Types of Rosacea: Subtype Classification, Symptoms & Treatment

If you’re trying to figure out what kind of rosacea you have, you’ve probably run into two different vocabularies. The older one talks about four “subtypes” — erythematotelangiectatic, papulopustular, phymatous, and ocular. The newer one, adopted internationally over the past decade, talks about “phenotypes” — individual features like persistent erythema, telangiectasia, papules, pustules, and phymatous changes that any given patient may show in any combination.

Both vocabularies describe the same disease. The newer one is more clinically useful because it matches how rosacea actually presents in real patients: as a mix of features that overlap and shift over time. This guide covers both, walks through each subtype/phenotype in depth, and connects each pattern to the treatment approach that fits it.

For a faster, plain-English version of this material, see our companion article types of rosacea (explained simply) — that piece is the explainer; this is the complete guide.

At a glance

• Subtype 1 — Erythematotelangiectatic rosacea (ETR): flushing, persistent central facial redness, visible small blood vessels (telangiectasias). Treatment focus: trigger management, sunscreen, topical brimonidine or oxymetazoline, vascular laser/IPL.
• Subtype 2 — Papulopustular rosacea (PPR): persistent central erythema with inflammatory papules and pustules, often mistaken for adult acne. Treatment focus: topical metronidazole, azelaic acid, ivermectin; oral doxycycline at sub-antimicrobial dose.
• Subtype 3 — Phymatous rosacea: thickening, irregular surface, and enlargement of the skin, most commonly on the nose (rhinophyma). Treatment focus: early — topical retinoids and oral isotretinoin; established — surgical/laser debulking.
• Subtype 4 — Ocular rosacea: dryness, burning, gritty feeling, light sensitivity, recurrent styes, blepharitis. Treatment focus: lid hygiene, warm compresses, artificial tears, topical and oral antibiotics under ophthalmologic supervision.
• Phenotype model (current consensus): any patient may show any combination of the features above. Treatment is matched to features present, not to a subtype label.
• Why this matters for you: the right treatment depends on which features you have. A patient with diffuse erythema and telangiectasia (ETR features) needs a fundamentally different approach than a patient with central erythema plus papulopustules (PPR features), even though both are “rosacea.”

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A short history of how rosacea is classified

Until the early 2000s, rosacea was discussed loosely — clinicians described what they saw and treated accordingly. In 2002, the National Rosacea Society Expert Committee published a standard classification system that defined four primary subtypes (ETR, PPR, phymatous, ocular) plus a fifth “granulomatous” variant. This subtype framework dominated rosacea research and clinical practice for the next fifteen years.

The problem with the subtype framework was clinical: most patients didn’t fit cleanly into one subtype. A typical rosacea patient had features of two or three. Treatment recommendations organized by subtype produced awkward conversations — “you have ETR with papulopustular features but mild phymatous changes” was a frequent reality. The framework was descriptive but not as useful as it could be for actually matching treatment to patient.

In 2017, the global ROSacea COnsensus (ROSCO) panel — an international group of dermatologists from Europe, North America, Asia, and Australia — published a phenotype-based classification framework. Instead of asking “which subtype does this patient have,” the framework asks “which features does this patient show, at what severity?” Treatment then matches features.

The 2016 Canadian Clinical Practice Guidelines for Rosacea, on which Dr. Rivers is a co-author (Asai et al, J Cutan Med Surg 2016, PMID 27207355), bridge both frameworks. The guidelines use subtype language as the organizing structure but recognize that real patients overlap, and provide treatment ladders that map cleanly onto the phenotype model.

The current international consensus is phenotype-based. The subtype labels remain useful shorthand and continue to appear in older literature, patient education, and many derm-clinic conversations. We’ll use both throughout this guide.

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Subtype 1 — Erythematotelangiectatic rosacea (ETR)

ETR is the rosacea phenotype most associated with the word “rosacea” in the lay imagination. Its hallmark features are:

• Persistent central facial erythema — a baseline redness that doesn’t go away even when you’re not flushing, concentrated in the central convexity of the face (cheeks, central forehead, nose, chin)
• Frequent flushing episodes — sudden temporary intensifications of the redness, often triggered by heat, alcohol, spicy food, emotional stress, or exercise
• Telangiectasias — visible dilated small blood vessels, most often on the cheeks, nasal alae (the sides of the nose), and around the nose
• Skin sensitivity — burning, stinging, or tightness in response to topical products that other people tolerate easily

Some ETR patients also have associated swelling (edema) of the central face, which can persist between flushing episodes.

Mechanism. ETR is fundamentally a problem of cutaneous vascular reactivity. The blood vessels in the upper dermis dilate too easily and stay dilated too long. Over years, this repeated dilation contributes to the formation of permanent telangiectasias — the small visible vessels that don’t blanch (whiten) when you press on them. The vasculature also appears to be primed to overrespond to neurogenic signals (heat sensors, pain sensors, stress responses), which is why so many ETR triggers operate through the nervous system rather than through inflammation.

Why ETR is often the hardest subtype to treat. ETR doesn’t respond well to the topical antibacterial and anti-inflammatory medications that work for the other subtypes. Metronidazole, azelaic acid, and ivermectin all target inflammatory pathways that aren’t the dominant problem in ETR. The treatments that do work — vascular lasers, intense pulsed light (IPL), topical alpha-agonists — are either expensive, time-limited, or have specific drawbacks that limit how patients use them.

