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Diagnosis of a Rapidly Growing Preauricular Nodule: Chondroid Syringoma or Pleomorphic Adenoma?
To the Editor:
Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.1 It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,2 while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.
A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.2 Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.3,4
Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.5 Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.6 Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.5
Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO2 laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.2 One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow9; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.
Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.
- Hirsch P, Helwig EB. Chondroid syringoma. Arch Dermatol. 1961;84:835-847.
 - Turhan-Haktanir N, Sahin O, Bukulmez A, et al. Chondroid syringoma in a child. Pediatr Dermatol. 2007;24:505-507.
 - Mathiasen RA, Rasgon BM, Rumore G. Malignant chondroid syringoma of the face: a first reported case. Otolaryngol Head Neck Surg. 2005;133:305-307.
 - Barnett MD, Wallack MK, Zuretti A, et al. Recurrent malignant chondroid syringoma of the foot: a case report and review of the literature. Am J Clin Oncol. 2000;23:227-232.
 - Dubb M, Michelow P. Cytologic features of chondroid syringoma in fine needle aspiration biopsies a report of 3 cases. Acta Cytol. 2010;54:183-186.
 - Rauso R, Santagata M, Tartaro G, et al. Chondroid syringoma: rare tumor of orofacial region. Minerva Stomatol. 2009;58:383-388.
 - Metzler G, Schaumburg-Lever G, Hornstein O, et al. Malignant chondroid syringoma: immunohistopathology. Am J Dermatopathol. 1996;18:83-89.
 - Argenyi ZB, Balogh K, Goeken JA. Immunohistochemical characterization of chondroid syringomas. Am J Clin Pathol. 1988;90:662-669.
 - Walls AC, Deng A, Geist DE. Mohs micrographic surgery for recurrent chondroid syringoma of the eyebrow. Dermatol Surg. 2012;38:800-802.
 
To the Editor:
Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.1 It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,2 while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.
A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.2 Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.3,4
Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.5 Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.6 Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.5
Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO2 laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.2 One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow9; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.
Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.
To the Editor:
Chondroid syringoma is a rare benign mixed tumor that originates from the sweat glands, typically presenting with both epithelial and mesenchymal components.1 It differs from pleomorphic adenoma, which arises from salivary glands. The surgical approach for complete excision is different for the 2 tumors; therefore, definitive diagnosis is important. For chondroid syringoma, total excision is recommended,2 while for pleomorphic adenoma, extracapsular dissection or superficial parotidectomy is commonly indicated. We report a case of a preauricular nodule at presentation and highlight the importance of differentiating a chondroid syringoma from a pleomorphic adenoma. This case is unique because of the anatomic location of the nodule, making diagnosis difficult because the tumor was abutting the parotid gland and a biopsy included normal salivary gland cells.
A 19-year-old man with a history of moderate acne on the shoulders, back, and face presented with a rapidly growing, painless nodule on right preauricular region of 6 months’ duration. The nodule was originally thought to be acne related and monitored, as the patient was asymptomatic. On examination the patient was found to have a firm, fixed, nontender, subcutaneous nodule overlying the right temporomandibular joint just anterior to the right tragus (Figure 1). Laboratory results were unremarkable. Computed tomography showed a subcutaneous nonaggressive-appearing soft-tissue mass measuring 16×17×12 mm just anterior and inferior to the external auditory canal cartilaginous segment with no bony abnormalities. The patient was initially treated with incomplete excision of the area for a presumed sebaceous cyst; 2 months later, an abnormal biopsy prompted a complete excisional biopsy.

Histologically, the initial incomplete excision biopsy revealed myxoid and chondroid tissue with glandular elements and adjacent lymph node with strong positivity for S-100 protein and moderate positivity for glial fibrillary acid protein, consistent with chondroid syringoma (Figure 2). Histological findings on second excision biopsy performed 2 months later showed tumor cells surrounded by normal salivary gland cells; therefore, it was difficult to define the origin of this tumor. Subsequent magnetic resonance imaging showed no evidence of the tumor and normal parotid gland borders.

Chondroid syringoma is a rare nonmelanoma skin tumor of the head and neck, mostly benign in nature but with malignant potential. Predominantly, it presents in males as an asymptomatic, slow-growing, nontender nodule.2 Malignant chondroid syringomas are more rare, typically appear on the trunk and legs of females, and present as rapidly growing hard nodules. They can arise de novo or from a preexisting chondroid syringoma and can metastasize.3,4
Clinically and histologically, chondroid syringoma resembles a pleomorphic adenoma. Its diagnosis is dependent on the clinical location to exclude origin in a salivary gland.5 Folliculosebaceous and myoepithelial differentiation within the tumor has been reported.6 Immunocytochemistry is the same in both types and is used to identify 2 prominent components—epithelial and mesenchymal—found in both chondroid syringoma and pleomorphic adenoma. Immunocytochemistry differentiates the epithelial component, which expresses cytokeratin, epithelial membrane antigen, and carcinoembryonic antigen. In contrast, the mesenchymal component expresses S-100, vimentin, and neuron‐specific enolase, and less often glial fibrillary acidic protein, smooth muscle actin, calponin, or p63.5,7,8 Identification of both layers is a distinctive trait of both tumors, rendering it apart from other conditions in the differential diagnosis.5
Typical treatment options include excision, electrodesiccation, dermabrasion, and argon or CO2 laser. Total excision is recommended if there is a benign tumor and complete excision is a cure.2 One case of recurrent benign chondroid syringoma was treated by Mohs micrographic surgery on the eyebrow9; however, Mohs surgery was not recommended in our case due to concerns of spread if malignant as well as an unknown tumor depth, as these tumors have a tendency for deep infiltration.
