B-cell lymphoma

A class of drugs targeting a protein found in the endoplasmic reticulum could be effective against B-cell malignancies, according to a study published in Cancer Research.

The protein, STING, plays a critical role in producing type I interferons that help regulate the immune system.

Previous research suggested that STING agonists can improve immune responses when used in cancer immunotherapy or as vaccine adjuvants.

However, the way B cells respond to STING agonists was not well understood.

Chih-Chi Andrew Hu, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues conducted a study to gain some insight.

The researchers found that normal B cells respond to STING agonists by undergoing mitochondria-mediated apoptosis, and STING agonists induce apoptosis in

malignant B cells through binding to STING.

STING agonists proved cytotoxic to B-cell leukemia, lymphoma, and multiple myeloma in vitro. But the drugs did not induce apoptosis in solid tumor malignancies or normal T cells.

The research also revealed that the IRE-1/XBP-1 stress response pathway is required for normal STING function. And B-cell leukemia, lymphoma, and myeloma require the IRE-1/XBP-1 pathway to be activated for survival.

Stimulation by STING agonists suppressed the IRE-1/XBP-1 pathway, which increased the level of apoptosis in malignant B cells.

The researchers confirmed these results in animal models, as treatment with STING agonists led to regression of chronic lymphocytic leukemia and multiple myeloma in mice.

“This specific cytotoxicity toward B cells strongly supports the use of STING agonists in the treatment of B-cell hematologic malignancies,” said Chih-Hang Anthony Tang, MD, PhD, of The Wistar Institute.

“We also believe that cytotoxicity in normal B cells can be managed with the administration of intravenous immunoglobulin that can help maintain normal levels of antibodies while treatment is being administered. This is something we plan on studying further.”

The Wistar Institute’s business development team is looking for a development partner for the advancement of novel STING agonists in treating B-cell hematologic malignancies.

B-cell lymphoma

A class of drugs targeting a protein found in the endoplasmic reticulum could be effective against B-cell malignancies, according to a study published in Cancer Research.

The protein, STING, plays a critical role in producing type I interferons that help regulate the immune system.

Previous research suggested that STING agonists can improve immune responses when used in cancer immunotherapy or as vaccine adjuvants.

However, the way B cells respond to STING agonists was not well understood.

Chih-Chi Andrew Hu, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues conducted a study to gain some insight.

The researchers found that normal B cells respond to STING agonists by undergoing mitochondria-mediated apoptosis, and STING agonists induce apoptosis in

malignant B cells through binding to STING.

STING agonists proved cytotoxic to B-cell leukemia, lymphoma, and multiple myeloma in vitro. But the drugs did not induce apoptosis in solid tumor malignancies or normal T cells.

The research also revealed that the IRE-1/XBP-1 stress response pathway is required for normal STING function. And B-cell leukemia, lymphoma, and myeloma require the IRE-1/XBP-1 pathway to be activated for survival.

Stimulation by STING agonists suppressed the IRE-1/XBP-1 pathway, which increased the level of apoptosis in malignant B cells.

The researchers confirmed these results in animal models, as treatment with STING agonists led to regression of chronic lymphocytic leukemia and multiple myeloma in mice.

“This specific cytotoxicity toward B cells strongly supports the use of STING agonists in the treatment of B-cell hematologic malignancies,” said Chih-Hang Anthony Tang, MD, PhD, of The Wistar Institute.

“We also believe that cytotoxicity in normal B cells can be managed with the administration of intravenous immunoglobulin that can help maintain normal levels of antibodies while treatment is being administered. This is something we plan on studying further.”

The Wistar Institute’s business development team is looking for a development partner for the advancement of novel STING agonists in treating B-cell hematologic malignancies.

B-cell lymphoma

A class of drugs targeting a protein found in the endoplasmic reticulum could be effective against B-cell malignancies, according to a study published in Cancer Research.

The protein, STING, plays a critical role in producing type I interferons that help regulate the immune system.

Previous research suggested that STING agonists can improve immune responses when used in cancer immunotherapy or as vaccine adjuvants.

However, the way B cells respond to STING agonists was not well understood.

Chih-Chi Andrew Hu, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues conducted a study to gain some insight.

The researchers found that normal B cells respond to STING agonists by undergoing mitochondria-mediated apoptosis, and STING agonists induce apoptosis in

malignant B cells through binding to STING.

STING agonists proved cytotoxic to B-cell leukemia, lymphoma, and multiple myeloma in vitro. But the drugs did not induce apoptosis in solid tumor malignancies or normal T cells.

The research also revealed that the IRE-1/XBP-1 stress response pathway is required for normal STING function. And B-cell leukemia, lymphoma, and myeloma require the IRE-1/XBP-1 pathway to be activated for survival.

Stimulation by STING agonists suppressed the IRE-1/XBP-1 pathway, which increased the level of apoptosis in malignant B cells.

The researchers confirmed these results in animal models, as treatment with STING agonists led to regression of chronic lymphocytic leukemia and multiple myeloma in mice.

“This specific cytotoxicity toward B cells strongly supports the use of STING agonists in the treatment of B-cell hematologic malignancies,” said Chih-Hang Anthony Tang, MD, PhD, of The Wistar Institute.

“We also believe that cytotoxicity in normal B cells can be managed with the administration of intravenous immunoglobulin that can help maintain normal levels of antibodies while treatment is being administered. This is something we plan on studying further.”

The Wistar Institute’s business development team is looking for a development partner for the advancement of novel STING agonists in treating B-cell hematologic malignancies.

There were four states at the highest level of influenza-like illness (ILI) activity for the week, more than any other week of the 2015-2016 flu season, according to the Centers for Disease Control and Prevention.

Arizona, Kentucky, New Jersey, and New Mexico, along with Puerto Rico, were all at level 10 on the CDC’s 1-10 scale of ILI activity for the week ending March 5, 2016. Other states in the “high” range were Arkansas, Illinois, Nevada, and North Carolina at level 9 and Alabama and Mississippi at level 8, the CDC reported.

The proportion of outpatient visits for ILI was 3.5% for the week, the highest of the season so far and well above the national baseline of 2.1%. In addition to the 10 states and Puerto Rico with ILI levels in the high range, there were 13 states in the “moderate” range (6 or 7 on the 1-10 scale) and 12 states in the “low” range (4 or 5), with a total of 44 states at level 2 or higher, data from the CDC’s Outpatient Influenza-like Illness Surveillance Network (ILINet) show.

Two flu-related pediatric deaths were reported during week 21 of the flu season, although both occurred earlier: one during the week ending Feb. 13 and one during the week ending Feb. 27. There have been a total of 20 pediatric deaths reported for the 2015-2016 season, with Florida (four deaths), California, (three), Arizona (two), and Nevada (two) the only states reporting more than one, the CDC report noted.

The continued rise in ILI activity is somewhat unusual. The only season out of the previous 10 with a peak later than the current one was 2011-2012, which peaked at only 2.4% on the week ending March 17, 2012. The earliest of the bunch came during the 2009-2010 season, which peaked at 7.7% during the week ending Oct. 24, 2009, according to ILINet data.

rfranki@frontlinemedcom.com

There were four states at the highest level of influenza-like illness (ILI) activity for the week, more than any other week of the 2015-2016 flu season, according to the Centers for Disease Control and Prevention.

Arizona, Kentucky, New Jersey, and New Mexico, along with Puerto Rico, were all at level 10 on the CDC’s 1-10 scale of ILI activity for the week ending March 5, 2016. Other states in the “high” range were Arkansas, Illinois, Nevada, and North Carolina at level 9 and Alabama and Mississippi at level 8, the CDC reported.

