Among patients with stage III renal cell carcinoma (RCC) by current staging criteria, survival outcomes are worse for those who have pathological nodal involvement, results of a retrospective study suggest.

Survival was significantly shorter for stage III patients with nodal involvement versus those with no involvement, and was “equivalent” to survival in stage IV RCC patients, according to study author Jose A. Karam, MD, of the University of Texas MD Anderson Cancer Center, Houston, and his coauthors.

“If these findings are validated in other studies, consideration should be given to reclassifying patients with stage III, pN1 disease as having stage IV disease,” Dr. Karam and his coauthors wrote in Cancer.

Dr. Karam and his colleagues looked at records for patients with RCC of any histologic subtype who had undergone radical or partial nephrectomy between 1993 and 2012. Their analysis included a total of 389 patients with stage III disease, including 274 with node-positive disease (pT3N0M0) and 115 with node-negative disease (pT123N1M0), along with 523 patients who had stage IV disease.

They found that median overall survival was just 2.4 years (95% confidence interval, 1.7-4.1) for stage III, node-positive disease patients, compared with 10.2 years (95% CI, 8.7-not estimable [NE]) for stage III, node-negative disease and 2.4 years (95% CI, 2.1-3.0) for stage IV disease.

There was a significant difference in overall survival between the three groups, but no significant difference between patients with stage III node-positive disease and stage IV disease, the investigators wrote.

Similarly, median cancer-specific survival was 2.8 years (95% CI, 1.8-4.8) for stage III node-positive disease, not reached (95% CI, 10.2-NE) for stage III node-negative disease, and 2.4 years (95% CI, 2.1-3.0) for stage IV disease, the investigators wrote.

In multivariate analysis, pathological lymph node involvement in the stage III patients was independently associated with worse overall and cancer-specific survival.

Dr. Karam and his coauthors wrote that it may be prudent to revise the current staging system to reclassify node-positive patients if further research confirms their findings. By the current American Joint Committee on Cancer tumor, nodes, and metastases staging manual, patients can be classified as stage III on the basis of either primary tumor status (pT3) or pathological lymph node involvement, they said.

The incidence of pathological, node-positive disease in RCC ranges from 2%-10% in studies, with 5-year survival rates that are “poor” at 5%-30%, the authors noted in their report.

“Even in the targeted therapy era, adjuvant therapy with tyrosine kinase inhibitors does not appear to improve on these outcomes in patients with pN-positive disease,” they wrote.

Funding support for the research came from the National Institutes of Health/National Cancer Institute. Dr. Karam reported serving as a consultant/advisory board member for Pfizer, EMD Serono, Novartis, and Roche/Genentech, and that the MD Anderson Cancer Center has received clinical trial research funding from Roche/Genentech, though none of these disclosures were related to the current report.

SOURCE: Karam JA et al. Cancer. 2018 Oct 1. doi: 10.1002/cncr.31661.

Among patients with stage III renal cell carcinoma (RCC) by current staging criteria, survival outcomes are worse for those who have pathological nodal involvement, results of a retrospective study suggest.

Survival was significantly shorter for stage III patients with nodal involvement versus those with no involvement, and was “equivalent” to survival in stage IV RCC patients, according to study author Jose A. Karam, MD, of the University of Texas MD Anderson Cancer Center, Houston, and his coauthors.

“If these findings are validated in other studies, consideration should be given to reclassifying patients with stage III, pN1 disease as having stage IV disease,” Dr. Karam and his coauthors wrote in Cancer.

Dr. Karam and his colleagues looked at records for patients with RCC of any histologic subtype who had undergone radical or partial nephrectomy between 1993 and 2012. Their analysis included a total of 389 patients with stage III disease, including 274 with node-positive disease (pT3N0M0) and 115 with node-negative disease (pT123N1M0), along with 523 patients who had stage IV disease.

They found that median overall survival was just 2.4 years (95% confidence interval, 1.7-4.1) for stage III, node-positive disease patients, compared with 10.2 years (95% CI, 8.7-not estimable [NE]) for stage III, node-negative disease and 2.4 years (95% CI, 2.1-3.0) for stage IV disease.

There was a significant difference in overall survival between the three groups, but no significant difference between patients with stage III node-positive disease and stage IV disease, the investigators wrote.

Similarly, median cancer-specific survival was 2.8 years (95% CI, 1.8-4.8) for stage III node-positive disease, not reached (95% CI, 10.2-NE) for stage III node-negative disease, and 2.4 years (95% CI, 2.1-3.0) for stage IV disease, the investigators wrote.

In multivariate analysis, pathological lymph node involvement in the stage III patients was independently associated with worse overall and cancer-specific survival.

Dr. Karam and his coauthors wrote that it may be prudent to revise the current staging system to reclassify node-positive patients if further research confirms their findings. By the current American Joint Committee on Cancer tumor, nodes, and metastases staging manual, patients can be classified as stage III on the basis of either primary tumor status (pT3) or pathological lymph node involvement, they said.

The incidence of pathological, node-positive disease in RCC ranges from 2%-10% in studies, with 5-year survival rates that are “poor” at 5%-30%, the authors noted in their report.

“Even in the targeted therapy era, adjuvant therapy with tyrosine kinase inhibitors does not appear to improve on these outcomes in patients with pN-positive disease,” they wrote.

Funding support for the research came from the National Institutes of Health/National Cancer Institute. Dr. Karam reported serving as a consultant/advisory board member for Pfizer, EMD Serono, Novartis, and Roche/Genentech, and that the MD Anderson Cancer Center has received clinical trial research funding from Roche/Genentech, though none of these disclosures were related to the current report.

SOURCE: Karam JA et al. Cancer. 2018 Oct 1. doi: 10.1002/cncr.31661.

Among patients with stage III renal cell carcinoma (RCC) by current staging criteria, survival outcomes are worse for those who have pathological nodal involvement, results of a retrospective study suggest.

Survival was significantly shorter for stage III patients with nodal involvement versus those with no involvement, and was “equivalent” to survival in stage IV RCC patients, according to study author Jose A. Karam, MD, of the University of Texas MD Anderson Cancer Center, Houston, and his coauthors.

“If these findings are validated in other studies, consideration should be given to reclassifying patients with stage III, pN1 disease as having stage IV disease,” Dr. Karam and his coauthors wrote in Cancer.

Dr. Karam and his colleagues looked at records for patients with RCC of any histologic subtype who had undergone radical or partial nephrectomy between 1993 and 2012. Their analysis included a total of 389 patients with stage III disease, including 274 with node-positive disease (pT3N0M0) and 115 with node-negative disease (pT123N1M0), along with 523 patients who had stage IV disease.

They found that median overall survival was just 2.4 years (95% confidence interval, 1.7-4.1) for stage III, node-positive disease patients, compared with 10.2 years (95% CI, 8.7-not estimable [NE]) for stage III, node-negative disease and 2.4 years (95% CI, 2.1-3.0) for stage IV disease.

There was a significant difference in overall survival between the three groups, but no significant difference between patients with stage III node-positive disease and stage IV disease, the investigators wrote.

Similarly, median cancer-specific survival was 2.8 years (95% CI, 1.8-4.8) for stage III node-positive disease, not reached (95% CI, 10.2-NE) for stage III node-negative disease, and 2.4 years (95% CI, 2.1-3.0) for stage IV disease, the investigators wrote.

In multivariate analysis, pathological lymph node involvement in the stage III patients was independently associated with worse overall and cancer-specific survival.

Dr. Karam and his coauthors wrote that it may be prudent to revise the current staging system to reclassify node-positive patients if further research confirms their findings. By the current American Joint Committee on Cancer tumor, nodes, and metastases staging manual, patients can be classified as stage III on the basis of either primary tumor status (pT3) or pathological lymph node involvement, they said.

The incidence of pathological, node-positive disease in RCC ranges from 2%-10% in studies, with 5-year survival rates that are “poor” at 5%-30%, the authors noted in their report.

“Even in the targeted therapy era, adjuvant therapy with tyrosine kinase inhibitors does not appear to improve on these outcomes in patients with pN-positive disease,” they wrote.

Funding support for the research came from the National Institutes of Health/National Cancer Institute. Dr. Karam reported serving as a consultant/advisory board member for Pfizer, EMD Serono, Novartis, and Roche/Genentech, and that the MD Anderson Cancer Center has received clinical trial research funding from Roche/Genentech, though none of these disclosures were related to the current report.

SOURCE: Karam JA et al. Cancer. 2018 Oct 1. doi: 10.1002/cncr.31661.

Lichen nitidus, which literally means “shiny moss,” is a relatively rare, chronic skin eruption that is characterized clinically by asymptomatic, flat-topped, sharply-demarcated, skin-colored papules, which are sometimes described as being “pinpoint.”

Lichen nitidus mainly affects children and young adults. The most common sites of involvement are the trunk, flexor aspects of upper extremities, dorsal aspects of hands, and genitalia, but lesions can occur anywhere on the skin. The lesions also can develop in sites of trauma (Koebner phenomenon), and this can be a significant clinical clue to aid in the diagnosis of lichen nitidus in favor of other conditions which may present as many small papules.¹ Nail changes can occur but are rare, presenting as dystrophy, pitting, riding, or loss of nail(s).²

Lichen nitidus can be a challenging diagnosis to make, especially if a practitioner is not used to seeing it. Many dermatologic conditions present with many fine papules, including the other answer choices in the given quiz question (molluscum contagiosum, keratosis pilaris, verruca vulgaris, papular eczema). What allows for a clearer diagnosis of lichen nitidus is the history provided by the patient as well as the exam. Lichen nitidus lesions typically arise without a known trigger and often persist for months while remaining asymptomatic.

Molluscum contagiosum tends to include papules that are larger and more substantial than lichen nitidus papules and may be accompanied by background hyperpigmentation or erythema, known as the “beginning of the end” sign. Keratosis pilaris is commonly thought of as a skin type more so than a skin condition, and is more commonly seen in fair-skinned individuals along the lateral arms and cheeks. It is commonly paired with a background of erythema and skin than tends to be more xerotic. Verruca are typically larger lesions, sometimes with a rough surface, and are not typically shiny. Verruca are more likely to present as a single lesion or a few lesions at a given location, as opposed to lichen nitidus which has many individual papules at a single location. Papular eczema typically is intensely pruritic and is associated with xerosis and atopy.

