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We are aware of the clinical importance of diagnosing psoriatic arthritis (PsA) as early as possible to initiate appropriate therapy. Because psoriasis precedes PsA in the majority of cases, it is incumbent on clinicians to seek any evidence of joint involvement at each clinical encounter.

In a study published online on February 25 in Annals of the Rheumatic Diseases. Faustini et al reported that patients with psoriasis but without PsA experience structural joint changes at the entheses. Therefore, evidence for structural joint alterations may already exist at the time of apparently exclusive skin involvement in psoriatic disease.

In the analysis, 85 participants without arthritis, including 55 with psoriasis and 30 healthy controls, received high-field magnetic resonance imaging (MRI) of the hand. These scans were scored for synovitis, osteitis, tenosynovitis, and periarticular inflammation. Participants with psoriasis also received complete clinical investigation as well as high-resolution peripheral quantitative computed tomography for detecting erosions and enthesiophytes. All participants were followed for at least 1 year to evaluate for the development of PsA.

Magnetic resonance imaging evaluation showed that 47% (26/55) of participants with psoriasis possessed at least 1 inflammatory lesion. Synovitis was the most prevalent inflammatory lesion (38% [21/55]), while osteitis (11% [6/55]), tenosynovitis (4% [2/55]), and periarticular inflammation (4% [2/55]) were less frequent.

The incidence of enthesiophytes and bone erosions did not differ between patients with psoriasis, with or without inflammatory changes on MRI. The risk for developing PsA was as high as 60% in those with subclinical synovitis and symptoms related to arthralgia. However, the risk was only 13% if the patients had normal MRIs and did not report arthralgia. Faustini et al concluded that the prevalence of subclinical inflammatory lesions is high in patients with cutaneous psoriasis. Specifically, arthralgia in conjunction with MRI synovitis constitutes a high-risk constellation for the development of PsA.

What’s the issue?

These findings are critical, as they indicate the nature of the potential genesis of PsA in many patients. If the data are confirmed in future investigations, it may change the way we evaluate or treat early PsA. How will these findings affect your workup for early PsA?

We want to know your views! Tell us what you think.

We are aware of the clinical importance of diagnosing psoriatic arthritis (PsA) as early as possible to initiate appropriate therapy. Because psoriasis precedes PsA in the majority of cases, it is incumbent on clinicians to seek any evidence of joint involvement at each clinical encounter.

In a study published online on February 25 in Annals of the Rheumatic Diseases. Faustini et al reported that patients with psoriasis but without PsA experience structural joint changes at the entheses. Therefore, evidence for structural joint alterations may already exist at the time of apparently exclusive skin involvement in psoriatic disease.

In the analysis, 85 participants without arthritis, including 55 with psoriasis and 30 healthy controls, received high-field magnetic resonance imaging (MRI) of the hand. These scans were scored for synovitis, osteitis, tenosynovitis, and periarticular inflammation. Participants with psoriasis also received complete clinical investigation as well as high-resolution peripheral quantitative computed tomography for detecting erosions and enthesiophytes. All participants were followed for at least 1 year to evaluate for the development of PsA.

Magnetic resonance imaging evaluation showed that 47% (26/55) of participants with psoriasis possessed at least 1 inflammatory lesion. Synovitis was the most prevalent inflammatory lesion (38% [21/55]), while osteitis (11% [6/55]), tenosynovitis (4% [2/55]), and periarticular inflammation (4% [2/55]) were less frequent.

The incidence of enthesiophytes and bone erosions did not differ between patients with psoriasis, with or without inflammatory changes on MRI. The risk for developing PsA was as high as 60% in those with subclinical synovitis and symptoms related to arthralgia. However, the risk was only 13% if the patients had normal MRIs and did not report arthralgia. Faustini et al concluded that the prevalence of subclinical inflammatory lesions is high in patients with cutaneous psoriasis. Specifically, arthralgia in conjunction with MRI synovitis constitutes a high-risk constellation for the development of PsA.

What’s the issue?

These findings are critical, as they indicate the nature of the potential genesis of PsA in many patients. If the data are confirmed in future investigations, it may change the way we evaluate or treat early PsA. How will these findings affect your workup for early PsA?

We want to know your views! Tell us what you think.

We are aware of the clinical importance of diagnosing psoriatic arthritis (PsA) as early as possible to initiate appropriate therapy. Because psoriasis precedes PsA in the majority of cases, it is incumbent on clinicians to seek any evidence of joint involvement at each clinical encounter.

In a study published online on February 25 in Annals of the Rheumatic Diseases. Faustini et al reported that patients with psoriasis but without PsA experience structural joint changes at the entheses. Therefore, evidence for structural joint alterations may already exist at the time of apparently exclusive skin involvement in psoriatic disease.

In the analysis, 85 participants without arthritis, including 55 with psoriasis and 30 healthy controls, received high-field magnetic resonance imaging (MRI) of the hand. These scans were scored for synovitis, osteitis, tenosynovitis, and periarticular inflammation. Participants with psoriasis also received complete clinical investigation as well as high-resolution peripheral quantitative computed tomography for detecting erosions and enthesiophytes. All participants were followed for at least 1 year to evaluate for the development of PsA.

Magnetic resonance imaging evaluation showed that 47% (26/55) of participants with psoriasis possessed at least 1 inflammatory lesion. Synovitis was the most prevalent inflammatory lesion (38% [21/55]), while osteitis (11% [6/55]), tenosynovitis (4% [2/55]), and periarticular inflammation (4% [2/55]) were less frequent.

The incidence of enthesiophytes and bone erosions did not differ between patients with psoriasis, with or without inflammatory changes on MRI. The risk for developing PsA was as high as 60% in those with subclinical synovitis and symptoms related to arthralgia. However, the risk was only 13% if the patients had normal MRIs and did not report arthralgia. Faustini et al concluded that the prevalence of subclinical inflammatory lesions is high in patients with cutaneous psoriasis. Specifically, arthralgia in conjunction with MRI synovitis constitutes a high-risk constellation for the development of PsA.

What’s the issue?

These findings are critical, as they indicate the nature of the potential genesis of PsA in many patients. If the data are confirmed in future investigations, it may change the way we evaluate or treat early PsA. How will these findings affect your workup for early PsA?

We want to know your views! Tell us what you think.

Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.

In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL^_1 vs 11.28 [2.74] ng/mL^_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.

For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.

What’s the issue?

Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?

We want to know your views! Tell us what you think.

Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.

In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL^_1 vs 11.28 [2.74] ng/mL^_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.

For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.

What’s the issue?

Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?

We want to know your views! Tell us what you think.

Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.

In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL^_1 vs 11.28 [2.74] ng/mL^_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.

For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.

What’s the issue?

Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?

We want to know your views! Tell us what you think.

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Le Gal et al (Sci Transl Med. 2015;7:308re8) discovered that antioxidant administration in mice not only increased lymph node metastases but also increased the migration and invasive properties of human melanoma cells. However, the antioxidant N-acetylcysteine (NAC) had no impact on the number and size of the primary tumors (in mice), and neither NAC nor Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), a structurally unrelated antioxidant and soluble vitamin E analogue, affected the proliferation of human melanoma cells. Hence, the progression of malignant melanoma (MM), a cancer that is sensitive to changes in reduction-oxidation status, may be influenced by exposure to antioxidants and vitamin E.

What’s the issue?

Healthy individuals and oncology patients commonly use supplements containing antioxidants to prevent cancer and fight malignancy, respectively. However, animal studies and human clinical trials have shown that antioxidants increase cancer risk and accelerate the progression of primary lung tumors. Le Gal et al’s study regarding progression of melanoma metastases following exposure to antioxidants extends the observations demonstrated for lung neoplasms. N-acetylcysteine was added to the drinking water of mice, whereas NAC and Trolox were added to a panel of human MM cell lines. N-acetylcysteine increased lymph node metastases in the endogenous mouse model of MM, and both NAC and Trolox markedly increased the migrations and invasive properties of human MM cells.

Cancers may be caused or exacerbated by free radicals. It has been assumed that antioxidants may protect against malignancy by destroying free radicals. Although prior studies have concluded that antioxidants prevent healthy cells from transforming into cancer after exposure to free radicals, Le Gal et al’s research suggests that antioxidants may not only protect but also enhance tumor progression once a cancer has developed.

If one extends the results of animal and tissue culture studies to humans, exposure to antioxidants may potentially influence the course of metastatic disease in patients who have already developed melanoma. In addition to systemic exposure after receiving oral antioxidants, melanoma patients also can be topically exposed to antioxidants. For example, nonprescription skin care products such as cutaneous rejuvenation treatments, emollients, and sunscreens can contain β-carotene, vitamin E, and other antioxidants. It remains to be determined whether topical exposure to antioxidants can cause the same observations that have occurred following systemic absorption in mice or tissue culture studies in human cell lines. Should we caution our melanoma patients with regards to what they apply to their skin?

