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CME/CE

Management of Rosacea

  • Authors: Guy F. Webster, MD, PhD; Diane Thiboutot, MD; James J. Leyden, MD
  • CME/CE Released: 8/28/2012
  • THIS ACTIVITY HAS EXPIRED
  • Valid for credit through: 8/28/2013
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Target Audience and Goal Statement

This activity is intended for dermatologists, primary care physicians, nurse practitioners, nurses, physician assistants, and other clinicians who treat patients with rosacea.

The goal of this program is to review the pathogenesis and treatment of rosacea, with an emphasis on emerging research on the molecular pathology of the disease.

Upon completion of this activity, participants will be able to:

  1. Describe the clinical subtypes of rosacea
  2. Review the evolving understanding of the pathogenesis of rosacea
  3. Examine treatment strategies that incorporate topical and systemic pharmacologic options for rosacea, as well as skin care practices and lifestyle modifications to help manage the disease


Disclosures

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Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.


Moderator

  • Guy F. Webster, MD, PhD

    Clinical Professor, Department of Dermatology, Jefferson Medical College, Philadelphia, Pennsylvania

    Disclosures

    Disclosure: Guy F. Webster, MD, PhD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Galderma Laboratories, L.P.; Allergan, Inc.; Ranbaxy Pharmaceuticals Inc.; GlaxoSmithKline; Valeant Pharmaceuticals International

    Dr Webster does intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Webster does intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

Panelists

  • Diane Thiboutot, MD

    Professor of Dermatology, Penn State College of Medicine, Hershey, Pennsylvania

    Disclosures

    Disclosure: Diane Thiboutot, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Allergan, Inc.; Intendis Inc; Galderma Laboratories, L.P.
    Received grants for clinical research from: Allergan, Inc.; Galderma Laboratories, L.P.

    Dr Thiboutot does intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Thiboutot does intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

  • James J. Leyden, MD

    Professor Emeritus, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

    Disclosures

    Disclosure: James J. Leyden, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Allergan, Inc.; Anacor Pharmaceuticals, Inc.; Obagi Medical Products, Inc.; Medicis Pharmaceutical Corporation; Unilever United States, Inc.

    Dr Leyden does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Leyden does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

Editors

  • Kristin M. Richardson

    Group Scientific Director, Medscape, LLC

    Disclosures

    Disclosure: Kristin M. Richardson has disclosed no relevant financial relationships.

  • Devon Schuyler

    Clinical Editor, Medscape, LLC

    Disclosures

    Disclosure: Devon Schuyler has disclosed no relevant financial relationships.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC

    Disclosures

    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

Nurse Planner

  • Laurie E. Scudder, DNP, NP

    Nurse Planner, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor, School of Nursing and Allied Health, George Washington University, Washington, DC

    Disclosures

    Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.


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CME/CE

Management of Rosacea

Authors: Guy F. Webster, MD, PhD; Diane Thiboutot, MD; James J. Leyden, MDFaculty and Disclosures
THIS ACTIVITY HAS EXPIRED

CME/CE Released: 8/28/2012

Valid for credit through: 8/28/2013

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  • Guy F. Webster, MD, PhD: Hello, I'm Dr Guy Webster, clinical professor, department of dermatology, Jefferson Medical College in Philadelphia. I would like to welcome you to this program titled "Management of Rosacea."

  • Slide 1.

    Slide 1.

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  • Joining me are Dr Diane Thiboutot, professor of dermatology at Penn State in Hershey, Pennsylvania, and Dr Jim Leyden, professor emeritus, University of Pennsylvania School of Medicine, department of dermatology, in Philadelphia.

  • Slide 2.

    Slide 2.

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  • We are going to talk about rosacea and associated diseases. Rosacea is a common disease. How common is hard to say exactly because it is difficult to define when a little blush on the cheek turns into rosacea. Depending on the study you look at, rosacea may affect from 5% to 15% of the population. We tend to think of rosacea as a disease that appears mainly in fair-skinned people, but as we'll talk about later, plenty of people with darker skin have aspects of rosacea that probably have gone unrecognized.