The cause of lichen nitidus is unknown, and there are no reported genetic factors that contribute to its presentation.³ It is thought to be a subtype of lichen planus, although this is still debated. There is more work that needs to be done to find answers to these questions and to assess what triggers these fine papules to present and in whom.

The dermatoscopic features of lichen nitidus were reported in a series of eight cases and include absent dermatoglyphics, radial ridges, ill-defined hypopigmentation, diffuse erythema, linear vessels within the lesion, and peripheral scaling.⁴ These features are distinctive in combination and can in some cases be used to clinically diagnose lichen nitidus without the need for a skin biopsy, which is an invasive procedure that should be avoided when possible, especially given the benign nature of lichen nitidus.

If a biopsy is performed, the histologic features that commonly are seen include well-circumscribed granuloma-like lymphohistiocytic infiltrates in the papillary dermis adjacent to ridges, mimicking a “ball-and-claw” formation.^1,5

Lichen nitidus generally is self-limiting, with minimal cosmetic disruption; therefore, treatment usually is not necessary. The lesions typically resolve within 1 year of presentation – and often sooner. Topical steroids can be used for symptomatic relief of pruritus, but generally do not hasten resolution of the papules themselves. Additionally, there have been reports in the literature of the successful resolution of lesions using topical calcineurin inhibitors and UVB therapy.

In a case report of an 8-year-old child with histologically confirmed lichen nitidus that had been present for 2 years, pimecrolimus 1% cream was used twice daily for 2 months with improvement and flattening of the papules.⁶ This report is compelling because the lesions persisted for twice the expected time of resolution without improvement and then showed relatively quick response to pimecrolimus. In a case of a 32-year-old male with lichen nitidus on his penis, tacrolimus 0.1% was used for 4 weeks with resolution of the papules.⁷ Although given that lichen nitidus can self-resolve in this same time period, it is unclear in this case whether the tacrolimus was the independent cause of the resolution.

With regard to UVB therapy, there have been reports of lichen nitidus resolution after 17-30 irradiation sessions in patients with lesions present for 3-6 months, although again, it is possible that the resolution observed was simply the natural course of the lichen nitidus for these patients rather than a therapeutic benefit of UVB therapy.^8,9

Given that lichen nitidus is benign and typically asymptomatic or with mild pruritus, it is reasonable to monitor the lesions without treating them. If the lesions persist beyond 1 year, it also is reasonable to trial therapies, such as topical calcineurin inhibitors and UVB therapy, although using these treatments earlier in the disease course has only limited supporting data and any improvement seen within 1 year of onset may be attributed to the natural disease course as opposed to an effect of the intervention. Considerations of the cost of therapy, as well as the degree to which the patient is bothered by the lesions and how long the lesions have persisted, should be undertaken when considering whether an intervention should be made.
 

Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Ms. Natsis or Dr. Eichenfield. Email them at [email protected].

References

1. Cutis. 1999 Aug 1;64(2):135-6.

2. J Am Acad Dermatol. 2004 Oct;51(4):606-24.

3. Papulosquamous diseases, in “Pediatric Dermatology,” 4th ed. (St Louis: Mosby; 2011, Vol. 2.

4. Pediatr Dermatol. 2018. doi: 10.1111/pde.13576.

5. Cutis. 2013 Dec;92(6):288, 297-8.

6. Dermatol Online J. 2011 Jul 15;17(7):11.

7. J Drugs Dermatol. 2004 Nov-Dec;3(6):683-4.

8. Int J Dermatol. 2004 Dec 23;45:615-7.

9. Photodermatol Photoimmunol Photomed. 2013 Aug;29(4):215-7.

Lichen nitidus, which literally means “shiny moss,” is a relatively rare, chronic skin eruption that is characterized clinically by asymptomatic, flat-topped, sharply-demarcated, skin-colored papules, which are sometimes described as being “pinpoint.”

Lichen nitidus mainly affects children and young adults. The most common sites of involvement are the trunk, flexor aspects of upper extremities, dorsal aspects of hands, and genitalia, but lesions can occur anywhere on the skin. The lesions also can develop in sites of trauma (Koebner phenomenon), and this can be a significant clinical clue to aid in the diagnosis of lichen nitidus in favor of other conditions which may present as many small papules.¹ Nail changes can occur but are rare, presenting as dystrophy, pitting, riding, or loss of nail(s).²

Lichen nitidus can be a challenging diagnosis to make, especially if a practitioner is not used to seeing it. Many dermatologic conditions present with many fine papules, including the other answer choices in the given quiz question (molluscum contagiosum, keratosis pilaris, verruca vulgaris, papular eczema). What allows for a clearer diagnosis of lichen nitidus is the history provided by the patient as well as the exam. Lichen nitidus lesions typically arise without a known trigger and often persist for months while remaining asymptomatic.

Molluscum contagiosum tends to include papules that are larger and more substantial than lichen nitidus papules and may be accompanied by background hyperpigmentation or erythema, known as the “beginning of the end” sign. Keratosis pilaris is commonly thought of as a skin type more so than a skin condition, and is more commonly seen in fair-skinned individuals along the lateral arms and cheeks. It is commonly paired with a background of erythema and skin than tends to be more xerotic. Verruca are typically larger lesions, sometimes with a rough surface, and are not typically shiny. Verruca are more likely to present as a single lesion or a few lesions at a given location, as opposed to lichen nitidus which has many individual papules at a single location. Papular eczema typically is intensely pruritic and is associated with xerosis and atopy.

The cause of lichen nitidus is unknown, and there are no reported genetic factors that contribute to its presentation.³ It is thought to be a subtype of lichen planus, although this is still debated. There is more work that needs to be done to find answers to these questions and to assess what triggers these fine papules to present and in whom.

The dermatoscopic features of lichen nitidus were reported in a series of eight cases and include absent dermatoglyphics, radial ridges, ill-defined hypopigmentation, diffuse erythema, linear vessels within the lesion, and peripheral scaling.⁴ These features are distinctive in combination and can in some cases be used to clinically diagnose lichen nitidus without the need for a skin biopsy, which is an invasive procedure that should be avoided when possible, especially given the benign nature of lichen nitidus.

If a biopsy is performed, the histologic features that commonly are seen include well-circumscribed granuloma-like lymphohistiocytic infiltrates in the papillary dermis adjacent to ridges, mimicking a “ball-and-claw” formation.^1,5

Lichen nitidus generally is self-limiting, with minimal cosmetic disruption; therefore, treatment usually is not necessary. The lesions typically resolve within 1 year of presentation – and often sooner. Topical steroids can be used for symptomatic relief of pruritus, but generally do not hasten resolution of the papules themselves. Additionally, there have been reports in the literature of the successful resolution of lesions using topical calcineurin inhibitors and UVB therapy.

In a case report of an 8-year-old child with histologically confirmed lichen nitidus that had been present for 2 years, pimecrolimus 1% cream was used twice daily for 2 months with improvement and flattening of the papules.⁶ This report is compelling because the lesions persisted for twice the expected time of resolution without improvement and then showed relatively quick response to pimecrolimus. In a case of a 32-year-old male with lichen nitidus on his penis, tacrolimus 0.1% was used for 4 weeks with resolution of the papules.⁷ Although given that lichen nitidus can self-resolve in this same time period, it is unclear in this case whether the tacrolimus was the independent cause of the resolution.

With regard to UVB therapy, there have been reports of lichen nitidus resolution after 17-30 irradiation sessions in patients with lesions present for 3-6 months, although again, it is possible that the resolution observed was simply the natural course of the lichen nitidus for these patients rather than a therapeutic benefit of UVB therapy.^8,9

Given that lichen nitidus is benign and typically asymptomatic or with mild pruritus, it is reasonable to monitor the lesions without treating them. If the lesions persist beyond 1 year, it also is reasonable to trial therapies, such as topical calcineurin inhibitors and UVB therapy, although using these treatments earlier in the disease course has only limited supporting data and any improvement seen within 1 year of onset may be attributed to the natural disease course as opposed to an effect of the intervention. Considerations of the cost of therapy, as well as the degree to which the patient is bothered by the lesions and how long the lesions have persisted, should be undertaken when considering whether an intervention should be made.
 

Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Ms. Natsis or Dr. Eichenfield. Email them at [email protected].

References

1. Cutis. 1999 Aug 1;64(2):135-6.

2. J Am Acad Dermatol. 2004 Oct;51(4):606-24.

3. Papulosquamous diseases, in “Pediatric Dermatology,” 4th ed. (St Louis: Mosby; 2011, Vol. 2.

4. Pediatr Dermatol. 2018. doi: 10.1111/pde.13576.

5. Cutis. 2013 Dec;92(6):288, 297-8.

6. Dermatol Online J. 2011 Jul 15;17(7):11.

7. J Drugs Dermatol. 2004 Nov-Dec;3(6):683-4.

8. Int J Dermatol. 2004 Dec 23;45:615-7.

9. Photodermatol Photoimmunol Photomed. 2013 Aug;29(4):215-7.

Lichen nitidus, which literally means “shiny moss,” is a relatively rare, chronic skin eruption that is characterized clinically by asymptomatic, flat-topped, sharply-demarcated, skin-colored papules, which are sometimes described as being “pinpoint.”

Lichen nitidus mainly affects children and young adults. The most common sites of involvement are the trunk, flexor aspects of upper extremities, dorsal aspects of hands, and genitalia, but lesions can occur anywhere on the skin. The lesions also can develop in sites of trauma (Koebner phenomenon), and this can be a significant clinical clue to aid in the diagnosis of lichen nitidus in favor of other conditions which may present as many small papules.¹ Nail changes can occur but are rare, presenting as dystrophy, pitting, riding, or loss of nail(s).²

Lichen nitidus can be a challenging diagnosis to make, especially if a practitioner is not used to seeing it. Many dermatologic conditions present with many fine papules, including the other answer choices in the given quiz question (molluscum contagiosum, keratosis pilaris, verruca vulgaris, papular eczema). What allows for a clearer diagnosis of lichen nitidus is the history provided by the patient as well as the exam. Lichen nitidus lesions typically arise without a known trigger and often persist for months while remaining asymptomatic.

