Rosacea is a common condition characterized by symptoms of facial flushing and a spectrum of clinical signs, including erythema, telangiectasia, coarseness of skin, and an inflammatory papulopustular eruption resembling acne (see the image below).[1, 2]
View Image
Rosacea: mild papules and erythema. Image from DermNet New Zealand (https://www.dermnetnz.org/imagedetail/2367).
Classification
On the basis of specific clinical signs and symptoms, an expert committee assembled by the National Rosacea Society explicitly defined and classified rosacea into the following subtypes:
Erythematotelangiectatic
Papulopustular
Phymatous
Ocular
Diagnostic criteria
The diagnosis of rosacea is made clinically on the basis of the updated classification developed by the global rosacea consensus panel in 2017, which specified that at least one diagnostic phenotype or two major phenotypes are required for diagnosis.[3, 4]
Diagnostic phenotypes (≥1 required) include the following:
Fixed centrofacial erythema in a characteristic pattern that may periodically intensify
Phymatous changes
Major phenotypes (≥2 required) include the following:
Papules and pustules
Flushing
Telangiectasia
Ocular manifestations
Secondary signs and symptoms that may appear with one or more diagnostic or major phenotypes include the following:
Burning and stinging
Edema (facial edema)
Dry-appearing skin
Ocular rosacea
Major features of ocular rosacea are as follows:
Lid margin telangiectasia
Interpalpebral conjunctival injection
Spade-shaped infiltrates in the cornea
Scleritis and sclerokeratitis
Secondary features of ocular rosacea are as follows:
"Honey crust" and collarette accumulation at the base of the lashes
Irregularity of the lid margin
Evaporative tear dysfunction
Although ocular manifestations may precede the cutaneous signs by years, in many cases they develop concurrently with dermatologic manifestations.
A skin biopsy is sometimes performed to exclude other cutaneous diseases, such as lupus or sarcoidosis.
See Clinical Presentation for more detail.
Histologic findings
Histologic findings include the following:
Nonpustular lesions show a nonspecific perivascular and perifollicular lymphohistiocytic infiltrate, accompanied by occasional multinucleated cells, plasma cells, neutrophils, and eosinophils
Papulopustular lesions demonstrate more pronounced granulomatous inflammation and sometimes perifollicular abscesses
Demodex folliculorum may be abundant in nearby follicles
See Workup for more detail.
Management
Deterrence
Before the initiation of therapy, the triggering factors that exacerbate the patient's rosacea should be identified and avoided if possible. Common triggering factors include the following[5, 6] :
Hot or cold temperatures
Wind
Hot drinks
Caffeine
Exercise
Spicy food
Alcohol
Emotions
Topical products that irritate the skin and decrease the barrier
Medications that cause flushing
In addition, daily use of broad-spectrum sunscreen is recommended for all patients with rosacea.[7]
Laser treatment
Vascular lasers, the mainstay of rosacea therapy, use wavelengths that allow selective absorption by oxyhemoglobin, leading to vessel reduction and causing minimal scarring or damage to surrounding tissue.
Pharmacologic therapy
Agents used to treat rosacea include topical acne agents, topical and oral antibiotics, topical alpha agonists, retinoidlike agents, calcineurin inhibitors, potassium-sparing diuretics, and corticosteroids. (See Medication.)
Surgery
Permanent telangiectasia may be treated by electrosurgery or the 585-nm pulsed dye laser. However, facial erythema is not improved, and new telangiectasias develop with the passage of time. Cosmetic improvement of rhinophyma may be produced by mechanical dermabrasion, carbon dioxide laser peel, and surgical shave techniques.
