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It is well established that increased body mass index and weight gain are risk factors for psoriasis, and the prevalence of obesity in patients with psoriasis is higher than in the general population. However, there are limited data concerning the role of diet and exercise in psoriasis.

Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of dietary intervention in combination with physical exercise for weight loss on improving psoriasis in overweight or obese individuals. The investigators evaluated 303 overweight or obese patients with moderate to severe chronic plaque psoriasis who did not achieve clearance after 4 weeks of continuous systemic treatment. Patients were randomized to 2 regimens: a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss, or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. The main outcome was any reduction of the psoriasis area and severity index (PASI) from baseline to week 20.

Analysis of the intention-to-treat population showed a median reduction in the PASI score of 48% (95% confidence interval, 33.3%-58.3%) in the diet arm and 25.5% (95% confidence interval, 18.2%-33.3%) in the counseling arm (P=.02). The weight-loss target (a ≥5% reduction from baseline) was reached by 29.8% of patients in the diet arm compared to 14.5% in the counseling arm (P=.001).

The authors concluded that a 20-week dietetic intervention associated with increased physical exercise reduced psoriasis severity in systemically treated overweight or obese patients with active psoriasis.

What’s the issue?

As we would expect, a direct dietary intervention had a great impact on the study population. Will you try to adopt a structured dietary intervention in your patient population?

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

It is well established that increased body mass index and weight gain are risk factors for psoriasis, and the prevalence of obesity in patients with psoriasis is higher than in the general population. However, there are limited data concerning the role of diet and exercise in psoriasis.

Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of dietary intervention in combination with physical exercise for weight loss on improving psoriasis in overweight or obese individuals. The investigators evaluated 303 overweight or obese patients with moderate to severe chronic plaque psoriasis who did not achieve clearance after 4 weeks of continuous systemic treatment. Patients were randomized to 2 regimens: a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss, or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. The main outcome was any reduction of the psoriasis area and severity index (PASI) from baseline to week 20.

Analysis of the intention-to-treat population showed a median reduction in the PASI score of 48% (95% confidence interval, 33.3%-58.3%) in the diet arm and 25.5% (95% confidence interval, 18.2%-33.3%) in the counseling arm (P=.02). The weight-loss target (a ≥5% reduction from baseline) was reached by 29.8% of patients in the diet arm compared to 14.5% in the counseling arm (P=.001).

The authors concluded that a 20-week dietetic intervention associated with increased physical exercise reduced psoriasis severity in systemically treated overweight or obese patients with active psoriasis.

What’s the issue?

As we would expect, a direct dietary intervention had a great impact on the study population. Will you try to adopt a structured dietary intervention in your patient population?

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

It is well established that increased body mass index and weight gain are risk factors for psoriasis, and the prevalence of obesity in patients with psoriasis is higher than in the general population. However, there are limited data concerning the role of diet and exercise in psoriasis.

Naldi et al (Br J Dermatol. 2014;170:634-642) assessed the impact of dietary intervention in combination with physical exercise for weight loss on improving psoriasis in overweight or obese individuals. The investigators evaluated 303 overweight or obese patients with moderate to severe chronic plaque psoriasis who did not achieve clearance after 4 weeks of continuous systemic treatment. Patients were randomized to 2 regimens: a 20-week quantitative and qualitative dietary plan associated with physical exercise for weight loss, or simple informative counseling at baseline about the utility of weight loss for clinical control of psoriatic disease. The main outcome was any reduction of the psoriasis area and severity index (PASI) from baseline to week 20.

Analysis of the intention-to-treat population showed a median reduction in the PASI score of 48% (95% confidence interval, 33.3%-58.3%) in the diet arm and 25.5% (95% confidence interval, 18.2%-33.3%) in the counseling arm (P=.02). The weight-loss target (a ≥5% reduction from baseline) was reached by 29.8% of patients in the diet arm compared to 14.5% in the counseling arm (P=.001).

The authors concluded that a 20-week dietetic intervention associated with increased physical exercise reduced psoriasis severity in systemically treated overweight or obese patients with active psoriasis.

What’s the issue?

As we would expect, a direct dietary intervention had a great impact on the study population. Will you try to adopt a structured dietary intervention in your patient population?

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

With the annual meeting of the American Academy of Dermatology (AAD) set in the “mile-high city” now behind us, we must begin to convert didactic sessions into improved outcomes in our daily patient encounters. The enormous variety of lectures and frequently overlapping schedules can make this event a whirlwind for unseasoned attendees. I aim to enlighten those attending future meetings about individual sessions of particularly high value to the dermatologist in training. As a disclaimer, my primary interests are in medical dermatology, so the content of the courses I recommend is by no means comprehensive; however, residents need to have a solid fund of medical knowledge to function in any practice setting and, perhaps more importantly, to pass the boards examination!