Due to its anatomical location and presentation as an anterior preauricular mass, it was difficult to differentiate between chondroid syringoma from sweat gland origin and pleomorphic adenoma from the salivary gland. As seen in our case, it is important for physicians to be aware of the differential diagnosis for mixed tumors because it can have a notable effect on the type of surgical therapy and follow-up management.
- Hirsch P, Helwig EB. Chondroid syringoma. Arch Dermatol. 1961;84:835-847.
 - Turhan-Haktanir N, Sahin O, Bukulmez A, et al. Chondroid syringoma in a child. Pediatr Dermatol. 2007;24:505-507.
 - Mathiasen RA, Rasgon BM, Rumore G. Malignant chondroid syringoma of the face: a first reported case. Otolaryngol Head Neck Surg. 2005;133:305-307.
 - Barnett MD, Wallack MK, Zuretti A, et al. Recurrent malignant chondroid syringoma of the foot: a case report and review of the literature. Am J Clin Oncol. 2000;23:227-232.
 - Dubb M, Michelow P. Cytologic features of chondroid syringoma in fine needle aspiration biopsies a report of 3 cases. Acta Cytol. 2010;54:183-186.
 - Rauso R, Santagata M, Tartaro G, et al. Chondroid syringoma: rare tumor of orofacial region. Minerva Stomatol. 2009;58:383-388.
 - Metzler G, Schaumburg-Lever G, Hornstein O, et al. Malignant chondroid syringoma: immunohistopathology. Am J Dermatopathol. 1996;18:83-89.
 - Argenyi ZB, Balogh K, Goeken JA. Immunohistochemical characterization of chondroid syringomas. Am J Clin Pathol. 1988;90:662-669.
 - Walls AC, Deng A, Geist DE. Mohs micrographic surgery for recurrent chondroid syringoma of the eyebrow. Dermatol Surg. 2012;38:800-802.
 
- Hirsch P, Helwig EB. Chondroid syringoma. Arch Dermatol. 1961;84:835-847.
 - Turhan-Haktanir N, Sahin O, Bukulmez A, et al. Chondroid syringoma in a child. Pediatr Dermatol. 2007;24:505-507.
 - Mathiasen RA, Rasgon BM, Rumore G. Malignant chondroid syringoma of the face: a first reported case. Otolaryngol Head Neck Surg. 2005;133:305-307.
 - Barnett MD, Wallack MK, Zuretti A, et al. Recurrent malignant chondroid syringoma of the foot: a case report and review of the literature. Am J Clin Oncol. 2000;23:227-232.
 - Dubb M, Michelow P. Cytologic features of chondroid syringoma in fine needle aspiration biopsies a report of 3 cases. Acta Cytol. 2010;54:183-186.
 - Rauso R, Santagata M, Tartaro G, et al. Chondroid syringoma: rare tumor of orofacial region. Minerva Stomatol. 2009;58:383-388.
 - Metzler G, Schaumburg-Lever G, Hornstein O, et al. Malignant chondroid syringoma: immunohistopathology. Am J Dermatopathol. 1996;18:83-89.
 - Argenyi ZB, Balogh K, Goeken JA. Immunohistochemical characterization of chondroid syringomas. Am J Clin Pathol. 1988;90:662-669.
 - Walls AC, Deng A, Geist DE. Mohs micrographic surgery for recurrent chondroid syringoma of the eyebrow. Dermatol Surg. 2012;38:800-802.
 
Practice Points
- Clinically and histologically, pleomorphic adenomas and chondroid syringoma both have identical presentations. Differentiation can be determined by knowing where the mixed tumor originated.
 - Both lesions warrant different surgical management techniques. Pleomorphic adenoma requires extracapsular dissection or superficial parotidectomy, while complete excision is recommended for chondroid syringoma.
 
Diagnostic error most common claim against internists
The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.
Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.
The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.
In cases that involved injury, a top contributing factor was patient assessment issues, such as failure to establish a differential diagnosis or inadequate assessment. Patient factors, such as noncompliance, were also a primary contributer to injuries. The third most common factor for injury was poor communication among providers, family, and patients, such as inadequate education about the risks of medications.
The findings hopefully will assist internists and risk managers in understanding common allegations and factors behind lawsuits so that improvements can be made, study coauthor David B. Troxel, MD, medical director for The Doctors Company said in a statement.
“With the data on patient allegations and the actual factors that led to injuries included in this study, physicians and risk managers can identify system weaknesses and reduce risk of harm to patients,” he said.
“Physicians, internists, would benefit from something we’re doing in my group where we talk about why it is that there are cognitive errors,” he said. “Is there a system problem here, rather than someone who just made a mistake?”
Dr. Marcus advised physicians to read a recent report by the National Academies of Sciences, Engineering, and Medicine, which calls for more emphasis on identifying and learning from diagnostic errors and near misses in clinical practice, a payment and care delivery environment that supports the diagnostic process, and a dedicated focus on new research.
Ensuring that patients understand the treatment plan and follow-up care management are also key risk mitigation steps, adds Dr. Troxel.
“Patient compliance is a major problem,” he said in an interview. “It’s not that patients are not listening to the doctor. Sometimes they don’t understand what the doctor is explaining. We encourage physicians to really make sure the patient understands by asking them to repeat back what you’ve told them. Make sure they got the information.”
[email protected]
On Twitter @legal_med
The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.
Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.
The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.
In cases that involved injury, a top contributing factor was patient assessment issues, such as failure to establish a differential diagnosis or inadequate assessment. Patient factors, such as noncompliance, were also a primary contributer to injuries. The third most common factor for injury was poor communication among providers, family, and patients, such as inadequate education about the risks of medications.
The findings hopefully will assist internists and risk managers in understanding common allegations and factors behind lawsuits so that improvements can be made, study coauthor David B. Troxel, MD, medical director for The Doctors Company said in a statement.
