interval compared with those treated in public hospitals (although the latter were more likely to survive). Patients who received treatment in hospitals with a low- to medium-service volume had a longer interval compared with those treated in hospitals with a high-service volume. Other predictors of longer survival included being female, younger, primary tumor site at the tongue, and earlier stage disease.

The researchers cite a study that found the median duration of clinical upstaging from early to late stage was 11.3 months, whereas the average period from advanced tumor to untreatable tumor was 3.8 months. That might explain why they found that the longer delay to treatment increased the risk of death, they suggest. The researchers also point to reasons such as pending second opinions, shortages of therapeutic instruments and manpower, and lack of public awareness.

Related: IBD and the Risk of Oral Cancer

All told however, the researchers conclude, the reasons for the increased time interval from diagnosis to treatment of OCSCC patients remain “multifaceted, integrated, and poorly understood.”

Source:
Tsai WC, Kung PT, Wang YH, Huang KH, Liu SA. PLoS One. 2017;12(4):e0175148.
doi: 10.1371/journal.pone.0175148.

Oral cancer has a low 5-year survival rate compared with other major types of cancer, and the rate hasn’t improved much in recent years, say researchers from China Medical University, Asia University, Taichung Veterans General Hospital, and National Yang-Ming University; all in Taichung, Taiwan. That may be due in part to delay in treatment, they say. Their analysis of data of 21,263 patients with oral cavity squamous cell carcinoma (OCSCC) bears out their theory.

Related: Predicting Tongue Cancer Recurrence

About 40% of the patients presented with stage IV disease. More than one-third had tongue cancer. The average time from diagnosis to treatment was 24 days. Most patients (86%) were treated within 30 days of diagnosis; 12% were treated between 31 and 120 days after diagnosis, and 2.7% received treatment 120 days after diagnosis. Surgery was usually the first treatment.

The time interval from diagnosis to treatment (the phrase the researchers prefer to “treatment delay” or “wait time”) was an independent prognostic factor in OCSCC patients. The average interval was 24 days. Those treated within 30 days tended to have a higher survival rate. Treatment after 120 days from diagnosis increased the risk of death by 1.32-fold.

The average follow-up period was 44 months. When the researchers stratified patients according to the time between diagnosis and treatment, they found patients aged ≥ 65 years or who had advanced cancer were more likely to be treated later. Patients treated initially with radiotherapy or chemotherapy were more likely to have a longer mean time interval when compared with those who were treated first with surgery.

Related: Shorter Length of Stay May Not Mean Higher Readmission Rates

The researchers also found that patients treated in private hospitals had a shorter time interval compared with those treated in public hospitals (although the latter were more likely to survive). Patients who received treatment in hospitals with a low- to medium-service volume had a longer interval compared with those treated in hospitals with a high-service volume. Other predictors of longer survival included being female, younger, primary tumor site at the tongue, and earlier stage disease.

The researchers cite a study that found the median duration of clinical upstaging from early to late stage was 11.3 months, whereas the average period from advanced tumor to untreatable tumor was 3.8 months. That might explain why they found that the longer delay to treatment increased the risk of death, they suggest. The researchers also point to reasons such as pending second opinions, shortages of therapeutic instruments and manpower, and lack of public awareness.

Related: IBD and the Risk of Oral Cancer

All told however, the researchers conclude, the reasons for the increased time interval from diagnosis to treatment of OCSCC patients remain “multifaceted, integrated, and poorly understood.”

Source:
Tsai WC, Kung PT, Wang YH, Huang KH, Liu SA. PLoS One. 2017;12(4):e0175148.
doi: 10.1371/journal.pone.0175148.

Oral cancer has a low 5-year survival rate compared with other major types of cancer, and the rate hasn’t improved much in recent years, say researchers from China Medical University, Asia University, Taichung Veterans General Hospital, and National Yang-Ming University; all in Taichung, Taiwan. That may be due in part to delay in treatment, they say. Their analysis of data of 21,263 patients with oral cavity squamous cell carcinoma (OCSCC) bears out their theory.

