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Pacific Dermatologic Association (PDA): Annual Meeting
Can patients be desensitized to nickel?
VANCOUVER, B.C. – Nickel has long ranked at the top of common contact allergens. In fact, it earned the No. 1 spot in the North American Contact Dermatitis Group patch test results in 2009-2010.
A team of Canadian researchers began to wonder: Is it feasible to induce tolerance to nickel, or to desensitize patients to this substance found in everything from jewelry and orthodontic devices to vitamins and herbal remedies? At the annual meeting of the Pacific Dermatologic Association, Dr. Gillian C. de Gannes, a dermatologist who directs the University of British Columbia Contact Dermatitis Clinic in Vancouver, discussed preliminary findings from a proof-of-principle study designed to answer that question.
“We have a nickel detection kit for our patients – the dimethylglyoxime test – but at this point, allergen avoidance counseling is how we treat nickel allergy,” she said. “The regulatory CD4-positive CD25-positive T cells (Tregs) modulate nickel sensitivity in humans, and topical application of calcipotriol induces Treg cells to prevent both the induction and elicitation of contact hypersensitivity in mice. It’s [also] been shown that topical vitamin D analogues prevented topical sensitization to DNCB [dinitrochlorobenzene] in humans: a very potent sensitizer,” she noted (Arch. Dermatol. 2006;142:1332-4).
In an effort to investigate whether topical immune modulators can stop preestablished contact hypersensitivity to nickel, Dr. de Gannes and her associates recruited 24 volunteers to participate in a double-blind, controlled trial, and randomized them to one of four groups: petrolatum ointment, betamethasone dipropionate ointment, calcipotriol ointment, and the combination of betamethasone dipropionate and calcipotriol ointments. “We first do a nickel patch test on the distal forearm to confirm that this person is sensitized to nickel,” she explained. “That’s our confirmation stage. On the opposite arm, we randomize them to one of the four groups of ointment, and we instruct them to apply a measured amount of ointment in a defined area twice daily for a week. They come back to us at the end of that week, and we repeat the nickel patch test where they applied their ointment to see whether they react or not.”
So far, preliminary results from 13 patients showed that application of some of the topical products induced tolerance and decreased reactivity to nickel, “but we’ve not yet been able to desensitize patients,” Dr. de Gannes noted. “This is just an interim analysis, and we have not unblinded the study yet. Hopefully we’ll have more meaningful results within the next year.”
The strategy is clinically relevant, she continued, because “we have hairstylists, for example, who come to us, allergic to the chemicals that they’re using. They really want to get back to their job. If this is a hand dermatitis caused by nickel or other contact allergens, and I can possibly give that hairstylist an ointment to apply to her hands in the morning and night and get back to her job, that’s a happy worker. That scenario would be a successful clinical outcome of this research, but we have a lot more work to do.”
Dr. de Gannes said that she had no relevant financial conflicts of interest to disclose.
On Twitter @dougbrunk
VANCOUVER, B.C. – Nickel has long ranked at the top of common contact allergens. In fact, it earned the No. 1 spot in the North American Contact Dermatitis Group patch test results in 2009-2010.
A team of Canadian researchers began to wonder: Is it feasible to induce tolerance to nickel, or to desensitize patients to this substance found in everything from jewelry and orthodontic devices to vitamins and herbal remedies? At the annual meeting of the Pacific Dermatologic Association, Dr. Gillian C. de Gannes, a dermatologist who directs the University of British Columbia Contact Dermatitis Clinic in Vancouver, discussed preliminary findings from a proof-of-principle study designed to answer that question.
“We have a nickel detection kit for our patients – the dimethylglyoxime test – but at this point, allergen avoidance counseling is how we treat nickel allergy,” she said. “The regulatory CD4-positive CD25-positive T cells (Tregs) modulate nickel sensitivity in humans, and topical application of calcipotriol induces Treg cells to prevent both the induction and elicitation of contact hypersensitivity in mice. It’s [also] been shown that topical vitamin D analogues prevented topical sensitization to DNCB [dinitrochlorobenzene] in humans: a very potent sensitizer,” she noted (Arch. Dermatol. 2006;142:1332-4).
In an effort to investigate whether topical immune modulators can stop preestablished contact hypersensitivity to nickel, Dr. de Gannes and her associates recruited 24 volunteers to participate in a double-blind, controlled trial, and randomized them to one of four groups: petrolatum ointment, betamethasone dipropionate ointment, calcipotriol ointment, and the combination of betamethasone dipropionate and calcipotriol ointments. “We first do a nickel patch test on the distal forearm to confirm that this person is sensitized to nickel,” she explained. “That’s our confirmation stage. On the opposite arm, we randomize them to one of the four groups of ointment, and we instruct them to apply a measured amount of ointment in a defined area twice daily for a week. They come back to us at the end of that week, and we repeat the nickel patch test where they applied their ointment to see whether they react or not.”
So far, preliminary results from 13 patients showed that application of some of the topical products induced tolerance and decreased reactivity to nickel, “but we’ve not yet been able to desensitize patients,” Dr. de Gannes noted. “This is just an interim analysis, and we have not unblinded the study yet. Hopefully we’ll have more meaningful results within the next year.”
The strategy is clinically relevant, she continued, because “we have hairstylists, for example, who come to us, allergic to the chemicals that they’re using. They really want to get back to their job. If this is a hand dermatitis caused by nickel or other contact allergens, and I can possibly give that hairstylist an ointment to apply to her hands in the morning and night and get back to her job, that’s a happy worker. That scenario would be a successful clinical outcome of this research, but we have a lot more work to do.”
Dr. de Gannes said that she had no relevant financial conflicts of interest to disclose.
On Twitter @dougbrunk
VANCOUVER, B.C. – Nickel has long ranked at the top of common contact allergens. In fact, it earned the No. 1 spot in the North American Contact Dermatitis Group patch test results in 2009-2010.
A team of Canadian researchers began to wonder: Is it feasible to induce tolerance to nickel, or to desensitize patients to this substance found in everything from jewelry and orthodontic devices to vitamins and herbal remedies? At the annual meeting of the Pacific Dermatologic Association, Dr. Gillian C. de Gannes, a dermatologist who directs the University of British Columbia Contact Dermatitis Clinic in Vancouver, discussed preliminary findings from a proof-of-principle study designed to answer that question.
“We have a nickel detection kit for our patients – the dimethylglyoxime test – but at this point, allergen avoidance counseling is how we treat nickel allergy,” she said. “The regulatory CD4-positive CD25-positive T cells (Tregs) modulate nickel sensitivity in humans, and topical application of calcipotriol induces Treg cells to prevent both the induction and elicitation of contact hypersensitivity in mice. It’s [also] been shown that topical vitamin D analogues prevented topical sensitization to DNCB [dinitrochlorobenzene] in humans: a very potent sensitizer,” she noted (Arch. Dermatol. 2006;142:1332-4).
In an effort to investigate whether topical immune modulators can stop preestablished contact hypersensitivity to nickel, Dr. de Gannes and her associates recruited 24 volunteers to participate in a double-blind, controlled trial, and randomized them to one of four groups: petrolatum ointment, betamethasone dipropionate ointment, calcipotriol ointment, and the combination of betamethasone dipropionate and calcipotriol ointments. “We first do a nickel patch test on the distal forearm to confirm that this person is sensitized to nickel,” she explained. “That’s our confirmation stage. On the opposite arm, we randomize them to one of the four groups of ointment, and we instruct them to apply a measured amount of ointment in a defined area twice daily for a week. They come back to us at the end of that week, and we repeat the nickel patch test where they applied their ointment to see whether they react or not.”
So far, preliminary results from 13 patients showed that application of some of the topical products induced tolerance and decreased reactivity to nickel, “but we’ve not yet been able to desensitize patients,” Dr. de Gannes noted. “This is just an interim analysis, and we have not unblinded the study yet. Hopefully we’ll have more meaningful results within the next year.”
The strategy is clinically relevant, she continued, because “we have hairstylists, for example, who come to us, allergic to the chemicals that they’re using. They really want to get back to their job. If this is a hand dermatitis caused by nickel or other contact allergens, and I can possibly give that hairstylist an ointment to apply to her hands in the morning and night and get back to her job, that’s a happy worker. That scenario would be a successful clinical outcome of this research, but we have a lot more work to do.”
Dr. de Gannes said that she had no relevant financial conflicts of interest to disclose.
On Twitter @dougbrunk
EXPERT ANALYSIS AT PDA 2014
Beta-blockers expand treatment options for infantile hemangiomas
VANCOUVER, B.C. – Propranolol may have revolutionized the treatment of infantile hemangiomas over the past decade, but other beta-blockers are making inroads in the treatment of these and other pediatric dermatologic disorders.
One such beta-blocker is atenolol, a hydrophilic cardioselective agent that acts principally on beta1-adrenergic receptors, “and theoretically has less chance of hypoglycemia and bronchoconstriction,” Dr. Joseph M. Lam said at the annual meeting of the Pacific Dermatologic Association. Atenolol does not cross the blood-brain barrier and features once-daily dosing, he noted.
A recent noninferiority trial in 23 patients with infantile hemangiomas compared atenolol 1 mg/kg/day with propranolol 2 mg/kg/day, and followed the patients for 6 months (J. Am. Acad. Dermatol. 2014;70:1045-9). Patients in both groups achieved a similar rate of complete response (54% in the atenolol group, compared with 60% in the propranolol group) and there were no significant adverse effects in either group. “There was rebound growth in 26% of patients once the medication was withdrawn,” said Dr. Lam of the department of pediatrics at British Columbia Children’s Hospital, Vancouver, who was not affiliated with the study. “Initially there was more rebound growth in the propranolol group versus the atenolol group (four vs. two cases, respectively), but that was not significant.”
Another study compared oral nadolol with propranolol in patients aged 1-12 months: 10 on nadolol and 9 matched controls on propranolol (Br. J. Dermatol; 2013:168:222-4). After 24 weeks of treatment patients in the nadolol group had statistically superior lesion shrinkage, compared with those in the propranolol group (P less than .0001). Dr. Lam described nadolol as a nonselective beta-blocker that “has no intrinsic sympathomimetic activity, little myocardial depressant activity, and does not cross the blood-brain barrier. So theoretically, you have less sleep disturbance than with propranolol. Practically, it’s easier dosing than propranolol. It’s 2 mg/kg per day and you divide that b.i.d. The solution is 10 mg/mL.”