“With the data on patient allegations and the actual factors that led to injuries included in this study, physicians and risk managers can identify system weaknesses and reduce risk of harm to patients,” he said.
“Physicians, internists, would benefit from something we’re doing in my group where we talk about why it is that there are cognitive errors,” he said. “Is there a system problem here, rather than someone who just made a mistake?”
Dr. Marcus advised physicians to read a recent report by the National Academies of Sciences, Engineering, and Medicine, which calls for more emphasis on identifying and learning from diagnostic errors and near misses in clinical practice, a payment and care delivery environment that supports the diagnostic process, and a dedicated focus on new research.
Ensuring that patients understand the treatment plan and follow-up care management are also key risk mitigation steps, adds Dr. Troxel.
“Patient compliance is a major problem,” he said in an interview. “It’s not that patients are not listening to the doctor. Sometimes they don’t understand what the doctor is explaining. We encourage physicians to really make sure the patient understands by asking them to repeat back what you’ve told them. Make sure they got the information.”
[email protected]
On Twitter @legal_med
The majority of lawsuits against internists stem from alleged diagnostics errors, results of a new study show.
Of 1,180 legal claims against internists, 39% were related to failed, delayed, or wrong diagnosis allegations, according to an analysis published by The Doctors Company, a nationwide medical malpractice insurer. Negligence associated with medical treatment accounted for 32% of the claims, while 19% were related to alleged medication errors.
The Doctors Company evaluated 1,180 claims from its database against internal medicine physicians that closed from 2007 to 2014. Of diagnostic-related cases, 56% alleged inadequate patient assessments, such as failure to order or delay in ordering diagnostic tests. The final diagnoses most commonly related to these allegations were myocardial infarction (6%), lung cancer (5%), and colorectal cancer (5%). More than 200 other diagnoses were seen in fewer than 2% of the claims, according to the study.
In cases that involved injury, a top contributing factor was patient assessment issues, such as failure to establish a differential diagnosis or inadequate assessment. Patient factors, such as noncompliance, were also a primary contributer to injuries. The third most common factor for injury was poor communication among providers, family, and patients, such as inadequate education about the risks of medications.
The findings hopefully will assist internists and risk managers in understanding common allegations and factors behind lawsuits so that improvements can be made, study coauthor David B. Troxel, MD, medical director for The Doctors Company said in a statement.
“With the data on patient allegations and the actual factors that led to injuries included in this study, physicians and risk managers can identify system weaknesses and reduce risk of harm to patients,” he said.
“Physicians, internists, would benefit from something we’re doing in my group where we talk about why it is that there are cognitive errors,” he said. “Is there a system problem here, rather than someone who just made a mistake?”
Dr. Marcus advised physicians to read a recent report by the National Academies of Sciences, Engineering, and Medicine, which calls for more emphasis on identifying and learning from diagnostic errors and near misses in clinical practice, a payment and care delivery environment that supports the diagnostic process, and a dedicated focus on new research.
Ensuring that patients understand the treatment plan and follow-up care management are also key risk mitigation steps, adds Dr. Troxel.
“Patient compliance is a major problem,” he said in an interview. “It’s not that patients are not listening to the doctor. Sometimes they don’t understand what the doctor is explaining. We encourage physicians to really make sure the patient understands by asking them to repeat back what you’ve told them. Make sure they got the information.”
[email protected]
On Twitter @legal_med
Four of five health care providers get flu shot
Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.
Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.
“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.
CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.
Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.
“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”
As a CDC employee, Dr. Black has no financial conflicts.
Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.
Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.
“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.
CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.
Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.
“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”
As a CDC employee, Dr. Black has no financial conflicts.
Influenza vaccine coverage among U.S. health care personnel increased very slightly during the 2015-2016 flu season, with 79% reporting that they received the shot, compared with 77% in 2014-2015.
Hospital personnel were most likely to be covered (91%) and long-term care personnel least likely to be covered (69%), Carla L. Black, PhD, wrote in the Sept. 30 issue of Morbidity and Mortality Weekly Report (2016;65:1026-31). Coverage among health care personnel working in long-term care settings did increase, however, from 64% in the 2014-2015 seasons to 69% in the 2015-2016 season, Dr. Black and colleagues noted.
“Although low, this is the only setting with an appreciable increase in coverage, compared with last season. Influenza vaccination among health care personnel in long-term care settings is especially important because influenza vaccine effectiveness is generally lowest in the elderly,” according to Dr Black, an epidemiologist with the Centers for Disease Control and Prevention.
CDC conducted the Internet survey of 2,258 health care workers from March to April, 2016.
Physicians had the highest level of coverage (95.6%), while health care assistants and aides had the lowest (64.5%). Employers also exerted an influence on coverage. Most respondents (73%) were vaccinated at work. Coverage was highest (96.5%) at facilities where vaccination was required and lowest (45%) where vaccination was not required, promoted, or offered on site.
“Employer vaccination requirements likely contributed to the observed gradual increase in vaccination among health care personnel working in settings with the lowest coverage,” the investigators noted. “In the absence of vaccination requirements, expanding the number of health care locations offering vaccination on site, over multiple days, and at no cost might help sustain and improve influenza vaccination coverage among health care personnel, including in long-term care settings.”
As a CDC employee, Dr. Black has no financial conflicts.
Key clinical point: 
Major finding: The flu vaccination rate was 79% among health care workers.
Data source: An Internet survey contained data on 2,258 people.
Disclosures: As a CDC employee, Dr. Black has no financial disclosures.
Many overweight Parkinson’s patients have insulin resistance
PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.
Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.