    Rosacea doesn't kill anybody, but it can make life quite miserable. Quality-of-life issues are key for many patients. Blushing and flushing can be painful and certainly unattractive. People with rosacea blush at the worst times, such as when they are under pressure and trying to be cool, yet they look the exact opposite of cool.

    Pustules and papules can form in the center of the face. Noses can get bulbous with sebaceous overgrowth called rhinophyma that approaches a W. C. Fields or J. P. Morgan look. Finally, the skin in rosacea is particularly irritable, resulting from a barrier defect.

  • Slide 3.

    Slide 3.

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  • There are clinical subtypes of rosacea. It is important to note that these are not stages of rosacea that progress from one stage to the next but rather different subtypes that we group together by symptom in patients with the disease we call rosacea.

    The first subtype is erythematotelangiectatic rosacea, which, to real people, means red. Patients get red cheeks and big blood vessels. There may be a component of sun damage.

  • Slide 4.

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  • Patients may also have papulopustular rosacea. It tends to be in the center of the face, and this subtype is usually what patients think of when they think of rosacea.

  • Slide 5.

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  • Phymatous rosacea, fortunately, is uncommon, especially in women. When diagnosing and treating patients, it is important to tell them that even though they have rosacea it is unlikely that they are going to end up looking like W. C. Fields.

  • Slide 6.

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  • Finally, there is ocular rosacea, which I think is an important subtype. Perhaps 30% of patients with cutaneous rosacea have ocular rosacea. It can manifest as styes or irritability or inability to tolerate contact lenses.

  • Slide 7.

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  • Rosacea does occur in darker skin, but the index of suspicion in darker-skinned patients is often very low because most of the dermatology textbooks were written by white men rather than people in pigmented countries. If you do a literature search in Medline, you will find that there are a lot of papers on rosacea from Turkey, Arab countries, and Asian countries, where the skin may be many shades darker than in the Northern European people we think of as typical rosacea patients.

    So clearly rosacea is not limited to the fair-skinned, but if you use a red face as the entry criterion for making a diagnosis of rosacea, you will miss the diagnosis in darker skin because you can't see the red through the pigment. In these cases, you need to ask patients about irritation. Do they become irritated when certain moisturizers are applied to their skin? Do they get a sense of warmth in the face? Do they have symptoms of ocular rosacea? A history of styes in childhood often predicts the development of rosacea in adults. Rosacea patients with darker skin are treated with the standard approaches that we will talk about in a few minutes.

    But before we do that, Dr Jim Leyden will talk about the pathogenesis of rosacea.

  • Slide 8.

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  • James J. Leyden, MD: Rosacea is a common disorder, and it is surprising that until relatively recently there has been very little study of the disease. Ronald Marks did some studies back in the day, about 45 years ago,[1,2] and Frank Powell has done some studies over the years.[3,4] More recently, the molecular biology techniques that have transformed our understanding of a variety of diseases have been applied to rosacea, so we are beginning to get glimpses of what may be going on at a more substantial level than we have understood in the past.

    You mentioned the subtypes of rosacea. There is a lot of discussion about whether these subtypes are part of a single disease process or whether they are separate entities with a common background of flushing. The point you made that there is a lot of evidence against the progression from one subtype to another is an important understanding that we have come to realize.

    There are good epidemiologic studies that show there is clearly a genetic component, but obviously no "rosacea gene" has been found yet. As I said, recent application of molecular biology techniques has started to give us an inkling of what may be happening in this process. I think it is worth mentioning that there have been relatively small numbers of patients in these studies, and for good reason. These are labor-intensive studies and they are expensive.

  • Slide 9.

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  • Gene array studies show that about 20% of the genes that are upregulated in the various forms of rosacea are linked with inflammation and immune defense. Surprisingly, there are genes involved in lipid and alcohol metabolism that have been identified.