We want to know your views! Tell us what you think.

Le Gal et al (Sci Transl Med. 2015;7:308re8) discovered that antioxidant administration in mice not only increased lymph node metastases but also increased the migration and invasive properties of human melanoma cells. However, the antioxidant N-acetylcysteine (NAC) had no impact on the number and size of the primary tumors (in mice), and neither NAC nor Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), a structurally unrelated antioxidant and soluble vitamin E analogue, affected the proliferation of human melanoma cells. Hence, the progression of malignant melanoma (MM), a cancer that is sensitive to changes in reduction-oxidation status, may be influenced by exposure to antioxidants and vitamin E.

What’s the issue?

Healthy individuals and oncology patients commonly use supplements containing antioxidants to prevent cancer and fight malignancy, respectively. However, animal studies and human clinical trials have shown that antioxidants increase cancer risk and accelerate the progression of primary lung tumors. Le Gal et al’s study regarding progression of melanoma metastases following exposure to antioxidants extends the observations demonstrated for lung neoplasms. N-acetylcysteine was added to the drinking water of mice, whereas NAC and Trolox were added to a panel of human MM cell lines. N-acetylcysteine increased lymph node metastases in the endogenous mouse model of MM, and both NAC and Trolox markedly increased the migrations and invasive properties of human MM cells.

Cancers may be caused or exacerbated by free radicals. It has been assumed that antioxidants may protect against malignancy by destroying free radicals. Although prior studies have concluded that antioxidants prevent healthy cells from transforming into cancer after exposure to free radicals, Le Gal et al’s research suggests that antioxidants may not only protect but also enhance tumor progression once a cancer has developed.

If one extends the results of animal and tissue culture studies to humans, exposure to antioxidants may potentially influence the course of metastatic disease in patients who have already developed melanoma. In addition to systemic exposure after receiving oral antioxidants, melanoma patients also can be topically exposed to antioxidants. For example, nonprescription skin care products such as cutaneous rejuvenation treatments, emollients, and sunscreens can contain β-carotene, vitamin E, and other antioxidants. It remains to be determined whether topical exposure to antioxidants can cause the same observations that have occurred following systemic absorption in mice or tissue culture studies in human cell lines. Should we caution our melanoma patients with regards to what they apply to their skin?

We want to know your views! Tell us what you think.

Le Gal et al (Sci Transl Med. 2015;7:308re8) discovered that antioxidant administration in mice not only increased lymph node metastases but also increased the migration and invasive properties of human melanoma cells. However, the antioxidant N-acetylcysteine (NAC) had no impact on the number and size of the primary tumors (in mice), and neither NAC nor Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), a structurally unrelated antioxidant and soluble vitamin E analogue, affected the proliferation of human melanoma cells. Hence, the progression of malignant melanoma (MM), a cancer that is sensitive to changes in reduction-oxidation status, may be influenced by exposure to antioxidants and vitamin E.

What’s the issue?

Healthy individuals and oncology patients commonly use supplements containing antioxidants to prevent cancer and fight malignancy, respectively. However, animal studies and human clinical trials have shown that antioxidants increase cancer risk and accelerate the progression of primary lung tumors. Le Gal et al’s study regarding progression of melanoma metastases following exposure to antioxidants extends the observations demonstrated for lung neoplasms. N-acetylcysteine was added to the drinking water of mice, whereas NAC and Trolox were added to a panel of human MM cell lines. N-acetylcysteine increased lymph node metastases in the endogenous mouse model of MM, and both NAC and Trolox markedly increased the migrations and invasive properties of human MM cells.

Cancers may be caused or exacerbated by free radicals. It has been assumed that antioxidants may protect against malignancy by destroying free radicals. Although prior studies have concluded that antioxidants prevent healthy cells from transforming into cancer after exposure to free radicals, Le Gal et al’s research suggests that antioxidants may not only protect but also enhance tumor progression once a cancer has developed.

If one extends the results of animal and tissue culture studies to humans, exposure to antioxidants may potentially influence the course of metastatic disease in patients who have already developed melanoma. In addition to systemic exposure after receiving oral antioxidants, melanoma patients also can be topically exposed to antioxidants. For example, nonprescription skin care products such as cutaneous rejuvenation treatments, emollients, and sunscreens can contain β-carotene, vitamin E, and other antioxidants. It remains to be determined whether topical exposure to antioxidants can cause the same observations that have occurred following systemic absorption in mice or tissue culture studies in human cell lines. Should we caution our melanoma patients with regards to what they apply to their skin?

We want to know your views! Tell us what you think.

In an article published online on January 26 in the Journal of the American Academy of Dermatology, my colleagues and I (Menge et al) reported on the use of reflectance confocal microscopy (RCM) for challenging facial lesions. We studied the diagnosis of lentigo maligna (LM) based on RCM versus the histopathologic diagnosis after biopsy.

In this study 17 patients were seen for evaluation of known or suspected LM at Memorial Sloan Kettering Cancer Center (New York, New York). Among these patients, a total of 63 sites on the skin were evaluated using RCM and a presumptive diagnosis was made. These sites were then biopsied to compare the diagnosis using RCM with that made by histopathology. When LM was present as determined by biopsy, RCM also was able to detect it 100% of the time (sensitivity). When LM was absent as determined by biopsy, RCM also indicated it was absent 71% of the time (specificity).

What’s the issue?

Lentigo maligna is a form of melanoma in situ occurring on sun-damaged skin. It can be quite subtle to detect clinically and therefore may go undiagnosed for a while. Lentigo maligna also has been shown to have notable subclinical extension with which traditional surgical margins for truncal melanoma may be too narrow to clear LM on the head and neck. Therefore, presurgical consultation may be difficult due to the amorphous borders. Random blind biopsies also are discouraged because of sampling error.

Additionally, repetitive biopsies over time, which may be frequently needed in individuals with heavy sun exposure, can be costly and cause adverse effects.

This study showed the usefulness and reliability of using RCM for challenging facial lesions that are suspicious for LM. The sensitivity and specificity of RCM in this study indicated that this technology performs well in detecting LM when present; however, false-positives were noted in this study. False-positives included pigmented actinic keratosis and melanocytosis. Dermatologists who are advanced in RCM technology and interpretation also were utilized in this study. More research is needed to understand how to best utilize this technology, but overall the ability of RCM to accurately identify LM without biopsy represents an exciting new development in how dermatologists can better diagnose, manage, and treat melanoma.

How will you adopt advances in cutaneous noninvasive imaging?

We want to know your views! Tell us what you think.

In an article published online on January 26 in the Journal of the American Academy of Dermatology, my colleagues and I (Menge et al) reported on the use of reflectance confocal microscopy (RCM) for challenging facial lesions. We studied the diagnosis of lentigo maligna (LM) based on RCM versus the histopathologic diagnosis after biopsy.

In this study 17 patients were seen for evaluation of known or suspected LM at Memorial Sloan Kettering Cancer Center (New York, New York). Among these patients, a total of 63 sites on the skin were evaluated using RCM and a presumptive diagnosis was made. These sites were then biopsied to compare the diagnosis using RCM with that made by histopathology. When LM was present as determined by biopsy, RCM also was able to detect it 100% of the time (sensitivity). When LM was absent as determined by biopsy, RCM also indicated it was absent 71% of the time (specificity).

What’s the issue?

Lentigo maligna is a form of melanoma in situ occurring on sun-damaged skin. It can be quite subtle to detect clinically and therefore may go undiagnosed for a while. Lentigo maligna also has been shown to have notable subclinical extension with which traditional surgical margins for truncal melanoma may be too narrow to clear LM on the head and neck. Therefore, presurgical consultation may be difficult due to the amorphous borders. Random blind biopsies also are discouraged because of sampling error.

Additionally, repetitive biopsies over time, which may be frequently needed in individuals with heavy sun exposure, can be costly and cause adverse effects.

This study showed the usefulness and reliability of using RCM for challenging facial lesions that are suspicious for LM. The sensitivity and specificity of RCM in this study indicated that this technology performs well in detecting LM when present; however, false-positives were noted in this study. False-positives included pigmented actinic keratosis and melanocytosis. Dermatologists who are advanced in RCM technology and interpretation also were utilized in this study. More research is needed to understand how to best utilize this technology, but overall the ability of RCM to accurately identify LM without biopsy represents an exciting new development in how dermatologists can better diagnose, manage, and treat melanoma.

How will you adopt advances in cutaneous noninvasive imaging?

We want to know your views! Tell us what you think.

In an article published online on January 26 in the Journal of the American Academy of Dermatology, my colleagues and I (Menge et al) reported on the use of reflectance confocal microscopy (RCM) for challenging facial lesions. We studied the diagnosis of lentigo maligna (LM) based on RCM versus the histopathologic diagnosis after biopsy.