Of the 93 patients (71 men), with an average age of 66 years, 9 were diabetic. Of the 84 nondiabetic patients, 49 (58%) had an abnormal HOMA-IR index, ranging from 2.01 to 9.92, which is consistent with IR. Of the 84, 63 were overweight (body mass index [BMI] greater than 25 kg/m2), and 60.3% had IR. Among the 27 nondiabetic, obese patients (BMI greater than 30 kg/m2), 96% had IR. Only 19% of patients with normal BMI had IR. All the nondiabetic subjects with abnormal HOMA-IR who had values available (n = 22) had normal fasting glucose and glycated hemoglobin levels.
The vast majority of subjects with IR had normal fasting glucose and insulin levels. “They’re using too much insulin to control the amount of glucose that they have even though their glucose itself is not abnormal,” Dr. Hogg said. “The relevance of this could be that this may promote some of the degenerative processes that are inherent to Parkinson’s and, more importantly, could potentially offer a reversible target, because if you can identify patients who are insulin resistant, you could, through diet and exercise and lifestyle changes or medications, potentially reverse this and potentially change their path from heading to Parkinson’s or worsening Parkinson’s to something else. That would be the ultimate hope for this research.”
Although overweight is a well known risk factor for insulin resistance, it may be particularly relevant in Parkinson’s disease “because it seems to promote aspects of the disease that could impact not just the motor features of Parkinson’s but also the nonmotor features. We’re most concerned about cognition. ... one of the most feared complications of Parkinson’s and something that we have very little to offer for right now,” Dr. Hogg explained.
He said he plans to look at brain glucose metabolism in Parkinson’s patients without insulin resistance and compare it to similar patients with insulin resistance using PET scanning to see if “these brains are potentially starved of energy.” He cited a British study that showed that exenatide, a glucagonlike peptide-1 (GLP-1) agonist used in diabetes, improved cognition in a treated group. He plans to test liraglutide, another GLP-1 agonist, to see if it will improve or at least stabilize motor or nonmotor symptoms of Parkinson’s disease in insulin-resistant patients.
He suggested that physicians may want to look at insulin and not just measures of blood glucose in appropriate patients.
Jori Fleisher, MD, a movement disorders neurologist at New York University Langone Medical Center in New York, commented that the study indicates that there may be a cohort of patients who are seen routinely but have an undiagnosed risk factor. “Potentially, if we could address it and get their insulin resistance under control, perhaps with weight loss, then we might be able to potentially affect the progression of the Parkinson’s disease,” she said.
As for a mechanism of the effect, she said it is known that there is a “huge role of oxidative stress and apoptosis in the progression of Parkinson’s disease,” and insulin resistance may contribute to it.
She said she would like to see the study replicated in a much larger cohort before routinely adopting insulin measures in clinical practice. If the findings are sufficiently validated, “this is something that seems fairly easy and innocuous to test for.”
Richard Smeyne, PhD, director of the Jefferson Comprehensive Parkinson’s Center at Thomas Jefferson University in Philadelphia, speculated that insulin may also have functions in the brain aside from its metabolic effects, specifically, promoting or maintaining neurons through neurotropic effects mediated through the insulinlike growth factor-1 receptors. Still, he cautioned that he would be “hesitant to look at insulin resistance peripherally and make some sort of comment about its relationship to Parkinson’s disease.”
The study was investigator initiated and had no commercial support. Dr. Hogg, Dr. Fleisher, and Dr. Smeyne reported having no financial disclosures.
PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.
Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.
Of the 93 patients (71 men), with an average age of 66 years, 9 were diabetic. Of the 84 nondiabetic patients, 49 (58%) had an abnormal HOMA-IR index, ranging from 2.01 to 9.92, which is consistent with IR. Of the 84, 63 were overweight (body mass index [BMI] greater than 25 kg/m2), and 60.3% had IR. Among the 27 nondiabetic, obese patients (BMI greater than 30 kg/m2), 96% had IR. Only 19% of patients with normal BMI had IR. All the nondiabetic subjects with abnormal HOMA-IR who had values available (n = 22) had normal fasting glucose and glycated hemoglobin levels.
The vast majority of subjects with IR had normal fasting glucose and insulin levels. “They’re using too much insulin to control the amount of glucose that they have even though their glucose itself is not abnormal,” Dr. Hogg said. “The relevance of this could be that this may promote some of the degenerative processes that are inherent to Parkinson’s and, more importantly, could potentially offer a reversible target, because if you can identify patients who are insulin resistant, you could, through diet and exercise and lifestyle changes or medications, potentially reverse this and potentially change their path from heading to Parkinson’s or worsening Parkinson’s to something else. That would be the ultimate hope for this research.”
Although overweight is a well known risk factor for insulin resistance, it may be particularly relevant in Parkinson’s disease “because it seems to promote aspects of the disease that could impact not just the motor features of Parkinson’s but also the nonmotor features. We’re most concerned about cognition. ... one of the most feared complications of Parkinson’s and something that we have very little to offer for right now,” Dr. Hogg explained.
He said he plans to look at brain glucose metabolism in Parkinson’s patients without insulin resistance and compare it to similar patients with insulin resistance using PET scanning to see if “these brains are potentially starved of energy.” He cited a British study that showed that exenatide, a glucagonlike peptide-1 (GLP-1) agonist used in diabetes, improved cognition in a treated group. He plans to test liraglutide, another GLP-1 agonist, to see if it will improve or at least stabilize motor or nonmotor symptoms of Parkinson’s disease in insulin-resistant patients.
He suggested that physicians may want to look at insulin and not just measures of blood glucose in appropriate patients.
Jori Fleisher, MD, a movement disorders neurologist at New York University Langone Medical Center in New York, commented that the study indicates that there may be a cohort of patients who are seen routinely but have an undiagnosed risk factor. “Potentially, if we could address it and get their insulin resistance under control, perhaps with weight loss, then we might be able to potentially affect the progression of the Parkinson’s disease,” she said.
