Perspectives

Clarke et al published a study online on March 2 in the Journal of Cutaneous Pathology regarding a novel diagnostic test for melanoma. Using quantitative reverse transcriptase–polymerase chain reaction targeting 23 preselected genes, biopsy samples from a variety of melanocytic skin lesions—464 lesions in a training set and 437 lesions in a separate validation set—were analyzed. The test assigned a single numeric score favoring either benign or malignant with sensitivity and specificity of 89% and 93%, respectively (training set), and 90% and 91%, respectively (validation set), when compared to expert consensus dermatopathology review.

What’s the issue?

Any clinician who biopsies multiple melanocytic lesions per day daydreams about a modality that will consistently and accurately distinguish the neoplasms that haunt us the most: the ones with no clear diagnosis and the lesions where intra- and interdepartmental histopathology results vary across the board. In fact, a patient recently told me that I “missed” her “dangerous” melanoma when our dermatopathology and outside consultant opinions stated that the lesion was a dysplastic nevus. The patient personally took the slides to another institution where they were deemed an “evolving” melanoma in situ. Are they all correct? How do we know that something is evolving? Which tumors will eventually be the sinister ones? If we don’t know, then how can a patient understand his/her predicament? What’s a clinician to do?

Reassuringly, in perusing the exhibit hall at the 73rd Annual Meeting of the American Academy of Dermatology, the climate has shifted somewhat. A new zone of molecular and genetic technology has emerged between the rows of pharmaceutical innovation and office supply hardware. The reverse transcriptase–polymerase chain reaction melanoma diagnostic test distinguishes itself with its large study set and measurement parameters, as it quantifies gene expression. Other adjunctive diagnostic modalities have been proven useful in atypical melanocytic proliferations, such as fluorescence in situ hybridization, comparative genomic hybridization, and DNA microarray technology, with focus on physical chromosomal copy alterations; however, it seems as though this new test provides a functional measure and straightforward plus/minus result that may be more universally and objectively relevant and interpretable from a simple skin biopsy. Perhaps the diagnostic technology has now outpaced our limited and confusing vocabulary for melanocytic lesions. Nonetheless, further clinical follow-up, prospective prognostic data, and cost analysis will define its evolving role. How do you think this gene signature test will ultimately influence our interpretation of melanocytic biopsy results?

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

Clarke et al published a study online on March 2 in the Journal of Cutaneous Pathology regarding a novel diagnostic test for melanoma. Using quantitative reverse transcriptase–polymerase chain reaction targeting 23 preselected genes, biopsy samples from a variety of melanocytic skin lesions—464 lesions in a training set and 437 lesions in a separate validation set—were analyzed. The test assigned a single numeric score favoring either benign or malignant with sensitivity and specificity of 89% and 93%, respectively (training set), and 90% and 91%, respectively (validation set), when compared to expert consensus dermatopathology review.

What’s the issue?

Any clinician who biopsies multiple melanocytic lesions per day daydreams about a modality that will consistently and accurately distinguish the neoplasms that haunt us the most: the ones with no clear diagnosis and the lesions where intra- and interdepartmental histopathology results vary across the board. In fact, a patient recently told me that I “missed” her “dangerous” melanoma when our dermatopathology and outside consultant opinions stated that the lesion was a dysplastic nevus. The patient personally took the slides to another institution where they were deemed an “evolving” melanoma in situ. Are they all correct? How do we know that something is evolving? Which tumors will eventually be the sinister ones? If we don’t know, then how can a patient understand his/her predicament? What’s a clinician to do?

Reassuringly, in perusing the exhibit hall at the 73rd Annual Meeting of the American Academy of Dermatology, the climate has shifted somewhat. A new zone of molecular and genetic technology has emerged between the rows of pharmaceutical innovation and office supply hardware. The reverse transcriptase–polymerase chain reaction melanoma diagnostic test distinguishes itself with its large study set and measurement parameters, as it quantifies gene expression. Other adjunctive diagnostic modalities have been proven useful in atypical melanocytic proliferations, such as fluorescence in situ hybridization, comparative genomic hybridization, and DNA microarray technology, with focus on physical chromosomal copy alterations; however, it seems as though this new test provides a functional measure and straightforward plus/minus result that may be more universally and objectively relevant and interpretable from a simple skin biopsy. Perhaps the diagnostic technology has now outpaced our limited and confusing vocabulary for melanocytic lesions. Nonetheless, further clinical follow-up, prospective prognostic data, and cost analysis will define its evolving role. How do you think this gene signature test will ultimately influence our interpretation of melanocytic biopsy results?

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

Clarke et al published a study online on March 2 in the Journal of Cutaneous Pathology regarding a novel diagnostic test for melanoma. Using quantitative reverse transcriptase–polymerase chain reaction targeting 23 preselected genes, biopsy samples from a variety of melanocytic skin lesions—464 lesions in a training set and 437 lesions in a separate validation set—were analyzed. The test assigned a single numeric score favoring either benign or malignant with sensitivity and specificity of 89% and 93%, respectively (training set), and 90% and 91%, respectively (validation set), when compared to expert consensus dermatopathology review.

What’s the issue?

Any clinician who biopsies multiple melanocytic lesions per day daydreams about a modality that will consistently and accurately distinguish the neoplasms that haunt us the most: the ones with no clear diagnosis and the lesions where intra- and interdepartmental histopathology results vary across the board. In fact, a patient recently told me that I “missed” her “dangerous” melanoma when our dermatopathology and outside consultant opinions stated that the lesion was a dysplastic nevus. The patient personally took the slides to another institution where they were deemed an “evolving” melanoma in situ. Are they all correct? How do we know that something is evolving? Which tumors will eventually be the sinister ones? If we don’t know, then how can a patient understand his/her predicament? What’s a clinician to do?