Related: Predicting Tongue Cancer Recurrence

About 40% of the patients presented with stage IV disease. More than one-third had tongue cancer. The average time from diagnosis to treatment was 24 days. Most patients (86%) were treated within 30 days of diagnosis; 12% were treated between 31 and 120 days after diagnosis, and 2.7% received treatment 120 days after diagnosis. Surgery was usually the first treatment.

The time interval from diagnosis to treatment (the phrase the researchers prefer to “treatment delay” or “wait time”) was an independent prognostic factor in OCSCC patients. The average interval was 24 days. Those treated within 30 days tended to have a higher survival rate. Treatment after 120 days from diagnosis increased the risk of death by 1.32-fold.

The average follow-up period was 44 months. When the researchers stratified patients according to the time between diagnosis and treatment, they found patients aged ≥ 65 years or who had advanced cancer were more likely to be treated later. Patients treated initially with radiotherapy or chemotherapy were more likely to have a longer mean time interval when compared with those who were treated first with surgery.

Related: Shorter Length of Stay May Not Mean Higher Readmission Rates

The researchers also found that patients treated in private hospitals had a shorter time interval compared with those treated in public hospitals (although the latter were more likely to survive). Patients who received treatment in hospitals with a low- to medium-service volume had a longer interval compared with those treated in hospitals with a high-service volume. Other predictors of longer survival included being female, younger, primary tumor site at the tongue, and earlier stage disease.

The researchers cite a study that found the median duration of clinical upstaging from early to late stage was 11.3 months, whereas the average period from advanced tumor to untreatable tumor was 3.8 months. That might explain why they found that the longer delay to treatment increased the risk of death, they suggest. The researchers also point to reasons such as pending second opinions, shortages of therapeutic instruments and manpower, and lack of public awareness.

Related: IBD and the Risk of Oral Cancer

All told however, the researchers conclude, the reasons for the increased time interval from diagnosis to treatment of OCSCC patients remain “multifaceted, integrated, and poorly understood.”

Source:
Tsai WC, Kung PT, Wang YH, Huang KH, Liu SA. PLoS One. 2017;12(4):e0175148.
doi: 10.1371/journal.pone.0175148.

Six years ago, a lesion appeared on this now 39-year-old woman’s forehead. It grew steadily to its current size, impinging on her brow line. Although it has been asymptomatic, the patient is concerned about malignancy, since she has a significant personal and family history of skin cancer. She has had several lesions removed from her face and back over the years.

EXAMINATION
There is a 2.2-cm, roughly round, white, cicatricial, concave lesion on the patient’s lower right forehead, extending into the brow line. Around the periphery are several 2- to 5-mm eroded papules. There are no palpable nodes on the head or neck.

Several scars are seen elsewhere on the patient’s face and back, consistent with her history. Her type II/VI skin is quite fair and sun-damaged.

A 6-mm deep punch biopsy of the lesion is obtained.

What is the diagnosis?

Of the different types of BCC, the most common are nodular. These present as pearly (ie, translucent) papules or nodules, with or without focal erosion or frank ulceration; they often have prominent telangiectasias coursing over their surfaces. BCCs can also appear as rashes (superficial BCC) that may not attract attention.

This patient’s lesion is one of the least common variations: It combines features of a morpheaform (scarlike) BCC with focal noduloulcerative papular lesions studding its periphery. The concavity of the scarlike portion, along with its prolonged presence, predicted deep involvement of adjacent tissue—confirmed by the biopsy results.

At a minimum, this patient will need Mohs micrographic surgical removal, with closure by skin graft or secondary intention. Given the deep perineural involvement, surgery alone may not clear the cancer; radiation therapy may be necessary.

TAKE-HOME LEARNING POINTS

• Morpheaform basal cell carcinoma (BCC), also known as cicatricial BCC, can present as a white, scarlike patch, often with an atrophic surface.
• This type of BCC is more aggressive than most, often requiring Mohs surgery.
• There are at least three other types of BCC, most of which involve nonhealing ulcerative papules or nodules.
• This patient’s history of sun-caused skin cancers makes recurrence likely.