Researchers also are studying topical application of beta-blockers for hemangiomas and other skin conditions, Dr. Lam noted. A pilot study of six patients with infantile hemangiomas on the face and neck demonstrated that twice-daily topical administration of timolol maleate 0.5% was safe and effective (Arch. Dermatol. 2010;146:564-5). Dr. Lam characterized timolol as “a hydrophilic molecule that permeates poorly across intact skin, but doesn’t work great for deep hemangiomas. It’s a good choice for superficial hemangiomas, and anyone can use this.”
A larger, retrospective, multicenter cohort study of timolol maleate 0.5% or 0.1% gel-forming solution for infantile hemangiomas also demonstrated positive results (Pediatr. Dermatol. 2012; 29:28-31). In that study, 72 of 73 treated patients improved, with better response seen in those who received the 0.5% solution.
In another pilot study, Chinese researchers assessed the efficacy of fractional carbon dioxide laser–assisted drug delivery of topical timolol solution for the treatment of deep infantile hemangioma (Pediatr. Dermatol. 2014;31:286-91). The regimen consisted of one pass without overlap delivered from a 10,600-nm fractional CO2 laser to a .12-mm spot size with a single pulse of 25-30 mJ. The researchers rated the results as “excellent” in 44% of patients. “good” in 44%, and “moderate” in 11%. Plasma timolol levels were detectable in all patients.
Additional data from an unrelated case series found that use of topical timolol successfully treated pediatric pyogenic granulomas (Pediatric Dermatol. 2014; 31:203-7). The agent “doesn’t work as fast as with hemangiomas, but it works as well, which is great because most pyogenic granulomas in young children are on the face or neck area,” Dr. Lam noted. “Some took up to 6 months to respond, but all patients in this series had no further bleeding. That’s usually the main concern for families.”
Current evidence suggests that timolol does not work well for port wine stains and other vascular malformations. To date, it has shown mixed results for other vascular tumors such as kaposiform hemangioendothelioma, tufted angioma, and Kasabach-Merritt phenomenon.
Dr. Lam disclosed that he is a member of the scientific advisory board for Johnson & Johnson, and is a speaker for the company. He also is a member of the Eczema Society of Canada’s Board of Directors.
VANCOUVER, B.C. – Propranolol may have revolutionized the treatment of infantile hemangiomas over the past decade, but other beta-blockers are making inroads in the treatment of these and other pediatric dermatologic disorders.
One such beta-blocker is atenolol, a hydrophilic cardioselective agent that acts principally on beta1-adrenergic receptors, “and theoretically has less chance of hypoglycemia and bronchoconstriction,” Dr. Joseph M. Lam said at the annual meeting of the Pacific Dermatologic Association. Atenolol does not cross the blood-brain barrier and features once-daily dosing, he noted.
A recent noninferiority trial in 23 patients with infantile hemangiomas compared atenolol 1 mg/kg/day with propranolol 2 mg/kg/day, and followed the patients for 6 months (J. Am. Acad. Dermatol. 2014;70:1045-9). Patients in both groups achieved a similar rate of complete response (54% in the atenolol group, compared with 60% in the propranolol group) and there were no significant adverse effects in either group. “There was rebound growth in 26% of patients once the medication was withdrawn,” said Dr. Lam of the department of pediatrics at British Columbia Children’s Hospital, Vancouver, who was not affiliated with the study. “Initially there was more rebound growth in the propranolol group versus the atenolol group (four vs. two cases, respectively), but that was not significant.”
Another study compared oral nadolol with propranolol in patients aged 1-12 months: 10 on nadolol and 9 matched controls on propranolol (Br. J. Dermatol; 2013:168:222-4). After 24 weeks of treatment patients in the nadolol group had statistically superior lesion shrinkage, compared with those in the propranolol group (P less than .0001). Dr. Lam described nadolol as a nonselective beta-blocker that “has no intrinsic sympathomimetic activity, little myocardial depressant activity, and does not cross the blood-brain barrier. So theoretically, you have less sleep disturbance than with propranolol. Practically, it’s easier dosing than propranolol. It’s 2 mg/kg per day and you divide that b.i.d. The solution is 10 mg/mL.”
Researchers also are studying topical application of beta-blockers for hemangiomas and other skin conditions, Dr. Lam noted. A pilot study of six patients with infantile hemangiomas on the face and neck demonstrated that twice-daily topical administration of timolol maleate 0.5% was safe and effective (Arch. Dermatol. 2010;146:564-5). Dr. Lam characterized timolol as “a hydrophilic molecule that permeates poorly across intact skin, but doesn’t work great for deep hemangiomas. It’s a good choice for superficial hemangiomas, and anyone can use this.”
A larger, retrospective, multicenter cohort study of timolol maleate 0.5% or 0.1% gel-forming solution for infantile hemangiomas also demonstrated positive results (Pediatr. Dermatol. 2012; 29:28-31). In that study, 72 of 73 treated patients improved, with better response seen in those who received the 0.5% solution.
In another pilot study, Chinese researchers assessed the efficacy of fractional carbon dioxide laser–assisted drug delivery of topical timolol solution for the treatment of deep infantile hemangioma (Pediatr. Dermatol. 2014;31:286-91). The regimen consisted of one pass without overlap delivered from a 10,600-nm fractional CO2 laser to a .12-mm spot size with a single pulse of 25-30 mJ. The researchers rated the results as “excellent” in 44% of patients. “good” in 44%, and “moderate” in 11%. Plasma timolol levels were detectable in all patients.
Additional data from an unrelated case series found that use of topical timolol successfully treated pediatric pyogenic granulomas (Pediatric Dermatol. 2014; 31:203-7). The agent “doesn’t work as fast as with hemangiomas, but it works as well, which is great because most pyogenic granulomas in young children are on the face or neck area,” Dr. Lam noted. “Some took up to 6 months to respond, but all patients in this series had no further bleeding. That’s usually the main concern for families.”
Current evidence suggests that timolol does not work well for port wine stains and other vascular malformations. To date, it has shown mixed results for other vascular tumors such as kaposiform hemangioendothelioma, tufted angioma, and Kasabach-Merritt phenomenon.
Dr. Lam disclosed that he is a member of the scientific advisory board for Johnson & Johnson, and is a speaker for the company. He also is a member of the Eczema Society of Canada’s Board of Directors.
VANCOUVER, B.C. – Propranolol may have revolutionized the treatment of infantile hemangiomas over the past decade, but other beta-blockers are making inroads in the treatment of these and other pediatric dermatologic disorders.
One such beta-blocker is atenolol, a hydrophilic cardioselective agent that acts principally on beta1-adrenergic receptors, “and theoretically has less chance of hypoglycemia and bronchoconstriction,” Dr. Joseph M. Lam said at the annual meeting of the Pacific Dermatologic Association. Atenolol does not cross the blood-brain barrier and features once-daily dosing, he noted.
A recent noninferiority trial in 23 patients with infantile hemangiomas compared atenolol 1 mg/kg/day with propranolol 2 mg/kg/day, and followed the patients for 6 months (J. Am. Acad. Dermatol. 2014;70:1045-9). Patients in both groups achieved a similar rate of complete response (54% in the atenolol group, compared with 60% in the propranolol group) and there were no significant adverse effects in either group. “There was rebound growth in 26% of patients once the medication was withdrawn,” said Dr. Lam of the department of pediatrics at British Columbia Children’s Hospital, Vancouver, who was not affiliated with the study. “Initially there was more rebound growth in the propranolol group versus the atenolol group (four vs. two cases, respectively), but that was not significant.”
Another study compared oral nadolol with propranolol in patients aged 1-12 months: 10 on nadolol and 9 matched controls on propranolol (Br. J. Dermatol; 2013:168:222-4). After 24 weeks of treatment patients in the nadolol group had statistically superior lesion shrinkage, compared with those in the propranolol group (P less than .0001). Dr. Lam described nadolol as a nonselective beta-blocker that “has no intrinsic sympathomimetic activity, little myocardial depressant activity, and does not cross the blood-brain barrier. So theoretically, you have less sleep disturbance than with propranolol. Practically, it’s easier dosing than propranolol. It’s 2 mg/kg per day and you divide that b.i.d. The solution is 10 mg/mL.”
Researchers also are studying topical application of beta-blockers for hemangiomas and other skin conditions, Dr. Lam noted. A pilot study of six patients with infantile hemangiomas on the face and neck demonstrated that twice-daily topical administration of timolol maleate 0.5% was safe and effective (Arch. Dermatol. 2010;146:564-5). Dr. Lam characterized timolol as “a hydrophilic molecule that permeates poorly across intact skin, but doesn’t work great for deep hemangiomas. It’s a good choice for superficial hemangiomas, and anyone can use this.”
A larger, retrospective, multicenter cohort study of timolol maleate 0.5% or 0.1% gel-forming solution for infantile hemangiomas also demonstrated positive results (Pediatr. Dermatol. 2012; 29:28-31). In that study, 72 of 73 treated patients improved, with better response seen in those who received the 0.5% solution.
In another pilot study, Chinese researchers assessed the efficacy of fractional carbon dioxide laser–assisted drug delivery of topical timolol solution for the treatment of deep infantile hemangioma (Pediatr. Dermatol. 2014;31:286-91). The regimen consisted of one pass without overlap delivered from a 10,600-nm fractional CO2 laser to a .12-mm spot size with a single pulse of 25-30 mJ. The researchers rated the results as “excellent” in 44% of patients. “good” in 44%, and “moderate” in 11%. Plasma timolol levels were detectable in all patients.
Additional data from an unrelated case series found that use of topical timolol successfully treated pediatric pyogenic granulomas (Pediatric Dermatol. 2014; 31:203-7). The agent “doesn’t work as fast as with hemangiomas, but it works as well, which is great because most pyogenic granulomas in young children are on the face or neck area,” Dr. Lam noted. “Some took up to 6 months to respond, but all patients in this series had no further bleeding. That’s usually the main concern for families.”
Current evidence suggests that timolol does not work well for port wine stains and other vascular malformations. To date, it has shown mixed results for other vascular tumors such as kaposiform hemangioendothelioma, tufted angioma, and Kasabach-Merritt phenomenon.