Reassuringly, in perusing the exhibit hall at the 73rd Annual Meeting of the American Academy of Dermatology, the climate has shifted somewhat. A new zone of molecular and genetic technology has emerged between the rows of pharmaceutical innovation and office supply hardware. The reverse transcriptase–polymerase chain reaction melanoma diagnostic test distinguishes itself with its large study set and measurement parameters, as it quantifies gene expression. Other adjunctive diagnostic modalities have been proven useful in atypical melanocytic proliferations, such as fluorescence in situ hybridization, comparative genomic hybridization, and DNA microarray technology, with focus on physical chromosomal copy alterations; however, it seems as though this new test provides a functional measure and straightforward plus/minus result that may be more universally and objectively relevant and interpretable from a simple skin biopsy. Perhaps the diagnostic technology has now outpaced our limited and confusing vocabulary for melanocytic lesions. Nonetheless, further clinical follow-up, prospective prognostic data, and cost analysis will define its evolving role. How do you think this gene signature test will ultimately influence our interpretation of melanocytic biopsy results?

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

With the advent of biologic therapies, there has been debate about the necessity to stop these therapies prior to elective surgery. The concern has been that there might be an increased risk for perioperative infections in the presence of these agents. Several current guidelines of care recommend a planned break from biologic therapy in patients undergoing major surgical procedures; for example, the British Association of Dermatologists and the British Society for Rheumatology recommend stopping biologics for at least 4 half-lives before surgery.

Bakkour et al published a study online on March 2 in the Journal of the European Academy of Dermatology and Venereology that audited the management of biologic therapy perioperatively in a tertiary referral psoriasis clinic against guidelines of care. In addition, they investigated the effects of continuing and stopping biologic therapy in psoriasis and psoriatic arthritis patients. Information was collected on the biologics used, whether they were held perioperatively, and whether patients developed postoperative complications and/or disease flare.

The authors identified 42 patients who had a total of 77 procedures performed. Procedures included cutaneous surgery, orthopedic procedures, and cardiothoracic surgery. Biologic therapy was continued in 76% of procedures. Comparing those who continued with those who stopped biologic therapy, there was no significant difference in postoperative risk for infection and delayed wound healing. This finding included patients who underwent major surgery. Interestingly, the interruption of biologic therapy perioperatively was associated with a significant (P=.003) risk for flare of psoriasis or psoriatic arthritis.

What’s the issue?

The authors concluded that continuing biologic therapy did not increase the risk for postoperative complications. However, stopping biologic therapy perioperatively significantly increased the risk for disease flare.

Although this study was small, it shed light on an issue of great interest in the use of biologic therapy. It showed that there is a potential downside to stopping these agents before surgery. Further data are needed to fully elucidate the proper management in these cases.

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

With the advent of biologic therapies, there has been debate about the necessity to stop these therapies prior to elective surgery. The concern has been that there might be an increased risk for perioperative infections in the presence of these agents. Several current guidelines of care recommend a planned break from biologic therapy in patients undergoing major surgical procedures; for example, the British Association of Dermatologists and the British Society for Rheumatology recommend stopping biologics for at least 4 half-lives before surgery.

Bakkour et al published a study online on March 2 in the Journal of the European Academy of Dermatology and Venereology that audited the management of biologic therapy perioperatively in a tertiary referral psoriasis clinic against guidelines of care. In addition, they investigated the effects of continuing and stopping biologic therapy in psoriasis and psoriatic arthritis patients. Information was collected on the biologics used, whether they were held perioperatively, and whether patients developed postoperative complications and/or disease flare.

The authors identified 42 patients who had a total of 77 procedures performed. Procedures included cutaneous surgery, orthopedic procedures, and cardiothoracic surgery. Biologic therapy was continued in 76% of procedures. Comparing those who continued with those who stopped biologic therapy, there was no significant difference in postoperative risk for infection and delayed wound healing. This finding included patients who underwent major surgery. Interestingly, the interruption of biologic therapy perioperatively was associated with a significant (P=.003) risk for flare of psoriasis or psoriatic arthritis.

What’s the issue?

The authors concluded that continuing biologic therapy did not increase the risk for postoperative complications. However, stopping biologic therapy perioperatively significantly increased the risk for disease flare.

Although this study was small, it shed light on an issue of great interest in the use of biologic therapy. It showed that there is a potential downside to stopping these agents before surgery. Further data are needed to fully elucidate the proper management in these cases.

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

With the advent of biologic therapies, there has been debate about the necessity to stop these therapies prior to elective surgery. The concern has been that there might be an increased risk for perioperative infections in the presence of these agents. Several current guidelines of care recommend a planned break from biologic therapy in patients undergoing major surgical procedures; for example, the British Association of Dermatologists and the British Society for Rheumatology recommend stopping biologics for at least 4 half-lives before surgery.

Bakkour et al published a study online on March 2 in the Journal of the European Academy of Dermatology and Venereology that audited the management of biologic therapy perioperatively in a tertiary referral psoriasis clinic against guidelines of care. In addition, they investigated the effects of continuing and stopping biologic therapy in psoriasis and psoriatic arthritis patients. Information was collected on the biologics used, whether they were held perioperatively, and whether patients developed postoperative complications and/or disease flare.

The authors identified 42 patients who had a total of 77 procedures performed. Procedures included cutaneous surgery, orthopedic procedures, and cardiothoracic surgery. Biologic therapy was continued in 76% of procedures. Comparing those who continued with those who stopped biologic therapy, there was no significant difference in postoperative risk for infection and delayed wound healing. This finding included patients who underwent major surgery. Interestingly, the interruption of biologic therapy perioperatively was associated with a significant (P=.003) risk for flare of psoriasis or psoriatic arthritis.

What’s the issue?

The authors concluded that continuing biologic therapy did not increase the risk for postoperative complications. However, stopping biologic therapy perioperatively significantly increased the risk for disease flare.