Rosacea is a common condition characterized by symptoms of facial flushing and a spectrum of clinical signs, including erythema, telangiectasia, coarseness of skin, and an inflammatory papulopustular eruption resembling acne.[1, 2]
Rosacea is defined by persistent erythema of the central portion of the face lasting for at least 3 months. Supporting criteria include flushing, papules, pustules, and telangiectasias on the convex surfaces. Secondary characteristics are burning and stinging, edema, plaques, a dry appearance, ocular manifestations, and phymatous changes. The prevalence of these findings designates the subclassification of the presentation, as well as the therapeutic options.[8, 9, 10]
An expert committee assembled by the National Rosacea Society explicitly defined and classified rosacea into four different subtypes (erythematotelangiectatic, papulopustular, phymatous, and ocular) on the basis of specific clinical signs and symptoms. Although didactically successful, the subtype designations were widely used individually and construed as distinct disorders, with the result that the frequent simultaneous occurrence of more than one subtype and the potential progression of one subtype to another were often ignored.
The diagnosis of rosacea is made clinically on the basis of the 2017 classification from the global rosacea consensus panel,[3] which specified that one diagnostic or two major phenotypes are required for the diagnosis (see Criteria for Clinical Diagnosis).
Skin biopsy may be necessary to exclude other disease states that mimic the clinical presentation of rosacea. For example, the clinician must exclude polycythemia vera, connective-tissue diseases (eg, lupus erythematosus, dermatomyositis, mixed connective-tissue disease), photosensitivity, carcinoid syndrome, mastocytosis, long-term use of topical steroids, contact dermatitis, and photosensitivity before making the diagnosis of rosacea.
Because the details of the pathophysiology of rosacea have not yet been fully elucidated, therapeutic approaches empirically target the signs and symptoms of the disease. The classification systems aid clinicians in treatment by highlighting the preponderance of one or more of the clustering signs of presentation and thereby helping to determine which therapeutic approach to initiate.
Central facial flushing, often accompanied by burning or stinging, is the predominant sign in erythematotelangiectatic rosacea (ETR). The redness usually spares the periocular skin. These patients typically have skin with a fine texture that lacks the sebaceous quality characteristic of other subtypes. The erythematous areas of the face at times appear rough with scale, likely due to chronic low-grade dermatitis. Frequent triggers to flushing include acutely felt emotional stress, hot drinks, alcohol, spicy foods, exercise, cold or hot weather, and hot baths and showers. These patients also report that the burning or stinging is exacerbated when topical agents are applied.
Papulopustular rosacea
Papulopustular rosacea (PPR) is the classic presentation of rosacea. Patients are typically women of middle age who predominately present with a red central portion of their face that contains small erythematous papules surmounted by pinpoint pustules. They may have a history of flushing. Telangiectasias are likely to be present but may be difficult to distinguish from the erythematous background in which they exist.
Phymatous rosacea
Phymatous rosacea is defined as marked skin thickenings and irregular surface nodularities of the nose, the chin, the forehead, one or both ears, or the eyelids. Four distinct histologic variants can occur with rhinophyma (associated changes of the nose): glandular, fibrous, fibroangiomatous, and actinic. The mainstays of treatment are topical isotretinoin and surgical correction. This differs from treatment of other rosacea subtypes.
Ocular rosacea
Although ocular manifestations may precede cutaneous signs by years, they frequently develop concurrently with dermatologic manifestations. Ocular manifestations include blepharitis, conjunctivitis, inflammation of the lids and meibomian glands, interpalpebral conjunctival hyperemia, and conjunctival telangiectasias. Patients may describe eye stinging or burning, dryness, irritation with light, or foreign body sensation. Ocular rosacea, like phymatous rosacea, requires its own distinct therapeutic management. Therefore, dermatologists must ask their patients specifically about ocular symptoms and must perform a thorough physical examination to rule out this type of rosacea.
The etiology of rosacea is unknown. It is likely, however, that several factors play a role in its development, including vasculature, climatic exposures, dermal matrix degeneration, chemicals and ingested agents, pilosebaceous unit abnormalities, microbial organisms, ferritin expression, reactive oxygen species (ROS), increased neoangiogenesis, and dysfunction of antimicrobial peptides (AMPs).[11] Furthermore, the distinct subtype of rosacea is likely determined by a patient's unique sensitivity to these triggers.