Dr. Lam disclosed that he is a member of the scientific advisory board for Johnson & Johnson, and is a speaker for the company. He also is a member of the Eczema Society of Canada’s Board of Directors.
‘Shotgun’ skin prick testing for food allergy held flawed
VANCOUVER, B.C. – The “shotgun” style of skin prick testing in children and adolescents with suspected IgE-mediated food allergy shows sensitization, but not necessarily allergy, according to Dr. James Bergman.
A positive skin test measures the presence of a specific IgE antibody, which does not necessarily equate to an allergy. Consequently, children may have multiple positive skin prick tests yet clinically tolerate the tested food, he said. “Sensitization is just the presence of a specific IgE to a food. Allergy is sensitization plus signs or symptoms upon exposure to the food.”
Dr. Bergman, who also holds a faculty position in the department of dermatology and skin science at the University of British Columbia, said the practice of shotgun skin prick testing can lead to unnecessary avoidance of specific foods. One group of researchers conducted oral food challenge tests in 125 children aged 1-9 years with a diagnosis of food allergy based on IgE tests. Nearly all of them (93%) had no reactivity when challenged with the suspect food (J. Peds. 2011; 158[4]:578-83). “Ninety-three percent of the children would have been avoiding their ‘allergic foods’ perhaps indefinitely,” said Dr. Bergman, who was not involved with the study.
“The general rule is, if you’re not having clinical symptoms that suggest an IgE-mediated reaction, then don’t test,” Dr. Bergman, a dermatologist who practices in Vancouver, said at the annual meeting of the Pacific Dermatologic Association.
“I explain to parents that if they want to test for a food in the situation where there is no IgE-mediated reaction, then it can be done, but there is a significant risk of a false positive or ‘fake allergy,’ ” he said. “In this situation the only way of knowing for sure whether it is an allergy is to undertake a formal oral food challenge, which is the (highest) standard for diagnosing food allergy.”
Telltale symptoms of an IgE-mediated food allergy include hives, vomiting, diarrhea, breathing problems, and change in level of consciousness. “These symptoms typically occur within minutes of ingestion, sometimes within 30 minutes and rarely up to 2 hours,” Dr. Bergman said. “If it’s beyond 2 hours, it’s unlikely to be IgE mediated.”
“If someone has a true food allergy, advise them to avoid the culprit food, give them an epinephrine injector, and refer them to an allergist for testing, education, and follow-up,” he advised.
Food allergies affect 6%-8% of pediatric patients, yet 35%- 90% of families self-report food allergies depending on the population studied. Milk, egg, wheat, peanuts, nuts, soy, and seafood account for 90% of food allergens. Most children outgrow allergy to milk, egg, wheat, and soy, while few outgrow allergy to peanuts, nuts, fish, and shellfish.
Most patients and many physicians believe that eczema is caused by food allergies. In fact, only a small minority of patients have food allergies that directly cause eczema. “Eczema could occur secondary to scratching induced by an urticarial food reaction or by a primary irritant reaction, but food directly causing isolated eczema is rare,” Dr. Bergman said. “The belief that food allergies directly cause eczema is completely understandable given that eczema patients do have an increased rate of allergies, the cyclic pattern of eczema, and the parent’s desire to find a cause for the child’s rash. Eczema’s cyclic nature can easily lead to a specific food being implicated due to recall bias. The parent will remember the flares that occurred with exposure to the specific food, while not recalling the times when the food was tolerated or the flares that were not associated with the food.”
If a parent is worried about a food causing eczema and there are no IgE mediated symptoms, then instead of testing he will often recommend that the family keep a formal food symptom diary while they are intermittently ingesting the food of concern. “The vast majority of parents will see no consistent direct correlation with the food and they can feel comfortable with ongoing future ingestion,” he said.
Some clinicians are offering oral immune therapy to patients with IgE-mediated food allergy. Dr. Bergman characterized such practice as “risky” at this point in time. “It’s like the traditional allergy shots you’d get for your pollen allergy, except it’s done orally,” he explained. “Research is being done in this area by introducing small amounts [of the allergen], in an attempt to induce tolerance. The results are encouraging, but the problem is that patients can have bad reactions. We also don’t know how well or for how long it will work. At this point, while promising, the field is not yet ready for prime time.”
He also said there is no current evidence supporting IgG testing, Vega testing, or muscle strength testing in the investigation of suspected IgE-mediated food allergy. “What I tell patients is that if any of these tests identifies something, it probably identifies something that’s mild and very temporary, because in my experience patients with positive IgG tests are usually told to avoid the food for 1-4 months and then to reintroduce that food in a rotation basis. Avoidance of food allergens based on this type of testing is not necessary. However, for patients who still wish to practice short term avoidance of the food then this is fine provided the diet does not compromise nutrition.”
Dr. Bergman reported having no financial disclosures.
On Twitter @dougbrunk
VANCOUVER, B.C. – The “shotgun” style of skin prick testing in children and adolescents with suspected IgE-mediated food allergy shows sensitization, but not necessarily allergy, according to Dr. James Bergman.
A positive skin test measures the presence of a specific IgE antibody, which does not necessarily equate to an allergy. Consequently, children may have multiple positive skin prick tests yet clinically tolerate the tested food, he said. “Sensitization is just the presence of a specific IgE to a food. Allergy is sensitization plus signs or symptoms upon exposure to the food.”
Dr. Bergman, who also holds a faculty position in the department of dermatology and skin science at the University of British Columbia, said the practice of shotgun skin prick testing can lead to unnecessary avoidance of specific foods. One group of researchers conducted oral food challenge tests in 125 children aged 1-9 years with a diagnosis of food allergy based on IgE tests. Nearly all of them (93%) had no reactivity when challenged with the suspect food (J. Peds. 2011; 158[4]:578-83). “Ninety-three percent of the children would have been avoiding their ‘allergic foods’ perhaps indefinitely,” said Dr. Bergman, who was not involved with the study.
“The general rule is, if you’re not having clinical symptoms that suggest an IgE-mediated reaction, then don’t test,” Dr. Bergman, a dermatologist who practices in Vancouver, said at the annual meeting of the Pacific Dermatologic Association.
“I explain to parents that if they want to test for a food in the situation where there is no IgE-mediated reaction, then it can be done, but there is a significant risk of a false positive or ‘fake allergy,’ ” he said. “In this situation the only way of knowing for sure whether it is an allergy is to undertake a formal oral food challenge, which is the (highest) standard for diagnosing food allergy.”
Telltale symptoms of an IgE-mediated food allergy include hives, vomiting, diarrhea, breathing problems, and change in level of consciousness. “These symptoms typically occur within minutes of ingestion, sometimes within 30 minutes and rarely up to 2 hours,” Dr. Bergman said. “If it’s beyond 2 hours, it’s unlikely to be IgE mediated.”
“If someone has a true food allergy, advise them to avoid the culprit food, give them an epinephrine injector, and refer them to an allergist for testing, education, and follow-up,” he advised.
Food allergies affect 6%-8% of pediatric patients, yet 35%- 90% of families self-report food allergies depending on the population studied. Milk, egg, wheat, peanuts, nuts, soy, and seafood account for 90% of food allergens. Most children outgrow allergy to milk, egg, wheat, and soy, while few outgrow allergy to peanuts, nuts, fish, and shellfish.
Most patients and many physicians believe that eczema is caused by food allergies. In fact, only a small minority of patients have food allergies that directly cause eczema. “Eczema could occur secondary to scratching induced by an urticarial food reaction or by a primary irritant reaction, but food directly causing isolated eczema is rare,” Dr. Bergman said. “The belief that food allergies directly cause eczema is completely understandable given that eczema patients do have an increased rate of allergies, the cyclic pattern of eczema, and the parent’s desire to find a cause for the child’s rash. Eczema’s cyclic nature can easily lead to a specific food being implicated due to recall bias. The parent will remember the flares that occurred with exposure to the specific food, while not recalling the times when the food was tolerated or the flares that were not associated with the food.”
If a parent is worried about a food causing eczema and there are no IgE mediated symptoms, then instead of testing he will often recommend that the family keep a formal food symptom diary while they are intermittently ingesting the food of concern. “The vast majority of parents will see no consistent direct correlation with the food and they can feel comfortable with ongoing future ingestion,” he said.
Some clinicians are offering oral immune therapy to patients with IgE-mediated food allergy. Dr. Bergman characterized such practice as “risky” at this point in time. “It’s like the traditional allergy shots you’d get for your pollen allergy, except it’s done orally,” he explained. “Research is being done in this area by introducing small amounts [of the allergen], in an attempt to induce tolerance. The results are encouraging, but the problem is that patients can have bad reactions. We also don’t know how well or for how long it will work. At this point, while promising, the field is not yet ready for prime time.”
He also said there is no current evidence supporting IgG testing, Vega testing, or muscle strength testing in the investigation of suspected IgE-mediated food allergy. “What I tell patients is that if any of these tests identifies something, it probably identifies something that’s mild and very temporary, because in my experience patients with positive IgG tests are usually told to avoid the food for 1-4 months and then to reintroduce that food in a rotation basis. Avoidance of food allergens based on this type of testing is not necessary. However, for patients who still wish to practice short term avoidance of the food then this is fine provided the diet does not compromise nutrition.”
Dr. Bergman reported having no financial disclosures.
On Twitter @dougbrunk
VANCOUVER, B.C. – The “shotgun” style of skin prick testing in children and adolescents with suspected IgE-mediated food allergy shows sensitization, but not necessarily allergy, according to Dr. James Bergman.
A positive skin test measures the presence of a specific IgE antibody, which does not necessarily equate to an allergy. Consequently, children may have multiple positive skin prick tests yet clinically tolerate the tested food, he said. “Sensitization is just the presence of a specific IgE to a food. Allergy is sensitization plus signs or symptoms upon exposure to the food.”
Dr. Bergman, who also holds a faculty position in the department of dermatology and skin science at the University of British Columbia, said the practice of shotgun skin prick testing can lead to unnecessary avoidance of specific foods. One group of researchers conducted oral food challenge tests in 125 children aged 1-9 years with a diagnosis of food allergy based on IgE tests. Nearly all of them (93%) had no reactivity when challenged with the suspect food (J. Peds. 2011; 158[4]:578-83). “Ninety-three percent of the children would have been avoiding their ‘allergic foods’ perhaps indefinitely,” said Dr. Bergman, who was not involved with the study.