Molluscum contagiosum tends to include papules that are larger and more substantial than lichen nitidus papules and may be accompanied by background hyperpigmentation or erythema, known as the “beginning of the end” sign. Keratosis pilaris is commonly thought of as a skin type more so than a skin condition, and is more commonly seen in fair-skinned individuals along the lateral arms and cheeks. It is commonly paired with a background of erythema and skin than tends to be more xerotic. Verruca are typically larger lesions, sometimes with a rough surface, and are not typically shiny. Verruca are more likely to present as a single lesion or a few lesions at a given location, as opposed to lichen nitidus which has many individual papules at a single location. Papular eczema typically is intensely pruritic and is associated with xerosis and atopy.

The cause of lichen nitidus is unknown, and there are no reported genetic factors that contribute to its presentation.³ It is thought to be a subtype of lichen planus, although this is still debated. There is more work that needs to be done to find answers to these questions and to assess what triggers these fine papules to present and in whom.

The dermatoscopic features of lichen nitidus were reported in a series of eight cases and include absent dermatoglyphics, radial ridges, ill-defined hypopigmentation, diffuse erythema, linear vessels within the lesion, and peripheral scaling.⁴ These features are distinctive in combination and can in some cases be used to clinically diagnose lichen nitidus without the need for a skin biopsy, which is an invasive procedure that should be avoided when possible, especially given the benign nature of lichen nitidus.

If a biopsy is performed, the histologic features that commonly are seen include well-circumscribed granuloma-like lymphohistiocytic infiltrates in the papillary dermis adjacent to ridges, mimicking a “ball-and-claw” formation.^1,5

Lichen nitidus generally is self-limiting, with minimal cosmetic disruption; therefore, treatment usually is not necessary. The lesions typically resolve within 1 year of presentation – and often sooner. Topical steroids can be used for symptomatic relief of pruritus, but generally do not hasten resolution of the papules themselves. Additionally, there have been reports in the literature of the successful resolution of lesions using topical calcineurin inhibitors and UVB therapy.

In a case report of an 8-year-old child with histologically confirmed lichen nitidus that had been present for 2 years, pimecrolimus 1% cream was used twice daily for 2 months with improvement and flattening of the papules.⁶ This report is compelling because the lesions persisted for twice the expected time of resolution without improvement and then showed relatively quick response to pimecrolimus. In a case of a 32-year-old male with lichen nitidus on his penis, tacrolimus 0.1% was used for 4 weeks with resolution of the papules.⁷ Although given that lichen nitidus can self-resolve in this same time period, it is unclear in this case whether the tacrolimus was the independent cause of the resolution.

With regard to UVB therapy, there have been reports of lichen nitidus resolution after 17-30 irradiation sessions in patients with lesions present for 3-6 months, although again, it is possible that the resolution observed was simply the natural course of the lichen nitidus for these patients rather than a therapeutic benefit of UVB therapy.^8,9

Given that lichen nitidus is benign and typically asymptomatic or with mild pruritus, it is reasonable to monitor the lesions without treating them. If the lesions persist beyond 1 year, it also is reasonable to trial therapies, such as topical calcineurin inhibitors and UVB therapy, although using these treatments earlier in the disease course has only limited supporting data and any improvement seen within 1 year of onset may be attributed to the natural disease course as opposed to an effect of the intervention. Considerations of the cost of therapy, as well as the degree to which the patient is bothered by the lesions and how long the lesions have persisted, should be undertaken when considering whether an intervention should be made.
 

Ms. Natsis is a medical student at the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. There are no conflicts of interest or financial disclosures for Ms. Natsis or Dr. Eichenfield. Email them at [email protected].

References

1. Cutis. 1999 Aug 1;64(2):135-6.

2. J Am Acad Dermatol. 2004 Oct;51(4):606-24.

3. Papulosquamous diseases, in “Pediatric Dermatology,” 4th ed. (St Louis: Mosby; 2011, Vol. 2.

4. Pediatr Dermatol. 2018. doi: 10.1111/pde.13576.

5. Cutis. 2013 Dec;92(6):288, 297-8.

6. Dermatol Online J. 2011 Jul 15;17(7):11.

7. J Drugs Dermatol. 2004 Nov-Dec;3(6):683-4.

8. Int J Dermatol. 2004 Dec 23;45:615-7.

9. Photodermatol Photoimmunol Photomed. 2013 Aug;29(4):215-7.

People using the federal healthcare.gov marketplace to buy health insurance in 2019 will see lower premiums for silver plans, the second-lowest cost option – the first such decline since the marketplace’s start in 2014 under the Affordable Care Act.

Mary Ellen Schneider/MDedge News

The Centers for Medicare & Medicaid Services reported that premiums will drop 1.5% on average, after an average increase of 25.4% in 2017 and an increase of 36.9% in 2018.

Tennessee saw the greatest reduction for the 2019 plan year, dropping 26.2%. North Dakota was at the opposite end, seeing premiums increase by 20.2%. CMS provided a state-by-state breakdown of premium changes for states in the federally facilitated marketplace.

CMS Administrator Seema Verma credits the decline to market stabilization actions taken by the agency.

“Despite predictions that our actions would increase rates and destabilize the markets, the opposite has happened,” she said in a statement. “The drop in benchmark plan premiums for plan year 2019 and the increased choices for Americans seeking insurance on the exchanges is proof positive that our actions are working.”

While the agency is “encouraged by this progress, we aren’t satisfied,” Ms. Verma added. “Even with this reduction, average rates are still too high. If we are going to truly offer affordable, high-quality health care, ultimately, the law needs to change.”

Some experts, however, were quick to dismiss Ms. Verma’s assertions that federal government action caused the decline.

In fact, the trend is more of a market correction, said Sara Collins, PhD, vice president of health coverage and access at the Commonwealth Fund, New York. It follows 2 years of premium increases by insurers anticipating government actions to intentionally destabilize the market.

“We saw a correction in premiums in 2017, which reflected the phase-out of the reinsurance program, so insurers adjusted their premiums to reflect that,” Dr. Collins said. “Also, insurers are getting to know their risk pools better. So, the prediction was that the markets would stabilize in the out-years of implementation.”

The individual market “is weathering very well the attempts by the Trump administration and Congress over the past year to weaken it,” Dr. Collins added. Those include repealing the individual mandate penalties, ending federal cost-sharing reduction payments, and promoting the sale of short-term, limited-duration health policies.

Efforts at the state level also have been helpful in stabilizing the marketplace, she noted, particularly in those states that implemented reinsurance plans. CMS noted its role in approving reinsurance waivers in seven states as a reason for the overall decline.

Matthew Fiedler, PhD, a fellow at the Brookings Institution, Washington, concurred that the reduction was more of a market correction than anything else.

It “is not that the repeal of the individual mandate and various other policy changes implemented by the administration haven’t hurt rates,” he said. “It’s that rates were far higher than they needed to be in 2018. Even with the headwind of those policy games, rates are declining this year. Without those policy changes, rates would be declining by more in 2018.”

[email protected]

People using the federal healthcare.gov marketplace to buy health insurance in 2019 will see lower premiums for silver plans, the second-lowest cost option – the first such decline since the marketplace’s start in 2014 under the Affordable Care Act.

Mary Ellen Schneider/MDedge News

The Centers for Medicare & Medicaid Services reported that premiums will drop 1.5% on average, after an average increase of 25.4% in 2017 and an increase of 36.9% in 2018.

Tennessee saw the greatest reduction for the 2019 plan year, dropping 26.2%. North Dakota was at the opposite end, seeing premiums increase by 20.2%. CMS provided a state-by-state breakdown of premium changes for states in the federally facilitated marketplace.

CMS Administrator Seema Verma credits the decline to market stabilization actions taken by the agency.

“Despite predictions that our actions would increase rates and destabilize the markets, the opposite has happened,” she said in a statement. “The drop in benchmark plan premiums for plan year 2019 and the increased choices for Americans seeking insurance on the exchanges is proof positive that our actions are working.”

While the agency is “encouraged by this progress, we aren’t satisfied,” Ms. Verma added. “Even with this reduction, average rates are still too high. If we are going to truly offer affordable, high-quality health care, ultimately, the law needs to change.”

Some experts, however, were quick to dismiss Ms. Verma’s assertions that federal government action caused the decline.

In fact, the trend is more of a market correction, said Sara Collins, PhD, vice president of health coverage and access at the Commonwealth Fund, New York. It follows 2 years of premium increases by insurers anticipating government actions to intentionally destabilize the market.

“We saw a correction in premiums in 2017, which reflected the phase-out of the reinsurance program, so insurers adjusted their premiums to reflect that,” Dr. Collins said. “Also, insurers are getting to know their risk pools better. So, the prediction was that the markets would stabilize in the out-years of implementation.”

The individual market “is weathering very well the attempts by the Trump administration and Congress over the past year to weaken it,” Dr. Collins added. Those include repealing the individual mandate penalties, ending federal cost-sharing reduction payments, and promoting the sale of short-term, limited-duration health policies.

Efforts at the state level also have been helpful in stabilizing the marketplace, she noted, particularly in those states that implemented reinsurance plans. CMS noted its role in approving reinsurance waivers in seven states as a reason for the overall decline.

Matthew Fiedler, PhD, a fellow at the Brookings Institution, Washington, concurred that the reduction was more of a market correction than anything else.

It “is not that the repeal of the individual mandate and various other policy changes implemented by the administration haven’t hurt rates,” he said. “It’s that rates were far higher than they needed to be in 2018. Even with the headwind of those policy games, rates are declining this year. Without those policy changes, rates would be declining by more in 2018.”

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People using the federal healthcare.gov marketplace to buy health insurance in 2019 will see lower premiums for silver plans, the second-lowest cost option – the first such decline since the marketplace’s start in 2014 under the Affordable Care Act.

Mary Ellen Schneider/MDedge News

The Centers for Medicare & Medicaid Services reported that premiums will drop 1.5% on average, after an average increase of 25.4% in 2017 and an increase of 36.9% in 2018.

Tennessee saw the greatest reduction for the 2019 plan year, dropping 26.2%. North Dakota was at the opposite end, seeing premiums increase by 20.2%. CMS provided a state-by-state breakdown of premium changes for states in the federally facilitated marketplace.

CMS Administrator Seema Verma credits the decline to market stabilization actions taken by the agency.

