Children with proliferative lupus nephritis appear to do similarly well after using induction treatment with mycophenolate mofetil or IV cyclophosphamide, according to findings in the real-world U.K. Juvenile Systemic Lupus Erythematosus Cohort Study.

HYWARDS/Getty Images

The study involved 34 patients who received mycophenolate mofetil and 17 who received IV cyclophosphamide as induction therapy for proliferative lupus nephritis in juvenile-onset systemic lupus erythematosus (JSLE). Along with her coinvestigators, first author Eve M.D. Smith, MD, PhD, of the University of Liverpool (England) and Alder Hey Children’s NHS Foundation Trust, described it as the largest study to date investigating induction treatments for proliferative lupus nephritis in JSLE.

The patients were aged 16 years or younger at diagnosis and monitored during 2006-2018 as part of the U.K. JSLE Cohort Study. They met four or more American College of Rheumatology SLE classification criteria and had a renal biopsy result demonstrating proliferative lupus nephritis, defined as class III or IV lupus nephritis by the International Society of Nephrology/Renal Pathology Society. Within the mycophenolate group, half received oral prednisolone only and half received both IV methylprednisolone and oral prednisolone, whereas 2 in the cyclophosphamide group received oral prednisolone only and 15 received both IV methylprednisolone and oral prednisolone.

All the patient demographic factors at baseline – including gender, ethnicity, age at diagnosis, and age at lupus nephritis onset – were similar in both treatment groups.

The investigators detected no significant differences between the two treatment groups at 4-8 and 10-14 months post renal biopsy and last follow-up in renal pediatric British Isles Lupus Assessment Grade scores, urine albumin/creatinine ratio, serum creatinine, erythrocyte sedimentation rate, anti-double stranded DNA antibody, Complement 3 levels, and patient/physician global scores. JSLE-related damage on the Systemic Lupus International Collaborating Clinics Standardized Damage Index also was no different between the groups after a median 13 months following renal biopsy. Lupus nephritis became inactive in 82%-85% of each group, taking a median of 262 days with mycophenolate and 151 days with IV cyclophosphamide, while flares occurred in 69% treated with mycophenolate at a median of 451 days and in 50% with cyclophosphamide at a median of 343 days.

“Results from the presented study highlight the need for prospective comparison of mycophenolate mofetil versus IV cyclophosphamide induction treatment to better inform lupus nephritis treatment protocols for children, especially given IV cyclophosphamide’s poor safety profile,” the investigators wrote.

[email protected]

SOURCE: Smith EMD et al. Lupus. 2019 Mar 14. doi: 10.1177/0961203319836712.

Children with proliferative lupus nephritis appear to do similarly well after using induction treatment with mycophenolate mofetil or IV cyclophosphamide, according to findings in the real-world U.K. Juvenile Systemic Lupus Erythematosus Cohort Study.

HYWARDS/Getty Images

The study involved 34 patients who received mycophenolate mofetil and 17 who received IV cyclophosphamide as induction therapy for proliferative lupus nephritis in juvenile-onset systemic lupus erythematosus (JSLE). Along with her coinvestigators, first author Eve M.D. Smith, MD, PhD, of the University of Liverpool (England) and Alder Hey Children’s NHS Foundation Trust, described it as the largest study to date investigating induction treatments for proliferative lupus nephritis in JSLE.

The patients were aged 16 years or younger at diagnosis and monitored during 2006-2018 as part of the U.K. JSLE Cohort Study. They met four or more American College of Rheumatology SLE classification criteria and had a renal biopsy result demonstrating proliferative lupus nephritis, defined as class III or IV lupus nephritis by the International Society of Nephrology/Renal Pathology Society. Within the mycophenolate group, half received oral prednisolone only and half received both IV methylprednisolone and oral prednisolone, whereas 2 in the cyclophosphamide group received oral prednisolone only and 15 received both IV methylprednisolone and oral prednisolone.

All the patient demographic factors at baseline – including gender, ethnicity, age at diagnosis, and age at lupus nephritis onset – were similar in both treatment groups.

The investigators detected no significant differences between the two treatment groups at 4-8 and 10-14 months post renal biopsy and last follow-up in renal pediatric British Isles Lupus Assessment Grade scores, urine albumin/creatinine ratio, serum creatinine, erythrocyte sedimentation rate, anti-double stranded DNA antibody, Complement 3 levels, and patient/physician global scores. JSLE-related damage on the Systemic Lupus International Collaborating Clinics Standardized Damage Index also was no different between the groups after a median 13 months following renal biopsy. Lupus nephritis became inactive in 82%-85% of each group, taking a median of 262 days with mycophenolate and 151 days with IV cyclophosphamide, while flares occurred in 69% treated with mycophenolate at a median of 451 days and in 50% with cyclophosphamide at a median of 343 days.

“Results from the presented study highlight the need for prospective comparison of mycophenolate mofetil versus IV cyclophosphamide induction treatment to better inform lupus nephritis treatment protocols for children, especially given IV cyclophosphamide’s poor safety profile,” the investigators wrote.

[email protected]

SOURCE: Smith EMD et al. Lupus. 2019 Mar 14. doi: 10.1177/0961203319836712.

Children with proliferative lupus nephritis appear to do similarly well after using induction treatment with mycophenolate mofetil or IV cyclophosphamide, according to findings in the real-world U.K. Juvenile Systemic Lupus Erythematosus Cohort Study.

HYWARDS/Getty Images

The study involved 34 patients who received mycophenolate mofetil and 17 who received IV cyclophosphamide as induction therapy for proliferative lupus nephritis in juvenile-onset systemic lupus erythematosus (JSLE). Along with her coinvestigators, first author Eve M.D. Smith, MD, PhD, of the University of Liverpool (England) and Alder Hey Children’s NHS Foundation Trust, described it as the largest study to date investigating induction treatments for proliferative lupus nephritis in JSLE.

The patients were aged 16 years or younger at diagnosis and monitored during 2006-2018 as part of the U.K. JSLE Cohort Study. They met four or more American College of Rheumatology SLE classification criteria and had a renal biopsy result demonstrating proliferative lupus nephritis, defined as class III or IV lupus nephritis by the International Society of Nephrology/Renal Pathology Society. Within the mycophenolate group, half received oral prednisolone only and half received both IV methylprednisolone and oral prednisolone, whereas 2 in the cyclophosphamide group received oral prednisolone only and 15 received both IV methylprednisolone and oral prednisolone.

All the patient demographic factors at baseline – including gender, ethnicity, age at diagnosis, and age at lupus nephritis onset – were similar in both treatment groups.

The investigators detected no significant differences between the two treatment groups at 4-8 and 10-14 months post renal biopsy and last follow-up in renal pediatric British Isles Lupus Assessment Grade scores, urine albumin/creatinine ratio, serum creatinine, erythrocyte sedimentation rate, anti-double stranded DNA antibody, Complement 3 levels, and patient/physician global scores. JSLE-related damage on the Systemic Lupus International Collaborating Clinics Standardized Damage Index also was no different between the groups after a median 13 months following renal biopsy. Lupus nephritis became inactive in 82%-85% of each group, taking a median of 262 days with mycophenolate and 151 days with IV cyclophosphamide, while flares occurred in 69% treated with mycophenolate at a median of 451 days and in 50% with cyclophosphamide at a median of 343 days.

“Results from the presented study highlight the need for prospective comparison of mycophenolate mofetil versus IV cyclophosphamide induction treatment to better inform lupus nephritis treatment protocols for children, especially given IV cyclophosphamide’s poor safety profile,” the investigators wrote.

[email protected]

SOURCE: Smith EMD et al. Lupus. 2019 Mar 14. doi: 10.1177/0961203319836712.

The Diagnosis:  Primary Cutaneous Perivascular Epithelioid Cell Tumor  

Perivascular epithelioid cell tumors (PEComas) were first described in 1996.¹ They comprise a family of rare mesenchymal neoplasms that have a unique characteristic of staining positive for melanocytic and smooth muscle markers on immunohistochemistry.² These neoplasms have been described in many areas of the body including the uterus, bladder, heart, pancreas, and prostate. The majority of PEComas are extracutaneous, with only 8% of reported cases originating on the skin.³ A case of primary cutaneous PEComa (pcPEComa) was described in 2003.⁴ The primary cutaneous form is extremely rare.^3,5-7  

A broad deep shave biopsy was performed in our patient in an attempt to sample the entire lesion. Histopathologic examination of the nodule demonstrated a dermal neoplasm comprised of a diffuse proliferation of large polygonal cells with abundant clear cytoplasm, fine chromatin, and prominent nucleoli (Figure 1A). Higher-power magnification showed moderate nuclear pleomorphism and only rare mitotic figures (Figure 1B).

Immunohistochemical staining revealed positivity for myomelanocytic markers with positivity for human melanoma black 45 (HMB-45)(Figure 2) and desmin (not shown). Additionally, the tumor was positive for CD163 and negative for smooth muscle actin, cytokeratin, and S-100 protein.  

Perivascular epithelioid cell tumors are characterized histologically as mesenchymal neoplasms containing large epithelioid to spindled cells with a slightly granular, vacuolated cytoplasm. These cells often are found in close proximity to vascular structures.^3,5,8 The hallmark of PEComas is the expression of both melanocytic and muscle markers.^3,8 A review of staining patterns of pcPEComas emphasized that immunophenotypes between visceral and primary cutaneous forms may vary considerably.^3,5,8 The most consistent and sensitive melanocytic marker is HMB-45 (88%-92% positive).^3,8 Positive Melan-A staining varies in the literature from 0% to 50% of cases.³ Our patient's neoplasm expressed the characteristic myomelanocytic immunophenotype with both HMB-45 and desmin positivity. 