I think the session that takes the cake for utility and value for residents is “High Yield ‘Power Hour’ for Residents,” which was led by a group of education-oriented Harvard University dermatologists. The power “hour” in fact lasted 2 hours, during which there was a variety of material presented covering pediatric dermatology, allergic dermatitis, infectious disease dermatology, blistering disorders, and pharmacology. The presenters showed incredible enthusiasm for their respective topics, and their passion also was evident in the high-yield handouts that they provided that were jam-packed with tables, bullet points, and frequently tested material. I would recommend that attendees save or print the handouts and avoid taking extensive notes on them during the session. Sit back, relax, and just soak in the lectures; later on, review the handouts. Also, be sure to arrive early—this session fills up fast—and fill out your evaluation! These lecturers deserve credit for their presentations and deserve a much larger room to accommodate residents that are otherwise willing to sit on the floor, crowd against the walls, and peek in through the doorway to listen.

I also feel residents benefit from lectures that provide us with practical information regarding complicated medical problems. I greatly enjoyed the symposium “Biologics: Perils and Promise” led by Canadian Dermatology Association President Richard Langley, MD. This conglomerate of experts addressed the risk for infection and malignancy with the use of biologics as well as pediatric use. The symposium also touched on the cardiovascular risk inherent in psoriasis and new developments suggesting that the treatment of psoriasis decreases overall systemic inflammation and possibly even cardiovascular risk. Another symposium in the same vein was “Systemic Therapies for Dermatologists: A Comprehensive Review and Update,” which was divided into short lectures discussing agents from acitretin to Zelboraf (vemurafenib). Expert insight on the use of these drugs was invaluable for those of us who train in programs where we are not frequently exposed to these agents.

For those residents interested in an overview of dermatopathology, “Dermatopathology Made Simple” led by Christine Ko, MD, was a lightning-fast tour through the subject. Dr. Ko categorized diagnoses based on pattern and also compared similar pathology side-by-side, focusing on key differences to help cinch the correct diagnosis. Although this talk was only 2 hours, it covered surprising breadth, as more than 170 different cases were presented. The handout accompanying this talk was excellent and served as a condensed review of all the material she covered.

Any resident attending an AAD meeting should first review the schedule carefully and then find topics that would be most beneficial during training and later on during practice. The recommendations I have made summarize material that will benefit all trainees in dermatology. Even those of us who will be continuing on to a fellowship need to have a handle on these topics to remain current and better communicate with colleagues. I look forward to seeing you all at future meetings!

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

With the annual meeting of the American Academy of Dermatology (AAD) set in the “mile-high city” now behind us, we must begin to convert didactic sessions into improved outcomes in our daily patient encounters. The enormous variety of lectures and frequently overlapping schedules can make this event a whirlwind for unseasoned attendees. I aim to enlighten those attending future meetings about individual sessions of particularly high value to the dermatologist in training. As a disclaimer, my primary interests are in medical dermatology, so the content of the courses I recommend is by no means comprehensive; however, residents need to have a solid fund of medical knowledge to function in any practice setting and, perhaps more importantly, to pass the boards examination!

I think the session that takes the cake for utility and value for residents is “High Yield ‘Power Hour’ for Residents,” which was led by a group of education-oriented Harvard University dermatologists. The power “hour” in fact lasted 2 hours, during which there was a variety of material presented covering pediatric dermatology, allergic dermatitis, infectious disease dermatology, blistering disorders, and pharmacology. The presenters showed incredible enthusiasm for their respective topics, and their passion also was evident in the high-yield handouts that they provided that were jam-packed with tables, bullet points, and frequently tested material. I would recommend that attendees save or print the handouts and avoid taking extensive notes on them during the session. Sit back, relax, and just soak in the lectures; later on, review the handouts. Also, be sure to arrive early—this session fills up fast—and fill out your evaluation! These lecturers deserve credit for their presentations and deserve a much larger room to accommodate residents that are otherwise willing to sit on the floor, crowd against the walls, and peek in through the doorway to listen.

I also feel residents benefit from lectures that provide us with practical information regarding complicated medical problems. I greatly enjoyed the symposium “Biologics: Perils and Promise” led by Canadian Dermatology Association President Richard Langley, MD. This conglomerate of experts addressed the risk for infection and malignancy with the use of biologics as well as pediatric use. The symposium also touched on the cardiovascular risk inherent in psoriasis and new developments suggesting that the treatment of psoriasis decreases overall systemic inflammation and possibly even cardiovascular risk. Another symposium in the same vein was “Systemic Therapies for Dermatologists: A Comprehensive Review and Update,” which was divided into short lectures discussing agents from acitretin to Zelboraf (vemurafenib). Expert insight on the use of these drugs was invaluable for those of us who train in programs where we are not frequently exposed to these agents.

For those residents interested in an overview of dermatopathology, “Dermatopathology Made Simple” led by Christine Ko, MD, was a lightning-fast tour through the subject. Dr. Ko categorized diagnoses based on pattern and also compared similar pathology side-by-side, focusing on key differences to help cinch the correct diagnosis. Although this talk was only 2 hours, it covered surprising breadth, as more than 170 different cases were presented. The handout accompanying this talk was excellent and served as a condensed review of all the material she covered.

Any resident attending an AAD meeting should first review the schedule carefully and then find topics that would be most beneficial during training and later on during practice. The recommendations I have made summarize material that will benefit all trainees in dermatology. Even those of us who will be continuing on to a fellowship need to have a handle on these topics to remain current and better communicate with colleagues. I look forward to seeing you all at future meetings!