“Despite predictions that our actions would increase rates and destabilize the markets, the opposite has happened,” she said in a statement. “The drop in benchmark plan premiums for plan year 2019 and the increased choices for Americans seeking insurance on the exchanges is proof positive that our actions are working.”

While the agency is “encouraged by this progress, we aren’t satisfied,” Ms. Verma added. “Even with this reduction, average rates are still too high. If we are going to truly offer affordable, high-quality health care, ultimately, the law needs to change.”

Some experts, however, were quick to dismiss Ms. Verma’s assertions that federal government action caused the decline.

In fact, the trend is more of a market correction, said Sara Collins, PhD, vice president of health coverage and access at the Commonwealth Fund, New York. It follows 2 years of premium increases by insurers anticipating government actions to intentionally destabilize the market.

“We saw a correction in premiums in 2017, which reflected the phase-out of the reinsurance program, so insurers adjusted their premiums to reflect that,” Dr. Collins said. “Also, insurers are getting to know their risk pools better. So, the prediction was that the markets would stabilize in the out-years of implementation.”

The individual market “is weathering very well the attempts by the Trump administration and Congress over the past year to weaken it,” Dr. Collins added. Those include repealing the individual mandate penalties, ending federal cost-sharing reduction payments, and promoting the sale of short-term, limited-duration health policies.

Efforts at the state level also have been helpful in stabilizing the marketplace, she noted, particularly in those states that implemented reinsurance plans. CMS noted its role in approving reinsurance waivers in seven states as a reason for the overall decline.

Matthew Fiedler, PhD, a fellow at the Brookings Institution, Washington, concurred that the reduction was more of a market correction than anything else.

It “is not that the repeal of the individual mandate and various other policy changes implemented by the administration haven’t hurt rates,” he said. “It’s that rates were far higher than they needed to be in 2018. Even with the headwind of those policy games, rates are declining this year. Without those policy changes, rates would be declining by more in 2018.”

[email protected]

“The Campus Cure: A Parent’s Guide to Mental Health and Wellness for College Students” (Lanham, Md.: Rowman & Littlefield Publishers, 2018) is written as a first-aid guide for parents of young people struggling with the mental health issues facing college students today. The importance of parents working collaboratively with the student/patient and the health care team is stressed throughout; Dr. Marcia Morris draws upon the medical literature and more than 20 years’ experience as a psychiatrist at the University of Florida, Gainesville, to provide clear guidance on a key theme: The continued support and involvement of caring parents in a young adult’s life can be crucial to her college success.

The book is well organized with separate chapters containing easy-to-understand explanations of the causes and treatments of common problems (anxiety, depression, substance use, academic failure to thrive), pressures (loneliness, perfectionism, financial stress, and culture/sexuality/gender issues), and crises (suicide, sexual assault, eating disorders, psychosis) affecting students today. Helpful background information about medications, resources for obtaining help on campuses, and legal issues about confidentiality is provided where appropriate. Each section is brought to life with vignettes of typical patients seen in the college mental health setting. Questions that ask the reader how they would respond in the situation illustrated are used effectively and encourage the reader to think through the information presented and retain what they have learned. Helpful summary lists of “tips” close most chapters.

In her introduction, Dr. Morris stresses that this book is not just for parents but also for family and friends who may find themselves in the role of being the caring adult in a student’s life. She encourages parents to read the whole book, even those chapters they may not think will apply to their child, explaining how common difficulties are in this age group and how important it is to know how to respond when an issue may arise.

Although this is good advice, I suspect that many parents without specific concerns are unlikely to proactively choose to read this book. Concerned parents who do pick this volume up “just in case” will find specific strategies for effective and helpful communication with their child and with professionals as well as stories of reassuring good outcomes from parental involvement. Dr. Morris recommends that parents ask their child to obtain access for the parents to the student’s grades and grant permission for parents to communicate with mental health care providers and school administration. However, she does not offer much guidance for the parent of the child who never signs the required forms to allow access to this information – and is generally not communicative with the parents.

Parents of a teenager who receives treatment (even prior to college) certainly should be encouraged to read this book. I also would recommend this book for many others working with young adults (even if they are not in college settings) for example, health care professionals without mental health training, educators, psychotherapist trainees, and mentors. Along with parents, they will find “The Campus Cure” to be a great resource for understanding and dealing with the mental health challenges of young adulthood.

Dr. Holland is board certified in child/adolescent and adult psychiatry. She is based in Boca Raton, Fla., where she is an affiliate assistant professor at Florida Atlantic University’s Schmidt College of Medicine. Click here to listen to a recent MDedge Psychcast interview with Dr. Morris about the prevalence of binge drinking on college campuses – and steps psychiatrists and other therapists can take to mitigate risk.

“The Campus Cure: A Parent’s Guide to Mental Health and Wellness for College Students” (Lanham, Md.: Rowman & Littlefield Publishers, 2018) is written as a first-aid guide for parents of young people struggling with the mental health issues facing college students today. The importance of parents working collaboratively with the student/patient and the health care team is stressed throughout; Dr. Marcia Morris draws upon the medical literature and more than 20 years’ experience as a psychiatrist at the University of Florida, Gainesville, to provide clear guidance on a key theme: The continued support and involvement of caring parents in a young adult’s life can be crucial to her college success.

The book is well organized with separate chapters containing easy-to-understand explanations of the causes and treatments of common problems (anxiety, depression, substance use, academic failure to thrive), pressures (loneliness, perfectionism, financial stress, and culture/sexuality/gender issues), and crises (suicide, sexual assault, eating disorders, psychosis) affecting students today. Helpful background information about medications, resources for obtaining help on campuses, and legal issues about confidentiality is provided where appropriate. Each section is brought to life with vignettes of typical patients seen in the college mental health setting. Questions that ask the reader how they would respond in the situation illustrated are used effectively and encourage the reader to think through the information presented and retain what they have learned. Helpful summary lists of “tips” close most chapters.

In her introduction, Dr. Morris stresses that this book is not just for parents but also for family and friends who may find themselves in the role of being the caring adult in a student’s life. She encourages parents to read the whole book, even those chapters they may not think will apply to their child, explaining how common difficulties are in this age group and how important it is to know how to respond when an issue may arise.

Although this is good advice, I suspect that many parents without specific concerns are unlikely to proactively choose to read this book. Concerned parents who do pick this volume up “just in case” will find specific strategies for effective and helpful communication with their child and with professionals as well as stories of reassuring good outcomes from parental involvement. Dr. Morris recommends that parents ask their child to obtain access for the parents to the student’s grades and grant permission for parents to communicate with mental health care providers and school administration. However, she does not offer much guidance for the parent of the child who never signs the required forms to allow access to this information – and is generally not communicative with the parents.

Parents of a teenager who receives treatment (even prior to college) certainly should be encouraged to read this book. I also would recommend this book for many others working with young adults (even if they are not in college settings) for example, health care professionals without mental health training, educators, psychotherapist trainees, and mentors. Along with parents, they will find “The Campus Cure” to be a great resource for understanding and dealing with the mental health challenges of young adulthood.

Dr. Holland is board certified in child/adolescent and adult psychiatry. She is based in Boca Raton, Fla., where she is an affiliate assistant professor at Florida Atlantic University’s Schmidt College of Medicine. Click here to listen to a recent MDedge Psychcast interview with Dr. Morris about the prevalence of binge drinking on college campuses – and steps psychiatrists and other therapists can take to mitigate risk.

“The Campus Cure: A Parent’s Guide to Mental Health and Wellness for College Students” (Lanham, Md.: Rowman & Littlefield Publishers, 2018) is written as a first-aid guide for parents of young people struggling with the mental health issues facing college students today. The importance of parents working collaboratively with the student/patient and the health care team is stressed throughout; Dr. Marcia Morris draws upon the medical literature and more than 20 years’ experience as a psychiatrist at the University of Florida, Gainesville, to provide clear guidance on a key theme: The continued support and involvement of caring parents in a young adult’s life can be crucial to her college success.

The book is well organized with separate chapters containing easy-to-understand explanations of the causes and treatments of common problems (anxiety, depression, substance use, academic failure to thrive), pressures (loneliness, perfectionism, financial stress, and culture/sexuality/gender issues), and crises (suicide, sexual assault, eating disorders, psychosis) affecting students today. Helpful background information about medications, resources for obtaining help on campuses, and legal issues about confidentiality is provided where appropriate. Each section is brought to life with vignettes of typical patients seen in the college mental health setting. Questions that ask the reader how they would respond in the situation illustrated are used effectively and encourage the reader to think through the information presented and retain what they have learned. Helpful summary lists of “tips” close most chapters.

In her introduction, Dr. Morris stresses that this book is not just for parents but also for family and friends who may find themselves in the role of being the caring adult in a student’s life. She encourages parents to read the whole book, even those chapters they may not think will apply to their child, explaining how common difficulties are in this age group and how important it is to know how to respond when an issue may arise.

Although this is good advice, I suspect that many parents without specific concerns are unlikely to proactively choose to read this book. Concerned parents who do pick this volume up “just in case” will find specific strategies for effective and helpful communication with their child and with professionals as well as stories of reassuring good outcomes from parental involvement. Dr. Morris recommends that parents ask their child to obtain access for the parents to the student’s grades and grant permission for parents to communicate with mental health care providers and school administration. However, she does not offer much guidance for the parent of the child who never signs the required forms to allow access to this information – and is generally not communicative with the parents.

Parents of a teenager who receives treatment (even prior to college) certainly should be encouraged to read this book. I also would recommend this book for many others working with young adults (even if they are not in college settings) for example, health care professionals without mental health training, educators, psychotherapist trainees, and mentors. Along with parents, they will find “The Campus Cure” to be a great resource for understanding and dealing with the mental health challenges of young adulthood.

Dr. Holland is board certified in child/adolescent and adult psychiatry. She is based in Boca Raton, Fla., where she is an affiliate assistant professor at Florida Atlantic University’s Schmidt College of Medicine. Click here to listen to a recent MDedge Psychcast interview with Dr. Morris about the prevalence of binge drinking on college campuses – and steps psychiatrists and other therapists can take to mitigate risk.

Oncologists are raising concerns about care access after the launch of a new company that links patients to cancer care options and clinical trials through mobile technology.

