CLINICAL POSTER HIGHLIGHTS: Advances in Treatment of Psoriasis Vulgaris and Actinic Keratosis

A poster review supplement to Dermatology News.

CLINICAL POSTER HIGHLIGHTS: Advances in Treatment of Psoriasis Vulgaris and Actinic Keratosis

A poster review supplement to Dermatology News.

CLINICAL POSTER HIGHLIGHTS: Advances in Treatment of Psoriasis Vulgaris and Actinic Keratosis

A poster review supplement to Dermatology News.

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

Massimo Federico, MD

Photo by Larry Young

SAN FRANCISCO—Outcomes remain dismal for the majority of patients with peripheral T-cell lymphoma (PTCL), according to a speaker at the 7th Annual T-cell Lymphoma Forum.

Massimo Federico, MD, of the Università di Modena e Reggio Emilia in Italy, presented an analysis of the first 1000 patients enrolled in the prospective T-Cell Project.

The data showed no improvements in survival for these patients compared to patients included in the retrospective International Peripheral T-Cell Lymphoma

Project.

The International Peripheral T-Cell Lymphoma Project included PTCL patients treated at various institutions between 1990 and 2002.

The T-Cell Project was designed to complement this retrospective analysis, providing prospective international data on PTCL patients.

“The main aim was to verify if a prospective collection of data would allow for more accurate information to better define prognosis of the most frequent subtypes of PTCL—PTCL not otherwise specified (NOS) and angioimmunoblastic T-cell lymphoma (AITL)—and improve our knowledge of clinical and biological characteristics and outcomes of the more uncommon subtypes of PTCL,” Dr Federico said.

He reported that, as of January 12, 2015, 73 institutions were recruiting patients for the project, and 6 institutions were active but not yet recruiting.

Of the 1308 patients registered at that point, 46% were from European countries (Italy, UK, Switzerland, Slovakia, Spain, and France), 20% were from the US, 20% were from South America (Argentina, Brazil, Chile, and Uruguay), and 14% were from the Middle East or Far East (South Korea, Hong Kong, and Israel).

Dr Federico went on to present data from the first 1000 patients registered in the project. The final analysis actually included 943 patients, as some patients withdrew consent, some did not have baseline data available, and some diagnoses could not be confirmed.

So of the 943 patients, 37% had PTCL-NOS, 17% had AITL, 15% had ALK-negative anaplastic large-cell lymphoma (ALCL), 7% had ALK-positive ALCL, 11% had natural killer/T-cell lymphoma (NKTCL), 8% had T-cell receptor γδ T-cell lymphoma, and 5% had other histologies.

The patients’ median age was 56 (range, 18-89), and 61% were male. Twenty-four percent of patients had an ECOG status greater than 1, 48% had B symptoms, and 71% had disease-related discomfort. Sixty-seven percent of patients had stage III-IV disease, 27% had nodal-only disease, 6% had bulky disease, 29% had more than 1 extranodal site, and 19% had bone marrow involvement.

The median follow-up was 41 months (range, 1-91). The 5-year overall survival (OS) was 44%, and the median OS was 39 months.

The 5-year OS was 35% for patients with PTCL-NOS, 42% for those with AITL, 45% for those with ALK-negative ALCL, 80% for those with ALK-positive ALCL, 48% for those with NKTCL (56% for nasal and 33% for extranasal), and 39% for those with T-cell receptor γδ T-cell lymphoma.

In comparison, the International Peripheral T-Cell Lymphoma Project showed a 5-year OS of 32% for patients with PTCL-NOS, 70% for patients with ALK-positive ALCL, and 49% for patients with ALK-negative ALCL (K. Savage et al. Blood 2008). The 5-year OS was 40% for patients with nasal NKTCL and 15% for those with extranasal NKTCL (W. Au et al. Blood 2008).

“[T]he outcome of PTCL continues to be dismal in the majority of cases, [with] no improvement in overall survival compared to older series,” Dr Federico summarized. “Treatment remains challenging, and new therapies are welcome.”

He added that the next steps for the T-Cell Project are to continue registration (with the goal of reaching 2000 assessable cases), extend the network to additional sites (particularly in under-represented areas such as Japan, China, India, and Oceania), and expand the collection of tissue.

“In particular, we intend to create an international tissue catalogue—including paraffin-embedded samples and, if possible, frozen ones—accessible to research groups with a solid reputation in investigating PTCLs at the molecular and translation level.”

Massimo Federico, MD

Photo by Larry Young

SAN FRANCISCO—Outcomes remain dismal for the majority of patients with peripheral T-cell lymphoma (PTCL), according to a speaker at the 7th Annual T-cell Lymphoma Forum.

Massimo Federico, MD, of the Università di Modena e Reggio Emilia in Italy, presented an analysis of the first 1000 patients enrolled in the prospective T-Cell Project.

The data showed no improvements in survival for these patients compared to patients included in the retrospective International Peripheral T-Cell Lymphoma

Project.

The International Peripheral T-Cell Lymphoma Project included PTCL patients treated at various institutions between 1990 and 2002.

The T-Cell Project was designed to complement this retrospective analysis, providing prospective international data on PTCL patients.

“The main aim was to verify if a prospective collection of data would allow for more accurate information to better define prognosis of the most frequent subtypes of PTCL—PTCL not otherwise specified (NOS) and angioimmunoblastic T-cell lymphoma (AITL)—and improve our knowledge of clinical and biological characteristics and outcomes of the more uncommon subtypes of PTCL,” Dr Federico said.

He reported that, as of January 12, 2015, 73 institutions were recruiting patients for the project, and 6 institutions were active but not yet recruiting.

Of the 1308 patients registered at that point, 46% were from European countries (Italy, UK, Switzerland, Slovakia, Spain, and France), 20% were from the US, 20% were from South America (Argentina, Brazil, Chile, and Uruguay), and 14% were from the Middle East or Far East (South Korea, Hong Kong, and Israel).

Dr Federico went on to present data from the first 1000 patients registered in the project. The final analysis actually included 943 patients, as some patients withdrew consent, some did not have baseline data available, and some diagnoses could not be confirmed.

So of the 943 patients, 37% had PTCL-NOS, 17% had AITL, 15% had ALK-negative anaplastic large-cell lymphoma (ALCL), 7% had ALK-positive ALCL, 11% had natural killer/T-cell lymphoma (NKTCL), 8% had T-cell receptor γδ T-cell lymphoma, and 5% had other histologies.

The patients’ median age was 56 (range, 18-89), and 61% were male. Twenty-four percent of patients had an ECOG status greater than 1, 48% had B symptoms, and 71% had disease-related discomfort. Sixty-seven percent of patients had stage III-IV disease, 27% had nodal-only disease, 6% had bulky disease, 29% had more than 1 extranodal site, and 19% had bone marrow involvement.

The median follow-up was 41 months (range, 1-91). The 5-year overall survival (OS) was 44%, and the median OS was 39 months.

The 5-year OS was 35% for patients with PTCL-NOS, 42% for those with AITL, 45% for those with ALK-negative ALCL, 80% for those with ALK-positive ALCL, 48% for those with NKTCL (56% for nasal and 33% for extranasal), and 39% for those with T-cell receptor γδ T-cell lymphoma.

In comparison, the International Peripheral T-Cell Lymphoma Project showed a 5-year OS of 32% for patients with PTCL-NOS, 70% for patients with ALK-positive ALCL, and 49% for patients with ALK-negative ALCL (K. Savage et al. Blood 2008). The 5-year OS was 40% for patients with nasal NKTCL and 15% for those with extranasal NKTCL (W. Au et al. Blood 2008).

“[T]he outcome of PTCL continues to be dismal in the majority of cases, [with] no improvement in overall survival compared to older series,” Dr Federico summarized. “Treatment remains challenging, and new therapies are welcome.”

He added that the next steps for the T-Cell Project are to continue registration (with the goal of reaching 2000 assessable cases), extend the network to additional sites (particularly in under-represented areas such as Japan, China, India, and Oceania), and expand the collection of tissue.

“In particular, we intend to create an international tissue catalogue—including paraffin-embedded samples and, if possible, frozen ones—accessible to research groups with a solid reputation in investigating PTCLs at the molecular and translation level.”