The proportion of outpatient visits for ILI was 3.5% for the week, the highest of the season so far and well above the national baseline of 2.1%. In addition to the 10 states and Puerto Rico with ILI levels in the high range, there were 13 states in the “moderate” range (6 or 7 on the 1-10 scale) and 12 states in the “low” range (4 or 5), with a total of 44 states at level 2 or higher, data from the CDC’s Outpatient Influenza-like Illness Surveillance Network (ILINet) show.

Two flu-related pediatric deaths were reported during week 21 of the flu season, although both occurred earlier: one during the week ending Feb. 13 and one during the week ending Feb. 27. There have been a total of 20 pediatric deaths reported for the 2015-2016 season, with Florida (four deaths), California, (three), Arizona (two), and Nevada (two) the only states reporting more than one, the CDC report noted.

The continued rise in ILI activity is somewhat unusual. The only season out of the previous 10 with a peak later than the current one was 2011-2012, which peaked at only 2.4% on the week ending March 17, 2012. The earliest of the bunch came during the 2009-2010 season, which peaked at 7.7% during the week ending Oct. 24, 2009, according to ILINet data.

rfranki@frontlinemedcom.com

There were four states at the highest level of influenza-like illness (ILI) activity for the week, more than any other week of the 2015-2016 flu season, according to the Centers for Disease Control and Prevention.

Arizona, Kentucky, New Jersey, and New Mexico, along with Puerto Rico, were all at level 10 on the CDC’s 1-10 scale of ILI activity for the week ending March 5, 2016. Other states in the “high” range were Arkansas, Illinois, Nevada, and North Carolina at level 9 and Alabama and Mississippi at level 8, the CDC reported.

The proportion of outpatient visits for ILI was 3.5% for the week, the highest of the season so far and well above the national baseline of 2.1%. In addition to the 10 states and Puerto Rico with ILI levels in the high range, there were 13 states in the “moderate” range (6 or 7 on the 1-10 scale) and 12 states in the “low” range (4 or 5), with a total of 44 states at level 2 or higher, data from the CDC’s Outpatient Influenza-like Illness Surveillance Network (ILINet) show.

Two flu-related pediatric deaths were reported during week 21 of the flu season, although both occurred earlier: one during the week ending Feb. 13 and one during the week ending Feb. 27. There have been a total of 20 pediatric deaths reported for the 2015-2016 season, with Florida (four deaths), California, (three), Arizona (two), and Nevada (two) the only states reporting more than one, the CDC report noted.

The continued rise in ILI activity is somewhat unusual. The only season out of the previous 10 with a peak later than the current one was 2011-2012, which peaked at only 2.4% on the week ending March 17, 2012. The earliest of the bunch came during the 2009-2010 season, which peaked at 7.7% during the week ending Oct. 24, 2009, according to ILINet data.

rfranki@frontlinemedcom.com

BOSTON – The day of the week a patient is discharged from the hospital may have an impact the likelihood of readmission.

Patients discharged home from the hospital on a Thursday after colorectal cancer surgery are more likely to be readmitted within 30 days than those discharged on any other day of the week, investigators found.

Neil Osterweil/Frontline Medical News

In contrast, there were no significant day-dependent differences in readmission rates among patients discharged to a skilled nursing facility or acute rehabilitation program, although patients admitted to clinical facilities had higher overall readmission rates, reported Anna Gustin and coinvestigators at the Levine Cancer Institute at the Carolinas Medical Center in Charlotte, N.C.

“For a patient discharged on a Thursday, if you’re going to get an infection, it’s going to be probably during the weekend, when it’s difficult to contact your primary physician, and when other resources are not as readily available,” said Ms. Gustin, who conducts epidemiologic research at Levine Cancer Center and is also a pre-med student and Japanese major at Wake Forest University in Winston-Salem, N.C.

In a study presented in a poster session at the annual Society of Surgical Oncology Cancer Symposium, Ms. Gustin and her coauthors looked at factors influencing readmission rates among patients undergoing surgery for primary, nonmetastatic colorectal cancer resections.

They drew on the to evaluate outcomes for 93,04 SEER-(Surveillance, Epidemiology, and End Results) Medicare database seven patients aged 66 years and older treated for primary colorectal cancer from 1998 through 2009.

They looked at potential contributing factors such as patient demographics, socioeconomic status, length of stay, days of admission and discharge, and discharge setting (home or clinical facility).

They use multivariate logistic regression models to analyze readmission rates at 14 and 30 days after initial discharge.

Focusing on home discharges, they found that as the week progressed, there was a significant likelihood that a patient discharged home would be readmitted (P less then .001 by chi-square and Cochran-Armitage tests). As noted before, the highest rate of readmission was for patients discharged on Thursday, at 12.4%, compared with 10.1% for patients discharged on Sunday, the discharge day least likely to be associated with rehospitalization.

In multivariate analysis, factors significantly associated with risk for 30-day readmission included male vs. female (hazard ratio, 1.16), black vs. other race (HR, 1.22), length of stay 5, 6-7, or 8-10 vs. 12 or more days (HR, 0.48, 0.59, 0.77, respectively), Charlson comorbidity index score 0, 1 or 3 vs. 3 (HR, 0.59, 0.73, 0.82, respectively), and home discharge vs. other (HR, 0.66; all above comparisons significant as shown by 95% confidence intervals).

The authors concluded that although home discharge itself reduces the likelihood of readmission, “improvements in preparing patients for discharge to home are needed. Additional outpatient interventions could rescue patients from readmission.”

They also suggested reexamining staffing policies and weekend availability of resources for patients, and call for addressing disparities in readmissions based on race, sex, length of stay, and comorbidities.

The study was internally supported. The authors reported having no relevant disclosures.

BOSTON – The day of the week a patient is discharged from the hospital may have an impact the likelihood of readmission.

Patients discharged home from the hospital on a Thursday after colorectal cancer surgery are more likely to be readmitted within 30 days than those discharged on any other day of the week, investigators found.

Neil Osterweil/Frontline Medical News

In contrast, there were no significant day-dependent differences in readmission rates among patients discharged to a skilled nursing facility or acute rehabilitation program, although patients admitted to clinical facilities had higher overall readmission rates, reported Anna Gustin and coinvestigators at the Levine Cancer Institute at the Carolinas Medical Center in Charlotte, N.C.

“For a patient discharged on a Thursday, if you’re going to get an infection, it’s going to be probably during the weekend, when it’s difficult to contact your primary physician, and when other resources are not as readily available,” said Ms. Gustin, who conducts epidemiologic research at Levine Cancer Center and is also a pre-med student and Japanese major at Wake Forest University in Winston-Salem, N.C.

In a study presented in a poster session at the annual Society of Surgical Oncology Cancer Symposium, Ms. Gustin and her coauthors looked at factors influencing readmission rates among patients undergoing surgery for primary, nonmetastatic colorectal cancer resections.

They drew on the to evaluate outcomes for 93,04 SEER-(Surveillance, Epidemiology, and End Results) Medicare database seven patients aged 66 years and older treated for primary colorectal cancer from 1998 through 2009.

They looked at potential contributing factors such as patient demographics, socioeconomic status, length of stay, days of admission and discharge, and discharge setting (home or clinical facility).

They use multivariate logistic regression models to analyze readmission rates at 14 and 30 days after initial discharge.

Focusing on home discharges, they found that as the week progressed, there was a significant likelihood that a patient discharged home would be readmitted (P less then .001 by chi-square and Cochran-Armitage tests). As noted before, the highest rate of readmission was for patients discharged on Thursday, at 12.4%, compared with 10.1% for patients discharged on Sunday, the discharge day least likely to be associated with rehospitalization.