“The general rule is, if you’re not having clinical symptoms that suggest an IgE-mediated reaction, then don’t test,” Dr. Bergman, a dermatologist who practices in Vancouver, said at the annual meeting of the Pacific Dermatologic Association.
“I explain to parents that if they want to test for a food in the situation where there is no IgE-mediated reaction, then it can be done, but there is a significant risk of a false positive or ‘fake allergy,’ ” he said. “In this situation the only way of knowing for sure whether it is an allergy is to undertake a formal oral food challenge, which is the (highest) standard for diagnosing food allergy.”
Telltale symptoms of an IgE-mediated food allergy include hives, vomiting, diarrhea, breathing problems, and change in level of consciousness. “These symptoms typically occur within minutes of ingestion, sometimes within 30 minutes and rarely up to 2 hours,” Dr. Bergman said. “If it’s beyond 2 hours, it’s unlikely to be IgE mediated.”
“If someone has a true food allergy, advise them to avoid the culprit food, give them an epinephrine injector, and refer them to an allergist for testing, education, and follow-up,” he advised.
Food allergies affect 6%-8% of pediatric patients, yet 35%- 90% of families self-report food allergies depending on the population studied. Milk, egg, wheat, peanuts, nuts, soy, and seafood account for 90% of food allergens. Most children outgrow allergy to milk, egg, wheat, and soy, while few outgrow allergy to peanuts, nuts, fish, and shellfish.
Most patients and many physicians believe that eczema is caused by food allergies. In fact, only a small minority of patients have food allergies that directly cause eczema. “Eczema could occur secondary to scratching induced by an urticarial food reaction or by a primary irritant reaction, but food directly causing isolated eczema is rare,” Dr. Bergman said. “The belief that food allergies directly cause eczema is completely understandable given that eczema patients do have an increased rate of allergies, the cyclic pattern of eczema, and the parent’s desire to find a cause for the child’s rash. Eczema’s cyclic nature can easily lead to a specific food being implicated due to recall bias. The parent will remember the flares that occurred with exposure to the specific food, while not recalling the times when the food was tolerated or the flares that were not associated with the food.”
If a parent is worried about a food causing eczema and there are no IgE mediated symptoms, then instead of testing he will often recommend that the family keep a formal food symptom diary while they are intermittently ingesting the food of concern. “The vast majority of parents will see no consistent direct correlation with the food and they can feel comfortable with ongoing future ingestion,” he said.
Some clinicians are offering oral immune therapy to patients with IgE-mediated food allergy. Dr. Bergman characterized such practice as “risky” at this point in time. “It’s like the traditional allergy shots you’d get for your pollen allergy, except it’s done orally,” he explained. “Research is being done in this area by introducing small amounts [of the allergen], in an attempt to induce tolerance. The results are encouraging, but the problem is that patients can have bad reactions. We also don’t know how well or for how long it will work. At this point, while promising, the field is not yet ready for prime time.”
He also said there is no current evidence supporting IgG testing, Vega testing, or muscle strength testing in the investigation of suspected IgE-mediated food allergy. “What I tell patients is that if any of these tests identifies something, it probably identifies something that’s mild and very temporary, because in my experience patients with positive IgG tests are usually told to avoid the food for 1-4 months and then to reintroduce that food in a rotation basis. Avoidance of food allergens based on this type of testing is not necessary. However, for patients who still wish to practice short term avoidance of the food then this is fine provided the diet does not compromise nutrition.”
Dr. Bergman reported having no financial disclosures.
On Twitter @dougbrunk
EXPERT ANALYSIS FROM THE PDA ANNUAL MEETING
Look to presentation, not pathology, for dermatomyositis diagnosis
VANCOUVER, B.C.– On histology, pathologists are unable to reliably differentiate between cutaneous lupus erythematosus and dermatomyositis. So it falls to clinicians to sort out what’s what based on the patient’s clinical presentation.
“Dermatomyositis is a disease of muscle and skin, but as dermatologists we should view this as primarily a dermatologic disorder, because the diagnosis is made on the skin,” Dr. Jan Dutz said at the annual meeting of the Pacific Dermatologic Association. “The pathology is not diagnostic. Therefore, it’s up to you to make the diagnosis based on the characteristic patterns of dermatomyositis: the changes of the violaceous erythema on the face and arms, the Gottron’s papules, and the changes in blood vessels.”
Enlarged and decreased capillaries are a hallmark clinical feature of dermatomyositis, which can be observed by examining the proximal nail folds. “It turns out that you can look at those capillaries and predict the severity of the disease, so that those who have improvement in the capillaries following early treatment usually have less severe disease,” said Dr. Dutz, professor of dermatology and skin science at the University of British Columbia, Vancouver.
Like cutaneous lupus erythematosus, dermatomyositis is a type 1 interferon-mediated disease. The genes inducible by type 1 interferon alpha have increased expression in muscle and in peripheral blood lymphocyte, and interferon alpha administration can induce disease. Researchers recently described a new subset of dermatomyositis based on an investigation of 77 patients with the disorder (J. Am. Acad. Dermatol. 2011;65:25-34). Of these, 10 (13%) had anti-MDA-5 (melanoma differentiation associated gene 5) antibodies, which are antibodies to a protein related to the interferon pathway. Most of the patients (8 of 10) tested negative for antinuclear antibody. The clinical features were palmar papules, ulcerations (usually on the back of the hands), MDA-5 antibody, and an increased risk of interstitial lung disease. “Ulceration had an odds ratio of almost 20 with being associated with this antibody and this syndrome,” said Dr. Dutz, who was not involved with the study. “So if you see these papules and you see these ulcerations on the hands, it increases the chance of interstitial lung disease.”
These clinical features also have been observed in cases of juvenile dermatomyositis (Arthritis Res. Ther. 2014;16:R138). “These patients get skin ulcerations, oral ulcerations, and have a high incidence for arthritis, mild muscle disease, and interstitial lung disease,” he said.
Dr. Dutz said that he often turns to antimalarial agents as the first treatment option for patients with dermatomyositis. If they don’t respond, he typically switches them to methotrexate. “If that doesn’t work, I usually try mycophenolate mofetil or IVIG [intravenous immunoglobulin], which is one of the most effective treatments for dermatomyositis,” he said. “Studies keep on emphasizing this. There’s also some interest in using rituximab in patients with resistant disease.”
Dr. Dutz disclosed that he is an advisory board member for Janssen, AbbVie, Amgen, Leo Pharma, Roche, and Novartis. He has also conducted clinical trials for Centocor and Ono Pharmaceutical Co.
On Twitter @dougbrunk
VANCOUVER, B.C.– On histology, pathologists are unable to reliably differentiate between cutaneous lupus erythematosus and dermatomyositis. So it falls to clinicians to sort out what’s what based on the patient’s clinical presentation.
“Dermatomyositis is a disease of muscle and skin, but as dermatologists we should view this as primarily a dermatologic disorder, because the diagnosis is made on the skin,” Dr. Jan Dutz said at the annual meeting of the Pacific Dermatologic Association. “The pathology is not diagnostic. Therefore, it’s up to you to make the diagnosis based on the characteristic patterns of dermatomyositis: the changes of the violaceous erythema on the face and arms, the Gottron’s papules, and the changes in blood vessels.”
Enlarged and decreased capillaries are a hallmark clinical feature of dermatomyositis, which can be observed by examining the proximal nail folds. “It turns out that you can look at those capillaries and predict the severity of the disease, so that those who have improvement in the capillaries following early treatment usually have less severe disease,” said Dr. Dutz, professor of dermatology and skin science at the University of British Columbia, Vancouver.
Like cutaneous lupus erythematosus, dermatomyositis is a type 1 interferon-mediated disease. The genes inducible by type 1 interferon alpha have increased expression in muscle and in peripheral blood lymphocyte, and interferon alpha administration can induce disease. Researchers recently described a new subset of dermatomyositis based on an investigation of 77 patients with the disorder (J. Am. Acad. Dermatol. 2011;65:25-34). Of these, 10 (13%) had anti-MDA-5 (melanoma differentiation associated gene 5) antibodies, which are antibodies to a protein related to the interferon pathway. Most of the patients (8 of 10) tested negative for antinuclear antibody. The clinical features were palmar papules, ulcerations (usually on the back of the hands), MDA-5 antibody, and an increased risk of interstitial lung disease. “Ulceration had an odds ratio of almost 20 with being associated with this antibody and this syndrome,” said Dr. Dutz, who was not involved with the study. “So if you see these papules and you see these ulcerations on the hands, it increases the chance of interstitial lung disease.”
These clinical features also have been observed in cases of juvenile dermatomyositis (Arthritis Res. Ther. 2014;16:R138). “These patients get skin ulcerations, oral ulcerations, and have a high incidence for arthritis, mild muscle disease, and interstitial lung disease,” he said.
Dr. Dutz said that he often turns to antimalarial agents as the first treatment option for patients with dermatomyositis. If they don’t respond, he typically switches them to methotrexate. “If that doesn’t work, I usually try mycophenolate mofetil or IVIG [intravenous immunoglobulin], which is one of the most effective treatments for dermatomyositis,” he said. “Studies keep on emphasizing this. There’s also some interest in using rituximab in patients with resistant disease.”
Dr. Dutz disclosed that he is an advisory board member for Janssen, AbbVie, Amgen, Leo Pharma, Roche, and Novartis. He has also conducted clinical trials for Centocor and Ono Pharmaceutical Co.
On Twitter @dougbrunk
VANCOUVER, B.C.– On histology, pathologists are unable to reliably differentiate between cutaneous lupus erythematosus and dermatomyositis. So it falls to clinicians to sort out what’s what based on the patient’s clinical presentation.
“Dermatomyositis is a disease of muscle and skin, but as dermatologists we should view this as primarily a dermatologic disorder, because the diagnosis is made on the skin,” Dr. Jan Dutz said at the annual meeting of the Pacific Dermatologic Association. “The pathology is not diagnostic. Therefore, it’s up to you to make the diagnosis based on the characteristic patterns of dermatomyositis: the changes of the violaceous erythema on the face and arms, the Gottron’s papules, and the changes in blood vessels.”