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

With the annual meeting of the American Academy of Dermatology (AAD) set in the “mile-high city” now behind us, we must begin to convert didactic sessions into improved outcomes in our daily patient encounters. The enormous variety of lectures and frequently overlapping schedules can make this event a whirlwind for unseasoned attendees. I aim to enlighten those attending future meetings about individual sessions of particularly high value to the dermatologist in training. As a disclaimer, my primary interests are in medical dermatology, so the content of the courses I recommend is by no means comprehensive; however, residents need to have a solid fund of medical knowledge to function in any practice setting and, perhaps more importantly, to pass the boards examination!

I think the session that takes the cake for utility and value for residents is “High Yield ‘Power Hour’ for Residents,” which was led by a group of education-oriented Harvard University dermatologists. The power “hour” in fact lasted 2 hours, during which there was a variety of material presented covering pediatric dermatology, allergic dermatitis, infectious disease dermatology, blistering disorders, and pharmacology. The presenters showed incredible enthusiasm for their respective topics, and their passion also was evident in the high-yield handouts that they provided that were jam-packed with tables, bullet points, and frequently tested material. I would recommend that attendees save or print the handouts and avoid taking extensive notes on them during the session. Sit back, relax, and just soak in the lectures; later on, review the handouts. Also, be sure to arrive early—this session fills up fast—and fill out your evaluation! These lecturers deserve credit for their presentations and deserve a much larger room to accommodate residents that are otherwise willing to sit on the floor, crowd against the walls, and peek in through the doorway to listen.

I also feel residents benefit from lectures that provide us with practical information regarding complicated medical problems. I greatly enjoyed the symposium “Biologics: Perils and Promise” led by Canadian Dermatology Association President Richard Langley, MD. This conglomerate of experts addressed the risk for infection and malignancy with the use of biologics as well as pediatric use. The symposium also touched on the cardiovascular risk inherent in psoriasis and new developments suggesting that the treatment of psoriasis decreases overall systemic inflammation and possibly even cardiovascular risk. Another symposium in the same vein was “Systemic Therapies for Dermatologists: A Comprehensive Review and Update,” which was divided into short lectures discussing agents from acitretin to Zelboraf (vemurafenib). Expert insight on the use of these drugs was invaluable for those of us who train in programs where we are not frequently exposed to these agents.

For those residents interested in an overview of dermatopathology, “Dermatopathology Made Simple” led by Christine Ko, MD, was a lightning-fast tour through the subject. Dr. Ko categorized diagnoses based on pattern and also compared similar pathology side-by-side, focusing on key differences to help cinch the correct diagnosis. Although this talk was only 2 hours, it covered surprising breadth, as more than 170 different cases were presented. The handout accompanying this talk was excellent and served as a condensed review of all the material she covered.

Any resident attending an AAD meeting should first review the schedule carefully and then find topics that would be most beneficial during training and later on during practice. The recommendations I have made summarize material that will benefit all trainees in dermatology. Even those of us who will be continuing on to a fellowship need to have a handle on these topics to remain current and better communicate with colleagues. I look forward to seeing you all at future meetings!

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

As one of the most common skin diseases, acne research, clinical guidelines, and therapeutic innovation are always a hot topic at the Annual Meeting of the American Academy of Dermatology (March 21-25, 2014). A new dimension in the chicken and egg, or rather microcomedone and inflammation, story of acne pathogenesis emerged in a recent Journal of Investigative Dermatology (2014;134:381-388) article, which demonstrated that Propionibacterium acnes triggers a key inflammatory mediator, IL-1β, via the inflammasome (a compilation of inflammatory proteins such as caspases and NOD-like receptors) activation, suggesting a role for inflammasome-mediated inflammation in acne pathogenesis in addition to and independent of toll-like receptor activation. A potential therapeutic target, perhaps?

Drs. Ted Rosen and Joshua Zeichner in 2 independent sessions (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics [Rosen] and Acne Treatment Controversies [Zeichner]) discussed the importance of purposeful utilization of oral antibiotics—less is more—to prevent the continued emergence of antimicrobial resistance. Dr. Rosen commented that doxycycline at doses ≥50 mg daily provides serum levels that have an impact on commensal or colonized organisms, while lower doses provide only the anti-inflammatory effects without any bacteriostatic impact. This finding highlights the importance of low-dose controlled-release formulations. Dr. Zeichner also stressed the importance of knowing when to quit; if a patient does not improve in 6 to 8 weeks of therapy, move on. He also commented on the importance of multimechanistic therapy (solo is a no-go), utilizing benzoyl peroxide–containing products and most importantly retinoids from day 1. Dr. Zeichner also stressed the importance of recognizing acne mimics, such as gram-negative folliculitis, and made it clear that hormonally driven acne must not be missed, especially in the adult female population.

