Blog

At the Society for General Microbiology Annual Conference (March 30–April 2, 2015), Harrison et al presented a paper describing their experience with a 1000-year-old antimicrobial remedy with antistaphylococcal activity (S19We1006). The unique team of investigators—consisting of an expert in Viking studies and 3 microbiologists from the University of Nottingham, England, and another microbiologist who performs mouse model studies from Texas Tech University (Lubbock, Texas)—pooled their talents to reconstruct and test an ancient recipe for treating eyelash follicle infection. The potion not only killed methicillin-resistant Staphylococcus aureus (MRSA) grown in established biofilms but also performed as good, if not better, than the conventional antibiotics on MRSA-infected skin wounds in mice.

“Take cropleek and garlic, of both equal quantities, pound them well together . . . take wine and bullocks gall, mix with the leek . . . let it stand 9 days in the brass vessel” is an excerpt of the recipe for treatment of a sty from the 9th century Anglo-Saxon text Bald’s Leechbook (translated from Old English). The modern day chefs cooked their potion using: (1) 2 Allium species (equal amounts of garlic and either leek or onion, finely chopped and crushed in a mortar for 2 minutes), (2) wine (add 25 mL [0.87 fl oz] of an organic vintage from a historic English vineyard near Glastonbury), (3) bullock gall (dissolve bile from a cow’s stomach in distilled water), and (4) brass (glass bottles with squares of brass sheets immersed in the mixture were used because a brass vessel would be not only hard to sterilize but also expensive). After brewing (in the “brass vessel”), the solution was purified by straining it and left to chill at 4^oC for 9 days before the mixture was used.

What’s the issue?

Advances in technology provide the opportunity to create new medical treatments. However, efficacious therapies may remain hidden in ancient texts, waiting to be discovered. Historic Chinese literature has been the source for modern day drugs such as artemisinin for Plasmodium falciparum malaria. The ancient recipe in Bald’s Leechbook may be the next major advance in the topical management of MRSA. I anticipate, in the future, that physicians may be prescribing “Bald’s potion” to treat impetigo. What do you think?

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

Suggested Readings

• AncientBiotics—a medieval remedy for modern day superbugs [news release]? United Kingdom: The University of Nottingham; March 30, 2015. http://www.nottingham.ac.uk/news/pressreleases/2015/march/ancientbiotics---a-medieval-remedy-for-modern-day-superbugs.aspx. Accessed August 12, 2015.
• Feilden T. 1,000-year-old onion and garlic eye remedy kills MRSA. BBC News. March 30, 2015. http://www.bbc.com/news/uk-england-nottinghamshire-32117815. Accessed August 12, 2015.
• Wilson C. Anglo-Saxon remedy kills hospital superbug MRSA. New Scientist. March 30, 2015. http://www.newscientist.com/article/dn27263-anglosaxon-remedy-kills-hospital-superbug-mrsa.html#.VTPpsqazDzl. Accessed August 12, 2015.

At the Society for General Microbiology Annual Conference (March 30–April 2, 2015), Harrison et al presented a paper describing their experience with a 1000-year-old antimicrobial remedy with antistaphylococcal activity (S19We1006). The unique team of investigators—consisting of an expert in Viking studies and 3 microbiologists from the University of Nottingham, England, and another microbiologist who performs mouse model studies from Texas Tech University (Lubbock, Texas)—pooled their talents to reconstruct and test an ancient recipe for treating eyelash follicle infection. The potion not only killed methicillin-resistant Staphylococcus aureus (MRSA) grown in established biofilms but also performed as good, if not better, than the conventional antibiotics on MRSA-infected skin wounds in mice.

“Take cropleek and garlic, of both equal quantities, pound them well together . . . take wine and bullocks gall, mix with the leek . . . let it stand 9 days in the brass vessel” is an excerpt of the recipe for treatment of a sty from the 9th century Anglo-Saxon text Bald’s Leechbook (translated from Old English). The modern day chefs cooked their potion using: (1) 2 Allium species (equal amounts of garlic and either leek or onion, finely chopped and crushed in a mortar for 2 minutes), (2) wine (add 25 mL [0.87 fl oz] of an organic vintage from a historic English vineyard near Glastonbury), (3) bullock gall (dissolve bile from a cow’s stomach in distilled water), and (4) brass (glass bottles with squares of brass sheets immersed in the mixture were used because a brass vessel would be not only hard to sterilize but also expensive). After brewing (in the “brass vessel”), the solution was purified by straining it and left to chill at 4^oC for 9 days before the mixture was used.

What’s the issue?

Advances in technology provide the opportunity to create new medical treatments. However, efficacious therapies may remain hidden in ancient texts, waiting to be discovered. Historic Chinese literature has been the source for modern day drugs such as artemisinin for Plasmodium falciparum malaria. The ancient recipe in Bald’s Leechbook may be the next major advance in the topical management of MRSA. I anticipate, in the future, that physicians may be prescribing “Bald’s potion” to treat impetigo. What do you think?

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

Suggested Readings

• AncientBiotics—a medieval remedy for modern day superbugs [news release]? United Kingdom: The University of Nottingham; March 30, 2015. http://www.nottingham.ac.uk/news/pressreleases/2015/march/ancientbiotics---a-medieval-remedy-for-modern-day-superbugs.aspx. Accessed August 12, 2015.
• Feilden T. 1,000-year-old onion and garlic eye remedy kills MRSA. BBC News. March 30, 2015. http://www.bbc.com/news/uk-england-nottinghamshire-32117815. Accessed August 12, 2015.
• Wilson C. Anglo-Saxon remedy kills hospital superbug MRSA. New Scientist. March 30, 2015. http://www.newscientist.com/article/dn27263-anglosaxon-remedy-kills-hospital-superbug-mrsa.html#.VTPpsqazDzl. Accessed August 12, 2015.

At the Society for General Microbiology Annual Conference (March 30–April 2, 2015), Harrison et al presented a paper describing their experience with a 1000-year-old antimicrobial remedy with antistaphylococcal activity (S19We1006). The unique team of investigators—consisting of an expert in Viking studies and 3 microbiologists from the University of Nottingham, England, and another microbiologist who performs mouse model studies from Texas Tech University (Lubbock, Texas)—pooled their talents to reconstruct and test an ancient recipe for treating eyelash follicle infection. The potion not only killed methicillin-resistant Staphylococcus aureus (MRSA) grown in established biofilms but also performed as good, if not better, than the conventional antibiotics on MRSA-infected skin wounds in mice.

“Take cropleek and garlic, of both equal quantities, pound them well together . . . take wine and bullocks gall, mix with the leek . . . let it stand 9 days in the brass vessel” is an excerpt of the recipe for treatment of a sty from the 9th century Anglo-Saxon text Bald’s Leechbook (translated from Old English). The modern day chefs cooked their potion using: (1) 2 Allium species (equal amounts of garlic and either leek or onion, finely chopped and crushed in a mortar for 2 minutes), (2) wine (add 25 mL [0.87 fl oz] of an organic vintage from a historic English vineyard near Glastonbury), (3) bullock gall (dissolve bile from a cow’s stomach in distilled water), and (4) brass (glass bottles with squares of brass sheets immersed in the mixture were used because a brass vessel would be not only hard to sterilize but also expensive). After brewing (in the “brass vessel”), the solution was purified by straining it and left to chill at 4^oC for 9 days before the mixture was used.

What’s the issue?

Advances in technology provide the opportunity to create new medical treatments. However, efficacious therapies may remain hidden in ancient texts, waiting to be discovered. Historic Chinese literature has been the source for modern day drugs such as artemisinin for Plasmodium falciparum malaria. The ancient recipe in Bald’s Leechbook may be the next major advance in the topical management of MRSA. I anticipate, in the future, that physicians may be prescribing “Bald’s potion” to treat impetigo. What do you think?