Massimo Federico, MD

Photo by Larry Young

SAN FRANCISCO—Outcomes remain dismal for the majority of patients with peripheral T-cell lymphoma (PTCL), according to a speaker at the 7th Annual T-cell Lymphoma Forum.

Massimo Federico, MD, of the Università di Modena e Reggio Emilia in Italy, presented an analysis of the first 1000 patients enrolled in the prospective T-Cell Project.

The data showed no improvements in survival for these patients compared to patients included in the retrospective International Peripheral T-Cell Lymphoma

Project.

The International Peripheral T-Cell Lymphoma Project included PTCL patients treated at various institutions between 1990 and 2002.

The T-Cell Project was designed to complement this retrospective analysis, providing prospective international data on PTCL patients.

“The main aim was to verify if a prospective collection of data would allow for more accurate information to better define prognosis of the most frequent subtypes of PTCL—PTCL not otherwise specified (NOS) and angioimmunoblastic T-cell lymphoma (AITL)—and improve our knowledge of clinical and biological characteristics and outcomes of the more uncommon subtypes of PTCL,” Dr Federico said.

He reported that, as of January 12, 2015, 73 institutions were recruiting patients for the project, and 6 institutions were active but not yet recruiting.

Of the 1308 patients registered at that point, 46% were from European countries (Italy, UK, Switzerland, Slovakia, Spain, and France), 20% were from the US, 20% were from South America (Argentina, Brazil, Chile, and Uruguay), and 14% were from the Middle East or Far East (South Korea, Hong Kong, and Israel).

Dr Federico went on to present data from the first 1000 patients registered in the project. The final analysis actually included 943 patients, as some patients withdrew consent, some did not have baseline data available, and some diagnoses could not be confirmed.

So of the 943 patients, 37% had PTCL-NOS, 17% had AITL, 15% had ALK-negative anaplastic large-cell lymphoma (ALCL), 7% had ALK-positive ALCL, 11% had natural killer/T-cell lymphoma (NKTCL), 8% had T-cell receptor γδ T-cell lymphoma, and 5% had other histologies.

The patients’ median age was 56 (range, 18-89), and 61% were male. Twenty-four percent of patients had an ECOG status greater than 1, 48% had B symptoms, and 71% had disease-related discomfort. Sixty-seven percent of patients had stage III-IV disease, 27% had nodal-only disease, 6% had bulky disease, 29% had more than 1 extranodal site, and 19% had bone marrow involvement.

The median follow-up was 41 months (range, 1-91). The 5-year overall survival (OS) was 44%, and the median OS was 39 months.

The 5-year OS was 35% for patients with PTCL-NOS, 42% for those with AITL, 45% for those with ALK-negative ALCL, 80% for those with ALK-positive ALCL, 48% for those with NKTCL (56% for nasal and 33% for extranasal), and 39% for those with T-cell receptor γδ T-cell lymphoma.

In comparison, the International Peripheral T-Cell Lymphoma Project showed a 5-year OS of 32% for patients with PTCL-NOS, 70% for patients with ALK-positive ALCL, and 49% for patients with ALK-negative ALCL (K. Savage et al. Blood 2008). The 5-year OS was 40% for patients with nasal NKTCL and 15% for those with extranasal NKTCL (W. Au et al. Blood 2008).

“[T]he outcome of PTCL continues to be dismal in the majority of cases, [with] no improvement in overall survival compared to older series,” Dr Federico summarized. “Treatment remains challenging, and new therapies are welcome.”

He added that the next steps for the T-Cell Project are to continue registration (with the goal of reaching 2000 assessable cases), extend the network to additional sites (particularly in under-represented areas such as Japan, China, India, and Oceania), and expand the collection of tissue.

“In particular, we intend to create an international tissue catalogue—including paraffin-embedded samples and, if possible, frozen ones—accessible to research groups with a solid reputation in investigating PTCLs at the molecular and translation level.”

Andrei Shustov, MD

Photo by Larry Young

SAN FRANCISCO—The distribution of peripheral T-cell lymphoma (PTCL) subtypes in the US varies greatly according to race and ethnicity, new research suggests.

The retrospective study showed that the overall incidence of PTCL and its subtypes is lower in American Indians and Alaskan Natives than in other ethnic groups.

And the black population has a significantly higher incidence of PTCL—and the most common subtype, PTCL-not otherwise specified (NOS)—than other populations.

Andrei Shustov, MD, of the University of Washington Medical Center in Seattle, presented these and other findings at the 7th Annual T-cell Lymphoma Forum.

The findings were derived from data collected by the Surveillance, Epidemiology, and End Results (SEER) Cancer Registries, which cover 28% of the US population. The data included patients older than 15 years of age who were treated at 18 centers from 2000 through 2011.

Of all cancer patients registered over the 12-year period, 60% were non-Hispanic whites (n=470,864,199), 17% were Hispanic whites (n=134,464,006), 12% were black (n=92,294,395), 10% were Asian/Pacific Islanders (n=74,973,831), and 1% were American Indian/Alaskan Natives (n=10,802,898).

The overall incidence of PTCL was highest in blacks—2.11 per 100,000 persons per year, compared to 1.63 in non-Hispanic whites, 1.53 in Hispanic whites, 1.46 in Asian/Pacific Islanders, and 0.97 in American Indian/Alaskan Natives.

Although American Indian/Alaskan Natives appear to have the lowest overall rate of PTCLs, some cases may have been misclassified, Dr Shustov noted.

“The data collected for ethnicity in the SEER registry are self-reported, and a lot of American Indian/Alaskan Natives misreport their ethnic background,” he said.

Subtype analyses

PTCL-NOS was the most common subtype among all the racial/ethnic groups. The highest rate of PTCL-NOS (per 100,000 persons per year) was in blacks—at 0.77, compared to 0.47 in non-Hispanic whites, 0.46 in Hispanic whites, 0.45 in Asian/Pacific Islanders, and 0.28 in American Indian/Alaskan Natives.

The proportion of PTCL-NOS cases was 29.5% in non-Hispanic whites, 35.7% in blacks, 29.8% in Asian/Pacific Islanders, 27% in Hispanic whites, and 23.1% in American Indian/Alaskan Natives.

The proportion of angioimmunoblastic T-cell lymphoma cases was 9.9% in non-Hispanic whites, 5.2% in blacks, 15.3% in Asian/Pacific Islanders, 9.9% in Hispanic whites, and 2.6% in American Indian/Alaskan Natives.

The proportion of anaplastic large-cell lymphoma cases was 17.6% in non-Hispanic whites, 17.3% in blacks, 12.4% in Asian/Pacific Islanders, 21.2% in Hispanic whites, and 28.2% in American Indian/Alaskan Natives.

And the proportion of NK/T-cell lymphoma cases was 3.4% in non-Hispanic whites, 2.0% in blacks, 13.9% in Asian/Pacific Islanders, 14.6% in Hispanic whites, and 14.1% in American Indian/Alaskan Natives.

“That data indicates that, given the overall incidence of T-cell lymphoma in Natives is lower than in whites, if you’re a Native American/Alaskan Native [with] T-cell lymphoma, you’re 4 times more likely to have nasal NK-cell lymphoma than non-Hispanic whites,” Dr Shustov said.

He then showed a pairwise comparison of the percentage of PTCL subtypes. All of the racial/ethnic groups were significantly different from one another (P<0.001), except when Hispanic whites were compared to American Indian/Alaskan Natives (P=0.14).

Dr Shustov said this might be explained by the fact that these two groups have similar genetic backgrounds.

Andrei Shustov, MD

Photo by Larry Young

SAN FRANCISCO—The distribution of peripheral T-cell lymphoma (PTCL) subtypes in the US varies greatly according to race and ethnicity, new research suggests.

The retrospective study showed that the overall incidence of PTCL and its subtypes is lower in American Indians and Alaskan Natives than in other ethnic groups.

And the black population has a significantly higher incidence of PTCL—and the most common subtype, PTCL-not otherwise specified (NOS)—than other populations.

Andrei Shustov, MD, of the University of Washington Medical Center in Seattle, presented these and other findings at the 7th Annual T-cell Lymphoma Forum.

The findings were derived from data collected by the Surveillance, Epidemiology, and End Results (SEER) Cancer Registries, which cover 28% of the US population. The data included patients older than 15 years of age who were treated at 18 centers from 2000 through 2011.