In multivariate analysis, factors significantly associated with risk for 30-day readmission included male vs. female (hazard ratio, 1.16), black vs. other race (HR, 1.22), length of stay 5, 6-7, or 8-10 vs. 12 or more days (HR, 0.48, 0.59, 0.77, respectively), Charlson comorbidity index score 0, 1 or 3 vs. 3 (HR, 0.59, 0.73, 0.82, respectively), and home discharge vs. other (HR, 0.66; all above comparisons significant as shown by 95% confidence intervals).

The authors concluded that although home discharge itself reduces the likelihood of readmission, “improvements in preparing patients for discharge to home are needed. Additional outpatient interventions could rescue patients from readmission.”

They also suggested reexamining staffing policies and weekend availability of resources for patients, and call for addressing disparities in readmissions based on race, sex, length of stay, and comorbidities.

The study was internally supported. The authors reported having no relevant disclosures.

BOSTON – The day of the week a patient is discharged from the hospital may have an impact the likelihood of readmission.

Patients discharged home from the hospital on a Thursday after colorectal cancer surgery are more likely to be readmitted within 30 days than those discharged on any other day of the week, investigators found.

Neil Osterweil/Frontline Medical News

In contrast, there were no significant day-dependent differences in readmission rates among patients discharged to a skilled nursing facility or acute rehabilitation program, although patients admitted to clinical facilities had higher overall readmission rates, reported Anna Gustin and coinvestigators at the Levine Cancer Institute at the Carolinas Medical Center in Charlotte, N.C.

“For a patient discharged on a Thursday, if you’re going to get an infection, it’s going to be probably during the weekend, when it’s difficult to contact your primary physician, and when other resources are not as readily available,” said Ms. Gustin, who conducts epidemiologic research at Levine Cancer Center and is also a pre-med student and Japanese major at Wake Forest University in Winston-Salem, N.C.

In a study presented in a poster session at the annual Society of Surgical Oncology Cancer Symposium, Ms. Gustin and her coauthors looked at factors influencing readmission rates among patients undergoing surgery for primary, nonmetastatic colorectal cancer resections.

They drew on the to evaluate outcomes for 93,04 SEER-(Surveillance, Epidemiology, and End Results) Medicare database seven patients aged 66 years and older treated for primary colorectal cancer from 1998 through 2009.

They looked at potential contributing factors such as patient demographics, socioeconomic status, length of stay, days of admission and discharge, and discharge setting (home or clinical facility).

They use multivariate logistic regression models to analyze readmission rates at 14 and 30 days after initial discharge.

Focusing on home discharges, they found that as the week progressed, there was a significant likelihood that a patient discharged home would be readmitted (P less then .001 by chi-square and Cochran-Armitage tests). As noted before, the highest rate of readmission was for patients discharged on Thursday, at 12.4%, compared with 10.1% for patients discharged on Sunday, the discharge day least likely to be associated with rehospitalization.

In multivariate analysis, factors significantly associated with risk for 30-day readmission included male vs. female (hazard ratio, 1.16), black vs. other race (HR, 1.22), length of stay 5, 6-7, or 8-10 vs. 12 or more days (HR, 0.48, 0.59, 0.77, respectively), Charlson comorbidity index score 0, 1 or 3 vs. 3 (HR, 0.59, 0.73, 0.82, respectively), and home discharge vs. other (HR, 0.66; all above comparisons significant as shown by 95% confidence intervals).

The authors concluded that although home discharge itself reduces the likelihood of readmission, “improvements in preparing patients for discharge to home are needed. Additional outpatient interventions could rescue patients from readmission.”

They also suggested reexamining staffing policies and weekend availability of resources for patients, and call for addressing disparities in readmissions based on race, sex, length of stay, and comorbidities.

The study was internally supported. The authors reported having no relevant disclosures.

Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.^1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.^1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.^2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.¹ In addition, spinal BFH appears to have no predilection for sex.

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.^4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.⁷ Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.⁶

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.^2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.^3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.^8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.^1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.^4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.^1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.^12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.^8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.⁴ GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.^12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.^1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.¹³

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.^14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.¹⁷ OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.¹³ In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern⁶ which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.^4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.^7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.^1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.^1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.¹ In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.^2,5,9,19 Clarke and colleagues⁹ reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.^2,9 The only case of lung metastasis, reported by Unni and Dahlin⁶ in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.^1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.^1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.^2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.¹ In addition, spinal BFH appears to have no predilection for sex.

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.^4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.⁷ Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.⁶

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.^2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.^3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.^8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.^1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.^4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.^1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.^12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.^8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.⁴ GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.^12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.^1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.¹³

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.^14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.¹⁷ OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.¹³ In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern⁶ which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.^4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.^7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.^1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.^1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.¹ In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.^2,5,9,19 Clarke and colleagues⁹ reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.^2,9 The only case of lung metastasis, reported by Unni and Dahlin⁶ in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

Benign fibrous histiocytoma (BFH) is a rare, well-recognized, primary skeletal tumor accounting for approximately 1% of all benign bone tumors. Spinal involvement is exceedingly rare with only 11 cases reported in the literature.^1,2 We present a case of BFH located in the cervical spine of a pediatric patient that was successfully treated with curretage through an anterior surgical approach, along with a review of the literature and appropriate management concerning BFH of the spine.

Case Report

A 14-year-old boy was tackled while playing football and noticed immediate neck pain and subjective paresthesia in the upper extremities. Examination revealed a nontender spine (cervical, thoracic, lumbar) and normal strength and range of motion in all extremities. Sensation was diffusely intact, long tract signs were absent, and gait was normal. On questioning, the patient endorsed mild antecedent neck pain but denied prior history of any trauma. Neck pain did not radiate and was slightly worsened by activity but was mostly intermittent and random. As the neck pain was very mild and was not interfering with daily activities, the patient had not sought care before presenting to the emergency department. He had no pertinent past medical or surgical history.

The patient presented with a computed tomography (CT) scan of his head and cervical spine and a magnetic resonance imaging (MRI) scan of the cervical spine. A magnetic resonance angiography (MRA) scan of the neck was ordered after his arrival.

Axial and sagittal CT (Figures 1A, 1B) showed a 1×1.2-cm discrete, expansile, lytic, radiolucent mass extending anterior from the left C2 vertebral body. The mass appeared to abut the left vertebral artery foramen. The cortical bone surrounding the lesion was thin but uniform. Sagittal and axial T1-weighted MRI (Figures 2A, 2B) showed the discrete, expansile, homogenous lesion with the same intensity as normal bone marrow. Sagittal and axial T2-weighted MRI (Figures 2C, 2D) showed a discrete, expansile, homogenous lesion with primarily high signal intensity. Sagittal short tau inversion recovery (STIR) MRI (Figure 2E) again showed the lesion with primarily low intensity. Given the close proximity of the lesion to the vertebral foramen, MRA was ordered; it showed the lesion was not interfering with the vertebral artery (Figure 2F).

The tumor’s location, in the left anterior aspect of the C2 vertebral body, was not conducive to percutaneous biopsy for establishing tissue diagnosis, so the decision was made to surgically excise the lesion. A left-sided anterior incision was made 2 fingerbreadths inferior to the jaw line in a neck crease. A head and neck surgeon assisted with dissection. Dissection was carried down through the skin, subcutaneous tissue, and platysma on to the anterior part of the spine medial to the carotid sheath. Superior thyroid nerve and vessels and superior laryngeal nerve were identified and preserved. Fluoroscopy confirmed correct location at C2. The tumor was easily visualized, and the outer shell broke easily with palpation. Gentle curettage was necessary when removing the tumor off the vertebral artery. A portion of the specimen was sent during surgery for frozen section, which showed infrequent mitotic figures and no other findings concerning for malignancy. No instability was created after curettage and excision of the tumor, so no grafting or instrumentation was necessary.