Lastly, new directions in acne are emerging, utilizing the science of nanotechnology (nano is equivalent to 1 billionth of a part). Drug delivery with nanomaterials is being fervently pursued across the globe in the field of acne. Nanoparticles can allow for sustained and controlled release of established products, increasing efficacy and stability, compliance due to decreased dosing, and safety by limiting associated irritation and dryness. In a session on nanotechnology, Dr. Rox Anderson presented his work utilizing gold nanoparticles to selectively destroy sebaceous glands via selective photothermolysis. He commented, “Do we really need our sebaceous glands,” citing that babies and infants do just fine without their activity. This work is currently in clinical trials in Europe. Nanotechnology also can be used to deliver previously undeliverable actives, such as the gaseous molecule nitric oxide. It was shown that a nitric oxide–releasing nanoparticle technology effectively penetrated the pilosebaceous unit, killed P acnes in culture, and inhibited inflammatory cytokine production by keratinocytes exposed to P acnes.

Stay tuned for more innovation coming soon!

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

As one of the most common skin diseases, acne research, clinical guidelines, and therapeutic innovation are always a hot topic at the Annual Meeting of the American Academy of Dermatology (March 21-25, 2014). A new dimension in the chicken and egg, or rather microcomedone and inflammation, story of acne pathogenesis emerged in a recent Journal of Investigative Dermatology (2014;134:381-388) article, which demonstrated that Propionibacterium acnes triggers a key inflammatory mediator, IL-1β, via the inflammasome (a compilation of inflammatory proteins such as caspases and NOD-like receptors) activation, suggesting a role for inflammasome-mediated inflammation in acne pathogenesis in addition to and independent of toll-like receptor activation. A potential therapeutic target, perhaps?

Drs. Ted Rosen and Joshua Zeichner in 2 independent sessions (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics [Rosen] and Acne Treatment Controversies [Zeichner]) discussed the importance of purposeful utilization of oral antibiotics—less is more—to prevent the continued emergence of antimicrobial resistance. Dr. Rosen commented that doxycycline at doses ≥50 mg daily provides serum levels that have an impact on commensal or colonized organisms, while lower doses provide only the anti-inflammatory effects without any bacteriostatic impact. This finding highlights the importance of low-dose controlled-release formulations. Dr. Zeichner also stressed the importance of knowing when to quit; if a patient does not improve in 6 to 8 weeks of therapy, move on. He also commented on the importance of multimechanistic therapy (solo is a no-go), utilizing benzoyl peroxide–containing products and most importantly retinoids from day 1. Dr. Zeichner also stressed the importance of recognizing acne mimics, such as gram-negative folliculitis, and made it clear that hormonally driven acne must not be missed, especially in the adult female population.

Lastly, new directions in acne are emerging, utilizing the science of nanotechnology (nano is equivalent to 1 billionth of a part). Drug delivery with nanomaterials is being fervently pursued across the globe in the field of acne. Nanoparticles can allow for sustained and controlled release of established products, increasing efficacy and stability, compliance due to decreased dosing, and safety by limiting associated irritation and dryness. In a session on nanotechnology, Dr. Rox Anderson presented his work utilizing gold nanoparticles to selectively destroy sebaceous glands via selective photothermolysis. He commented, “Do we really need our sebaceous glands,” citing that babies and infants do just fine without their activity. This work is currently in clinical trials in Europe. Nanotechnology also can be used to deliver previously undeliverable actives, such as the gaseous molecule nitric oxide. It was shown that a nitric oxide–releasing nanoparticle technology effectively penetrated the pilosebaceous unit, killed P acnes in culture, and inhibited inflammatory cytokine production by keratinocytes exposed to P acnes.

Stay tuned for more innovation coming soon!

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

As one of the most common skin diseases, acne research, clinical guidelines, and therapeutic innovation are always a hot topic at the Annual Meeting of the American Academy of Dermatology (March 21-25, 2014). A new dimension in the chicken and egg, or rather microcomedone and inflammation, story of acne pathogenesis emerged in a recent Journal of Investigative Dermatology (2014;134:381-388) article, which demonstrated that Propionibacterium acnes triggers a key inflammatory mediator, IL-1β, via the inflammasome (a compilation of inflammatory proteins such as caspases and NOD-like receptors) activation, suggesting a role for inflammasome-mediated inflammation in acne pathogenesis in addition to and independent of toll-like receptor activation. A potential therapeutic target, perhaps?

Drs. Ted Rosen and Joshua Zeichner in 2 independent sessions (Treating Tumors and Inflammatory Skin Diseases With Immunomodulators and Biologics [Rosen] and Acne Treatment Controversies [Zeichner]) discussed the importance of purposeful utilization of oral antibiotics—less is more—to prevent the continued emergence of antimicrobial resistance. Dr. Rosen commented that doxycycline at doses ≥50 mg daily provides serum levels that have an impact on commensal or colonized organisms, while lower doses provide only the anti-inflammatory effects without any bacteriostatic impact. This finding highlights the importance of low-dose controlled-release formulations. Dr. Zeichner also stressed the importance of knowing when to quit; if a patient does not improve in 6 to 8 weeks of therapy, move on. He also commented on the importance of multimechanistic therapy (solo is a no-go), utilizing benzoyl peroxide–containing products and most importantly retinoids from day 1. Dr. Zeichner also stressed the importance of recognizing acne mimics, such as gram-negative folliculitis, and made it clear that hormonally driven acne must not be missed, especially in the adult female population.

