When wounds won’t heal, try these strategies

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When wounds won’t heal, try these strategies

SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

Dr. Theodora Mauro

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

 

 

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

Dr. Theodora Mauro

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

 

 

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

Dr. Theodora Mauro

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

 

 

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE PACIFIC DERMATOLOGIC ASSOCIATION

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Female hair loss differs by age

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SAN FRANCISCO – Three distinct stages of pattern hair loss in women are related to the age of onset, and are not necessarily androgen related.

Between puberty and age 40 years, hair miniaturization in females tends to be caused by androgenetic alopecia, a common hereditary thinning or balding induced by androgens in genetically susceptible people of both sexes. By contrast, women in their 60s or older may develop hair thinning from age-related, or "senescent" alopecia, which is distinct from androgenetic alopecia because senescent alopecia is not mediated by dihydrotestosterone, Dr. Vera H. Price said at the annual meeting of the Pacific Dermatologic Association.

However, a newly identified stage that often occurs between 45 and 55 years of age is gaining popularity in the lexicon of hair loss. In this stage, called "female pattern hair loss," the role of androgens is less clear-cut, and other hormonal and nonhormonal factors may play a role, said Dr. Price, professor of dermatology at the University of California, San Francisco.

All three stages show similar histopathology, with follicular downsizing, normal sebaceous glands, and no significant inflammation. However, recognizing and understanding the three stages help inform management, said Dr. Price.

Treatment with minoxidil is suitable for all three stages of hair loss, for example, but androgen blockade via off-label treatment with finasteride is not helpful in senescent alopecia. "I don’t use it after 60 years of age in women or men," she said.

Millions of men who have taken finasteride 5 mg/day for benign prostatic hypertrophy have not regrown scalp hair, evidence that senescent alopecia is not dihydrotestosterone mediated, she noted.

Androgenetic alopecia. To screen for suspected androgenetic alopecia in women, check for menstrual irregularities, infertility, hirsutism, severe cystic acne, galactorrhea, and virilization. "If none are present, you do not have to do a single hormonal test" because it’s not androgenetic alopecia causing the hair loss, Dr. Price said.

If any one of those conditions is present, however, check levels of testosterone, dehydroepiandrosterone sulfate (DHEAS), and prolactin.

In all hair loss patients, get a complete blood count and check for normal levels of thyroid-stimulating hormone (TSH), ferritin, and 25-hydroxyvitamin D; the latter two are required for a normal hair cycle. Be sure to order the ferritin level specifically, because ordering "iron studies" won’t include a ferritin level, she added.

Female pattern hair loss. The pathogenesis behind female pattern hair loss is not well understood. As women go through menopause, hair growth parameters change. The hair growth rate slows, the anagen/telogen ratio decreases, and hair diameters become smaller, Dr. Price explained.

Hormonal and molecular factors that may influence female pattern hair loss need to be better defined, including the possible roles of estrogen, estrogen receptor (ER)-beta, aromatase, 5-alpha-reductase, dihydrotestosterone, and androgen receptors, she said.

"When we understand that, we’ll understand this group a little more clearly," she added. "I’ve always been puzzled a little bit when the onset is in this age group."

Senescent alopecia. "I call it ‘wisdom-related’ alopecia," quipped Dr. Price. The gene expression profiles of androgenetic alopecia and senescent alopecia differ. In the former, hair growth cycle genes are differentially expressed. In the latter, systemic senescent/aging genes are differentially expressed, suggesting these are two distinct disorders.

Management. For any stage of hair loss, minoxidil (Rogaine) may help if used properly over an extended period of time, said Dr. Price. Apply the 2% or 5% solution every single day directly to a dry scalp, not right after a shower, and spread it gently across the scalp, she advised. Give minoxidil time to absorb without spraying, moussing, or blow-drying the hair while it absorbs. Once-daily minoxidil foam 5% also has been approved for women and is less oily and absorbed faster.

Of note, androgen blockade via off-label oral finasteride 1 mg/day for confirmed androgenetic alopecia is contraindicated in women who may be or may become pregnant because it will cause hypospadias in a male fetus, said Dr. Price. Prescribe concurrent oral contraception in premenopausal women or make sure the woman is postmenopausal when using finasteride.

"Do I use it in women? I do, but I’m very careful," she said. "They have to be post hysterectomy or post tubal ligation. I want to be certain that they’re not going to conceive."

In appropriate patients, minoxidil and finasteride could be used together if the patient can afford it, she added.