As for a mechanism of the effect, she said it is known that there is a “huge role of oxidative stress and apoptosis in the progression of Parkinson’s disease,” and insulin resistance may contribute to it.
She said she would like to see the study replicated in a much larger cohort before routinely adopting insulin measures in clinical practice. If the findings are sufficiently validated, “this is something that seems fairly easy and innocuous to test for.”
Richard Smeyne, PhD, director of the Jefferson Comprehensive Parkinson’s Center at Thomas Jefferson University in Philadelphia, speculated that insulin may also have functions in the brain aside from its metabolic effects, specifically, promoting or maintaining neurons through neurotropic effects mediated through the insulinlike growth factor-1 receptors. Still, he cautioned that he would be “hesitant to look at insulin resistance peripherally and make some sort of comment about its relationship to Parkinson’s disease.”
The study was investigator initiated and had no commercial support. Dr. Hogg, Dr. Fleisher, and Dr. Smeyne reported having no financial disclosures.
PORTLAND, ORE. – More than half of overweight, nondiabetic people with Parkinson’s disease were insulin resistant even though most had normal fasting glucose and insulin levels in a prospective, observational study, raising concerns about the potential role of insulin resistance in accelerating the progression of neurodegenerative diseases, including certain features of Parkinson’s disease.
Researchers at Cedars-Sinai Medical Center in Los Angeles tested 93 patients with Parkinson’s disease to determine the prevalence of undiagnosed insulin resistance (IR). They used the homeostatic model assessment of insulin resistance (HOMA-IR) formula, with a HOMA-IR index of 2.0 as a cut-off for abnormal insulin sensitivity. The index is a measure of how much insulin is needed to control blood sugar and uses just blood fasting insulin and glucose levels for the calculation.
Of the 93 patients (71 men), with an average age of 66 years, 9 were diabetic. Of the 84 nondiabetic patients, 49 (58%) had an abnormal HOMA-IR index, ranging from 2.01 to 9.92, which is consistent with IR. Of the 84, 63 were overweight (body mass index [BMI] greater than 25 kg/m2), and 60.3% had IR. Among the 27 nondiabetic, obese patients (BMI greater than 30 kg/m2), 96% had IR. Only 19% of patients with normal BMI had IR. All the nondiabetic subjects with abnormal HOMA-IR who had values available (n = 22) had normal fasting glucose and glycated hemoglobin levels.
The vast majority of subjects with IR had normal fasting glucose and insulin levels. “They’re using too much insulin to control the amount of glucose that they have even though their glucose itself is not abnormal,” Dr. Hogg said. “The relevance of this could be that this may promote some of the degenerative processes that are inherent to Parkinson’s and, more importantly, could potentially offer a reversible target, because if you can identify patients who are insulin resistant, you could, through diet and exercise and lifestyle changes or medications, potentially reverse this and potentially change their path from heading to Parkinson’s or worsening Parkinson’s to something else. That would be the ultimate hope for this research.”
Although overweight is a well known risk factor for insulin resistance, it may be particularly relevant in Parkinson’s disease “because it seems to promote aspects of the disease that could impact not just the motor features of Parkinson’s but also the nonmotor features. We’re most concerned about cognition. ... one of the most feared complications of Parkinson’s and something that we have very little to offer for right now,” Dr. Hogg explained.
He said he plans to look at brain glucose metabolism in Parkinson’s patients without insulin resistance and compare it to similar patients with insulin resistance using PET scanning to see if “these brains are potentially starved of energy.” He cited a British study that showed that exenatide, a glucagonlike peptide-1 (GLP-1) agonist used in diabetes, improved cognition in a treated group. He plans to test liraglutide, another GLP-1 agonist, to see if it will improve or at least stabilize motor or nonmotor symptoms of Parkinson’s disease in insulin-resistant patients.
He suggested that physicians may want to look at insulin and not just measures of blood glucose in appropriate patients.
Jori Fleisher, MD, a movement disorders neurologist at New York University Langone Medical Center in New York, commented that the study indicates that there may be a cohort of patients who are seen routinely but have an undiagnosed risk factor. “Potentially, if we could address it and get their insulin resistance under control, perhaps with weight loss, then we might be able to potentially affect the progression of the Parkinson’s disease,” she said.
As for a mechanism of the effect, she said it is known that there is a “huge role of oxidative stress and apoptosis in the progression of Parkinson’s disease,” and insulin resistance may contribute to it.
She said she would like to see the study replicated in a much larger cohort before routinely adopting insulin measures in clinical practice. If the findings are sufficiently validated, “this is something that seems fairly easy and innocuous to test for.”
Richard Smeyne, PhD, director of the Jefferson Comprehensive Parkinson’s Center at Thomas Jefferson University in Philadelphia, speculated that insulin may also have functions in the brain aside from its metabolic effects, specifically, promoting or maintaining neurons through neurotropic effects mediated through the insulinlike growth factor-1 receptors. Still, he cautioned that he would be “hesitant to look at insulin resistance peripherally and make some sort of comment about its relationship to Parkinson’s disease.”
The study was investigator initiated and had no commercial support. Dr. Hogg, Dr. Fleisher, and Dr. Smeyne reported having no financial disclosures.
AT WPC 2016
Key clinical point: 
Major finding: Among 84 nondiabetic, Parkinson’s patients, 58% had insulin resistance, although their blood glucose and insulin levels were not abnormal.
Data source: Prospective, observational study of a total of 93 Parkinson’s patients.
Disclosures: The study was investigator initiated and had no commercial support. Dr. Hogg, Dr. Fleisher, and Dr. Smeyne reported having no financial disclosures.
Paulo Fontoura, MD, PhD
Biomarkers predict Parkinson’s among high-risk individuals
PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.
These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.
The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.