Enlarged and decreased capillaries are a hallmark clinical feature of dermatomyositis, which can be observed by examining the proximal nail folds. “It turns out that you can look at those capillaries and predict the severity of the disease, so that those who have improvement in the capillaries following early treatment usually have less severe disease,” said Dr. Dutz, professor of dermatology and skin science at the University of British Columbia, Vancouver.
Like cutaneous lupus erythematosus, dermatomyositis is a type 1 interferon-mediated disease. The genes inducible by type 1 interferon alpha have increased expression in muscle and in peripheral blood lymphocyte, and interferon alpha administration can induce disease. Researchers recently described a new subset of dermatomyositis based on an investigation of 77 patients with the disorder (J. Am. Acad. Dermatol. 2011;65:25-34). Of these, 10 (13%) had anti-MDA-5 (melanoma differentiation associated gene 5) antibodies, which are antibodies to a protein related to the interferon pathway. Most of the patients (8 of 10) tested negative for antinuclear antibody. The clinical features were palmar papules, ulcerations (usually on the back of the hands), MDA-5 antibody, and an increased risk of interstitial lung disease. “Ulceration had an odds ratio of almost 20 with being associated with this antibody and this syndrome,” said Dr. Dutz, who was not involved with the study. “So if you see these papules and you see these ulcerations on the hands, it increases the chance of interstitial lung disease.”
These clinical features also have been observed in cases of juvenile dermatomyositis (Arthritis Res. Ther. 2014;16:R138). “These patients get skin ulcerations, oral ulcerations, and have a high incidence for arthritis, mild muscle disease, and interstitial lung disease,” he said.
Dr. Dutz said that he often turns to antimalarial agents as the first treatment option for patients with dermatomyositis. If they don’t respond, he typically switches them to methotrexate. “If that doesn’t work, I usually try mycophenolate mofetil or IVIG [intravenous immunoglobulin], which is one of the most effective treatments for dermatomyositis,” he said. “Studies keep on emphasizing this. There’s also some interest in using rituximab in patients with resistant disease.”
Dr. Dutz disclosed that he is an advisory board member for Janssen, AbbVie, Amgen, Leo Pharma, Roche, and Novartis. He has also conducted clinical trials for Centocor and Ono Pharmaceutical Co.
On Twitter @dougbrunk
EXPERT ANALYSIS FROM PDA 2014
Ergonomic solutions limit Mohs surgeons’ aches and pains
VANCOUVER, B.C. – Attention to ergonomics may reduce risks for a wide range of musculoskeletal problems and headaches that afflict Mohs surgeons, Dr. Mariusz Sapijaszko said at the annual meeting of the Pacific Dermatologic Association.
The demands of performing Mohs surgery were first detailed in a study of 17 Mohs surgeons at the Mayo Clinic. Nearly two-thirds (59%) had chronic neck pain, half had shoulder pain (53%), and nearly half had lower back pain (41%). About a third experienced eye fatigue and one-fourth had headaches (Dermatol. Surg. 2007;33:1304-13).
Since then, a survey of American College of Mohs Surgery members found that 90% reported some type of musculoskeletal symptoms or injuries (Dermatol. Surg. 2012;38:240-8).
Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alberta, offered the following ergonomic tips based on his own clinical practice as well as recommendations offered by researchers who conducted the 2007 Mayo Clinic study and those focused on optimizing the operating theater environment (ANZ J. Surg. 2010;80:917-24).
To reduce neck-related symptoms:
• Keep your gaze angle between 15 and 30 degrees below horizontal.
• Position the patient close to you.
• Take short surgery breaks to stretch and adjust your posture.
• Use a stool with sternal support or a sit/stand stool.
To avoid lower back pain:
• Change positions frequently.
• Use a foot rest or foot rail.
• Use a stool with sternal support.
To prevent eye fatigue:
• Decrease the intensity of surgical lighting with a dimmer switch.
• Use goggles or glasses that contain antiglare film.
• Use brushed steel instead of polished steel instruments.
To minimize peripheral edema:
• Wear compression stockings.
• Use a foot rest or foot rail.
• Use gel insoles, or antifatigue floor mats.
To reduce headaches:
• Keep ambient noise below 56 dB.
• Select music based on the preference of the surgeon, patient, and other OR staff.
To optimize your comfort, optimize patient comfort:
• Select a procedure table that has adjustable positions for knee, hip, and neck angles as well as good lower back and lumbar support and a comfortable pillow type and position.
"You need to lie down on your own table and find out how good or bad it feels," Dr. Sapijaszko advised. He favors fully adjustable tables such as those used in the massage industry, and recommends a 12-degree tilt for the patient’s head.
On Twitter @dougbrunk
VANCOUVER, B.C. – Attention to ergonomics may reduce risks for a wide range of musculoskeletal problems and headaches that afflict Mohs surgeons, Dr. Mariusz Sapijaszko said at the annual meeting of the Pacific Dermatologic Association.
The demands of performing Mohs surgery were first detailed in a study of 17 Mohs surgeons at the Mayo Clinic. Nearly two-thirds (59%) had chronic neck pain, half had shoulder pain (53%), and nearly half had lower back pain (41%). About a third experienced eye fatigue and one-fourth had headaches (Dermatol. Surg. 2007;33:1304-13).
Since then, a survey of American College of Mohs Surgery members found that 90% reported some type of musculoskeletal symptoms or injuries (Dermatol. Surg. 2012;38:240-8).
Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alberta, offered the following ergonomic tips based on his own clinical practice as well as recommendations offered by researchers who conducted the 2007 Mayo Clinic study and those focused on optimizing the operating theater environment (ANZ J. Surg. 2010;80:917-24).
To reduce neck-related symptoms:
• Keep your gaze angle between 15 and 30 degrees below horizontal.
• Position the patient close to you.
• Take short surgery breaks to stretch and adjust your posture.
• Use a stool with sternal support or a sit/stand stool.
To avoid lower back pain:
• Change positions frequently.
• Use a foot rest or foot rail.
• Use a stool with sternal support.
To prevent eye fatigue:
• Decrease the intensity of surgical lighting with a dimmer switch.
• Use goggles or glasses that contain antiglare film.
• Use brushed steel instead of polished steel instruments.
To minimize peripheral edema:
• Wear compression stockings.
• Use a foot rest or foot rail.
• Use gel insoles, or antifatigue floor mats.
To reduce headaches:
• Keep ambient noise below 56 dB.
• Select music based on the preference of the surgeon, patient, and other OR staff.
To optimize your comfort, optimize patient comfort:
• Select a procedure table that has adjustable positions for knee, hip, and neck angles as well as good lower back and lumbar support and a comfortable pillow type and position.
"You need to lie down on your own table and find out how good or bad it feels," Dr. Sapijaszko advised. He favors fully adjustable tables such as those used in the massage industry, and recommends a 12-degree tilt for the patient’s head.
On Twitter @dougbrunk
VANCOUVER, B.C. – Attention to ergonomics may reduce risks for a wide range of musculoskeletal problems and headaches that afflict Mohs surgeons, Dr. Mariusz Sapijaszko said at the annual meeting of the Pacific Dermatologic Association.
The demands of performing Mohs surgery were first detailed in a study of 17 Mohs surgeons at the Mayo Clinic. Nearly two-thirds (59%) had chronic neck pain, half had shoulder pain (53%), and nearly half had lower back pain (41%). About a third experienced eye fatigue and one-fourth had headaches (Dermatol. Surg. 2007;33:1304-13).
Since then, a survey of American College of Mohs Surgery members found that 90% reported some type of musculoskeletal symptoms or injuries (Dermatol. Surg. 2012;38:240-8).
Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alberta, offered the following ergonomic tips based on his own clinical practice as well as recommendations offered by researchers who conducted the 2007 Mayo Clinic study and those focused on optimizing the operating theater environment (ANZ J. Surg. 2010;80:917-24).
To reduce neck-related symptoms:
• Keep your gaze angle between 15 and 30 degrees below horizontal.
• Position the patient close to you.
• Take short surgery breaks to stretch and adjust your posture.
• Use a stool with sternal support or a sit/stand stool.
To avoid lower back pain:
• Change positions frequently.
• Use a foot rest or foot rail.
• Use a stool with sternal support.
To prevent eye fatigue:
• Decrease the intensity of surgical lighting with a dimmer switch.
• Use goggles or glasses that contain antiglare film.
• Use brushed steel instead of polished steel instruments.
To minimize peripheral edema:
• Wear compression stockings.
• Use a foot rest or foot rail.
• Use gel insoles, or antifatigue floor mats.
To reduce headaches:
• Keep ambient noise below 56 dB.
• Select music based on the preference of the surgeon, patient, and other OR staff.
To optimize your comfort, optimize patient comfort:
• Select a procedure table that has adjustable positions for knee, hip, and neck angles as well as good lower back and lumbar support and a comfortable pillow type and position.
"You need to lie down on your own table and find out how good or bad it feels," Dr. Sapijaszko advised. He favors fully adjustable tables such as those used in the massage industry, and recommends a 12-degree tilt for the patient’s head.
On Twitter @dougbrunk
EXPERT ANALYSIS AT THE PDA ANNUAL MEETING
Early treatment key to halting progression of cicatricial alopecia
VANCOUVER, B.C. – Cicatricial alopecia should be considered a "trichologic emergency," Dr. Jerry Shapiro advised at the annual meeting of the Pacific Dermatologic Association. The hair loss may be permanent, "so it’s important to get on top of this, and not just sit out the condition."
Cicatricial alopecia is characterized by a loss of follicular ostia with replacement by fibrous tissue. Primary cicatricial alopecia targets the hair follicle and involves preferential destruction of the follicular epithelium with sparing of interfollicular dermis. In secondary cicatricial alopecia, "the follicle is an innocent bystander" that is destroyed in the course of infectious tinea capitis, infiltrative diseases such as metastatic disease and sarcoidosis, trauma such as radiation exposure and burns, and inflammatory conditions such as pemphigus vulgaris.
The North American Hair Research Society consensus classification of cicatricial alopecia is based on the infiltrate: lymphocytic, neutrophilic, mixed, or nonspecific.