Vasculature
Increased blood flow to the blood vessels of the face and an increased number of blood vessels closer to the surface of the face are thought to be responsible for the redness and flushing associated with rosacea. Furthermore, vasodilatation, the normal response to hyperthermia, is thought to be more pronounced or exaggerated in individuals with rosacea.
Climatic exposures
Some studies have suggested that harsh climatic exposures (eg, from wind or ultraviolet [UV] light) damage cutaneous blood vessels and dermal connective tissue. This also includes exposure to solar irradiation, which may explain why rosacea predominately affects the facial convexities and has a tendency to flare in the spring. However, other studies have suggested the contrary, finding that most patients' symptoms do not worsen in the sunlight and do not flare with an acute exposure to UV light.
Dermal matrix degeneration
Rosacea involves associated damage to the endothelium and degeneration of the dermal matrix. However, it is not known whether (A) the initial damage is in the dermal matrix, leading to poor tissue support of cutaneous vessels and causing pooling of serum, inflammatory mediators, and metabolic waste; or (B) the initial abnormality exists in the cutaneous vasculature, leading to leaky vessels and delayed clearance of serum proteins, inflammatory mediators, and metabolic waste, thus resulting in matrix degeneration.
Chemicals and ingested agents
Spicy foods, alcohol, and hot beverages have traditionally been thought to trigger flushing in patients with rosacea. Most of the evidence, however, has not supported a central role for dietary factors in the pathogenesis. Moreover, certain medications (eg, amiodarone, topical steroids, nasal steroids, and high doses of vitamins B6 and B12) may cause flares for patients with rosacea. A rosacealike syndrome (including perioral dermatitis) can result from the indiscriminate use of potent corticosteroids on the face.
Perivascular vs perifollicular inflammation
An inflammatory infiltrate may exist in a perivascular location, a perifollicular location, or both; however, studies to date have yielded conflicting answers to the question of which location predominates. There is a need for more studies designed to categorize subtypes of rosacea, in that the answer to this question varies according to the subclassification.
Microbial organisms
Demodex species (mites that normally inhabit human hair follicles) may play a role in the pathogenesis of rosacea. Some studies have suggested that Demodex prefers the skin regions that are affected in rosacea (eg, nose and cheeks).[12] Some evidence indicates that an immune response of helper-inducer T-cell infiltrates occurs, surrounding the Demodex antigens in patients with rosacea. There is, however, conflicting evidence indicating that Demodex does not induce an inflammatory response in patients with rosacea. Moreover, Demodex is found in large numbers of healthy individuals without rosacea. Further study is required to determine whether Demodex truly is pathogenic.
Some studies have suggested that Helicobacter pylori may be associated with the etiology of rosacea. However, many of these studies were not controlled for confounding variables that influence H pylori prevalence (eg, sex, age, socioeconomic status, and medications). Furthermore, these studies did not have sufficient statistical power to account for the ubiquitous nature of H pylori infection.
Ferritin expression
Iron catalyzes the conversion of hydrogen peroxide to free radicals, which leads to tissue injury by damaging cellular membranes, proteins, and DNA. At the cellular level, unmetabolized iron is stored as ferritin. In a 2009 study, skin biopsy specimens from patients with rosacea were immunohistochemically analyzed, and the number of ferritin-positive cells was significantly higher in affected individuals than in control subjects.[13] Additionally, higher ferritin positivity correlated with more advanced subtypes of rosacea. Thus, increased release of free iron from proteolysis of ferritin can result in oxidative damage to the skin, which may contribute to the pathogenesis of rosacea.