Although this study was small, it shed light on an issue of great interest in the use of biologic therapy. It showed that there is a potential downside to stopping these agents before surgery. Further data are needed to fully elucidate the proper management in these cases.

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

At the recent 73rd Annual Meeting of the American Academy of Dermatology (AAD) in San Francisco, California, acne was once again a hot topic. Considerably more attention was paid to the role of androgens and, by default, antihormonal therapy as compared to prior years. Here are some of the highlights.

Spironolactone for Acne

Although not US Food and Drug Administration approved for the treatment of acne, spironolactone can be quite effective in the treatment of adult female acne due to its ability to block androgen receptors, decrease androgen production, inhibit 5α-reductase, and increase sexual hormone–binding protein. The question that often comes up is, how frequently do you need to check serum potassium levels, given that this drug is a potassium-sparing diuretic? According to both a poster at the AAD (P1296) and a study (the largest of its kind) published online on March 22 by Plovanich et al in JAMA Dermatology, the answer is not often or possibly not at all in young, otherwise-healthy women. Who should be checked then? Patients who have known cardiac and renal disease or impaired hepatic functioning as well as patients taking angiotensin-converting enzyme inhibitors, aldosterone blockers, angiotensin II antagonists, nonsteroidal anti-inflammatory drugs, or potassium supplementation. Be cautious with patients on digoxin and lithium, as spironolactone can increase their serum concentration and half-life.

Isotretinoin Risk

During a symposium (Acne Treatment Controversies), Dr. Diane M. Thiboutot discussed what’s new in the world of isotretinoin safety myths as well as useful tips to improve outcomes. The most recent data do not support a link between isotretinoin and inflammatory bowel disease. Prednisone and lower doses of isotretinoin can be used when initiating in a patient with severe inflammatory acne. Isotretinoin use also can be considered in patients with prior history of pseudotumor from tetracycline antibiotics with appropriate consultation. No significant issues regarding wound healing have been demonstrated or reported with isotretinoin, so the need to stop before cutaneous surgery is unlikely. Additionally, there are limited reports of complications with rhinoplasty, a possible slight increased risk for dry socket, and few cases of keloidal scarring with dermabrasion.

Updates in Pathophysiology

New immunologic targets for therapy and a better understanding of the role of the sebocyte in acne pathogenesis dominated the discussions at the AAD. In a workshop (Translating Evidence Into Practice: Acne Guidelines), Dr. Rachel V. Reynolds discussed the many hats worn by the sebocyte from an endocrine organ responsive to melanocortins, vitamin D, and corticotropin-releasing hormone to an immune cell responsible for secreting antimicrobial peptides and a broad array of inflammatory mediators implicated in the pathogenesis of acne. Fitting in with the recent excitement surrounding the identification of a key inflammasome (NLRP3 [NOD-like receptor family, pyrin domain containing 3]) in the IL-1β-induced subclinical inflammation in acne (Qin et al. J Invest Dermatol. 2014;134:381-388), it also was found that the sebocyte can participate in the same pathway. Propionibacterium acnes–induced NLRP3-derived IL-1β activation in sebocytes also has a role in acne pathogenesis (Li et al. J Invest Dermatol. 2014;134:2747-2756).

With respect to targeting elements of the inflammasome, during a forum (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics) I had the opportunity to discuss my collaboration with Dr. Jenny Kim of the University of California, Los Angeles, using nitric oxide–releasing nanoparticles (P1691). We found that not only do nitric oxide–releasing nanoparticles prevent the release of inflammatory cytokines from P acnes–stimulated human keratinocytes and monocytes, but even more importantly, this nanotechnology can inhibit multiple elements of the inflammasome cascade at the gene level. For example, caspase-1 and IL-1β suggests a mechanism(s) by which this technology could serve as not only a treatment of acne but of other inflammatory dermatoses.

That’s all for now! Stay tuned for more updates and hot topics in the world of acne.

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

At the recent 73rd Annual Meeting of the American Academy of Dermatology (AAD) in San Francisco, California, acne was once again a hot topic. Considerably more attention was paid to the role of androgens and, by default, antihormonal therapy as compared to prior years. Here are some of the highlights.

Spironolactone for Acne

Although not US Food and Drug Administration approved for the treatment of acne, spironolactone can be quite effective in the treatment of adult female acne due to its ability to block androgen receptors, decrease androgen production, inhibit 5α-reductase, and increase sexual hormone–binding protein. The question that often comes up is, how frequently do you need to check serum potassium levels, given that this drug is a potassium-sparing diuretic? According to both a poster at the AAD (P1296) and a study (the largest of its kind) published online on March 22 by Plovanich et al in JAMA Dermatology, the answer is not often or possibly not at all in young, otherwise-healthy women. Who should be checked then? Patients who have known cardiac and renal disease or impaired hepatic functioning as well as patients taking angiotensin-converting enzyme inhibitors, aldosterone blockers, angiotensin II antagonists, nonsteroidal anti-inflammatory drugs, or potassium supplementation. Be cautious with patients on digoxin and lithium, as spironolactone can increase their serum concentration and half-life.

Isotretinoin Risk

During a symposium (Acne Treatment Controversies), Dr. Diane M. Thiboutot discussed what’s new in the world of isotretinoin safety myths as well as useful tips to improve outcomes. The most recent data do not support a link between isotretinoin and inflammatory bowel disease. Prednisone and lower doses of isotretinoin can be used when initiating in a patient with severe inflammatory acne. Isotretinoin use also can be considered in patients with prior history of pseudotumor from tetracycline antibiotics with appropriate consultation. No significant issues regarding wound healing have been demonstrated or reported with isotretinoin, so the need to stop before cutaneous surgery is unlikely. Additionally, there are limited reports of complications with rhinoplasty, a possible slight increased risk for dry socket, and few cases of keloidal scarring with dermabrasion.