Given the histologic characteristics, these lesions can be mistaken for melanocytic and other nonmelanocytic tumors with a clear cell morphology such as balloon cell nevus, hypomelanotic blue nevus, and melanoma.^2,3 A pigmented case of pcPEComa was reported in 2015 and was originally diagnosed as metastatic melanoma.⁶ Unlike pcPEComa, melanoma usually stains positive with S-100 protein in up to 99% of cases⁸ and is negative for muscle markers; however, a case series reported S-100 protein positivity in 38% of pcPEComas.³ Nonmelanocytic neoplasms in the histologic differential diagnosis include clear cell sarcoma and clear cell renal cell carcinoma, both of which show immunoreactivity for cytokeratin.⁹  

Histologic criteria exist for establishing malignancy potential for visceral PEComas but not for pcPEComas, though it has been suggested that the same malignancy criteria should be applied to pcPEComas.^3,9 Features associated with malignancy include size greater than 8 cm, mitotic activity greater than 1 mitosis per 50 high-power fields, infiltrative growth pattern, high nuclear grade, necrosis, and vascular invasion. Based on these criteria, fulfilling 2 or more features technically classifies the lesion as malignant, 1 feature classifies it as uncertain malignant potential, and a lack of these features renders the lesion benign.⁹  

The overwhelming majority of pcPEComas are considered benign. One case of pcPEComa was considered malignant with a high mitotic rate (5 mitoses per 10 high-power fields) and nuclear atypia.¹⁰ Further workup with thoracic computed tomography and positron emission tomography-computed tomography was negative for metastasis. Treatment with wide excision and radiotherapy was performed with no sign of recurrence at 24-month follow-up.¹⁰  

Although pcPEComas arising from the dermis seem to be benign overall, PEComas originating from the subcutaneous tissue may have greater malignancy potential. Two cases of subcutaneous PEComas presenting as nodules resulted in metastasis; one case had local nodal metastasis and another developed metastasis to the lungs months later.^10,11 

The Diagnosis:  Primary Cutaneous Perivascular Epithelioid Cell Tumor  

Perivascular epithelioid cell tumors (PEComas) were first described in 1996.¹ They comprise a family of rare mesenchymal neoplasms that have a unique characteristic of staining positive for melanocytic and smooth muscle markers on immunohistochemistry.² These neoplasms have been described in many areas of the body including the uterus, bladder, heart, pancreas, and prostate. The majority of PEComas are extracutaneous, with only 8% of reported cases originating on the skin.³ A case of primary cutaneous PEComa (pcPEComa) was described in 2003.⁴ The primary cutaneous form is extremely rare.^3,5-7  

A broad deep shave biopsy was performed in our patient in an attempt to sample the entire lesion. Histopathologic examination of the nodule demonstrated a dermal neoplasm comprised of a diffuse proliferation of large polygonal cells with abundant clear cytoplasm, fine chromatin, and prominent nucleoli (Figure 1A). Higher-power magnification showed moderate nuclear pleomorphism and only rare mitotic figures (Figure 1B).

Immunohistochemical staining revealed positivity for myomelanocytic markers with positivity for human melanoma black 45 (HMB-45)(Figure 2) and desmin (not shown). Additionally, the tumor was positive for CD163 and negative for smooth muscle actin, cytokeratin, and S-100 protein.  

Perivascular epithelioid cell tumors are characterized histologically as mesenchymal neoplasms containing large epithelioid to spindled cells with a slightly granular, vacuolated cytoplasm. These cells often are found in close proximity to vascular structures.^3,5,8 The hallmark of PEComas is the expression of both melanocytic and muscle markers.^3,8 A review of staining patterns of pcPEComas emphasized that immunophenotypes between visceral and primary cutaneous forms may vary considerably.^3,5,8 The most consistent and sensitive melanocytic marker is HMB-45 (88%-92% positive).^3,8 Positive Melan-A staining varies in the literature from 0% to 50% of cases.³ Our patient's neoplasm expressed the characteristic myomelanocytic immunophenotype with both HMB-45 and desmin positivity. 

Given the histologic characteristics, these lesions can be mistaken for melanocytic and other nonmelanocytic tumors with a clear cell morphology such as balloon cell nevus, hypomelanotic blue nevus, and melanoma.^2,3 A pigmented case of pcPEComa was reported in 2015 and was originally diagnosed as metastatic melanoma.⁶ Unlike pcPEComa, melanoma usually stains positive with S-100 protein in up to 99% of cases⁸ and is negative for muscle markers; however, a case series reported S-100 protein positivity in 38% of pcPEComas.³ Nonmelanocytic neoplasms in the histologic differential diagnosis include clear cell sarcoma and clear cell renal cell carcinoma, both of which show immunoreactivity for cytokeratin.⁹  

Histologic criteria exist for establishing malignancy potential for visceral PEComas but not for pcPEComas, though it has been suggested that the same malignancy criteria should be applied to pcPEComas.^3,9 Features associated with malignancy include size greater than 8 cm, mitotic activity greater than 1 mitosis per 50 high-power fields, infiltrative growth pattern, high nuclear grade, necrosis, and vascular invasion. Based on these criteria, fulfilling 2 or more features technically classifies the lesion as malignant, 1 feature classifies it as uncertain malignant potential, and a lack of these features renders the lesion benign.⁹  

The overwhelming majority of pcPEComas are considered benign. One case of pcPEComa was considered malignant with a high mitotic rate (5 mitoses per 10 high-power fields) and nuclear atypia.¹⁰ Further workup with thoracic computed tomography and positron emission tomography-computed tomography was negative for metastasis. Treatment with wide excision and radiotherapy was performed with no sign of recurrence at 24-month follow-up.¹⁰  

Although pcPEComas arising from the dermis seem to be benign overall, PEComas originating from the subcutaneous tissue may have greater malignancy potential. Two cases of subcutaneous PEComas presenting as nodules resulted in metastasis; one case had local nodal metastasis and another developed metastasis to the lungs months later.^10,11 

The Diagnosis:  Primary Cutaneous Perivascular Epithelioid Cell Tumor  

Perivascular epithelioid cell tumors (PEComas) were first described in 1996.¹ They comprise a family of rare mesenchymal neoplasms that have a unique characteristic of staining positive for melanocytic and smooth muscle markers on immunohistochemistry.² These neoplasms have been described in many areas of the body including the uterus, bladder, heart, pancreas, and prostate. The majority of PEComas are extracutaneous, with only 8% of reported cases originating on the skin.³ A case of primary cutaneous PEComa (pcPEComa) was described in 2003.⁴ The primary cutaneous form is extremely rare.^3,5-7  

A broad deep shave biopsy was performed in our patient in an attempt to sample the entire lesion. Histopathologic examination of the nodule demonstrated a dermal neoplasm comprised of a diffuse proliferation of large polygonal cells with abundant clear cytoplasm, fine chromatin, and prominent nucleoli (Figure 1A). Higher-power magnification showed moderate nuclear pleomorphism and only rare mitotic figures (Figure 1B).

Immunohistochemical staining revealed positivity for myomelanocytic markers with positivity for human melanoma black 45 (HMB-45)(Figure 2) and desmin (not shown). Additionally, the tumor was positive for CD163 and negative for smooth muscle actin, cytokeratin, and S-100 protein.  

Perivascular epithelioid cell tumors are characterized histologically as mesenchymal neoplasms containing large epithelioid to spindled cells with a slightly granular, vacuolated cytoplasm. These cells often are found in close proximity to vascular structures.^3,5,8 The hallmark of PEComas is the expression of both melanocytic and muscle markers.^3,8 A review of staining patterns of pcPEComas emphasized that immunophenotypes between visceral and primary cutaneous forms may vary considerably.^3,5,8 The most consistent and sensitive melanocytic marker is HMB-45 (88%-92% positive).^3,8 Positive Melan-A staining varies in the literature from 0% to 50% of cases.³ Our patient's neoplasm expressed the characteristic myomelanocytic immunophenotype with both HMB-45 and desmin positivity. 

Given the histologic characteristics, these lesions can be mistaken for melanocytic and other nonmelanocytic tumors with a clear cell morphology such as balloon cell nevus, hypomelanotic blue nevus, and melanoma.^2,3 A pigmented case of pcPEComa was reported in 2015 and was originally diagnosed as metastatic melanoma.⁶ Unlike pcPEComa, melanoma usually stains positive with S-100 protein in up to 99% of cases⁸ and is negative for muscle markers; however, a case series reported S-100 protein positivity in 38% of pcPEComas.³ Nonmelanocytic neoplasms in the histologic differential diagnosis include clear cell sarcoma and clear cell renal cell carcinoma, both of which show immunoreactivity for cytokeratin.⁹  

Histologic criteria exist for establishing malignancy potential for visceral PEComas but not for pcPEComas, though it has been suggested that the same malignancy criteria should be applied to pcPEComas.^3,9 Features associated with malignancy include size greater than 8 cm, mitotic activity greater than 1 mitosis per 50 high-power fields, infiltrative growth pattern, high nuclear grade, necrosis, and vascular invasion. Based on these criteria, fulfilling 2 or more features technically classifies the lesion as malignant, 1 feature classifies it as uncertain malignant potential, and a lack of these features renders the lesion benign.⁹  

The overwhelming majority of pcPEComas are considered benign. One case of pcPEComa was considered malignant with a high mitotic rate (5 mitoses per 10 high-power fields) and nuclear atypia.¹⁰ Further workup with thoracic computed tomography and positron emission tomography-computed tomography was negative for metastasis. Treatment with wide excision and radiotherapy was performed with no sign of recurrence at 24-month follow-up.¹⁰  

Although pcPEComas arising from the dermis seem to be benign overall, PEComas originating from the subcutaneous tissue may have greater malignancy potential. Two cases of subcutaneous PEComas presenting as nodules resulted in metastasis; one case had local nodal metastasis and another developed metastasis to the lungs months later.^10,11 

Improvements to the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) food package guidelines in 2009 appear responsible for reversing the upward trend in obesity prevalence among WIC toddler participants, Madeleine I.G. Daepp, of the Massachusetts Institute of Technology, Cambridge, and her associates reported in Pediatrics.