Of all cancer patients registered over the 12-year period, 60% were non-Hispanic whites (n=470,864,199), 17% were Hispanic whites (n=134,464,006), 12% were black (n=92,294,395), 10% were Asian/Pacific Islanders (n=74,973,831), and 1% were American Indian/Alaskan Natives (n=10,802,898).

The overall incidence of PTCL was highest in blacks—2.11 per 100,000 persons per year, compared to 1.63 in non-Hispanic whites, 1.53 in Hispanic whites, 1.46 in Asian/Pacific Islanders, and 0.97 in American Indian/Alaskan Natives.

Although American Indian/Alaskan Natives appear to have the lowest overall rate of PTCLs, some cases may have been misclassified, Dr Shustov noted.

“The data collected for ethnicity in the SEER registry are self-reported, and a lot of American Indian/Alaskan Natives misreport their ethnic background,” he said.

Subtype analyses

PTCL-NOS was the most common subtype among all the racial/ethnic groups. The highest rate of PTCL-NOS (per 100,000 persons per year) was in blacks—at 0.77, compared to 0.47 in non-Hispanic whites, 0.46 in Hispanic whites, 0.45 in Asian/Pacific Islanders, and 0.28 in American Indian/Alaskan Natives.

The proportion of PTCL-NOS cases was 29.5% in non-Hispanic whites, 35.7% in blacks, 29.8% in Asian/Pacific Islanders, 27% in Hispanic whites, and 23.1% in American Indian/Alaskan Natives.

The proportion of angioimmunoblastic T-cell lymphoma cases was 9.9% in non-Hispanic whites, 5.2% in blacks, 15.3% in Asian/Pacific Islanders, 9.9% in Hispanic whites, and 2.6% in American Indian/Alaskan Natives.

The proportion of anaplastic large-cell lymphoma cases was 17.6% in non-Hispanic whites, 17.3% in blacks, 12.4% in Asian/Pacific Islanders, 21.2% in Hispanic whites, and 28.2% in American Indian/Alaskan Natives.

And the proportion of NK/T-cell lymphoma cases was 3.4% in non-Hispanic whites, 2.0% in blacks, 13.9% in Asian/Pacific Islanders, 14.6% in Hispanic whites, and 14.1% in American Indian/Alaskan Natives.

“That data indicates that, given the overall incidence of T-cell lymphoma in Natives is lower than in whites, if you’re a Native American/Alaskan Native [with] T-cell lymphoma, you’re 4 times more likely to have nasal NK-cell lymphoma than non-Hispanic whites,” Dr Shustov said.

He then showed a pairwise comparison of the percentage of PTCL subtypes. All of the racial/ethnic groups were significantly different from one another (P<0.001), except when Hispanic whites were compared to American Indian/Alaskan Natives (P=0.14).

Dr Shustov said this might be explained by the fact that these two groups have similar genetic backgrounds.

Andrei Shustov, MD

Photo by Larry Young

SAN FRANCISCO—The distribution of peripheral T-cell lymphoma (PTCL) subtypes in the US varies greatly according to race and ethnicity, new research suggests.

The retrospective study showed that the overall incidence of PTCL and its subtypes is lower in American Indians and Alaskan Natives than in other ethnic groups.

And the black population has a significantly higher incidence of PTCL—and the most common subtype, PTCL-not otherwise specified (NOS)—than other populations.

Andrei Shustov, MD, of the University of Washington Medical Center in Seattle, presented these and other findings at the 7th Annual T-cell Lymphoma Forum.

The findings were derived from data collected by the Surveillance, Epidemiology, and End Results (SEER) Cancer Registries, which cover 28% of the US population. The data included patients older than 15 years of age who were treated at 18 centers from 2000 through 2011.

Of all cancer patients registered over the 12-year period, 60% were non-Hispanic whites (n=470,864,199), 17% were Hispanic whites (n=134,464,006), 12% were black (n=92,294,395), 10% were Asian/Pacific Islanders (n=74,973,831), and 1% were American Indian/Alaskan Natives (n=10,802,898).

The overall incidence of PTCL was highest in blacks—2.11 per 100,000 persons per year, compared to 1.63 in non-Hispanic whites, 1.53 in Hispanic whites, 1.46 in Asian/Pacific Islanders, and 0.97 in American Indian/Alaskan Natives.

Although American Indian/Alaskan Natives appear to have the lowest overall rate of PTCLs, some cases may have been misclassified, Dr Shustov noted.

“The data collected for ethnicity in the SEER registry are self-reported, and a lot of American Indian/Alaskan Natives misreport their ethnic background,” he said.

Subtype analyses

PTCL-NOS was the most common subtype among all the racial/ethnic groups. The highest rate of PTCL-NOS (per 100,000 persons per year) was in blacks—at 0.77, compared to 0.47 in non-Hispanic whites, 0.46 in Hispanic whites, 0.45 in Asian/Pacific Islanders, and 0.28 in American Indian/Alaskan Natives.

The proportion of PTCL-NOS cases was 29.5% in non-Hispanic whites, 35.7% in blacks, 29.8% in Asian/Pacific Islanders, 27% in Hispanic whites, and 23.1% in American Indian/Alaskan Natives.

The proportion of angioimmunoblastic T-cell lymphoma cases was 9.9% in non-Hispanic whites, 5.2% in blacks, 15.3% in Asian/Pacific Islanders, 9.9% in Hispanic whites, and 2.6% in American Indian/Alaskan Natives.

The proportion of anaplastic large-cell lymphoma cases was 17.6% in non-Hispanic whites, 17.3% in blacks, 12.4% in Asian/Pacific Islanders, 21.2% in Hispanic whites, and 28.2% in American Indian/Alaskan Natives.

And the proportion of NK/T-cell lymphoma cases was 3.4% in non-Hispanic whites, 2.0% in blacks, 13.9% in Asian/Pacific Islanders, 14.6% in Hispanic whites, and 14.1% in American Indian/Alaskan Natives.

“That data indicates that, given the overall incidence of T-cell lymphoma in Natives is lower than in whites, if you’re a Native American/Alaskan Native [with] T-cell lymphoma, you’re 4 times more likely to have nasal NK-cell lymphoma than non-Hispanic whites,” Dr Shustov said.

He then showed a pairwise comparison of the percentage of PTCL subtypes. All of the racial/ethnic groups were significantly different from one another (P<0.001), except when Hispanic whites were compared to American Indian/Alaskan Natives (P=0.14).

Dr Shustov said this might be explained by the fact that these two groups have similar genetic backgrounds.

Need another reason to make your toddler dinner instead of feeding him a prepackaged meal? New research shows a large number of dinners, snacks, and desserts sold in the United States that are designed for toddlers contain added sugar and salt, leaving them at risk for developing hypertension and diabetes later on in life.

Fortunately, commercial foods made for infants (vegetables, dinners, plain fruit without grains, dry cereals) sold in the United States tend to have little sugar and sodium added. But parents should still try to limit salty snacks, sweet desserts, and juice drinks, because they often contain more salt and sugar than kids need.

Approximately 79% of U.S. children aged 1-3 years eat more sodium than is recommended by the Institute of Medicine, noted Mary E. Cogswell, DrPH, a researcher from the Centers for Disease Control and Prevention in a study published in Pediatrics.

©Purestock/thinkstockphotos.com

Dr. Cogswell and her team of researchers looked at package information for 1,074 food products sold in the United States in 2012 that was marketed to infants, toddlers, or both.

Seventy-two percent of toddler dinners examined contained added sodium, and 32% percent of toddler dinners contained added sugar; 52% of ready-to-serve mixed grains and fruits contained too much added sugar. The majority of dairy-based desserts (70%) and fruit juices (88%) intended for both infant and toddler consumption also contained added sugar.

Limiting how much sugar and salt your children are exposed to can go a long way in preventing obesity and high blood pressure, so parents should look carefully at labels when selecting what foods to buy for toddlers.

“Key advice for parents includes limiting juice and avoiding sugar-sweetened beverages and energy-dense, nutrient-poor snacks; if purchasing commercial toddler foods, the labels should be checked for sodium and added sugar,” the authors wrote.

[email protected]

Need another reason to make your toddler dinner instead of feeding him a prepackaged meal? New research shows a large number of dinners, snacks, and desserts sold in the United States that are designed for toddlers contain added sugar and salt, leaving them at risk for developing hypertension and diabetes later on in life.