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

Suggested Readings

• AncientBiotics—a medieval remedy for modern day superbugs [news release]? United Kingdom: The University of Nottingham; March 30, 2015. http://www.nottingham.ac.uk/news/pressreleases/2015/march/ancientbiotics---a-medieval-remedy-for-modern-day-superbugs.aspx. Accessed August 12, 2015.
• Feilden T. 1,000-year-old onion and garlic eye remedy kills MRSA. BBC News. March 30, 2015. http://www.bbc.com/news/uk-england-nottinghamshire-32117815. Accessed August 12, 2015.
• Wilson C. Anglo-Saxon remedy kills hospital superbug MRSA. New Scientist. March 30, 2015. http://www.newscientist.com/article/dn27263-anglosaxon-remedy-kills-hospital-superbug-mrsa.html#.VTPpsqazDzl. Accessed August 12, 2015.

We are all aware of the association of psoriasis with systemic comorbidities. Psoriasis, psoriatic arthritis (PsA), and uveitis are inflammatory disorders that have notable overlap in their inflammatory pathways. In an article published online on July 29 in JAMA Dermatology, Egeberg et al investigated the potential bidirectional relationship between psoriatic disease and uveitis.

The researchers conducted a study (1997-2011) of 74,129 patients aged 18 years and older with incident psoriasis who were identified through administrative registries. There also were 13,114 patients with uveitis identified from the study cohort.

Incidence rates for uveitis per 10,000 person-years were 2.02 (95% CI [confidence interval], 1.99-2.06) for the reference population, 2.88 (95% CI, 2.33-3.56) for patients with mild psoriasis, 4.23 (2.40-7.45) for severe psoriasis, and 5.49 (95% CI, 3.36-8.96) for PsA. Incidence rate ratios per 10,000 person-years for the reference population, which included participants without uveitis, were 9.37 (95% CI, 9.30-9.45) for patients with mild psoriasis, 1.12 (95% CI, 1.10-1.15) for severe psoriasis, and 1.04 (95% CI, 1.01-1.06) for PsA. Patients with uveitis had corresponding incidence rates of 15.51 (95% CI, 12.92-18.62) for mild psoriasis, 2.66 (95% CI, 1.72-4.13) for severe psoriasis, and 4.25 (95% CI, 3.00-6.01) for PsA. Incidence rate ratios per 10,000 person-years for patients with uveitis were 1.59 (95% CI, 1.32-1.91) for mild psoriasis, 2.17 (95% CI, 1.40-3.38) for severe psoriasis, and 3.77 (95% CI, 2.66-5.34) for PsA.

The authors concluded that there is a bidirectional association between psoriatic disease and uveitis. They noted that increased focus on ocular symptoms in patients with psoriasis and PsA and on cutaneous and joint symptoms in patients with prior or current uveitis may be appropriate.

What’s the issue?

This research adds to the potential comorbidities of psoriasis and also adds a potential comorbidity of uveitis itself. Therefore, it would be helpful to add ocular symptoms to our review of systems in those with psoriatic disease. How will this information affect your workup of psoriasis patients?

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

We are all aware of the association of psoriasis with systemic comorbidities. Psoriasis, psoriatic arthritis (PsA), and uveitis are inflammatory disorders that have notable overlap in their inflammatory pathways. In an article published online on July 29 in JAMA Dermatology, Egeberg et al investigated the potential bidirectional relationship between psoriatic disease and uveitis.

The researchers conducted a study (1997-2011) of 74,129 patients aged 18 years and older with incident psoriasis who were identified through administrative registries. There also were 13,114 patients with uveitis identified from the study cohort.

Incidence rates for uveitis per 10,000 person-years were 2.02 (95% CI [confidence interval], 1.99-2.06) for the reference population, 2.88 (95% CI, 2.33-3.56) for patients with mild psoriasis, 4.23 (2.40-7.45) for severe psoriasis, and 5.49 (95% CI, 3.36-8.96) for PsA. Incidence rate ratios per 10,000 person-years for the reference population, which included participants without uveitis, were 9.37 (95% CI, 9.30-9.45) for patients with mild psoriasis, 1.12 (95% CI, 1.10-1.15) for severe psoriasis, and 1.04 (95% CI, 1.01-1.06) for PsA. Patients with uveitis had corresponding incidence rates of 15.51 (95% CI, 12.92-18.62) for mild psoriasis, 2.66 (95% CI, 1.72-4.13) for severe psoriasis, and 4.25 (95% CI, 3.00-6.01) for PsA. Incidence rate ratios per 10,000 person-years for patients with uveitis were 1.59 (95% CI, 1.32-1.91) for mild psoriasis, 2.17 (95% CI, 1.40-3.38) for severe psoriasis, and 3.77 (95% CI, 2.66-5.34) for PsA.

The authors concluded that there is a bidirectional association between psoriatic disease and uveitis. They noted that increased focus on ocular symptoms in patients with psoriasis and PsA and on cutaneous and joint symptoms in patients with prior or current uveitis may be appropriate.

What’s the issue?

This research adds to the potential comorbidities of psoriasis and also adds a potential comorbidity of uveitis itself. Therefore, it would be helpful to add ocular symptoms to our review of systems in those with psoriatic disease. How will this information affect your workup of psoriasis patients?

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

We are all aware of the association of psoriasis with systemic comorbidities. Psoriasis, psoriatic arthritis (PsA), and uveitis are inflammatory disorders that have notable overlap in their inflammatory pathways. In an article published online on July 29 in JAMA Dermatology, Egeberg et al investigated the potential bidirectional relationship between psoriatic disease and uveitis.

The researchers conducted a study (1997-2011) of 74,129 patients aged 18 years and older with incident psoriasis who were identified through administrative registries. There also were 13,114 patients with uveitis identified from the study cohort.

Incidence rates for uveitis per 10,000 person-years were 2.02 (95% CI [confidence interval], 1.99-2.06) for the reference population, 2.88 (95% CI, 2.33-3.56) for patients with mild psoriasis, 4.23 (2.40-7.45) for severe psoriasis, and 5.49 (95% CI, 3.36-8.96) for PsA. Incidence rate ratios per 10,000 person-years for the reference population, which included participants without uveitis, were 9.37 (95% CI, 9.30-9.45) for patients with mild psoriasis, 1.12 (95% CI, 1.10-1.15) for severe psoriasis, and 1.04 (95% CI, 1.01-1.06) for PsA. Patients with uveitis had corresponding incidence rates of 15.51 (95% CI, 12.92-18.62) for mild psoriasis, 2.66 (95% CI, 1.72-4.13) for severe psoriasis, and 4.25 (95% CI, 3.00-6.01) for PsA. Incidence rate ratios per 10,000 person-years for patients with uveitis were 1.59 (95% CI, 1.32-1.91) for mild psoriasis, 2.17 (95% CI, 1.40-3.38) for severe psoriasis, and 3.77 (95% CI, 2.66-5.34) for PsA.

The authors concluded that there is a bidirectional association between psoriatic disease and uveitis. They noted that increased focus on ocular symptoms in patients with psoriasis and PsA and on cutaneous and joint symptoms in patients with prior or current uveitis may be appropriate.

What’s the issue?

This research adds to the potential comorbidities of psoriasis and also adds a potential comorbidity of uveitis itself. Therefore, it would be helpful to add ocular symptoms to our review of systems in those with psoriatic disease. How will this information affect your workup of psoriasis patients?

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

Martin et al recently presented a study at the 2015 American Society of Clinical Oncology Annual Meeting (J Clin Oncol. 2015;33[suppl]:9000) that reported on a phase 3 double-blind randomized trial to assess the use of oral nicotinamide to reduce actinic skin cancers, namely basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).

This study was conducted in 2 tertiary treatment centers in Sydney, Australia, from 2012 to 2014, and it included 386 immunocompetent participants with 2 or more histologically confirmed nonmelanoma skin cancers (NMSCs) in the last 5 years. Two groups were randomized (1:1 ratio) to either receive oral nicotinamide 500 mg twice daily or matched placebo for 12 months. The primary end point measured was the number of new NMSCs to 12 months. Other secondary end points included number of SCCs, BCCs, and actinic keratoses to 12 months. Dermatologists performed skin checks every 3 months on the participants.