Four individuals out of the 22 reached the primary endpoint, which was a diagnosis of PD by a neurologist unaware of the biomarker data. Two of the four individuals with PD also had Lewy body dementia.
“All of the people who went on to convert [to PD], all of them, had at least three of those biomarkers positive. And among the 18 who so far haven’t developed Parkinson’s, none of them had three or more biomarkers. Most of them had none,” said Dr. Goldstein, director of the clinical neurocardiology section at the NINDS. He presented this first look at the PDRisk Study outcome data at the World Parkinson Congress.
Among 10 healthy control subjects without any risk factors for PD, 1 had two positive biomarkers, and the rest had none. Individuals who converted to PD could be distinguished from those who did not by low values for the posterior/anterior ratio of putamen 18F-DOPA–derived radioactivity, CSF DOPA, CSF 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine), and septal myocardial 18F-dopamine-derived radioactivity. Almost 20 years ago, Dr. Goldstein found that there is a substantial loss of sympathetic noradrenergic nerves in the heart in PD.
He has weighted all the biomarkers as if they had equal contributions, which “is not fair,” he said. All four biomarkers were predictive on their own, but some were more potent than others, notably the ratio of DOPA in the anterior to posterior putamen and low values for DOPA in the CSF. He noted that this finding is the first time CSF DOPA has been documented as a biomarker for the development of PD.
The question remains about what to do with these predictors of PD if they are validated. Dr. Goldstein said they could be used to track the efficacy of any intervention to slow the decline to PD.
The study was run by the NINDS and had no outside support. Dr. Goldstein is a U.S. government employee and reported having no financial disclosures.
 
PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.
These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.
The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.
Four individuals out of the 22 reached the primary endpoint, which was a diagnosis of PD by a neurologist unaware of the biomarker data. Two of the four individuals with PD also had Lewy body dementia.
“All of the people who went on to convert [to PD], all of them, had at least three of those biomarkers positive. And among the 18 who so far haven’t developed Parkinson’s, none of them had three or more biomarkers. Most of them had none,” said Dr. Goldstein, director of the clinical neurocardiology section at the NINDS. He presented this first look at the PDRisk Study outcome data at the World Parkinson Congress.
Among 10 healthy control subjects without any risk factors for PD, 1 had two positive biomarkers, and the rest had none. Individuals who converted to PD could be distinguished from those who did not by low values for the posterior/anterior ratio of putamen 18F-DOPA–derived radioactivity, CSF DOPA, CSF 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine), and septal myocardial 18F-dopamine-derived radioactivity. Almost 20 years ago, Dr. Goldstein found that there is a substantial loss of sympathetic noradrenergic nerves in the heart in PD.
He has weighted all the biomarkers as if they had equal contributions, which “is not fair,” he said. All four biomarkers were predictive on their own, but some were more potent than others, notably the ratio of DOPA in the anterior to posterior putamen and low values for DOPA in the CSF. He noted that this finding is the first time CSF DOPA has been documented as a biomarker for the development of PD.
The question remains about what to do with these predictors of PD if they are validated. Dr. Goldstein said they could be used to track the efficacy of any intervention to slow the decline to PD.
The study was run by the NINDS and had no outside support. Dr. Goldstein is a U.S. government employee and reported having no financial disclosures.
 
PORTLAND, ORE. – The presence of at least three out of four chemical biomarkers can predict the development of Parkinson’s disease at 3 years of follow-up in people with multiple risk factors for the disease, according to David Goldstein, MD.
These biomarkers, found in the cerebrospinal fluid and in the heart, represent catecholaminergic neurodegeneration.
The PDRisk study of the National Institute of Neurological Disorders and Stroke (NINDS) is investigating whether individuals with at least three out of four statistical risk factors for Parkinson’s disease (PD) develop the disease, based on chemical biomarkers of neurodegeneration. The risk factors are family history of the disease, olfactory dysfunction, dream enactment behavior, and orthostatic hypotension. The biomarkers are PET neuroimaging or cerebrospinal fluid (CSF) neurochemical indicators of catecholamine deficiency in the brain or heart. All the biomarkers are related to dopamine, its precursor, or its metabolites.
Four individuals out of the 22 reached the primary endpoint, which was a diagnosis of PD by a neurologist unaware of the biomarker data. Two of the four individuals with PD also had Lewy body dementia.
“All of the people who went on to convert [to PD], all of them, had at least three of those biomarkers positive. And among the 18 who so far haven’t developed Parkinson’s, none of them had three or more biomarkers. Most of them had none,” said Dr. Goldstein, director of the clinical neurocardiology section at the NINDS. He presented this first look at the PDRisk Study outcome data at the World Parkinson Congress.
Among 10 healthy control subjects without any risk factors for PD, 1 had two positive biomarkers, and the rest had none. Individuals who converted to PD could be distinguished from those who did not by low values for the posterior/anterior ratio of putamen 18F-DOPA–derived radioactivity, CSF DOPA, CSF 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine), and septal myocardial 18F-dopamine-derived radioactivity. Almost 20 years ago, Dr. Goldstein found that there is a substantial loss of sympathetic noradrenergic nerves in the heart in PD.
He has weighted all the biomarkers as if they had equal contributions, which “is not fair,” he said. All four biomarkers were predictive on their own, but some were more potent than others, notably the ratio of DOPA in the anterior to posterior putamen and low values for DOPA in the CSF. He noted that this finding is the first time CSF DOPA has been documented as a biomarker for the development of PD.
The question remains about what to do with these predictors of PD if they are validated. Dr. Goldstein said they could be used to track the efficacy of any intervention to slow the decline to PD.
The study was run by the NINDS and had no outside support. Dr. Goldstein is a U.S. government employee and reported having no financial disclosures.