Fortunately, commercial foods made for infants (vegetables, dinners, plain fruit without grains, dry cereals) sold in the United States tend to have little sugar and sodium added. But parents should still try to limit salty snacks, sweet desserts, and juice drinks, because they often contain more salt and sugar than kids need.

Approximately 79% of U.S. children aged 1-3 years eat more sodium than is recommended by the Institute of Medicine, noted Mary E. Cogswell, DrPH, a researcher from the Centers for Disease Control and Prevention in a study published in Pediatrics.

©Purestock/thinkstockphotos.com

Dr. Cogswell and her team of researchers looked at package information for 1,074 food products sold in the United States in 2012 that was marketed to infants, toddlers, or both.

Seventy-two percent of toddler dinners examined contained added sodium, and 32% percent of toddler dinners contained added sugar; 52% of ready-to-serve mixed grains and fruits contained too much added sugar. The majority of dairy-based desserts (70%) and fruit juices (88%) intended for both infant and toddler consumption also contained added sugar.

Limiting how much sugar and salt your children are exposed to can go a long way in preventing obesity and high blood pressure, so parents should look carefully at labels when selecting what foods to buy for toddlers.

“Key advice for parents includes limiting juice and avoiding sugar-sweetened beverages and energy-dense, nutrient-poor snacks; if purchasing commercial toddler foods, the labels should be checked for sodium and added sugar,” the authors wrote.

[email protected]

Need another reason to make your toddler dinner instead of feeding him a prepackaged meal? New research shows a large number of dinners, snacks, and desserts sold in the United States that are designed for toddlers contain added sugar and salt, leaving them at risk for developing hypertension and diabetes later on in life.

Fortunately, commercial foods made for infants (vegetables, dinners, plain fruit without grains, dry cereals) sold in the United States tend to have little sugar and sodium added. But parents should still try to limit salty snacks, sweet desserts, and juice drinks, because they often contain more salt and sugar than kids need.

Approximately 79% of U.S. children aged 1-3 years eat more sodium than is recommended by the Institute of Medicine, noted Mary E. Cogswell, DrPH, a researcher from the Centers for Disease Control and Prevention in a study published in Pediatrics.

©Purestock/thinkstockphotos.com

Dr. Cogswell and her team of researchers looked at package information for 1,074 food products sold in the United States in 2012 that was marketed to infants, toddlers, or both.

Seventy-two percent of toddler dinners examined contained added sodium, and 32% percent of toddler dinners contained added sugar; 52% of ready-to-serve mixed grains and fruits contained too much added sugar. The majority of dairy-based desserts (70%) and fruit juices (88%) intended for both infant and toddler consumption also contained added sugar.

Limiting how much sugar and salt your children are exposed to can go a long way in preventing obesity and high blood pressure, so parents should look carefully at labels when selecting what foods to buy for toddlers.

“Key advice for parents includes limiting juice and avoiding sugar-sweetened beverages and energy-dense, nutrient-poor snacks; if purchasing commercial toddler foods, the labels should be checked for sodium and added sugar,” the authors wrote.

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I read with interest Dr. Hickner’s editorial, “How to avoid diagnostic errors” (J Fam Pract. 2014;63:625), and was fascinated by the diagnostic checklists developed by John Ely, MD, which are available at www.improvediagnosis.org/resource/resmgr/docs/diffdx.doc.

On his checklists, Dr. Ely suggests the material could be adapted for use on a handheld device, so I decided to convert Dr. Ely’s checklists from Microsoft Word to a PDF with hyperlinks so they would be easy to view on most tablets and smartphones. I kept the content exactly the same, but formatted each diagnostic problem as a “header,” which became the table of contents. Each of these table of contents headers is hyperlinked, so a user can simply tap on the item in the table of contents and jump to the correct page (“card”) in the document.

After converting Dr. Ely’s checklists to a PDF, I found them easy to use on both an iPhone and Google tablet.

Thank you again, Drs. Ely and Hickner, for your work in this area.

E. Chris Vincent, MD
Seattle, Wash

Dr. Vincent is one of the assistant editors for Clinical Inquiries, a monthly column in The Journal of Family Practice.

When patients can communicate with their physician via an online portal, the diagnostic process is greatly enhanced.Dr. Hickner’s list of 7 ways to avoid diagnostic errors was excellent. I would augment his sixth tip (“Follow up, follow up, follow up, and do so in a timely manner”) with something we tell all of our patients: “Keep me informed via our online portal.” When patients have such easy access to communication with their physician, the diagnostic process is greatly enhanced.

Joseph E. Scherger, MD, MPH
Rancho Mirage, Calif

I read with interest Dr. Hickner’s editorial, “How to avoid diagnostic errors” (J Fam Pract. 2014;63:625), and was fascinated by the diagnostic checklists developed by John Ely, MD, which are available at www.improvediagnosis.org/resource/resmgr/docs/diffdx.doc.

On his checklists, Dr. Ely suggests the material could be adapted for use on a handheld device, so I decided to convert Dr. Ely’s checklists from Microsoft Word to a PDF with hyperlinks so they would be easy to view on most tablets and smartphones. I kept the content exactly the same, but formatted each diagnostic problem as a “header,” which became the table of contents. Each of these table of contents headers is hyperlinked, so a user can simply tap on the item in the table of contents and jump to the correct page (“card”) in the document.

After converting Dr. Ely’s checklists to a PDF, I found them easy to use on both an iPhone and Google tablet.

Thank you again, Drs. Ely and Hickner, for your work in this area.

E. Chris Vincent, MD
Seattle, Wash

Dr. Vincent is one of the assistant editors for Clinical Inquiries, a monthly column in The Journal of Family Practice.

When patients can communicate with their physician via an online portal, the diagnostic process is greatly enhanced.Dr. Hickner’s list of 7 ways to avoid diagnostic errors was excellent. I would augment his sixth tip (“Follow up, follow up, follow up, and do so in a timely manner”) with something we tell all of our patients: “Keep me informed via our online portal.” When patients have such easy access to communication with their physician, the diagnostic process is greatly enhanced.

Joseph E. Scherger, MD, MPH
Rancho Mirage, Calif

I read with interest Dr. Hickner’s editorial, “How to avoid diagnostic errors” (J Fam Pract. 2014;63:625), and was fascinated by the diagnostic checklists developed by John Ely, MD, which are available at www.improvediagnosis.org/resource/resmgr/docs/diffdx.doc.

On his checklists, Dr. Ely suggests the material could be adapted for use on a handheld device, so I decided to convert Dr. Ely’s checklists from Microsoft Word to a PDF with hyperlinks so they would be easy to view on most tablets and smartphones. I kept the content exactly the same, but formatted each diagnostic problem as a “header,” which became the table of contents. Each of these table of contents headers is hyperlinked, so a user can simply tap on the item in the table of contents and jump to the correct page (“card”) in the document.

After converting Dr. Ely’s checklists to a PDF, I found them easy to use on both an iPhone and Google tablet.

Thank you again, Drs. Ely and Hickner, for your work in this area.

E. Chris Vincent, MD
Seattle, Wash

Dr. Vincent is one of the assistant editors for Clinical Inquiries, a monthly column in The Journal of Family Practice.

When patients can communicate with their physician via an online portal, the diagnostic process is greatly enhanced.Dr. Hickner’s list of 7 ways to avoid diagnostic errors was excellent. I would augment his sixth tip (“Follow up, follow up, follow up, and do so in a timely manner”) with something we tell all of our patients: “Keep me informed via our online portal.” When patients have such easy access to communication with their physician, the diagnostic process is greatly enhanced.

Joseph E. Scherger, MD, MPH
Rancho Mirage, Calif

Illustrative case

A 57-year-old man with diabetes refuses to fast before coming to the clinic for lipid testing because he’s afraid he’ll become hypoglycemic. You have not been able to obtain a lipid panel on him for more than a year and you want to determine his LDL level. Will a nonfasting lipid panel be useful?

Approximately 71 million US adults have high LDL.² The 2013 American College of Cardiology/American Heart Association guidelines recommend fasting cholesterol checks for all adults ages 21 and older for primary prevention of cardiovascular disease.³ The US Preventive Services Task Force (USPSTF) has long recommended screening cholesterol in adults to prevent atherosclerotic vascular disease.