Grossly, the tumor was pale tan and firm. Histologic examination with hematoxylin-eosin staining revealed a bland spindle-cell neoplasm that focally involved bone. A storiform pattern was present. The cells had scant cytoplasm and oval to elongate nuclei with tapered ends. Significant nuclear pleomorphism was not seen. The stroma was loose, with focal myxoid change. Benign multinucleated giant cells were present. Mitotic activity was infrequent (Figures 3A–3D). Two attending pathologists reviewed the case material and the frozen and formalin-fixed specimens independently and concurred with the diagnosis of BFH. In addition, the case was reviewed at the surgical pathology consensus conference; the reviewers agreed on BFH, and additional studies were deemed unnecessary.

Given the patient’s complete clinical picture, the differential diagnosis included nonossifying fibroma (NOF), eosinophilic granuloma (EG), BFH, fibrous dysplasia, giant cell tumor (GCT), aneurysmal bone cyst (ABC), and osteoblastoma (OB).

Discussion

BFH is an extremely rare bone lesion, accounting for only 1% of all surgically managed bone tumors; not counting the present case, only 11 spine cases have been reported in the literature.^1,2 BFH of the spine traditionally causes nonspecific, poorly localized pain. The Table lists the reported cases of spinal BFH and their presenting symptoms, location, and treatment. BFH usually occurs in young adults, but the age range is 5 to 75 years.^2-4 Mean age of the 12 patients with spinal BFH in the literature (including ours) is 25 years.¹ In addition, spinal BFH appears to have no predilection for sex.

Skeletal BFH presents as a discrete, well-defined, osteolytic lesion with sharp borders and potentially a sclerotic rim.^4-6 Cortical expansion and even cortical disruption with invasion into adjacent tissue have occurred in flat bones.⁷ Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in storiform pattern.⁶

BFH shares many of its radiologic and histologic characteristics and clinical symptoms with other benign bone lesions (the tumors listed above). Therefore, accurate diagnosis of BFH requires appropriate correlation of clinical, radiographic, and histologic data.^2,3,8 Below is a comparison of BFH with related bone lesions.

Spinal BFH causes a nonspecific, poorly localized pain similar to that of EG, ABC, GCT, and OB.^3,9 NOF and fibrous dysplasia generally do not cause pain, unless these lesions are discovered secondary to a pathologic fracture.^8,10,11 Our patient had minor antecedent neck pain, which was brought to light by his football accident. ABC and OB are more locally aggressive than BFH and can cause neurologic symptoms by mass effect and spinal cord or nerve root compression.^1,8 In this case and in the 6 other cases of BFH of the cervical spine, there were no neurologic changes.^4,10

Of the tumors mentioned, NOF and EG almost always occur in children. However, NOF usually occurs in the metaphyseal region of long bones, and EG is usually accompanied by systemic symptoms, such as lymphadenopathy, hepatomegaly, and increased inflammatory markers.^1,8 Fibrous dysplasia usually presents in childhood but does not become symptomatic until adulthood. GCTs and OB predominantly occur in adulthood.^12,13 Our patient’s age and lack of other systemic symptoms supported the diagnosis of BFH.

Appearance on MRI is reported less with BFH than with other tumors, but heterogenous signal intensity similar to that of skeletal muscle on T1-weighted images and high signal intensity on T2-weighted images is typically reported.^8,14 NOF and fibrous dysplasia do not disrupt the bony cortex unless a pathologic fracture has occurred.⁴ GCTs are more aggressive lytic lesions with more aggressive radiologic features. GCTs generally cause cortical expansion/attenuation, and lack a sclerotic rim. GCTs also have a heterogenous appearance on MRI and give a low to intermediate signal on both T1- and T2-weighted images.^12,15 The appearance of EG is similar to that of BFH as an osteolytic lesion with a sclerotic rim, though EGs typically break through the cortex and acquire a “punched-out” look.^1,8 ABC typically is described as an expansile osteolytic lesion with a “soap-bubble” appearance on radiographs; periosteal elevation and cortical attenuation can also be visualized. MRI shows the typical multilobular appearance of the lesion with fluid levels.¹³

OB appears as a radiolucent lesion, with or without calcifications, surrounded by a thin margin of reactive bone.^14,16 A distinguishing characteristic of OB was thought to be intense radioisotope uptake on bone scintigraphy, but recently a bony BFH demonstrated intense uptake.¹⁷ OBs typically demonstrate nonspecific MRI results similar to those of BFH: low to intermediate signal on T1-weighted images and intermediate to high signal on T2-weighted images.¹³ In our patient’s case, the radiographic appearance and lack of specific radiographic findings consistent with the other tumors supported the diagnosis of BFH.

Histologically, BFHs contain spindle cells, multinucleated giant cells, and foam cells in a storiform pattern⁶ which was demonstrated in our patient’s case. In addition, significant nuclear pleomorphism, mitotic activity, and necrosis were absent—a difference between BFH and malignant fibrous histiocytoma.^4,15 The microscopic characteristics of BFH readily differentiate it from OB, ABC, EG, and GCT, but not from NOF on microscopic appearance alone. Clinical and radiographic findings must be consistent, as mentioned.^7,18

Complete surgical excision is the reported treatment for BFH. Prognosis after resection or curettage is usually good, and recurrences have been rare.^1,2 Depending on the intraspinous location of BFH, stabilization after resection or curettage may be necessary to prevent residual instability. Three of the 11 reported cases of spinal BFH required stabilization by anterior fusion or posterior pedicle screw fixation after resection.^1,2 The other 8 cases underwent excision alone or excision and grafting. All 11 patients were disease-free at a mean follow-up of 3.5 years.¹ In nonspinal BFH, however, both local recurrence and lung metastasis have been reported.^2,5,9,19 Clarke and colleagues⁹ reported local recurrences in 3 of 8 cases. These recurrences involved BFH in long bones of the leg, which had been treated with curettage and grafting. There has been no reliable report of a malignant change in BFH.^2,9 The only case of lung metastasis, reported by Unni and Dahlin⁶ in their study of 10 cases, occurred 2 years after local recurrence in the distal femur.Our patient was doing well at most recent follow-up, 6 months after surgery. He had no pain and had returned to normal activities. Although there are no reported cases of spinal BFH recurrence, we will follow this patient with imaging on an annual basis. His case is of particular interest to orthopedic surgeons because they encounter benign bone lesions every day, and many of these lesions are in difficult anatomical locations. Knowing the characteristics, differential diagnoses, and appropriate diagnostic workups for benign bone lesions is important for optimal and timely patient care.

At this ripe point in my career, many new patients come referred by Dr. Google. “I checked the Internet,” they say. “You have great reviews.”

I don’t read my reviews. The abusive ones make me ill. People must filter out the bile and focus on the positives.

Laymen have little sense of how good the professionals they consult really are. Unless I’m audited and lose, how would I know how skillful my accountant is? My urologist is a nice man. How good is he at prostate surgery? I hope not to find out. Nevertheless, reviews are here to stay, as are physician evaluations by insurers and professional agencies.

Some office days highlight the gap, really the chasm, between the truth of the professional matter and what makes patients decide to trust or mistrust us. Last Thursday was one of those days.

Marla brought in her daughter, aged 3 years. Zoe had a scaly rash and some red papules on her arms and legs.

“Did your pediatrician treat this?” I asked.

“No, I came right to you,” said Marla. “You diagnosed her with bedbugs when she was an infant. The pediatricians had no idea what was going on. I trust you.”

That is flattering, but if I were being fully honest, I would tell Marla:

•  Bedbug bites are tricky to diagnose. I’ve missed my share.

•  What helped me diagnose them in her daughter was that the pediatrician had already tried several remedies that hadn’t helped.

Even if I said these things, though – and why waste all that wonderful transference? – Marla would probably have said, “Maybe so, but you got it right, and I trust you.” Nothing succeeds like success.