 
AT WPC 2016
Key clinical point: 
Major finding: Among 22 individuals followed for at least 3 years, biomarkers were 100% positively or negatively predictive of developing Parkinson’s disease.
Data source: A prospective cohort study of 3,176 individuals supplying risk factor data, of whom 31 had three or more risk factors and biomarkers testing, and of whom 22 were followed for at least 3 years.
Disclosures: The study was run by the National Institute of Neurological Disorders and Stroke and had no outside support. Dr. Goldstein is a U.S. government employee and reported having no financial disclosures.
Steroids could reduce death rate for TB patients with acute respiratory failure
Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.
An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan. 
Mortality rates were similar between the steroid-treated and non–steroid-treated groups (48.6% and 50%, respectively), and unadjusted 90-day mortality risk was not affected by steroid administration (odds ratio, 0.94; 95% CI, 0.46-1.92; P = .875), reported Dr. Yang and colleagues (Clin Infect Dis. 2016 Sep 8. doi: 10.1093/cid/ciw616).
The study involved the examination of records of 124 patients (mean age 62, 64% men) admitted to a single center over a 25-year period ending in 2014. Of these, 56.5% received corticosteroids, and 49.2% of the cohort died within 90 days.
The investigators acknowledged that their study was limited by various factors, including its small size, its use of data from a single center, and its lack of a standardized approach to steroid treatment.
“Further prospective randomized controlled trials will therefore be necessary to clarify the role of steroids in the management of these patients,” they wrote in their analysis. However, Dr. Yang and colleagues argued, in acute respiratory failure – a rare but dangerous complication in TB – “corticosteroids represent an attractive option because they can suppress cytokine expression and are effective in managing the inflammatory complications of extrapulmonary tuberculosis. Moreover, corticosteroids have been recently been shown to reduce mortality or treatment failure in patients with tuberculosis or severe pneumonia.”
Robert C. Hyzy, MD, director of the critical care medicine unit at the University of Michigan, Ann Arbor, said the findings “should be considered hypothesis generating.
“Clinicians should wait for prospective validation of this observation before considering the use of corticosteroids in hospitalized patients with tuberculosis,” he added.
Dr. Yang and colleagues disclosed no conflicts of interest or outside funding for their study.
Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.
An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan. 
Mortality rates were similar between the steroid-treated and non–steroid-treated groups (48.6% and 50%, respectively), and unadjusted 90-day mortality risk was not affected by steroid administration (odds ratio, 0.94; 95% CI, 0.46-1.92; P = .875), reported Dr. Yang and colleagues (Clin Infect Dis. 2016 Sep 8. doi: 10.1093/cid/ciw616).
The study involved the examination of records of 124 patients (mean age 62, 64% men) admitted to a single center over a 25-year period ending in 2014. Of these, 56.5% received corticosteroids, and 49.2% of the cohort died within 90 days.
The investigators acknowledged that their study was limited by various factors, including its small size, its use of data from a single center, and its lack of a standardized approach to steroid treatment.
“Further prospective randomized controlled trials will therefore be necessary to clarify the role of steroids in the management of these patients,” they wrote in their analysis. However, Dr. Yang and colleagues argued, in acute respiratory failure – a rare but dangerous complication in TB – “corticosteroids represent an attractive option because they can suppress cytokine expression and are effective in managing the inflammatory complications of extrapulmonary tuberculosis. Moreover, corticosteroids have been recently been shown to reduce mortality or treatment failure in patients with tuberculosis or severe pneumonia.”
Robert C. Hyzy, MD, director of the critical care medicine unit at the University of Michigan, Ann Arbor, said the findings “should be considered hypothesis generating.
“Clinicians should wait for prospective validation of this observation before considering the use of corticosteroids in hospitalized patients with tuberculosis,” he added.
Dr. Yang and colleagues disclosed no conflicts of interest or outside funding for their study.
Tuberculosis patients admitted to intensive care units with acute respiratory failure had significantly better survival at 90 days after treatment with corticosteroids and anti-TB drugs, compared with patients not treated with the steroids, according to a retrospective study.
An adjusted inverse probability of treatment weighted analysis using propensity scores revealed corticosteroid use to be independently associated with a significantly reduced 90-day mortality rate (OR = 0.47; 95% CI, 0.22-0.98). This statistical approach was used because it reduces selection bias and other potential confounding factors in a way that a multivariate analysis cannot, wrote Ji Young Yang, MD, of Busan (South Korea) Paik Hospital and Inje University College of Medicine in Busan. 
Mortality rates were similar between the steroid-treated and non–steroid-treated groups (48.6% and 50%, respectively), and unadjusted 90-day mortality risk was not affected by steroid administration (odds ratio, 0.94; 95% CI, 0.46-1.92; P = .875), reported Dr. Yang and colleagues (Clin Infect Dis. 2016 Sep 8. doi: 10.1093/cid/ciw616).
The study involved the examination of records of 124 patients (mean age 62, 64% men) admitted to a single center over a 25-year period ending in 2014. Of these, 56.5% received corticosteroids, and 49.2% of the cohort died within 90 days.
The investigators acknowledged that their study was limited by various factors, including its small size, its use of data from a single center, and its lack of a standardized approach to steroid treatment.
“Further prospective randomized controlled trials will therefore be necessary to clarify the role of steroids in the management of these patients,” they wrote in their analysis. However, Dr. Yang and colleagues argued, in acute respiratory failure – a rare but dangerous complication in TB – “corticosteroids represent an attractive option because they can suppress cytokine expression and are effective in managing the inflammatory complications of extrapulmonary tuberculosis. Moreover, corticosteroids have been recently been shown to reduce mortality or treatment failure in patients with tuberculosis or severe pneumonia.”
Robert C. Hyzy, MD, director of the critical care medicine unit at the University of Michigan, Ann Arbor, said the findings “should be considered hypothesis generating.