In this study 17 patients were seen for evaluation of known or suspected LM at Memorial Sloan Kettering Cancer Center (New York, New York). Among these patients, a total of 63 sites on the skin were evaluated using RCM and a presumptive diagnosis was made. These sites were then biopsied to compare the diagnosis using RCM with that made by histopathology. When LM was present as determined by biopsy, RCM also was able to detect it 100% of the time (sensitivity). When LM was absent as determined by biopsy, RCM also indicated it was absent 71% of the time (specificity).

What’s the issue?

Lentigo maligna is a form of melanoma in situ occurring on sun-damaged skin. It can be quite subtle to detect clinically and therefore may go undiagnosed for a while. Lentigo maligna also has been shown to have notable subclinical extension with which traditional surgical margins for truncal melanoma may be too narrow to clear LM on the head and neck. Therefore, presurgical consultation may be difficult due to the amorphous borders. Random blind biopsies also are discouraged because of sampling error.

Additionally, repetitive biopsies over time, which may be frequently needed in individuals with heavy sun exposure, can be costly and cause adverse effects.

This study showed the usefulness and reliability of using RCM for challenging facial lesions that are suspicious for LM. The sensitivity and specificity of RCM in this study indicated that this technology performs well in detecting LM when present; however, false-positives were noted in this study. False-positives included pigmented actinic keratosis and melanocytosis. Dermatologists who are advanced in RCM technology and interpretation also were utilized in this study. More research is needed to understand how to best utilize this technology, but overall the ability of RCM to accurately identify LM without biopsy represents an exciting new development in how dermatologists can better diagnose, manage, and treat melanoma.

How will you adopt advances in cutaneous noninvasive imaging?

We want to know your views! Tell us what you think.

In a study published online on April 14 in Arteriosclerosis, Thrombosis, and Vascular Biology, Khalid et al evaluated the risk for AAA in patients with psoriasis in a nationwide cohort study in Denmark. The study participants were Danish residents 18 years and older who were observed from January 1, 1997 until diagnosis of AAA; December 31, 2011; migration; or death. Incidence rates for AAA were calculated, and incidence rate ratios were adjusted for age, sex, comorbidity, medications, socioeconomic status, and smoking.

A total of 5,495,203 individuals were eligible for this study. Of them, Khalid et al identified 59,423 patients with mild psoriasis and 11,566 patients with severe psoriasis. The overall incidence rates of AAA were 3.72, 7.30, and 9.87 per 10,000 person-years for the reference population (23,696 cases), mild psoriasis (240 cases), and severe psoriasis (50 cases), respectively. The corresponding adjusted incidence rate ratios for AAA were increased in patients with psoriasis with incidence rate ratios of 1.20 (95% CI, 1.03-1.39) and 1.67 (95% CI, 1.21-2.32) for individuals with mild and severe disease, respectively.

Khalid et al concluded that psoriasis was associated with a disease severity–dependent increased risk for AAA; however, the mechanisms and consequences of this novel finding require further investigation.

What’s the issue?

Another example of an association of a comorbidity with psoriasis, this finding emphasizes the need for cardiovascular referral in psoriasis patients with risk factors such as hypertension and diabetes mellitus. How will these data influence your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

In a study published online on April 14 in Arteriosclerosis, Thrombosis, and Vascular Biology, Khalid et al evaluated the risk for AAA in patients with psoriasis in a nationwide cohort study in Denmark. The study participants were Danish residents 18 years and older who were observed from January 1, 1997 until diagnosis of AAA; December 31, 2011; migration; or death. Incidence rates for AAA were calculated, and incidence rate ratios were adjusted for age, sex, comorbidity, medications, socioeconomic status, and smoking.

A total of 5,495,203 individuals were eligible for this study. Of them, Khalid et al identified 59,423 patients with mild psoriasis and 11,566 patients with severe psoriasis. The overall incidence rates of AAA were 3.72, 7.30, and 9.87 per 10,000 person-years for the reference population (23,696 cases), mild psoriasis (240 cases), and severe psoriasis (50 cases), respectively. The corresponding adjusted incidence rate ratios for AAA were increased in patients with psoriasis with incidence rate ratios of 1.20 (95% CI, 1.03-1.39) and 1.67 (95% CI, 1.21-2.32) for individuals with mild and severe disease, respectively.

Khalid et al concluded that psoriasis was associated with a disease severity–dependent increased risk for AAA; however, the mechanisms and consequences of this novel finding require further investigation.

What’s the issue?

Another example of an association of a comorbidity with psoriasis, this finding emphasizes the need for cardiovascular referral in psoriasis patients with risk factors such as hypertension and diabetes mellitus. How will these data influence your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

In a study published online on April 14 in Arteriosclerosis, Thrombosis, and Vascular Biology, Khalid et al evaluated the risk for AAA in patients with psoriasis in a nationwide cohort study in Denmark. The study participants were Danish residents 18 years and older who were observed from January 1, 1997 until diagnosis of AAA; December 31, 2011; migration; or death. Incidence rates for AAA were calculated, and incidence rate ratios were adjusted for age, sex, comorbidity, medications, socioeconomic status, and smoking.

A total of 5,495,203 individuals were eligible for this study. Of them, Khalid et al identified 59,423 patients with mild psoriasis and 11,566 patients with severe psoriasis. The overall incidence rates of AAA were 3.72, 7.30, and 9.87 per 10,000 person-years for the reference population (23,696 cases), mild psoriasis (240 cases), and severe psoriasis (50 cases), respectively. The corresponding adjusted incidence rate ratios for AAA were increased in patients with psoriasis with incidence rate ratios of 1.20 (95% CI, 1.03-1.39) and 1.67 (95% CI, 1.21-2.32) for individuals with mild and severe disease, respectively.

Khalid et al concluded that psoriasis was associated with a disease severity–dependent increased risk for AAA; however, the mechanisms and consequences of this novel finding require further investigation.

What’s the issue?

Another example of an association of a comorbidity with psoriasis, this finding emphasizes the need for cardiovascular referral in psoriasis patients with risk factors such as hypertension and diabetes mellitus. How will these data influence your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

One of the determinants of a successful surgical outcome is the perception, on the part of the patient, of the cosmesis of a scar. The use of Z-plasty is an accepted means by which to break a scar up into smaller geometric segments. In some instances, a Z-plasty is used for scar revision to elongate a scar that may be pulling. However, a study published online in JAMA Facial Plastic Surgery on April 7 mentions the lack of studies measuring the perception of these scars among the normal population after surgery.

Ratnarathorn et al designed a prospective Internet-based survey with a goal of 580 responses to give a power of 90%. The survey was distributed to a diverse sample of the US population. Using editing software, Ratnarathorn et al superimposed a mature linear scar and a mature zigzag scar onto the faces of standardized headshots from 4 individuals (2 males, 2 females). Each individual had 1 image of the linear scar and 1 image of the zigzag scars superimposed onto each of 3 anatomical areas—forehead (flat surface), cheek (convex surface), and temple (concave surface)—yielding 24 images for the respondents to assess.

A 24.5% (n=876) response rate was achieved with 3575 surveys distributed. Of the 876 respondents, 810 (92.5%) completed the survey (46.1% male, 53.9% female). Respondents were asked to rate the scars on a scale of 1 to 10 (1=normal skin; 10=worst scar imaginable).

Results were statistically significantly lower (better) for the linear scars compared to the zigzag scars in all 3 anatomic areas and across both male and female groups with a mean score of 2.9 versus 4.5 (P<.001). A multivariable regression model of respondent age, sex, educational level, and income showed no statistically significant effect on the rating of the scars.

What’s the issue?

This study highlights some interesting points. Coming from an academic practice, we oftentimes find ourselves teaching residents a variety of skin closure techniques to deal with defects from skin cancer excisions. It is both challenging and fun to design complex closures; however, we must keep in mind what is in the best interest of the patient. One of the points I try to emphasize is that we must understand that there are no true straight lines on the face. In fact, when scars from procedures appear as geometric shapes on the face, our eyes tend to be drawn to them. For this reason, it often is best to use curvilinear lines wherever possible. Ratnarathorn et al highlights that point exactly. More studies of this nature are needed to assess what is perceived as a successful outcome, by both physicians and patients.

As you follow your patients for the long-term, have you noticed that you perform more or fewer zigzag scars?

We want to know your views! Tell us what you think.

One of the determinants of a successful surgical outcome is the perception, on the part of the patient, of the cosmesis of a scar. The use of Z-plasty is an accepted means by which to break a scar up into smaller geometric segments. In some instances, a Z-plasty is used for scar revision to elongate a scar that may be pulling. However, a study published online in JAMA Facial Plastic Surgery on April 7 mentions the lack of studies measuring the perception of these scars among the normal population after surgery.