Spironolactone, an androgen receptor inhibitor, also has been used in a dose of 200 mg/day to retard hair thinning due to androgenetic alopecia. Data show that spironolactone 50-200 mg/day can be used successfully to treat acne and hirsutism, but there are no evidence-based studies showing that it helps hair regrowth.

 

 

"I use very little spironolactone for androgenetic alopecia," Dr. Price said. "It will not grow hair. I think it’s used a lot because people aren’t familiar with minoxidil or don’t know about using finasteride if there’s no possibility of pregnancy."

Dr. Price reported having financial associations with Allergan and Follica, neither of which was pertinent to this topic.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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SAN FRANCISCO – Three distinct stages of pattern hair loss in women are related to the age of onset, and are not necessarily androgen related.

Between puberty and age 40 years, hair miniaturization in females tends to be caused by androgenetic alopecia, a common hereditary thinning or balding induced by androgens in genetically susceptible people of both sexes. By contrast, women in their 60s or older may develop hair thinning from age-related, or "senescent" alopecia, which is distinct from androgenetic alopecia because senescent alopecia is not mediated by dihydrotestosterone, Dr. Vera H. Price said at the annual meeting of the Pacific Dermatologic Association.

However, a newly identified stage that often occurs between 45 and 55 years of age is gaining popularity in the lexicon of hair loss. In this stage, called "female pattern hair loss," the role of androgens is less clear-cut, and other hormonal and nonhormonal factors may play a role, said Dr. Price, professor of dermatology at the University of California, San Francisco.

All three stages show similar histopathology, with follicular downsizing, normal sebaceous glands, and no significant inflammation. However, recognizing and understanding the three stages help inform management, said Dr. Price.

Treatment with minoxidil is suitable for all three stages of hair loss, for example, but androgen blockade via off-label treatment with finasteride is not helpful in senescent alopecia. "I don’t use it after 60 years of age in women or men," she said.

Millions of men who have taken finasteride 5 mg/day for benign prostatic hypertrophy have not regrown scalp hair, evidence that senescent alopecia is not dihydrotestosterone mediated, she noted.

Androgenetic alopecia. To screen for suspected androgenetic alopecia in women, check for menstrual irregularities, infertility, hirsutism, severe cystic acne, galactorrhea, and virilization. "If none are present, you do not have to do a single hormonal test" because it’s not androgenetic alopecia causing the hair loss, Dr. Price said.

If any one of those conditions is present, however, check levels of testosterone, dehydroepiandrosterone sulfate (DHEAS), and prolactin.

In all hair loss patients, get a complete blood count and check for normal levels of thyroid-stimulating hormone (TSH), ferritin, and 25-hydroxyvitamin D; the latter two are required for a normal hair cycle. Be sure to order the ferritin level specifically, because ordering "iron studies" won’t include a ferritin level, she added.

Female pattern hair loss. The pathogenesis behind female pattern hair loss is not well understood. As women go through menopause, hair growth parameters change. The hair growth rate slows, the anagen/telogen ratio decreases, and hair diameters become smaller, Dr. Price explained.

Hormonal and molecular factors that may influence female pattern hair loss need to be better defined, including the possible roles of estrogen, estrogen receptor (ER)-beta, aromatase, 5-alpha-reductase, dihydrotestosterone, and androgen receptors, she said.

"When we understand that, we’ll understand this group a little more clearly," she added. "I’ve always been puzzled a little bit when the onset is in this age group."

Senescent alopecia. "I call it ‘wisdom-related’ alopecia," quipped Dr. Price. The gene expression profiles of androgenetic alopecia and senescent alopecia differ. In the former, hair growth cycle genes are differentially expressed. In the latter, systemic senescent/aging genes are differentially expressed, suggesting these are two distinct disorders.

Management. For any stage of hair loss, minoxidil (Rogaine) may help if used properly over an extended period of time, said Dr. Price. Apply the 2% or 5% solution every single day directly to a dry scalp, not right after a shower, and spread it gently across the scalp, she advised. Give minoxidil time to absorb without spraying, moussing, or blow-drying the hair while it absorbs. Once-daily minoxidil foam 5% also has been approved for women and is less oily and absorbed faster.

Of note, androgen blockade via off-label oral finasteride 1 mg/day for confirmed androgenetic alopecia is contraindicated in women who may be or may become pregnant because it will cause hypospadias in a male fetus, said Dr. Price. Prescribe concurrent oral contraception in premenopausal women or make sure the woman is postmenopausal when using finasteride.