“Clinicians should wait for prospective validation of this observation before considering the use of corticosteroids in hospitalized patients with tuberculosis,” he added.
Dr. Yang and colleagues disclosed no conflicts of interest or outside funding for their study.
Key clinical point: Corticosteroids used in combination with anti-TB treatment appeared to lower 90-day mortality in TB patients with ARF.
Major finding: Reduced 90-day mortality was associated with corticosteroid use (odds ratio, 0.47; 95% CI, 0.22-0.98; P = .049).
Data source: A retrospective cohort study of 124 patients admitted to intensive care units with TB and ARF in a single Korean center from 1989 to 2014.
Disclosures: The investigators reported no outside funding or conflicts of interest.
Midterm results of thoracic stenting for acute type B dissection promising
LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.
Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.
One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).
Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.
Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.
The primary safety endpoint was all-cause mortality within 30 days from the index procedure.
A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.
At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.
One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.
Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.
The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.
LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.
Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.
One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).
Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.
Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.
The primary safety endpoint was all-cause mortality within 30 days from the index procedure.
A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.
At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.
One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.
Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.
The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.
LAS VEGAS – Patients with acute, complicated type B aortic dissections are reported to have a greater than 50% likelihood of dying from their condition. Three-year results of the Valiant thoracic stent graft in the treatment of these dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%, according to Ali Azizzadeh, MD.
Dr. Azizzadeh presented the midterm results of the Medtronic Dissection US IDE trial of endovascular treatment with the Valiant Captivia thoracic stent graft (Medtronic) in acute, complicated type B aortic dissection patients at the 2016 Vascular Interventional Advances meeting.
One-year outcomes of the trial were reported last year in the Annals of Thoracic Surgery (2015 Sep;100:802-9).
Dr. Azizzadeh is a vascular surgeon at the Memorial Hermann Heart and Vascular Institute, Houston.
Between June 2010 and May 2012, 50 patients with acute, complicated type B aortic dissection were enrolled at 16 clinical sites in the United States in this multicenter, prospective, nonrandomized trial with a planned 5-year follow-up.
The primary safety endpoint was all-cause mortality within 30 days from the index procedure.
A total of 28 patients completed their 3-year follow-up. Through 3 years, there were no postindex ruptures or conversions to open surgical repair reported in the trial.
At 3 years, true lumen diameter over the stented region (or endograft segment) remained stable or increased in 92.3% of patients, according to Dr. Azizzadeh. False lumen diameter remained stable or decreased in 69.3% of patients, and the false lumen was partially or completely thrombosed in 75% of patients.
One death (from sepsis) occurred between years 2 and 3; and was adjudicated by the clinical events committee as unrelated to the device, the procedure, or the dissection.
Although these midterm results are encouraging, said Dr. Azizzadeh, longer-term outcomes are needed to assess the durability of the stent graft in this indication.
The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.
AT VIVA16 LAS VEGAS
Key clinical point: 
Major finding: Three-year results of the Valiant thoracic stent graft in the treatment of acute type B dissections showed freedom from all-cause mortality of 79.4%, and a freedom from dissection-related mortality of 90%.
Data source: Midterm results were presented from the multicenter, prospective, nonrandomized Medtronic Dissection US IDE trial.
Disclosures: The trial was sponsored by Medtronic. Dr. Azizzadeh has consulted for and received research/trial funding from W.L. Gore & Associates and Medtronic.
VIDEO: Is your patient clinically depressed, or is there something else?
Is your 42-year-old patient with well-controlled hypertension and type 2 diabetes dealing with a mood disorder that should be regarded as a psychiatric illness – or is she experiencing demoralization and grief?
In this installment of Mental Health Consult, the patient screens positive for depression but is ambivalent about taking antidepressants. In addition, the patient believes she has a number of coping resources that she can utilize. Finding out whether there is a need for an evidence-based psychotherapy, medication, or if other interventions are appropriate requires four key questions when taking a history.
Our expert panel from George Washington University, Washington, includes James L. Griffith, MD, chair of psychiatry and behavioral sciences; April Barbour, MD, MPH, director of the division of general internal medicine; and Lorenzo Norris, MD, medical director of psychiatric and behavioral services.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
[email protected]
On Twitter @whitneymcknight
Is your 42-year-old patient with well-controlled hypertension and type 2 diabetes dealing with a mood disorder that should be regarded as a psychiatric illness – or is she experiencing demoralization and grief?
In this installment of Mental Health Consult, the patient screens positive for depression but is ambivalent about taking antidepressants. In addition, the patient believes she has a number of coping resources that she can utilize. Finding out whether there is a need for an evidence-based psychotherapy, medication, or if other interventions are appropriate requires four key questions when taking a history.
Our expert panel from George Washington University, Washington, includes James L. Griffith, MD, chair of psychiatry and behavioral sciences; April Barbour, MD, MPH, director of the division of general internal medicine; and Lorenzo Norris, MD, medical director of psychiatric and behavioral services.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
[email protected]
On Twitter @whitneymcknight
Is your 42-year-old patient with well-controlled hypertension and type 2 diabetes dealing with a mood disorder that should be regarded as a psychiatric illness – or is she experiencing demoralization and grief?
In this installment of Mental Health Consult, the patient screens positive for depression but is ambivalent about taking antidepressants. In addition, the patient believes she has a number of coping resources that she can utilize. Finding out whether there is a need for an evidence-based psychotherapy, medication, or if other interventions are appropriate requires four key questions when taking a history.
Our expert panel from George Washington University, Washington, includes James L. Griffith, MD, chair of psychiatry and behavioral sciences; April Barbour, MD, MPH, director of the division of general internal medicine; and Lorenzo Norris, MD, medical director of psychiatric and behavioral services.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
[email protected]
On Twitter @whitneymcknight