In 2008, the USPSTF recommended lipid screening for all men ages 35 years and older, for all men ages 20 to 35 years who are at increased risk for coronary heart disease, and for all women ages 20 years and older who are at increased risk for coronary heart disease.⁴ The USPSTF recommends TC and HDL as the preferred screening tests and states that these tests can be performed on fasting or nonfasting samples, but if LDL is added, a fasting sample is recommended.⁴ Other national and international guidelines on cholesterol management also recommend a fasting lipid panel to stratify patients’ risk and determine treatment options.^5-7

LDL usually is reported as a calculated value using the Friedewald equation (LDL equals TC minus HDL minus [triglycerides divided by 5]).⁸ This calculation is not accurate for patients with triglyceride levels >400 mg/dL, which has prompted most authorities to recommend a fasting sample. That’s because while TC and HDL are not affected by food (and LDL may vary by only 10% or less), triglycerides can fluctuate by 20% to 30%, which would influence the calculation of a nonfasting LDL.^9,10 LDL can be measured directly, but the process is generally expensive and not commonly used.¹¹

The Centers for Disease Control and Prevention (CDC) estimates that over 20% of US adults (more than 48 million people) have not had a screening lipid panel in the previous 5 years.¹² One barrier to screening is that both physicians and patients often believe that a fasting specimen is required. Yet fasting specimens are difficult to obtain because they often require a separate visit to the clinic, which can result in lost time from work and additional transportation costs.

STUDY SUMMARY: There’s no difference between fasting and nonfasting LDL

Doran et al¹ used data from the NHANES-III survey to compare the prognostic value of fasting vs nonfasting LDL for all-cause mortality and cardiovascular mortality. NHANES-III is a nationally representative cross-sectional survey that was performed from 1988 to 1994.¹³ Doran et al¹ included 16,161 US adults ages 18 years and older for whom data on fasting time were available. Participants for whom LDL calculations were not possible due to missing HDL, TC, or triglyceride levels were excluded. Those with triglycerides ≥400 mg/dL were excluded from the primary analysis.

Participants were stratified based on fasting status (≥8 hours or <8 hours) and followed for a mean of 14 (± .22) years. To control for possible cofounders, researchers used propensity score matching to identify 4299 pairs of fasting and nonfasting individuals with similar cardiovascular risk factors, including race, smoking history, prior cardiovascular disease, cholesterol medication use, diabetes, elevated TC, low HDL, hypertension, enlarged waist circumference, and low socioeconomic status. After matching, the baseline characteristics of the fasting and nonfasting groups were similar.

The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar.The primary outcome was all-cause mortality, and the secondary outcome was cardiovascular mortality. The prognostic value of fasting and nonfasting LDL for these outcomes was evaluated as the area under the receiver operator curve (ROC) using the Hosmer-Lemeshow C-statistic.¹⁴ (In this case, similar C-statistics indicate that the tests have similar prognostic values.*) Kaplan-Meier curves were used to assess survival. The association of LDL with mortality, after adjustment of potential confounders, was evaluated using Cox proportional hazard models. The groups were divided into tertiles based on LDL levels (<100 mg/dL, 100-130 mg/dL, and >130 mg/dL).

As expected, compared to individuals in the first LDL tertile (<100 mg/dL), those with a higher LDL had an increased risk of all-cause mortality (hazard ratio [HR]=1.61; 95% confidence interval [CI], 1.25-2.08 [second tertile] and HR=2.10;  95% CI, 1.70-2.61 [third tertile]). The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar, as suggested by the C-statistics (0.59 [95% CI, 0.56-0.61] vs 0.58 [95% CI, 0.56-0.60]; P=.73).

The risk of cardiovascular mortality also increased with increasing LDL tertiles. As was the case with all-cause mortality, the prognostic value of fasting vs nonfasting status was similar for predicting cardiovascular mortality as observed by similar C-statistics (0.64 [95% CI, 0.62-0.66] vs 0.63 [95% CI, 0.60-0.65]; P=.49). In addition, fasting vs nonfasting C-statistics were similar for both diabetic and non-diabetic patients.

WHAT’S NEW: Results suggest fasting may no longer be necessary

While obtaining a fasting lipid panel is recommended by multiple guidelines and has become traditional practice, the need for fasting originated primarily out of concern for the effect of postprandial triglycerides on calculating LDL. This is the first study that compared the prognostic value of fasting and nonfasting LDL values for predicting mortality; it demonstrated that they are essentially the same.

CAVEATS: Fasting and nonfasting measurements were taken from different patients

The only challenge: It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles.The fasting and nonfasting lipids were not collected from the same individuals. However, to decrease confounding, Doran et al¹ factored in multiple cardiovascular risk factors as covariables.

Another caveat is that individuals with triglyceride levels >400 mg/dL were excluded. However, investigators ran a sensitivity analysis that included individuals with triglycerides >400 mg/dL and found no significant difference in C-statistics between the fasting and nonfasting groups.

CHALLENGES TO IMPLEMENTATION: Dropping the requirement to fast goes against established practice

It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles, but we see no other barriers to adopting this recommendation.

* The C-statistic is the probability that predicting the outcome is better than chance and is used to compare the goodness of fit of logistic regression models. Values for this measure range from 0.5 to 1.0. A value of 0.5 indicates that the model is no better than chance at making a prediction of membership in a group and a value of 1.0 indicates that the model perfectly identifies those within a group and those not.

ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Illustrative case

A 57-year-old man with diabetes refuses to fast before coming to the clinic for lipid testing because he’s afraid he’ll become hypoglycemic. You have not been able to obtain a lipid panel on him for more than a year and you want to determine his LDL level. Will a nonfasting lipid panel be useful?

Approximately 71 million US adults have high LDL.² The 2013 American College of Cardiology/American Heart Association guidelines recommend fasting cholesterol checks for all adults ages 21 and older for primary prevention of cardiovascular disease.³ The US Preventive Services Task Force (USPSTF) has long recommended screening cholesterol in adults to prevent atherosclerotic vascular disease.

In 2008, the USPSTF recommended lipid screening for all men ages 35 years and older, for all men ages 20 to 35 years who are at increased risk for coronary heart disease, and for all women ages 20 years and older who are at increased risk for coronary heart disease.⁴ The USPSTF recommends TC and HDL as the preferred screening tests and states that these tests can be performed on fasting or nonfasting samples, but if LDL is added, a fasting sample is recommended.⁴ Other national and international guidelines on cholesterol management also recommend a fasting lipid panel to stratify patients’ risk and determine treatment options.^5-7

LDL usually is reported as a calculated value using the Friedewald equation (LDL equals TC minus HDL minus [triglycerides divided by 5]).⁸ This calculation is not accurate for patients with triglyceride levels >400 mg/dL, which has prompted most authorities to recommend a fasting sample. That’s because while TC and HDL are not affected by food (and LDL may vary by only 10% or less), triglycerides can fluctuate by 20% to 30%, which would influence the calculation of a nonfasting LDL.^9,10 LDL can be measured directly, but the process is generally expensive and not commonly used.¹¹

The Centers for Disease Control and Prevention (CDC) estimates that over 20% of US adults (more than 48 million people) have not had a screening lipid panel in the previous 5 years.¹² One barrier to screening is that both physicians and patients often believe that a fasting specimen is required. Yet fasting specimens are difficult to obtain because they often require a separate visit to the clinic, which can result in lost time from work and additional transportation costs.

STUDY SUMMARY: There’s no difference between fasting and nonfasting LDL

Doran et al¹ used data from the NHANES-III survey to compare the prognostic value of fasting vs nonfasting LDL for all-cause mortality and cardiovascular mortality. NHANES-III is a nationally representative cross-sectional survey that was performed from 1988 to 1994.¹³ Doran et al¹ included 16,161 US adults ages 18 years and older for whom data on fasting time were available. Participants for whom LDL calculations were not possible due to missing HDL, TC, or triglyceride levels were excluded. Those with triglycerides ≥400 mg/dL were excluded from the primary analysis.