The results of the study showed that the average NMSC rate was significantly lower for the oral nicotinamide group (1.77) compared to the placebo group (2.42). The estimated relative rate reduction (RRR) was 0.23 (95% confidence interval [CI], 0.04-0.38; P=.02) adjusting for center and NMSC history, and 0.27 (95% CI, 0.05-0.44; P=.02) with no adjustment. The effects for BCC were comparable to SCC: BCC (RRR, 0.20; 95% CI, -0.06 to 0.39; P=.1) and SCC (RRR, 0.30; 95% CI, 0-0.51; P=.05). Additionally, actinic keratosis counts were reduced by 11% at 3 months (P=.01), 14% at 6 months (P<.001), 20% at 9 months (P<.0001), and 13% at 12 months (P<.005) for the oral nicotinamide group compared to the placebo group. There was no difference in the adverse event rates between the 2 groups.

What’s the issue?

This study reported the results of a double-blind randomized study of nicotinamide (vitamin B₃) to reduce actinic cancer, called the ONTRAC (Oral Nicotinamide to Reduce Actinic Cancer) study, with favorable results for the use of oral nicotinamide, an inexpensive vitamin. There was a 20% reduction in BCC and a 30% reduction in SCC in the nicotinamide group compared to the group taking a placebo with no active ingredients. This study was conducted in a heavily sun-damaged group and it is postulated that nicotinamide helps cells repair DNA damage.

The thought of using a vitamin to reduce skin cancer rates is exciting; however, this study is singular, and while it did show promising results, the number of participants is not very large. There also was no evidence that nicotinamide prevents melanoma formation. Also, there was no protective effect seen once the vitamin B₃ treatment was stopped. One must be cognizant that nicotinamide is not interchangeable with other forms of vitamin B₃ such as niacin.

Although this study is promising, more research is needed to determine nicotinamide’s preventative effects. Of course, strict sun protection and skin checks are the first line in the prevention of skin cancer. Will you be prescribing oral nicotinamide to your patients to prevent NMSC?

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

Martin et al recently presented a study at the 2015 American Society of Clinical Oncology Annual Meeting (J Clin Oncol. 2015;33[suppl]:9000) that reported on a phase 3 double-blind randomized trial to assess the use of oral nicotinamide to reduce actinic skin cancers, namely basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).

This study was conducted in 2 tertiary treatment centers in Sydney, Australia, from 2012 to 2014, and it included 386 immunocompetent participants with 2 or more histologically confirmed nonmelanoma skin cancers (NMSCs) in the last 5 years. Two groups were randomized (1:1 ratio) to either receive oral nicotinamide 500 mg twice daily or matched placebo for 12 months. The primary end point measured was the number of new NMSCs to 12 months. Other secondary end points included number of SCCs, BCCs, and actinic keratoses to 12 months. Dermatologists performed skin checks every 3 months on the participants.

The results of the study showed that the average NMSC rate was significantly lower for the oral nicotinamide group (1.77) compared to the placebo group (2.42). The estimated relative rate reduction (RRR) was 0.23 (95% confidence interval [CI], 0.04-0.38; P=.02) adjusting for center and NMSC history, and 0.27 (95% CI, 0.05-0.44; P=.02) with no adjustment. The effects for BCC were comparable to SCC: BCC (RRR, 0.20; 95% CI, -0.06 to 0.39; P=.1) and SCC (RRR, 0.30; 95% CI, 0-0.51; P=.05). Additionally, actinic keratosis counts were reduced by 11% at 3 months (P=.01), 14% at 6 months (P<.001), 20% at 9 months (P<.0001), and 13% at 12 months (P<.005) for the oral nicotinamide group compared to the placebo group. There was no difference in the adverse event rates between the 2 groups.

What’s the issue?

This study reported the results of a double-blind randomized study of nicotinamide (vitamin B₃) to reduce actinic cancer, called the ONTRAC (Oral Nicotinamide to Reduce Actinic Cancer) study, with favorable results for the use of oral nicotinamide, an inexpensive vitamin. There was a 20% reduction in BCC and a 30% reduction in SCC in the nicotinamide group compared to the group taking a placebo with no active ingredients. This study was conducted in a heavily sun-damaged group and it is postulated that nicotinamide helps cells repair DNA damage.

The thought of using a vitamin to reduce skin cancer rates is exciting; however, this study is singular, and while it did show promising results, the number of participants is not very large. There also was no evidence that nicotinamide prevents melanoma formation. Also, there was no protective effect seen once the vitamin B₃ treatment was stopped. One must be cognizant that nicotinamide is not interchangeable with other forms of vitamin B₃ such as niacin.

Although this study is promising, more research is needed to determine nicotinamide’s preventative effects. Of course, strict sun protection and skin checks are the first line in the prevention of skin cancer. Will you be prescribing oral nicotinamide to your patients to prevent NMSC?

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

Martin et al recently presented a study at the 2015 American Society of Clinical Oncology Annual Meeting (J Clin Oncol. 2015;33[suppl]:9000) that reported on a phase 3 double-blind randomized trial to assess the use of oral nicotinamide to reduce actinic skin cancers, namely basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).

This study was conducted in 2 tertiary treatment centers in Sydney, Australia, from 2012 to 2014, and it included 386 immunocompetent participants with 2 or more histologically confirmed nonmelanoma skin cancers (NMSCs) in the last 5 years. Two groups were randomized (1:1 ratio) to either receive oral nicotinamide 500 mg twice daily or matched placebo for 12 months. The primary end point measured was the number of new NMSCs to 12 months. Other secondary end points included number of SCCs, BCCs, and actinic keratoses to 12 months. Dermatologists performed skin checks every 3 months on the participants.

The results of the study showed that the average NMSC rate was significantly lower for the oral nicotinamide group (1.77) compared to the placebo group (2.42). The estimated relative rate reduction (RRR) was 0.23 (95% confidence interval [CI], 0.04-0.38; P=.02) adjusting for center and NMSC history, and 0.27 (95% CI, 0.05-0.44; P=.02) with no adjustment. The effects for BCC were comparable to SCC: BCC (RRR, 0.20; 95% CI, -0.06 to 0.39; P=.1) and SCC (RRR, 0.30; 95% CI, 0-0.51; P=.05). Additionally, actinic keratosis counts were reduced by 11% at 3 months (P=.01), 14% at 6 months (P<.001), 20% at 9 months (P<.0001), and 13% at 12 months (P<.005) for the oral nicotinamide group compared to the placebo group. There was no difference in the adverse event rates between the 2 groups.

What’s the issue?

This study reported the results of a double-blind randomized study of nicotinamide (vitamin B₃) to reduce actinic cancer, called the ONTRAC (Oral Nicotinamide to Reduce Actinic Cancer) study, with favorable results for the use of oral nicotinamide, an inexpensive vitamin. There was a 20% reduction in BCC and a 30% reduction in SCC in the nicotinamide group compared to the group taking a placebo with no active ingredients. This study was conducted in a heavily sun-damaged group and it is postulated that nicotinamide helps cells repair DNA damage.

The thought of using a vitamin to reduce skin cancer rates is exciting; however, this study is singular, and while it did show promising results, the number of participants is not very large. There also was no evidence that nicotinamide prevents melanoma formation. Also, there was no protective effect seen once the vitamin B₃ treatment was stopped. One must be cognizant that nicotinamide is not interchangeable with other forms of vitamin B₃ such as niacin.

Although this study is promising, more research is needed to determine nicotinamide’s preventative effects. Of course, strict sun protection and skin checks are the first line in the prevention of skin cancer. Will you be prescribing oral nicotinamide to your patients to prevent NMSC?

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

Of all the comorbidities associated with psoriasis, psoriatic arthritis (PsA) is the most common and one of the most problematic. Early recognition, diagnosis, and treatment of PsA can help prevent or limit extensive joint damage that occurs in later stages of the disease. Because cutaneous psoriasis precedes the onset of PsA in 84% of patients with psoriasis, it is incumbent upon dermatologists to be the first line of defense in the screening for joint problems. However, the efficacy of PsA screening remains unknown.