"Do I use it in women? I do, but I’m very careful," she said. "They have to be post hysterectomy or post tubal ligation. I want to be certain that they’re not going to conceive."

In appropriate patients, minoxidil and finasteride could be used together if the patient can afford it, she added.

Spironolactone, an androgen receptor inhibitor, also has been used in a dose of 200 mg/day to retard hair thinning due to androgenetic alopecia. Data show that spironolactone 50-200 mg/day can be used successfully to treat acne and hirsutism, but there are no evidence-based studies showing that it helps hair regrowth.

 

 

"I use very little spironolactone for androgenetic alopecia," Dr. Price said. "It will not grow hair. I think it’s used a lot because people aren’t familiar with minoxidil or don’t know about using finasteride if there’s no possibility of pregnancy."

Dr. Price reported having financial associations with Allergan and Follica, neither of which was pertinent to this topic.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SAN FRANCISCO – Three distinct stages of pattern hair loss in women are related to the age of onset, and are not necessarily androgen related.

Between puberty and age 40 years, hair miniaturization in females tends to be caused by androgenetic alopecia, a common hereditary thinning or balding induced by androgens in genetically susceptible people of both sexes. By contrast, women in their 60s or older may develop hair thinning from age-related, or "senescent" alopecia, which is distinct from androgenetic alopecia because senescent alopecia is not mediated by dihydrotestosterone, Dr. Vera H. Price said at the annual meeting of the Pacific Dermatologic Association.

However, a newly identified stage that often occurs between 45 and 55 years of age is gaining popularity in the lexicon of hair loss. In this stage, called "female pattern hair loss," the role of androgens is less clear-cut, and other hormonal and nonhormonal factors may play a role, said Dr. Price, professor of dermatology at the University of California, San Francisco.

All three stages show similar histopathology, with follicular downsizing, normal sebaceous glands, and no significant inflammation. However, recognizing and understanding the three stages help inform management, said Dr. Price.

Treatment with minoxidil is suitable for all three stages of hair loss, for example, but androgen blockade via off-label treatment with finasteride is not helpful in senescent alopecia. "I don’t use it after 60 years of age in women or men," she said.

Millions of men who have taken finasteride 5 mg/day for benign prostatic hypertrophy have not regrown scalp hair, evidence that senescent alopecia is not dihydrotestosterone mediated, she noted.

Androgenetic alopecia. To screen for suspected androgenetic alopecia in women, check for menstrual irregularities, infertility, hirsutism, severe cystic acne, galactorrhea, and virilization. "If none are present, you do not have to do a single hormonal test" because it’s not androgenetic alopecia causing the hair loss, Dr. Price said.

If any one of those conditions is present, however, check levels of testosterone, dehydroepiandrosterone sulfate (DHEAS), and prolactin.

In all hair loss patients, get a complete blood count and check for normal levels of thyroid-stimulating hormone (TSH), ferritin, and 25-hydroxyvitamin D; the latter two are required for a normal hair cycle. Be sure to order the ferritin level specifically, because ordering "iron studies" won’t include a ferritin level, she added.

Female pattern hair loss. The pathogenesis behind female pattern hair loss is not well understood. As women go through menopause, hair growth parameters change. The hair growth rate slows, the anagen/telogen ratio decreases, and hair diameters become smaller, Dr. Price explained.

Hormonal and molecular factors that may influence female pattern hair loss need to be better defined, including the possible roles of estrogen, estrogen receptor (ER)-beta, aromatase, 5-alpha-reductase, dihydrotestosterone, and androgen receptors, she said.

"When we understand that, we’ll understand this group a little more clearly," she added. "I’ve always been puzzled a little bit when the onset is in this age group."

Senescent alopecia. "I call it ‘wisdom-related’ alopecia," quipped Dr. Price. The gene expression profiles of androgenetic alopecia and senescent alopecia differ. In the former, hair growth cycle genes are differentially expressed. In the latter, systemic senescent/aging genes are differentially expressed, suggesting these are two distinct disorders.

Management. For any stage of hair loss, minoxidil (Rogaine) may help if used properly over an extended period of time, said Dr. Price. Apply the 2% or 5% solution every single day directly to a dry scalp, not right after a shower, and spread it gently across the scalp, she advised. Give minoxidil time to absorb without spraying, moussing, or blow-drying the hair while it absorbs. Once-daily minoxidil foam 5% also has been approved for women and is less oily and absorbed faster.