Participants were stratified based on fasting status (≥8 hours or <8 hours) and followed for a mean of 14 (± .22) years. To control for possible cofounders, researchers used propensity score matching to identify 4299 pairs of fasting and nonfasting individuals with similar cardiovascular risk factors, including race, smoking history, prior cardiovascular disease, cholesterol medication use, diabetes, elevated TC, low HDL, hypertension, enlarged waist circumference, and low socioeconomic status. After matching, the baseline characteristics of the fasting and nonfasting groups were similar.

The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar.The primary outcome was all-cause mortality, and the secondary outcome was cardiovascular mortality. The prognostic value of fasting and nonfasting LDL for these outcomes was evaluated as the area under the receiver operator curve (ROC) using the Hosmer-Lemeshow C-statistic.¹⁴ (In this case, similar C-statistics indicate that the tests have similar prognostic values.*) Kaplan-Meier curves were used to assess survival. The association of LDL with mortality, after adjustment of potential confounders, was evaluated using Cox proportional hazard models. The groups were divided into tertiles based on LDL levels (<100 mg/dL, 100-130 mg/dL, and >130 mg/dL).

As expected, compared to individuals in the first LDL tertile (<100 mg/dL), those with a higher LDL had an increased risk of all-cause mortality (hazard ratio [HR]=1.61; 95% confidence interval [CI], 1.25-2.08 [second tertile] and HR=2.10;  95% CI, 1.70-2.61 [third tertile]). The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar, as suggested by the C-statistics (0.59 [95% CI, 0.56-0.61] vs 0.58 [95% CI, 0.56-0.60]; P=.73).

The risk of cardiovascular mortality also increased with increasing LDL tertiles. As was the case with all-cause mortality, the prognostic value of fasting vs nonfasting status was similar for predicting cardiovascular mortality as observed by similar C-statistics (0.64 [95% CI, 0.62-0.66] vs 0.63 [95% CI, 0.60-0.65]; P=.49). In addition, fasting vs nonfasting C-statistics were similar for both diabetic and non-diabetic patients.

WHAT’S NEW: Results suggest fasting may no longer be necessary

While obtaining a fasting lipid panel is recommended by multiple guidelines and has become traditional practice, the need for fasting originated primarily out of concern for the effect of postprandial triglycerides on calculating LDL. This is the first study that compared the prognostic value of fasting and nonfasting LDL values for predicting mortality; it demonstrated that they are essentially the same.

CAVEATS: Fasting and nonfasting measurements were taken from different patients

The only challenge: It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles.The fasting and nonfasting lipids were not collected from the same individuals. However, to decrease confounding, Doran et al¹ factored in multiple cardiovascular risk factors as covariables.

Another caveat is that individuals with triglyceride levels >400 mg/dL were excluded. However, investigators ran a sensitivity analysis that included individuals with triglycerides >400 mg/dL and found no significant difference in C-statistics between the fasting and nonfasting groups.

CHALLENGES TO IMPLEMENTATION: Dropping the requirement to fast goes against established practice

It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles, but we see no other barriers to adopting this recommendation.

* The C-statistic is the probability that predicting the outcome is better than chance and is used to compare the goodness of fit of logistic regression models. Values for this measure range from 0.5 to 1.0. A value of 0.5 indicates that the model is no better than chance at making a prediction of membership in a group and a value of 1.0 indicates that the model perfectly identifies those within a group and those not.

ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Illustrative case

A 57-year-old man with diabetes refuses to fast before coming to the clinic for lipid testing because he’s afraid he’ll become hypoglycemic. You have not been able to obtain a lipid panel on him for more than a year and you want to determine his LDL level. Will a nonfasting lipid panel be useful?

Approximately 71 million US adults have high LDL.² The 2013 American College of Cardiology/American Heart Association guidelines recommend fasting cholesterol checks for all adults ages 21 and older for primary prevention of cardiovascular disease.³ The US Preventive Services Task Force (USPSTF) has long recommended screening cholesterol in adults to prevent atherosclerotic vascular disease.

In 2008, the USPSTF recommended lipid screening for all men ages 35 years and older, for all men ages 20 to 35 years who are at increased risk for coronary heart disease, and for all women ages 20 years and older who are at increased risk for coronary heart disease.⁴ The USPSTF recommends TC and HDL as the preferred screening tests and states that these tests can be performed on fasting or nonfasting samples, but if LDL is added, a fasting sample is recommended.⁴ Other national and international guidelines on cholesterol management also recommend a fasting lipid panel to stratify patients’ risk and determine treatment options.^5-7

LDL usually is reported as a calculated value using the Friedewald equation (LDL equals TC minus HDL minus [triglycerides divided by 5]).⁸ This calculation is not accurate for patients with triglyceride levels >400 mg/dL, which has prompted most authorities to recommend a fasting sample. That’s because while TC and HDL are not affected by food (and LDL may vary by only 10% or less), triglycerides can fluctuate by 20% to 30%, which would influence the calculation of a nonfasting LDL.^9,10 LDL can be measured directly, but the process is generally expensive and not commonly used.¹¹

The Centers for Disease Control and Prevention (CDC) estimates that over 20% of US adults (more than 48 million people) have not had a screening lipid panel in the previous 5 years.¹² One barrier to screening is that both physicians and patients often believe that a fasting specimen is required. Yet fasting specimens are difficult to obtain because they often require a separate visit to the clinic, which can result in lost time from work and additional transportation costs.

STUDY SUMMARY: There’s no difference between fasting and nonfasting LDL

Doran et al¹ used data from the NHANES-III survey to compare the prognostic value of fasting vs nonfasting LDL for all-cause mortality and cardiovascular mortality. NHANES-III is a nationally representative cross-sectional survey that was performed from 1988 to 1994.¹³ Doran et al¹ included 16,161 US adults ages 18 years and older for whom data on fasting time were available. Participants for whom LDL calculations were not possible due to missing HDL, TC, or triglyceride levels were excluded. Those with triglycerides ≥400 mg/dL were excluded from the primary analysis.

Participants were stratified based on fasting status (≥8 hours or <8 hours) and followed for a mean of 14 (± .22) years. To control for possible cofounders, researchers used propensity score matching to identify 4299 pairs of fasting and nonfasting individuals with similar cardiovascular risk factors, including race, smoking history, prior cardiovascular disease, cholesterol medication use, diabetes, elevated TC, low HDL, hypertension, enlarged waist circumference, and low socioeconomic status. After matching, the baseline characteristics of the fasting and nonfasting groups were similar.

The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar.The primary outcome was all-cause mortality, and the secondary outcome was cardiovascular mortality. The prognostic value of fasting and nonfasting LDL for these outcomes was evaluated as the area under the receiver operator curve (ROC) using the Hosmer-Lemeshow C-statistic.¹⁴ (In this case, similar C-statistics indicate that the tests have similar prognostic values.*) Kaplan-Meier curves were used to assess survival. The association of LDL with mortality, after adjustment of potential confounders, was evaluated using Cox proportional hazard models. The groups were divided into tertiles based on LDL levels (<100 mg/dL, 100-130 mg/dL, and >130 mg/dL).

As expected, compared to individuals in the first LDL tertile (<100 mg/dL), those with a higher LDL had an increased risk of all-cause mortality (hazard ratio [HR]=1.61; 95% confidence interval [CI], 1.25-2.08 [second tertile] and HR=2.10;  95% CI, 1.70-2.61 [third tertile]). The prognostic value of fasting vs nonfasting status for predicting all-cause mortality was similar, as suggested by the C-statistics (0.59 [95% CI, 0.56-0.61] vs 0.58 [95% CI, 0.56-0.60]; P=.73).

The risk of cardiovascular mortality also increased with increasing LDL tertiles. As was the case with all-cause mortality, the prognostic value of fasting vs nonfasting status was similar for predicting cardiovascular mortality as observed by similar C-statistics (0.64 [95% CI, 0.62-0.66] vs 0.63 [95% CI, 0.60-0.65]; P=.49). In addition, fasting vs nonfasting C-statistics were similar for both diabetic and non-diabetic patients.

WHAT’S NEW: Results suggest fasting may no longer be necessary

While obtaining a fasting lipid panel is recommended by multiple guidelines and has become traditional practice, the need for fasting originated primarily out of concern for the effect of postprandial triglycerides on calculating LDL. This is the first study that compared the prognostic value of fasting and nonfasting LDL values for predicting mortality; it demonstrated that they are essentially the same.