    Diane Thiboutot, MD: It is interesting that there are now gene array data for different diseases of the skin. There are array data for acne, rosacea, and psoriasis. We are now able to compare those array data among the different diseases to find similarities and differences, which is exciting.

    Dr Leyden: And 50 years from now, they will say, "Can you imagine? Back then, they didn't even know ..."

    There is some suggestion that certain cytokines and chemokines may be central to the disease. Perhaps we will see with further study if interleukin 7 and interleukin 26 are really central to the disease, the way we've learned in psoriasis, for example, which has led to substantial differences in treatment.

  • Slide 10.

    Slide 10.

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  • There is an emerging concept that neurogenic inflammation is involved in rosacea. Interestingly, there is a marked increase in mast cells. There is also a marked increase in fibroblasts.

    One of the more interesting recent discoveries is the novel class of nonselective nerve receptors called transient receptor channels. One of them, for example, responds to capsaicin and things that we recognize as triggers in rosacea patients -- spicy foods, temperature changes, and various chemicals. When they are upregulated or stimulated they release substance P and calcitonin gene-related peptide, which is a potent vasodilator.

    Dr Thiboutot: Have any of them been shown to relate to ultraviolet exposure?

    Dr Webster: Or up-regulated by it?

    Dr Leyden: That would be another one of the possible triggers.

  • Slide 11.

    Slide 11.

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  • The emerging hypothesis, which has to be tested before it becomes a theory -- or a dogma -- is that there may be a genetic predisposition and either an overexpression of these receptors and/or a different threshold for activation, resulting in neurogenic inflammation.

  • Slide 12.

    Slide 12.

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  • The other idea being talked about in our field is the possibility that the innate immune system is involved in rosacea. There are data showing increased Toll-like receptor 2, increased amounts of cathelicidin -- the antimicrobial peptide -- and increased amounts of various other peptides in rosacea skin compared with nonrosacea skin.There is also increased kallikrein processing of cathelicidin, resulting in increased peptides.

    Dr Thiboutot: There is sometimes a bit of confusion because the cathelicidins are antimicrobial peptides, and people think that is generally good because they are killing bacteria that might relate to the disease process. But a lot of people don't realize that these same cathelicidins are proinflammatory, and that is what is thought to be playing a role in rosacea.

    Dr Leyden: And that is what the innate immune system is all about. It's a defensive mechanism, so if an invading microbe is trying to get into us, it's fortunate that we have that system before a specific immune defense is developed.

    Dr Webster: It makes a lot of sense too that cathelicidin gets cleaved into other active agents, just like the complement cascade where you have a component that binds to a cell and casts off an active inflammatory component. A lot of different things happen with inflammation, and it's never as simple as we think it is. There are wheels turning within wheels, and I think that one day we'll find that maybe the cathelicidin story is only part of it, maybe even an epiphenomenon.

  • Slide 13.

    Slide 13.

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  • Dr Leyden: One of the things that has not been totally worked out yet is the role of ultraviolet radiation, although there is at least 1 good study just reported at the recent Society of Investigative Dermatology meeting.

    When Ronald Marks did his classic histology work[2] in rosacea, he emphasized the solar elastosis in the biopsies of patients. That could be because they were more prone to rosacea and more prone to photodamage. One of the studies done in our department many years ago by Albert Kligman, MD, PhD, and Robert Lavker, PhD,[5] looked at biopsies of skin from the back of the necks of North Carolina farmers, and they noticed a marked increase in mast cells and apposition of those mast cells with fibroblasts. Now we're seeing this in rosacea, and there is the possibility that it may be photodamage.

    The recent study from the University of Michigan looked at patients with photo damage without flushing and blushing vs patients who might have had some photodamage but clearly had what we would call erythematotelangiectatic rosacea. The investigators found a marked increase in mast cells in those with rosacea compared with those with photodamage. In addition, there was an almost 10-fold increase in calcitonin gene-related peptide in the skin of subjects with erythematotelangiectatic rosacea compared with subjects with photodamage. They also found a marked increase in substance P, but interestingly, they did not find an increase in cathelicidin or the other peptides that have been described. So, as is often the case, as more people start doing studies we get more questions. So while it's beginning to get clearer, it's also getting muddier.