Six years ago, a lesion appeared on this now 39-year-old woman’s forehead. It grew steadily to its current size, impinging on her brow line. Although it has been asymptomatic, the patient is concerned about malignancy, since she has a significant personal and family history of skin cancer. She has had several lesions removed from her face and back over the years.

EXAMINATION
There is a 2.2-cm, roughly round, white, cicatricial, concave lesion on the patient’s lower right forehead, extending into the brow line. Around the periphery are several 2- to 5-mm eroded papules. There are no palpable nodes on the head or neck.

Several scars are seen elsewhere on the patient’s face and back, consistent with her history. Her type II/VI skin is quite fair and sun-damaged.

A 6-mm deep punch biopsy of the lesion is obtained.

What is the diagnosis?

Of the different types of BCC, the most common are nodular. These present as pearly (ie, translucent) papules or nodules, with or without focal erosion or frank ulceration; they often have prominent telangiectasias coursing over their surfaces. BCCs can also appear as rashes (superficial BCC) that may not attract attention.

This patient’s lesion is one of the least common variations: It combines features of a morpheaform (scarlike) BCC with focal noduloulcerative papular lesions studding its periphery. The concavity of the scarlike portion, along with its prolonged presence, predicted deep involvement of adjacent tissue—confirmed by the biopsy results.

At a minimum, this patient will need Mohs micrographic surgical removal, with closure by skin graft or secondary intention. Given the deep perineural involvement, surgery alone may not clear the cancer; radiation therapy may be necessary.

TAKE-HOME LEARNING POINTS

• Morpheaform basal cell carcinoma (BCC), also known as cicatricial BCC, can present as a white, scarlike patch, often with an atrophic surface.
• This type of BCC is more aggressive than most, often requiring Mohs surgery.
• There are at least three other types of BCC, most of which involve nonhealing ulcerative papules or nodules.
• This patient’s history of sun-caused skin cancers makes recurrence likely.

Six years ago, a lesion appeared on this now 39-year-old woman’s forehead. It grew steadily to its current size, impinging on her brow line. Although it has been asymptomatic, the patient is concerned about malignancy, since she has a significant personal and family history of skin cancer. She has had several lesions removed from her face and back over the years.

EXAMINATION
There is a 2.2-cm, roughly round, white, cicatricial, concave lesion on the patient’s lower right forehead, extending into the brow line. Around the periphery are several 2- to 5-mm eroded papules. There are no palpable nodes on the head or neck.

Several scars are seen elsewhere on the patient’s face and back, consistent with her history. Her type II/VI skin is quite fair and sun-damaged.

A 6-mm deep punch biopsy of the lesion is obtained.

What is the diagnosis?

Of the different types of BCC, the most common are nodular. These present as pearly (ie, translucent) papules or nodules, with or without focal erosion or frank ulceration; they often have prominent telangiectasias coursing over their surfaces. BCCs can also appear as rashes (superficial BCC) that may not attract attention.

This patient’s lesion is one of the least common variations: It combines features of a morpheaform (scarlike) BCC with focal noduloulcerative papular lesions studding its periphery. The concavity of the scarlike portion, along with its prolonged presence, predicted deep involvement of adjacent tissue—confirmed by the biopsy results.

At a minimum, this patient will need Mohs micrographic surgical removal, with closure by skin graft or secondary intention. Given the deep perineural involvement, surgery alone may not clear the cancer; radiation therapy may be necessary.

TAKE-HOME LEARNING POINTS

• Morpheaform basal cell carcinoma (BCC), also known as cicatricial BCC, can present as a white, scarlike patch, often with an atrophic surface.
• This type of BCC is more aggressive than most, often requiring Mohs surgery.
• There are at least three other types of BCC, most of which involve nonhealing ulcerative papules or nodules.
• This patient’s history of sun-caused skin cancers makes recurrence likely.

Patients with at least five biopsies showing nondysplastic Barrett’s esophagus were statistically as likely to progress to high-grade dysplasia or esophageal adenocarcinoma as patients with a single such biopsy, according to a multicenter prospective registry study reported in the June issue of Clinical Gastroenterology and Hepatology (doi: org/10.1016/j.cgh.2017.02.019).