Courtesy National Cancer Institute

Using data.gov files from 2008, 2010, 2012, and 2014, Ms. Daepp and her colleagues conducted a quasi-experimental interrupted time series analysis to compare state-level population trends in obesity prevalence among children aged 2-4 years before and after 2009. The goal of the study was to determine whether the WIC package changes had any influence on obesity trends among program participants. Altogether, data from 2,253,471 children in 2000 and 3,152,137 children in 2012 was included in the analysis.

Among the guidelines updated to encourage healthier eating habits were the addition of cash allowances for the purchase of more fruits and vegetables, reduction by half in the allowable portions of juice, reduction in cheese, transition of toddlers aged 2-4 years to low-fat or skim milk, and replacement of refined-grain products with healthier whole grain products.

Across all states included in the study, the authors reported average obesity prevalence of 13% in 2000 and 15% in 2008. Although no change was observed in 2010, by 2014 the obesity prevalence decreased to 14%. Hawaii was excluded because of concerns about data quality.

Ms. Daepp and her associates “estimated a pre-2009 annual trend of a 0.23% increase in childhood obesity prevalence.” After the 2009 package revision, they estimated “a decline in childhood obesity of 0.34% per year [P less than .001].”

This change could not be explained by racial-ethnic makeup or child poverty, changes in maternal prepregnancy body mass indices, or prevalence of macrosomia. Speculating that “unmeasured heterogeneity in WIC populations across states” might explain the difference, the authors also suggested that variance in how effectively the package changes were implemented from state to state could be a factor.

Ms. Daepp and her associates recommended that future studies should focus on evaluating differences in how closely vendors follow the package changes, as well as considering whether any other implementation factors could have an influence on state-by-state trends in childhood obesity.

Study limitations noted included an absence of individual body mass index data and information on changes in energy intake and expenditure.

This study was funded by the National Institutes of Health. Ms. Daepp was supported by a National Science Foundation Graduate Research Fellowship grant. Three coauthors were supported by the JPB Foundation; a fourth was supported by an NIH grant.

SOURCE: Daepp MIG et al. Pediatrics. 2019 Apr 1. doi: 10.1542/peds.2018-2841.

Improvements to the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) food package guidelines in 2009 appear responsible for reversing the upward trend in obesity prevalence among WIC toddler participants, Madeleine I.G. Daepp, of the Massachusetts Institute of Technology, Cambridge, and her associates reported in Pediatrics.

Courtesy National Cancer Institute

Using data.gov files from 2008, 2010, 2012, and 2014, Ms. Daepp and her colleagues conducted a quasi-experimental interrupted time series analysis to compare state-level population trends in obesity prevalence among children aged 2-4 years before and after 2009. The goal of the study was to determine whether the WIC package changes had any influence on obesity trends among program participants. Altogether, data from 2,253,471 children in 2000 and 3,152,137 children in 2012 was included in the analysis.

Among the guidelines updated to encourage healthier eating habits were the addition of cash allowances for the purchase of more fruits and vegetables, reduction by half in the allowable portions of juice, reduction in cheese, transition of toddlers aged 2-4 years to low-fat or skim milk, and replacement of refined-grain products with healthier whole grain products.

Across all states included in the study, the authors reported average obesity prevalence of 13% in 2000 and 15% in 2008. Although no change was observed in 2010, by 2014 the obesity prevalence decreased to 14%. Hawaii was excluded because of concerns about data quality.

Ms. Daepp and her associates “estimated a pre-2009 annual trend of a 0.23% increase in childhood obesity prevalence.” After the 2009 package revision, they estimated “a decline in childhood obesity of 0.34% per year [P less than .001].”

This change could not be explained by racial-ethnic makeup or child poverty, changes in maternal prepregnancy body mass indices, or prevalence of macrosomia. Speculating that “unmeasured heterogeneity in WIC populations across states” might explain the difference, the authors also suggested that variance in how effectively the package changes were implemented from state to state could be a factor.

Ms. Daepp and her associates recommended that future studies should focus on evaluating differences in how closely vendors follow the package changes, as well as considering whether any other implementation factors could have an influence on state-by-state trends in childhood obesity.

Study limitations noted included an absence of individual body mass index data and information on changes in energy intake and expenditure.

This study was funded by the National Institutes of Health. Ms. Daepp was supported by a National Science Foundation Graduate Research Fellowship grant. Three coauthors were supported by the JPB Foundation; a fourth was supported by an NIH grant.

SOURCE: Daepp MIG et al. Pediatrics. 2019 Apr 1. doi: 10.1542/peds.2018-2841.

Improvements to the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) food package guidelines in 2009 appear responsible for reversing the upward trend in obesity prevalence among WIC toddler participants, Madeleine I.G. Daepp, of the Massachusetts Institute of Technology, Cambridge, and her associates reported in Pediatrics.

Courtesy National Cancer Institute

Using data.gov files from 2008, 2010, 2012, and 2014, Ms. Daepp and her colleagues conducted a quasi-experimental interrupted time series analysis to compare state-level population trends in obesity prevalence among children aged 2-4 years before and after 2009. The goal of the study was to determine whether the WIC package changes had any influence on obesity trends among program participants. Altogether, data from 2,253,471 children in 2000 and 3,152,137 children in 2012 was included in the analysis.

Among the guidelines updated to encourage healthier eating habits were the addition of cash allowances for the purchase of more fruits and vegetables, reduction by half in the allowable portions of juice, reduction in cheese, transition of toddlers aged 2-4 years to low-fat or skim milk, and replacement of refined-grain products with healthier whole grain products.

Across all states included in the study, the authors reported average obesity prevalence of 13% in 2000 and 15% in 2008. Although no change was observed in 2010, by 2014 the obesity prevalence decreased to 14%. Hawaii was excluded because of concerns about data quality.

Ms. Daepp and her associates “estimated a pre-2009 annual trend of a 0.23% increase in childhood obesity prevalence.” After the 2009 package revision, they estimated “a decline in childhood obesity of 0.34% per year [P less than .001].”

This change could not be explained by racial-ethnic makeup or child poverty, changes in maternal prepregnancy body mass indices, or prevalence of macrosomia. Speculating that “unmeasured heterogeneity in WIC populations across states” might explain the difference, the authors also suggested that variance in how effectively the package changes were implemented from state to state could be a factor.

Ms. Daepp and her associates recommended that future studies should focus on evaluating differences in how closely vendors follow the package changes, as well as considering whether any other implementation factors could have an influence on state-by-state trends in childhood obesity.

Study limitations noted included an absence of individual body mass index data and information on changes in energy intake and expenditure.

This study was funded by the National Institutes of Health. Ms. Daepp was supported by a National Science Foundation Graduate Research Fellowship grant. Three coauthors were supported by the JPB Foundation; a fourth was supported by an NIH grant.

SOURCE: Daepp MIG et al. Pediatrics. 2019 Apr 1. doi: 10.1542/peds.2018-2841.

NEW ORLEANS – When HIV-negative children born to mothers infected with HIV are evaluated in adolescence, they are found to have far higher rates of obesity and reactive airway disease than are those with no such exposure, according to research that provides a compelling link between inflammatory activity in utero and subsequent risk of metabolic disorders.

Most supportive of that link was a near-linear inverse relationship between CD4 counts during the time of pregnancy and risk of both obesity and reactive respiratory disease more than a decade later, according to research presented by Lindsay Fourman, MD, an instructor in medicine at Massachusetts General Hospital, Boston, during the annual meeting of the Endocrine Society.

In this video interview, Dr. Fourman discusses the effort to understand the long-term health consequences of being exposed to HIV and antiretroviral therapies while in utero, a group known by the acronym HIV-exposed uninfected (HEU). With effective therapies now routinely preventing mother-to-child transmission, this population of children is growing quickly.

For this study, 50 HEU individuals were identified from a patient database. They were matched in a 3:1 ratio to a control group for a variety of demographic and socioeconomic variables. At a median age of 18 years, the HEU population was found to have a “strikingly” higher rate of obesity, compared with controls (42% vs. 25%, respectively; P = .04). The rate of reactive airway disease was similarly increased in the HEU group (40% vs. 24%; P = .04).

These data are important for considering health risks in an HEU population, but Dr. Fourman explained that it provides support for looking at metabolic risks from other in utero exposures linked to upregulated inflammation, such as gestational diabetes or obesity.

Dr Fourman and her colleagues reported no disclosures or financial conflicts of interest.