  • Slide 14.

    Slide 14.

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  • It was thought for a long time that papulopustular rosacea is not a follicular disease. I think Frank Powell has clearly shown that it is a follicular inflammatory process.[4] The question is, what triggers it? Right now, Demodex seems to be the most likely candidate -- perhaps the only candidate. There are data that topical ivermectin, which is an anti-Demodex, works, but it may have other activity.

    Dr Webster: But topical lindane doesn't do much.

    Dr Leyden: Well, there you go. Who knows? And whatever the trigger is, it may be reacting via Toll-like receptors in follicular epithelium.

    A question I have an interest in is, if you have a patient with what we call papulopustular rosacea, when the papules and pustules go away, does the patient still have papulopustular rosacea or is it erythematotelangiectatic rosacea? Maybe they are the same, and then for whatever reason waves of papules and pustules are overlaid on that. We'll see in time.

  • Slide 15.

    Slide 15.

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  • There is not as much research on the phymatous subtype, and the molecular techniques have not been applied to the same degree in that area. One hypothesis is that receptors for cytokines and chemokines can switch from an inflammatory to a fibrotic response.

    Dr Thiboutot: That's what I was thinking about because you have all those mediators. Maybe they are mediated by the mast cells in part. On the one hand, you have possible breakdown of collagen where you have the solar elastosis. Yet on the other hand, in the nose, you end up getting this fibrotic response.

  • Slide 16.

    Slide 16.

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  • Dr Leyden: In ocular rosacea, there are some advances in terms of molecular studies. Several investigators have shown that there is increased interleukin 1.Some older studies suggest there is a decrease in tear production.The studies that interest me show that the meibomian secretion -- meibum -- is different; there is an increase in certain fatty acids which makes sense to some people in terms of tear stability. When you look at patients with ocular rosacea, you see this inspissated concrete-like stuff in the follicles with inflammation around it. There are studies showing that systemic antibiotics like azithromycin and minocycline actually have an effect on the fluidity of the meibum -- that it becomes more fluid, less waxy, less thick. We need more work in that area.

    Dr Thiboutot: You wonder if it's the inflammatory response to the bacteria, and that inflammatory response is somehow affecting lipid production in the meibomian glands.

    Dr Leyden: We did a study in Guy's earlier years -- in childhood when he was getting his PhD -- at the Wills Eye Institute in Philadelphia. We were hell bent to find P acnes or something in those follicles that was responding to tetracyclines and we couldn't, we failed. So if there's an organism in there, we couldn't find it. And there are only 2 or 3 studies suggesting that the lipid composition of the meibomian gland is different.

    Dr Webster: Of course, those kind of studies are "fiddling studies," and there's a lot of room for technical error, as we both well know. I'd want to see a preponderance of data.

    Dr Leyden: Right, but at least we're beginning to have studies. In the past we just had talk.

    Dr Webster: Talk is easy.

    Dr Leyden: Talk is easy, and studies are hard. And the more you look, the more you have to look. That's what research means: look again.

    Dr Webster: Well, enough with research already. Let's talk about patients. Diane, would you tell us how you treat rosacea topically?

  • Slide 17.

    Slide 17.

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  • Dr Thiboutot: We have a variety of medications and a variety of formulations. There is clindamycin, erythromycin, sodium sulfacetamide/sulfur. Probably the 2 mainstays of topical therapy are metronidazole and azelaic acid.

  • Slide 18.

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  • Metronidazole is available as a cream and gel in a 1% formulation. The generics are mostly available in a 0.75% formulation. Metronidazole 1% gel is indicated for the inflammatory lesions of rosacea -- not for erythema -- and it is generally dosed once a day.