Of note, androgen blockade via off-label oral finasteride 1 mg/day for confirmed androgenetic alopecia is contraindicated in women who may be or may become pregnant because it will cause hypospadias in a male fetus, said Dr. Price. Prescribe concurrent oral contraception in premenopausal women or make sure the woman is postmenopausal when using finasteride.

"Do I use it in women? I do, but I’m very careful," she said. "They have to be post hysterectomy or post tubal ligation. I want to be certain that they’re not going to conceive."

In appropriate patients, minoxidil and finasteride could be used together if the patient can afford it, she added.

Spironolactone, an androgen receptor inhibitor, also has been used in a dose of 200 mg/day to retard hair thinning due to androgenetic alopecia. Data show that spironolactone 50-200 mg/day can be used successfully to treat acne and hirsutism, but there are no evidence-based studies showing that it helps hair regrowth.

 

 

"I use very little spironolactone for androgenetic alopecia," Dr. Price said. "It will not grow hair. I think it’s used a lot because people aren’t familiar with minoxidil or don’t know about using finasteride if there’s no possibility of pregnancy."

Dr. Price reported having financial associations with Allergan and Follica, neither of which was pertinent to this topic.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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SAN FRANCISCO – Five practice tips can help physicians consider systemic therapy for the subset of children with psoriasis who develop severe disease at some point, Dr. Kelly M. Cordoro said.

The key is to weigh the risks and benefits to decide which is worse, the treatment or the disease, in terms of how it affects the patient medically, psychosocially, and physically, she said at the annual meeting of the Pacific Dermatologic Association.

Approximately a quarter of the physicians in the audience had treated patients younger than 18 years with systemic therapy for psoriasis, an informal poll showed.*"

Dr. Kelly M. Cordoro

The exact approach varies per patient, and not all cases of severe pediatric psoriasis need systemic treatment. "It’s an art as much as it is a science," said Dr. Cordoro of the University of California, San Francisco.

It’s often a good idea to start with nonimmunosuppressive systemic agents for psoriasis in children, such as phototherapy or acitretin, before trying immunosuppressive treatments such as cyclosporine, methotrexate, or biologics, she suggested. Systemic therapy should be added to a multimodal care plan that includes identification and treatment of triggers and comorbidities, topical therapy, lifestyle modifications, education, and support. Keep in mind that no systemic medications are approved to treat psoriasis in children, and management is based on expert opinion, Dr. Cordoro noted.

Dr. Cordoro offered the following five pearls and principles to guide physicians managing severe pediatric psoriasis:

Don’t just do something, stand there! Treat these children conservatively at first and observe the response, especially in patients with new-onset psoriasis and in particular if they have a family history of psoriasis, said Dr. Cordoro. It’s also a good approach in patients who’ve had a recent infection – group A streptococcal infection is a very common trigger of pediatric psoriasis, for example – or a recent viral illness or skin trauma.

"If you can find the trigger" and treat it, "you may be able to prevent the use of systemic therapy" for the psoriasis, she said. Conservative, yet aggressive, treatment might include a combination of topical therapy, wet wraps, itch control, and managing the triggers. Let the disease evolve for a few days to weeks before moving to systemic therapy, she suggested.

Don’t just stand there, do something! The psychological impact of chronic disease can be as disabling as the physical impact, and uncontrolled inflammation can cause long-term health consequences, Dr. Cordoro said. No systemic therapies are approved for pediatric psoriasis because of a lack of studies, "but I encourage you to treat these kids" with severe disease who fail topical and other treatment strategies, she said.

Off-label use of methotrexate can help children with any form of psoriasis, in a dose range of 0.2-0.7 mg/kg per week, with a maximum of 25 mg/week, said Dr. Cordoro. Consider this a rescue phase, and then try to taper to the lowest effective dose or off of systemic therapy.

"Methotrexate doesn’t have to be forever," Dr. Cordoro emphasized. In children, methotrexate’s side effects commonly include GI symptoms and anorexia, and the drug very rarely causes pulmonary and hepatotoxicity. Dr. Cordoro recommended a supplemental folate dose of 1-5 mg every day, except methotrexate dose days, to ameliorate some of the GI side effects and the potential bone marrow toxicity. Monitoring is less intense than in adults, and involves frequent lab evaluations but no liver biopsies. Drug interactions with NSAIDs or trimethoprim/sulfamethoxazole can cause bone marrow toxicity, so be sure to send a letter to the child’s pediatrician and parents to alert them, she said.