SOURCE: Fourman L et al. ENDO 2019, Session P10 (SAT-256).

NEW ORLEANS – When HIV-negative children born to mothers infected with HIV are evaluated in adolescence, they are found to have far higher rates of obesity and reactive airway disease than are those with no such exposure, according to research that provides a compelling link between inflammatory activity in utero and subsequent risk of metabolic disorders.

Most supportive of that link was a near-linear inverse relationship between CD4 counts during the time of pregnancy and risk of both obesity and reactive respiratory disease more than a decade later, according to research presented by Lindsay Fourman, MD, an instructor in medicine at Massachusetts General Hospital, Boston, during the annual meeting of the Endocrine Society.

In this video interview, Dr. Fourman discusses the effort to understand the long-term health consequences of being exposed to HIV and antiretroviral therapies while in utero, a group known by the acronym HIV-exposed uninfected (HEU). With effective therapies now routinely preventing mother-to-child transmission, this population of children is growing quickly.

For this study, 50 HEU individuals were identified from a patient database. They were matched in a 3:1 ratio to a control group for a variety of demographic and socioeconomic variables. At a median age of 18 years, the HEU population was found to have a “strikingly” higher rate of obesity, compared with controls (42% vs. 25%, respectively; P = .04). The rate of reactive airway disease was similarly increased in the HEU group (40% vs. 24%; P = .04).

These data are important for considering health risks in an HEU population, but Dr. Fourman explained that it provides support for looking at metabolic risks from other in utero exposures linked to upregulated inflammation, such as gestational diabetes or obesity.

Dr Fourman and her colleagues reported no disclosures or financial conflicts of interest.

SOURCE: Fourman L et al. ENDO 2019, Session P10 (SAT-256).

NEW ORLEANS – When HIV-negative children born to mothers infected with HIV are evaluated in adolescence, they are found to have far higher rates of obesity and reactive airway disease than are those with no such exposure, according to research that provides a compelling link between inflammatory activity in utero and subsequent risk of metabolic disorders.

Most supportive of that link was a near-linear inverse relationship between CD4 counts during the time of pregnancy and risk of both obesity and reactive respiratory disease more than a decade later, according to research presented by Lindsay Fourman, MD, an instructor in medicine at Massachusetts General Hospital, Boston, during the annual meeting of the Endocrine Society.

In this video interview, Dr. Fourman discusses the effort to understand the long-term health consequences of being exposed to HIV and antiretroviral therapies while in utero, a group known by the acronym HIV-exposed uninfected (HEU). With effective therapies now routinely preventing mother-to-child transmission, this population of children is growing quickly.

For this study, 50 HEU individuals were identified from a patient database. They were matched in a 3:1 ratio to a control group for a variety of demographic and socioeconomic variables. At a median age of 18 years, the HEU population was found to have a “strikingly” higher rate of obesity, compared with controls (42% vs. 25%, respectively; P = .04). The rate of reactive airway disease was similarly increased in the HEU group (40% vs. 24%; P = .04).

These data are important for considering health risks in an HEU population, but Dr. Fourman explained that it provides support for looking at metabolic risks from other in utero exposures linked to upregulated inflammation, such as gestational diabetes or obesity.

Dr Fourman and her colleagues reported no disclosures or financial conflicts of interest.

SOURCE: Fourman L et al. ENDO 2019, Session P10 (SAT-256).

“Doctor, I have a question for you.”

“Yes?”

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

Mr. B thought he felt too well to have an aggressive cancer infiltrating his liver, abdominal wall, and lungs. He lived an active life, going to church, volunteering, and playing with his grandchildren. But the biopsy results were back. It wasn’t an infection. It wasn’t inflammation. It was stage 4 cancer.

And just like that, his life changed.

His prognosis was likely months, with a best case scenario of several years. But gone were the days of thinking 10, 20, and 30 years ahead.

It’s not a bad thing. It’s an adaptive mechanism and positive outlooks can even be associated with better medical outcomes. There’s almost always a “but” if you look hard enough. And in the face of life-changing news, we are incentivized to look really, really hard.

Yet Mr. B caught me off guard because he wasn’t asking me to maintain hope. He was pushing me one step further.

At one point in our conversation, he revealed this clearly. “Doctor, I don’t even care if it’s false hope – just tell me the cancer will disappear.”

Mr. B was asking me to lie to him.

The last thing I wanted was to take away hope, closing the door on a future that truly was clouded in uncertainty. But I also couldn’t look him in the eye and tell him his incurable disease was, in fact, curable.

That doesn’t mean there aren’t ways to phrase things kindly. Patients respond differently to “there’s a 90% chance of survival” and “there’s a 10% chance of death” even though the facts are identical.

When I sense a person like Mr. B is looking to me for hope, I try to frame that initial conversation in the style of the first statement. It’s not dishonest. With an already overwhelming piece of information, it’s choosing to share the most positive version of a narrative that can be told in many different ways and will evolve over time.

Moreover, being hopeful and realistic are not mutually exclusive. Just because someone is seeking the rare chance of a good outcome doesn’t mean he or she doesn’t understand the seriousness of the situation. It is possible to seek out experimental drugs while also considering hospice. It is possible to hope for a plan A while preparing for a plan B. Those are two compatible beliefs, and it’s OK – preferred, even – to hold them at once.

The challenge is avoiding getting pulled into an outlook that is not just positive, not just unlikely – but one with no basis in reality. There’s hope – and then there’s false hope. There’s a positive take – and then there’s lying. It can be a fine line, and with the intention of being kind it can be all too easy to “yes, but” our way into untruths.

The best we can do is set limits with compassion, and understand that telling the truth doesn’t always mean that someone hears it.

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

The chances of Mr. B’s cancer responding to chemotherapy were not good but hardly impossible. But without any therapy at all?

“I have not.”

“What about at other places ... in other states or countries. Have you ever heard of a person like me who was cured without treatment?”

“I have not.”

“I guess what I’m asking, Doctor, is ... have you ever seen where the cancer was there and then one day was not ... have you ever seen a miracle?”

Reaching. Grasping.

“I have not.”

“Well,” he said, “Maybe I will be the first.”

We look at each other, pondering this. In my silence is the answer.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

“Doctor, I have a question for you.”

“Yes?”

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

Mr. B thought he felt too well to have an aggressive cancer infiltrating his liver, abdominal wall, and lungs. He lived an active life, going to church, volunteering, and playing with his grandchildren. But the biopsy results were back. It wasn’t an infection. It wasn’t inflammation. It was stage 4 cancer.

And just like that, his life changed.

His prognosis was likely months, with a best case scenario of several years. But gone were the days of thinking 10, 20, and 30 years ahead.

It’s not a bad thing. It’s an adaptive mechanism and positive outlooks can even be associated with better medical outcomes. There’s almost always a “but” if you look hard enough. And in the face of life-changing news, we are incentivized to look really, really hard.

Yet Mr. B caught me off guard because he wasn’t asking me to maintain hope. He was pushing me one step further.

At one point in our conversation, he revealed this clearly. “Doctor, I don’t even care if it’s false hope – just tell me the cancer will disappear.”

Mr. B was asking me to lie to him.

The last thing I wanted was to take away hope, closing the door on a future that truly was clouded in uncertainty. But I also couldn’t look him in the eye and tell him his incurable disease was, in fact, curable.

That doesn’t mean there aren’t ways to phrase things kindly. Patients respond differently to “there’s a 90% chance of survival” and “there’s a 10% chance of death” even though the facts are identical.

When I sense a person like Mr. B is looking to me for hope, I try to frame that initial conversation in the style of the first statement. It’s not dishonest. With an already overwhelming piece of information, it’s choosing to share the most positive version of a narrative that can be told in many different ways and will evolve over time.

Moreover, being hopeful and realistic are not mutually exclusive. Just because someone is seeking the rare chance of a good outcome doesn’t mean he or she doesn’t understand the seriousness of the situation. It is possible to seek out experimental drugs while also considering hospice. It is possible to hope for a plan A while preparing for a plan B. Those are two compatible beliefs, and it’s OK – preferred, even – to hold them at once.

The challenge is avoiding getting pulled into an outlook that is not just positive, not just unlikely – but one with no basis in reality. There’s hope – and then there’s false hope. There’s a positive take – and then there’s lying. It can be a fine line, and with the intention of being kind it can be all too easy to “yes, but” our way into untruths.

The best we can do is set limits with compassion, and understand that telling the truth doesn’t always mean that someone hears it.

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

The chances of Mr. B’s cancer responding to chemotherapy were not good but hardly impossible. But without any therapy at all?

“I have not.”

“What about at other places ... in other states or countries. Have you ever heard of a person like me who was cured without treatment?”

“I have not.”

“I guess what I’m asking, Doctor, is ... have you ever seen where the cancer was there and then one day was not ... have you ever seen a miracle?”

Reaching. Grasping.

“I have not.”

“Well,” he said, “Maybe I will be the first.”

We look at each other, pondering this. In my silence is the answer.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

“Doctor, I have a question for you.”

“Yes?”

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

Mr. B thought he felt too well to have an aggressive cancer infiltrating his liver, abdominal wall, and lungs. He lived an active life, going to church, volunteering, and playing with his grandchildren. But the biopsy results were back. It wasn’t an infection. It wasn’t inflammation. It was stage 4 cancer.

And just like that, his life changed.

His prognosis was likely months, with a best case scenario of several years. But gone were the days of thinking 10, 20, and 30 years ahead.