In a recent article published online on June 5 in the Journal of the American Academy of Dermatology, Villani et al performed an analysis to determine the point prevalence of undiagnosed PsA in patients with psoriasis, utilizing a systematic search of the literature and meta-analysis. Searching PubMed, Cochrane, and Embase databases, the authors identified 394 studies for review. None of the studies sought to determine the prevalence of undiagnosed PsA in patients with psoriasis.

The investigators made the assumption that the prevalence of newly diagnosed PsA in patients with psoriasis at the time they sought medical care could be a reasonable estimate of this value. Seven epidemiological studies and 5 studies on PsA screening questionnaires were selected for review and were used to clearly identify patients with newly diagnosed PsA.

The authors found that the prevalence of undiagnosed PsA was 15.5% when all studies were analyzed and 10.1% when only epidemiological studies were included. The high prevalence of undiagnosed PsA in patients with psoriasis reinforces the recommendation that dermatologists need to screen all patients with psoriasis for PsA.

What’s the issue?

The findings of this study are not surprising. Therefore, it is important that we double our efforts to screen patients for PsA to address this comorbidity as early as possible. Improved algorithms for screening of patients for PsA would be a welcome advancement. How will you improve your screening methods for PsA?

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

Of all the comorbidities associated with psoriasis, psoriatic arthritis (PsA) is the most common and one of the most problematic. Early recognition, diagnosis, and treatment of PsA can help prevent or limit extensive joint damage that occurs in later stages of the disease. Because cutaneous psoriasis precedes the onset of PsA in 84% of patients with psoriasis, it is incumbent upon dermatologists to be the first line of defense in the screening for joint problems. However, the efficacy of PsA screening remains unknown.

In a recent article published online on June 5 in the Journal of the American Academy of Dermatology, Villani et al performed an analysis to determine the point prevalence of undiagnosed PsA in patients with psoriasis, utilizing a systematic search of the literature and meta-analysis. Searching PubMed, Cochrane, and Embase databases, the authors identified 394 studies for review. None of the studies sought to determine the prevalence of undiagnosed PsA in patients with psoriasis.

The investigators made the assumption that the prevalence of newly diagnosed PsA in patients with psoriasis at the time they sought medical care could be a reasonable estimate of this value. Seven epidemiological studies and 5 studies on PsA screening questionnaires were selected for review and were used to clearly identify patients with newly diagnosed PsA.

The authors found that the prevalence of undiagnosed PsA was 15.5% when all studies were analyzed and 10.1% when only epidemiological studies were included. The high prevalence of undiagnosed PsA in patients with psoriasis reinforces the recommendation that dermatologists need to screen all patients with psoriasis for PsA.

What’s the issue?

The findings of this study are not surprising. Therefore, it is important that we double our efforts to screen patients for PsA to address this comorbidity as early as possible. Improved algorithms for screening of patients for PsA would be a welcome advancement. How will you improve your screening methods for PsA?

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

Of all the comorbidities associated with psoriasis, psoriatic arthritis (PsA) is the most common and one of the most problematic. Early recognition, diagnosis, and treatment of PsA can help prevent or limit extensive joint damage that occurs in later stages of the disease. Because cutaneous psoriasis precedes the onset of PsA in 84% of patients with psoriasis, it is incumbent upon dermatologists to be the first line of defense in the screening for joint problems. However, the efficacy of PsA screening remains unknown.

In a recent article published online on June 5 in the Journal of the American Academy of Dermatology, Villani et al performed an analysis to determine the point prevalence of undiagnosed PsA in patients with psoriasis, utilizing a systematic search of the literature and meta-analysis. Searching PubMed, Cochrane, and Embase databases, the authors identified 394 studies for review. None of the studies sought to determine the prevalence of undiagnosed PsA in patients with psoriasis.

The investigators made the assumption that the prevalence of newly diagnosed PsA in patients with psoriasis at the time they sought medical care could be a reasonable estimate of this value. Seven epidemiological studies and 5 studies on PsA screening questionnaires were selected for review and were used to clearly identify patients with newly diagnosed PsA.

The authors found that the prevalence of undiagnosed PsA was 15.5% when all studies were analyzed and 10.1% when only epidemiological studies were included. The high prevalence of undiagnosed PsA in patients with psoriasis reinforces the recommendation that dermatologists need to screen all patients with psoriasis for PsA.

What’s the issue?

The findings of this study are not surprising. Therefore, it is important that we double our efforts to screen patients for PsA to address this comorbidity as early as possible. Improved algorithms for screening of patients for PsA would be a welcome advancement. How will you improve your screening methods for PsA?

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

The use of gauges to expand or alter the shape of the earlobe is a relatively popular trend in this day and age. However, as with tattoos, patients sometimes request removal of this physical alteration out of regret or a change in lifestyle. Managing these patients poses a challenge for dermatologists due to the variable degree of tissue ptosis left behind.

Collins et al published a retrospective review in JAMA Facial Plastic Surgery (2015;17:144-148) of their last 20 patients treated for earlobe reconstruction that had at least 1 year of follow-up. The earlobe deformities were classified as small, medium, or large. Small defects were those that were small enough to be treated with an elliptical excision and primary closure. Medium defects were those that had a disruption of the natural curve of the inferior earlobe and a more distinct soft tissue loss of the lobule. A primary closure of this type of defect may cause an unnaturally long lobule. The authors suggested excising the opening and then using a posterior-based advancement flap to restore the natural earlobe contour while improving some of the soft tissue loss. Large defects were those with a lot of volume loss and tissue redundancy. These defects required a wedge excision of the elongated piercing site and a posterior-superior–based advancement flap with 2 arms to it.

Results showed that all 20 patients did well after at least 1 year without the need for further reconstruction or excisional scar revision. Two patients did undergo dermabrasion at 1 year to help blend the final scar.

What’s the issue?

Trends such as the placement of earlobe gauges may wane at some point, resulting in a number of patients seeking our help to repair their earlobes. The approach presented in this study tailors the method of repair to the size of the defect. By doing so, one can hope to restore the natural shape and volume to achieve a natural-appearing earlobe. Have you seen an increase in the number of patients seeking this type of repair?

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

The use of gauges to expand or alter the shape of the earlobe is a relatively popular trend in this day and age. However, as with tattoos, patients sometimes request removal of this physical alteration out of regret or a change in lifestyle. Managing these patients poses a challenge for dermatologists due to the variable degree of tissue ptosis left behind.

Collins et al published a retrospective review in JAMA Facial Plastic Surgery (2015;17:144-148) of their last 20 patients treated for earlobe reconstruction that had at least 1 year of follow-up. The earlobe deformities were classified as small, medium, or large. Small defects were those that were small enough to be treated with an elliptical excision and primary closure. Medium defects were those that had a disruption of the natural curve of the inferior earlobe and a more distinct soft tissue loss of the lobule. A primary closure of this type of defect may cause an unnaturally long lobule. The authors suggested excising the opening and then using a posterior-based advancement flap to restore the natural earlobe contour while improving some of the soft tissue loss. Large defects were those with a lot of volume loss and tissue redundancy. These defects required a wedge excision of the elongated piercing site and a posterior-superior–based advancement flap with 2 arms to it.

Results showed that all 20 patients did well after at least 1 year without the need for further reconstruction or excisional scar revision. Two patients did undergo dermabrasion at 1 year to help blend the final scar.

What’s the issue?

Trends such as the placement of earlobe gauges may wane at some point, resulting in a number of patients seeking our help to repair their earlobes. The approach presented in this study tailors the method of repair to the size of the defect. By doing so, one can hope to restore the natural shape and volume to achieve a natural-appearing earlobe. Have you seen an increase in the number of patients seeking this type of repair?

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

The use of gauges to expand or alter the shape of the earlobe is a relatively popular trend in this day and age. However, as with tattoos, patients sometimes request removal of this physical alteration out of regret or a change in lifestyle. Managing these patients poses a challenge for dermatologists due to the variable degree of tissue ptosis left behind.