Updates in Pathophysiology

New immunologic targets for therapy and a better understanding of the role of the sebocyte in acne pathogenesis dominated the discussions at the AAD. In a workshop (Translating Evidence Into Practice: Acne Guidelines), Dr. Rachel V. Reynolds discussed the many hats worn by the sebocyte from an endocrine organ responsive to melanocortins, vitamin D, and corticotropin-releasing hormone to an immune cell responsible for secreting antimicrobial peptides and a broad array of inflammatory mediators implicated in the pathogenesis of acne. Fitting in with the recent excitement surrounding the identification of a key inflammasome (NLRP3 [NOD-like receptor family, pyrin domain containing 3]) in the IL-1β-induced subclinical inflammation in acne (Qin et al. J Invest Dermatol. 2014;134:381-388), it also was found that the sebocyte can participate in the same pathway. Propionibacterium acnes–induced NLRP3-derived IL-1β activation in sebocytes also has a role in acne pathogenesis (Li et al. J Invest Dermatol. 2014;134:2747-2756).

With respect to targeting elements of the inflammasome, during a forum (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics) I had the opportunity to discuss my collaboration with Dr. Jenny Kim of the University of California, Los Angeles, using nitric oxide–releasing nanoparticles (P1691). We found that not only do nitric oxide–releasing nanoparticles prevent the release of inflammatory cytokines from P acnes–stimulated human keratinocytes and monocytes, but even more importantly, this nanotechnology can inhibit multiple elements of the inflammasome cascade at the gene level. For example, caspase-1 and IL-1β suggests a mechanism(s) by which this technology could serve as not only a treatment of acne but of other inflammatory dermatoses.

That’s all for now! Stay tuned for more updates and hot topics in the world of acne.

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

At the recent 73rd Annual Meeting of the American Academy of Dermatology (AAD) in San Francisco, California, acne was once again a hot topic. Considerably more attention was paid to the role of androgens and, by default, antihormonal therapy as compared to prior years. Here are some of the highlights.

Spironolactone for Acne

Although not US Food and Drug Administration approved for the treatment of acne, spironolactone can be quite effective in the treatment of adult female acne due to its ability to block androgen receptors, decrease androgen production, inhibit 5α-reductase, and increase sexual hormone–binding protein. The question that often comes up is, how frequently do you need to check serum potassium levels, given that this drug is a potassium-sparing diuretic? According to both a poster at the AAD (P1296) and a study (the largest of its kind) published online on March 22 by Plovanich et al in JAMA Dermatology, the answer is not often or possibly not at all in young, otherwise-healthy women. Who should be checked then? Patients who have known cardiac and renal disease or impaired hepatic functioning as well as patients taking angiotensin-converting enzyme inhibitors, aldosterone blockers, angiotensin II antagonists, nonsteroidal anti-inflammatory drugs, or potassium supplementation. Be cautious with patients on digoxin and lithium, as spironolactone can increase their serum concentration and half-life.

Isotretinoin Risk

During a symposium (Acne Treatment Controversies), Dr. Diane M. Thiboutot discussed what’s new in the world of isotretinoin safety myths as well as useful tips to improve outcomes. The most recent data do not support a link between isotretinoin and inflammatory bowel disease. Prednisone and lower doses of isotretinoin can be used when initiating in a patient with severe inflammatory acne. Isotretinoin use also can be considered in patients with prior history of pseudotumor from tetracycline antibiotics with appropriate consultation. No significant issues regarding wound healing have been demonstrated or reported with isotretinoin, so the need to stop before cutaneous surgery is unlikely. Additionally, there are limited reports of complications with rhinoplasty, a possible slight increased risk for dry socket, and few cases of keloidal scarring with dermabrasion.

Updates in Pathophysiology

New immunologic targets for therapy and a better understanding of the role of the sebocyte in acne pathogenesis dominated the discussions at the AAD. In a workshop (Translating Evidence Into Practice: Acne Guidelines), Dr. Rachel V. Reynolds discussed the many hats worn by the sebocyte from an endocrine organ responsive to melanocortins, vitamin D, and corticotropin-releasing hormone to an immune cell responsible for secreting antimicrobial peptides and a broad array of inflammatory mediators implicated in the pathogenesis of acne. Fitting in with the recent excitement surrounding the identification of a key inflammasome (NLRP3 [NOD-like receptor family, pyrin domain containing 3]) in the IL-1β-induced subclinical inflammation in acne (Qin et al. J Invest Dermatol. 2014;134:381-388), it also was found that the sebocyte can participate in the same pathway. Propionibacterium acnes–induced NLRP3-derived IL-1β activation in sebocytes also has a role in acne pathogenesis (Li et al. J Invest Dermatol. 2014;134:2747-2756).

With respect to targeting elements of the inflammasome, during a forum (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics) I had the opportunity to discuss my collaboration with Dr. Jenny Kim of the University of California, Los Angeles, using nitric oxide–releasing nanoparticles (P1691). We found that not only do nitric oxide–releasing nanoparticles prevent the release of inflammatory cytokines from P acnes–stimulated human keratinocytes and monocytes, but even more importantly, this nanotechnology can inhibit multiple elements of the inflammasome cascade at the gene level. For example, caspase-1 and IL-1β suggests a mechanism(s) by which this technology could serve as not only a treatment of acne but of other inflammatory dermatoses.

That’s all for now! Stay tuned for more updates and hot topics in the world of acne.

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

Recently there has been a lot of interest and attention given to the rejuvenation of the face utilizing autologous fat. Much of this interest stems from the understanding of the aging process on facial fat volume, bone density, and muscle thickness. Even in your 30s, volume deficit begins to show as undereye circles and the cheeks take on a submalar hollow, which continues to progress with time.