It’s not a bad thing. It’s an adaptive mechanism and positive outlooks can even be associated with better medical outcomes. There’s almost always a “but” if you look hard enough. And in the face of life-changing news, we are incentivized to look really, really hard.

Yet Mr. B caught me off guard because he wasn’t asking me to maintain hope. He was pushing me one step further.

At one point in our conversation, he revealed this clearly. “Doctor, I don’t even care if it’s false hope – just tell me the cancer will disappear.”

Mr. B was asking me to lie to him.

The last thing I wanted was to take away hope, closing the door on a future that truly was clouded in uncertainty. But I also couldn’t look him in the eye and tell him his incurable disease was, in fact, curable.

That doesn’t mean there aren’t ways to phrase things kindly. Patients respond differently to “there’s a 90% chance of survival” and “there’s a 10% chance of death” even though the facts are identical.

When I sense a person like Mr. B is looking to me for hope, I try to frame that initial conversation in the style of the first statement. It’s not dishonest. With an already overwhelming piece of information, it’s choosing to share the most positive version of a narrative that can be told in many different ways and will evolve over time.

Moreover, being hopeful and realistic are not mutually exclusive. Just because someone is seeking the rare chance of a good outcome doesn’t mean he or she doesn’t understand the seriousness of the situation. It is possible to seek out experimental drugs while also considering hospice. It is possible to hope for a plan A while preparing for a plan B. Those are two compatible beliefs, and it’s OK – preferred, even – to hold them at once.

The challenge is avoiding getting pulled into an outlook that is not just positive, not just unlikely – but one with no basis in reality. There’s hope – and then there’s false hope. There’s a positive take – and then there’s lying. It can be a fine line, and with the intention of being kind it can be all too easy to “yes, but” our way into untruths.

The best we can do is set limits with compassion, and understand that telling the truth doesn’t always mean that someone hears it.

“Have you ever had a patient – I mean, someone like me, someone in my ... state ... get cured without any treatment?”

The chances of Mr. B’s cancer responding to chemotherapy were not good but hardly impossible. But without any therapy at all?

“I have not.”

“What about at other places ... in other states or countries. Have you ever heard of a person like me who was cured without treatment?”

“I have not.”

“I guess what I’m asking, Doctor, is ... have you ever seen where the cancer was there and then one day was not ... have you ever seen a miracle?”

Reaching. Grasping.

“I have not.”

“Well,” he said, “Maybe I will be the first.”

We look at each other, pondering this. In my silence is the answer.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

I recall in college we used to talk a lot about the relationship between town and gown, that is, the town community and the academic community, and how they relate to each other. This remains pertinent today as we consider the dermatology academic community and practicing dermatologists. There should be a virtuous circle between dermatologists in their community and their academic medical center.

Academic medical centers are up to date and on the cutting edge of science and treatments – and happy to share with community dermatologists. This is where you will learn about teledermatology and how to use the latest biologics.

They provide educational opportunities such as grand rounds and visiting speakers. They allow community physicians to attend staff and resident lectures, bring their most challenging cases to grand rounds, and get feedback and suggestions, with everyone learning from the experience. They host dermatology events for all. They allow community physicians to staff resident clinics where both benefit from the interaction. The academic center provides a charity care network for the community – and usually provides the experts of last resort for difficult cases as they are often on the cutting edge of research and newest treatments.

Large multispecialty practices– and private equity groups – are not going to fill this role.

Dermatology is a highly isolated specialty and the interaction with others at the academic center may be the only physical link to the outside world of medicine. Having an academic dermatology program in your community is a serious asset that community dermatologists should appreciate and support.

However, as the gown supports the town, so should the town support the gown. There is a pervasive inaccuracy in the community that these academic dermatology departments are supported by government funds or a “state line” of support. This is incorrect. These departments support themselves with clinical work. In addition, the dean and/or the medical school takes a generous cut out of their profits, and the departments also must compete – furiously – for grants, of which the medical school immediately takes about 55% for indirect “overhead,” a frequent complaint of academic physicians.

If you practice near such an academic center and benefit from its virtuous circle, you can consider sending them some of your dermatopathology or Mohs, even if you are a large group and could handle them yourselves. You can join the local dermatologic society and bring cases to grand rounds. You can offer to teach the residents in their clinic, or in your office, and expose them to real life practice.

If you have the means, you could consider funding a lectureship or an endowed departmental chair. No matter the virtual content available online, the quality of learning one on one from another specialist cannot be beat. So make the effort to visit the gown from the town. You will be warmly welcomed and join a virtuous circle of lifelong learners.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

I recall in college we used to talk a lot about the relationship between town and gown, that is, the town community and the academic community, and how they relate to each other. This remains pertinent today as we consider the dermatology academic community and practicing dermatologists. There should be a virtuous circle between dermatologists in their community and their academic medical center.

Academic medical centers are up to date and on the cutting edge of science and treatments – and happy to share with community dermatologists. This is where you will learn about teledermatology and how to use the latest biologics.

They provide educational opportunities such as grand rounds and visiting speakers. They allow community physicians to attend staff and resident lectures, bring their most challenging cases to grand rounds, and get feedback and suggestions, with everyone learning from the experience. They host dermatology events for all. They allow community physicians to staff resident clinics where both benefit from the interaction. The academic center provides a charity care network for the community – and usually provides the experts of last resort for difficult cases as they are often on the cutting edge of research and newest treatments.

Large multispecialty practices– and private equity groups – are not going to fill this role.

Dermatology is a highly isolated specialty and the interaction with others at the academic center may be the only physical link to the outside world of medicine. Having an academic dermatology program in your community is a serious asset that community dermatologists should appreciate and support.

However, as the gown supports the town, so should the town support the gown. There is a pervasive inaccuracy in the community that these academic dermatology departments are supported by government funds or a “state line” of support. This is incorrect. These departments support themselves with clinical work. In addition, the dean and/or the medical school takes a generous cut out of their profits, and the departments also must compete – furiously – for grants, of which the medical school immediately takes about 55% for indirect “overhead,” a frequent complaint of academic physicians.

If you practice near such an academic center and benefit from its virtuous circle, you can consider sending them some of your dermatopathology or Mohs, even if you are a large group and could handle them yourselves. You can join the local dermatologic society and bring cases to grand rounds. You can offer to teach the residents in their clinic, or in your office, and expose them to real life practice.

If you have the means, you could consider funding a lectureship or an endowed departmental chair. No matter the virtual content available online, the quality of learning one on one from another specialist cannot be beat. So make the effort to visit the gown from the town. You will be warmly welcomed and join a virtuous circle of lifelong learners.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

I recall in college we used to talk a lot about the relationship between town and gown, that is, the town community and the academic community, and how they relate to each other. This remains pertinent today as we consider the dermatology academic community and practicing dermatologists. There should be a virtuous circle between dermatologists in their community and their academic medical center.

Academic medical centers are up to date and on the cutting edge of science and treatments – and happy to share with community dermatologists. This is where you will learn about teledermatology and how to use the latest biologics.

They provide educational opportunities such as grand rounds and visiting speakers. They allow community physicians to attend staff and resident lectures, bring their most challenging cases to grand rounds, and get feedback and suggestions, with everyone learning from the experience. They host dermatology events for all. They allow community physicians to staff resident clinics where both benefit from the interaction. The academic center provides a charity care network for the community – and usually provides the experts of last resort for difficult cases as they are often on the cutting edge of research and newest treatments.

Large multispecialty practices– and private equity groups – are not going to fill this role.

Dermatology is a highly isolated specialty and the interaction with others at the academic center may be the only physical link to the outside world of medicine. Having an academic dermatology program in your community is a serious asset that community dermatologists should appreciate and support.

However, as the gown supports the town, so should the town support the gown. There is a pervasive inaccuracy in the community that these academic dermatology departments are supported by government funds or a “state line” of support. This is incorrect. These departments support themselves with clinical work. In addition, the dean and/or the medical school takes a generous cut out of their profits, and the departments also must compete – furiously – for grants, of which the medical school immediately takes about 55% for indirect “overhead,” a frequent complaint of academic physicians.

If you practice near such an academic center and benefit from its virtuous circle, you can consider sending them some of your dermatopathology or Mohs, even if you are a large group and could handle them yourselves. You can join the local dermatologic society and bring cases to grand rounds. You can offer to teach the residents in their clinic, or in your office, and expose them to real life practice.

If you have the means, you could consider funding a lectureship or an endowed departmental chair. No matter the virtual content available online, the quality of learning one on one from another specialist cannot be beat. So make the effort to visit the gown from the town. You will be warmly welcomed and join a virtuous circle of lifelong learners.

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

NEW ORLEANS – A hormone that is oversecreted in obesity may provide a pathway from adipose to lung tissue in individuals with both obesity and asthma, according to new research presented at the annual meeting of the Endocrine Society.

“Obesity-related asthma is a really understudied and new phenomenon. It’s a unique complication of obesity,” said Furkan Burak, MD, in a video interview after an obesity-focused press conference.

“In addition to being a standalone disease, obesity mostly comes as a package. And that’s the problem,” said Dr. Burak, pointing to obesity-related asthma’s clustering with diseases such as diabetes and atherosclerosis.

Asthma affects 10% of the world population, and it’s becoming increasingly understood that obesity-related, adult-onset asthma is a separate disease entity from allergic asthma, which usually begins in childhood, said Dr. Burak, an endocrinology fellow at Brigham and Women’s Hospital, Boston.