    In terms of lesion reduction, the data are quite comparable between metronidazole and azelaic acid, with about a 50% to 65% decrease in the inflammatory lesions of rosacea.

  • Slide 19.

    Slide 19.

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  • Dr Leyden: That brings up an interesting point. The papulopustular lesions are interesting in terms of their natural history because they are more likely to get better.

    Dr Thiboutot: Right.

    Dr Leyden: So when we look at data, people say "maybe we should just sell the vehicle." But what it really shows is the natural history of the disease.

    Dr Webster: It's a disease that tends to get better.

    Dr Leyden: The natural history is characterized by waxing and waning with significant periods of freedom from lesions.

    Dr Thiboutot: Many of my patients might have 2 or 3 flares a year, and the rest of the time they are doing pretty well. So it makes it difficult to do studies because you don't know where the patients are falling along that continuum.

    Dr Webster: The one aspect of rosacea that seems pretty even in intensity is ocular rosacea. If patients are bad in January, they're going to be bad in June.

    Dr Thiboutot: It's pretty consistent.

    Dr Leyden: They don't wax and wane so much; that's right. I always thought it would be good if we had studies looking earlier in the disease process. The time points in rosacea studies are pretty much the same as in acne studies -- we pick people at their worst. If there is an anti-inflammatory effect, I think we would see more if we had earlier time points. We might be able to distinguish between the natural history of the disease and the activity of the active ingredient by looking more thoroughly at an earlier time point.

  • Slide 20.

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  • Dr Thiboutot: Azelaic acid is also used topically for rosacea, and it comes as a 15% gel. There are data to suggest that it has antimicrobial activity. It may have some effects on keratinization, and some recent studies in animal models suggest that azelaic acid may have some effect on the kallikrein 5 enzyme and the Toll-like receptor 2 that Dr Leyden was talking about earlier. There is about a 55% reduction in inflammatory lesions after about 10 weeks of treatment.

  • Slide 21.

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  • Another topical agent that is often used as a wash or a lotion is sodium sulfacetamide/sulfur. There have been some studies done, but many of them were not vehicle-controlled. I often find that it works well in patients who have seborrheic dermatitis along with their rosacea -- that is where I use it most.

    Dr Webster: That is something that I find a lot -- a mixture of rosacea and seborrheic dermatitis or rosacea and eczema. And if you don't take care of the second disease, the rosacea ends up being very resistant. It is as though the other disease is itself a trigger for rosacea.

  • Slide 22.

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  • Dr Thiboutot: A Cochrane review of rosacea therapies looked at 58 controlled trials in more than 6000 patients.The conclusions were that there was evidence that topical metronidazole and azelaic acid were better than placebo, and there was 1 study that reported the use of cyclosporine in an ophthalmic formulation for the treatment of ocular rosacea. Azelaic acid and metronidazole are approved by the US Food and Drug Administration (FDA) for the treatment of rosacea. Ophthalmic cyclosporine is not, but has been reported to be beneficial.

  • Slide 23.

    Slide 23.

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  • In terms of other topical therapies for ocular rosacea, ophthalmologists often recommend lid hygiene -- warm soaks, sometimes using baby shampoo to remove the crusts. I think artificial tears are important. A lot of people have dry eye, and as I mentioned, cyclosporine has been used and so has ocular azithromycin.

    Dr Leyden: The dry eye is a result of the meibum not getting to spread?

    Dr Webster: There's dry eye, and there's dry eye. The eye has a limited vocabulary. It can say it hurts. It can say it's dry. It can say it's itchy. A lot of times the dry sensation is a reflection of inflammation, and it's not actually dry when you measure the tear level. The lack of meibum, which is the outer layer on the tear film, will make tears evaporate more quickly.

    Dr Webster: Let's talk a bit about oral rosacea therapy -- what you would do when topical therapy fails or if you have a patient who says, "I don't want creams. I want to take pills." This is what a lot of men say.

  • Slide 24.