Ratnarathorn et al designed a prospective Internet-based survey with a goal of 580 responses to give a power of 90%. The survey was distributed to a diverse sample of the US population. Using editing software, Ratnarathorn et al superimposed a mature linear scar and a mature zigzag scar onto the faces of standardized headshots from 4 individuals (2 males, 2 females). Each individual had 1 image of the linear scar and 1 image of the zigzag scars superimposed onto each of 3 anatomical areas—forehead (flat surface), cheek (convex surface), and temple (concave surface)—yielding 24 images for the respondents to assess.

A 24.5% (n=876) response rate was achieved with 3575 surveys distributed. Of the 876 respondents, 810 (92.5%) completed the survey (46.1% male, 53.9% female). Respondents were asked to rate the scars on a scale of 1 to 10 (1=normal skin; 10=worst scar imaginable).

Results were statistically significantly lower (better) for the linear scars compared to the zigzag scars in all 3 anatomic areas and across both male and female groups with a mean score of 2.9 versus 4.5 (P<.001). A multivariable regression model of respondent age, sex, educational level, and income showed no statistically significant effect on the rating of the scars.

What’s the issue?

This study highlights some interesting points. Coming from an academic practice, we oftentimes find ourselves teaching residents a variety of skin closure techniques to deal with defects from skin cancer excisions. It is both challenging and fun to design complex closures; however, we must keep in mind what is in the best interest of the patient. One of the points I try to emphasize is that we must understand that there are no true straight lines on the face. In fact, when scars from procedures appear as geometric shapes on the face, our eyes tend to be drawn to them. For this reason, it often is best to use curvilinear lines wherever possible. Ratnarathorn et al highlights that point exactly. More studies of this nature are needed to assess what is perceived as a successful outcome, by both physicians and patients.

As you follow your patients for the long-term, have you noticed that you perform more or fewer zigzag scars?

We want to know your views! Tell us what you think.

One of the determinants of a successful surgical outcome is the perception, on the part of the patient, of the cosmesis of a scar. The use of Z-plasty is an accepted means by which to break a scar up into smaller geometric segments. In some instances, a Z-plasty is used for scar revision to elongate a scar that may be pulling. However, a study published online in JAMA Facial Plastic Surgery on April 7 mentions the lack of studies measuring the perception of these scars among the normal population after surgery.

Ratnarathorn et al designed a prospective Internet-based survey with a goal of 580 responses to give a power of 90%. The survey was distributed to a diverse sample of the US population. Using editing software, Ratnarathorn et al superimposed a mature linear scar and a mature zigzag scar onto the faces of standardized headshots from 4 individuals (2 males, 2 females). Each individual had 1 image of the linear scar and 1 image of the zigzag scars superimposed onto each of 3 anatomical areas—forehead (flat surface), cheek (convex surface), and temple (concave surface)—yielding 24 images for the respondents to assess.

A 24.5% (n=876) response rate was achieved with 3575 surveys distributed. Of the 876 respondents, 810 (92.5%) completed the survey (46.1% male, 53.9% female). Respondents were asked to rate the scars on a scale of 1 to 10 (1=normal skin; 10=worst scar imaginable).

Results were statistically significantly lower (better) for the linear scars compared to the zigzag scars in all 3 anatomic areas and across both male and female groups with a mean score of 2.9 versus 4.5 (P<.001). A multivariable regression model of respondent age, sex, educational level, and income showed no statistically significant effect on the rating of the scars.

What’s the issue?

This study highlights some interesting points. Coming from an academic practice, we oftentimes find ourselves teaching residents a variety of skin closure techniques to deal with defects from skin cancer excisions. It is both challenging and fun to design complex closures; however, we must keep in mind what is in the best interest of the patient. One of the points I try to emphasize is that we must understand that there are no true straight lines on the face. In fact, when scars from procedures appear as geometric shapes on the face, our eyes tend to be drawn to them. For this reason, it often is best to use curvilinear lines wherever possible. Ratnarathorn et al highlights that point exactly. More studies of this nature are needed to assess what is perceived as a successful outcome, by both physicians and patients.

As you follow your patients for the long-term, have you noticed that you perform more or fewer zigzag scars?

We want to know your views! Tell us what you think.

According to a study by Ji et al published online on February 11 in the International Journal of Impotence Research, men with psoriasis may be more prone to erectile dysfunction (ED) than those without this skin disease, and their odds of sexual difficulties are even higher if they are depressed or have other health problems such as diabetes mellitus or high blood pressure.

The investigators evaluated 191 psoriasis patients and 191 healthy men. Of the 191 patients with psoriasis, 52.9% had symptoms of ED compared with 40.3% of the control group, reflecting an age-adjusted odds ratio of 1.965 in favor of the psoriasis group. A univariate analysis of the psoriasis cohort demonstrated that age, hypertension, hyperlipidemia, diabetes mellitus, and depressive symptoms were risk factors for ED. A multivariate logistic regression model indicated that increasing age, hypertension, hyperlipidemia, and depressive symptoms were independent risk factors for ED in those with psoriasis. More severe depressive symptoms increased the risk of ED, especially moderate to severe ED.

Ji et al noted that ED is a predictor of future cardiovascular disease; therefore, it is important to identify ED early in treatment to evaluate cardiovascular issues in psoriasis patients. They noted that screening of ED may become a part of routine care in the management of psoriasis patients.

What’s the issue?

Even though it was a small study from one location, it still sheds light on many important issues. Psoriasis and its comorbidities appear to increase the risk for ED. In addition, ED also may be an indicator of cardiovascular disease.

How will these data impact your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

According to a study by Ji et al published online on February 11 in the International Journal of Impotence Research, men with psoriasis may be more prone to erectile dysfunction (ED) than those without this skin disease, and their odds of sexual difficulties are even higher if they are depressed or have other health problems such as diabetes mellitus or high blood pressure.

The investigators evaluated 191 psoriasis patients and 191 healthy men. Of the 191 patients with psoriasis, 52.9% had symptoms of ED compared with 40.3% of the control group, reflecting an age-adjusted odds ratio of 1.965 in favor of the psoriasis group. A univariate analysis of the psoriasis cohort demonstrated that age, hypertension, hyperlipidemia, diabetes mellitus, and depressive symptoms were risk factors for ED. A multivariate logistic regression model indicated that increasing age, hypertension, hyperlipidemia, and depressive symptoms were independent risk factors for ED in those with psoriasis. More severe depressive symptoms increased the risk of ED, especially moderate to severe ED.

Ji et al noted that ED is a predictor of future cardiovascular disease; therefore, it is important to identify ED early in treatment to evaluate cardiovascular issues in psoriasis patients. They noted that screening of ED may become a part of routine care in the management of psoriasis patients.

What’s the issue?

Even though it was a small study from one location, it still sheds light on many important issues. Psoriasis and its comorbidities appear to increase the risk for ED. In addition, ED also may be an indicator of cardiovascular disease.

How will these data impact your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

According to a study by Ji et al published online on February 11 in the International Journal of Impotence Research, men with psoriasis may be more prone to erectile dysfunction (ED) than those without this skin disease, and their odds of sexual difficulties are even higher if they are depressed or have other health problems such as diabetes mellitus or high blood pressure.

The investigators evaluated 191 psoriasis patients and 191 healthy men. Of the 191 patients with psoriasis, 52.9% had symptoms of ED compared with 40.3% of the control group, reflecting an age-adjusted odds ratio of 1.965 in favor of the psoriasis group. A univariate analysis of the psoriasis cohort demonstrated that age, hypertension, hyperlipidemia, diabetes mellitus, and depressive symptoms were risk factors for ED. A multivariate logistic regression model indicated that increasing age, hypertension, hyperlipidemia, and depressive symptoms were independent risk factors for ED in those with psoriasis. More severe depressive symptoms increased the risk of ED, especially moderate to severe ED.

Ji et al noted that ED is a predictor of future cardiovascular disease; therefore, it is important to identify ED early in treatment to evaluate cardiovascular issues in psoriasis patients. They noted that screening of ED may become a part of routine care in the management of psoriasis patients.

What’s the issue?

Even though it was a small study from one location, it still sheds light on many important issues. Psoriasis and its comorbidities appear to increase the risk for ED. In addition, ED also may be an indicator of cardiovascular disease.

How will these data impact your evaluation of psoriasis patients?

We want to know your views! Tell us what you think.

In addition to the standard fare at the 74th Annual Meeting of the American Academy of Dermatology (AAD) in Washington, DC (March 4–8, 2016), this year there were several lectures addressing the use of nitric oxide (NO) for the treatment of acne. Therefore, I would like to review how NO gets delivered and the therapeutic implications as well as provide some context and understanding of the varying NO delivery systems being investigated.

Let’s start with some basics: Why should we even consider NO, a diatomic lipophilic gaseous molecule, for acne? It may be a surprise, but you already use NO for this purpose.