“There are two types of asthma related to obesity,” he said. Classic allergic asthma can get worse with obesity; however, asthma can sometimes occur de novo in adults, particularly women, with obesity. “What is important is … that they are less responsive to classic treatments,” such as steroids and beta-agonists. “And the problem is not small: Of asthmatics, 40% are obese. It’s a therapeutic problem, and we are not able to treat them well.”

The fatty acid binding protein 4, aP2, a hormone that is released by adipose tissue, travels to distant organs and regulates metabolic responses. Levels of aP2 are known to be increased in obesity, particularly in individuals with asthma, said Dr. Burak.

Citing work done at Brigham and Women’s Hospital and at Boston’s Harvard Medical School, as well as elsewhere, Dr. Burak and his collaborators noted in the abstract accompanying the presentation that “increased serum aP2 levels strongly correlate with poor metabolic, inflammatory, and cardiovascular outcomes in multiple independent human studies.”

Dr. Burak said he and his colleagues are trying to sort out “how a fat-tissue–borne hormone could potentially cause a problem in the lung.”

A big clue came with the discovery that patients with asthma and obesity have elevated levels of aP2 within their airways when bronchoalveolar lavage is performed, suggesting that the hormone may be the pathological mediator linking obesity to asthma – “a direct link between the fat tissue and the lung,” he said.

Serum aP2 levels were available from the Nurse’s Health Study, so Dr. Burak and his colleagues looked at those levels in randomly selected study participants. “We found that aP2 levels were elevated 25.6% – significantly – in asthmatics, compared with nonasthmatics, but only in obese and overweight [participants, and] not in lean” participants, he said.

Dr. Burak and his colleagues compared 525 individuals with body mass indices of less than 25 kg/m², of whom 15 had asthma, with 385 individuals with body mass indices of more than 25, of whom 15 of whom had asthma.

Collecting bronchoalveolar lavage fluid from individuals with asthma showed a mean increase of 23% in aP2 levels in patients with obesity compared with lean individuals.

These data taken together show both systemic and local elevations of aP2 in human obesity. “That could contribute to the airway hyperreactivity and to the asthma pathogenesis,” which would confirm findings from animal studies, said Dr. Burak.

Further investigation will focus on individuals who are haploinsufficient for aP2. The group already is known to have lower risk for dyslipidemia, diabetes, and cardiovascular disease, but Dr. Burak and his collaborators also will determine whether asthma incidence is also lower.

The eventual goal is to attack aP2 as a therapeutic target. “Can we inhibit and target aP2 therapeutically in the context of obesity to treat obesity-related asthma? We have a big hope for that.”

Dr. Burak and his colleagues reported no disclosures or financial conflicts of interest.

[email protected]

SOURCE: Burak MF et al. ENDO 2019, Session OR01-1.

NEW ORLEANS – A hormone that is oversecreted in obesity may provide a pathway from adipose to lung tissue in individuals with both obesity and asthma, according to new research presented at the annual meeting of the Endocrine Society.

“Obesity-related asthma is a really understudied and new phenomenon. It’s a unique complication of obesity,” said Furkan Burak, MD, in a video interview after an obesity-focused press conference.

“In addition to being a standalone disease, obesity mostly comes as a package. And that’s the problem,” said Dr. Burak, pointing to obesity-related asthma’s clustering with diseases such as diabetes and atherosclerosis.

Asthma affects 10% of the world population, and it’s becoming increasingly understood that obesity-related, adult-onset asthma is a separate disease entity from allergic asthma, which usually begins in childhood, said Dr. Burak, an endocrinology fellow at Brigham and Women’s Hospital, Boston.

“There are two types of asthma related to obesity,” he said. Classic allergic asthma can get worse with obesity; however, asthma can sometimes occur de novo in adults, particularly women, with obesity. “What is important is … that they are less responsive to classic treatments,” such as steroids and beta-agonists. “And the problem is not small: Of asthmatics, 40% are obese. It’s a therapeutic problem, and we are not able to treat them well.”

The fatty acid binding protein 4, aP2, a hormone that is released by adipose tissue, travels to distant organs and regulates metabolic responses. Levels of aP2 are known to be increased in obesity, particularly in individuals with asthma, said Dr. Burak.

Citing work done at Brigham and Women’s Hospital and at Boston’s Harvard Medical School, as well as elsewhere, Dr. Burak and his collaborators noted in the abstract accompanying the presentation that “increased serum aP2 levels strongly correlate with poor metabolic, inflammatory, and cardiovascular outcomes in multiple independent human studies.”

Dr. Burak said he and his colleagues are trying to sort out “how a fat-tissue–borne hormone could potentially cause a problem in the lung.”

A big clue came with the discovery that patients with asthma and obesity have elevated levels of aP2 within their airways when bronchoalveolar lavage is performed, suggesting that the hormone may be the pathological mediator linking obesity to asthma – “a direct link between the fat tissue and the lung,” he said.

Serum aP2 levels were available from the Nurse’s Health Study, so Dr. Burak and his colleagues looked at those levels in randomly selected study participants. “We found that aP2 levels were elevated 25.6% – significantly – in asthmatics, compared with nonasthmatics, but only in obese and overweight [participants, and] not in lean” participants, he said.

Dr. Burak and his colleagues compared 525 individuals with body mass indices of less than 25 kg/m², of whom 15 had asthma, with 385 individuals with body mass indices of more than 25, of whom 15 of whom had asthma.

Collecting bronchoalveolar lavage fluid from individuals with asthma showed a mean increase of 23% in aP2 levels in patients with obesity compared with lean individuals.

These data taken together show both systemic and local elevations of aP2 in human obesity. “That could contribute to the airway hyperreactivity and to the asthma pathogenesis,” which would confirm findings from animal studies, said Dr. Burak.

Further investigation will focus on individuals who are haploinsufficient for aP2. The group already is known to have lower risk for dyslipidemia, diabetes, and cardiovascular disease, but Dr. Burak and his collaborators also will determine whether asthma incidence is also lower.

The eventual goal is to attack aP2 as a therapeutic target. “Can we inhibit and target aP2 therapeutically in the context of obesity to treat obesity-related asthma? We have a big hope for that.”

Dr. Burak and his colleagues reported no disclosures or financial conflicts of interest.

[email protected]

SOURCE: Burak MF et al. ENDO 2019, Session OR01-1.

NEW ORLEANS – A hormone that is oversecreted in obesity may provide a pathway from adipose to lung tissue in individuals with both obesity and asthma, according to new research presented at the annual meeting of the Endocrine Society.

“Obesity-related asthma is a really understudied and new phenomenon. It’s a unique complication of obesity,” said Furkan Burak, MD, in a video interview after an obesity-focused press conference.

“In addition to being a standalone disease, obesity mostly comes as a package. And that’s the problem,” said Dr. Burak, pointing to obesity-related asthma’s clustering with diseases such as diabetes and atherosclerosis.

Asthma affects 10% of the world population, and it’s becoming increasingly understood that obesity-related, adult-onset asthma is a separate disease entity from allergic asthma, which usually begins in childhood, said Dr. Burak, an endocrinology fellow at Brigham and Women’s Hospital, Boston.

“There are two types of asthma related to obesity,” he said. Classic allergic asthma can get worse with obesity; however, asthma can sometimes occur de novo in adults, particularly women, with obesity. “What is important is … that they are less responsive to classic treatments,” such as steroids and beta-agonists. “And the problem is not small: Of asthmatics, 40% are obese. It’s a therapeutic problem, and we are not able to treat them well.”

The fatty acid binding protein 4, aP2, a hormone that is released by adipose tissue, travels to distant organs and regulates metabolic responses. Levels of aP2 are known to be increased in obesity, particularly in individuals with asthma, said Dr. Burak.

Citing work done at Brigham and Women’s Hospital and at Boston’s Harvard Medical School, as well as elsewhere, Dr. Burak and his collaborators noted in the abstract accompanying the presentation that “increased serum aP2 levels strongly correlate with poor metabolic, inflammatory, and cardiovascular outcomes in multiple independent human studies.”

Dr. Burak said he and his colleagues are trying to sort out “how a fat-tissue–borne hormone could potentially cause a problem in the lung.”

A big clue came with the discovery that patients with asthma and obesity have elevated levels of aP2 within their airways when bronchoalveolar lavage is performed, suggesting that the hormone may be the pathological mediator linking obesity to asthma – “a direct link between the fat tissue and the lung,” he said.

Serum aP2 levels were available from the Nurse’s Health Study, so Dr. Burak and his colleagues looked at those levels in randomly selected study participants. “We found that aP2 levels were elevated 25.6% – significantly – in asthmatics, compared with nonasthmatics, but only in obese and overweight [participants, and] not in lean” participants, he said.

Dr. Burak and his colleagues compared 525 individuals with body mass indices of less than 25 kg/m², of whom 15 had asthma, with 385 individuals with body mass indices of more than 25, of whom 15 of whom had asthma.

Collecting bronchoalveolar lavage fluid from individuals with asthma showed a mean increase of 23% in aP2 levels in patients with obesity compared with lean individuals.

These data taken together show both systemic and local elevations of aP2 in human obesity. “That could contribute to the airway hyperreactivity and to the asthma pathogenesis,” which would confirm findings from animal studies, said Dr. Burak.

Further investigation will focus on individuals who are haploinsufficient for aP2. The group already is known to have lower risk for dyslipidemia, diabetes, and cardiovascular disease, but Dr. Burak and his collaborators also will determine whether asthma incidence is also lower.