Reactive oxygen species
Early in the inflammatory process, ROS are released by neutrophils, which are postulated to play a central role in the inflammation associated with rosacea. Free radicals (eg, superoxide anions and hydroxyl radicals), in addition to other reactive molecules (eg, molecular oxygen, singlet oxygen, and hydrogen peroxide), make up many of the ROS that lead to oxidative tissue damage. Several mechanisms have been adduced to explain how ROS result in skin inflammation, most notably the following[14, 15] :
Deactivation of natural defenses caused by excessive oxidant stress from ROS
Chemical and oxidative modification of proteins and lipids by ROS
Alteration of the lipid balance, which, when normal, would suppress the creation of ROS
Production of cytokines and other inflammatory mediators by keratinocytes, fibroblasts, and endothelial cells damaged by ROS
Generation of ROS by cathelicidins, which are found in greater amounts in the facial skin of affected individuals
Neoangiogenesis and vascular endothelial growth factor (VEGF) overexpression
Studies performed using video capillaroscopy on ETR lesions showed increased neoangiogenesis and blood-vessel enlargement. Multiple immunohistochemistry studies showed increased vascular endothelial growth factor (VEGF) expression in vascular endothelium in lesional skin of rosacea patients as compared with nonlesional skin. Cuevas et al used topical dobesilate, an inhibitor of angiogenic growth factor, for the treatment of ETR and reported an improvement in erythema and telangiectasia after 2 weeks.[16]
Antimicrobial peptides
AMPs are low-molecular-weight proteins that are a part of the innate immune response and have demonstrated broad-spectrum antimicrobial activity against bacteria, viruses, and fungi. They are rapidly released upon injury or infection of the skin and have been implicated in the pathogenesis of many inflammatory skin diseases. Two of the best-known AMP types are the cathelicidins and the β-defensins; the former are known to be expressed at abnormally high levels in patients with rosacea.
Specifically, the LL-37 peptide form of cathelicidin, in addition to proteolytically processed forms of LL-37, has been found in significantly higher amounts in rosacea patients than in healthy individuals. LL-37 is expressed by polymorphonuclear leukocytes and lymphocytes. It interacts with endothelial cells and stimulates angiogenesis both in vitro and in vivo; it also modulates the expression of VEGF.[11] Injection of LL-37 and these peptides derived from LL-37 into mice was found to induce inflammation, erythema, and telangiectasia; accordingly, researchers hypothesized that an excess of cathelicidins coupled with abnormal processing caused disease.[17]
Accurate incidence data for rosacea are not available; however, rosacea is known to be a common skin condition that disproportionately affects persons of fair-skinned European and Celtic origin. In the United States, it has been estimated that more than 16 million people are affected by rosacea; worldwide, the prevalence is estimated to exceed 5% overall and may be as high as 18% in some areas.[18] A study in Sweden revealed an incidence of one case in 10 middle-class workers. The caseating granulomatous variant (acne agminata) may occur more commonly in people of Asian or African origin.
Rosacea also occurs in people with dark skin but is less frequently diagnosed in such populations. It is unknown whether factors such as masking of facial redness by abundant skin pigment, protective effects of melanin against UV light, and genetic predisposition to rosacea contribute to the lower rate of diagnosis in people with skin color.
Both males and females are affected by rosacea; however, females appear to be affected with slightly greater frequency.[19] different lesions appear to have some age- or sex-related predilections.[18] In younger patients, the first signs are more likely to be flushing and erythema, whereas in older patients, the first lesions are more likely to be telangiectasias. Phymatous rosacea is predominantly found in males.[19]
A spectrum of clinical features is seen, and progression may be stepwise. The condition ranges from minor cosmetic disability to severe disfiguring disease. In most patients who receive treatment, a stable state is reached with variable residual symptoms. In some patients, the disease takes a chronic relapsing or progressive course.
Patients should be advised to avoid known exacerbating factors, such as hot or cold temperatures, wind, hot drinks, caffeine, exercise, spicy food, alcohol, strong emotions, topical products that irritate the skin and decrease the barrier, and medications that cause flushing. Patients should be encouraged to use a noncomedogenic high-factor sunscreen when exposed to sunlight and wind.
Patients with rosacea are likely to have a background of facial flushing, often dating to childhood or the early teens. In adult life, flushing may be increasingly precipitated by hot drinks, heat, emotion, and other causes of rapid body temperature changes. Some patients report flushing with alcohol, which is not a specific symptom.
The symptoms are usually intermittent but can progressively lead to permanently flushed skin. The latter may be described as high-color and is associated with the development of permanent telangiectasia. Additionally, a few individuals report a gritty quality to the eyes, as well as facial edema.