• NO is produced on the surface of the skin by action of commensal bacteria and plays a physiologic role in inhibition of infection by pathogenic organisms including bacteria, fungi, and viruses, and a microbicidal role against Propionibacterium acnes.
• NO minimizes inflammation by inhibiting neutrophil chemotaxis; production of lipases by P acnes (minimizes production of immunogenic free fatty acids); production of multiple cytokines such as tumor necrosis factor α, IL-8, and IL-6; antigen-presenting cell recognition of P acnes; and multiple elements of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome, the specific inflammasome reported to be impressively activated when monocytes, and even sebocytes, are exposed to P acnes, thereby inhibiting the conversion of pro–IL-1β to IL-1β.

However, NO’s direct biological action is not enough to explain these effects. It is S-nitrosylation, the covalent modification of a protein cysteine thiol by a NO group to generate an S-nitrosothiol such as nitrosoglutathione, that explains NO’s potent modulation of gene expression and enzymatic functions.

Nitric oxide was first featured in the late-breaking research session presented by Lawrence F. Eichenfield, MD, at the AAD (Efficacy and Safety of SB204 Gel in the Treatment of Acne Vulgaris)(F053). Results were presented from a phase 2b, multicenter, randomized, double-blind study comparing the efficacy, safety, and tolerability of SB204 NO-releasing gel 4% to vehicle in participants with acne vulgaris. The investigators concluded that SB204 once daily was safe and effective for the treatment of acne vulgaris, though they did not present data on the technology itself.

The NO-releasing technology being used in SB204 is an NO donor that falls under a class of NO donors called the diazeniumdiolates, or NONOates, which have been used experimentally for more than 50 years. These compounds consist of a diolate group (N[O-]N=O) bound to a nucleophile adduct (a primary or secondary amine or polyamine) by means of a nitrogen atom. Thus, you have NO bound to a donor that under appropriate environmental conditions will release its NO following first-order kinetics. It simply releases NO, rather then generate or create it.

Two issues are to be raised in relation to Dr. Eichenfield’s presentation:

Accumulation of amines and their metabolites released from NONOates have been shown to induce cytotoxicity in a study by Saavedra et al (J Med Chem. 1997;40:1947-1954). In the study by Blecher et al (Nanomedicine. 2012;8:1364-1371), topical application of DETA (diethylenetriamine) NONOate, another type of NONOate, actually delayed wound closure in NOD-SCID (nonobese diabetic severe combined immunodeficiency) mice as compared to untreated controls in a study by Blecher et al. Systemic infusion at concentrations required to reduce blood pressure resulted in methemoglobinemia and diminished oxygen-carrying capacity in a study by Cabrales et al (Free Radic Biol Med. 2010;49:530-538). The NONOate utilized in SB204 is encapsulated in a hydrogel particle to prevent permeation of said metabolites and donor compounds through the skin; however, a 12-week safety evaluation is certainly not long enough to determine whether local or systemic absorption has occurred. Of note, the NO-np has undergone extensive safety testing from cell culture of embryonic zebra fish to Syrian hamsters and even pigs showing no significant toxicity at any of the effective concentrations in animal studies.

Data published on the NO-np’s preclinical efficacy for the treatment of acne, infected excisions, and burn wounds were presented in 2 of my lectures at the AAD (Nanotechnology and Immunomodulators [F085] and Antimicrobial Dressings: Silver and Beyond [S056])(Chouake et al [J Drugs Dermatol. 2012;11:1471-1477]; Friedman et al [Virulence. 2011;2:217-221]; Han et al [PLoS One. 2009;4:e7804]; Marcherla et al [Front Microbiol. 2012;3:193]; Martinez et al [J Invest Dermatol. 2009;129:2463-2469]; Qin et al [J Invest Dermatol. 2015;135:2723-2731]; Blecher et al [Nanomedicine. 2012;8:1364-1371]). These data can be found within the suggested reading below.

What’s the issue?

Know the awesome biological power of NO. Know the differences between delivery systems, including donors and generators. Know the differences in therapeutic relevance, including efficacy and safety.

Do you know NO?

We want to know your views! Tell us what you think.

Suggested Readings

Multidrug-Resistant Bacterial and Fungal Skin and Soft Tissue Infections

1. Ahmadi M, Lee H, Sanchez D, et al. Sustained nitric oxide releasing nanoparticles induce cell death in Candida albicans yeast and hyphal cells preventing biofilm formation in vitro and in a rodent central venous catheter model. Antimicrob Agents Chemother. 2016;60:2185-2194.
2. Chouake J, Schairer D, Kutner A, et al. Nitrosoglutathione generating nitric oxide nanoparticles as an improved strategy for combating Pseudomonas aeruginosa–infected wounds. J Drugs Dermatol. 2012;11:1471-1477.
3. Friedman A, Blecher K, Sanchez D, et al. Susceptibility of gram positive and negative bacteria to novel nitric oxide-releasing nanoparticle technology. Virulence. 2011;2:217-221.
4. Friedman A, Blecher K, Schairer D, et al. Improved antimicrobial efficacy with nitric oxide releasing nanoparticle generated S-nitrosoglutathione. Nitric Oxide. 2011;25:381-386.
5. Han G, Martinez LM, Mihu MR, et al. Nitric oxide releasing nanoparticles are therapeutic for Staphylococcus aureus abscesses in murine model of infection. PLoS One. 2009;4:e7804.
6. Landriscina A, Rosen J, Blecher-Paz K, et al. Nitric oxide-releasing nanoparticles as a treatment for cutaneous dermatophyte infections. Sci Lett. 2015,4:193.
7. Marcherla C, Sanchez DA, Ahmadi M, et al. Nitric oxide releasing nanoparticles for the treatment of Candida albicans burn infections [published online June 8, 2012]. Front Microbiol. 2012;3:193.
8. Martinez L, Han G, Chacko M, et al. Antimicrobial and healing efficacy of sustained release nitric oxide nanoparticles against Staphylococcus aureus skin infections. J Invest Dermatol. 2009;129:2463-2469.
9. Mihu MR, Sandkovsky U, Han G, et al. The use of nitric oxide releasing nanoparticles as a treatment against Acinetobacter baumannii in wound infections. Virulence. 2010;1:62-67.
10. Mordorski B, Pelgrift R, Adler B, et al. S-nitrosocaptopril nanoparticles as nitric oxide-liberating and transnitrosylating anti-infective technology. Nanomedicine. 2015;11:283-291.
11. Qin M, Landriscina A, Rosen JM, et al. Nitric oxide-releasing nanoparticles prevent Propionibacterium acnes-induced inflammation by both clearing the organism and inhibiting microbial stimulation of the innate immune response. J Invest Dermatol. 2015;135:2723-2731.
12. Schairer D, Martinez L, Blecher K, et al. Nitric oxide nanoparticles: pre-clinical utility as a therapeutic for intramuscular abscesses. Virulence. 2012;3:1-6.

Wound Healing

1. Blecher K, Martinez LR, Tuckman-Vernon C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing in NOD-SCID mice. Nanomedicine. 2012;8:1364-1371.
2. Han G, Nguyen LN, Macherla C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing by promoting fibroblast migration and collagen deposition. Am J Pathol. 2012;180:1465-1473.

Erectile Dysfunction

1. Han G, Tar M, Kuppam DS, et al. Nanoparticles as a novel delivery vehicle for therapeutics targeting erectile dysfunction [published online September 18, 2009. J Sex Med. 2010;7(1 pt 1):224-333.
2. Tar M, CabralesP, Navati M, et al. Topically applied NO-releasing nanoparticles can increase intracorporal pressure and elicit spontaneous erections in a rat model of radical prostatectomy. J Sex Med. 2014;11:2903-2914.

Cardiovascular Disease

1. Cabrales P, Han G, Nacharaju P, et al. Reversal of hemoglobin-induced vasoconstriction with sustained release of nitric oxide [published online November 5, 2010]. Am J Physiol Heart Circ Physiol. 2011;300:H49-H56.
2. Cabrales P, Han G, Roche C, et al. Sustained release nitric oxide from long-lived circulation nanoparticles. Free Radic Biol Med. 2010;49:530-538.
3. Nacharaju P, Friedman AJ, Friedman JM, et al. Exogenous nitric oxide prevents collapse during hemorrhagic shock. Resuscitation. 2011;82:607-613.

Safety of NO Donors

1. Friedman A, Friedman JM. Novel biomaterials for the sustained release of nitric oxide: past, present, and future. Expert Opin Drug Deliv. 2009;6:1113-1122.
2. Liang H, Nacharaju P, Friedman A, et al. Nitric oxide generating/releasing materials. Future Sci OA. 2015;1. doi:10.4155/fso.15.54.
3. Saavedra JE, Billiar TR, Williams DL, et al. Targeting nitric oxide (NO) delivery in vivo. design of a liver-selective NO donor prodrug that blocks tumor necrosis factor-alpha-induced apoptosis and toxicity in the liver. J Med Chem. 1997;40:1947-1954.