Collins et al published a retrospective review in JAMA Facial Plastic Surgery (2015;17:144-148) of their last 20 patients treated for earlobe reconstruction that had at least 1 year of follow-up. The earlobe deformities were classified as small, medium, or large. Small defects were those that were small enough to be treated with an elliptical excision and primary closure. Medium defects were those that had a disruption of the natural curve of the inferior earlobe and a more distinct soft tissue loss of the lobule. A primary closure of this type of defect may cause an unnaturally long lobule. The authors suggested excising the opening and then using a posterior-based advancement flap to restore the natural earlobe contour while improving some of the soft tissue loss. Large defects were those with a lot of volume loss and tissue redundancy. These defects required a wedge excision of the elongated piercing site and a posterior-superior–based advancement flap with 2 arms to it.

Results showed that all 20 patients did well after at least 1 year without the need for further reconstruction or excisional scar revision. Two patients did undergo dermabrasion at 1 year to help blend the final scar.

What’s the issue?

Trends such as the placement of earlobe gauges may wane at some point, resulting in a number of patients seeking our help to repair their earlobes. The approach presented in this study tailors the method of repair to the size of the defect. By doing so, one can hope to restore the natural shape and volume to achieve a natural-appearing earlobe. Have you seen an increase in the number of patients seeking this type of repair?

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

At the recent American Society of Clinical Oncology Annual Meeting, Martin et al presented data from the Australian Oral Nicotinamide to Reduce Actinic Cancer (ONTRAC) study. This prospective double-blind, randomized, controlled trial examined 386 immunocompetent patients with 2 or more nonmelanoma skin cancers (NMSCs) in the last 5 years (average, 8). The patients were randomized to receive oral nicotinamide 500 mg twice daily or placebo for 1 year, resulting in significant reduction of new NMSCs (average rate 1.77 vs 2.42; relative rate reduction, 23%; P=.02), with similar results for basal and squamous cell carcinomas. Actinic keratosis counts were reduced throughout the year by up to 20%, peaking at 9 months. No differences in adverse events were noted between the treatment and placebo groups.

What’s the issue?

High-risk NMSC patients present a challenge to dermatologists, as their need for constant surveillance, field therapy for actinic keratoses, and revolving visits between skin examinations and procedural modalities such as Mohs micrographic surgery can be staggering. Chemopreventive strategies pose difficulties, especially for elderly patients, due to tolerability and adherence, skin irritation and cosmetic limitations of topical therapies such as 5-fluorouracil, and inadequacy or financial inaccessibility of oral therapies such as acitretin.

Nicotinamide is a confusing supplement, as it is also called niacinamide. One of the 2 forms of vitamin B₃, nicotinic acid (or niacin) is the other form and can be converted to nicotinamide in the body. It has cholesterol and vasodilatory/flushing effects that nicotinamide itself does not. Therefore, these supplement subtypes are not generally interchangeable.

Nicotinamide is postulated to enhance DNA repair and reverse UV immunosuppression in NMSC patients and is a well-tolerated and inexpensive supplement (approximately $10 a month for the dosage in this study). Although the decrease in skin cancer number per year seems modest in this study, my patients would likely welcome at least 1 fewer surgery per year and much less cryotherapy or 5-fluorouracil cream, especially if it is as simple as buying the supplement at the grocery store as they do for their fish oil capsules and probiotics. Does vitamin B₃ hold promise for your high-risk NMSC patients?

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

At the recent American Society of Clinical Oncology Annual Meeting, Martin et al presented data from the Australian Oral Nicotinamide to Reduce Actinic Cancer (ONTRAC) study. This prospective double-blind, randomized, controlled trial examined 386 immunocompetent patients with 2 or more nonmelanoma skin cancers (NMSCs) in the last 5 years (average, 8). The patients were randomized to receive oral nicotinamide 500 mg twice daily or placebo for 1 year, resulting in significant reduction of new NMSCs (average rate 1.77 vs 2.42; relative rate reduction, 23%; P=.02), with similar results for basal and squamous cell carcinomas. Actinic keratosis counts were reduced throughout the year by up to 20%, peaking at 9 months. No differences in adverse events were noted between the treatment and placebo groups.

What’s the issue?

High-risk NMSC patients present a challenge to dermatologists, as their need for constant surveillance, field therapy for actinic keratoses, and revolving visits between skin examinations and procedural modalities such as Mohs micrographic surgery can be staggering. Chemopreventive strategies pose difficulties, especially for elderly patients, due to tolerability and adherence, skin irritation and cosmetic limitations of topical therapies such as 5-fluorouracil, and inadequacy or financial inaccessibility of oral therapies such as acitretin.

Nicotinamide is a confusing supplement, as it is also called niacinamide. One of the 2 forms of vitamin B₃, nicotinic acid (or niacin) is the other form and can be converted to nicotinamide in the body. It has cholesterol and vasodilatory/flushing effects that nicotinamide itself does not. Therefore, these supplement subtypes are not generally interchangeable.

Nicotinamide is postulated to enhance DNA repair and reverse UV immunosuppression in NMSC patients and is a well-tolerated and inexpensive supplement (approximately $10 a month for the dosage in this study). Although the decrease in skin cancer number per year seems modest in this study, my patients would likely welcome at least 1 fewer surgery per year and much less cryotherapy or 5-fluorouracil cream, especially if it is as simple as buying the supplement at the grocery store as they do for their fish oil capsules and probiotics. Does vitamin B₃ hold promise for your high-risk NMSC patients?

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

At the recent American Society of Clinical Oncology Annual Meeting, Martin et al presented data from the Australian Oral Nicotinamide to Reduce Actinic Cancer (ONTRAC) study. This prospective double-blind, randomized, controlled trial examined 386 immunocompetent patients with 2 or more nonmelanoma skin cancers (NMSCs) in the last 5 years (average, 8). The patients were randomized to receive oral nicotinamide 500 mg twice daily or placebo for 1 year, resulting in significant reduction of new NMSCs (average rate 1.77 vs 2.42; relative rate reduction, 23%; P=.02), with similar results for basal and squamous cell carcinomas. Actinic keratosis counts were reduced throughout the year by up to 20%, peaking at 9 months. No differences in adverse events were noted between the treatment and placebo groups.

What’s the issue?

High-risk NMSC patients present a challenge to dermatologists, as their need for constant surveillance, field therapy for actinic keratoses, and revolving visits between skin examinations and procedural modalities such as Mohs micrographic surgery can be staggering. Chemopreventive strategies pose difficulties, especially for elderly patients, due to tolerability and adherence, skin irritation and cosmetic limitations of topical therapies such as 5-fluorouracil, and inadequacy or financial inaccessibility of oral therapies such as acitretin.

Nicotinamide is a confusing supplement, as it is also called niacinamide. One of the 2 forms of vitamin B₃, nicotinic acid (or niacin) is the other form and can be converted to nicotinamide in the body. It has cholesterol and vasodilatory/flushing effects that nicotinamide itself does not. Therefore, these supplement subtypes are not generally interchangeable.

Nicotinamide is postulated to enhance DNA repair and reverse UV immunosuppression in NMSC patients and is a well-tolerated and inexpensive supplement (approximately $10 a month for the dosage in this study). Although the decrease in skin cancer number per year seems modest in this study, my patients would likely welcome at least 1 fewer surgery per year and much less cryotherapy or 5-fluorouracil cream, especially if it is as simple as buying the supplement at the grocery store as they do for their fish oil capsules and probiotics. Does vitamin B₃ hold promise for your high-risk NMSC patients?

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

Lower eyelid malposition is both a cosmetic and functional issue for many patients. It often arises from normal aging; however, it also can be due to thyroid disease, trauma, and surgery (iatrogenic). Correction of lower eyelid malposition requires a variety of surgical approaches to elevate the lower eyelid position. These procedures are not without risk. There have been reports of hyaluronic acid injections being used to help stretch the skin and give support to the sagging eyelid.