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  • Tetracycline antibiotics are clearly effective. The only FDA-approved drug for treating rosacea orally is doxycycline 40 mg, and we believe that it works directly by being anti-inflammatory. Tetracyclines are a family of drugs that have a lot of activities in addition to the one they are famous for. In addition to being antibiotics, they are also antimalarial and they are anti-inflammatory in many different ways. One of them, perhaps the one that's most relevant to rosacea, is inhibition of granulomas and inhibition of protease activity, which they do quite effectively.

    Doxycycline has been developed in a dose so low that it is not antimicrobial, so you don't have to worry about raising up resistant populations in your rosacea patients. It seems to be every bit as effective as the antimicrobial-dose doxycycline in treating rosacea.

  • Slide 25.

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  • Other oral drugs used are ciprofloxacin, trimethoprim sulfamethoxazole, and isotretinoin, which have all been used in patients who have not responded to doxycycline. To my way of thinking, it is hard to rationalize using ciprofloxacin or trimethoprim sulfamethoxazole very often. Ciprofloxacin and trimethoprim sulfamethoxazole are both drugs that we use for serious infections, and because rosacea is a chronic disease, you wouldn't want to have many patients on these drugs long-term. But if your back is against the wall and you can't get somebody better, that's something to think about.

    Granulomatous rosacea often responds to isotretinoin in a lower dose than you would use for acne. You're looking for a low, long-term suppressive dose; 10 or 20 mg a day is often sufficient. You don't get the long-term cure that you do in acne when you use isotretinoin in rosacea. When you take patients off the drug, the rosacea often comes right back.

    There are other drugs that are occasionally effective, such as β-blockers in patients who have a particular problem with flushing and blushing due to excitement. You can take away one of the feedbacks for increasing emotional excitement by using a β-blocker. It's actually a performance-enhancing drug.

    Selective serotonin reuptake inhibitors are often helpful in patients whose rosacea exacerbates when they are depressed. I have had several rosacea patients whose chronic depression was diagnosed because they came to the dermatologist saying, "Why is my face always red?" and it turned out they were always crying.

  • Slide 26.

    Slide 26.

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  • One of the questions that comes up when you think about using low-dose doxycycline is, "Is it as good as high-dose doxycycline?" Naturally we all think that more is better, so why not use more? Well, there are reasons not to use more. Higher-dose doxycycline is phototoxic. It can upset the stomach in some patients, and there is at least the possibility of generating antibiotic-resistant bacteria.

    This slide is a plot of the body weight of patients in a doxycycline study vs their clinical response. It basically shows that really thin people and really heavy people with about a 4-fold difference in body mass had the exact same clinical response to 40-mg doxycycline, which is sort of like saying that 40-mg doxycycline is as good as 160-mg doxycycline. My clinical experience seems to bear that out, and in the average rosacea patient, low-dose doxycycline is every bit as good as the higher dose.

    Dr Leyden: That doesn't answer the question of why in the clinical studies for 40-mg doxycycline there seemed to be groups of patients who did well and those who did fair to not so well. What's missing in that analysis is that we don't know about absorption. There is about a 35% coefficient of variation of absorption of that particular form of doxycycline, so if you're a poor absorber, that would explain a lot. That would mean that a higher dose would give you the same plasma level as someone who is a better absorber. So there is still some work to be done.

    Dr Webster: In addition, you don't know that 40 mg is the lowest dose that works.

    Dr Thiboutot: The other thing that's been a source of confusion for our residents in training and other folks is that the 40-mg formulation we're talking about is a sustained-release formulation. So it's not the same as taking two 20s at the same time. Again, it gets back to the release.

    Dr Leyden: And the absorption.

    Dr Webster: Rounding out the therapeutic options are laser and light treatments, which are particularly effective in some forms of rosacea. Diane,would you talk about that?

  • Slide 27.