For severe, diffuse plaque psoriasis in children, any of the conventional systemic or biologic treatments can be effective, and the choice depends on patient and clinical factors, Dr. Cordoro said. The goal is to gain control, taper the systemic treatment, and hold it at the lowest effective dose or transition to topical therapy or phototherapy.

Don’t forget oral retinoids. Often a forgotten choice for therapy, short-term oral retinoids can be the best first systemic treatment for severe guttate psoriasis if phototherapy is not indicated or unavailable, or for palmoplantar psoriasis or pustular psoriasis, Dr. Cordoro said. In some cases, there can be synergistic effects from combining a low-dose retinoid with low-dose narrow-band UVB phototherapy.

Acitretin is not immunosuppressive but is teratogenic, so it should be avoided in girls older than 8 years, Dr. Cordoro noted. Reversible, dose-dependent side effects include mucocutaneous effects, dyslipidemia, or transaminitis. "Kids cannot tolerate high doses of retinoids, so 1 mg/kg per day or less is where you need to be," she said. Much-feared potential skeletal effects are very rare at doses that low when the medication is used for no more than a year or two, she added.

 

 

When you need speed, try cyclosporine. Cyclosporine acts rapidly. An initial high dose of 5 mg/kg per day can take control of refractory plaque psoriasis, rapidly moving pustular psoriasis, or severe, rapidly progressive psoriasis. No more than a year of continuous use is the guideline, so you don’t want to start low and go slow. "Kids and typically tolerate and need higher doses" compared with adults, Dr. Cordoro said. Use the modified form (Neoral) for better oral bioavailability and better sustained drug levels, she suggested.

This, too, is a rescue treatment intended to control and stabilize the disease, followed by tapering and transitioning to other therapies. The most serious potential side effects include nephrotoxicity, hypertension, and immunosuppression. The most common side effects include nausea, vomiting and diarrhea, anorexia, and headache. Less often, cyclosporine can cause myalgia, arthralgia, paresthesia, gingival hyperplasia, or hypertrichosis. "My colleagues in oncology assure me that at the doses we’re using for psoriasis, we’re not at risk for giving these kids carcinomas down the road," she said.

Biologics play an important role. Biologics are potent, but wouldn’t be the first choice for systemic therapy because they don’t have prolonged efficacy, said Dr. Cordoro. Their precise place in the therapeutic armamentarium is yet to be defined. "I like to reserve a biologic for when I don’t necessarily have a better choice, because I know I have a finite period of time for biologics," she said.

Nonetheless, anti–tumor necrosis factor agents can play a role in treating refractory plaque psoriasis, severe or refractory generalized pustular psoriasis, or psoriatic arthritis, Dr. Cordoro said. Anecdotal reports suggest that IL-12 and IL-23 inhibitors may help with pediatric psoriasis, but there are no study data yet.

The potential advantages of using biologics include less frequent dosing, less laboratory monitoring, and targeted treatment. On the other hand, biologics are expensive, require injection or infusion, have as-yet-unknown long-term risks, and are not approved for treating pediatric psoriasis (so insurance coverage is a battle), said Dr. Cordoro. Questions remain about standardized dosing and monitoring protocols, and about the endpoints of biologic therapy in this setting, although experience with biologics and evidence of their efficacy and safety in children are accumulating, she said.

Dr. Cordoro recommended two articles that she coauthored that provide expert consensus guidelines, tables, and charts for systemic treatment and monitoring of children with psoriasis (Dermatol. Clin. 2013;31:267-88 and Skin Therapy Lett. 2013;18:1-4).

Dr. Cordoro reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

*CORRECTION, 11/4/2013: An earlier version of this article imprecisely stated the results of the informal study.

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SAN FRANCISCO – Five practice tips can help physicians consider systemic therapy for the subset of children with psoriasis who develop severe disease at some point, Dr. Kelly M. Cordoro said.

The key is to weigh the risks and benefits to decide which is worse, the treatment or the disease, in terms of how it affects the patient medically, psychosocially, and physically, she said at the annual meeting of the Pacific Dermatologic Association.

Approximately a quarter of the physicians in the audience had treated patients younger than 18 years with systemic therapy for psoriasis, an informal poll showed.*"

Dr. Kelly M. Cordoro

The exact approach varies per patient, and not all cases of severe pediatric psoriasis need systemic treatment. "It’s an art as much as it is a science," said Dr. Cordoro of the University of California, San Francisco.