Le et al published a study (Ophthal Plast Reconstr Surg. 2014;30:504-507) on the effect of autologous fat injection on lower eyelid position. They performed a retrospective pilot study of autologous fat injections to support the lower eyelid in patients presenting for cosmetic reasons. A retrospective chart review was performed identifying 70 patients that had undergone lower eyelid and malar autologous fat injections for cosmetic improvement performed by a single surgeon. Patients were excluded if they had prior eyelid surgery. Photographs were taken in a standardized fashion and evaluated by 2 blinded evaluators. The measurements evaluated were the lower eyelid position (marginal reflex distance 2 [MRD2]) and inferior scleral show (SS).

The fat was harvested from the inner thigh and knee under tumescent anesthesia, strained, and injected with a 1.2-mm blunt cannula into various planes of the facial soft tissues. Approximately 0 to 2 mL was injected into the tear trough areas and 3 to 7 mL into the malar region, both per side. Photographs were repeated at an average of 117, 125, and 316 days.

Results showed that the MRD2 distance improved 0.5 mm bilaterally and was maintained at 316 days. Similarly, the SS measurement improved by 0.5 mm and was maintained at 125 days. Results improved slightly more in patients who had simultaneous face-lifts, but the difference was not statistically significant.

What’s the issue?

Lower eyelid malposition can make patients appear aged or tired while functionally causing dry eye or excessive tearing. Finding a way to improve this condition without surgery is key because the surgeries are fraught with risk. This study suggests that we should look more critically at lower eyelid positions in our patients who are receiving synthetic fillers or autologous fat to see if we are improving the MRD2 and SS measurements. Have you been seeing an increase in patients seeking improvement for “tired-looking eyes,” or do patients know they look tired but cannot pinpoint why?

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

Lower eyelid malposition is both a cosmetic and functional issue for many patients. It often arises from normal aging; however, it also can be due to thyroid disease, trauma, and surgery (iatrogenic). Correction of lower eyelid malposition requires a variety of surgical approaches to elevate the lower eyelid position. These procedures are not without risk. There have been reports of hyaluronic acid injections being used to help stretch the skin and give support to the sagging eyelid.

Le et al published a study (Ophthal Plast Reconstr Surg. 2014;30:504-507) on the effect of autologous fat injection on lower eyelid position. They performed a retrospective pilot study of autologous fat injections to support the lower eyelid in patients presenting for cosmetic reasons. A retrospective chart review was performed identifying 70 patients that had undergone lower eyelid and malar autologous fat injections for cosmetic improvement performed by a single surgeon. Patients were excluded if they had prior eyelid surgery. Photographs were taken in a standardized fashion and evaluated by 2 blinded evaluators. The measurements evaluated were the lower eyelid position (marginal reflex distance 2 [MRD2]) and inferior scleral show (SS).

The fat was harvested from the inner thigh and knee under tumescent anesthesia, strained, and injected with a 1.2-mm blunt cannula into various planes of the facial soft tissues. Approximately 0 to 2 mL was injected into the tear trough areas and 3 to 7 mL into the malar region, both per side. Photographs were repeated at an average of 117, 125, and 316 days.

Results showed that the MRD2 distance improved 0.5 mm bilaterally and was maintained at 316 days. Similarly, the SS measurement improved by 0.5 mm and was maintained at 125 days. Results improved slightly more in patients who had simultaneous face-lifts, but the difference was not statistically significant.

What’s the issue?

Lower eyelid malposition can make patients appear aged or tired while functionally causing dry eye or excessive tearing. Finding a way to improve this condition without surgery is key because the surgeries are fraught with risk. This study suggests that we should look more critically at lower eyelid positions in our patients who are receiving synthetic fillers or autologous fat to see if we are improving the MRD2 and SS measurements. Have you been seeing an increase in patients seeking improvement for “tired-looking eyes,” or do patients know they look tired but cannot pinpoint why?

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

Lower eyelid malposition is both a cosmetic and functional issue for many patients. It often arises from normal aging; however, it also can be due to thyroid disease, trauma, and surgery (iatrogenic). Correction of lower eyelid malposition requires a variety of surgical approaches to elevate the lower eyelid position. These procedures are not without risk. There have been reports of hyaluronic acid injections being used to help stretch the skin and give support to the sagging eyelid.

Le et al published a study (Ophthal Plast Reconstr Surg. 2014;30:504-507) on the effect of autologous fat injection on lower eyelid position. They performed a retrospective pilot study of autologous fat injections to support the lower eyelid in patients presenting for cosmetic reasons. A retrospective chart review was performed identifying 70 patients that had undergone lower eyelid and malar autologous fat injections for cosmetic improvement performed by a single surgeon. Patients were excluded if they had prior eyelid surgery. Photographs were taken in a standardized fashion and evaluated by 2 blinded evaluators. The measurements evaluated were the lower eyelid position (marginal reflex distance 2 [MRD2]) and inferior scleral show (SS).

The fat was harvested from the inner thigh and knee under tumescent anesthesia, strained, and injected with a 1.2-mm blunt cannula into various planes of the facial soft tissues. Approximately 0 to 2 mL was injected into the tear trough areas and 3 to 7 mL into the malar region, both per side. Photographs were repeated at an average of 117, 125, and 316 days.

Results showed that the MRD2 distance improved 0.5 mm bilaterally and was maintained at 316 days. Similarly, the SS measurement improved by 0.5 mm and was maintained at 125 days. Results improved slightly more in patients who had simultaneous face-lifts, but the difference was not statistically significant.

What’s the issue?

Lower eyelid malposition can make patients appear aged or tired while functionally causing dry eye or excessive tearing. Finding a way to improve this condition without surgery is key because the surgeries are fraught with risk. This study suggests that we should look more critically at lower eyelid positions in our patients who are receiving synthetic fillers or autologous fat to see if we are improving the MRD2 and SS measurements. Have you been seeing an increase in patients seeking improvement for “tired-looking eyes,” or do patients know they look tired but cannot pinpoint why?

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

We are currently in the midst of a new wave of drug developments and approvals for psoriasis; however, we recently have been reminded of the tenuous nature of bringing a new drug to market. Last month, Amgen Inc announced it was pulling out of the long-running collaboration on the high-profile IL-17 program after evaluating the likely commercial impact it would face in light of the suicidal thoughts some patients reported during the studies.

Brodalumab had successfully completed 3 phase 3 studies in patients with moderate to severe plaque psoriasis known as the AMAGINE program. Top-line results from AMAGINE-1 comparing brodalumab with placebo were released in May 2014. Top-line results from AMAGINE-2 and AMAGINE-3 comparing brodalumab with ustekinumab and placebo were announced in November 2014. AMAGINE-2 and AMAGINE-3 are identical in design. “During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” said Amgen Executive Vice President of Research and Development Sean Harper in a statement. AstraZeneca must now decide whether to pursue brodalumab independently.

Once the exact data are publicly released, we will be able to better evaluate the issues of suicidal ideation involved.

What’s the issue?

Brodalumab was eagerly anticipated in the dermatology community. In an instant, the drug’s future is in doubt, which once again demonstrates the fragility of the drug development process. How will this recent announcement affect your use of new biologics?

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

We are currently in the midst of a new wave of drug developments and approvals for psoriasis; however, we recently have been reminded of the tenuous nature of bringing a new drug to market. Last month, Amgen Inc announced it was pulling out of the long-running collaboration on the high-profile IL-17 program after evaluating the likely commercial impact it would face in light of the suicidal thoughts some patients reported during the studies.

Brodalumab had successfully completed 3 phase 3 studies in patients with moderate to severe plaque psoriasis known as the AMAGINE program. Top-line results from AMAGINE-1 comparing brodalumab with placebo were released in May 2014. Top-line results from AMAGINE-2 and AMAGINE-3 comparing brodalumab with ustekinumab and placebo were announced in November 2014. AMAGINE-2 and AMAGINE-3 are identical in design. “During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” said Amgen Executive Vice President of Research and Development Sean Harper in a statement. AstraZeneca must now decide whether to pursue brodalumab independently.

Once the exact data are publicly released, we will be able to better evaluate the issues of suicidal ideation involved.