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  • Dr Thiboutot: The erythema of rosacea is difficult to treat. The medical treatments that we have tend to not do as good a job with erythematotelangiectatic rosacea as they do with the papules and pustules. I think lasers and lights may be a little bit more effective in this area. The pulsed-dye laser and intense pulsed light have been used. I want to talk a little bit about the comparison because I think most commonly, people are using pulsed-dye lasers or intense pulsed light. A side-by-side comparison of the 2 modalities was done in 2009. Basically they found that both pulsed-dye lasers and intense pulsed light were effective, and there was no difference between the two in this particular study. The study was well done; it was a split-face comparison.

  • Slide 28.

    Slide 28.

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  • In terms of rhinophyma, the other subtype of rosacea, most treatments are surgical. Surgeons use excision, the carbon dioxide laser, the cauterizing scalpel, or sometimes combinations of these.

  • Slide 29.

    Slide 29.

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  • The other aspect of rosacea treatment that we haven't touched on is lifestyle modification. I think patient education is very important. We need to educate our patients about sun protection and avoiding trigger factors, and we should give them recommendations for skin and eye care.

    I often ask my rosacea patients if they have any eye symptoms because I think a lot of them are unaware that their eye problems are related to their skin problems.

    Dr Leyden: And they wouldn't think of telling it to a dermatologist.

    Dr Thiboutot: Right, so I make it a point to ask.

    Dr Webster: And look.

    Dr Thiboutot: And look. Exactly. In terms of eye care, we generally recommend artificial tears -- that is my starting point. Doxycycline can also help for the eye symptoms.

  • Slide 30.

    Slide 30.

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  • In terms of facial cleansers, for the most part rosacea patients have sensitive skin, so I generally recommend a mild cleansing agent. Oftentimes, as we talked about, UV radiation may play a role, so the use of sunscreen is important. You can also find moisturizers that contain sunscreens.

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    Slide 31.

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  • Dr Webster: So what's left? Well, what's left is the future. Current research is looking at different mechanisms of inflammation. It's tempting to think that what we know today is the answer. But we have figured out over a few centuries that that's not true -- nobody leeches anything anymore.

    What treatments are coming? There are products being developed to directly address the erythema of rosacea. Previously, the thought was that you can make some redness go away by making a pimple go away, and the reactive erythema goes along with it, but that's not the redness that rosacea patients complain about. They're complaining about the basic red face without pimples. What do you do about that?

    Two products in late-stage development are oxymetazoline and brimonidine. Both work quite well in making redness go away for 8 or 12 hours. They seem to be safe, and I'm excited about this new option coming.

    Ivermectin is coming too. It is known as an antiparasitic, and it was developed based on the idea that Demodex is important in rosacea. I'm a Demodex agnostic. I don't think it's important in rosacea, and I think the fact that ivermectin works means it's doing something else antiinflammatory. But I've been wrong at least once before. Do you have anything that you would like to add?

    Dr Leyden: As I said earlier, we need a lot more molecular studies, and if they are funded and done we may get to the point that we have specific cytokines that become targets, the way we do in psoriasis. The way we are talking now about rosacea is the way we were talking about psoriasis 10, 15, 20 years ago. Now we have a whole host of drugs for psoriasis that are very specific. If molecular studies in rosacea continue, we should be in the position we are in now with psoriasis.

    Dr Webster: Yes, and 20 years ago, there were a million different mediators that were measured and found to be elevated in psoriasis, but only one or two have been found to be critically important for making psoriasis better. And the others are just bystanders doing what they're told.

    Dr Leyden: So the future may be bright.

    Dr Webster: The future is definitely bright, we just can't predict it.

    Dr Thiboutot: Hopefully, we'll be ready.

    Dr Leyden: Hopefully, I'll be around for it.

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    Slide 32.

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  • Dr Webster: Thank you for participating in this activity. You may now take the posttest by clicking on the "Earn CME/CNE Credit" link. Please also take a moment to complete the program evaluation that follows. Thank you very much.

  • Slide 33.

    Slide 33.

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This transcript has been edited for style and clarity.

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