It’s often a good idea to start with nonimmunosuppressive systemic agents for psoriasis in children, such as phototherapy or acitretin, before trying immunosuppressive treatments such as cyclosporine, methotrexate, or biologics, she suggested. Systemic therapy should be added to a multimodal care plan that includes identification and treatment of triggers and comorbidities, topical therapy, lifestyle modifications, education, and support. Keep in mind that no systemic medications are approved to treat psoriasis in children, and management is based on expert opinion, Dr. Cordoro noted.

Dr. Cordoro offered the following five pearls and principles to guide physicians managing severe pediatric psoriasis:

Don’t just do something, stand there! Treat these children conservatively at first and observe the response, especially in patients with new-onset psoriasis and in particular if they have a family history of psoriasis, said Dr. Cordoro. It’s also a good approach in patients who’ve had a recent infection – group A streptococcal infection is a very common trigger of pediatric psoriasis, for example – or a recent viral illness or skin trauma.

"If you can find the trigger" and treat it, "you may be able to prevent the use of systemic therapy" for the psoriasis, she said. Conservative, yet aggressive, treatment might include a combination of topical therapy, wet wraps, itch control, and managing the triggers. Let the disease evolve for a few days to weeks before moving to systemic therapy, she suggested.

Don’t just stand there, do something! The psychological impact of chronic disease can be as disabling as the physical impact, and uncontrolled inflammation can cause long-term health consequences, Dr. Cordoro said. No systemic therapies are approved for pediatric psoriasis because of a lack of studies, "but I encourage you to treat these kids" with severe disease who fail topical and other treatment strategies, she said.

Off-label use of methotrexate can help children with any form of psoriasis, in a dose range of 0.2-0.7 mg/kg per week, with a maximum of 25 mg/week, said Dr. Cordoro. Consider this a rescue phase, and then try to taper to the lowest effective dose or off of systemic therapy.

"Methotrexate doesn’t have to be forever," Dr. Cordoro emphasized. In children, methotrexate’s side effects commonly include GI symptoms and anorexia, and the drug very rarely causes pulmonary and hepatotoxicity. Dr. Cordoro recommended a supplemental folate dose of 1-5 mg every day, except methotrexate dose days, to ameliorate some of the GI side effects and the potential bone marrow toxicity. Monitoring is less intense than in adults, and involves frequent lab evaluations but no liver biopsies. Drug interactions with NSAIDs or trimethoprim/sulfamethoxazole can cause bone marrow toxicity, so be sure to send a letter to the child’s pediatrician and parents to alert them, she said.

For severe, diffuse plaque psoriasis in children, any of the conventional systemic or biologic treatments can be effective, and the choice depends on patient and clinical factors, Dr. Cordoro said. The goal is to gain control, taper the systemic treatment, and hold it at the lowest effective dose or transition to topical therapy or phototherapy.

Don’t forget oral retinoids. Often a forgotten choice for therapy, short-term oral retinoids can be the best first systemic treatment for severe guttate psoriasis if phototherapy is not indicated or unavailable, or for palmoplantar psoriasis or pustular psoriasis, Dr. Cordoro said. In some cases, there can be synergistic effects from combining a low-dose retinoid with low-dose narrow-band UVB phototherapy.

Acitretin is not immunosuppressive but is teratogenic, so it should be avoided in girls older than 8 years, Dr. Cordoro noted. Reversible, dose-dependent side effects include mucocutaneous effects, dyslipidemia, or transaminitis. "Kids cannot tolerate high doses of retinoids, so 1 mg/kg per day or less is where you need to be," she said. Much-feared potential skeletal effects are very rare at doses that low when the medication is used for no more than a year or two, she added.

 

 

When you need speed, try cyclosporine. Cyclosporine acts rapidly. An initial high dose of 5 mg/kg per day can take control of refractory plaque psoriasis, rapidly moving pustular psoriasis, or severe, rapidly progressive psoriasis. No more than a year of continuous use is the guideline, so you don’t want to start low and go slow. "Kids and typically tolerate and need higher doses" compared with adults, Dr. Cordoro said. Use the modified form (Neoral) for better oral bioavailability and better sustained drug levels, she suggested.