Lastly, new directions in acne are emerging, utilizing the science of nanotechnology (nano is equivalent to 1 billionth of a part). Drug delivery with nanomaterials is being fervently pursued across the globe in the field of acne. Nanoparticles can allow for sustained and controlled release of established products, increasing efficacy and stability, compliance due to decreased dosing, and safety by limiting associated irritation and dryness. In a session on nanotechnology, Dr. Rox Anderson presented his work utilizing gold nanoparticles to selectively destroy sebaceous glands via selective photothermolysis. He commented, “Do we really need our sebaceous glands,” citing that babies and infants do just fine without their activity. This work is currently in clinical trials in Europe. Nanotechnology also can be used to deliver previously undeliverable actives, such as the gaseous molecule nitric oxide. It was shown that a nitric oxide–releasing nanoparticle technology effectively penetrated the pilosebaceous unit, killed P acnes in culture, and inhibited inflammatory cytokine production by keratinocytes exposed to P acnes.

Stay tuned for more innovation coming soon!

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

Prostate tumorigenesis is related to sex hormones, particularly androgens. It also has been suggested that melanoma may be androgen dependent. Postulated mechanisms of pathogenesis include androgen level imbalance (for which early evidence may present as severe teenaged acne), chromosome telomere length alteration (for which increased risk for melanoma is associated with long telomeres), and host immune response modification.

In a December 2013 article published in the Journal of Clinical Oncology, Li et al (2013;31:4394-4399) confirmed that a personal history of prostate cancer was associated with an increased risk for subsequent melanoma. Among patients with prostate cancer whose median age at diagnosis was 68 years or younger, a higher hazard ratio of melanoma was noted. Also, similar to prostate cancer, they observed a positive association between melanoma risk and severe teenaged acne defined by the use of tetracycline for 4 or more years.

What’s the issue?

Are there clinical implications to the confirmation that there is an increased risk for patients with prostate cancer to subsequently develop melanoma? Specifically, should there be increased surveillance for melanoma in these individuals? Perhaps it would be reasonable to regularly perform a complete skin examination in all patients with a history of prostate cancer, especially men who had prostate cancer diagnosed before 68 years of age.

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

Prostate tumorigenesis is related to sex hormones, particularly androgens. It also has been suggested that melanoma may be androgen dependent. Postulated mechanisms of pathogenesis include androgen level imbalance (for which early evidence may present as severe teenaged acne), chromosome telomere length alteration (for which increased risk for melanoma is associated with long telomeres), and host immune response modification.

In a December 2013 article published in the Journal of Clinical Oncology, Li et al (2013;31:4394-4399) confirmed that a personal history of prostate cancer was associated with an increased risk for subsequent melanoma. Among patients with prostate cancer whose median age at diagnosis was 68 years or younger, a higher hazard ratio of melanoma was noted. Also, similar to prostate cancer, they observed a positive association between melanoma risk and severe teenaged acne defined by the use of tetracycline for 4 or more years.

What’s the issue?

Are there clinical implications to the confirmation that there is an increased risk for patients with prostate cancer to subsequently develop melanoma? Specifically, should there be increased surveillance for melanoma in these individuals? Perhaps it would be reasonable to regularly perform a complete skin examination in all patients with a history of prostate cancer, especially men who had prostate cancer diagnosed before 68 years of age.

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

Prostate tumorigenesis is related to sex hormones, particularly androgens. It also has been suggested that melanoma may be androgen dependent. Postulated mechanisms of pathogenesis include androgen level imbalance (for which early evidence may present as severe teenaged acne), chromosome telomere length alteration (for which increased risk for melanoma is associated with long telomeres), and host immune response modification.

In a December 2013 article published in the Journal of Clinical Oncology, Li et al (2013;31:4394-4399) confirmed that a personal history of prostate cancer was associated with an increased risk for subsequent melanoma. Among patients with prostate cancer whose median age at diagnosis was 68 years or younger, a higher hazard ratio of melanoma was noted. Also, similar to prostate cancer, they observed a positive association between melanoma risk and severe teenaged acne defined by the use of tetracycline for 4 or more years.

What’s the issue?

Are there clinical implications to the confirmation that there is an increased risk for patients with prostate cancer to subsequently develop melanoma? Specifically, should there be increased surveillance for melanoma in these individuals? Perhaps it would be reasonable to regularly perform a complete skin examination in all patients with a history of prostate cancer, especially men who had prostate cancer diagnosed before 68 years of age.

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

A recent study in the Journal of Drugs in Dermatology (2014;13:56-61) featured long-term data regarding use of brimonidine gel, which was approved by the US Food and Drug Administration last year as the only topical agent on the market to treat erythema associated with rosacea. Compared to the initial safety and efficacy in phase 2 and 3 trials with 4-week use, this study spanned 12 months and assessed the erythema and adverse events associated with the drug. The decrease in erythema with once-daily application was observed after first use and was durable until the end of the study with no tachyphylaxis. The side-effect profile was mild and included flushing and irritancy events that typically improved over time.

What’s the issue?