Rosacea consists of a spectrum of symptoms and signs, and most patients do not develop every possible stage of disease. Variable erythema and telangiectasia are seen over the cheeks and the forehead. Inflammatory papules and pustules may be predominantly observed over the nose, the forehead, and the cheeks. (See the images below.) Extrafacial involvement uncommonly occurs over the neck and the upper part of the chest.
View Image
Rosacea: mild papules and erythema. Image from DermNet New Zealand (https://www.dermnetnz.org/imagedetail/2367).
View Image
Rosacea: moderate papules and early pustules. Image from DermNet New Zealand (https://www.dermnetnz.org/imagedetail/2369).
View Image
Rosacea: severe erythema, papules, and pustules. Image from DermNet New Zealand (https://www.dermnetnz.org/imagedetail/2371).
Prominence of sebaceous glands may be noted, with the development of thickened and disfigured noses (rhinophyma) in extreme cases. Unlike patietns with acne, patients with rosacea generally do not report greasiness of the skin; instead, they may experience drying and peeling. The absence of comedones is another helpful distinguishing feature. Ocular lymphedema may be prominent but is uncommon. The condition generally does not produce scarring.
Rhinophyma may occur as an isolated entity, without other symptoms or signs of rosacea. It can be disfiguring and thus distressing for patients. Some authorities consider rhinophyma to represent a different disease process, even though phymatous rosacea is considered one of the four subtypes of rosacea.[20]
Lymphedema may be marked periorbitally; on occasion, it is the presenting symptom.
Symptoms of ocular rosacea may be accompanied by conjunctival injection; rarely, chalazion and episcleritis may occur.
Rosacea fulminans (pyoderma faciale) is, fortunately, a rare complication and is characterized by the development of nodules and abscesses with sinus tract formation accompanied by systemic signs. Patients often have low-grade fever, an elevated erythrocyte sedimentation rate (ESR), and possibly an elevated white blood cell (WBC) count.
Not uncommonly, both seborrhea and seborrheic dermatitis/blepharitis may be observed in patients with rosacea. The reasons for these associations are not well understood.
A rare granulomatous variant of rosacea (acne agminata/lupus miliaris disseminatus faciei) can manifest with inflammatory erythematous or flesh-colored papules distributed symmetrically across the upper part of the face, particularly around the eyes and the nose. The lesions tend to be discrete, and surrounding erythema, though not a marked feature, may be present. These patients often do not have a history of flushing. This pattern of rosacea is sometimes associated with scarring and may be resistant to conventional treatment.
An expert committee assembled by the National Rosacea Society explicitly defined and classified rosacea into the following four subtypes on the basis of specific clinical signs and symptoms:
Erythematotelangiectatic
Papulopustular
Phymatous
Ocular
In 2017, the global rosacea consensus panel recommended an updated classification, in which at least one diagnostic phenotype or, in the absence of a diagnostic phenotype, two major phenotypes are required for the diagnosis of rosacea.[3, 4]
Diagnostic phenotypes
A diagnosis of rosacea may be considered in the presence of one of the following diagnostic cutaneous signs:
Fixed centrofacial erythema in a characteristic pattern that may periodically intensify
Phymatous changes - Patulous follicles, skin thickening or fibrosis, glandular hyperplasia, and bulbous appearance of the nose (rhinophyma is the most common form)
Major phenotypes
Without a diagnostic phenotype, the presence of two or more of the following major features may be considered diagnostic:
Papules and pustules
Flushing - Frequent and typically prolonged
Telangiectasia - Predominantly centrofacial in phenotypes I-IV; rarely seen in darker phenotypes
Ocular manifestations
Secondary phenotypes
The following secondary signs and symptoms may appear with one or more diagnostic or major phenotypes:
Burning and stinging
Edema - Facial edema
Dry appearance - Central facial skin may be rough and scaly
Ocular rosacea
Major features of ocular rosacea are as follows:
Lid margin telangiectasia
Interpalpebral conjunctival injection
Spade-shaped infiltrates in the cornea
Scleritis and sclerokeratitis
Secondary features of ocular rosacea are as follows:
"Honey crust" and collarette accumulation at the base of the lashes
Rosacea keratitis and keratoconjunctivitis sicca are recognized complications. Rosacea fulminans is a rare complication. Scarring generally does not occur. A genetic analysis found rosacea to be associated with an increased risk of hypertension.[21] There is evidence for an association of rosacea with headaches, with different rosacea subtypes possibly asociated with different headache types (eg, migraine, tension, cluster, secondary).[22]
The diagnosis of rosacea is made clinically (see Presentation). In some cases, a skin biopsy is performed to exclude other cutaneous diseases, such as lupus or sarcoidosis.