Charles-de-Sá et al (Plast Reconstr Surg. 2015;135:999-1009) looked at the direct antiaging effects that autologous fat grafting has on skin. The authors observed 6 consecutive patients (5 women and 1 man; mixed ethnic backgrounds; aged 45–65 years; nonsmokers) who presented for face-lifts. A small skin and fat biopsy from the preauricular area on each patient was taken for baseline histologic analysis.

The patients had abdominal fat harvested and processed in 2 manners. One portion was centrifuged at 3000 rpm for 3 minutes. The pellet at the base of the syringe (stromal vascular fraction) was then taken and mixed with 1 mL of adipose tissue and injected into the right preauricular skin in a subdermal fanning technique using a small cannula (1.5 mm) on a 3-mL syringe. The second portion of the fat was sent for stem cell expansion (2×10⁶ mesenchymal cells). Five weeks later, the solution of stem cells (0.4 mL) was diluted with normal saline to a volume of 1 mL and injected in the left preauricular area, also 2 cm in front of the tragus.

Three months after the injections, repeat biopsies in the grafted areas were taken and sent for hematoxylin and eosin stain and electron microscopy. Results showed that at baseline on hematoxylin and eosin, the skin showed evidence of mild solar elastosis. However, after both methods of fat processing, the treated areas showed a reduction in solar elastosis, increased elastin fibers in the papillary dermis, and increased vasculature in the reticular dermis (near the subcutaneous fat). The results were similar in both types of fat processing; there was no statistically significant difference between modalities.

What’s the issue?

Those of us who have performed autologous fat grafting on patients have remarked for years on the improved appearance of the skin and the slowing down of the aging process that is not accounted for by volume replacement alone. This study has shown that fat grafting or stem cell injection in the subcutaneous layer has a beneficial effect on the overlying skin. The fact that both techniques showed similar results is helpful because it demonstrates that improvement can be achieved without having to expand the cells in vitro, thus eliminating all the regulatory issues that accompany cell cultures. A larger study would be extremely beneficial at this point. How does this procedure compare to platelet-rich plasma injections that are also the big fad for skin rejuvenation?

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

Recently there has been a lot of interest and attention given to the rejuvenation of the face utilizing autologous fat. Much of this interest stems from the understanding of the aging process on facial fat volume, bone density, and muscle thickness. Even in your 30s, volume deficit begins to show as undereye circles and the cheeks take on a submalar hollow, which continues to progress with time.

Charles-de-Sá et al (Plast Reconstr Surg. 2015;135:999-1009) looked at the direct antiaging effects that autologous fat grafting has on skin. The authors observed 6 consecutive patients (5 women and 1 man; mixed ethnic backgrounds; aged 45–65 years; nonsmokers) who presented for face-lifts. A small skin and fat biopsy from the preauricular area on each patient was taken for baseline histologic analysis.

The patients had abdominal fat harvested and processed in 2 manners. One portion was centrifuged at 3000 rpm for 3 minutes. The pellet at the base of the syringe (stromal vascular fraction) was then taken and mixed with 1 mL of adipose tissue and injected into the right preauricular skin in a subdermal fanning technique using a small cannula (1.5 mm) on a 3-mL syringe. The second portion of the fat was sent for stem cell expansion (2×10⁶ mesenchymal cells). Five weeks later, the solution of stem cells (0.4 mL) was diluted with normal saline to a volume of 1 mL and injected in the left preauricular area, also 2 cm in front of the tragus.

Three months after the injections, repeat biopsies in the grafted areas were taken and sent for hematoxylin and eosin stain and electron microscopy. Results showed that at baseline on hematoxylin and eosin, the skin showed evidence of mild solar elastosis. However, after both methods of fat processing, the treated areas showed a reduction in solar elastosis, increased elastin fibers in the papillary dermis, and increased vasculature in the reticular dermis (near the subcutaneous fat). The results were similar in both types of fat processing; there was no statistically significant difference between modalities.

What’s the issue?

Those of us who have performed autologous fat grafting on patients have remarked for years on the improved appearance of the skin and the slowing down of the aging process that is not accounted for by volume replacement alone. This study has shown that fat grafting or stem cell injection in the subcutaneous layer has a beneficial effect on the overlying skin. The fact that both techniques showed similar results is helpful because it demonstrates that improvement can be achieved without having to expand the cells in vitro, thus eliminating all the regulatory issues that accompany cell cultures. A larger study would be extremely beneficial at this point. How does this procedure compare to platelet-rich plasma injections that are also the big fad for skin rejuvenation?

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

Recently there has been a lot of interest and attention given to the rejuvenation of the face utilizing autologous fat. Much of this interest stems from the understanding of the aging process on facial fat volume, bone density, and muscle thickness. Even in your 30s, volume deficit begins to show as undereye circles and the cheeks take on a submalar hollow, which continues to progress with time.

Charles-de-Sá et al (Plast Reconstr Surg. 2015;135:999-1009) looked at the direct antiaging effects that autologous fat grafting has on skin. The authors observed 6 consecutive patients (5 women and 1 man; mixed ethnic backgrounds; aged 45–65 years; nonsmokers) who presented for face-lifts. A small skin and fat biopsy from the preauricular area on each patient was taken for baseline histologic analysis.

The patients had abdominal fat harvested and processed in 2 manners. One portion was centrifuged at 3000 rpm for 3 minutes. The pellet at the base of the syringe (stromal vascular fraction) was then taken and mixed with 1 mL of adipose tissue and injected into the right preauricular skin in a subdermal fanning technique using a small cannula (1.5 mm) on a 3-mL syringe. The second portion of the fat was sent for stem cell expansion (2×10⁶ mesenchymal cells). Five weeks later, the solution of stem cells (0.4 mL) was diluted with normal saline to a volume of 1 mL and injected in the left preauricular area, also 2 cm in front of the tragus.