"We determine our treatment decisions based on the infiltrate," said Dr. Shapiro, whose New York– and Vancouver–based practices are devoted exclusively to hair and scalp disorders. "A biopsy can be crucial when you’re managing these patients, so you know how actively inflamed the lesions are and what the primary infiltrate is. We always take a 4-mm punch biopsy, and we may take two. We’ll do one for transverse sectioning and another one for longitudinal sectioning."
"Sometimes there’s (histologic) overlap between lupus erythematosus or lichen planopilaris," he said. The clinical and pathologic findings can be variable, so the differential diagnosis is difficult. "There are no cures, and the cause of these conditions is unknown."
Discoid lupus erythematosus often presents with atrophy and extensive hair loss. A hallmark feature is central follicular hyperkeratosis. If less than 10% of the scalp is involved, Dr. Shapiro uses ultrapotent topical corticosteroids such as clobetasol with or without triamcinolone acetonide (TCA) injections (10 mg/cc for a maximum total of 2 ccs per sitting once a month). "We inject into the areas that are red as well as the surrounding areas so that it doesn’t spread," he said.
If a patient responds to this regimen he continues to use it on an as-needed basis. For nonresponders, Dr. Shapiro resorts to hydroxychloroquine 200 mg b.i.d. or isotretinoin 40 mg b.i.d. Other alternatives can include topical tacrolimus. Others have used tazarotene and imiquimod, he said, but "I find the latter two too irritating."
For patients with 10% or greater scalp involvement, Dr. Shapiro uses hydroxychloroquine plus ultrapotent topical steroids, plus TCA injections, plus bridging therapy with prednisone, usually with 40 mg prednisone tapered.
Patients with lichen planopilaris typically present with peripheral hyperkeratosis, or frontal fibrosing alopecia, which is marked by loss of a strip of hair at the front and/or the sides of the scalp. Frontal fibrosing alopecia is "a silent epidemic. In Vancouver, I’m seeing about seven cases per day of this, and three to four cases per day in New York. Sometimes, the eyebrows are the first sign of hair loss. Many times it can go completely around the scalp, so it’s [considered] marginally fibrosing," Dr. Shapiro said.
Frontal fibrosing alopecia primarily affects postmenopausal women. "We think there is a hormonal component that is causing this, but there is also a trigger in the environment," Dr. Shapiro said. "We don’t know what the trigger is, but certain countries have less of it. China does not see that much of it, nor does Saudi Arabia."
Dr. Shapiro and his associates recently published a retrospective study of 62 cases of frontal fibrosing alopecia seen between January 2004 and March 2012. Of the 62 patients, 61 were women (Int. J. Dermatol. 2014 [doi:10.1111/ijd.12479]). Their average age was 61 years and the age of onset ranged from 18 to 81 years. In terms of symptoms, 22 (35%) patients were asymptomatic, 42 (68%) had a history of female pattern hair loss, and 50 (81%) patients’ eyebrows were affected.
In Dr. Shapiro’s experience, intralesional TCA with or without oral tetracycline or hydroxychloroquine may help to halt or slow the progression of frontal fibrosing alopecia. He typically uses intralesional Kenalog 2.5 mL/cc. "I do 30 injections for 3 ccs total: 0.1 cc/injection site and I go from one ear to the other," Dr. Shapiro said. "We’ll also use clobetasol solution at the beginning and taper to a betamethasone solution. Other things to consider are tacrolimus, Cetaphil cleanser, and finasteride."
Dr. Shapiro disclosed that he is a consultant to Johnson & Johnson, GSK/Stiefel, Allergan, MSD, and Applied Biology.
On Twitter @dougbrunk
VANCOUVER, B.C. – Cicatricial alopecia should be considered a "trichologic emergency," Dr. Jerry Shapiro advised at the annual meeting of the Pacific Dermatologic Association. The hair loss may be permanent, "so it’s important to get on top of this, and not just sit out the condition."
Cicatricial alopecia is characterized by a loss of follicular ostia with replacement by fibrous tissue. Primary cicatricial alopecia targets the hair follicle and involves preferential destruction of the follicular epithelium with sparing of interfollicular dermis. In secondary cicatricial alopecia, "the follicle is an innocent bystander" that is destroyed in the course of infectious tinea capitis, infiltrative diseases such as metastatic disease and sarcoidosis, trauma such as radiation exposure and burns, and inflammatory conditions such as pemphigus vulgaris.
The North American Hair Research Society consensus classification of cicatricial alopecia is based on the infiltrate: lymphocytic, neutrophilic, mixed, or nonspecific.
"We determine our treatment decisions based on the infiltrate," said Dr. Shapiro, whose New York– and Vancouver–based practices are devoted exclusively to hair and scalp disorders. "A biopsy can be crucial when you’re managing these patients, so you know how actively inflamed the lesions are and what the primary infiltrate is. We always take a 4-mm punch biopsy, and we may take two. We’ll do one for transverse sectioning and another one for longitudinal sectioning."
"Sometimes there’s (histologic) overlap between lupus erythematosus or lichen planopilaris," he said. The clinical and pathologic findings can be variable, so the differential diagnosis is difficult. "There are no cures, and the cause of these conditions is unknown."
Discoid lupus erythematosus often presents with atrophy and extensive hair loss. A hallmark feature is central follicular hyperkeratosis. If less than 10% of the scalp is involved, Dr. Shapiro uses ultrapotent topical corticosteroids such as clobetasol with or without triamcinolone acetonide (TCA) injections (10 mg/cc for a maximum total of 2 ccs per sitting once a month). "We inject into the areas that are red as well as the surrounding areas so that it doesn’t spread," he said.
If a patient responds to this regimen he continues to use it on an as-needed basis. For nonresponders, Dr. Shapiro resorts to hydroxychloroquine 200 mg b.i.d. or isotretinoin 40 mg b.i.d. Other alternatives can include topical tacrolimus. Others have used tazarotene and imiquimod, he said, but "I find the latter two too irritating."
For patients with 10% or greater scalp involvement, Dr. Shapiro uses hydroxychloroquine plus ultrapotent topical steroids, plus TCA injections, plus bridging therapy with prednisone, usually with 40 mg prednisone tapered.
Patients with lichen planopilaris typically present with peripheral hyperkeratosis, or frontal fibrosing alopecia, which is marked by loss of a strip of hair at the front and/or the sides of the scalp. Frontal fibrosing alopecia is "a silent epidemic. In Vancouver, I’m seeing about seven cases per day of this, and three to four cases per day in New York. Sometimes, the eyebrows are the first sign of hair loss. Many times it can go completely around the scalp, so it’s [considered] marginally fibrosing," Dr. Shapiro said.
Frontal fibrosing alopecia primarily affects postmenopausal women. "We think there is a hormonal component that is causing this, but there is also a trigger in the environment," Dr. Shapiro said. "We don’t know what the trigger is, but certain countries have less of it. China does not see that much of it, nor does Saudi Arabia."
Dr. Shapiro and his associates recently published a retrospective study of 62 cases of frontal fibrosing alopecia seen between January 2004 and March 2012. Of the 62 patients, 61 were women (Int. J. Dermatol. 2014 [doi:10.1111/ijd.12479]). Their average age was 61 years and the age of onset ranged from 18 to 81 years. In terms of symptoms, 22 (35%) patients were asymptomatic, 42 (68%) had a history of female pattern hair loss, and 50 (81%) patients’ eyebrows were affected.
In Dr. Shapiro’s experience, intralesional TCA with or without oral tetracycline or hydroxychloroquine may help to halt or slow the progression of frontal fibrosing alopecia. He typically uses intralesional Kenalog 2.5 mL/cc. "I do 30 injections for 3 ccs total: 0.1 cc/injection site and I go from one ear to the other," Dr. Shapiro said. "We’ll also use clobetasol solution at the beginning and taper to a betamethasone solution. Other things to consider are tacrolimus, Cetaphil cleanser, and finasteride."
Dr. Shapiro disclosed that he is a consultant to Johnson & Johnson, GSK/Stiefel, Allergan, MSD, and Applied Biology.
On Twitter @dougbrunk
VANCOUVER, B.C. – Cicatricial alopecia should be considered a "trichologic emergency," Dr. Jerry Shapiro advised at the annual meeting of the Pacific Dermatologic Association. The hair loss may be permanent, "so it’s important to get on top of this, and not just sit out the condition."
Cicatricial alopecia is characterized by a loss of follicular ostia with replacement by fibrous tissue. Primary cicatricial alopecia targets the hair follicle and involves preferential destruction of the follicular epithelium with sparing of interfollicular dermis. In secondary cicatricial alopecia, "the follicle is an innocent bystander" that is destroyed in the course of infectious tinea capitis, infiltrative diseases such as metastatic disease and sarcoidosis, trauma such as radiation exposure and burns, and inflammatory conditions such as pemphigus vulgaris.
The North American Hair Research Society consensus classification of cicatricial alopecia is based on the infiltrate: lymphocytic, neutrophilic, mixed, or nonspecific.
"We determine our treatment decisions based on the infiltrate," said Dr. Shapiro, whose New York– and Vancouver–based practices are devoted exclusively to hair and scalp disorders. "A biopsy can be crucial when you’re managing these patients, so you know how actively inflamed the lesions are and what the primary infiltrate is. We always take a 4-mm punch biopsy, and we may take two. We’ll do one for transverse sectioning and another one for longitudinal sectioning."
"Sometimes there’s (histologic) overlap between lupus erythematosus or lichen planopilaris," he said. The clinical and pathologic findings can be variable, so the differential diagnosis is difficult. "There are no cures, and the cause of these conditions is unknown."
Discoid lupus erythematosus often presents with atrophy and extensive hair loss. A hallmark feature is central follicular hyperkeratosis. If less than 10% of the scalp is involved, Dr. Shapiro uses ultrapotent topical corticosteroids such as clobetasol with or without triamcinolone acetonide (TCA) injections (10 mg/cc for a maximum total of 2 ccs per sitting once a month). "We inject into the areas that are red as well as the surrounding areas so that it doesn’t spread," he said.
If a patient responds to this regimen he continues to use it on an as-needed basis. For nonresponders, Dr. Shapiro resorts to hydroxychloroquine 200 mg b.i.d. or isotretinoin 40 mg b.i.d. Other alternatives can include topical tacrolimus. Others have used tazarotene and imiquimod, he said, but "I find the latter two too irritating."