The reverse, however, is also true: Nothing fails like failure.

Later the same day Brian brought in Luke, aged 6 years. Luke has severe atopic dermatitis. As usual, he was scratching up a storm. “I think it’s infected,” Brian said. “Shouldn’t he take antibiotics?”

I examined Luke and found subacute eczema. “I don’t think so,” I said. “This is what Luke’s eczema flares look like. Let’s treat him with a topical steroid cream and see how he does.”

“But he had staph last year,” said Brian.

“I recall,” I said, “but most of his outbreaks have not been infected, and it doesn’t look like staph now. Let’s treat it as we usually do and see what happens over the next week.”

Two weeks later Brian brought back Luke, still scratching. There were still no pustules or deeper inflammatory lesions. We started Luke on an antibiotic, and swabbed scratched areas. Two days later the culture grew staph. By the time I called Brian with the results, he had brought Luke to an emergency room. “He has abscesses,” he told me.

The next day the sensitivities were back, confirming staph. I called Brian, who had this to say: “He should have been on antibiotics 2 weeks ago. From now on, whenever he starts scratching, he should be started on them right away. I won’t be bringing him back to your practice. I don’t trust you. I trust the doctors in the ER more.”

Is it really a good idea to start every eczema patient on antibiotics? How about every eczema patient who once had staph? Based on my own clinical experience with both conditions, I would answer both questions in the negative. Others might disagree.

One thing is sure, though: Like most patients, Brian sees the situation not through the eyes of my experience but through his own case series, with an n of 1. But that 1 carries a lot of weight, because the 1 is Luke, his son. It is therefore clear – to him – that his son should be treated preemptively with antibiotics for every eczema flare.

At this point I might too, for Luke, but I will not get the chance. Once trust is gone, the clinical relationship is over. Sometimes it’s one strike and you’re out.

For her part, Marla sees things through her single case report as well, drawing the opposite conclusion: that my success earned me the trust her pediatrician lost.

The subtleties and nuances of such cases, which every clinician knows, are lost in the often black-and-white world of lay reviews and pay-for-performance algorithms. That’s clinical life.

Trust me.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. Write to him at dermnews@frontlinemedcom.com.

At this ripe point in my career, many new patients come referred by Dr. Google. “I checked the Internet,” they say. “You have great reviews.”

I don’t read my reviews. The abusive ones make me ill. People must filter out the bile and focus on the positives.

Laymen have little sense of how good the professionals they consult really are. Unless I’m audited and lose, how would I know how skillful my accountant is? My urologist is a nice man. How good is he at prostate surgery? I hope not to find out. Nevertheless, reviews are here to stay, as are physician evaluations by insurers and professional agencies.

Some office days highlight the gap, really the chasm, between the truth of the professional matter and what makes patients decide to trust or mistrust us. Last Thursday was one of those days.

Marla brought in her daughter, aged 3 years. Zoe had a scaly rash and some red papules on her arms and legs.

“Did your pediatrician treat this?” I asked.

“No, I came right to you,” said Marla. “You diagnosed her with bedbugs when she was an infant. The pediatricians had no idea what was going on. I trust you.”

That is flattering, but if I were being fully honest, I would tell Marla:

•  Bedbug bites are tricky to diagnose. I’ve missed my share.

•  What helped me diagnose them in her daughter was that the pediatrician had already tried several remedies that hadn’t helped.

Even if I said these things, though – and why waste all that wonderful transference? – Marla would probably have said, “Maybe so, but you got it right, and I trust you.” Nothing succeeds like success.

The reverse, however, is also true: Nothing fails like failure.

Later the same day Brian brought in Luke, aged 6 years. Luke has severe atopic dermatitis. As usual, he was scratching up a storm. “I think it’s infected,” Brian said. “Shouldn’t he take antibiotics?”

I examined Luke and found subacute eczema. “I don’t think so,” I said. “This is what Luke’s eczema flares look like. Let’s treat him with a topical steroid cream and see how he does.”

“But he had staph last year,” said Brian.

“I recall,” I said, “but most of his outbreaks have not been infected, and it doesn’t look like staph now. Let’s treat it as we usually do and see what happens over the next week.”

Two weeks later Brian brought back Luke, still scratching. There were still no pustules or deeper inflammatory lesions. We started Luke on an antibiotic, and swabbed scratched areas. Two days later the culture grew staph. By the time I called Brian with the results, he had brought Luke to an emergency room. “He has abscesses,” he told me.

The next day the sensitivities were back, confirming staph. I called Brian, who had this to say: “He should have been on antibiotics 2 weeks ago. From now on, whenever he starts scratching, he should be started on them right away. I won’t be bringing him back to your practice. I don’t trust you. I trust the doctors in the ER more.”

Is it really a good idea to start every eczema patient on antibiotics? How about every eczema patient who once had staph? Based on my own clinical experience with both conditions, I would answer both questions in the negative. Others might disagree.

One thing is sure, though: Like most patients, Brian sees the situation not through the eyes of my experience but through his own case series, with an n of 1. But that 1 carries a lot of weight, because the 1 is Luke, his son. It is therefore clear – to him – that his son should be treated preemptively with antibiotics for every eczema flare.

At this point I might too, for Luke, but I will not get the chance. Once trust is gone, the clinical relationship is over. Sometimes it’s one strike and you’re out.

For her part, Marla sees things through her single case report as well, drawing the opposite conclusion: that my success earned me the trust her pediatrician lost.

The subtleties and nuances of such cases, which every clinician knows, are lost in the often black-and-white world of lay reviews and pay-for-performance algorithms. That’s clinical life.

Trust me.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. Write to him at dermnews@frontlinemedcom.com.

At this ripe point in my career, many new patients come referred by Dr. Google. “I checked the Internet,” they say. “You have great reviews.”

I don’t read my reviews. The abusive ones make me ill. People must filter out the bile and focus on the positives.

Laymen have little sense of how good the professionals they consult really are. Unless I’m audited and lose, how would I know how skillful my accountant is? My urologist is a nice man. How good is he at prostate surgery? I hope not to find out. Nevertheless, reviews are here to stay, as are physician evaluations by insurers and professional agencies.

Some office days highlight the gap, really the chasm, between the truth of the professional matter and what makes patients decide to trust or mistrust us. Last Thursday was one of those days.

Marla brought in her daughter, aged 3 years. Zoe had a scaly rash and some red papules on her arms and legs.

“Did your pediatrician treat this?” I asked.

“No, I came right to you,” said Marla. “You diagnosed her with bedbugs when she was an infant. The pediatricians had no idea what was going on. I trust you.”

That is flattering, but if I were being fully honest, I would tell Marla:

•  Bedbug bites are tricky to diagnose. I’ve missed my share.

•  What helped me diagnose them in her daughter was that the pediatrician had already tried several remedies that hadn’t helped.

Even if I said these things, though – and why waste all that wonderful transference? – Marla would probably have said, “Maybe so, but you got it right, and I trust you.” Nothing succeeds like success.

The reverse, however, is also true: Nothing fails like failure.

Later the same day Brian brought in Luke, aged 6 years. Luke has severe atopic dermatitis. As usual, he was scratching up a storm. “I think it’s infected,” Brian said. “Shouldn’t he take antibiotics?”

I examined Luke and found subacute eczema. “I don’t think so,” I said. “This is what Luke’s eczema flares look like. Let’s treat him with a topical steroid cream and see how he does.”

“But he had staph last year,” said Brian.

“I recall,” I said, “but most of his outbreaks have not been infected, and it doesn’t look like staph now. Let’s treat it as we usually do and see what happens over the next week.”