This, too, is a rescue treatment intended to control and stabilize the disease, followed by tapering and transitioning to other therapies. The most serious potential side effects include nephrotoxicity, hypertension, and immunosuppression. The most common side effects include nausea, vomiting and diarrhea, anorexia, and headache. Less often, cyclosporine can cause myalgia, arthralgia, paresthesia, gingival hyperplasia, or hypertrichosis. "My colleagues in oncology assure me that at the doses we’re using for psoriasis, we’re not at risk for giving these kids carcinomas down the road," she said.

Biologics play an important role. Biologics are potent, but wouldn’t be the first choice for systemic therapy because they don’t have prolonged efficacy, said Dr. Cordoro. Their precise place in the therapeutic armamentarium is yet to be defined. "I like to reserve a biologic for when I don’t necessarily have a better choice, because I know I have a finite period of time for biologics," she said.

Nonetheless, anti–tumor necrosis factor agents can play a role in treating refractory plaque psoriasis, severe or refractory generalized pustular psoriasis, or psoriatic arthritis, Dr. Cordoro said. Anecdotal reports suggest that IL-12 and IL-23 inhibitors may help with pediatric psoriasis, but there are no study data yet.

The potential advantages of using biologics include less frequent dosing, less laboratory monitoring, and targeted treatment. On the other hand, biologics are expensive, require injection or infusion, have as-yet-unknown long-term risks, and are not approved for treating pediatric psoriasis (so insurance coverage is a battle), said Dr. Cordoro. Questions remain about standardized dosing and monitoring protocols, and about the endpoints of biologic therapy in this setting, although experience with biologics and evidence of their efficacy and safety in children are accumulating, she said.

Dr. Cordoro recommended two articles that she coauthored that provide expert consensus guidelines, tables, and charts for systemic treatment and monitoring of children with psoriasis (Dermatol. Clin. 2013;31:267-88 and Skin Therapy Lett. 2013;18:1-4).

Dr. Cordoro reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

*CORRECTION, 11/4/2013: An earlier version of this article imprecisely stated the results of the informal study.

SAN FRANCISCO – Five practice tips can help physicians consider systemic therapy for the subset of children with psoriasis who develop severe disease at some point, Dr. Kelly M. Cordoro said.

The key is to weigh the risks and benefits to decide which is worse, the treatment or the disease, in terms of how it affects the patient medically, psychosocially, and physically, she said at the annual meeting of the Pacific Dermatologic Association.

Approximately a quarter of the physicians in the audience had treated patients younger than 18 years with systemic therapy for psoriasis, an informal poll showed.*"

Dr. Kelly M. Cordoro

The exact approach varies per patient, and not all cases of severe pediatric psoriasis need systemic treatment. "It’s an art as much as it is a science," said Dr. Cordoro of the University of California, San Francisco.

It’s often a good idea to start with nonimmunosuppressive systemic agents for psoriasis in children, such as phototherapy or acitretin, before trying immunosuppressive treatments such as cyclosporine, methotrexate, or biologics, she suggested. Systemic therapy should be added to a multimodal care plan that includes identification and treatment of triggers and comorbidities, topical therapy, lifestyle modifications, education, and support. Keep in mind that no systemic medications are approved to treat psoriasis in children, and management is based on expert opinion, Dr. Cordoro noted.

Dr. Cordoro offered the following five pearls and principles to guide physicians managing severe pediatric psoriasis:

Don’t just do something, stand there! Treat these children conservatively at first and observe the response, especially in patients with new-onset psoriasis and in particular if they have a family history of psoriasis, said Dr. Cordoro. It’s also a good approach in patients who’ve had a recent infection – group A streptococcal infection is a very common trigger of pediatric psoriasis, for example – or a recent viral illness or skin trauma.

"If you can find the trigger" and treat it, "you may be able to prevent the use of systemic therapy" for the psoriasis, she said. Conservative, yet aggressive, treatment might include a combination of topical therapy, wet wraps, itch control, and managing the triggers. Let the disease evolve for a few days to weeks before moving to systemic therapy, she suggested.

Don’t just stand there, do something! The psychological impact of chronic disease can be as disabling as the physical impact, and uncontrolled inflammation can cause long-term health consequences, Dr. Cordoro said. No systemic therapies are approved for pediatric psoriasis because of a lack of studies, "but I encourage you to treat these kids" with severe disease who fail topical and other treatment strategies, she said.

Off-label use of methotrexate can help children with any form of psoriasis, in a dose range of 0.2-0.7 mg/kg per week, with a maximum of 25 mg/week, said Dr. Cordoro. Consider this a rescue phase, and then try to taper to the lowest effective dose or off of systemic therapy.