The findings, which contradict those from another recent multicenter cohort study (Gastroenterology. 2013;145[3]:548-53), highlight the need for more studies before lengthening the time between surveillance biopsies in patients with nondysplastic Barrett’s esophagus, Rajesh Krishnamoorthi, MD, of Mayo Clinic in Rochester, Minn., wrote with his associates.

Barrett’s esophagus is the strongest predictor of esophageal adenocarcinoma, but studies have reported mixed results as to whether the risk of this cancer increases over time or wanes with consecutive biopsies that indicate nondysplasia, the researchers noted. Therefore, they studied the prospective, multicenter Mayo Clinic Esophageal Adenocarcinoma and Barrett’s Esophagus registry, excluding patients who progressed to adenocarcinoma within 12 months, had missing data, or had no follow-up biopsies. This approach left 480 subjects for analysis. Patients averaged 63 years of age, 78% were male, the mean length of Barrett’s esophagus was 5.7 cm, and the average time between biopsies was 1.8 years, with a standard deviation of 1.3 years.

A total of 16 patients progressed to high-grade dysplasia or esophageal adenocarcinoma over 1,832 patient-years of follow-up, for an overall annual risk of progression of 0.87%. Two patients progressed to esophageal adenocarcinoma (annual risk, 0.11%; 95% confidence interval, 0.03% to 0.44%), while 14 patients progressed to high-grade dysplasia (annual risk, 0.76%; 95% CI, 0.45% to 1.29%). Eight patients progressed to one of these two outcomes after a single nondysplastic biopsy, three progressed after two such biopsies, three progressed after three such biopsies, none progressed after four such biopsies, and two progressed after five such biopsies. Statistically, patients with at least five consecutive nondysplastic biopsies were no less likely to progress than were patients with only one nondysplastic biopsy (hazard ratio, 0.48; 95% CI, 0.07 to 1.92; P = .32). Hazard ratios for the other groups ranged between 0.0 and 0.85, with no significant difference in estimated risk between groups (P = .68) after controlling for age, sex, and length of Barrett’s esophagus.

The previous multicenter cohort study linked persistently nondysplastic Barrett’s esophagus with a lower rate of progression to esophageal adenocarcinoma, and, based on those findings, the authors suggested lengthening intervals between biopsy surveillance or even stopping surveillance, Dr. Krishnamoorthi and his associates noted. However, that study did not have mutually exclusive groups. “Additional data are required before increasing the interval between surveillance endoscopies based on persistence of nondysplastic Barrett’s esophagus,” they concluded.

The study lacked misclassification bias given long-segment Barrett’s esophagus, and specialized gastrointestinal pathologists interpreted all histology specimens, the researchers noted. “The small number of progressors is a potential limitation, reducing power to assess associations,” they added.

The investigators did not report funding sources. They reported having no conflicts of interest.

Patients with at least five biopsies showing nondysplastic Barrett’s esophagus were statistically as likely to progress to high-grade dysplasia or esophageal adenocarcinoma as patients with a single such biopsy, according to a multicenter prospective registry study reported in the June issue of Clinical Gastroenterology and Hepatology (doi: org/10.1016/j.cgh.2017.02.019).

The findings, which contradict those from another recent multicenter cohort study (Gastroenterology. 2013;145[3]:548-53), highlight the need for more studies before lengthening the time between surveillance biopsies in patients with nondysplastic Barrett’s esophagus, Rajesh Krishnamoorthi, MD, of Mayo Clinic in Rochester, Minn., wrote with his associates.

Barrett’s esophagus is the strongest predictor of esophageal adenocarcinoma, but studies have reported mixed results as to whether the risk of this cancer increases over time or wanes with consecutive biopsies that indicate nondysplasia, the researchers noted. Therefore, they studied the prospective, multicenter Mayo Clinic Esophageal Adenocarcinoma and Barrett’s Esophagus registry, excluding patients who progressed to adenocarcinoma within 12 months, had missing data, or had no follow-up biopsies. This approach left 480 subjects for analysis. Patients averaged 63 years of age, 78% were male, the mean length of Barrett’s esophagus was 5.7 cm, and the average time between biopsies was 1.8 years, with a standard deviation of 1.3 years.