For patients with 10% or greater scalp involvement, Dr. Shapiro uses hydroxychloroquine plus ultrapotent topical steroids, plus TCA injections, plus bridging therapy with prednisone, usually with 40 mg prednisone tapered.
Patients with lichen planopilaris typically present with peripheral hyperkeratosis, or frontal fibrosing alopecia, which is marked by loss of a strip of hair at the front and/or the sides of the scalp. Frontal fibrosing alopecia is "a silent epidemic. In Vancouver, I’m seeing about seven cases per day of this, and three to four cases per day in New York. Sometimes, the eyebrows are the first sign of hair loss. Many times it can go completely around the scalp, so it’s [considered] marginally fibrosing," Dr. Shapiro said.
Frontal fibrosing alopecia primarily affects postmenopausal women. "We think there is a hormonal component that is causing this, but there is also a trigger in the environment," Dr. Shapiro said. "We don’t know what the trigger is, but certain countries have less of it. China does not see that much of it, nor does Saudi Arabia."
Dr. Shapiro and his associates recently published a retrospective study of 62 cases of frontal fibrosing alopecia seen between January 2004 and March 2012. Of the 62 patients, 61 were women (Int. J. Dermatol. 2014 [doi:10.1111/ijd.12479]). Their average age was 61 years and the age of onset ranged from 18 to 81 years. In terms of symptoms, 22 (35%) patients were asymptomatic, 42 (68%) had a history of female pattern hair loss, and 50 (81%) patients’ eyebrows were affected.
In Dr. Shapiro’s experience, intralesional TCA with or without oral tetracycline or hydroxychloroquine may help to halt or slow the progression of frontal fibrosing alopecia. He typically uses intralesional Kenalog 2.5 mL/cc. "I do 30 injections for 3 ccs total: 0.1 cc/injection site and I go from one ear to the other," Dr. Shapiro said. "We’ll also use clobetasol solution at the beginning and taper to a betamethasone solution. Other things to consider are tacrolimus, Cetaphil cleanser, and finasteride."
Dr. Shapiro disclosed that he is a consultant to Johnson & Johnson, GSK/Stiefel, Allergan, MSD, and Applied Biology.
On Twitter @dougbrunk
EXPERT ANALYSIS AT THE PDA ANNUAL MEETING
Jury still out on effect of systemic psoriasis meds on MI risk
VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.
"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.
Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.
Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.
Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.
A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).
A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).
"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."
One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.
Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.
On Twitter @dougbrunk
VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.
"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.
Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.
Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.
Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.
A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).
A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).
"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."
One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.
Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.
On Twitter @dougbrunk
VANCOUVER, B.C. – Results from some studies have concluded that treatment with conventional systemic or biologic therapy improves the elevated risk of cardiovascular disease in patients with psoriasis, but the association is not yet definitive, according to Dr. Robert Kalb.
"Current evidence is suggestive, but certainly our patients with psoriasis need intensive management of cardiovascular risk factors and appropriate psoriasis therapy, which may also produce benefits from a cardiovascular standpoint," Dr. Kalb said at the annual meeting of the Pacific Dermatologic Association.
Researchers who conducted the earliest study to explore the association between psoriasis and increased risk for cardiovascular death found that when they controlled for risk factors including age, sex, smoking, diabetes, hypertension, and hyperlipidemia, having psoriasis led to a hazard ratio of 1.57 for cardiovascular death (Eur. Heart J. 2010;31:1000-6). Since that time, six meta-analyses have appeared in the medical literature showing that psoriasis is linked to an increased risk of cardiovascular disease. Most of these studies defined severe psoriasis as patients who had received a systemic agent. Body surface area or other objective measures of psoriasis were not part of the definition, said Dr. Kalb, a dermatologist in group practice in Buffalo.
Emerging evidence supports the idea that increased risk factors are associated with the severity of psoriasis. As part of the landmark Incident Health Outcomes and Psoriasis Events (iHope) study, investigators found that patients with disease affecting 10% or more body surface area had an increased risk of myocardial infarction. One study defined psoriasis severity by body surface area (JAMA Dermatol. 2013;149:1173-9). The investigators found that the burdens of MI and other comorbid diseases increase with increasing disease severity, particularly in those with 10% body surface area or more affected.
Investigators are also working to determine if systemic therapy reduces the risk of MI in psoriasis patients. The Consortium of Rheumatology Researchers of North America (CORRONA) registry database found that in patients with rheumatoid arthritis, anti–tumor necrosis factor (TNF) agents reduced the risk of cardiovascular events (HR, 0.39), compared with nonbiologic disease-modifying antirheumatic drugs. Methotrexate did not reduce the risk of cardiovascular events, while the use of prednisone increased the risk (Ann. Rheum. Dis. 2011;70:576-82). Another review showed that anti-TNF therapy decreased the risk, but the use of methotrexate decreased the risk slightly more (Rheumatology 2011;50:518-31). "Reassuringly, there was no increased risk of congestive heart failure, which has always been [included] in the label of [anti-]TNF agents," Dr. Kalb said.
A cohort study of 25,554 patients with moderate to severe psoriasis used U.S. administrative and pharmacy claims data to examine the risk of acute myocardial infarction in those who underwent systemic therapy, compared with those who underwent phototherapy. The investigators found a trend toward an increased risk of MI in those who received systemic therapy, but there were no significant differences in risk between the two treatment groups (Br. J. Dermatol. 2011;165:1066-73). On the other hand, a retrospective, longitudinal cohort study of 2,400 patients with severe psoriasis in Denmark showed that the use of biologic agents and methotrexate was associated with fewer cardiovascular events (hazard ratios, 0.48 and 0.50, respectively), but the use of other antipsoriatic therapies – including cyclosporine, retinoids, phototherapy, and topicals – were not (J. Intern Med. 2013;273:197-204).
A retrospective cohort study of 8,845 Kaiser Permanente psoriasis patients set out to determine whether treatment with TNF inhibitors was associated with a decreased risk of MI, compared with those who did not receive TNF inhibitors (Arch. Dermatol. 2012;148:1244-50) . After adjusting for MI risk factors, the researchers found that those who received TNF inhibitors had a significantly lower risk of MI, compared with those who received topical therapy (adjusted HR, 0.50).
"Why do different studies reach different conclusions?" Dr. Kalb asked. "Different populations were studied, and there were differences in terms of how reference groups were defined and in the methods for categorizing therapy and severity of disease. Data from population studies are not yet sufficient to determine whether [anti-]TNF agents will reduce the incidence of MI."
One conundrum for researchers is how to measure this decreased risk. "What surrogate markers should we use?" Dr. Kalb asked. "One study showed a significant decrease in CRP [C-reactive protein] and ESR [erythrocyte sedimentation rate] in patients receiving therapy. The gold standard of decrease in mortality in this type of study will not be done because it requires thousands of patients studied over at least 10 years." However, in cardiology, 18-fluorodeoxyglucose PET scanning shows decreased inflammation in patients taking statins. Whether the same effect can be shown in psoriasis patients taking systemic medications for their disease remains unknown, but prospective studies are ongoing.
Dr. Kalb disclosed that he is an investigator and/or consultant for AbbVie, Amgen, Celgene, Dermira, Janssen, Leo, Merck, Pfizer, and Taro. He is also on the dermatology safety monitoring board for ApoPharma and Eli Lilly.
On Twitter @dougbrunk
EXPERT ANALYSIS AT PDA 2014
Field therapy preferred when treating actinic keratoses
VANCOUVER, B.C. – In the clinical opinion of Dr. Mariusz Sapijaszko, treating actinic keratosis without field therapy creates a disadvantage "because this is not an individual lesion disease," he maintained at the annual meeting of the Pacific Dermatologic Association.
Actinic keratosis "is a field concept disease. I tell patients ‘the sun has not been shining only on your left temple. It’s been shining all over your face and scalp, neck, and arms. ... It’s time to start looking after your skin with sun protection and lesion-directed field therapies.’"
An estimated 11% of all dermatologic visits in the United States are for actinic keratosis (AK) and "we worry about it because the natural course of AK lesions is unpredictable," said Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alta. It’s not easy to predict which lesions will progress to in situ or invasive squamous cell carcinomas (SCCs).
An estimated 40%-80% of cutaneous SCCs arise from, or near, an AK lesion, which supports the concept of field UV damage. AK lesions may persist, regress, or progress, depending on the patient’s immune status. Some lesions that regress will recur, from 32% within 1 year to 92% within 5 years. Progression can lead to hypertrophic AKs, in situ SCC, or invasive SCC. It can be difficult to distinguish AKs and early forms of SCC or even other nonmelanoma skin cancers, "so it’s important to treat all AKs," Dr. Sapijaszko said. Lesions that can progress to SCC include those that are hyperkeratotic, painful, have atypical features such as broader or deeper presentations, as well as those difficult to clear with standard therapies and those that occur in immunocompromised patients.
Locally destructive, mechanical ways to treat AKs include liquid nitrogen cryosurgery, electrodessication and curettage, and excision. "All of these treatments are highly operator dependent, because clearly if you use liquid nitrogen cryotherapy enough you will destroy that lesion but you will not destroy the surrounding DNA damage that has been present," he said.
Field-directed therapies, however, provide an opportunity for a more complete treatment effect. Options include 5-FU (5-fluorouracil), imiquimod, ingenol mebutate, and photodynamic therapy as well as chemical peels and laser resurfacing. Chemical peels and laser resurfacing "have less robust data, but they’re operator dependent, because you can do laser resurfacing with 100 microns or 300 microns," Dr. Sapijaszko said.
"That can depend on the technique you use, and the laser you use, and the patient in front of you." Some of the field treatment options are easier to apply than others. For example, 5-FU is applied twice daily, while imiquimod is applied twice weekly; yet all boast complete clearance rates in the 40%-50% range. "Side effects are also similar between these agents," he said. "Pain is not a big issue except with 5-FU; some patients experience a significant burning sensation."
The newest approved field therapy option, ingenol mebutate, has a dual mechanism of action: it causes cell death within 24 hours and it has been shown to reduce the number of UV-induced mutated p53 patches in mice. "This is important because we’re not just treating the lesions that we see, we want to treat the molecular changes that lead to the actual problem," Dr. Sapijaszko said. "Having decreased mutations is a huge advantage. Direct cell death leads to secondary inflammation. The immune response is characterized by cytokine release and activation of endothelial cells, leading to infiltration of lymphocytes and neutrophils, which contributes to clearance of tumor cells."