The manufacturers of this new product tout that “Red is Wrong” (http://www.rediswrong.com). Although this strong statement virtually forces people to sprint to the Web site to see how they could improve their facial erythema and my patients have reported quite favorably on its efficacy and tolerability, obtaining the medication has been problematic. Similar to many of the coupon cards and assistance provided by pharmaceutical companies, the true segment of the population for which they serve is more limited than it appears, as health insurance plans with prescription deductibles, Medicare, Medicaid (and any spin-offs of the sort in the last few months involving US health care cost-management gymnastics) typically are excluded from discounts, and the out-of-pocket cost can be well over $200 per month. In an era when we have heroically developed a new and effective drug for a common and problematic indication, how will we practically provide it to the masses?

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

A recent study in the Journal of Drugs in Dermatology (2014;13:56-61) featured long-term data regarding use of brimonidine gel, which was approved by the US Food and Drug Administration last year as the only topical agent on the market to treat erythema associated with rosacea. Compared to the initial safety and efficacy in phase 2 and 3 trials with 4-week use, this study spanned 12 months and assessed the erythema and adverse events associated with the drug. The decrease in erythema with once-daily application was observed after first use and was durable until the end of the study with no tachyphylaxis. The side-effect profile was mild and included flushing and irritancy events that typically improved over time.

What’s the issue?

The manufacturers of this new product tout that “Red is Wrong” (http://www.rediswrong.com). Although this strong statement virtually forces people to sprint to the Web site to see how they could improve their facial erythema and my patients have reported quite favorably on its efficacy and tolerability, obtaining the medication has been problematic. Similar to many of the coupon cards and assistance provided by pharmaceutical companies, the true segment of the population for which they serve is more limited than it appears, as health insurance plans with prescription deductibles, Medicare, Medicaid (and any spin-offs of the sort in the last few months involving US health care cost-management gymnastics) typically are excluded from discounts, and the out-of-pocket cost can be well over $200 per month. In an era when we have heroically developed a new and effective drug for a common and problematic indication, how will we practically provide it to the masses?

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

A recent study in the Journal of Drugs in Dermatology (2014;13:56-61) featured long-term data regarding use of brimonidine gel, which was approved by the US Food and Drug Administration last year as the only topical agent on the market to treat erythema associated with rosacea. Compared to the initial safety and efficacy in phase 2 and 3 trials with 4-week use, this study spanned 12 months and assessed the erythema and adverse events associated with the drug. The decrease in erythema with once-daily application was observed after first use and was durable until the end of the study with no tachyphylaxis. The side-effect profile was mild and included flushing and irritancy events that typically improved over time.

What’s the issue?

The manufacturers of this new product tout that “Red is Wrong” (http://www.rediswrong.com). Although this strong statement virtually forces people to sprint to the Web site to see how they could improve their facial erythema and my patients have reported quite favorably on its efficacy and tolerability, obtaining the medication has been problematic. Similar to many of the coupon cards and assistance provided by pharmaceutical companies, the true segment of the population for which they serve is more limited than it appears, as health insurance plans with prescription deductibles, Medicare, Medicaid (and any spin-offs of the sort in the last few months involving US health care cost-management gymnastics) typically are excluded from discounts, and the out-of-pocket cost can be well over $200 per month. In an era when we have heroically developed a new and effective drug for a common and problematic indication, how will we practically provide it to the masses?

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

In an article published online on February 27, 2014, in JAMA Facial Plastic Surgery, Jiang et al reported on a potentially fatal complication during the use of autologous fat transfer for facial augmentation. They described 3 patients with a nonthrombotic pulmonary embolism during autologous fat injection to the temple area. Two of 3 patients were under local anesthesia and 1 patient was under general anesthesia. The 2 patients under local anesthesia complained of sudden diaphoresis, dyspnea, and tachypnea. The other patient who was under general anesthesia had sudden cardiac and respiratory arrest and subsequently died. Autopsy confirmed a pulmonary embolism. The authors identified the middle temporal vein (MTV) as the culprit vessel that was cannulized. In this report, 10 cadaveric dissections were done to identify and characterize the MTV.

What’s the issue?

Facial augmentation with autologous fat as well as other filler materials has become increasingly popular. Therefore, knowledge of anatomy and vasculature are of utmost importance to help mitigate potential complications. The anatomic levels of the temporal region from superficial to deep include the epidermis, dermis, subcutaneous adipose, superficial musculoaponeurotic system, superficial temporal fascia, superficial layer of the deep temporal fascia, superficial temporal fat-pad, deep layer of the deep temporal fascia, and temporalis muscle. The MTV arises from 2 to 4 tributaries at the area of the lateral orbital angle. It is lifted by the superficial temporal fat-pad, and because it lies between the superficial and deep layers of the deep temporal fascia, the vein walls are kept patent and do not collapse during injection. The sentinel vein is one of the MTV’s tributaries and has the same characteristics. It lies lateral to the lateral orbital rim and perforates through the superficial layer of the deep temporal fascia. Another reason why the MTV is a risk factor for cannulization is its large caliber. The stem can be as wide as 3.15 +/- 0.13 mm. This study found a mean (standard deviation) of 2.06 (0.17) mm from the point of origin and 3.02 (0.23) mm at the palpebral fissure plane. The authors made the recommendation to use blunt-tipped needles during fat augmentation in this area as well as multiple injection sites with slow injection. This technique also can be applied to filling with other materials. Pulling back on the syringe before injection also can help as well as injecting small amounts in a steady retrograde fashion. Before your next filler patient, is it time for an anatomy review?