In addition to the standard fare at the 74th Annual Meeting of the American Academy of Dermatology (AAD) in Washington, DC (March 4–8, 2016), this year there were several lectures addressing the use of nitric oxide (NO) for the treatment of acne. Therefore, I would like to review how NO gets delivered and the therapeutic implications as well as provide some context and understanding of the varying NO delivery systems being investigated.

Let’s start with some basics: Why should we even consider NO, a diatomic lipophilic gaseous molecule, for acne? It may be a surprise, but you already use NO for this purpose.

• NO is produced on the surface of the skin by action of commensal bacteria and plays a physiologic role in inhibition of infection by pathogenic organisms including bacteria, fungi, and viruses, and a microbicidal role against Propionibacterium acnes.
• NO minimizes inflammation by inhibiting neutrophil chemotaxis; production of lipases by P acnes (minimizes production of immunogenic free fatty acids); production of multiple cytokines such as tumor necrosis factor α, IL-8, and IL-6; antigen-presenting cell recognition of P acnes; and multiple elements of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome, the specific inflammasome reported to be impressively activated when monocytes, and even sebocytes, are exposed to P acnes, thereby inhibiting the conversion of pro–IL-1β to IL-1β.

However, NO’s direct biological action is not enough to explain these effects. It is S-nitrosylation, the covalent modification of a protein cysteine thiol by a NO group to generate an S-nitrosothiol such as nitrosoglutathione, that explains NO’s potent modulation of gene expression and enzymatic functions.

Nitric oxide was first featured in the late-breaking research session presented by Lawrence F. Eichenfield, MD, at the AAD (Efficacy and Safety of SB204 Gel in the Treatment of Acne Vulgaris)(F053). Results were presented from a phase 2b, multicenter, randomized, double-blind study comparing the efficacy, safety, and tolerability of SB204 NO-releasing gel 4% to vehicle in participants with acne vulgaris. The investigators concluded that SB204 once daily was safe and effective for the treatment of acne vulgaris, though they did not present data on the technology itself.

The NO-releasing technology being used in SB204 is an NO donor that falls under a class of NO donors called the diazeniumdiolates, or NONOates, which have been used experimentally for more than 50 years. These compounds consist of a diolate group (N[O-]N=O) bound to a nucleophile adduct (a primary or secondary amine or polyamine) by means of a nitrogen atom. Thus, you have NO bound to a donor that under appropriate environmental conditions will release its NO following first-order kinetics. It simply releases NO, rather then generate or create it.

Two issues are to be raised in relation to Dr. Eichenfield’s presentation:

Accumulation of amines and their metabolites released from NONOates have been shown to induce cytotoxicity in a study by Saavedra et al (J Med Chem. 1997;40:1947-1954). In the study by Blecher et al (Nanomedicine. 2012;8:1364-1371), topical application of DETA (diethylenetriamine) NONOate, another type of NONOate, actually delayed wound closure in NOD-SCID (nonobese diabetic severe combined immunodeficiency) mice as compared to untreated controls in a study by Blecher et al. Systemic infusion at concentrations required to reduce blood pressure resulted in methemoglobinemia and diminished oxygen-carrying capacity in a study by Cabrales et al (Free Radic Biol Med. 2010;49:530-538). The NONOate utilized in SB204 is encapsulated in a hydrogel particle to prevent permeation of said metabolites and donor compounds through the skin; however, a 12-week safety evaluation is certainly not long enough to determine whether local or systemic absorption has occurred. Of note, the NO-np has undergone extensive safety testing from cell culture of embryonic zebra fish to Syrian hamsters and even pigs showing no significant toxicity at any of the effective concentrations in animal studies.

Data published on the NO-np’s preclinical efficacy for the treatment of acne, infected excisions, and burn wounds were presented in 2 of my lectures at the AAD (Nanotechnology and Immunomodulators [F085] and Antimicrobial Dressings: Silver and Beyond [S056])(Chouake et al [J Drugs Dermatol. 2012;11:1471-1477]; Friedman et al [Virulence. 2011;2:217-221]; Han et al [PLoS One. 2009;4:e7804]; Marcherla et al [Front Microbiol. 2012;3:193]; Martinez et al [J Invest Dermatol. 2009;129:2463-2469]; Qin et al [J Invest Dermatol. 2015;135:2723-2731]; Blecher et al [Nanomedicine. 2012;8:1364-1371]). These data can be found within the suggested reading below.

What’s the issue?

Know the awesome biological power of NO. Know the differences between delivery systems, including donors and generators. Know the differences in therapeutic relevance, including efficacy and safety.

Do you know NO?

We want to know your views! Tell us what you think.

Suggested Readings

Multidrug-Resistant Bacterial and Fungal Skin and Soft Tissue Infections

1. Ahmadi M, Lee H, Sanchez D, et al. Sustained nitric oxide releasing nanoparticles induce cell death in Candida albicans yeast and hyphal cells preventing biofilm formation in vitro and in a rodent central venous catheter model. Antimicrob Agents Chemother. 2016;60:2185-2194.
2. Chouake J, Schairer D, Kutner A, et al. Nitrosoglutathione generating nitric oxide nanoparticles as an improved strategy for combating Pseudomonas aeruginosa–infected wounds. J Drugs Dermatol. 2012;11:1471-1477.
3. Friedman A, Blecher K, Sanchez D, et al. Susceptibility of gram positive and negative bacteria to novel nitric oxide-releasing nanoparticle technology. Virulence. 2011;2:217-221.
4. Friedman A, Blecher K, Schairer D, et al. Improved antimicrobial efficacy with nitric oxide releasing nanoparticle generated S-nitrosoglutathione. Nitric Oxide. 2011;25:381-386.
5. Han G, Martinez LM, Mihu MR, et al. Nitric oxide releasing nanoparticles are therapeutic for Staphylococcus aureus abscesses in murine model of infection. PLoS One. 2009;4:e7804.
6. Landriscina A, Rosen J, Blecher-Paz K, et al. Nitric oxide-releasing nanoparticles as a treatment for cutaneous dermatophyte infections. Sci Lett. 2015,4:193.
7. Marcherla C, Sanchez DA, Ahmadi M, et al. Nitric oxide releasing nanoparticles for the treatment of Candida albicans burn infections [published online June 8, 2012]. Front Microbiol. 2012;3:193.
8. Martinez L, Han G, Chacko M, et al. Antimicrobial and healing efficacy of sustained release nitric oxide nanoparticles against Staphylococcus aureus skin infections. J Invest Dermatol. 2009;129:2463-2469.
9. Mihu MR, Sandkovsky U, Han G, et al. The use of nitric oxide releasing nanoparticles as a treatment against Acinetobacter baumannii in wound infections. Virulence. 2010;1:62-67.
10. Mordorski B, Pelgrift R, Adler B, et al. S-nitrosocaptopril nanoparticles as nitric oxide-liberating and transnitrosylating anti-infective technology. Nanomedicine. 2015;11:283-291.
11. Qin M, Landriscina A, Rosen JM, et al. Nitric oxide-releasing nanoparticles prevent Propionibacterium acnes-induced inflammation by both clearing the organism and inhibiting microbial stimulation of the innate immune response. J Invest Dermatol. 2015;135:2723-2731.
12. Schairer D, Martinez L, Blecher K, et al. Nitric oxide nanoparticles: pre-clinical utility as a therapeutic for intramuscular abscesses. Virulence. 2012;3:1-6.

Wound Healing

1. Blecher K, Martinez LR, Tuckman-Vernon C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing in NOD-SCID mice. Nanomedicine. 2012;8:1364-1371.
2. Han G, Nguyen LN, Macherla C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing by promoting fibroblast migration and collagen deposition. Am J Pathol. 2012;180:1465-1473.

Erectile Dysfunction

1. Han G, Tar M, Kuppam DS, et al. Nanoparticles as a novel delivery vehicle for therapeutics targeting erectile dysfunction [published online September 18, 2009. J Sex Med. 2010;7(1 pt 1):224-333.
2. Tar M, CabralesP, Navati M, et al. Topically applied NO-releasing nanoparticles can increase intracorporal pressure and elicit spontaneous erections in a rat model of radical prostatectomy. J Sex Med. 2014;11:2903-2914.

Cardiovascular Disease

1. Cabrales P, Han G, Nacharaju P, et al. Reversal of hemoglobin-induced vasoconstriction with sustained release of nitric oxide [published online November 5, 2010]. Am J Physiol Heart Circ Physiol. 2011;300:H49-H56.
2. Cabrales P, Han G, Roche C, et al. Sustained release nitric oxide from long-lived circulation nanoparticles. Free Radic Biol Med. 2010;49:530-538.
3. Nacharaju P, Friedman AJ, Friedman JM, et al. Exogenous nitric oxide prevents collapse during hemorrhagic shock. Resuscitation. 2011;82:607-613.