Driver, which began in September in the U.S. and China, is a global technology platform that allows patients to access treatment options across a broad network of cancer centers without leaving home. Cancer patients join the platform using a mobile app, through which Driver obtains the required consent to acquire medical records and tumor samples, and the company uses the information to recommend treatment options and clinical trials.

ljubaphoto/Getty Images

A separate app called Driver for Clinic enables oncologists who belong to Driver’s partner hospitals to manage their institution’s clinical trial information and quickly filter that information based on patients’ medical history to determine the patient’s eligibility for treatments.

Driver’s mission is to connect more patients to the best cancer treatments, regardless of location, said Will Polkinghorn, MD, Driver cofounder and CEO.

“Driver’s cofounders met at Harvard Medical School [in Boston] and saw firsthand the challenges of patients getting access to the latest, cutting-edge treatments available,” Dr. Polkinghorn said in an interview. “As doctors, [we] also witnessed how difficult it was for doctors to manage information in clinic and know about all the treatments that become available all around the world. Driver was created as a platform, with an app for the patient and an app for the doctor, to solve this broken marketplace.”

As part of the model, patients can review their recommended treatment options through video with an expert oncologist and select a hospital within Driver’s network for further evaluation. The company’s global network includes more than 30 leading U.S. cancer centers, including the Cleveland Clinic; multiple locations of the Mayo Clinic; the University of California, San Francisco; and Massachusetts General Hospital, Boston. The U.S. National Cancer Institute (NCI) and the Chinese National Cancer Center are founding members of Driver’s global network, according to the company.

Making more information and treatment options available is a positive for patients, said Walter Stadler, MD, chief of hematology/oncology and director of the genitourinary oncology program at the University of Chicago. However, he noted that the cost for patients to use Driver is prohibitive for many patients. Driver charges patients $3,000 up front and then a $20 monthly fee to use its service. Insurance does not subsidize the cost, nor does Driver help with travel or treatment costs, according to its website.

“It’s inequality of access,” Dr. Stadler said in an interview. “Many of us are very concerned that the clinical trials currently being conducted do not represent the general population well because they don’t represent patients with disparities … Here, we further exacerbate the problem by saying, ‘Okay, we’ll take the 5% of patients who can afford the service and expand their access, and the others, well, that’s not our problem.’ ”

“Access to clinical trials for patients residing in rural areas, as well as those getting their treatment in community based clinics, would not change,” Dr. Patel said in an interview. “Hence, challenges of social and demographic disparities and inequalities in clinical trial access and participation would be altered minimally. There is much greater need for such [platforms to include] community cancer clinics that would be more inclusive and encompass larger geographic areas where the majority of patients receive their care.”

Disadvantaged populations with limited access are not being overlooked by the company, according to Driver leaders. A branch of the company called Driver for All aims to increase access to optimal treatments for free through partnerships with local communities, Dr. Polkinghorn said. Driver for All has thus far partnered with Howard University Hospital in Washington to connect Howard patients to clinical trials at NCI. A partnership with Beijing Children’s Hospital and the Futang Research Center of Pediatric Development, meanwhile, is working to connect patients with rare-disease experts. Driver has funded 100% of the cost of these projects to date, according to its website.

Outside of Driver for All, Dr. Polkinghorn acknowledges that patients must bear the cost of Driver’s consumer products; however, the price should be viewed in context, he said.

“It’s important to remember that today, in order to be evaluated by 30 [plus] centers for treatment options, patients would need to fly to these centers, make appointments, and be seen by a doctor – this would require both time and resources for flights/hotels, which would cost much more than our sticker price,” he said. “So while $3,000 is a lot of money for some patients, Driver’s product is ultimately able to provide more visibility to options that simply would not be realistic today.”

James Gulley, MD, of the National Cancer Institute Center for Cancer Research, said any platform that can efficiently provide access to clinical trial options yields another source of information for patients to utilize in decision making with their health provider. Dr. Gulley, who heads the center’s genitourinary malignancies branch, declined to comment about access-to-care concerns with Driver’s model. He emphasized that patients who participate in NIH research studies are treated without charge.

“The key to finding better [cancer] treatment is to perform science-driven clinical trials,” Dr. Gulley said in an interview. “However, there are many barriers for enrollment in clinical trials. … As a government agency, NCI is open to partnering with any organization that seeks to improve access to clinical trials for cancer patients.”

NCI and Driver recently conducted a study to validate Driver’s platform; it showed that Driver’s technology successfully predicted the eligibility of patients in NCI Center for Cancer Research clinical trials. The study, presented at a recent American Society of Clinical Oncology meeting, evaluated Driver’s processing of 21 metastatic prostate cancer patients enrolled in a therapeutic NCI clinical trial within the last five years. Results showed Driver correctly predicted that 20 of the patients were “potentially eligible” for the trial in which they were enrolled, and that one was ineligible. Based on the study, a protocol is now in development for a new clinical study, which will seek to further determine the efficiency and accuracy of the clinical trial access program created by Driver, according to Dr. Gulley.

“We need breakthrough technologies and opportunities for patients to be able to access the most successful and promising cancer treatments, regardless of where they live,” Dr. Ryan said in an interview. “Companies like Driver are attempting to bridge that gap by connecting patients to doctors at world class cancer institutes and direct them toward the best care for their particular condition.”

Driver’s model also allows researchers the opportunity to develop specific, unique treatment for less common cancers and remain optimistic that they can attract patients to receive such treatments as they are developed, Dr. Ryan said.

Dr. Stadler, however, worries that Driver may be giving patients the wrong perception that all it takes is a computer and medical records to determine their best treatment route.

“There’s a lot more subtlety to treatment decisions than most people would like to admit,” Dr. Stadler said. “It’s more than just a bunch of data from sophisticated laboratory tests and the written medical record. Obtaining objective information is the first step, but it’s far from the only step.”

Patients may have significant limitations in functional status that is apparent only during an in-person assessment, for example, he said. In other cases, family members may be essential in conveying information about a patient’s cognitive disabilities. Even when such information is documented, it is sometimes difficult to extract the full picture from the record alone, he said. Dr. Stadler is also bothered that the model requires physicians and hospitals to provide their skilled analyses to a for-profit company, which in turn, charges patients to review the information.

“This is our work,” he said. “I agree that patients should have the information, and I don’t mind sharing anything I have with patients, but now I’m going to share it with another business that essentially is competing with me in terms of providing guidance to patients.”

Oncologists are raising concerns about care access after the launch of a new company that links patients to cancer care options and clinical trials through mobile technology.

Driver, which began in September in the U.S. and China, is a global technology platform that allows patients to access treatment options across a broad network of cancer centers without leaving home. Cancer patients join the platform using a mobile app, through which Driver obtains the required consent to acquire medical records and tumor samples, and the company uses the information to recommend treatment options and clinical trials.

ljubaphoto/Getty Images

A separate app called Driver for Clinic enables oncologists who belong to Driver’s partner hospitals to manage their institution’s clinical trial information and quickly filter that information based on patients’ medical history to determine the patient’s eligibility for treatments.

Driver’s mission is to connect more patients to the best cancer treatments, regardless of location, said Will Polkinghorn, MD, Driver cofounder and CEO.

“Driver’s cofounders met at Harvard Medical School [in Boston] and saw firsthand the challenges of patients getting access to the latest, cutting-edge treatments available,” Dr. Polkinghorn said in an interview. “As doctors, [we] also witnessed how difficult it was for doctors to manage information in clinic and know about all the treatments that become available all around the world. Driver was created as a platform, with an app for the patient and an app for the doctor, to solve this broken marketplace.”

As part of the model, patients can review their recommended treatment options through video with an expert oncologist and select a hospital within Driver’s network for further evaluation. The company’s global network includes more than 30 leading U.S. cancer centers, including the Cleveland Clinic; multiple locations of the Mayo Clinic; the University of California, San Francisco; and Massachusetts General Hospital, Boston. The U.S. National Cancer Institute (NCI) and the Chinese National Cancer Center are founding members of Driver’s global network, according to the company.

Making more information and treatment options available is a positive for patients, said Walter Stadler, MD, chief of hematology/oncology and director of the genitourinary oncology program at the University of Chicago. However, he noted that the cost for patients to use Driver is prohibitive for many patients. Driver charges patients $3,000 up front and then a $20 monthly fee to use its service. Insurance does not subsidize the cost, nor does Driver help with travel or treatment costs, according to its website.

“It’s inequality of access,” Dr. Stadler said in an interview. “Many of us are very concerned that the clinical trials currently being conducted do not represent the general population well because they don’t represent patients with disparities … Here, we further exacerbate the problem by saying, ‘Okay, we’ll take the 5% of patients who can afford the service and expand their access, and the others, well, that’s not our problem.’ ”

“Access to clinical trials for patients residing in rural areas, as well as those getting their treatment in community based clinics, would not change,” Dr. Patel said in an interview. “Hence, challenges of social and demographic disparities and inequalities in clinical trial access and participation would be altered minimally. There is much greater need for such [platforms to include] community cancer clinics that would be more inclusive and encompass larger geographic areas where the majority of patients receive their care.”

Disadvantaged populations with limited access are not being overlooked by the company, according to Driver leaders. A branch of the company called Driver for All aims to increase access to optimal treatments for free through partnerships with local communities, Dr. Polkinghorn said. Driver for All has thus far partnered with Howard University Hospital in Washington to connect Howard patients to clinical trials at NCI. A partnership with Beijing Children’s Hospital and the Futang Research Center of Pediatric Development, meanwhile, is working to connect patients with rare-disease experts. Driver has funded 100% of the cost of these projects to date, according to its website.

Outside of Driver for All, Dr. Polkinghorn acknowledges that patients must bear the cost of Driver’s consumer products; however, the price should be viewed in context, he said.

“It’s important to remember that today, in order to be evaluated by 30 [plus] centers for treatment options, patients would need to fly to these centers, make appointments, and be seen by a doctor – this would require both time and resources for flights/hotels, which would cost much more than our sticker price,” he said. “So while $3,000 is a lot of money for some patients, Driver’s product is ultimately able to provide more visibility to options that simply would not be realistic today.”

James Gulley, MD, of the National Cancer Institute Center for Cancer Research, said any platform that can efficiently provide access to clinical trial options yields another source of information for patients to utilize in decision making with their health provider. Dr. Gulley, who heads the center’s genitourinary malignancies branch, declined to comment about access-to-care concerns with Driver’s model. He emphasized that patients who participate in NIH research studies are treated without charge.