"Methotrexate doesn’t have to be forever," Dr. Cordoro emphasized. In children, methotrexate’s side effects commonly include GI symptoms and anorexia, and the drug very rarely causes pulmonary and hepatotoxicity. Dr. Cordoro recommended a supplemental folate dose of 1-5 mg every day, except methotrexate dose days, to ameliorate some of the GI side effects and the potential bone marrow toxicity. Monitoring is less intense than in adults, and involves frequent lab evaluations but no liver biopsies. Drug interactions with NSAIDs or trimethoprim/sulfamethoxazole can cause bone marrow toxicity, so be sure to send a letter to the child’s pediatrician and parents to alert them, she said.

For severe, diffuse plaque psoriasis in children, any of the conventional systemic or biologic treatments can be effective, and the choice depends on patient and clinical factors, Dr. Cordoro said. The goal is to gain control, taper the systemic treatment, and hold it at the lowest effective dose or transition to topical therapy or phototherapy.

Don’t forget oral retinoids. Often a forgotten choice for therapy, short-term oral retinoids can be the best first systemic treatment for severe guttate psoriasis if phototherapy is not indicated or unavailable, or for palmoplantar psoriasis or pustular psoriasis, Dr. Cordoro said. In some cases, there can be synergistic effects from combining a low-dose retinoid with low-dose narrow-band UVB phototherapy.

Acitretin is not immunosuppressive but is teratogenic, so it should be avoided in girls older than 8 years, Dr. Cordoro noted. Reversible, dose-dependent side effects include mucocutaneous effects, dyslipidemia, or transaminitis. "Kids cannot tolerate high doses of retinoids, so 1 mg/kg per day or less is where you need to be," she said. Much-feared potential skeletal effects are very rare at doses that low when the medication is used for no more than a year or two, she added.

 

 

When you need speed, try cyclosporine. Cyclosporine acts rapidly. An initial high dose of 5 mg/kg per day can take control of refractory plaque psoriasis, rapidly moving pustular psoriasis, or severe, rapidly progressive psoriasis. No more than a year of continuous use is the guideline, so you don’t want to start low and go slow. "Kids and typically tolerate and need higher doses" compared with adults, Dr. Cordoro said. Use the modified form (Neoral) for better oral bioavailability and better sustained drug levels, she suggested.

This, too, is a rescue treatment intended to control and stabilize the disease, followed by tapering and transitioning to other therapies. The most serious potential side effects include nephrotoxicity, hypertension, and immunosuppression. The most common side effects include nausea, vomiting and diarrhea, anorexia, and headache. Less often, cyclosporine can cause myalgia, arthralgia, paresthesia, gingival hyperplasia, or hypertrichosis. "My colleagues in oncology assure me that at the doses we’re using for psoriasis, we’re not at risk for giving these kids carcinomas down the road," she said.

Biologics play an important role. Biologics are potent, but wouldn’t be the first choice for systemic therapy because they don’t have prolonged efficacy, said Dr. Cordoro. Their precise place in the therapeutic armamentarium is yet to be defined. "I like to reserve a biologic for when I don’t necessarily have a better choice, because I know I have a finite period of time for biologics," she said.

Nonetheless, anti–tumor necrosis factor agents can play a role in treating refractory plaque psoriasis, severe or refractory generalized pustular psoriasis, or psoriatic arthritis, Dr. Cordoro said. Anecdotal reports suggest that IL-12 and IL-23 inhibitors may help with pediatric psoriasis, but there are no study data yet.

The potential advantages of using biologics include less frequent dosing, less laboratory monitoring, and targeted treatment. On the other hand, biologics are expensive, require injection or infusion, have as-yet-unknown long-term risks, and are not approved for treating pediatric psoriasis (so insurance coverage is a battle), said Dr. Cordoro. Questions remain about standardized dosing and monitoring protocols, and about the endpoints of biologic therapy in this setting, although experience with biologics and evidence of their efficacy and safety in children are accumulating, she said.

Dr. Cordoro recommended two articles that she coauthored that provide expert consensus guidelines, tables, and charts for systemic treatment and monitoring of children with psoriasis (Dermatol. Clin. 2013;31:267-88 and Skin Therapy Lett. 2013;18:1-4).

Dr. Cordoro reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

*CORRECTION, 11/4/2013: An earlier version of this article imprecisely stated the results of the informal study.

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