What’s the issue?

Brodalumab was eagerly anticipated in the dermatology community. In an instant, the drug’s future is in doubt, which once again demonstrates the fragility of the drug development process. How will this recent announcement affect your use of new biologics?

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

We are currently in the midst of a new wave of drug developments and approvals for psoriasis; however, we recently have been reminded of the tenuous nature of bringing a new drug to market. Last month, Amgen Inc announced it was pulling out of the long-running collaboration on the high-profile IL-17 program after evaluating the likely commercial impact it would face in light of the suicidal thoughts some patients reported during the studies.

Brodalumab had successfully completed 3 phase 3 studies in patients with moderate to severe plaque psoriasis known as the AMAGINE program. Top-line results from AMAGINE-1 comparing brodalumab with placebo were released in May 2014. Top-line results from AMAGINE-2 and AMAGINE-3 comparing brodalumab with ustekinumab and placebo were announced in November 2014. AMAGINE-2 and AMAGINE-3 are identical in design. “During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” said Amgen Executive Vice President of Research and Development Sean Harper in a statement. AstraZeneca must now decide whether to pursue brodalumab independently.

Once the exact data are publicly released, we will be able to better evaluate the issues of suicidal ideation involved.

What’s the issue?

Brodalumab was eagerly anticipated in the dermatology community. In an instant, the drug’s future is in doubt, which once again demonstrates the fragility of the drug development process. How will this recent announcement affect your use of new biologics?

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

Who is tired of the same old stuff when it comes to acne? Innovation in therapy has been stagnant with a flurry of “me too” reformulated fixed combinations. The only true advance has been in drug delivery, with new vehicles allowing for the solubilization of established drugs such as dapsone or the combination of incompatible actives such as benzoyl peroxide and a retinoid. Before we can welcome new drugs with open arms, we must first expand the construct of acne pathophysiology to identify more appropriate targets for said new drugs. In a recent article published online in the Journal of the American Academy of Dermatology in June, Metiko et al highlight this sentiment. Generations of dermatologists were taught the 3- to 4-step process (depending on the teacher) through which an acne lesion forms: (1) follicular epidermal hyperproliferation, (2) Propionibacterium acnes colonization, and (3) inflammation. However, the molecular underpinnings of this theory have been challenged for more than a decade, with research highlighting the presence of preclinical inflammation, most recently found to be mediated by IL-1ß through a specific inflammasome pathway, NLRP3 (NOD-like receptor family, pyrin domain containing 3). Maybe we are missing a bridge between this stellar basic science and the clinical dermatologist who contends that the pesky microcomedone is the acne instigator. This short but sweet letter once again calls this antiquated prose into question in a highly visible clinical dermatology journal.

In thinking of new pathways and targets, Gupta et al published an article online in Archives of Dermatological Research on May 19 on the role of peroxisome proliferator-activated receptors (PPARs) and PPAR agonists in the treatment of multiple dermatologic diseases. For our purposes, I will highlight the section on acne and will start at the end: More research is needed. Peroxisome proliferator-activated receptors are nuclear hormone receptors that regulate gene expression, cell growth and differentiation, apoptosis, inflammatory responses, and tumorigenesis after binding with specific ligands. With respect to acne specifically, PPARs influence 2 of the pathophysiologic factors—sebum production and inflammation—due to their effect on lipid deposition in the sebocytes and inhibition of proinflammatory gene expression and downregulation of inflammatory cytokines. It appears that activation or inhibition of specific PPAR subtypes can either increase or decrease sebum production or be pro- or anti-inflammatory. The tough part is which receptors to activate and which to inhibit. This review related to an interesting clinical study that evaluated oral zileuton 600 mg administered 4 times daily for 3 months for acne. Zileuton inhibits leukotriene B4 production, which, as it turns out, is a natural ligand for PPARα. The idea here is that this blockade would be anti-inflammatory and indirectly inhibit the sebum production via PPARα suppression. The pilot study was reported as successful, with a decrease in the papulopustular acne severity index in a time-dependent manner in subjects evaluated.

What’s the issue?

So, what’s the point of this long-winded, double-paper review? We need to expand our acne horizons. We need new bench-to-bedside approaches. Which is your favorite target?

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

Who is tired of the same old stuff when it comes to acne? Innovation in therapy has been stagnant with a flurry of “me too” reformulated fixed combinations. The only true advance has been in drug delivery, with new vehicles allowing for the solubilization of established drugs such as dapsone or the combination of incompatible actives such as benzoyl peroxide and a retinoid. Before we can welcome new drugs with open arms, we must first expand the construct of acne pathophysiology to identify more appropriate targets for said new drugs. In a recent article published online in the Journal of the American Academy of Dermatology in June, Metiko et al highlight this sentiment. Generations of dermatologists were taught the 3- to 4-step process (depending on the teacher) through which an acne lesion forms: (1) follicular epidermal hyperproliferation, (2) Propionibacterium acnes colonization, and (3) inflammation. However, the molecular underpinnings of this theory have been challenged for more than a decade, with research highlighting the presence of preclinical inflammation, most recently found to be mediated by IL-1ß through a specific inflammasome pathway, NLRP3 (NOD-like receptor family, pyrin domain containing 3). Maybe we are missing a bridge between this stellar basic science and the clinical dermatologist who contends that the pesky microcomedone is the acne instigator. This short but sweet letter once again calls this antiquated prose into question in a highly visible clinical dermatology journal.

In thinking of new pathways and targets, Gupta et al published an article online in Archives of Dermatological Research on May 19 on the role of peroxisome proliferator-activated receptors (PPARs) and PPAR agonists in the treatment of multiple dermatologic diseases. For our purposes, I will highlight the section on acne and will start at the end: More research is needed. Peroxisome proliferator-activated receptors are nuclear hormone receptors that regulate gene expression, cell growth and differentiation, apoptosis, inflammatory responses, and tumorigenesis after binding with specific ligands. With respect to acne specifically, PPARs influence 2 of the pathophysiologic factors—sebum production and inflammation—due to their effect on lipid deposition in the sebocytes and inhibition of proinflammatory gene expression and downregulation of inflammatory cytokines. It appears that activation or inhibition of specific PPAR subtypes can either increase or decrease sebum production or be pro- or anti-inflammatory. The tough part is which receptors to activate and which to inhibit. This review related to an interesting clinical study that evaluated oral zileuton 600 mg administered 4 times daily for 3 months for acne. Zileuton inhibits leukotriene B4 production, which, as it turns out, is a natural ligand for PPARα. The idea here is that this blockade would be anti-inflammatory and indirectly inhibit the sebum production via PPARα suppression. The pilot study was reported as successful, with a decrease in the papulopustular acne severity index in a time-dependent manner in subjects evaluated.

What’s the issue?

So, what’s the point of this long-winded, double-paper review? We need to expand our acne horizons. We need new bench-to-bedside approaches. Which is your favorite target?

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

Who is tired of the same old stuff when it comes to acne? Innovation in therapy has been stagnant with a flurry of “me too” reformulated fixed combinations. The only true advance has been in drug delivery, with new vehicles allowing for the solubilization of established drugs such as dapsone or the combination of incompatible actives such as benzoyl peroxide and a retinoid. Before we can welcome new drugs with open arms, we must first expand the construct of acne pathophysiology to identify more appropriate targets for said new drugs. In a recent article published online in the Journal of the American Academy of Dermatology in June, Metiko et al highlight this sentiment. Generations of dermatologists were taught the 3- to 4-step process (depending on the teacher) through which an acne lesion forms: (1) follicular epidermal hyperproliferation, (2) Propionibacterium acnes colonization, and (3) inflammation. However, the molecular underpinnings of this theory have been challenged for more than a decade, with research highlighting the presence of preclinical inflammation, most recently found to be mediated by IL-1ß through a specific inflammasome pathway, NLRP3 (NOD-like receptor family, pyrin domain containing 3). Maybe we are missing a bridge between this stellar basic science and the clinical dermatologist who contends that the pesky microcomedone is the acne instigator. This short but sweet letter once again calls this antiquated prose into question in a highly visible clinical dermatology journal.