“The key to finding better [cancer] treatment is to perform science-driven clinical trials,” Dr. Gulley said in an interview. “However, there are many barriers for enrollment in clinical trials. … As a government agency, NCI is open to partnering with any organization that seeks to improve access to clinical trials for cancer patients.”

NCI and Driver recently conducted a study to validate Driver’s platform; it showed that Driver’s technology successfully predicted the eligibility of patients in NCI Center for Cancer Research clinical trials. The study, presented at a recent American Society of Clinical Oncology meeting, evaluated Driver’s processing of 21 metastatic prostate cancer patients enrolled in a therapeutic NCI clinical trial within the last five years. Results showed Driver correctly predicted that 20 of the patients were “potentially eligible” for the trial in which they were enrolled, and that one was ineligible. Based on the study, a protocol is now in development for a new clinical study, which will seek to further determine the efficiency and accuracy of the clinical trial access program created by Driver, according to Dr. Gulley.

“We need breakthrough technologies and opportunities for patients to be able to access the most successful and promising cancer treatments, regardless of where they live,” Dr. Ryan said in an interview. “Companies like Driver are attempting to bridge that gap by connecting patients to doctors at world class cancer institutes and direct them toward the best care for their particular condition.”

Driver’s model also allows researchers the opportunity to develop specific, unique treatment for less common cancers and remain optimistic that they can attract patients to receive such treatments as they are developed, Dr. Ryan said.

Dr. Stadler, however, worries that Driver may be giving patients the wrong perception that all it takes is a computer and medical records to determine their best treatment route.

“There’s a lot more subtlety to treatment decisions than most people would like to admit,” Dr. Stadler said. “It’s more than just a bunch of data from sophisticated laboratory tests and the written medical record. Obtaining objective information is the first step, but it’s far from the only step.”

Patients may have significant limitations in functional status that is apparent only during an in-person assessment, for example, he said. In other cases, family members may be essential in conveying information about a patient’s cognitive disabilities. Even when such information is documented, it is sometimes difficult to extract the full picture from the record alone, he said. Dr. Stadler is also bothered that the model requires physicians and hospitals to provide their skilled analyses to a for-profit company, which in turn, charges patients to review the information.

“This is our work,” he said. “I agree that patients should have the information, and I don’t mind sharing anything I have with patients, but now I’m going to share it with another business that essentially is competing with me in terms of providing guidance to patients.”

Oncologists are raising concerns about care access after the launch of a new company that links patients to cancer care options and clinical trials through mobile technology.

Driver, which began in September in the U.S. and China, is a global technology platform that allows patients to access treatment options across a broad network of cancer centers without leaving home. Cancer patients join the platform using a mobile app, through which Driver obtains the required consent to acquire medical records and tumor samples, and the company uses the information to recommend treatment options and clinical trials.

ljubaphoto/Getty Images

A separate app called Driver for Clinic enables oncologists who belong to Driver’s partner hospitals to manage their institution’s clinical trial information and quickly filter that information based on patients’ medical history to determine the patient’s eligibility for treatments.

Driver’s mission is to connect more patients to the best cancer treatments, regardless of location, said Will Polkinghorn, MD, Driver cofounder and CEO.

“Driver’s cofounders met at Harvard Medical School [in Boston] and saw firsthand the challenges of patients getting access to the latest, cutting-edge treatments available,” Dr. Polkinghorn said in an interview. “As doctors, [we] also witnessed how difficult it was for doctors to manage information in clinic and know about all the treatments that become available all around the world. Driver was created as a platform, with an app for the patient and an app for the doctor, to solve this broken marketplace.”

As part of the model, patients can review their recommended treatment options through video with an expert oncologist and select a hospital within Driver’s network for further evaluation. The company’s global network includes more than 30 leading U.S. cancer centers, including the Cleveland Clinic; multiple locations of the Mayo Clinic; the University of California, San Francisco; and Massachusetts General Hospital, Boston. The U.S. National Cancer Institute (NCI) and the Chinese National Cancer Center are founding members of Driver’s global network, according to the company.

Making more information and treatment options available is a positive for patients, said Walter Stadler, MD, chief of hematology/oncology and director of the genitourinary oncology program at the University of Chicago. However, he noted that the cost for patients to use Driver is prohibitive for many patients. Driver charges patients $3,000 up front and then a $20 monthly fee to use its service. Insurance does not subsidize the cost, nor does Driver help with travel or treatment costs, according to its website.

“It’s inequality of access,” Dr. Stadler said in an interview. “Many of us are very concerned that the clinical trials currently being conducted do not represent the general population well because they don’t represent patients with disparities … Here, we further exacerbate the problem by saying, ‘Okay, we’ll take the 5% of patients who can afford the service and expand their access, and the others, well, that’s not our problem.’ ”

“Access to clinical trials for patients residing in rural areas, as well as those getting their treatment in community based clinics, would not change,” Dr. Patel said in an interview. “Hence, challenges of social and demographic disparities and inequalities in clinical trial access and participation would be altered minimally. There is much greater need for such [platforms to include] community cancer clinics that would be more inclusive and encompass larger geographic areas where the majority of patients receive their care.”

Disadvantaged populations with limited access are not being overlooked by the company, according to Driver leaders. A branch of the company called Driver for All aims to increase access to optimal treatments for free through partnerships with local communities, Dr. Polkinghorn said. Driver for All has thus far partnered with Howard University Hospital in Washington to connect Howard patients to clinical trials at NCI. A partnership with Beijing Children’s Hospital and the Futang Research Center of Pediatric Development, meanwhile, is working to connect patients with rare-disease experts. Driver has funded 100% of the cost of these projects to date, according to its website.

Outside of Driver for All, Dr. Polkinghorn acknowledges that patients must bear the cost of Driver’s consumer products; however, the price should be viewed in context, he said.

“It’s important to remember that today, in order to be evaluated by 30 [plus] centers for treatment options, patients would need to fly to these centers, make appointments, and be seen by a doctor – this would require both time and resources for flights/hotels, which would cost much more than our sticker price,” he said. “So while $3,000 is a lot of money for some patients, Driver’s product is ultimately able to provide more visibility to options that simply would not be realistic today.”

James Gulley, MD, of the National Cancer Institute Center for Cancer Research, said any platform that can efficiently provide access to clinical trial options yields another source of information for patients to utilize in decision making with their health provider. Dr. Gulley, who heads the center’s genitourinary malignancies branch, declined to comment about access-to-care concerns with Driver’s model. He emphasized that patients who participate in NIH research studies are treated without charge.

“The key to finding better [cancer] treatment is to perform science-driven clinical trials,” Dr. Gulley said in an interview. “However, there are many barriers for enrollment in clinical trials. … As a government agency, NCI is open to partnering with any organization that seeks to improve access to clinical trials for cancer patients.”

NCI and Driver recently conducted a study to validate Driver’s platform; it showed that Driver’s technology successfully predicted the eligibility of patients in NCI Center for Cancer Research clinical trials. The study, presented at a recent American Society of Clinical Oncology meeting, evaluated Driver’s processing of 21 metastatic prostate cancer patients enrolled in a therapeutic NCI clinical trial within the last five years. Results showed Driver correctly predicted that 20 of the patients were “potentially eligible” for the trial in which they were enrolled, and that one was ineligible. Based on the study, a protocol is now in development for a new clinical study, which will seek to further determine the efficiency and accuracy of the clinical trial access program created by Driver, according to Dr. Gulley.

“We need breakthrough technologies and opportunities for patients to be able to access the most successful and promising cancer treatments, regardless of where they live,” Dr. Ryan said in an interview. “Companies like Driver are attempting to bridge that gap by connecting patients to doctors at world class cancer institutes and direct them toward the best care for their particular condition.”

Driver’s model also allows researchers the opportunity to develop specific, unique treatment for less common cancers and remain optimistic that they can attract patients to receive such treatments as they are developed, Dr. Ryan said.

Dr. Stadler, however, worries that Driver may be giving patients the wrong perception that all it takes is a computer and medical records to determine their best treatment route.

“There’s a lot more subtlety to treatment decisions than most people would like to admit,” Dr. Stadler said. “It’s more than just a bunch of data from sophisticated laboratory tests and the written medical record. Obtaining objective information is the first step, but it’s far from the only step.”

Patients may have significant limitations in functional status that is apparent only during an in-person assessment, for example, he said. In other cases, family members may be essential in conveying information about a patient’s cognitive disabilities. Even when such information is documented, it is sometimes difficult to extract the full picture from the record alone, he said. Dr. Stadler is also bothered that the model requires physicians and hospitals to provide their skilled analyses to a for-profit company, which in turn, charges patients to review the information.

“This is our work,” he said. “I agree that patients should have the information, and I don’t mind sharing anything I have with patients, but now I’m going to share it with another business that essentially is competing with me in terms of providing guidance to patients.”

Venous thromboembolism (VTE) is the No. 1 cause of preventable deaths in hospitals, and 60% of all VTE cases occur during or following hospitalization, according to Jeffrey I. Weitz, MD, of McMaster University in Hamilton, Ont.

CDC/Janice Haney Carr

Hospitalized patients should receive prophylaxis to reduce their risk for VTE, he said in a webinar to promote World Thrombosis Day.

“To prevent VTE, people need to be aware of the problem,” he said. Hospitalization for any reason increases the risk of VTE, but thromboprophylaxis may be underused in medical patients, compared with surgical patients, because most surgical patients are automatically considered at risk.

Prevention of VTE involves understanding the risk factors, Dr. Weitz said. He pointed to a triad of conditions that promote clotting: slow blood flow, injury to the vessel wall, and increased clotability of the blood.

In a study of VTE risk factors, recent surgery with hospitalization and trauma topped the list, but hospitalization without recent surgery was associated with a nearly 8-fold increase in risk (Arch Intern Med. 2000;160[6]:809-15).

Evidence supports the value of anticoagulant prophylaxis, Dr. Weitz said. In a 2007 meta-analysis, use of anticoagulants reduced the risk of VTE by approximately 60% (Ann Intern Med. 2007 Feb 20;146[4]:278-88), and a 2011 update showed a reduction in risk of approximately 30% (Ann Intern Med. 2011 Nov 1;155[9]:602-15).