Safety of NO Donors

1. Friedman A, Friedman JM. Novel biomaterials for the sustained release of nitric oxide: past, present, and future. Expert Opin Drug Deliv. 2009;6:1113-1122.
2. Liang H, Nacharaju P, Friedman A, et al. Nitric oxide generating/releasing materials. Future Sci OA. 2015;1. doi:10.4155/fso.15.54.
3. Saavedra JE, Billiar TR, Williams DL, et al. Targeting nitric oxide (NO) delivery in vivo. design of a liver-selective NO donor prodrug that blocks tumor necrosis factor-alpha-induced apoptosis and toxicity in the liver. J Med Chem. 1997;40:1947-1954.

In addition to the standard fare at the 74th Annual Meeting of the American Academy of Dermatology (AAD) in Washington, DC (March 4–8, 2016), this year there were several lectures addressing the use of nitric oxide (NO) for the treatment of acne. Therefore, I would like to review how NO gets delivered and the therapeutic implications as well as provide some context and understanding of the varying NO delivery systems being investigated.

Let’s start with some basics: Why should we even consider NO, a diatomic lipophilic gaseous molecule, for acne? It may be a surprise, but you already use NO for this purpose.

• NO is produced on the surface of the skin by action of commensal bacteria and plays a physiologic role in inhibition of infection by pathogenic organisms including bacteria, fungi, and viruses, and a microbicidal role against Propionibacterium acnes.
• NO minimizes inflammation by inhibiting neutrophil chemotaxis; production of lipases by P acnes (minimizes production of immunogenic free fatty acids); production of multiple cytokines such as tumor necrosis factor α, IL-8, and IL-6; antigen-presenting cell recognition of P acnes; and multiple elements of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome, the specific inflammasome reported to be impressively activated when monocytes, and even sebocytes, are exposed to P acnes, thereby inhibiting the conversion of pro–IL-1β to IL-1β.

However, NO’s direct biological action is not enough to explain these effects. It is S-nitrosylation, the covalent modification of a protein cysteine thiol by a NO group to generate an S-nitrosothiol such as nitrosoglutathione, that explains NO’s potent modulation of gene expression and enzymatic functions.

Nitric oxide was first featured in the late-breaking research session presented by Lawrence F. Eichenfield, MD, at the AAD (Efficacy and Safety of SB204 Gel in the Treatment of Acne Vulgaris)(F053). Results were presented from a phase 2b, multicenter, randomized, double-blind study comparing the efficacy, safety, and tolerability of SB204 NO-releasing gel 4% to vehicle in participants with acne vulgaris. The investigators concluded that SB204 once daily was safe and effective for the treatment of acne vulgaris, though they did not present data on the technology itself.

The NO-releasing technology being used in SB204 is an NO donor that falls under a class of NO donors called the diazeniumdiolates, or NONOates, which have been used experimentally for more than 50 years. These compounds consist of a diolate group (N[O-]N=O) bound to a nucleophile adduct (a primary or secondary amine or polyamine) by means of a nitrogen atom. Thus, you have NO bound to a donor that under appropriate environmental conditions will release its NO following first-order kinetics. It simply releases NO, rather then generate or create it.

Two issues are to be raised in relation to Dr. Eichenfield’s presentation:

Accumulation of amines and their metabolites released from NONOates have been shown to induce cytotoxicity in a study by Saavedra et al (J Med Chem. 1997;40:1947-1954). In the study by Blecher et al (Nanomedicine. 2012;8:1364-1371), topical application of DETA (diethylenetriamine) NONOate, another type of NONOate, actually delayed wound closure in NOD-SCID (nonobese diabetic severe combined immunodeficiency) mice as compared to untreated controls in a study by Blecher et al. Systemic infusion at concentrations required to reduce blood pressure resulted in methemoglobinemia and diminished oxygen-carrying capacity in a study by Cabrales et al (Free Radic Biol Med. 2010;49:530-538). The NONOate utilized in SB204 is encapsulated in a hydrogel particle to prevent permeation of said metabolites and donor compounds through the skin; however, a 12-week safety evaluation is certainly not long enough to determine whether local or systemic absorption has occurred. Of note, the NO-np has undergone extensive safety testing from cell culture of embryonic zebra fish to Syrian hamsters and even pigs showing no significant toxicity at any of the effective concentrations in animal studies.

Data published on the NO-np’s preclinical efficacy for the treatment of acne, infected excisions, and burn wounds were presented in 2 of my lectures at the AAD (Nanotechnology and Immunomodulators [F085] and Antimicrobial Dressings: Silver and Beyond [S056])(Chouake et al [J Drugs Dermatol. 2012;11:1471-1477]; Friedman et al [Virulence. 2011;2:217-221]; Han et al [PLoS One. 2009;4:e7804]; Marcherla et al [Front Microbiol. 2012;3:193]; Martinez et al [J Invest Dermatol. 2009;129:2463-2469]; Qin et al [J Invest Dermatol. 2015;135:2723-2731]; Blecher et al [Nanomedicine. 2012;8:1364-1371]). These data can be found within the suggested reading below.

What’s the issue?

Know the awesome biological power of NO. Know the differences between delivery systems, including donors and generators. Know the differences in therapeutic relevance, including efficacy and safety.

Do you know NO?

We want to know your views! Tell us what you think.

Suggested Readings

Multidrug-Resistant Bacterial and Fungal Skin and Soft Tissue Infections

1. Ahmadi M, Lee H, Sanchez D, et al. Sustained nitric oxide releasing nanoparticles induce cell death in Candida albicans yeast and hyphal cells preventing biofilm formation in vitro and in a rodent central venous catheter model. Antimicrob Agents Chemother. 2016;60:2185-2194.
2. Chouake J, Schairer D, Kutner A, et al. Nitrosoglutathione generating nitric oxide nanoparticles as an improved strategy for combating Pseudomonas aeruginosa–infected wounds. J Drugs Dermatol. 2012;11:1471-1477.
3. Friedman A, Blecher K, Sanchez D, et al. Susceptibility of gram positive and negative bacteria to novel nitric oxide-releasing nanoparticle technology. Virulence. 2011;2:217-221.
4. Friedman A, Blecher K, Schairer D, et al. Improved antimicrobial efficacy with nitric oxide releasing nanoparticle generated S-nitrosoglutathione. Nitric Oxide. 2011;25:381-386.
5. Han G, Martinez LM, Mihu MR, et al. Nitric oxide releasing nanoparticles are therapeutic for Staphylococcus aureus abscesses in murine model of infection. PLoS One. 2009;4:e7804.
6. Landriscina A, Rosen J, Blecher-Paz K, et al. Nitric oxide-releasing nanoparticles as a treatment for cutaneous dermatophyte infections. Sci Lett. 2015,4:193.
7. Marcherla C, Sanchez DA, Ahmadi M, et al. Nitric oxide releasing nanoparticles for the treatment of Candida albicans burn infections [published online June 8, 2012]. Front Microbiol. 2012;3:193.
8. Martinez L, Han G, Chacko M, et al. Antimicrobial and healing efficacy of sustained release nitric oxide nanoparticles against Staphylococcus aureus skin infections. J Invest Dermatol. 2009;129:2463-2469.
9. Mihu MR, Sandkovsky U, Han G, et al. The use of nitric oxide releasing nanoparticles as a treatment against Acinetobacter baumannii in wound infections. Virulence. 2010;1:62-67.
10. Mordorski B, Pelgrift R, Adler B, et al. S-nitrosocaptopril nanoparticles as nitric oxide-liberating and transnitrosylating anti-infective technology. Nanomedicine. 2015;11:283-291.
11. Qin M, Landriscina A, Rosen JM, et al. Nitric oxide-releasing nanoparticles prevent Propionibacterium acnes-induced inflammation by both clearing the organism and inhibiting microbial stimulation of the innate immune response. J Invest Dermatol. 2015;135:2723-2731.
12. Schairer D, Martinez L, Blecher K, et al. Nitric oxide nanoparticles: pre-clinical utility as a therapeutic for intramuscular abscesses. Virulence. 2012;3:1-6.

Wound Healing

1. Blecher K, Martinez LR, Tuckman-Vernon C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing in NOD-SCID mice. Nanomedicine. 2012;8:1364-1371.
2. Han G, Nguyen LN, Macherla C, et al. Nitric oxide-releasing nanoparticles accelerate wound healing by promoting fibroblast migration and collagen deposition. Am J Pathol. 2012;180:1465-1473.

Erectile Dysfunction

1. Han G, Tar M, Kuppam DS, et al. Nanoparticles as a novel delivery vehicle for therapeutics targeting erectile dysfunction [published online September 18, 2009. J Sex Med. 2010;7(1 pt 1):224-333.
2. Tar M, CabralesP, Navati M, et al. Topically applied NO-releasing nanoparticles can increase intracorporal pressure and elicit spontaneous erections in a rat model of radical prostatectomy. J Sex Med. 2014;11:2903-2914.