Three months after the injections, repeat biopsies in the grafted areas were taken and sent for hematoxylin and eosin stain and electron microscopy. Results showed that at baseline on hematoxylin and eosin, the skin showed evidence of mild solar elastosis. However, after both methods of fat processing, the treated areas showed a reduction in solar elastosis, increased elastin fibers in the papillary dermis, and increased vasculature in the reticular dermis (near the subcutaneous fat). The results were similar in both types of fat processing; there was no statistically significant difference between modalities.

What’s the issue?

Those of us who have performed autologous fat grafting on patients have remarked for years on the improved appearance of the skin and the slowing down of the aging process that is not accounted for by volume replacement alone. This study has shown that fat grafting or stem cell injection in the subcutaneous layer has a beneficial effect on the overlying skin. The fact that both techniques showed similar results is helpful because it demonstrates that improvement can be achieved without having to expand the cells in vitro, thus eliminating all the regulatory issues that accompany cell cultures. A larger study would be extremely beneficial at this point. How does this procedure compare to platelet-rich plasma injections that are also the big fad for skin rejuvenation?

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

Gerami et al (Clin Cancer Res. 2015;21:175-183) discussed the development and use of a genetic signature to predict the likelihood of metastasis from cutaneous melanoma. A genetic signature comprised of 28 prognostic genetic targets and 3 control genes was developed from the expression data available and reverse transcriptase–polymerase chain reaction analysis of more than 260 primary cutaneous melanoma cases was performed. Genetic expression data from public databases were used to identify genes that were similarly upregulated or downregulated in metastatic disease. The analysis of cutaneous melanoma and uveal melanoma tumors led to the selection of 54 gene targets that had different expression profiles for primary tumors compared with metastatic tumors. Of the 54 targets of interest, 20 were selected for further reverse transcriptase–polymerase chain reaction analysis based on genetic loci. Additionally, analysis of metastatic and nonmetastatic primary cutaneous melanoma tumors using a profile assay for uveal melanoma led to the selection of 5 additional gene targets. The sample set of cases included 107 stage I and stage II primary melanomas. Twenty cases had metastatic disease and 5 cases had regional recurrence.

Prediction of metastatic risk for this test was classified either as class 1 (low risk) or class 2 (high risk). In the development cohort, 43 of 107 cases were predicted to be class 2. All cases with documented metastatic progression were called class 2 (100% sensitivity), whereas 64 of 82 nonmetastatic cases were called class 1 (78% specificity; accuracy determined by the area under the receiver operating characteristic curve, 0.93). Kaplan-Meier survival analysis revealed that disease-free survival for the predicted classes was significantly different (P<.0001). Also, the median time to metastasis for class 2 cases was 2.5 years, whereas the median time for class 1 cases was not reached. Five-year disease-free survival was 100% for class 1 cases compared with 38% for class 2 cases.

What’s the issue?

Stage I cutaneous melanoma tumors have a 5-year overall survival rate of 91% to 97%. Although the majority of clinical stage I patients will be disease free at 5 years, some stage I patients will develop advanced disease. Furthermore, prognosis for clinical stage II and stage III cases by the TNM staging system is highly variable, as evidenced by a 5-year survival rate of 53% to 82% for stage II patients and a 5-year survival rate of 22% to 68% for stage III patients. However, up to 20% of stage I and stage II patients will die from the disease within 4 years of the initial diagnosis. This statistic can be difficult for patients, as it can be unclear which stage I and stage II patients are more at risk.

This test had a limited number of samples that were used to create this predictive tool. Would patients with stage I and stage II disease deemed to be high risk by this test benefit from adjuvant therapy and/or enhanced imaging protocols to allow for early detection of metastasis? Will you be recommending this test to your melanoma patients?

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

Gerami et al (Clin Cancer Res. 2015;21:175-183) discussed the development and use of a genetic signature to predict the likelihood of metastasis from cutaneous melanoma. A genetic signature comprised of 28 prognostic genetic targets and 3 control genes was developed from the expression data available and reverse transcriptase–polymerase chain reaction analysis of more than 260 primary cutaneous melanoma cases was performed. Genetic expression data from public databases were used to identify genes that were similarly upregulated or downregulated in metastatic disease. The analysis of cutaneous melanoma and uveal melanoma tumors led to the selection of 54 gene targets that had different expression profiles for primary tumors compared with metastatic tumors. Of the 54 targets of interest, 20 were selected for further reverse transcriptase–polymerase chain reaction analysis based on genetic loci. Additionally, analysis of metastatic and nonmetastatic primary cutaneous melanoma tumors using a profile assay for uveal melanoma led to the selection of 5 additional gene targets. The sample set of cases included 107 stage I and stage II primary melanomas. Twenty cases had metastatic disease and 5 cases had regional recurrence.

Prediction of metastatic risk for this test was classified either as class 1 (low risk) or class 2 (high risk). In the development cohort, 43 of 107 cases were predicted to be class 2. All cases with documented metastatic progression were called class 2 (100% sensitivity), whereas 64 of 82 nonmetastatic cases were called class 1 (78% specificity; accuracy determined by the area under the receiver operating characteristic curve, 0.93). Kaplan-Meier survival analysis revealed that disease-free survival for the predicted classes was significantly different (P<.0001). Also, the median time to metastasis for class 2 cases was 2.5 years, whereas the median time for class 1 cases was not reached. Five-year disease-free survival was 100% for class 1 cases compared with 38% for class 2 cases.

What’s the issue?

Stage I cutaneous melanoma tumors have a 5-year overall survival rate of 91% to 97%. Although the majority of clinical stage I patients will be disease free at 5 years, some stage I patients will develop advanced disease. Furthermore, prognosis for clinical stage II and stage III cases by the TNM staging system is highly variable, as evidenced by a 5-year survival rate of 53% to 82% for stage II patients and a 5-year survival rate of 22% to 68% for stage III patients. However, up to 20% of stage I and stage II patients will die from the disease within 4 years of the initial diagnosis. This statistic can be difficult for patients, as it can be unclear which stage I and stage II patients are more at risk.