CAVEATS: Fasting and nonfasting measurements were taken from different patients

The only challenge: It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles.The fasting and nonfasting lipids were not collected from the same individuals. However, to decrease confounding, Doran et al¹ factored in multiple cardiovascular risk factors as covariables.

Another caveat is that individuals with triglyceride levels >400 mg/dL were excluded. However, investigators ran a sensitivity analysis that included individuals with triglycerides >400 mg/dL and found no significant difference in C-statistics between the fasting and nonfasting groups.

CHALLENGES TO IMPLEMENTATION: Dropping the requirement to fast goes against established practice

It may be difficult for physicians to change a longstanding practice of checking fasting lipid profiles, but we see no other barriers to adopting this recommendation.

* The C-statistic is the probability that predicting the outcome is better than chance and is used to compare the goodness of fit of logistic regression models. Values for this measure range from 0.5 to 1.0. A value of 0.5 indicates that the model is no better than chance at making a prediction of membership in a group and a value of 1.0 indicates that the model perfectly identifies those within a group and those not.

ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

THE CASE

An 84-year old woman came to the emergency department (ED) with sharp back pain on her left side that she’d had for 4 days. The pain radiated to her posterior hips when standing. She said her whole body felt achy and she was experiencing weakness in both legs.

The patient had a history of hypertension, coronary artery disease, and aortic stenosis; she’d received a bioprosthetic aortic valve 7 years ago. She was not immunocompromised or receiving steroids but was taking docusate, oxybutynin, carvedilol, amlodipine, atorvastatin, furosemide, rivaroxaban, and a multivitamin. Her physical exam, vital signs, and complete blood count (CBC) were normal. An x-ray of the lumbar spine showed degenerative joint/disc disease and spondylosis at L4-L5 and L5-S1. The patient was sent home with oxycodone/acetaminophen 5 mg/325 mg every 6 hours as needed for pain and told to follow up with her family physician (FP).

Six days later, the patient went to see her FP and told her that her symptoms hadn’t improved. She was afebrile and her blood pressure was 150/80 mm Hg. Her muscle strength was 4/5 with hip flexion bilaterally; the rest of her strength was 5/5. There was no lumbar paraspinal tenderness and she had a negative straight leg raise test. No other neurologic deficits were noted. The FP prescribed physical therapy at home with a licensed therapist, which consisted of stretching exercises and active, dynamic exercise to improve the patient’s range of motion. She also ordered outpatient lumbar magnetic resonance imaging (MRI).

THE DIAGNOSIS

We are unaware of any other case reports that describe S. salivarius as having caused osteomyelitis without concurrent endocarditis.Approximately 3 weeks later, the patient’s MRI revealed osteomyelitis/discitis at the L3-L4 level and severe tricompartmental stenosis from L2-L3 through L4-L5. A day after receiving the results—and about a month after having first gone to the ED—the patient was admitted to the hospital. She was afebrile and her blood pressure was 148/75 mm Hg. Her physical exam revealed no leukocytosis or neurologic deficits, but did show a systolic murmur from her aortic valve.

She had an erythrocyte sedimentation rate (ESR) of 77 mm/hr (normal range for women, <30 mm/hr) and her C-reactive protein (CRP) level was 5.88 mg/dL (<.50 mg/dL indicates average risk for cardiovascular disease). A transesophageal echocardiogram was performed and there was no sign of vegetation or thrombi. However, blood cultures were positive for Streptococcus salivarius—a bacterium found on human dental plaque—which we determined was the cause of the osteomyelitis.

To the best of our knowledge, there have been no other case reports that described S. salivarius as having caused osteomyelitis without concurrent endocarditis.

DISCUSSION

Back pain is a common and costly issue among primary care patients. More than two-thirds of adults suffer from low back pain at some point, primarily without underlying malignancy or neurologic deficits.^1,2 Acute low back pain is often mechanical (97%); however, other causes, including infection, may be to blame (TABLE).¹ Most acute back pain will improve with conservative treatment and patients need only reassurance of a favorable prognosis, but 20% of patients may develop chronic back pain.²

The diagnostic approach to low back pain varies widely.³ Some data indicate that early imaging of back pain can lead to unneeded follow-up testing, radiation exposure, unnecessary surgery, patient “labeling,” and increased health care costs, all of which suggest that routine imaging shouldn’t be pursued in acute low back pain.⁴

Red flags for acute low back pain that warrant imaging include age >50 years, fever, weight loss, elevated ESR, history of malignancy, trauma, motor deficits, steroid or illicit drug use, and litigation.¹ If not already done, it’s also important to order a CBC, ESR, and CRP for patients with any of these red flags.

Imaging studies are important, but clinical correlation is crucial because imaging can reveal disk abnormalities even in healthy, asymptomatic patients.⁵ Computed tomography scans or MRI is indicated for patients with neurologic deficits or nerve root tension signs, but only if a patient is a potential candidate for surgery or epidural steroid injection.^6,7 If you suspect an infection (such as spondylodiscitis or osteomyelitis), diagnosing the condition quickly is key.

Our patient had 2 red flags (age >50 years and elevated ESR) that helped us reach an unlikely diagnosis of lumbar osteomyelitis with S. salivarius as the cause. Degenerative spinal disease seen on x-ray may have delayed our patient’s diagnosis. If our patient had had an ESR or CRP test earlier, or if further imaging had been conducted sooner (given her proximal muscle weakness), the correct diagnosis would have been made more quickly and appropriate treatment provided sooner.

Our patient

The patient was started on a 6-week course of intravenous ceftriaxone 2g/d, which she continued to receive at home via a peripherally inserted central catheter. The patient was instructed at discharge (on Day 8) to follow up with her FP, which she did 12 days later. At that visit, her back pain was improved and her ESR and CRP levels were within normal ranges.

THE TAKEAWAY

When evaluating a patient who presents with low back pain, perform a focused history and be on the lookout for “red flags” that warrant further imaging and testing. Routine imaging is not recommended for patients with nonspecific low back pain, but imaging may be indicated for patients with neurologic deficits or nerve root tension signs.

A patient with low back pain caused by osteomyelitis may present with fever, elevated ESR, and/or motor deficits. Identifying the bacteria underlying the infection will help guide selection of appropriate antibiotics.

THE CASE

An 84-year old woman came to the emergency department (ED) with sharp back pain on her left side that she’d had for 4 days. The pain radiated to her posterior hips when standing. She said her whole body felt achy and she was experiencing weakness in both legs.

The patient had a history of hypertension, coronary artery disease, and aortic stenosis; she’d received a bioprosthetic aortic valve 7 years ago. She was not immunocompromised or receiving steroids but was taking docusate, oxybutynin, carvedilol, amlodipine, atorvastatin, furosemide, rivaroxaban, and a multivitamin. Her physical exam, vital signs, and complete blood count (CBC) were normal. An x-ray of the lumbar spine showed degenerative joint/disc disease and spondylosis at L4-L5 and L5-S1. The patient was sent home with oxycodone/acetaminophen 5 mg/325 mg every 6 hours as needed for pain and told to follow up with her family physician (FP).

Six days later, the patient went to see her FP and told her that her symptoms hadn’t improved. She was afebrile and her blood pressure was 150/80 mm Hg. Her muscle strength was 4/5 with hip flexion bilaterally; the rest of her strength was 5/5. There was no lumbar paraspinal tenderness and she had a negative straight leg raise test. No other neurologic deficits were noted. The FP prescribed physical therapy at home with a licensed therapist, which consisted of stretching exercises and active, dynamic exercise to improve the patient’s range of motion. She also ordered outpatient lumbar magnetic resonance imaging (MRI).

THE DIAGNOSIS

We are unaware of any other case reports that describe S. salivarius as having caused osteomyelitis without concurrent endocarditis.Approximately 3 weeks later, the patient’s MRI revealed osteomyelitis/discitis at the L3-L4 level and severe tricompartmental stenosis from L2-L3 through L4-L5. A day after receiving the results—and about a month after having first gone to the ED—the patient was admitted to the hospital. She was afebrile and her blood pressure was 148/75 mm Hg. Her physical exam revealed no leukocytosis or neurologic deficits, but did show a systolic murmur from her aortic valve.