While risk assessment remains a challenge, several models can help, said Dr. Weitz.

Current guidelines from the American College of Chest Physicians suggest a shift toward individualized assessment of VTE risk, and the Centers for Medicare & Medicaid Services mandates VTE risk assessment, Dr. Weitz said.

He offered seven steps to improve prophylaxis in the hospital:

1. Obtain commitment from hospital leadership, including formation of a committee.

2. Have a written hospital policy on thromboprophylaxis.

3. Keep the policy simple and standard in terms of who gets prophylaxis and when.

4. Use order sets, computer order entry, and decision support.

5. Make the prophylaxis decision mandatory.

6. Involve of all the members of the care team and patients.

7. Use audits to measure improvement.

Several risk assessment models for VTE in hospitalized medical patients have been studied, including the Padua and IMPROVE models, Dr. Weitz said. For any model, factoring in the D-dimer can provide more information. “If D-dimer is increased more than twice the upper limit of normal, it is a risk factor for VTE,” he said.

Another consideration in thromboprophylaxis involves extending the duration of prophylaxis beyond the hospital stay, which is becoming a larger issue because of the pressure to move patients out of the hospital as quickly as possible, Dr. Weitz said. However, trials of extended thromboprophylaxis have yielded mixed results. Extended doses of medications, including rivaroxaban, enoxaparin, apixaban, and betrixaban can reduce the risk of VTE, but can also increase the risk of major bleeding.

“I think at this point we are not yet there at identifying patients who should have thromboprophylaxis beyond the hospital stay,” Dr. Weitz said.

But VTE risk should be assessed in all hospitalized patients, and “appropriate thromboprophylaxis is essential for reducing the burden of hospital-associated VTE,” he said.

Dr. Weitz encouraged clinicians to explore more resources for managing VTE risk at worldthrombosisday.org.

Dr. Weitz reported relationships with companies including Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Pfizer, Portola, Ionis Pharmaceuticals, Janssen, Merck, Novartis, and Servier. He also reported research support from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, and the Canadian Fund for Innovation.

Venous thromboembolism (VTE) is the No. 1 cause of preventable deaths in hospitals, and 60% of all VTE cases occur during or following hospitalization, according to Jeffrey I. Weitz, MD, of McMaster University in Hamilton, Ont.

CDC/Janice Haney Carr

Hospitalized patients should receive prophylaxis to reduce their risk for VTE, he said in a webinar to promote World Thrombosis Day.

“To prevent VTE, people need to be aware of the problem,” he said. Hospitalization for any reason increases the risk of VTE, but thromboprophylaxis may be underused in medical patients, compared with surgical patients, because most surgical patients are automatically considered at risk.

Prevention of VTE involves understanding the risk factors, Dr. Weitz said. He pointed to a triad of conditions that promote clotting: slow blood flow, injury to the vessel wall, and increased clotability of the blood.

In a study of VTE risk factors, recent surgery with hospitalization and trauma topped the list, but hospitalization without recent surgery was associated with a nearly 8-fold increase in risk (Arch Intern Med. 2000;160[6]:809-15).

Evidence supports the value of anticoagulant prophylaxis, Dr. Weitz said. In a 2007 meta-analysis, use of anticoagulants reduced the risk of VTE by approximately 60% (Ann Intern Med. 2007 Feb 20;146[4]:278-88), and a 2011 update showed a reduction in risk of approximately 30% (Ann Intern Med. 2011 Nov 1;155[9]:602-15).

While risk assessment remains a challenge, several models can help, said Dr. Weitz.

Current guidelines from the American College of Chest Physicians suggest a shift toward individualized assessment of VTE risk, and the Centers for Medicare & Medicaid Services mandates VTE risk assessment, Dr. Weitz said.

He offered seven steps to improve prophylaxis in the hospital:

1. Obtain commitment from hospital leadership, including formation of a committee.

2. Have a written hospital policy on thromboprophylaxis.

3. Keep the policy simple and standard in terms of who gets prophylaxis and when.

4. Use order sets, computer order entry, and decision support.

5. Make the prophylaxis decision mandatory.

6. Involve of all the members of the care team and patients.

7. Use audits to measure improvement.

Several risk assessment models for VTE in hospitalized medical patients have been studied, including the Padua and IMPROVE models, Dr. Weitz said. For any model, factoring in the D-dimer can provide more information. “If D-dimer is increased more than twice the upper limit of normal, it is a risk factor for VTE,” he said.

Another consideration in thromboprophylaxis involves extending the duration of prophylaxis beyond the hospital stay, which is becoming a larger issue because of the pressure to move patients out of the hospital as quickly as possible, Dr. Weitz said. However, trials of extended thromboprophylaxis have yielded mixed results. Extended doses of medications, including rivaroxaban, enoxaparin, apixaban, and betrixaban can reduce the risk of VTE, but can also increase the risk of major bleeding.

“I think at this point we are not yet there at identifying patients who should have thromboprophylaxis beyond the hospital stay,” Dr. Weitz said.

But VTE risk should be assessed in all hospitalized patients, and “appropriate thromboprophylaxis is essential for reducing the burden of hospital-associated VTE,” he said.

Dr. Weitz encouraged clinicians to explore more resources for managing VTE risk at worldthrombosisday.org.

Dr. Weitz reported relationships with companies including Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Pfizer, Portola, Ionis Pharmaceuticals, Janssen, Merck, Novartis, and Servier. He also reported research support from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, and the Canadian Fund for Innovation.

Venous thromboembolism (VTE) is the No. 1 cause of preventable deaths in hospitals, and 60% of all VTE cases occur during or following hospitalization, according to Jeffrey I. Weitz, MD, of McMaster University in Hamilton, Ont.

CDC/Janice Haney Carr

Hospitalized patients should receive prophylaxis to reduce their risk for VTE, he said in a webinar to promote World Thrombosis Day.

“To prevent VTE, people need to be aware of the problem,” he said. Hospitalization for any reason increases the risk of VTE, but thromboprophylaxis may be underused in medical patients, compared with surgical patients, because most surgical patients are automatically considered at risk.

Prevention of VTE involves understanding the risk factors, Dr. Weitz said. He pointed to a triad of conditions that promote clotting: slow blood flow, injury to the vessel wall, and increased clotability of the blood.

In a study of VTE risk factors, recent surgery with hospitalization and trauma topped the list, but hospitalization without recent surgery was associated with a nearly 8-fold increase in risk (Arch Intern Med. 2000;160[6]:809-15).

Evidence supports the value of anticoagulant prophylaxis, Dr. Weitz said. In a 2007 meta-analysis, use of anticoagulants reduced the risk of VTE by approximately 60% (Ann Intern Med. 2007 Feb 20;146[4]:278-88), and a 2011 update showed a reduction in risk of approximately 30% (Ann Intern Med. 2011 Nov 1;155[9]:602-15).

While risk assessment remains a challenge, several models can help, said Dr. Weitz.

Current guidelines from the American College of Chest Physicians suggest a shift toward individualized assessment of VTE risk, and the Centers for Medicare & Medicaid Services mandates VTE risk assessment, Dr. Weitz said.

He offered seven steps to improve prophylaxis in the hospital:

1. Obtain commitment from hospital leadership, including formation of a committee.

2. Have a written hospital policy on thromboprophylaxis.

3. Keep the policy simple and standard in terms of who gets prophylaxis and when.

4. Use order sets, computer order entry, and decision support.

5. Make the prophylaxis decision mandatory.

6. Involve of all the members of the care team and patients.

7. Use audits to measure improvement.

Several risk assessment models for VTE in hospitalized medical patients have been studied, including the Padua and IMPROVE models, Dr. Weitz said. For any model, factoring in the D-dimer can provide more information. “If D-dimer is increased more than twice the upper limit of normal, it is a risk factor for VTE,” he said.

Another consideration in thromboprophylaxis involves extending the duration of prophylaxis beyond the hospital stay, which is becoming a larger issue because of the pressure to move patients out of the hospital as quickly as possible, Dr. Weitz said. However, trials of extended thromboprophylaxis have yielded mixed results. Extended doses of medications, including rivaroxaban, enoxaparin, apixaban, and betrixaban can reduce the risk of VTE, but can also increase the risk of major bleeding.

“I think at this point we are not yet there at identifying patients who should have thromboprophylaxis beyond the hospital stay,” Dr. Weitz said.

But VTE risk should be assessed in all hospitalized patients, and “appropriate thromboprophylaxis is essential for reducing the burden of hospital-associated VTE,” he said.

Dr. Weitz encouraged clinicians to explore more resources for managing VTE risk at worldthrombosisday.org.

Dr. Weitz reported relationships with companies including Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, Pfizer, Portola, Ionis Pharmaceuticals, Janssen, Merck, Novartis, and Servier. He also reported research support from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, and the Canadian Fund for Innovation.

Results of the phase 3 KEYNOTE-048 trial investigating pembrolizumab (Keytruda) for first-line treatment of recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) will be presented during a presidential symposium at the European Society for Medical Oncology Congress.

The drug is currently approved for second-line treatment of HNSCC. Merck, the maker of the anti–programmed cell death protein therapy, announced in July that the primary endpoint of overall survival as monotherapy in the first-line setting of advanced HNSCC had been met in patients whose tumors expressed programmed death–ligand 1.

More than 800 patients in KEYNOTE-048 were randomized to receive pembrolizumab as monotherapy or in combination with cisplatin or carboplatin and 5-FU, or cetuximab plus cisplatin or carboplatin and 5-FU.

The dual primary endpoints were overall survival and progression-free survival. The secondary endpoints of the study were PFS (at 6 months and 12 months), objective response rate, and time to deterioration in Quality of Life Global Health Status/Quality of Life Scales of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire, according to the company.

Further details from the interim analysis of KEYNOTE-048 will be presented by Barbara Burtness, MD, of Yale Cancer Center, New Haven, Conn., during Presidential Symposium 3 at ESMO 2018 on Oct. 22 in Munich.

Results of the phase 3 KEYNOTE-048 trial investigating pembrolizumab (Keytruda) for first-line treatment of recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) will be presented during a presidential symposium at the European Society for Medical Oncology Congress.

The drug is currently approved for second-line treatment of HNSCC. Merck, the maker of the anti–programmed cell death protein therapy, announced in July that the primary endpoint of overall survival as monotherapy in the first-line setting of advanced HNSCC had been met in patients whose tumors expressed programmed death–ligand 1.