This test had a limited number of samples that were used to create this predictive tool. Would patients with stage I and stage II disease deemed to be high risk by this test benefit from adjuvant therapy and/or enhanced imaging protocols to allow for early detection of metastasis? Will you be recommending this test to your melanoma patients?

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

Gerami et al (Clin Cancer Res. 2015;21:175-183) discussed the development and use of a genetic signature to predict the likelihood of metastasis from cutaneous melanoma. A genetic signature comprised of 28 prognostic genetic targets and 3 control genes was developed from the expression data available and reverse transcriptase–polymerase chain reaction analysis of more than 260 primary cutaneous melanoma cases was performed. Genetic expression data from public databases were used to identify genes that were similarly upregulated or downregulated in metastatic disease. The analysis of cutaneous melanoma and uveal melanoma tumors led to the selection of 54 gene targets that had different expression profiles for primary tumors compared with metastatic tumors. Of the 54 targets of interest, 20 were selected for further reverse transcriptase–polymerase chain reaction analysis based on genetic loci. Additionally, analysis of metastatic and nonmetastatic primary cutaneous melanoma tumors using a profile assay for uveal melanoma led to the selection of 5 additional gene targets. The sample set of cases included 107 stage I and stage II primary melanomas. Twenty cases had metastatic disease and 5 cases had regional recurrence.

Prediction of metastatic risk for this test was classified either as class 1 (low risk) or class 2 (high risk). In the development cohort, 43 of 107 cases were predicted to be class 2. All cases with documented metastatic progression were called class 2 (100% sensitivity), whereas 64 of 82 nonmetastatic cases were called class 1 (78% specificity; accuracy determined by the area under the receiver operating characteristic curve, 0.93). Kaplan-Meier survival analysis revealed that disease-free survival for the predicted classes was significantly different (P<.0001). Also, the median time to metastasis for class 2 cases was 2.5 years, whereas the median time for class 1 cases was not reached. Five-year disease-free survival was 100% for class 1 cases compared with 38% for class 2 cases.

What’s the issue?

Stage I cutaneous melanoma tumors have a 5-year overall survival rate of 91% to 97%. Although the majority of clinical stage I patients will be disease free at 5 years, some stage I patients will develop advanced disease. Furthermore, prognosis for clinical stage II and stage III cases by the TNM staging system is highly variable, as evidenced by a 5-year survival rate of 53% to 82% for stage II patients and a 5-year survival rate of 22% to 68% for stage III patients. However, up to 20% of stage I and stage II patients will die from the disease within 4 years of the initial diagnosis. This statistic can be difficult for patients, as it can be unclear which stage I and stage II patients are more at risk.

This test had a limited number of samples that were used to create this predictive tool. Would patients with stage I and stage II disease deemed to be high risk by this test benefit from adjuvant therapy and/or enhanced imaging protocols to allow for early detection of metastasis? Will you be recommending this test to your melanoma patients?

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

Do you greet your patients when you enter the examination room in your office or their room in the hospital? “Of course I do,” most physicians reply. And, do you shake hands? If your answer is yes, should you? Perhaps a fist bump would be a more hygienic alternative.

Mela and Whitworth (Am J Infect Control. 2014;42:916-917) demonstrated that “dap greetings” such as the high five and the fist bump dramatically reduced the transfer of bacteria during greeting exchange compared with the traditional handshake. Transmission of bacteria during the handshake was influenced not only by the large contact area but also the duration of the activity and the strength of the grip. Specifically, they observed the following about bacterial transfer: (1) it positively correlated with the area of contact made during the greeting, (2) it increased for greetings lasting longer than 3 seconds (handshakes and prolonged fist bumps), and (3) it was greater following handshakes with a strong grip as compared to those with a moderate-strength grip.

What’s the issue?

The potential spread of infection by physicians to their patients is an issue of concern. The transmission of health care–associated microorganisms by fomites in the hospital environment may contribute to this problem. Indeed, contaminated apparel of health care personnel may result in cross-transmission of bacteria.

A physician’s attire is influenced by culture and tradition. Many medical schools still conduct “white coat ceremonies” for their students to acknowledge the beginning of clinical training. However, physicians’ white coats may increase nosocomial infection transmission. It was shown that 91.3% of swabs taken from the cuffs and pocket mouths of white coats worn by physicians at an acute care hospital had bacterial contamination (World Health Popul. 2010;11:44-54).

Another potential vector for the transmission of infections by physicians is the necktie. Bacteria often colonize the neckties of health care workers; therefore, they can become a source of nosocomial infections in hospitalized individuals. Perhaps physicians, while providing patient care in a clinical setting, should not only hang up their white coats but also abandon their neckties in an effort to keep their patients safe.

Now, in addition to the physician’s attire, it has been shown that the physical interaction during the initial moments of the physician-patient encounter also may have the potential to transmit infectious organisms directly between 2 individuals. Indeed, an increased risk for infection transmission may be associated with the greeting type (particularly, the handshake), the greeting longevity (often >3 seconds), and the greeting contact force (eg, a strong grip). Therefore, following the salutation with patients, perhaps physicians should consider a fist bump instead of a handshake.

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

Suggested Readings

• Abuannadi M, O’Keefe JH, Brewer J. Neckties for physicians: yes? no? maybe? Mo Med. 2010;107:366-367.
• Bearman G, Bryant K, Leekha S, et al. Healthcare personnel attire in non-operating-room settings. Infect Control Hosp Epidemiol. 2014;35:107-121.
• Bi G, Wilson AB. Deadly ties and the rise of multi-drug resistant infections: a case for a new health care practitioner hygienic dress code. Independent Democratic Conference. https://www.yumpu.com/en/document/view/24854102/deadly-ties-and-the-rise-of-multi-drug-resistant-infections-a-case-. Published May 2011. Accessed March 12, 2015.