A total of 16 patients progressed to high-grade dysplasia or esophageal adenocarcinoma over 1,832 patient-years of follow-up, for an overall annual risk of progression of 0.87%. Two patients progressed to esophageal adenocarcinoma (annual risk, 0.11%; 95% confidence interval, 0.03% to 0.44%), while 14 patients progressed to high-grade dysplasia (annual risk, 0.76%; 95% CI, 0.45% to 1.29%). Eight patients progressed to one of these two outcomes after a single nondysplastic biopsy, three progressed after two such biopsies, three progressed after three such biopsies, none progressed after four such biopsies, and two progressed after five such biopsies. Statistically, patients with at least five consecutive nondysplastic biopsies were no less likely to progress than were patients with only one nondysplastic biopsy (hazard ratio, 0.48; 95% CI, 0.07 to 1.92; P = .32). Hazard ratios for the other groups ranged between 0.0 and 0.85, with no significant difference in estimated risk between groups (P = .68) after controlling for age, sex, and length of Barrett’s esophagus.

The previous multicenter cohort study linked persistently nondysplastic Barrett’s esophagus with a lower rate of progression to esophageal adenocarcinoma, and, based on those findings, the authors suggested lengthening intervals between biopsy surveillance or even stopping surveillance, Dr. Krishnamoorthi and his associates noted. However, that study did not have mutually exclusive groups. “Additional data are required before increasing the interval between surveillance endoscopies based on persistence of nondysplastic Barrett’s esophagus,” they concluded.

The study lacked misclassification bias given long-segment Barrett’s esophagus, and specialized gastrointestinal pathologists interpreted all histology specimens, the researchers noted. “The small number of progressors is a potential limitation, reducing power to assess associations,” they added.

The investigators did not report funding sources. They reported having no conflicts of interest.

Patients with at least five biopsies showing nondysplastic Barrett’s esophagus were statistically as likely to progress to high-grade dysplasia or esophageal adenocarcinoma as patients with a single such biopsy, according to a multicenter prospective registry study reported in the June issue of Clinical Gastroenterology and Hepatology (doi: org/10.1016/j.cgh.2017.02.019).

The findings, which contradict those from another recent multicenter cohort study (Gastroenterology. 2013;145[3]:548-53), highlight the need for more studies before lengthening the time between surveillance biopsies in patients with nondysplastic Barrett’s esophagus, Rajesh Krishnamoorthi, MD, of Mayo Clinic in Rochester, Minn., wrote with his associates.

Barrett’s esophagus is the strongest predictor of esophageal adenocarcinoma, but studies have reported mixed results as to whether the risk of this cancer increases over time or wanes with consecutive biopsies that indicate nondysplasia, the researchers noted. Therefore, they studied the prospective, multicenter Mayo Clinic Esophageal Adenocarcinoma and Barrett’s Esophagus registry, excluding patients who progressed to adenocarcinoma within 12 months, had missing data, or had no follow-up biopsies. This approach left 480 subjects for analysis. Patients averaged 63 years of age, 78% were male, the mean length of Barrett’s esophagus was 5.7 cm, and the average time between biopsies was 1.8 years, with a standard deviation of 1.3 years.

A total of 16 patients progressed to high-grade dysplasia or esophageal adenocarcinoma over 1,832 patient-years of follow-up, for an overall annual risk of progression of 0.87%. Two patients progressed to esophageal adenocarcinoma (annual risk, 0.11%; 95% confidence interval, 0.03% to 0.44%), while 14 patients progressed to high-grade dysplasia (annual risk, 0.76%; 95% CI, 0.45% to 1.29%). Eight patients progressed to one of these two outcomes after a single nondysplastic biopsy, three progressed after two such biopsies, three progressed after three such biopsies, none progressed after four such biopsies, and two progressed after five such biopsies. Statistically, patients with at least five consecutive nondysplastic biopsies were no less likely to progress than were patients with only one nondysplastic biopsy (hazard ratio, 0.48; 95% CI, 0.07 to 1.92; P = .32). Hazard ratios for the other groups ranged between 0.0 and 0.85, with no significant difference in estimated risk between groups (P = .68) after controlling for age, sex, and length of Barrett’s esophagus.