In thinking of new pathways and targets, Gupta et al published an article online in Archives of Dermatological Research on May 19 on the role of peroxisome proliferator-activated receptors (PPARs) and PPAR agonists in the treatment of multiple dermatologic diseases. For our purposes, I will highlight the section on acne and will start at the end: More research is needed. Peroxisome proliferator-activated receptors are nuclear hormone receptors that regulate gene expression, cell growth and differentiation, apoptosis, inflammatory responses, and tumorigenesis after binding with specific ligands. With respect to acne specifically, PPARs influence 2 of the pathophysiologic factors—sebum production and inflammation—due to their effect on lipid deposition in the sebocytes and inhibition of proinflammatory gene expression and downregulation of inflammatory cytokines. It appears that activation or inhibition of specific PPAR subtypes can either increase or decrease sebum production or be pro- or anti-inflammatory. The tough part is which receptors to activate and which to inhibit. This review related to an interesting clinical study that evaluated oral zileuton 600 mg administered 4 times daily for 3 months for acne. Zileuton inhibits leukotriene B4 production, which, as it turns out, is a natural ligand for PPARα. The idea here is that this blockade would be anti-inflammatory and indirectly inhibit the sebum production via PPARα suppression. The pilot study was reported as successful, with a decrease in the papulopustular acne severity index in a time-dependent manner in subjects evaluated.

What’s the issue?

So, what’s the point of this long-winded, double-paper review? We need to expand our acne horizons. We need new bench-to-bedside approaches. Which is your favorite target?

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

“An apple a day keeps the doctor away,” and coffee each day keeps the melanoma away. A recent analysis of data by Loftfield et al from a food frequency questionnaire published online on January 20 in the Journal of the National Cancer Institute demonstrated that caffeinated coffee intake was inversely associated with melanoma. Specifically, consuming 4 or more cups of caffeinated coffee each day was found to decrease the risk for melanoma by 20%.

The authors’ reference groups were derived from a National Institutes of Health–AARP prospective cohort diet and health study that commenced in 1995 to 1996 and concluded on December 31, 2006. They observed that the lower risk for melanoma was only associated with caffeinated coffee. Unexpectedly, they also observed that caffeinated coffee drinking only decreased the risk for melanoma but not melanoma in situ.

There is scientific evidence that coffee has a role in decreasing UVB-induced carcinogenesis. Caffeine (both orally and topically) inhibits UVB-induced carcinogenesis by absorbing UV radiation. Also, 5-O-caffeoylquinic acid (the major chlorogenic acid in coffee) and its metabolite caffeic acid inhibit cyclooxygenase 2 expression, which is overexpressed in human melanoma cells and in response to UVB exposure. In addition to caffeine, coffee also contains several bioactive compounds: diterpenes, polyphenols, and trigonelline. Topical diterpenes inhibit inflammation in epidermal cells. During coffee roasting, trigonelline generates nicotinic acid and nicotinamide, both of which are protective against UVB-induced skin carcinogenesis in mice and UVB-induced immunosuppression in both humans and mice.

What’s the issue?

According to an article in The Washington Post, the “apple” adage originated in the 1860s; the original phrase was “Eat an apple on going to bed, and you’ll keep the doctor from earning his bread,” which evolved to “An apple a day, no doctor to pay,” then “An apple a day sends the doctor away” before the current version was first used in 1922. As one who enjoys having a cup of caffeinated coffee next to my computer in the office or at home, I can easily welcome the prospect of a few additional cups each day to prevent melanoma. And, as advocates for a possible benefit to our patients’ better health, should we should provide complimentary caffeinated coffee in our office waiting rooms to encourage our dermatology patients to decrease their risk for developing melanoma?

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

“An apple a day keeps the doctor away,” and coffee each day keeps the melanoma away. A recent analysis of data by Loftfield et al from a food frequency questionnaire published online on January 20 in the Journal of the National Cancer Institute demonstrated that caffeinated coffee intake was inversely associated with melanoma. Specifically, consuming 4 or more cups of caffeinated coffee each day was found to decrease the risk for melanoma by 20%.

The authors’ reference groups were derived from a National Institutes of Health–AARP prospective cohort diet and health study that commenced in 1995 to 1996 and concluded on December 31, 2006. They observed that the lower risk for melanoma was only associated with caffeinated coffee. Unexpectedly, they also observed that caffeinated coffee drinking only decreased the risk for melanoma but not melanoma in situ.

There is scientific evidence that coffee has a role in decreasing UVB-induced carcinogenesis. Caffeine (both orally and topically) inhibits UVB-induced carcinogenesis by absorbing UV radiation. Also, 5-O-caffeoylquinic acid (the major chlorogenic acid in coffee) and its metabolite caffeic acid inhibit cyclooxygenase 2 expression, which is overexpressed in human melanoma cells and in response to UVB exposure. In addition to caffeine, coffee also contains several bioactive compounds: diterpenes, polyphenols, and trigonelline. Topical diterpenes inhibit inflammation in epidermal cells. During coffee roasting, trigonelline generates nicotinic acid and nicotinamide, both of which are protective against UVB-induced skin carcinogenesis in mice and UVB-induced immunosuppression in both humans and mice.

What’s the issue?

According to an article in The Washington Post, the “apple” adage originated in the 1860s; the original phrase was “Eat an apple on going to bed, and you’ll keep the doctor from earning his bread,” which evolved to “An apple a day, no doctor to pay,” then “An apple a day sends the doctor away” before the current version was first used in 1922. As one who enjoys having a cup of caffeinated coffee next to my computer in the office or at home, I can easily welcome the prospect of a few additional cups each day to prevent melanoma. And, as advocates for a possible benefit to our patients’ better health, should we should provide complimentary caffeinated coffee in our office waiting rooms to encourage our dermatology patients to decrease their risk for developing melanoma?

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

“An apple a day keeps the doctor away,” and coffee each day keeps the melanoma away. A recent analysis of data by Loftfield et al from a food frequency questionnaire published online on January 20 in the Journal of the National Cancer Institute demonstrated that caffeinated coffee intake was inversely associated with melanoma. Specifically, consuming 4 or more cups of caffeinated coffee each day was found to decrease the risk for melanoma by 20%.

The authors’ reference groups were derived from a National Institutes of Health–AARP prospective cohort diet and health study that commenced in 1995 to 1996 and concluded on December 31, 2006. They observed that the lower risk for melanoma was only associated with caffeinated coffee. Unexpectedly, they also observed that caffeinated coffee drinking only decreased the risk for melanoma but not melanoma in situ.

There is scientific evidence that coffee has a role in decreasing UVB-induced carcinogenesis. Caffeine (both orally and topically) inhibits UVB-induced carcinogenesis by absorbing UV radiation. Also, 5-O-caffeoylquinic acid (the major chlorogenic acid in coffee) and its metabolite caffeic acid inhibit cyclooxygenase 2 expression, which is overexpressed in human melanoma cells and in response to UVB exposure. In addition to caffeine, coffee also contains several bioactive compounds: diterpenes, polyphenols, and trigonelline. Topical diterpenes inhibit inflammation in epidermal cells. During coffee roasting, trigonelline generates nicotinic acid and nicotinamide, both of which are protective against UVB-induced skin carcinogenesis in mice and UVB-induced immunosuppression in both humans and mice.

What’s the issue?

According to an article in The Washington Post, the “apple” adage originated in the 1860s; the original phrase was “Eat an apple on going to bed, and you’ll keep the doctor from earning his bread,” which evolved to “An apple a day, no doctor to pay,” then “An apple a day sends the doctor away” before the current version was first used in 1922. As one who enjoys having a cup of caffeinated coffee next to my computer in the office or at home, I can easily welcome the prospect of a few additional cups each day to prevent melanoma. And, as advocates for a possible benefit to our patients’ better health, should we should provide complimentary caffeinated coffee in our office waiting rooms to encourage our dermatology patients to decrease their risk for developing melanoma?

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