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

In an article published online on February 27, 2014, in JAMA Facial Plastic Surgery, Jiang et al reported on a potentially fatal complication during the use of autologous fat transfer for facial augmentation. They described 3 patients with a nonthrombotic pulmonary embolism during autologous fat injection to the temple area. Two of 3 patients were under local anesthesia and 1 patient was under general anesthesia. The 2 patients under local anesthesia complained of sudden diaphoresis, dyspnea, and tachypnea. The other patient who was under general anesthesia had sudden cardiac and respiratory arrest and subsequently died. Autopsy confirmed a pulmonary embolism. The authors identified the middle temporal vein (MTV) as the culprit vessel that was cannulized. In this report, 10 cadaveric dissections were done to identify and characterize the MTV.

What’s the issue?

Facial augmentation with autologous fat as well as other filler materials has become increasingly popular. Therefore, knowledge of anatomy and vasculature are of utmost importance to help mitigate potential complications. The anatomic levels of the temporal region from superficial to deep include the epidermis, dermis, subcutaneous adipose, superficial musculoaponeurotic system, superficial temporal fascia, superficial layer of the deep temporal fascia, superficial temporal fat-pad, deep layer of the deep temporal fascia, and temporalis muscle. The MTV arises from 2 to 4 tributaries at the area of the lateral orbital angle. It is lifted by the superficial temporal fat-pad, and because it lies between the superficial and deep layers of the deep temporal fascia, the vein walls are kept patent and do not collapse during injection. The sentinel vein is one of the MTV’s tributaries and has the same characteristics. It lies lateral to the lateral orbital rim and perforates through the superficial layer of the deep temporal fascia. Another reason why the MTV is a risk factor for cannulization is its large caliber. The stem can be as wide as 3.15 +/- 0.13 mm. This study found a mean (standard deviation) of 2.06 (0.17) mm from the point of origin and 3.02 (0.23) mm at the palpebral fissure plane. The authors made the recommendation to use blunt-tipped needles during fat augmentation in this area as well as multiple injection sites with slow injection. This technique also can be applied to filling with other materials. Pulling back on the syringe before injection also can help as well as injecting small amounts in a steady retrograde fashion. Before your next filler patient, is it time for an anatomy review?

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

In an article published online on February 27, 2014, in JAMA Facial Plastic Surgery, Jiang et al reported on a potentially fatal complication during the use of autologous fat transfer for facial augmentation. They described 3 patients with a nonthrombotic pulmonary embolism during autologous fat injection to the temple area. Two of 3 patients were under local anesthesia and 1 patient was under general anesthesia. The 2 patients under local anesthesia complained of sudden diaphoresis, dyspnea, and tachypnea. The other patient who was under general anesthesia had sudden cardiac and respiratory arrest and subsequently died. Autopsy confirmed a pulmonary embolism. The authors identified the middle temporal vein (MTV) as the culprit vessel that was cannulized. In this report, 10 cadaveric dissections were done to identify and characterize the MTV.

What’s the issue?

Facial augmentation with autologous fat as well as other filler materials has become increasingly popular. Therefore, knowledge of anatomy and vasculature are of utmost importance to help mitigate potential complications. The anatomic levels of the temporal region from superficial to deep include the epidermis, dermis, subcutaneous adipose, superficial musculoaponeurotic system, superficial temporal fascia, superficial layer of the deep temporal fascia, superficial temporal fat-pad, deep layer of the deep temporal fascia, and temporalis muscle. The MTV arises from 2 to 4 tributaries at the area of the lateral orbital angle. It is lifted by the superficial temporal fat-pad, and because it lies between the superficial and deep layers of the deep temporal fascia, the vein walls are kept patent and do not collapse during injection. The sentinel vein is one of the MTV’s tributaries and has the same characteristics. It lies lateral to the lateral orbital rim and perforates through the superficial layer of the deep temporal fascia. Another reason why the MTV is a risk factor for cannulization is its large caliber. The stem can be as wide as 3.15 +/- 0.13 mm. This study found a mean (standard deviation) of 2.06 (0.17) mm from the point of origin and 3.02 (0.23) mm at the palpebral fissure plane. The authors made the recommendation to use blunt-tipped needles during fat augmentation in this area as well as multiple injection sites with slow injection. This technique also can be applied to filling with other materials. Pulling back on the syringe before injection also can help as well as injecting small amounts in a steady retrograde fashion. Before your next filler patient, is it time for an anatomy review?

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

There is a growing amount of literature demonstrating that psoriasis is a chronic and debilitating inflammatory disease associated with serious comorbidities. Emerging comorbidities of psoriasis include cardiovascular disease and metabolic syndrome. Psoriasis patients have an increased prevalence of the core components of metabolic syndrome, including obesity, dyslipidemia, and insulin resistance.

According to van der Voort et al (J Am Acad Dermatol. 2014;70:517-524), prior case-controlled studies observed an increased prevalence of nonalcoholic fatty liver disease (NAFLD) in patients with psoriasis, which they noted as a relevant factor in selecting optimal psoriasis treatment. Their study sought to compare the prevalence of NAFLD in participants with psoriasis and those without psoriasis. They conducted a large prospective population-based cohort study that enrolled elderly participants (>55 years). Nonalcoholic fatty liver disease was diagnosed as fatty liver on ultrasonography in the absence of other liver diseases. A multivariable logistic regression model was used to assess if psoriasis was associated with NAFLD after adjusting for demographic and lifestyle characteristics as well as laboratory findings.