Two weeks later Brian brought back Luke, still scratching. There were still no pustules or deeper inflammatory lesions. We started Luke on an antibiotic, and swabbed scratched areas. Two days later the culture grew staph. By the time I called Brian with the results, he had brought Luke to an emergency room. “He has abscesses,” he told me.

The next day the sensitivities were back, confirming staph. I called Brian, who had this to say: “He should have been on antibiotics 2 weeks ago. From now on, whenever he starts scratching, he should be started on them right away. I won’t be bringing him back to your practice. I don’t trust you. I trust the doctors in the ER more.”

Is it really a good idea to start every eczema patient on antibiotics? How about every eczema patient who once had staph? Based on my own clinical experience with both conditions, I would answer both questions in the negative. Others might disagree.

One thing is sure, though: Like most patients, Brian sees the situation not through the eyes of my experience but through his own case series, with an n of 1. But that 1 carries a lot of weight, because the 1 is Luke, his son. It is therefore clear – to him – that his son should be treated preemptively with antibiotics for every eczema flare.

At this point I might too, for Luke, but I will not get the chance. Once trust is gone, the clinical relationship is over. Sometimes it’s one strike and you’re out.

For her part, Marla sees things through her single case report as well, drawing the opposite conclusion: that my success earned me the trust her pediatrician lost.

The subtleties and nuances of such cases, which every clinician knows, are lost in the often black-and-white world of lay reviews and pay-for-performance algorithms. That’s clinical life.

Trust me.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. Write to him at dermnews@frontlinemedcom.com.

When an adolescent presents with a history of sudden decline in academic performance, be sure to consider serious mental illness.

According to Dr. David Pickar, a psychiatrist and former (retired) director of intramural research at the National Institute of Mental Health, 90%of cases – particularly of schizophrenia – occur between the ages of 16 and 24 years.

“As a scientist, I’ve spent my career thinking about that, but for the primary care doc, if the family comes in and reports that their kid was a good student, and he’s now terrible,” first-episode psychosis should be considered, said Dr. Pickar, who produced a documentary short film describing how to recognize schizophrenia and psychosis. In this video, Dr. Pickar also explains how the use of marijuana also can precipitate psychosis in some people with a genetic predisposition to the illness.

When an adolescent presents with a history of sudden decline in academic performance, be sure to consider serious mental illness.

According to Dr. David Pickar, a psychiatrist and former (retired) director of intramural research at the National Institute of Mental Health, 90%of cases – particularly of schizophrenia – occur between the ages of 16 and 24 years.

“As a scientist, I’ve spent my career thinking about that, but for the primary care doc, if the family comes in and reports that their kid was a good student, and he’s now terrible,” first-episode psychosis should be considered, said Dr. Pickar, who produced a documentary short film describing how to recognize schizophrenia and psychosis. In this video, Dr. Pickar also explains how the use of marijuana also can precipitate psychosis in some people with a genetic predisposition to the illness.

When an adolescent presents with a history of sudden decline in academic performance, be sure to consider serious mental illness.

According to Dr. David Pickar, a psychiatrist and former (retired) director of intramural research at the National Institute of Mental Health, 90%of cases – particularly of schizophrenia – occur between the ages of 16 and 24 years.

“As a scientist, I’ve spent my career thinking about that, but for the primary care doc, if the family comes in and reports that their kid was a good student, and he’s now terrible,” first-episode psychosis should be considered, said Dr. Pickar, who produced a documentary short film describing how to recognize schizophrenia and psychosis. In this video, Dr. Pickar also explains how the use of marijuana also can precipitate psychosis in some people with a genetic predisposition to the illness.

Presenter: Kyung E. Rhee, MD, MSc, MA

Summary: Eating disorders (ED) are common and have significant morbidity and mortality. EDs are the third most common psychiatric disorder of adolescents with a prevalence of 0.5-2% for anorexia and 0.9-3% for bulimia; 90% of patients are female. Mortality rate can be as high as 10% for anorexia and 1% for bulimia. Diagnosis is formally guided by DSM 5 criteria, but the mnemonic SCOFF can be useful:

1. Do you feel or make yourself SICK when eating?
2. Do you feel you’ve lost CONTROL of your eating?
3. Have you lost one STONE (14 lbs. developed by the British) of weight?
4. Do you feel FAT?
5. Does FOOD dominate your life?

A detailed history is needed as patients with ED may engage in secretive behaviors to hide their illness. After diagnosis, treatment may be outpatient or inpatient. Medical issues hospitalists are likely to see with inpatients include re-feeding syndrome, various metabolic disturbances, secondary amenorrhea, sleep disturbances, and for patients with bulimia, evidence of dental or esophageal trauma from purging. Differential diagnoses include: IBD, thyroid disease, celiac, diabetes, and Addison’s disease.

Hospitalists’ role in treatment is as part of a multidisciplinary group to manage the medical complications. Inpatient management includes individual and group therapy, monitored group meals, daily blind weights, bathroom visits, and focused lab studies. There is no “cure” and only ~50% of patients are free of ongoing symptoms after treatment.

Key Takeaways

• Eating disorders are common in adolescent females and have significant morbidity and mortality.
• Hospitalists’ role is diagnosis via careful history and management of medical complications with an eating disorder team. TH

Dr. Pressel is a pediatric hospitalist and inpatient medical director at Nemours/Alfred I. duPont Hospital for Children in Wilmington, Del., and a member of Team Hospitalist.

Presenter: Kyung E. Rhee, MD, MSc, MA

Summary: Eating disorders (ED) are common and have significant morbidity and mortality. EDs are the third most common psychiatric disorder of adolescents with a prevalence of 0.5-2% for anorexia and 0.9-3% for bulimia; 90% of patients are female. Mortality rate can be as high as 10% for anorexia and 1% for bulimia. Diagnosis is formally guided by DSM 5 criteria, but the mnemonic SCOFF can be useful:

1. Do you feel or make yourself SICK when eating?
2. Do you feel you’ve lost CONTROL of your eating?
3. Have you lost one STONE (14 lbs. developed by the British) of weight?
4. Do you feel FAT?
5. Does FOOD dominate your life?

A detailed history is needed as patients with ED may engage in secretive behaviors to hide their illness. After diagnosis, treatment may be outpatient or inpatient. Medical issues hospitalists are likely to see with inpatients include re-feeding syndrome, various metabolic disturbances, secondary amenorrhea, sleep disturbances, and for patients with bulimia, evidence of dental or esophageal trauma from purging. Differential diagnoses include: IBD, thyroid disease, celiac, diabetes, and Addison’s disease.

Hospitalists’ role in treatment is as part of a multidisciplinary group to manage the medical complications. Inpatient management includes individual and group therapy, monitored group meals, daily blind weights, bathroom visits, and focused lab studies. There is no “cure” and only ~50% of patients are free of ongoing symptoms after treatment.

Key Takeaways

• Eating disorders are common in adolescent females and have significant morbidity and mortality.
• Hospitalists’ role is diagnosis via careful history and management of medical complications with an eating disorder team. TH

Dr. Pressel is a pediatric hospitalist and inpatient medical director at Nemours/Alfred I. duPont Hospital for Children in Wilmington, Del., and a member of Team Hospitalist.

Presenter: Kyung E. Rhee, MD, MSc, MA

Summary: Eating disorders (ED) are common and have significant morbidity and mortality. EDs are the third most common psychiatric disorder of adolescents with a prevalence of 0.5-2% for anorexia and 0.9-3% for bulimia; 90% of patients are female. Mortality rate can be as high as 10% for anorexia and 1% for bulimia. Diagnosis is formally guided by DSM 5 criteria, but the mnemonic SCOFF can be useful:

1. Do you feel or make yourself SICK when eating?
2. Do you feel you’ve lost CONTROL of your eating?
3. Have you lost one STONE (14 lbs. developed by the British) of weight?
4. Do you feel FAT?
5. Does FOOD dominate your life?