The eventual goal is to attack aP2 as a therapeutic target. “Can we inhibit and target aP2 therapeutically in the context of obesity to treat obesity-related asthma? We have a big hope for that.”

Dr. Burak and his colleagues reported no disclosures or financial conflicts of interest.

[email protected]

SOURCE: Burak MF et al. ENDO 2019, Session OR01-1.

PHILADELPHIA – Although the new ulcerative colitis guidelines make no current recommendations on probiotics and curcumin because of gaps in knowledge, both may be beneficial today in selected patients, an expert said at the meeting jointly provided by Rutgers and Global Academy for Medical Education.

Andrew D. Bowser/MDedge News

“Probiotics can be added, in my opinion, to patients on mesalamine with mild to moderate ulcerative colitis in order to help induce remission without having to go to immunosuppressive medication,” said Steven R. Brant, MD, chief of the division of gastroenterology and hepatology at Robert Wood Johnson Medical School, New Brunswick, N.J.

Likewise, curcumin has shown “minimal harm” in mild ulcerative colitis and may help nudge patients toward disease control without having to resort to corticosteroids or other immunosuppressive therapy, Dr. Brant said.

The new American Gastroenterological Association guidelines for treatment of mild to moderate ulcerative colitis, published in February in the journal Gastroenterology, declined to make recommendations on either probiotics or curcumin, citing “knowledge gaps and areas for future research.”

“Although these modalities appear to be safe, their use risks delaying proven effective therapy with the potential for worsening symptoms or complications,” Cynthia W. Ko, MD, and guideline coauthors said in the recommendations.

From the patient perspective, probiotics are “popular,” Dr. Brant said in his presentation, noting that some patients will request probiotics as a first-line therapy or even ask to be taken off mesalamine and put on probiotics.

Meta-analyses have provided differing conclusions on the benefits of probiotics. One recently published analysis of probiotics versus mesalamine showed a slight trend to favor mesalamine, but when looking at good-quality studies only, the meta-analysis showed a nonsignificant trend in favor of probiotics, Dr. Brant said.

By contrast, in a Cochrane meta-analysis of mesalamine at standard doses versus placebo, there was consistent evidence for a benefit of mesalamine: “so the main problem with giving probiotics as a choice is that you’re going to put the patient at risk for progressive symptoms and complications,” said Dr. Brant.

However, looking specifically at the probiotic VSL#3, the Toronto Ulcerative Colitis Consensus Group said that it was linked to significantly improved remission (44% vs. 25%; odds ratio, 2.4; P = .0007). Coverage issues could be a snag, since the amount of the probiotic associated with improved remission was equivalent to four double-strength packets. “Try getting that approved,” Dr. Brant told attendees. “You’ll have some challenges.”

Curcumin was evaluated in a multicenter trial showing that, when added to maximal mesalamine, it may be helpful in avoiding an advance in therapy, with 54% achieving clinical remission at week 4 versus 0% of placebo-treated patients.

That was a “reasonable study” but more research needs to be done, Dr. Brant said.

“I think that given the minimal harm, it may be worth a trial, though not in patients that are really having systemic symptoms, severe bleeding, and are getting worse,” he said. “It’s patients that have some response on mesalamine where it may be valuable, if you have time to spare to give them curcumin.”

Dr. Brant indicated that he had no relevant financial relationships to disclose.

Global Academy and this news organization are owned by the same parent company.

PHILADELPHIA – Although the new ulcerative colitis guidelines make no current recommendations on probiotics and curcumin because of gaps in knowledge, both may be beneficial today in selected patients, an expert said at the meeting jointly provided by Rutgers and Global Academy for Medical Education.

Andrew D. Bowser/MDedge News

“Probiotics can be added, in my opinion, to patients on mesalamine with mild to moderate ulcerative colitis in order to help induce remission without having to go to immunosuppressive medication,” said Steven R. Brant, MD, chief of the division of gastroenterology and hepatology at Robert Wood Johnson Medical School, New Brunswick, N.J.

Likewise, curcumin has shown “minimal harm” in mild ulcerative colitis and may help nudge patients toward disease control without having to resort to corticosteroids or other immunosuppressive therapy, Dr. Brant said.

The new American Gastroenterological Association guidelines for treatment of mild to moderate ulcerative colitis, published in February in the journal Gastroenterology, declined to make recommendations on either probiotics or curcumin, citing “knowledge gaps and areas for future research.”

“Although these modalities appear to be safe, their use risks delaying proven effective therapy with the potential for worsening symptoms or complications,” Cynthia W. Ko, MD, and guideline coauthors said in the recommendations.

From the patient perspective, probiotics are “popular,” Dr. Brant said in his presentation, noting that some patients will request probiotics as a first-line therapy or even ask to be taken off mesalamine and put on probiotics.

Meta-analyses have provided differing conclusions on the benefits of probiotics. One recently published analysis of probiotics versus mesalamine showed a slight trend to favor mesalamine, but when looking at good-quality studies only, the meta-analysis showed a nonsignificant trend in favor of probiotics, Dr. Brant said.

By contrast, in a Cochrane meta-analysis of mesalamine at standard doses versus placebo, there was consistent evidence for a benefit of mesalamine: “so the main problem with giving probiotics as a choice is that you’re going to put the patient at risk for progressive symptoms and complications,” said Dr. Brant.

However, looking specifically at the probiotic VSL#3, the Toronto Ulcerative Colitis Consensus Group said that it was linked to significantly improved remission (44% vs. 25%; odds ratio, 2.4; P = .0007). Coverage issues could be a snag, since the amount of the probiotic associated with improved remission was equivalent to four double-strength packets. “Try getting that approved,” Dr. Brant told attendees. “You’ll have some challenges.”

Curcumin was evaluated in a multicenter trial showing that, when added to maximal mesalamine, it may be helpful in avoiding an advance in therapy, with 54% achieving clinical remission at week 4 versus 0% of placebo-treated patients.

That was a “reasonable study” but more research needs to be done, Dr. Brant said.

“I think that given the minimal harm, it may be worth a trial, though not in patients that are really having systemic symptoms, severe bleeding, and are getting worse,” he said. “It’s patients that have some response on mesalamine where it may be valuable, if you have time to spare to give them curcumin.”

Dr. Brant indicated that he had no relevant financial relationships to disclose.

Global Academy and this news organization are owned by the same parent company.

PHILADELPHIA – Although the new ulcerative colitis guidelines make no current recommendations on probiotics and curcumin because of gaps in knowledge, both may be beneficial today in selected patients, an expert said at the meeting jointly provided by Rutgers and Global Academy for Medical Education.

Andrew D. Bowser/MDedge News

“Probiotics can be added, in my opinion, to patients on mesalamine with mild to moderate ulcerative colitis in order to help induce remission without having to go to immunosuppressive medication,” said Steven R. Brant, MD, chief of the division of gastroenterology and hepatology at Robert Wood Johnson Medical School, New Brunswick, N.J.

Likewise, curcumin has shown “minimal harm” in mild ulcerative colitis and may help nudge patients toward disease control without having to resort to corticosteroids or other immunosuppressive therapy, Dr. Brant said.

The new American Gastroenterological Association guidelines for treatment of mild to moderate ulcerative colitis, published in February in the journal Gastroenterology, declined to make recommendations on either probiotics or curcumin, citing “knowledge gaps and areas for future research.”

“Although these modalities appear to be safe, their use risks delaying proven effective therapy with the potential for worsening symptoms or complications,” Cynthia W. Ko, MD, and guideline coauthors said in the recommendations.

From the patient perspective, probiotics are “popular,” Dr. Brant said in his presentation, noting that some patients will request probiotics as a first-line therapy or even ask to be taken off mesalamine and put on probiotics.

Meta-analyses have provided differing conclusions on the benefits of probiotics. One recently published analysis of probiotics versus mesalamine showed a slight trend to favor mesalamine, but when looking at good-quality studies only, the meta-analysis showed a nonsignificant trend in favor of probiotics, Dr. Brant said.

By contrast, in a Cochrane meta-analysis of mesalamine at standard doses versus placebo, there was consistent evidence for a benefit of mesalamine: “so the main problem with giving probiotics as a choice is that you’re going to put the patient at risk for progressive symptoms and complications,” said Dr. Brant.

However, looking specifically at the probiotic VSL#3, the Toronto Ulcerative Colitis Consensus Group said that it was linked to significantly improved remission (44% vs. 25%; odds ratio, 2.4; P = .0007). Coverage issues could be a snag, since the amount of the probiotic associated with improved remission was equivalent to four double-strength packets. “Try getting that approved,” Dr. Brant told attendees. “You’ll have some challenges.”

Curcumin was evaluated in a multicenter trial showing that, when added to maximal mesalamine, it may be helpful in avoiding an advance in therapy, with 54% achieving clinical remission at week 4 versus 0% of placebo-treated patients.

That was a “reasonable study” but more research needs to be done, Dr. Brant said.

“I think that given the minimal harm, it may be worth a trial, though not in patients that are really having systemic symptoms, severe bleeding, and are getting worse,” he said. “It’s patients that have some response on mesalamine where it may be valuable, if you have time to spare to give them curcumin.”

Dr. Brant indicated that he had no relevant financial relationships to disclose.

Global Academy and this news organization are owned by the same parent company.

DENVER – Combining gold microparticles with energy from a standard dermatology laser represents a new in-office treatment option for patients with mild to moderate acne, according to Jill S. Waibel, MD.