The previous multicenter cohort study linked persistently nondysplastic Barrett’s esophagus with a lower rate of progression to esophageal adenocarcinoma, and, based on those findings, the authors suggested lengthening intervals between biopsy surveillance or even stopping surveillance, Dr. Krishnamoorthi and his associates noted. However, that study did not have mutually exclusive groups. “Additional data are required before increasing the interval between surveillance endoscopies based on persistence of nondysplastic Barrett’s esophagus,” they concluded.

The study lacked misclassification bias given long-segment Barrett’s esophagus, and specialized gastrointestinal pathologists interpreted all histology specimens, the researchers noted. “The small number of progressors is a potential limitation, reducing power to assess associations,” they added.

The investigators did not report funding sources. They reported having no conflicts of interest.

Click here to access Combating Public Pathogens in Federal Health Care Systems

Table of Contents

• Open Clinical Trials for Patients With HIV and/or Viral Hepatitis
• HIV Update: Which Single-Tablet Regimens, and When
• Improving Veteran Access to Treatment for Hepatitis C Virus Infection
• Strategies to Improve Hepatocellular Carcinoma Surveillance in Veterans With Hepatitis B Virus Infection
• Heart Transplantation Outcomes in Patients With Hepatitis C Virus Infection: Potential Impact of Newer Antiviral Treatments After Transplantation

Click here to access Combating Public Pathogens in Federal Health Care Systems

Table of Contents

• Open Clinical Trials for Patients With HIV and/or Viral Hepatitis
• HIV Update: Which Single-Tablet Regimens, and When
• Improving Veteran Access to Treatment for Hepatitis C Virus Infection
• Strategies to Improve Hepatocellular Carcinoma Surveillance in Veterans With Hepatitis B Virus Infection
• Heart Transplantation Outcomes in Patients With Hepatitis C Virus Infection: Potential Impact of Newer Antiviral Treatments After Transplantation

Click here to access Combating Public Pathogens in Federal Health Care Systems

Table of Contents

• Open Clinical Trials for Patients With HIV and/or Viral Hepatitis
• HIV Update: Which Single-Tablet Regimens, and When
• Improving Veteran Access to Treatment for Hepatitis C Virus Infection
• Strategies to Improve Hepatocellular Carcinoma Surveillance in Veterans With Hepatitis B Virus Infection
• Heart Transplantation Outcomes in Patients With Hepatitis C Virus Infection: Potential Impact of Newer Antiviral Treatments After Transplantation

Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

Click here to access the June 2017 Digital Edition.

Table of Contents

• A Pathway to Full Practice Authority for Physician Assistants in the VA
• Outcomes Associated With a Multidisciplinary Pain Oversight Committee to Facilitate Management of Chronic Opioid Therapy
• Quality of Chronic Obstructive Pulmonary Disease-Related Health Care in Rural and Urban Clinics
• Three Anomalies and a Complication: Ruptured Noncoronary Sinus of Valsalva Aneurysm, Atrial Septal Aneurysm, and Patent Foramen Ovale
• Orthorexia Nervosa: An Obsession With Healthy Eating
• Interprofessional Education in PACT Primary Care-Mental Health Integration

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

What are the long-term clinical effects of wartime traumatic brain injuries (TBIs)? Most are mild, but in general all are incompletely described, say researchers from University of Washington in Seattle and Washington University in St. Louis, Missouri. However, their own study found that service members with even mild concussive TBI often “experienced evolution, not resolution” of symptoms.

The researchers compared the results of 1-year and 5-year clinical evaluations of 50 active-duty U.S. military with acute to subacute concussive blast injury and 44 deployed but uninjured service members. The evaluations included neurobehavioral and neuropsychological performance and mental health burden.