A detailed history is needed as patients with ED may engage in secretive behaviors to hide their illness. After diagnosis, treatment may be outpatient or inpatient. Medical issues hospitalists are likely to see with inpatients include re-feeding syndrome, various metabolic disturbances, secondary amenorrhea, sleep disturbances, and for patients with bulimia, evidence of dental or esophageal trauma from purging. Differential diagnoses include: IBD, thyroid disease, celiac, diabetes, and Addison’s disease.

Hospitalists’ role in treatment is as part of a multidisciplinary group to manage the medical complications. Inpatient management includes individual and group therapy, monitored group meals, daily blind weights, bathroom visits, and focused lab studies. There is no “cure” and only ~50% of patients are free of ongoing symptoms after treatment.

Key Takeaways

• Eating disorders are common in adolescent females and have significant morbidity and mortality.
• Hospitalists’ role is diagnosis via careful history and management of medical complications with an eating disorder team. TH

Dr. Pressel is a pediatric hospitalist and inpatient medical director at Nemours/Alfred I. duPont Hospital for Children in Wilmington, Del., and a member of Team Hospitalist.

Serious mental illness can present slowly and in ways that might not look serious, which is why primary care physicians would do well to educate themselves about what psychosis looks like.

The problem, according to Dr. David Pickar, psychiatrist and former (retired) intramural research director for the National Institute of Mental Health, is the lack of information about recognizing the signs and symptoms, and about proper interventions.

“Knowing about it is enormously important for all docs,” Dr. Pickar says. “What’s fascinating is many of the first breaks occur, not necessarily quietly, but can be a little insidious. They can be brought to primary care. It is not uncommon. With serious mental illness, particularly schizophrenia, 1% of the population has it. That makes it a very common disorder.”

Serious mental illness can present slowly and in ways that might not look serious, which is why primary care physicians would do well to educate themselves about what psychosis looks like.

The problem, according to Dr. David Pickar, psychiatrist and former (retired) intramural research director for the National Institute of Mental Health, is the lack of information about recognizing the signs and symptoms, and about proper interventions.

“Knowing about it is enormously important for all docs,” Dr. Pickar says. “What’s fascinating is many of the first breaks occur, not necessarily quietly, but can be a little insidious. They can be brought to primary care. It is not uncommon. With serious mental illness, particularly schizophrenia, 1% of the population has it. That makes it a very common disorder.”

Serious mental illness can present slowly and in ways that might not look serious, which is why primary care physicians would do well to educate themselves about what psychosis looks like.

The problem, according to Dr. David Pickar, psychiatrist and former (retired) intramural research director for the National Institute of Mental Health, is the lack of information about recognizing the signs and symptoms, and about proper interventions.

“Knowing about it is enormously important for all docs,” Dr. Pickar says. “What’s fascinating is many of the first breaks occur, not necessarily quietly, but can be a little insidious. They can be brought to primary care. It is not uncommon. With serious mental illness, particularly schizophrenia, 1% of the population has it. That makes it a very common disorder.”

AUSTIN, TEX. – The shift from volume- to value-based care has become a regular hot topic among the medical community. But one rarely discussed question is how quality-based care will impact physician contracts with health plans, according to Bloomfield Hills, Mich., health law attorney Mark S. Kopson.

In a video interview at an American Health Lawyers Association meeting, Mr. Kopson discusses how to navigate payer contracts when operating within value-based care models. He addresses ideal terms to include in quality-based care contracts and how to mitigate legal risks with health plans.

“The contract language that works in volume-based contracts doesn’t work in value-based contracts,” Mr. Kopson explains. “We have to make a distinction between the two and recognize that there are risks and issues that have to be addressed in value-based arrangements.”

agallegos@frontlinemedcom.com

On Twitter @legal_med

AUSTIN, TEX. – The shift from volume- to value-based care has become a regular hot topic among the medical community. But one rarely discussed question is how quality-based care will impact physician contracts with health plans, according to Bloomfield Hills, Mich., health law attorney Mark S. Kopson.

In a video interview at an American Health Lawyers Association meeting, Mr. Kopson discusses how to navigate payer contracts when operating within value-based care models. He addresses ideal terms to include in quality-based care contracts and how to mitigate legal risks with health plans.

“The contract language that works in volume-based contracts doesn’t work in value-based contracts,” Mr. Kopson explains. “We have to make a distinction between the two and recognize that there are risks and issues that have to be addressed in value-based arrangements.”

agallegos@frontlinemedcom.com

On Twitter @legal_med

AUSTIN, TEX. – The shift from volume- to value-based care has become a regular hot topic among the medical community. But one rarely discussed question is how quality-based care will impact physician contracts with health plans, according to Bloomfield Hills, Mich., health law attorney Mark S. Kopson.

In a video interview at an American Health Lawyers Association meeting, Mr. Kopson discusses how to navigate payer contracts when operating within value-based care models. He addresses ideal terms to include in quality-based care contracts and how to mitigate legal risks with health plans.

“The contract language that works in volume-based contracts doesn’t work in value-based contracts,” Mr. Kopson explains. “We have to make a distinction between the two and recognize that there are risks and issues that have to be addressed in value-based arrangements.”

agallegos@frontlinemedcom.com

On Twitter @legal_med

View summaries from the event on the following pages.

Thursday, March 10, 2016

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder
Roueen Rafeyan, MD, Feinberg School of Medicine at Northwestern University

Successful Aging
George T. Grossberg, MD, Saint Louis University 

Psychopharmacology and Pregnancy: The New Labeling Changes and Implications for Clinical Practice
Marlene P. Freeman, MD, Massachusetts General Hospital

Anxiety Disorders in Women Across the Lifecycle
Marlene P. Freeman, MD, Massachusetts General Hospital

Mild Cognitive Impairment: “Senior Moments” and DSM-5
George T. Grossberg, MD, Saint Louis University

Assessing major depressive disorder and an option for treatment
Jay D. Fawver, MD, Indiana University School of Medicine

Innovative Treatments of Anxiety, Part 1 (Use of Benzodiazepines)
Mark H. Pollack, MD, Rush University Medical Center

Innovative Treatments of Anxiety, Part 2 (Other Standard and Novel Therapeutic Approaches)
Mark H. Pollack, MD, Rush University Medical Center

Treatment of Chronic Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital

Friday, March 11, 2016

Subtypes of Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Managing ADHD: What Matters Most When Selecting a Treatment Option
Michael Feld, MD, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Dr. Feld discussed the utility of the brand-name extended-release (ER) methylphenidate HCl (Aptensio) for its value in children—specifically, its ability to “extend the day” without additional dosing of a short-action medication. The design of Aptensio—a multilayered beaded delivery system in which every bead is both an immediate- and an extended-release vehicle—allows an early peak serum drug level and later peak level (at 8 hours). Aptensio is administered by sprinkling the contents of a capsule on applesauce; it is is safe practice, Dr. Feld explained, to augment the ER drug delivery with an immediate-release agent when deemed necessary, by observing how difficult it is for the patient to make it through the day at home, school, or work.