“Why do we need lasers and light for acne? We have compliance issues, particularly in the pubertal population,” she said at the annual conference of the American Society for Laser Medicine and Surgery. “We also have systemic side effects from medications and antibiotic resistance. Acne is still the number one reason people see a dermatologist.”

The gold microparticles were cleared by the Food and Drug Administration in September 2018 for the treatment of mild to moderate inflammatory acne. Based on European study data and ongoing studies in the United States, the optimal treatment approach begins with putting on a topical retinoid nightly and benzoyl peroxide (BPO) wash to clear follicular debris and reduce bacterial load prior to the application of gold microparticles and laser energy.

Dr. Waibel, director of the Miami Dermatology and Laser Institute, presented results from a clinical trial of 64 patients with mild to moderate acne that was conducted at seven European centers. All patients applied topical 0.1% adapalene/2.5% benzoyl peroxide daily for 2-4 weeks, then they underwent three microparticles plus laser procedures over a 2-week period. “It takes about 10 minutes to put the gold nanoparticles on,” Dr. Waibel said. “They’re rubbed in by a massager, the particles get in down into the follicle. Once it’s in the follicle, you wipe the gold completely off and you activate the FDA-approved 1064 nm Nd:YAG laser.”

Energy was delivered at a fluency of 25-34 J/cm² and a pulse duration of 30 seconds. Concomitant rescue medications were allowed at the discretion of the investigator after the 2-month evaluation. Formal evaluations included inflammatory lesion counts at baseline, 2, 3, and 6 months; the Investigator Global Assessment scale at baseline, 2, 3, and 6 months; and safety and tolerability. Most of the patients (78%) were female, and their average age was 23 years, with a range between 13 and 38 years. The average level of pain reported by patients was 4 on a scale between 0 and 10, and mild, transient erythema and edema were reported post procedure. There were no adverse events otherwise.

Dr. Waibel reported that the interim mean improvement of inflammatory lesion counts was 66% at 3 months and 79% at 6 months. “At six months, 63% of patients were clear or almost clear according to the Investigator Global Assessment scale,” she added.

After the three treatment sessions, researchers observed a 63% reduction in acne at 2 months, a 74% reduction at 6 months, and an 85% reduction at 12 months. By comparison, a subset of 26 patients who received gold microparticle monotherapy had a 49% reduction in acne at 2 months and a 65% reduction at 6 months.

“A short course of retinoid and benzoyl peroxide prior to gold microparticles treatment improved the inflammatory lesion count reduction, compared with historical studies,” Dr. Waibel said (J Invest Dermatol. 2015;135[7]:1727-34). “Gold microparticles treatment for acne may be part of a multitherapy approach for patients with mild to moderate facial acne. Clinical outcomes are predictable and durable through 12 months.”

The approach is being further studied in the United States and researchers are exploring the potential for fewer treatments over a period of two weeks. Dr. Waibel disclosed that she has served on the advisory board for Sebacia, which developed the gold microparticles, and has received clinical trials funding from the company. She also reported having financial relationships with numerous other device and pharmaceutical companies.

[email protected]

DENVER – Combining gold microparticles with energy from a standard dermatology laser represents a new in-office treatment option for patients with mild to moderate acne, according to Jill S. Waibel, MD.

“Why do we need lasers and light for acne? We have compliance issues, particularly in the pubertal population,” she said at the annual conference of the American Society for Laser Medicine and Surgery. “We also have systemic side effects from medications and antibiotic resistance. Acne is still the number one reason people see a dermatologist.”

The gold microparticles were cleared by the Food and Drug Administration in September 2018 for the treatment of mild to moderate inflammatory acne. Based on European study data and ongoing studies in the United States, the optimal treatment approach begins with putting on a topical retinoid nightly and benzoyl peroxide (BPO) wash to clear follicular debris and reduce bacterial load prior to the application of gold microparticles and laser energy.

Dr. Waibel, director of the Miami Dermatology and Laser Institute, presented results from a clinical trial of 64 patients with mild to moderate acne that was conducted at seven European centers. All patients applied topical 0.1% adapalene/2.5% benzoyl peroxide daily for 2-4 weeks, then they underwent three microparticles plus laser procedures over a 2-week period. “It takes about 10 minutes to put the gold nanoparticles on,” Dr. Waibel said. “They’re rubbed in by a massager, the particles get in down into the follicle. Once it’s in the follicle, you wipe the gold completely off and you activate the FDA-approved 1064 nm Nd:YAG laser.”

Energy was delivered at a fluency of 25-34 J/cm² and a pulse duration of 30 seconds. Concomitant rescue medications were allowed at the discretion of the investigator after the 2-month evaluation. Formal evaluations included inflammatory lesion counts at baseline, 2, 3, and 6 months; the Investigator Global Assessment scale at baseline, 2, 3, and 6 months; and safety and tolerability. Most of the patients (78%) were female, and their average age was 23 years, with a range between 13 and 38 years. The average level of pain reported by patients was 4 on a scale between 0 and 10, and mild, transient erythema and edema were reported post procedure. There were no adverse events otherwise.

Dr. Waibel reported that the interim mean improvement of inflammatory lesion counts was 66% at 3 months and 79% at 6 months. “At six months, 63% of patients were clear or almost clear according to the Investigator Global Assessment scale,” she added.

After the three treatment sessions, researchers observed a 63% reduction in acne at 2 months, a 74% reduction at 6 months, and an 85% reduction at 12 months. By comparison, a subset of 26 patients who received gold microparticle monotherapy had a 49% reduction in acne at 2 months and a 65% reduction at 6 months.

“A short course of retinoid and benzoyl peroxide prior to gold microparticles treatment improved the inflammatory lesion count reduction, compared with historical studies,” Dr. Waibel said (J Invest Dermatol. 2015;135[7]:1727-34). “Gold microparticles treatment for acne may be part of a multitherapy approach for patients with mild to moderate facial acne. Clinical outcomes are predictable and durable through 12 months.”

The approach is being further studied in the United States and researchers are exploring the potential for fewer treatments over a period of two weeks. Dr. Waibel disclosed that she has served on the advisory board for Sebacia, which developed the gold microparticles, and has received clinical trials funding from the company. She also reported having financial relationships with numerous other device and pharmaceutical companies.

[email protected]

DENVER – Combining gold microparticles with energy from a standard dermatology laser represents a new in-office treatment option for patients with mild to moderate acne, according to Jill S. Waibel, MD.

“Why do we need lasers and light for acne? We have compliance issues, particularly in the pubertal population,” she said at the annual conference of the American Society for Laser Medicine and Surgery. “We also have systemic side effects from medications and antibiotic resistance. Acne is still the number one reason people see a dermatologist.”

The gold microparticles were cleared by the Food and Drug Administration in September 2018 for the treatment of mild to moderate inflammatory acne. Based on European study data and ongoing studies in the United States, the optimal treatment approach begins with putting on a topical retinoid nightly and benzoyl peroxide (BPO) wash to clear follicular debris and reduce bacterial load prior to the application of gold microparticles and laser energy.

Dr. Waibel, director of the Miami Dermatology and Laser Institute, presented results from a clinical trial of 64 patients with mild to moderate acne that was conducted at seven European centers. All patients applied topical 0.1% adapalene/2.5% benzoyl peroxide daily for 2-4 weeks, then they underwent three microparticles plus laser procedures over a 2-week period. “It takes about 10 minutes to put the gold nanoparticles on,” Dr. Waibel said. “They’re rubbed in by a massager, the particles get in down into the follicle. Once it’s in the follicle, you wipe the gold completely off and you activate the FDA-approved 1064 nm Nd:YAG laser.”

Energy was delivered at a fluency of 25-34 J/cm² and a pulse duration of 30 seconds. Concomitant rescue medications were allowed at the discretion of the investigator after the 2-month evaluation. Formal evaluations included inflammatory lesion counts at baseline, 2, 3, and 6 months; the Investigator Global Assessment scale at baseline, 2, 3, and 6 months; and safety and tolerability. Most of the patients (78%) were female, and their average age was 23 years, with a range between 13 and 38 years. The average level of pain reported by patients was 4 on a scale between 0 and 10, and mild, transient erythema and edema were reported post procedure. There were no adverse events otherwise.

Dr. Waibel reported that the interim mean improvement of inflammatory lesion counts was 66% at 3 months and 79% at 6 months. “At six months, 63% of patients were clear or almost clear according to the Investigator Global Assessment scale,” she added.

After the three treatment sessions, researchers observed a 63% reduction in acne at 2 months, a 74% reduction at 6 months, and an 85% reduction at 12 months. By comparison, a subset of 26 patients who received gold microparticle monotherapy had a 49% reduction in acne at 2 months and a 65% reduction at 6 months.

“A short course of retinoid and benzoyl peroxide prior to gold microparticles treatment improved the inflammatory lesion count reduction, compared with historical studies,” Dr. Waibel said (J Invest Dermatol. 2015;135[7]:1727-34). “Gold microparticles treatment for acne may be part of a multitherapy approach for patients with mild to moderate facial acne. Clinical outcomes are predictable and durable through 12 months.”

The approach is being further studied in the United States and researchers are exploring the potential for fewer treatments over a period of two weeks. Dr. Waibel disclosed that she has served on the advisory board for Sebacia, which developed the gold microparticles, and has received clinical trials funding from the company. She also reported having financial relationships with numerous other device and pharmaceutical companies.

[email protected]