She had an erythrocyte sedimentation rate (ESR) of 77 mm/hr (normal range for women, <30 mm/hr) and her C-reactive protein (CRP) level was 5.88 mg/dL (<.50 mg/dL indicates average risk for cardiovascular disease). A transesophageal echocardiogram was performed and there was no sign of vegetation or thrombi. However, blood cultures were positive for Streptococcus salivarius—a bacterium found on human dental plaque—which we determined was the cause of the osteomyelitis.

To the best of our knowledge, there have been no other case reports that described S. salivarius as having caused osteomyelitis without concurrent endocarditis.

DISCUSSION

Back pain is a common and costly issue among primary care patients. More than two-thirds of adults suffer from low back pain at some point, primarily without underlying malignancy or neurologic deficits.^1,2 Acute low back pain is often mechanical (97%); however, other causes, including infection, may be to blame (TABLE).¹ Most acute back pain will improve with conservative treatment and patients need only reassurance of a favorable prognosis, but 20% of patients may develop chronic back pain.²

The diagnostic approach to low back pain varies widely.³ Some data indicate that early imaging of back pain can lead to unneeded follow-up testing, radiation exposure, unnecessary surgery, patient “labeling,” and increased health care costs, all of which suggest that routine imaging shouldn’t be pursued in acute low back pain.⁴

Red flags for acute low back pain that warrant imaging include age >50 years, fever, weight loss, elevated ESR, history of malignancy, trauma, motor deficits, steroid or illicit drug use, and litigation.¹ If not already done, it’s also important to order a CBC, ESR, and CRP for patients with any of these red flags.

Imaging studies are important, but clinical correlation is crucial because imaging can reveal disk abnormalities even in healthy, asymptomatic patients.⁵ Computed tomography scans or MRI is indicated for patients with neurologic deficits or nerve root tension signs, but only if a patient is a potential candidate for surgery or epidural steroid injection.^6,7 If you suspect an infection (such as spondylodiscitis or osteomyelitis), diagnosing the condition quickly is key.

Our patient had 2 red flags (age >50 years and elevated ESR) that helped us reach an unlikely diagnosis of lumbar osteomyelitis with S. salivarius as the cause. Degenerative spinal disease seen on x-ray may have delayed our patient’s diagnosis. If our patient had had an ESR or CRP test earlier, or if further imaging had been conducted sooner (given her proximal muscle weakness), the correct diagnosis would have been made more quickly and appropriate treatment provided sooner.

Our patient

The patient was started on a 6-week course of intravenous ceftriaxone 2g/d, which she continued to receive at home via a peripherally inserted central catheter. The patient was instructed at discharge (on Day 8) to follow up with her FP, which she did 12 days later. At that visit, her back pain was improved and her ESR and CRP levels were within normal ranges.

THE TAKEAWAY

When evaluating a patient who presents with low back pain, perform a focused history and be on the lookout for “red flags” that warrant further imaging and testing. Routine imaging is not recommended for patients with nonspecific low back pain, but imaging may be indicated for patients with neurologic deficits or nerve root tension signs.

A patient with low back pain caused by osteomyelitis may present with fever, elevated ESR, and/or motor deficits. Identifying the bacteria underlying the infection will help guide selection of appropriate antibiotics.

THE CASE

An 84-year old woman came to the emergency department (ED) with sharp back pain on her left side that she’d had for 4 days. The pain radiated to her posterior hips when standing. She said her whole body felt achy and she was experiencing weakness in both legs.

The patient had a history of hypertension, coronary artery disease, and aortic stenosis; she’d received a bioprosthetic aortic valve 7 years ago. She was not immunocompromised or receiving steroids but was taking docusate, oxybutynin, carvedilol, amlodipine, atorvastatin, furosemide, rivaroxaban, and a multivitamin. Her physical exam, vital signs, and complete blood count (CBC) were normal. An x-ray of the lumbar spine showed degenerative joint/disc disease and spondylosis at L4-L5 and L5-S1. The patient was sent home with oxycodone/acetaminophen 5 mg/325 mg every 6 hours as needed for pain and told to follow up with her family physician (FP).

Six days later, the patient went to see her FP and told her that her symptoms hadn’t improved. She was afebrile and her blood pressure was 150/80 mm Hg. Her muscle strength was 4/5 with hip flexion bilaterally; the rest of her strength was 5/5. There was no lumbar paraspinal tenderness and she had a negative straight leg raise test. No other neurologic deficits were noted. The FP prescribed physical therapy at home with a licensed therapist, which consisted of stretching exercises and active, dynamic exercise to improve the patient’s range of motion. She also ordered outpatient lumbar magnetic resonance imaging (MRI).

THE DIAGNOSIS

We are unaware of any other case reports that describe S. salivarius as having caused osteomyelitis without concurrent endocarditis.Approximately 3 weeks later, the patient’s MRI revealed osteomyelitis/discitis at the L3-L4 level and severe tricompartmental stenosis from L2-L3 through L4-L5. A day after receiving the results—and about a month after having first gone to the ED—the patient was admitted to the hospital. She was afebrile and her blood pressure was 148/75 mm Hg. Her physical exam revealed no leukocytosis or neurologic deficits, but did show a systolic murmur from her aortic valve.

She had an erythrocyte sedimentation rate (ESR) of 77 mm/hr (normal range for women, <30 mm/hr) and her C-reactive protein (CRP) level was 5.88 mg/dL (<.50 mg/dL indicates average risk for cardiovascular disease). A transesophageal echocardiogram was performed and there was no sign of vegetation or thrombi. However, blood cultures were positive for Streptococcus salivarius—a bacterium found on human dental plaque—which we determined was the cause of the osteomyelitis.

To the best of our knowledge, there have been no other case reports that described S. salivarius as having caused osteomyelitis without concurrent endocarditis.

DISCUSSION

Back pain is a common and costly issue among primary care patients. More than two-thirds of adults suffer from low back pain at some point, primarily without underlying malignancy or neurologic deficits.^1,2 Acute low back pain is often mechanical (97%); however, other causes, including infection, may be to blame (TABLE).¹ Most acute back pain will improve with conservative treatment and patients need only reassurance of a favorable prognosis, but 20% of patients may develop chronic back pain.²

The diagnostic approach to low back pain varies widely.³ Some data indicate that early imaging of back pain can lead to unneeded follow-up testing, radiation exposure, unnecessary surgery, patient “labeling,” and increased health care costs, all of which suggest that routine imaging shouldn’t be pursued in acute low back pain.⁴

Red flags for acute low back pain that warrant imaging include age >50 years, fever, weight loss, elevated ESR, history of malignancy, trauma, motor deficits, steroid or illicit drug use, and litigation.¹ If not already done, it’s also important to order a CBC, ESR, and CRP for patients with any of these red flags.

Imaging studies are important, but clinical correlation is crucial because imaging can reveal disk abnormalities even in healthy, asymptomatic patients.⁵ Computed tomography scans or MRI is indicated for patients with neurologic deficits or nerve root tension signs, but only if a patient is a potential candidate for surgery or epidural steroid injection.^6,7 If you suspect an infection (such as spondylodiscitis or osteomyelitis), diagnosing the condition quickly is key.

Our patient had 2 red flags (age >50 years and elevated ESR) that helped us reach an unlikely diagnosis of lumbar osteomyelitis with S. salivarius as the cause. Degenerative spinal disease seen on x-ray may have delayed our patient’s diagnosis. If our patient had had an ESR or CRP test earlier, or if further imaging had been conducted sooner (given her proximal muscle weakness), the correct diagnosis would have been made more quickly and appropriate treatment provided sooner.

Our patient

The patient was started on a 6-week course of intravenous ceftriaxone 2g/d, which she continued to receive at home via a peripherally inserted central catheter. The patient was instructed at discharge (on Day 8) to follow up with her FP, which she did 12 days later. At that visit, her back pain was improved and her ESR and CRP levels were within normal ranges.

THE TAKEAWAY

When evaluating a patient who presents with low back pain, perform a focused history and be on the lookout for “red flags” that warrant further imaging and testing. Routine imaging is not recommended for patients with nonspecific low back pain, but imaging may be indicated for patients with neurologic deficits or nerve root tension signs.

A patient with low back pain caused by osteomyelitis may present with fever, elevated ESR, and/or motor deficits. Identifying the bacteria underlying the infection will help guide selection of appropriate antibiotics.