The histologic features of rosacea depend on the stage of disease. Nonpustular lesions show a nonspecific perivascular and perifollicular lymphohistiocytic infiltrate, accompanied by occasional multinucleated cells, plasma cells, neutrophils, and eosinophils. Papulopustular lesions demonstrate more pronounced granulomatous inflammation and sometimes perifollicular abscesses. Demodex folliculorum may be abundant in nearby follicles. (See the image below.)
View Image
Histopathology of rosacea. Perifollicular chronic inflammation and vascular ectasia. Image from Dirk Elston, MD.
Before the initiation of therapy, the triggering factors that exacerbate the patient's rosacea should be identified and avoided if possible.[4] These factors may be unique to each individual patient. Common triggering factors include the following[5, 6] :
Hot or cold temperatures
Wind
Hot drinks
Caffeine
Exercise
Spicy food
Alcohol
Emotions
Topical products that irritate the skin and decrease the barrier
Medications that cause flushing
Some patients find that regular facial massage reduces lymphedema.
Laser therapy
Nonablative laser therapy acts against rosacea by remodeling of the dermal connective tissue and improving the epidermal barrier.[23] The major disadvantage of this therapy is its cost; it is not covered by insurance. One to three treatments 4-8 weeks apart are required to achieve the best results.
Vascular lasers are the mainstay of rosacea therapy. These include the pulsed dye laser (585 or 595 nm), the potassium-titanyl-phosphate laser (532 nm), and the diode-pumped frequency-doubled laser (532 nm). These wavelengths allow selective absorption by oxyhemoglobin, which leads to vessel reduction with minimal damage to surrounding tissue or scarring. To be effective against deeper facial vessels, lasers using longer wavelengths are required, including the diode laser (810 nm), the long-pulsed Alexandrite laser (755 nm), and the long-pulsed Nd:YAG laser (1064 nm).
Intense pulsed-light therapy is a multichromatic laser with different targets, including melanin and hemoglobin. It is also useful for facial rejuvenation, affecting vascular lesions, pigmented lesions, and hair.
Pharmacologic therapy
Topical metronidazole is commonly used as a first-line agent.[4] A study by De Grau-Bassal et al described the development of an emulgel formulation containing both metronidazole and clindamycin as a possible treatment alternative for rosacea, once the necessary preclinical and clinical studies are done.[24]
Topical azelaic acid, sulfacetamide products, and topical acne medications are also commonly used. (See Medication.)
Topical and oral antibiotics are also very effective, and for oral rosacea, they are usually considered a first-line therapy. Generally, long-term use of oral antibiotics for rosacea should be avoided if possible.[4] In many cases, oral and topical antibiotics are used in combination. The oral treatment may be eventually withdrawn and the topical treatment then used alone as maintenance therapy; however, in patients with ocular involvement, the oral therapy must be maintained.
In patients who require a systemic antibiotic, a doxycycline dosage of 20-50 mg q12h appears to be as effective as the higher dosage (100 mg) previously used.[25] For many patients, this could represent a significant cost reduction.