Overview of Autism Spectrum Disorder
Robert L. Hendren, DO, University of California, San Francisco

Comorbidity of Schizophrenia and Substance Abuse
Henry A. Nasrallah, MD, Saint Louis University

Overview of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Bipolar Depression: Presentation, Diagnosis, and Treatment in the Outpatient Psychiatry Practice Setting
Peter J. Weiden, MD, University of Illinois at Chicago

Neuroinflammation and Oxidative Stress in Schizophrenia and Mood Disorders: Biomarkers and Therapeutic Targets
Henry A. Nasrallah, MD, Saint Louis University

Clinical Management of Autism Spectrum Disorders: What Happens Over Time/Borderline Intellectual Functioning
Robert L. Hendren, DO, University of California, San Francisco

Management of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Saturday, March 12, 2015

Managing the Difficult Child
Anthony L. Rostain, MD, MA, University of Pennsylvania

Major Depression With Subsyndromal Mania/Hypomania: Implications for Diagnosis and Management
Trisha Suppes, MD, PhD, Stanford University School of Medicine, Roger S. McIntyre, MD, FRCPC, University of Toronto, and J. Craig Nelson, MD, University of California, San Francisco

General Overview of Sleep Disorders
Thomas Roth, PhD, Henry Ford Hospital

Comorbid ADHD with Substance Abuse 
Anthony L. Rostain, MD, MA, University of Pennsylvania

How to Treat Patients with Insomnia
Thomas Roth, PhD, Henry Ford Hospital

View summaries from the event on the following pages.

Thursday, March 10, 2016

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder
Roueen Rafeyan, MD, Feinberg School of Medicine at Northwestern University

Successful Aging
George T. Grossberg, MD, Saint Louis University 

Psychopharmacology and Pregnancy: The New Labeling Changes and Implications for Clinical Practice
Marlene P. Freeman, MD, Massachusetts General Hospital

Anxiety Disorders in Women Across the Lifecycle
Marlene P. Freeman, MD, Massachusetts General Hospital

Mild Cognitive Impairment: “Senior Moments” and DSM-5
George T. Grossberg, MD, Saint Louis University

Assessing major depressive disorder and an option for treatment
Jay D. Fawver, MD, Indiana University School of Medicine

Innovative Treatments of Anxiety, Part 1 (Use of Benzodiazepines)
Mark H. Pollack, MD, Rush University Medical Center

Innovative Treatments of Anxiety, Part 2 (Other Standard and Novel Therapeutic Approaches)
Mark H. Pollack, MD, Rush University Medical Center

Treatment of Chronic Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital

Friday, March 11, 2016

Subtypes of Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Managing ADHD: What Matters Most When Selecting a Treatment Option
Michael Feld, MD, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Dr. Feld discussed the utility of the brand-name extended-release (ER) methylphenidate HCl (Aptensio) for its value in children—specifically, its ability to “extend the day” without additional dosing of a short-action medication. The design of Aptensio—a multilayered beaded delivery system in which every bead is both an immediate- and an extended-release vehicle—allows an early peak serum drug level and later peak level (at 8 hours). Aptensio is administered by sprinkling the contents of a capsule on applesauce; it is is safe practice, Dr. Feld explained, to augment the ER drug delivery with an immediate-release agent when deemed necessary, by observing how difficult it is for the patient to make it through the day at home, school, or work.

Overview of Autism Spectrum Disorder
Robert L. Hendren, DO, University of California, San Francisco

Comorbidity of Schizophrenia and Substance Abuse
Henry A. Nasrallah, MD, Saint Louis University

Overview of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Bipolar Depression: Presentation, Diagnosis, and Treatment in the Outpatient Psychiatry Practice Setting
Peter J. Weiden, MD, University of Illinois at Chicago

Neuroinflammation and Oxidative Stress in Schizophrenia and Mood Disorders: Biomarkers and Therapeutic Targets
Henry A. Nasrallah, MD, Saint Louis University

Clinical Management of Autism Spectrum Disorders: What Happens Over Time/Borderline Intellectual Functioning
Robert L. Hendren, DO, University of California, San Francisco

Management of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Saturday, March 12, 2015

Managing the Difficult Child
Anthony L. Rostain, MD, MA, University of Pennsylvania

Major Depression With Subsyndromal Mania/Hypomania: Implications for Diagnosis and Management
Trisha Suppes, MD, PhD, Stanford University School of Medicine, Roger S. McIntyre, MD, FRCPC, University of Toronto, and J. Craig Nelson, MD, University of California, San Francisco

General Overview of Sleep Disorders
Thomas Roth, PhD, Henry Ford Hospital

Comorbid ADHD with Substance Abuse 
Anthony L. Rostain, MD, MA, University of Pennsylvania

How to Treat Patients with Insomnia
Thomas Roth, PhD, Henry Ford Hospital

View summaries from the event on the following pages.

Thursday, March 10, 2016

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder
Roueen Rafeyan, MD, Feinberg School of Medicine at Northwestern University

Successful Aging
George T. Grossberg, MD, Saint Louis University 

Psychopharmacology and Pregnancy: The New Labeling Changes and Implications for Clinical Practice
Marlene P. Freeman, MD, Massachusetts General Hospital

Anxiety Disorders in Women Across the Lifecycle
Marlene P. Freeman, MD, Massachusetts General Hospital

Mild Cognitive Impairment: “Senior Moments” and DSM-5
George T. Grossberg, MD, Saint Louis University

Assessing major depressive disorder and an option for treatment
Jay D. Fawver, MD, Indiana University School of Medicine

Innovative Treatments of Anxiety, Part 1 (Use of Benzodiazepines)
Mark H. Pollack, MD, Rush University Medical Center

Innovative Treatments of Anxiety, Part 2 (Other Standard and Novel Therapeutic Approaches)
Mark H. Pollack, MD, Rush University Medical Center

Treatment of Chronic Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital

Friday, March 11, 2016

Subtypes of Depression
Andrew A. Nierenberg, MD, Massachusetts General Hospital, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Managing ADHD: What Matters Most When Selecting a Treatment Option
Michael Feld, MD, Alexian Brothers Behavioral Health Hospital for Violence Prevention Clinic/Program and ADHD Clinic

Dr. Feld discussed the utility of the brand-name extended-release (ER) methylphenidate HCl (Aptensio) for its value in children—specifically, its ability to “extend the day” without additional dosing of a short-action medication. The design of Aptensio—a multilayered beaded delivery system in which every bead is both an immediate- and an extended-release vehicle—allows an early peak serum drug level and later peak level (at 8 hours). Aptensio is administered by sprinkling the contents of a capsule on applesauce; it is is safe practice, Dr. Feld explained, to augment the ER drug delivery with an immediate-release agent when deemed necessary, by observing how difficult it is for the patient to make it through the day at home, school, or work.

Overview of Autism Spectrum Disorder
Robert L. Hendren, DO, University of California, San Francisco

Comorbidity of Schizophrenia and Substance Abuse
Henry A. Nasrallah, MD, Saint Louis University

Overview of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Bipolar Depression: Presentation, Diagnosis, and Treatment in the Outpatient Psychiatry Practice Setting
Peter J. Weiden, MD, University of Illinois at Chicago

Neuroinflammation and Oxidative Stress in Schizophrenia and Mood Disorders: Biomarkers and Therapeutic Targets
Henry A. Nasrallah, MD, Saint Louis University

Clinical Management of Autism Spectrum Disorders: What Happens Over Time/Borderline Intellectual Functioning
Robert L. Hendren, DO, University of California, San Francisco

Management of PTSD
Carol S. North, MD, MPE, DFAPA, University of Texas Southwestern Medical Center

Saturday, March 12, 2015

Managing the Difficult Child
Anthony L. Rostain, MD, MA, University of Pennsylvania

Major Depression With Subsyndromal Mania/Hypomania: Implications for Diagnosis and Management
Trisha Suppes, MD, PhD, Stanford University School of Medicine, Roger S. McIntyre, MD, FRCPC, University of Toronto, and J. Craig Nelson, MD, University of California, San Francisco

General Overview of Sleep Disorders
Thomas Roth, PhD, Henry Ford Hospital

Comorbid ADHD with Substance Abuse 
Anthony L. Rostain, MD, MA, University of Pennsylvania

How to Treat Patients with Insomnia
Thomas Roth, PhD, Henry Ford Hospital