In total, 2292 participants were included in the study; 118 (5.1%) participants had psoriasis. The prevalence of NAFLD was 46.2% in participants with psoriasis compared to 33.3% in those without psoriasis (P=.005); psoriasis was significantly associated with NAFLD. After the authors adjusted for alcohol consumption, pack-years and smoking status, presence of metabolic syndrome, and alanine aminotransferase levels, psoriasis remained a significant predictor of NAFLD (adjusted odds ratio, 1.7; 95% confidence interval, 1.1-2.6). The authors concluded that elderly participants with psoriasis were 70% more likely to have NAFLD than those without psoriasis independent of common NAFLD risk factors.

What’s the issue?

This study gives us a new comorbidity to be aware of and monitor. In considering therapy in this population, it also is important to consider the risk for NAFLD when selecting treatments that may have hepatic toxicity or are metabolized by the liver. How will this study change your approach to patients with psoriasis?

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

There is a growing amount of literature demonstrating that psoriasis is a chronic and debilitating inflammatory disease associated with serious comorbidities. Emerging comorbidities of psoriasis include cardiovascular disease and metabolic syndrome. Psoriasis patients have an increased prevalence of the core components of metabolic syndrome, including obesity, dyslipidemia, and insulin resistance.

According to van der Voort et al (J Am Acad Dermatol. 2014;70:517-524), prior case-controlled studies observed an increased prevalence of nonalcoholic fatty liver disease (NAFLD) in patients with psoriasis, which they noted as a relevant factor in selecting optimal psoriasis treatment. Their study sought to compare the prevalence of NAFLD in participants with psoriasis and those without psoriasis. They conducted a large prospective population-based cohort study that enrolled elderly participants (>55 years). Nonalcoholic fatty liver disease was diagnosed as fatty liver on ultrasonography in the absence of other liver diseases. A multivariable logistic regression model was used to assess if psoriasis was associated with NAFLD after adjusting for demographic and lifestyle characteristics as well as laboratory findings.

In total, 2292 participants were included in the study; 118 (5.1%) participants had psoriasis. The prevalence of NAFLD was 46.2% in participants with psoriasis compared to 33.3% in those without psoriasis (P=.005); psoriasis was significantly associated with NAFLD. After the authors adjusted for alcohol consumption, pack-years and smoking status, presence of metabolic syndrome, and alanine aminotransferase levels, psoriasis remained a significant predictor of NAFLD (adjusted odds ratio, 1.7; 95% confidence interval, 1.1-2.6). The authors concluded that elderly participants with psoriasis were 70% more likely to have NAFLD than those without psoriasis independent of common NAFLD risk factors.

What’s the issue?

This study gives us a new comorbidity to be aware of and monitor. In considering therapy in this population, it also is important to consider the risk for NAFLD when selecting treatments that may have hepatic toxicity or are metabolized by the liver. How will this study change your approach to patients with psoriasis?

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

There is a growing amount of literature demonstrating that psoriasis is a chronic and debilitating inflammatory disease associated with serious comorbidities. Emerging comorbidities of psoriasis include cardiovascular disease and metabolic syndrome. Psoriasis patients have an increased prevalence of the core components of metabolic syndrome, including obesity, dyslipidemia, and insulin resistance.

According to van der Voort et al (J Am Acad Dermatol. 2014;70:517-524), prior case-controlled studies observed an increased prevalence of nonalcoholic fatty liver disease (NAFLD) in patients with psoriasis, which they noted as a relevant factor in selecting optimal psoriasis treatment. Their study sought to compare the prevalence of NAFLD in participants with psoriasis and those without psoriasis. They conducted a large prospective population-based cohort study that enrolled elderly participants (>55 years). Nonalcoholic fatty liver disease was diagnosed as fatty liver on ultrasonography in the absence of other liver diseases. A multivariable logistic regression model was used to assess if psoriasis was associated with NAFLD after adjusting for demographic and lifestyle characteristics as well as laboratory findings.

In total, 2292 participants were included in the study; 118 (5.1%) participants had psoriasis. The prevalence of NAFLD was 46.2% in participants with psoriasis compared to 33.3% in those without psoriasis (P=.005); psoriasis was significantly associated with NAFLD. After the authors adjusted for alcohol consumption, pack-years and smoking status, presence of metabolic syndrome, and alanine aminotransferase levels, psoriasis remained a significant predictor of NAFLD (adjusted odds ratio, 1.7; 95% confidence interval, 1.1-2.6). The authors concluded that elderly participants with psoriasis were 70% more likely to have NAFLD than those without psoriasis independent of common NAFLD risk factors.

What’s the issue?

This study gives us a new comorbidity to be aware of and monitor. In considering therapy in this population, it also is important to consider the risk for NAFLD when selecting treatments that may have hepatic toxicity or are metabolized by the liver. How will this study change your approach to patients with psoriasis?

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

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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