In two phase 3 randomized controlled trials (RCTs), a modified low-dose oral formulation of minocycline was found to be more effective than than either placebo or doxycycline 40 mg in the treatment of papulopustular rosacea (PPR) and to have a favorable risk-benefit profile.[26]
Retinoids have been advocated by some authorities.[27, 28, 29]
A topical form of the alpha-2 agonist brimonidine was approved by the US Food and Drug Administration (FDA) in August 2013 for treatment of erythema associated with rosacea. In two phase 3 clinical studies of 1 month's duration, which included more than 550 patients, adults who used brimonidine topical gel demonstrated significantly greater improvement in the facial redness of rosacea than those who used vehicle gel alone.[30] In addition, a long-term study of 276 subjects who used brimonidine topical gel for up to 12-months was conducted.
Another topical alpha agonist, oxymetazoline, was approved in 2017 for persistent facial erythema associated with rosacea in adults. In two randomized clinical trials (N = 885) comparing the active drug with the cream vehicle, once-daily topical application of 1% cream was found to reduce persistent facial erythema associated with rosacea through 12 hours.[31] The primary measure of efficacy was the proportion of patients with at least a two-grade reduction in erythema (improvement) from baseline on both the clinician erythema assessment (CEA) and subject self-assessment (SSA) (composite success).
The 2021 rosacea guidelines from the British Association of Dermatologists (BAD) recommended that topical brimonidine or oxymetazoline be considered in cases where facial erythema is the primary presentation.[4]
Topical ivermectin is FDA-approved for treatment of the inflammatory lesions of rosacea. It was recommended as a first-line therapy for rosacea in the 2021 BAD guidelines.[4] Stein et al reported in 2014 that ivermectin 1% cream was safe and effective for the treatment of inflammatory lesions from papulopustular rosacea, on the basis of two identically designed double-blind RCTs of ivermectin 1% cream vs vehicle applied once daily for 12 weeks.[32]
Several case reports have described successful treatment with oral ivermectin plus topical acaricidal agents.[33, 34, 35] A 2014 report described a 12-year-old girl with D folliculorum–associated rosacea who had complete resolution of her symptoms after a single oral dose of ivermectin.[36]
An RCT by Wang et al (N = 34) found that 30% supramolecular salicylic acid (SSA) was effective and safe for the management of PPR.[37]
Rosacea fulminans is treated with moderately high doses of prednisolone (30-60 mg/d) followed by oral isotretinoin.
There is some anecdotal evidence to suggest that rosacea can be effectively treated with medications that reduce flushing, including beta blockers, clonidine, naloxone, ondansetron, and selective serotonin reuptake inhibitors (SSRIs).
Topical and ophthalmic fusidic acid is available in Canada but not in the United States. It is used for the treatment of ocular rosacea. Fusidic acid is a topical antibacterial that inhibits bacterial protein synthesis, causing bacterial death. Rosacea may respond to topical fusidic acid for at least 3 months.
Oral contraceptive therapy has been helpful in patients who provide historical information of worsening rosacea with their hormonal cycle.
Dapsone has been used to treat severe, refractory rosacea; it has been particularly beneficial for patients who cannot take isotretinoin.[38]
Sunscreen
The use of daily broad-spectrum sunscreen is recommended for all patients with rosacea.[7] A sunscreen that protects against both UV-A and UV-B light should be selected. Physical blockers such as titanium dioxide and zinc oxide are well tolerated. Additionally, the sunscreen should contain protective silicones such as dimethicone or cyclomethicone. Green-tinted sunscreens can provide coverage of the erythema.
The patient is encouraged to avoid astringents, toners, menthols, camphor, waterproof cosmetics requiring solvents for removal, or products containing sodium lauryl sulfate.
Permanent telangiectasia may be treated by means of electrosurgery or the 585-nm pulsed dye laser. However, facial erythema is not improved, and new telangiectasias develop with the passage of time.
Cosmetic improvement of rhinophyma may be produced by mechanical dermabrasion, carbon dioxide laser peel, and surgical shave techniques. For those with significant rhinophyma, nasal debulking by means of laser ablation or surgical intervention may be considered.[4]
The following organization has released guidelines for the management of rosacea. Key diagnostic and treatment recommendations have been reviewed and integrated throughout the article.