Before ingenol mebutate came on the market, investigators randomized patients with AKs to one of three treatment groups: imiquimod 5% cream, 5-FU 5% ointment, or cryotherapy (Br. J. Dermatol. 2007; 157 [suppl. 2]:34-40). Compared with their counterparts, patients in the imiquimod group fared significantly better in terms of sustained clearance of cleared lesions (73% vs. 54% in the 5-FU group, vs. 28% in the cryosurgery group (P less than .01).
"I wish we had comparative data to ingenol mebutate, but to me, of these three modalities, imiquimod stands out as the favorite," Dr. Sapijaszko said.
He went on to note that combining the available mechanical and field treatments for AK simultaneously or sequentially can lead to optimal outcomes. "Combination therapy, in particular cryotherapy, has been successfully used with a variety of topicals and has been shown to be highly advantageous, compared with placebo or to some of these agents alone," he said. "In addition, cryotherapy can be used with PDT, chemical peels, and laser resurfacing. Almost nobody in my practice gets one treatment, unless it’s a single individual lesion. Everybody gets recommendations on appropriate sun protection – just being sun smart."
Dr. Sapijaszko disclosed that he has received honoraria from and is an advisor to Galderma, Leo Pharma, and Valeant.
On Twitter @dougbrunk
VANCOUVER, B.C. – In the clinical opinion of Dr. Mariusz Sapijaszko, treating actinic keratosis without field therapy creates a disadvantage "because this is not an individual lesion disease," he maintained at the annual meeting of the Pacific Dermatologic Association.
Actinic keratosis "is a field concept disease. I tell patients ‘the sun has not been shining only on your left temple. It’s been shining all over your face and scalp, neck, and arms. ... It’s time to start looking after your skin with sun protection and lesion-directed field therapies.’"
An estimated 11% of all dermatologic visits in the United States are for actinic keratosis (AK) and "we worry about it because the natural course of AK lesions is unpredictable," said Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alta. It’s not easy to predict which lesions will progress to in situ or invasive squamous cell carcinomas (SCCs).
An estimated 40%-80% of cutaneous SCCs arise from, or near, an AK lesion, which supports the concept of field UV damage. AK lesions may persist, regress, or progress, depending on the patient’s immune status. Some lesions that regress will recur, from 32% within 1 year to 92% within 5 years. Progression can lead to hypertrophic AKs, in situ SCC, or invasive SCC. It can be difficult to distinguish AKs and early forms of SCC or even other nonmelanoma skin cancers, "so it’s important to treat all AKs," Dr. Sapijaszko said. Lesions that can progress to SCC include those that are hyperkeratotic, painful, have atypical features such as broader or deeper presentations, as well as those difficult to clear with standard therapies and those that occur in immunocompromised patients.
Locally destructive, mechanical ways to treat AKs include liquid nitrogen cryosurgery, electrodessication and curettage, and excision. "All of these treatments are highly operator dependent, because clearly if you use liquid nitrogen cryotherapy enough you will destroy that lesion but you will not destroy the surrounding DNA damage that has been present," he said.
Field-directed therapies, however, provide an opportunity for a more complete treatment effect. Options include 5-FU (5-fluorouracil), imiquimod, ingenol mebutate, and photodynamic therapy as well as chemical peels and laser resurfacing. Chemical peels and laser resurfacing "have less robust data, but they’re operator dependent, because you can do laser resurfacing with 100 microns or 300 microns," Dr. Sapijaszko said.
"That can depend on the technique you use, and the laser you use, and the patient in front of you." Some of the field treatment options are easier to apply than others. For example, 5-FU is applied twice daily, while imiquimod is applied twice weekly; yet all boast complete clearance rates in the 40%-50% range. "Side effects are also similar between these agents," he said. "Pain is not a big issue except with 5-FU; some patients experience a significant burning sensation."
The newest approved field therapy option, ingenol mebutate, has a dual mechanism of action: it causes cell death within 24 hours and it has been shown to reduce the number of UV-induced mutated p53 patches in mice. "This is important because we’re not just treating the lesions that we see, we want to treat the molecular changes that lead to the actual problem," Dr. Sapijaszko said. "Having decreased mutations is a huge advantage. Direct cell death leads to secondary inflammation. The immune response is characterized by cytokine release and activation of endothelial cells, leading to infiltration of lymphocytes and neutrophils, which contributes to clearance of tumor cells."
Before ingenol mebutate came on the market, investigators randomized patients with AKs to one of three treatment groups: imiquimod 5% cream, 5-FU 5% ointment, or cryotherapy (Br. J. Dermatol. 2007; 157 [suppl. 2]:34-40). Compared with their counterparts, patients in the imiquimod group fared significantly better in terms of sustained clearance of cleared lesions (73% vs. 54% in the 5-FU group, vs. 28% in the cryosurgery group (P less than .01).
"I wish we had comparative data to ingenol mebutate, but to me, of these three modalities, imiquimod stands out as the favorite," Dr. Sapijaszko said.
He went on to note that combining the available mechanical and field treatments for AK simultaneously or sequentially can lead to optimal outcomes. "Combination therapy, in particular cryotherapy, has been successfully used with a variety of topicals and has been shown to be highly advantageous, compared with placebo or to some of these agents alone," he said. "In addition, cryotherapy can be used with PDT, chemical peels, and laser resurfacing. Almost nobody in my practice gets one treatment, unless it’s a single individual lesion. Everybody gets recommendations on appropriate sun protection – just being sun smart."
Dr. Sapijaszko disclosed that he has received honoraria from and is an advisor to Galderma, Leo Pharma, and Valeant.
On Twitter @dougbrunk
VANCOUVER, B.C. – In the clinical opinion of Dr. Mariusz Sapijaszko, treating actinic keratosis without field therapy creates a disadvantage "because this is not an individual lesion disease," he maintained at the annual meeting of the Pacific Dermatologic Association.
Actinic keratosis "is a field concept disease. I tell patients ‘the sun has not been shining only on your left temple. It’s been shining all over your face and scalp, neck, and arms. ... It’s time to start looking after your skin with sun protection and lesion-directed field therapies.’"
An estimated 11% of all dermatologic visits in the United States are for actinic keratosis (AK) and "we worry about it because the natural course of AK lesions is unpredictable," said Dr. Sapijaszko of the Western Canada Dermatology Institute, Edmonton, Alta. It’s not easy to predict which lesions will progress to in situ or invasive squamous cell carcinomas (SCCs).
An estimated 40%-80% of cutaneous SCCs arise from, or near, an AK lesion, which supports the concept of field UV damage. AK lesions may persist, regress, or progress, depending on the patient’s immune status. Some lesions that regress will recur, from 32% within 1 year to 92% within 5 years. Progression can lead to hypertrophic AKs, in situ SCC, or invasive SCC. It can be difficult to distinguish AKs and early forms of SCC or even other nonmelanoma skin cancers, "so it’s important to treat all AKs," Dr. Sapijaszko said. Lesions that can progress to SCC include those that are hyperkeratotic, painful, have atypical features such as broader or deeper presentations, as well as those difficult to clear with standard therapies and those that occur in immunocompromised patients.
Locally destructive, mechanical ways to treat AKs include liquid nitrogen cryosurgery, electrodessication and curettage, and excision. "All of these treatments are highly operator dependent, because clearly if you use liquid nitrogen cryotherapy enough you will destroy that lesion but you will not destroy the surrounding DNA damage that has been present," he said.
Field-directed therapies, however, provide an opportunity for a more complete treatment effect. Options include 5-FU (5-fluorouracil), imiquimod, ingenol mebutate, and photodynamic therapy as well as chemical peels and laser resurfacing. Chemical peels and laser resurfacing "have less robust data, but they’re operator dependent, because you can do laser resurfacing with 100 microns or 300 microns," Dr. Sapijaszko said.
"That can depend on the technique you use, and the laser you use, and the patient in front of you." Some of the field treatment options are easier to apply than others. For example, 5-FU is applied twice daily, while imiquimod is applied twice weekly; yet all boast complete clearance rates in the 40%-50% range. "Side effects are also similar between these agents," he said. "Pain is not a big issue except with 5-FU; some patients experience a significant burning sensation."
The newest approved field therapy option, ingenol mebutate, has a dual mechanism of action: it causes cell death within 24 hours and it has been shown to reduce the number of UV-induced mutated p53 patches in mice. "This is important because we’re not just treating the lesions that we see, we want to treat the molecular changes that lead to the actual problem," Dr. Sapijaszko said. "Having decreased mutations is a huge advantage. Direct cell death leads to secondary inflammation. The immune response is characterized by cytokine release and activation of endothelial cells, leading to infiltration of lymphocytes and neutrophils, which contributes to clearance of tumor cells."
Before ingenol mebutate came on the market, investigators randomized patients with AKs to one of three treatment groups: imiquimod 5% cream, 5-FU 5% ointment, or cryotherapy (Br. J. Dermatol. 2007; 157 [suppl. 2]:34-40). Compared with their counterparts, patients in the imiquimod group fared significantly better in terms of sustained clearance of cleared lesions (73% vs. 54% in the 5-FU group, vs. 28% in the cryosurgery group (P less than .01).
"I wish we had comparative data to ingenol mebutate, but to me, of these three modalities, imiquimod stands out as the favorite," Dr. Sapijaszko said.
He went on to note that combining the available mechanical and field treatments for AK simultaneously or sequentially can lead to optimal outcomes. "Combination therapy, in particular cryotherapy, has been successfully used with a variety of topicals and has been shown to be highly advantageous, compared with placebo or to some of these agents alone," he said. "In addition, cryotherapy can be used with PDT, chemical peels, and laser resurfacing. Almost nobody in my practice gets one treatment, unless it’s a single individual lesion. Everybody gets recommendations on appropriate sun protection – just being sun smart."
Dr. Sapijaszko disclosed that he has received honoraria from and is an advisor to Galderma, Leo Pharma, and Valeant.
On Twitter @dougbrunk
EXPERT ANALYSIS AT THE PDA ANNUAL MEETING