More than 800 patients in KEYNOTE-048 were randomized to receive pembrolizumab as monotherapy or in combination with cisplatin or carboplatin and 5-FU, or cetuximab plus cisplatin or carboplatin and 5-FU.

The dual primary endpoints were overall survival and progression-free survival. The secondary endpoints of the study were PFS (at 6 months and 12 months), objective response rate, and time to deterioration in Quality of Life Global Health Status/Quality of Life Scales of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire, according to the company.

Further details from the interim analysis of KEYNOTE-048 will be presented by Barbara Burtness, MD, of Yale Cancer Center, New Haven, Conn., during Presidential Symposium 3 at ESMO 2018 on Oct. 22 in Munich.

Results of the phase 3 KEYNOTE-048 trial investigating pembrolizumab (Keytruda) for first-line treatment of recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) will be presented during a presidential symposium at the European Society for Medical Oncology Congress.

The drug is currently approved for second-line treatment of HNSCC. Merck, the maker of the anti–programmed cell death protein therapy, announced in July that the primary endpoint of overall survival as monotherapy in the first-line setting of advanced HNSCC had been met in patients whose tumors expressed programmed death–ligand 1.

More than 800 patients in KEYNOTE-048 were randomized to receive pembrolizumab as monotherapy or in combination with cisplatin or carboplatin and 5-FU, or cetuximab plus cisplatin or carboplatin and 5-FU.

The dual primary endpoints were overall survival and progression-free survival. The secondary endpoints of the study were PFS (at 6 months and 12 months), objective response rate, and time to deterioration in Quality of Life Global Health Status/Quality of Life Scales of the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire, according to the company.

Further details from the interim analysis of KEYNOTE-048 will be presented by Barbara Burtness, MD, of Yale Cancer Center, New Haven, Conn., during Presidential Symposium 3 at ESMO 2018 on Oct. 22 in Munich.

BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

BERLIN – Spinal cord volume deficits in patients with multiple sclerosis may contribute to clinical disability that appears out of proportion to lesion load on brain imaging, according to new research.

Kari Oakes/MDedge News

In a pool of 362 patients with mild to moderate MS-related disability but identical white matter lesion load identified by MRI, those with higher disability had significantly lower spinal cord volumes when compared against those with disability scores in the mild range (P less than .001).

Though brain MRI is a key tool used to track disease severity and progression in MS, some patients have relatively high disability but a low burden of white matter intracerebral lesions on MRI. Little is known about spinal cord volume in MS patients with pronounced dissociation between intracerebral lesion load and disability, Michaela Andelova, MD, said in an interview during a poster session at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Dr. Andelova, of Charles University, Prague, said that she and her colleagues hypothesized that spinal cord volume would differ between patients who had varying levels of disability, despite identical white matter lesion load.

To test this, she and her colleagues looked at records of 1,245 patients with relapsing-remitting MS. They divided them into three groups by severity of clinical disability, and also by extent of cerebral T2 hyperintense lesion load. The investigators identified a group of patients (n = 53) whose total volume of T2-weighted hyperintense lesions was less than 3 mL, but whose Expanded Disability Status Scale (EDSS) scores were at least 3.5; this was the low lesion load/high disability (LLHD) group.

Dr. Andelova and her colleagues then identified another group of patients (n = 71) who had a volume of T2-weighted hyperintensities that was greater than 9 mL, but whose EDSS score was less than 1.5. This was the high lesion load/low disability (HLLD) group.

The remaining patients (n = 1,121), who did not have these paradoxical associations, were analyzed separately.

For all patients, mean upper cervical cord area (MUCCA) was also measured. Using images acquired by a 3 T MRI scanner, MUCCA was calculated as the mean sum of spinal cord area in 21 slices centered at the C3/4 intervertebral disk, using an in-house, semiautomated method.

“Despite higher disability, LLHD patients demonstrated significantly higher normalized total brain volume, higher normalized volumes of thalamus and callosum, and smaller lateral ventricles than [the] HLLD group,” wrote Dr. Andelova and her collaborators.

However, the LLHD patients had MUCCA values that were significantly lower than the other groups: The nonparadoxical group’s mean MUCCA was 84.02 mm², while the HLLD group had a mean MUCCA of 85.75 mm². This difference was not statistically significant. By contrast, the LLHD group’s mean MUCCA was significantly smaller, at 80.40 mm² (P = .023 versus nonparadoxical patients, and P = .007 versus HLLD patients).

Looking at the data another way, Dr. Andelova and her colleagues compared 362 evenly divided patients with moderate disability (EDSS 3.5-6.5) with matched patients who had mild MS-related disability (EDSS less than 3) and identical cerebral lesion loads. They found that MUCCA was significantly smaller in the moderate disability group (78.86 versus 84.44 mm²; P less than .001).

In addition to having identical lesions loads, the mild and moderate disability groups didn’t differ significantly in normalized total brain volume or regional brain volumes. The group with moderate disability did have slightly less white matter volume (P = .039), Dr. Andelova pointed out.

All differences found between groups retained statistical significance even after adjustment for such potential confounders as age, sex, and duration of disease, Dr. Andelova said.

“Reduced spinal cord volume may explain part of the clinical-radiological paradox in patients who have high disability despite low intracranial lesion load,” Dr. Andelova and her collaborators wrote. “In line with this finding, relatively preserved spinal cord volume may be associated with functional reserve and less physical disability in patients with low disability despite high cerebral lesion load.”

Further work looking more precisely at cerebral lesion distribution and quantitative MRI investigation of lesion distribution is in the works for Dr. Andelova and her collaborators. They are hoping to see some association between various distribution patterns and accelerated spinal atrophy.

The research was supported by the Czech government. Dr. Andelova and several of her collaborators reported financial relationships with pharmaceutical companies.

[email protected]

SOURCE: Andelova M et al. Mult Scler. 2018;24(Suppl 2):211, Abstract P477.

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

The Food and Drug Administration has approved ID CORE XT, a molecular-based assay that uses DNA to test for non-ABO red blood cell types for use in transfusion.

It’s the second molecular test for blood compatibility but the first to report genotype in its results, according to an announcement from the agency.

The test is important because it evaluates patients – especially those who receive repeated blood transfusions for conditions such as sickle cell anemia – for non-ABO antigens, but it does so without using antisera, which is sometimes unavailable.

A study found comparable performance between the ID CORE XT, licensed serologic reagents, and DNA sequencing tests, according to the FDA.

The ID CORE XT test is marketed by Progenika Biopharma, a Grifols company.

More information can be found in the full FDA press announcement.

[email protected]

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.

BERLIN – Children with acute disseminated encephalomyelitis have a significantly increased risk of subsequent epilepsy when it occurs with oligoclonal bands in cerebrospinal fluid and seizures at presentation, Thomas Rossor, MD, reported at the annual congress of the European Committee for Treatment and Research in Multiple Sclerosis.

Michele G. Sullivan/MDedge News

But fortunately, the seizures of postacute disseminated encephalomyelitis (post-ADEM) epilepsy are relatively easy to control and not clinically devastating, said Dr. Rossor of Great Ormond Street Hospital, London.

Of the 12 who developed epilepsy in Dr. Rossor’s retrospective, multicenter review of 74 children with ADEM, 11 were well controlled on one drug and 1 on two drugs.

Pediatric ADEM is usually monophasic with good clinical outcome, he said. But a benign course is not set in stone: Up to 40% of children experience seizures during the acute presentation. “In contrast,” Dr. Rossor said, “adult patients with relapsing-remitting multiple sclerosis have the same risk of developing epilepsy as the general population.” Among adults with cortical encephalitis, antibodies against myelin oligodendrocyte glycoprotein (MOG) have been associated with seizures and the need for antiepileptic medications, he added.

That finding was part of what spurred Dr. Rossor’s study, which aimed to identify predictors of relapse and post-ADEM epilepsy in children. The patients in the review had a median age of 4.5 years. All were tested for anti-MOG antibodies, and most (about 68%) were positive. Oligoclonal bands in cerebrospinal fluid (CSF) occurred in 22%. The median follow-up period was 5 years.

A total of 41% (n = 31) relapsed after the initial acute phase. Among these, the final diagnosis included multiphasic disseminated encephalomyelitis (n = 19); ADEM-optic neuritis (n = 3); and neuromyelitis optica spectrum disorder (n = 6).

Of the 74 patients, 16 (22%) had seizures during the acute phase, and 12 (16%) developed post-ADEM epilepsy at a median of 3 months. The most common clinical characteristics with post-ADEM epilepsy included oligoclonal bands (57% vs. 13%), anti-MOG antibodies (92% vs. 16%), and seizures at presentation (50% vs. 16%). When these were entered into a regression model, oligoclonal bands and initial seizures significantly predicted epilepsy, increasing the risk by 20.7 and 13.5 times, respectively.

Since relapse is known to be associated with post-ADEM epilepsy, Dr. Rossor first looked at relapse risk. He conducted a multivariate analysis that included several clinical characteristics: age, prodrome, increased CSF white cells and protein, oligoclonal bands, anti-MOG antibodies, and seizures both at presentation and after the acute phase.

Anti-MOG antibodies were significantly more common among the relapsed patients than among the monophasic patients (87% vs. 53%). Seizures at presentation also were more common among the relapsed patients (32% vs. 14%). These two factors were entered into a binary regression analysis; only anti-MOG antibodies remained significantly associated with relapse, increasing the risk fivefold (odds ratio = 5.4; P = .007).

Anti-MOG antibodies also were associated with both earlier and more relapses. Overall, 40% of anti–MOG-antibody–positive patients relapsed by 24 months. In contrast, only 20% of anti–MOG-antibody–negative patients had relapsed by 24 months, and this number remained steady throughout the follow-up period.

By 96 months, almost all the anti–MOG-antibody–positive patients had relapsed, and some experienced many relapses. “In the antibody-negative group, four patients did relapse, but they had relatively few relapses. In the antibody-positive group, some had relatively few relapses, but several had 15, 20, or 25 clinical relapses in the follow-up period,” he said.

Dr. Rossor and his coauthors had no financial disclosures.

[email protected]

SOURCE: Rossor T et al. Mult Scler. 2018;24(Suppl 2):27. Abstract 62.