British Association of Dermatologists guidelines for the management of people with rosacea 2021[4]
What is the rosacea?How is rosacea classified?What are the diagnostic criteria for rosacea?What are secondary signs and symptoms in rosacea?What are the signs and symptoms of ocular rosacea?How is rosacea diagnosed?Which histological findings are characteristic of rosacea?What is the role of laser treatment in the treatment of rosacea?What is the role of surgery in the treatment of rosacea?What are the common triggering factors for rosacea?What is the role of sunscreen in the treatment of rosacea?What is rosacea?How is rosacea diagnosed?What is erythematotelangiectatic rosacea (ETR)?What is papulopustular rosacea (PPR)?What is phymatous rosacea?What is ocular rosacea?What is the pathophysiology of rosacea?What is the role of vasculature in the pathophysiology of rosacea?What is the role of climate in the pathophysiology of rosacea?What is the role of dermal matrix degeneration in the pathophysiology of rosacea?What is the role of chemicals and ingested agents in the pathophysiology of rosacea?What is the role of inflammation in the pathophysiology of rosacea?What is the role of microbial organisms in the pathophysiology of rosacea?What is the role of ferritin in the pathophysiology of rosacea?What is the role of reactive oxygen species (ROS) in the pathophysiology of rosacea?What is the role of vascular endothelial growth factor (VEGF) in the pathophysiology of rosacea?What is the role of antimicrobial peptides (AMPs) in the pathophysiology of rosacea?What causes rosacea?What is the prevalence of rosacea?What is the prognosis of rosacea?What is included in patient education about rosacea?Which clinical history findings are characteristic of rosacea?Which physical findings are characteristic of rosacea?Which physical findings are characteristic of ocular rosacea?Which physical findings are characteristic of rosacea fulminans (pyoderma faciale)?Which dermatologic disorders are common comorbidities of rosacea?Which physical findings are characteristic of a granulomatous variant of rosacea (acne agminata/lupus miliaris disseminatus faciei)?What are the possible complications of rosacea?Which disorders should be included in the differential diagnoses of rosacea?What are the differential diagnoses for Rosacea?What is the role of lab testing in the workup of rosacea?What is the role of skin biopsy in the workup of rosacea?Which histologic findings are characteristic of rosacea?How is rosacea treated?What is the role of sunscreen in the treatment of rosacea?What is the role of laser therapy in the treatment of rosacea?What is the role of surgery in the treatment of rosacea?Which dietary modifications are used in the treatment of rosacea?What are the treatment guidelines for patients with rosacea?What are goals of drug treatment for rosacea?What is the role of metronidazole and retinoids in the treatment of rosacea?What is the role of brimonidine in the treatment of rosacea?What is the role of oxymetazoline in the treatment of rosacea?What is the role of ivermectin (Soolantra) in the treatment of rosacea?Which oral medications are used in the treatment of rosacea?Which medications in the drug class Diuretics, Potassium-Sparing are used in the treatment of Rosacea?Which medications in the drug class Corticosteroids are used in the treatment of Rosacea?Which medications in the drug class Calcineurin Inhibitors are used in the treatment of Rosacea?Which medications in the drug class Antibacterials, Topical are used in the treatment of Rosacea?Which medications in the drug class Alpha Agonists, Topical are used in the treatment of Rosacea?Which medications in the drug class Acne Agents, Topical Combos are used in the treatment of Rosacea?Which medications in the drug class Acne Agents, Topical are used in the treatment of Rosacea?
Danielle Bolton, BS, Medical Assistant, Georgetown Dermatology
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Christen M Mowad, MD, Professor, Department of Dermatology, Geisinger Medical Center
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Emeritus Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier<br/>Served as a speaker for various universities, dermatology societies, and dermatology departments.
Additional Contributors
Saurabh Singh, MD, Staff Physician, Department of Dermatology, Georgetown University/Washington Hospital Center
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Ravi Ratnavel, MD, Mana Ogholikhan, MD, and Saurabh Singh, MD, to the development and writing of this article.
){kind=link}
){kind=link}
){kind=link}
){kind=link}