Do you greet your patients when you enter the examination room in your office or their room in the hospital? “Of course I do,” most physicians reply. And, do you shake hands? If your answer is yes, should you? Perhaps a fist bump would be a more hygienic alternative.

Mela and Whitworth (Am J Infect Control. 2014;42:916-917) demonstrated that “dap greetings” such as the high five and the fist bump dramatically reduced the transfer of bacteria during greeting exchange compared with the traditional handshake. Transmission of bacteria during the handshake was influenced not only by the large contact area but also the duration of the activity and the strength of the grip. Specifically, they observed the following about bacterial transfer: (1) it positively correlated with the area of contact made during the greeting, (2) it increased for greetings lasting longer than 3 seconds (handshakes and prolonged fist bumps), and (3) it was greater following handshakes with a strong grip as compared to those with a moderate-strength grip.

What’s the issue?

The potential spread of infection by physicians to their patients is an issue of concern. The transmission of health care–associated microorganisms by fomites in the hospital environment may contribute to this problem. Indeed, contaminated apparel of health care personnel may result in cross-transmission of bacteria.

A physician’s attire is influenced by culture and tradition. Many medical schools still conduct “white coat ceremonies” for their students to acknowledge the beginning of clinical training. However, physicians’ white coats may increase nosocomial infection transmission. It was shown that 91.3% of swabs taken from the cuffs and pocket mouths of white coats worn by physicians at an acute care hospital had bacterial contamination (World Health Popul. 2010;11:44-54).

Another potential vector for the transmission of infections by physicians is the necktie. Bacteria often colonize the neckties of health care workers; therefore, they can become a source of nosocomial infections in hospitalized individuals. Perhaps physicians, while providing patient care in a clinical setting, should not only hang up their white coats but also abandon their neckties in an effort to keep their patients safe.

Now, in addition to the physician’s attire, it has been shown that the physical interaction during the initial moments of the physician-patient encounter also may have the potential to transmit infectious organisms directly between 2 individuals. Indeed, an increased risk for infection transmission may be associated with the greeting type (particularly, the handshake), the greeting longevity (often >3 seconds), and the greeting contact force (eg, a strong grip). Therefore, following the salutation with patients, perhaps physicians should consider a fist bump instead of a handshake.

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

Suggested Readings

• Abuannadi M, O’Keefe JH, Brewer J. Neckties for physicians: yes? no? maybe? Mo Med. 2010;107:366-367.
• Bearman G, Bryant K, Leekha S, et al. Healthcare personnel attire in non-operating-room settings. Infect Control Hosp Epidemiol. 2014;35:107-121.
• Bi G, Wilson AB. Deadly ties and the rise of multi-drug resistant infections: a case for a new health care practitioner hygienic dress code. Independent Democratic Conference. https://www.yumpu.com/en/document/view/24854102/deadly-ties-and-the-rise-of-multi-drug-resistant-infections-a-case-. Published May 2011. Accessed March 12, 2015.

Do you greet your patients when you enter the examination room in your office or their room in the hospital? “Of course I do,” most physicians reply. And, do you shake hands? If your answer is yes, should you? Perhaps a fist bump would be a more hygienic alternative.

Mela and Whitworth (Am J Infect Control. 2014;42:916-917) demonstrated that “dap greetings” such as the high five and the fist bump dramatically reduced the transfer of bacteria during greeting exchange compared with the traditional handshake. Transmission of bacteria during the handshake was influenced not only by the large contact area but also the duration of the activity and the strength of the grip. Specifically, they observed the following about bacterial transfer: (1) it positively correlated with the area of contact made during the greeting, (2) it increased for greetings lasting longer than 3 seconds (handshakes and prolonged fist bumps), and (3) it was greater following handshakes with a strong grip as compared to those with a moderate-strength grip.

What’s the issue?

The potential spread of infection by physicians to their patients is an issue of concern. The transmission of health care–associated microorganisms by fomites in the hospital environment may contribute to this problem. Indeed, contaminated apparel of health care personnel may result in cross-transmission of bacteria.

A physician’s attire is influenced by culture and tradition. Many medical schools still conduct “white coat ceremonies” for their students to acknowledge the beginning of clinical training. However, physicians’ white coats may increase nosocomial infection transmission. It was shown that 91.3% of swabs taken from the cuffs and pocket mouths of white coats worn by physicians at an acute care hospital had bacterial contamination (World Health Popul. 2010;11:44-54).

Another potential vector for the transmission of infections by physicians is the necktie. Bacteria often colonize the neckties of health care workers; therefore, they can become a source of nosocomial infections in hospitalized individuals. Perhaps physicians, while providing patient care in a clinical setting, should not only hang up their white coats but also abandon their neckties in an effort to keep their patients safe.

Now, in addition to the physician’s attire, it has been shown that the physical interaction during the initial moments of the physician-patient encounter also may have the potential to transmit infectious organisms directly between 2 individuals. Indeed, an increased risk for infection transmission may be associated with the greeting type (particularly, the handshake), the greeting longevity (often >3 seconds), and the greeting contact force (eg, a strong grip). Therefore, following the salutation with patients, perhaps physicians should consider a fist bump instead of a handshake.

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

Suggested Readings

• Abuannadi M, O’Keefe JH, Brewer J. Neckties for physicians: yes? no? maybe? Mo Med. 2010;107:366-367.
• Bearman G, Bryant K, Leekha S, et al. Healthcare personnel attire in non-operating-room settings. Infect Control Hosp Epidemiol. 2014;35:107-121.
• Bi G, Wilson AB. Deadly ties and the rise of multi-drug resistant infections: a case for a new health care practitioner hygienic dress code. Independent Democratic Conference. https://www.yumpu.com/en/document/view/24854102/deadly-ties-and-the-rise-of-multi-drug-resistant-infections-a-case-. Published May 2011. Accessed March 12, 2015.