At 5 years, global disability, satisfaction with life, neurobehavioral symptom severity, psychiatric symptom severity, and sleep impairment were significantly worse in patients with concussive blast TBI. Of the patients with concussive blast TBI, 36 (72%) showed decline, compared with only 5 of the combat-deployed group (11%). The researchers also found symptoms of PTSD and depression worsened in the concussive TBI patients. Performance on cognitive measures was no different between the 2 groups. A combination of factors, including neurobehavioral symptom severity, walking ability, and verbal fluency at 1 year after injury, was highly predictive of poor outcomes 5 years later.

“This is one of the first studies to connect the dots from injury to longer term outcomes and it shows that even mild concussions can lead to long-term impairment and continued decline in satisfaction with life,” said lead author Christine L. Mac Donald, PhD. “Most physicians believe that patients will stabilize 6 to 12 months postinjury, but this study challenges that.”

The researchers also found that, although 80% of service members with concussions had sought mental health treatment, only 19% reported that those programs were helpful. The findings advocate for new treatment strategies, the researchers say, to “combat the long-term and extremely costly effect” of these wartime injuries.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The AGA recently partnered with CommonBond (studentloans.gastro.org) to help its members save thousands by refinancing their student loans. Kevin Tin, MD, who is an AGA member, has a student loan story that can certainly offer guidance and perspective to others. Kevin earned his B.S. in health sciences from Stony Brook University and his M.D. from American University of Antigua. He completed his residency at Maimonides Medical Center in Brooklyn, N.Y., where he is currently a gastroenterology fellow.

How was your medical school experience?

My medical school experience was memorable for many reasons, particularly because I had an opportunity to study in Antigua. My time there allowed me to experience a different culture and, ultimately, a different perspective. I believe this taught me how to relate to each of my patients’ individual situations and to see things from their eyes. But, the overall cost of medical school (i.e., tuition, cost of living, medical supplies, and study resources) caught me off guard. By the time I graduated, I had amassed more than $200,000 in student loans; this was not something that I felt prepared to deal with.

How would you describe your initial experience with student loans?

BrianAJackson/Thinkstock

What strategies have you implemented to pay off your student loans?

I’ve learned a few crucial strategies that any physician could, and should, take advantage of to save money on their student loans. First, be sure to spend responsibly while in medical school. I focused on finding free study resources and medical supplies as well as sharing materials with friends and roommates whenever possible. As I mentioned earlier, make small payments when you can; as soon as I entered residency, I started making interest payments on my loans. I wanted to contribute as much as I could, as early as I could, to get out of debt. Second, after graduation, endeavor to live frugally. Although I knew my salary would ultimately increase, I saved as much money as I could and put money toward paying off my loans. Finally, try to refinance your student loans; I refinanced mine with CommonBond. It was an unexpectedly pleasant experience: the website was extremely easy to navigate and any time I needed help, a representative was available to answer my questions. CommonBond also gave me the best rates I could find.
 

What were the benefits of refinancing your student loans?

What is your advice to early-career GIs who have or need to take out loans?

Do your research and do it early. While in medical school, understand what options are available to you and learn to live within your means. In your residency, plan to use a portion of your salary for paying off your student loans, even if it is only a small amount each month. This will reduce the volume of interest that will capitalize, so your loan balance doesn’t grow over time. When you start your full-time job, be financially responsible and limit your spending so you can devote additional funds to paying off your student loans.

If you would like to learn more about student loan refinancing with CommonBond, please visit studentloans.gastro.org. AGA members get a $200 cash bonus for refinancing!
 

Ms. Duggal is vice president of marketing for CommonBond.

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

The correct answer is C: colonic ischemia.

AGA Institute

AGA Institute

References

1. Zuckerman G.R., et al. Am J Gastroenterol. 2003;98:2018-22.

2. Tanapanpanit O., Pongpirul K. BMJ Case Rep. 2015 Sept. 17;2015.

This article has an accompanying continuing medical education activity, also eligible for MOC credit (see gastrojournal.org for details). Learning Objective: Upon completion of this activity, successful learners will be able to recognize colon single-stripe sign as an endoscopic feature of colonic ischemia.
 

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.