Cardiovascular Disease

1. Cabrales P, Han G, Nacharaju P, et al. Reversal of hemoglobin-induced vasoconstriction with sustained release of nitric oxide [published online November 5, 2010]. Am J Physiol Heart Circ Physiol. 2011;300:H49-H56.
2. Cabrales P, Han G, Roche C, et al. Sustained release nitric oxide from long-lived circulation nanoparticles. Free Radic Biol Med. 2010;49:530-538.
3. Nacharaju P, Friedman AJ, Friedman JM, et al. Exogenous nitric oxide prevents collapse during hemorrhagic shock. Resuscitation. 2011;82:607-613.

Safety of NO Donors

1. Friedman A, Friedman JM. Novel biomaterials for the sustained release of nitric oxide: past, present, and future. Expert Opin Drug Deliv. 2009;6:1113-1122.
2. Liang H, Nacharaju P, Friedman A, et al. Nitric oxide generating/releasing materials. Future Sci OA. 2015;1. doi:10.4155/fso.15.54.
3. Saavedra JE, Billiar TR, Williams DL, et al. Targeting nitric oxide (NO) delivery in vivo. design of a liver-selective NO donor prodrug that blocks tumor necrosis factor-alpha-induced apoptosis and toxicity in the liver. J Med Chem. 1997;40:1947-1954.

Many male and female patients seek therapy for androgenetic alopecia (AGA) at some point. Results are rarely achieved with single-modality therapy. In fact, the treatment of AGA often requires a combination approach of systemic medications and supplements; topical therapy; and if indicated, some type of minimally invasive procedure or surgical option.

The use of platelet-rich plasma (PRP) to pretreat follicular unit hair grafts may increase hair growth and density. Although the method by which PRP helps promote hair growth remains a source of speculation, it is known that platelets contain many growth factors in the platelet α granules. When these granules become activated, they release many types of growth factors ranging from vascular endothelial growth factor, transforming growth factor ß, epidermal growth factor, platelet-derived growth factor, and insulinlike growth factor.

Injection or topical application of PRP has become a popular treatment for skin rejuvenation, alopecia, and autologous fat grafting; however, many of these treatments are being done without the studies to support them.

Alves and Grimalt (Dermatol Surg. 2016;42:491-497) conducted a prospective, split-scalp, placebo-controlled study evaluating the use of PRP injections in the treatment of AGA in 25 patients (12 men, 13 women) with a mean age of 39 years (age range, 21–62 years). Photographs were taken and 4 areas per split scalp were marked with red tattoo dots. The patients were randomized to receive PRP on 1 side and saline injections on the other side. Patients were blinded, but the physician performing the treatment was not blinded. Treatments were performed monthly for 3 sessions. Follow-up photographs and hair density counts were performed at 3 and 6 months after treatment.

Results showed that after 6 months there was a statistically significant (P<.05) increase in the total hair density and terminal hair counts on the PRP-treated side compared to baseline and to the placebo-treated side. When broken down by demographics, patients who did best were men 40 years or younger with AGA beginning at 25 years or older, a positive family history of AGA, and AGA duration of greater than 10 years.

What’s the issue?

The results of this study suggest that PRP has a mild to modest effect (approximately 10% increase) on increasing hair density in a specific patient population. This split-scalp, placebo-controlled study is one of the few of its kind in the field of PRP research and the authors should be applauded for the design of this study. However, it would be beneficial to have a 1-year follow-up to see if the results are maintained and to better help determine if maintenance injections would be needed to sustain the results.

The field of hair restoration and regeneration will continue to grow as newer technologies in hair stem cell injections come to the forefront as well. Rigorous studies will be needed to better help physicians and patients make the right treatment decisions.

Have patients been asking you about PRP for skin rejuvenation and hair restoration?

We want to know your views! Tell us what you think.

Many male and female patients seek therapy for androgenetic alopecia (AGA) at some point. Results are rarely achieved with single-modality therapy. In fact, the treatment of AGA often requires a combination approach of systemic medications and supplements; topical therapy; and if indicated, some type of minimally invasive procedure or surgical option.

The use of platelet-rich plasma (PRP) to pretreat follicular unit hair grafts may increase hair growth and density. Although the method by which PRP helps promote hair growth remains a source of speculation, it is known that platelets contain many growth factors in the platelet α granules. When these granules become activated, they release many types of growth factors ranging from vascular endothelial growth factor, transforming growth factor ß, epidermal growth factor, platelet-derived growth factor, and insulinlike growth factor.

Injection or topical application of PRP has become a popular treatment for skin rejuvenation, alopecia, and autologous fat grafting; however, many of these treatments are being done without the studies to support them.

Alves and Grimalt (Dermatol Surg. 2016;42:491-497) conducted a prospective, split-scalp, placebo-controlled study evaluating the use of PRP injections in the treatment of AGA in 25 patients (12 men, 13 women) with a mean age of 39 years (age range, 21–62 years). Photographs were taken and 4 areas per split scalp were marked with red tattoo dots. The patients were randomized to receive PRP on 1 side and saline injections on the other side. Patients were blinded, but the physician performing the treatment was not blinded. Treatments were performed monthly for 3 sessions. Follow-up photographs and hair density counts were performed at 3 and 6 months after treatment.

Results showed that after 6 months there was a statistically significant (P<.05) increase in the total hair density and terminal hair counts on the PRP-treated side compared to baseline and to the placebo-treated side. When broken down by demographics, patients who did best were men 40 years or younger with AGA beginning at 25 years or older, a positive family history of AGA, and AGA duration of greater than 10 years.

What’s the issue?

The results of this study suggest that PRP has a mild to modest effect (approximately 10% increase) on increasing hair density in a specific patient population. This split-scalp, placebo-controlled study is one of the few of its kind in the field of PRP research and the authors should be applauded for the design of this study. However, it would be beneficial to have a 1-year follow-up to see if the results are maintained and to better help determine if maintenance injections would be needed to sustain the results.

The field of hair restoration and regeneration will continue to grow as newer technologies in hair stem cell injections come to the forefront as well. Rigorous studies will be needed to better help physicians and patients make the right treatment decisions.

Have patients been asking you about PRP for skin rejuvenation and hair restoration?

We want to know your views! Tell us what you think.

Many male and female patients seek therapy for androgenetic alopecia (AGA) at some point. Results are rarely achieved with single-modality therapy. In fact, the treatment of AGA often requires a combination approach of systemic medications and supplements; topical therapy; and if indicated, some type of minimally invasive procedure or surgical option.

The use of platelet-rich plasma (PRP) to pretreat follicular unit hair grafts may increase hair growth and density. Although the method by which PRP helps promote hair growth remains a source of speculation, it is known that platelets contain many growth factors in the platelet α granules. When these granules become activated, they release many types of growth factors ranging from vascular endothelial growth factor, transforming growth factor ß, epidermal growth factor, platelet-derived growth factor, and insulinlike growth factor.

Injection or topical application of PRP has become a popular treatment for skin rejuvenation, alopecia, and autologous fat grafting; however, many of these treatments are being done without the studies to support them.

Alves and Grimalt (Dermatol Surg. 2016;42:491-497) conducted a prospective, split-scalp, placebo-controlled study evaluating the use of PRP injections in the treatment of AGA in 25 patients (12 men, 13 women) with a mean age of 39 years (age range, 21–62 years). Photographs were taken and 4 areas per split scalp were marked with red tattoo dots. The patients were randomized to receive PRP on 1 side and saline injections on the other side. Patients were blinded, but the physician performing the treatment was not blinded. Treatments were performed monthly for 3 sessions. Follow-up photographs and hair density counts were performed at 3 and 6 months after treatment.

Results showed that after 6 months there was a statistically significant (P<.05) increase in the total hair density and terminal hair counts on the PRP-treated side compared to baseline and to the placebo-treated side. When broken down by demographics, patients who did best were men 40 years or younger with AGA beginning at 25 years or older, a positive family history of AGA, and AGA duration of greater than 10 years.

What’s the issue?

The results of this study suggest that PRP has a mild to modest effect (approximately 10% increase) on increasing hair density in a specific patient population. This split-scalp, placebo-controlled study is one of the few of its kind in the field of PRP research and the authors should be applauded for the design of this study. However, it would be beneficial to have a 1-year follow-up to see if the results are maintained and to better help determine if maintenance injections would be needed to sustain the results.

The field of hair restoration and regeneration will continue to grow as newer technologies in hair stem cell injections come to the forefront as well. Rigorous studies will be needed to better help physicians and patients make the right treatment decisions.

Have patients been asking you about PRP for skin rejuvenation and hair restoration?

We want to know your views! Tell us what you think.