Treatment approach for ETR features:

1. Trigger management. Heat, alcohol, spicy food, hot beverages, stress, and UV exposure all reliably worsen ETR. Identifying personal triggers via a structured trigger diary (see rosacea triggers: the short list that matters) is the cheapest highest-leverage intervention.
2. Daily mineral sunscreen. UV is the single most consistent ETR trigger documented in the literature. See our mineral sunscreen for rosacea primer.
3. Topical alpha-agonists. Brimonidine 0.33% gel (Mirvaso) and oxymetazoline 1% cream (Rhofade) cause cutaneous vasoconstriction and reduce visible redness within an hour, lasting 8–12 hours. Both have meaningful side effect profiles — rebound flushing is the main issue with brimonidine — and require careful patient education.
4. Vascular laser or IPL. For the visible telangiectasias and the persistent baseline erythema, pulsed-dye laser (595 nm), KTP laser (532 nm), and IPL (broadband, with vascular filter) all have strong evidence. Treatment series usually requires three to five sessions; results last years but are not permanent.
5. Coverage cosmetics. Green-tinted color correctors (such as the Dr. Jart Cicapair Color Correcting Treatment) optically neutralize redness and improve daily comfort.

For the visual primer on what diffuse central erythema actually looks like and how to distinguish it from non-rosacea facial redness, see our rosacea redness on face and redness 101: rosacea vs. irritation explainers.

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Subtype 2 — Papulopustular rosacea (PPR)

PPR is the rosacea phenotype that most commonly gets confused with adult acne. Its hallmark features are:

• Persistent central facial erythema (shared with ETR)
• Inflammatory papules — small red bumps without a visible whitehead, distributed across the central face
• Pustules — small white-headed bumps that look like acne pustules but lack comedones (blackheads/whiteheads)
• Notably absent: comedones. Rosacea does not produce blackheads or closed-comedone whiteheads. If you have those, the diagnosis is acne or perioral dermatitis, not rosacea.

PPR often (though not always) overlaps with ETR features — the patient has both the diffuse erythema and the papulopustular elements. The treatment approach changes meaningfully based on whether papulopustules are present.

Mechanism. PPR is dominated by inflammation. The current model involves the innate immune system (specifically, abnormal cathelicidin processing producing inflammatory peptides), the Demodex folliculorum mite (which is present at higher density in rosacea-prone skin and may serve as an inflammatory trigger), and possibly the bacterium Bacillus oleronius associated with Demodex. Unlike ETR, the dominant problem is not vascular reactivity but immune dysregulation in the skin.

Why PPR usually responds well to treatment. Multiple topical and systemic medications target the underlying inflammation effectively. Most PPR patients see meaningful improvement within eight to twelve weeks of starting an appropriate regimen.

Treatment approach for PPR features:

1. Topical azelaic acid 15% gel or foam (Finacea). First-line for many dermatologists. Anti-inflammatory and modestly antibacterial. Applied twice daily. The OTC 10% strength (such as The Ordinary Azelaic Acid Suspension 10%) is a reasonable starting point if prescription access is limited. See our azelaic acid for rosacea full guide.
2. Topical metronidazole 0.75–1% (Metrogel, MetroCream, Rosadan). Longest-tenured prescription topical for rosacea. Modest efficacy, very well tolerated.
3. Topical ivermectin 1% cream (Soolantra). Targets the Demodex population. Often produces striking improvement over twelve weeks, particularly in patients with denser papulopustular involvement. See our Demodex mites and rosacea explainer for the mechanism.
4. Topical minocycline foam 1.5% (FMX103, Zilxi). Newer topical antibiotic; useful when oral antibiotics are not appropriate.
5. Oral doxycycline 40 mg modified-release (Oracea, Apprilon). Sub-antimicrobial dose used for the anti-inflammatory effect. Standard for moderate-to-severe PPR. The sub-antimicrobial dosing avoids antibiotic resistance concerns.
6. Standard supportive care. Daily mineral sunscreen, gentle cleanser, bland moisturizer — see best products for rosacea.

For the visual disambiguation of PPR from acne and perioral dermatitis, see our rosacea vs acne and dermatitis guide.

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Subtype 3 — Phymatous rosacea

Phymatous rosacea is the least common subtype but the most visually distinctive. The characteristic features:

• Skin thickening — the skin develops a coarse, irregular surface texture
• Patulous (enlarged) follicular openings — the pores appear visibly enlarged
• Sebaceous hyperplasia — the sebaceous glands themselves enlarge
• Increased volume / nodularity — in advanced cases, the skin develops grossly enlarged, lobulated nodules
• Distribution: the nose (rhinophyma) is by far the most common location, accounting for around 95% of phymatous rosacea cases. The chin (gnathophyma), forehead (metophyma), ears (otophyma), and eyelids (blepharophyma) are described but rare.

Phymatous rosacea is dramatically more common in men than women (estimates range from 12:1 to 30:1 male predominance). It typically appears later in the rosacea course — patients usually have years of erythema and/or papulopustules before phymatous changes develop.

Mechanism. The pathophysiology of phymatous rosacea is the least well-understood of the four subtypes. It appears to involve a combination of chronic inflammation, fibroblast activation, sebaceous gland hypertrophy, and lymphedema. The role of the Demodex mite — which is found at very high density within the patulous follicles of rhinophyma — is debated but possibly contributes to the inflammatory drive.

Why phymatous rosacea is the hardest to reverse. Once the connective tissue and sebaceous gland enlargement is established, topical and systemic medications cannot reduce the volume meaningfully. Early-stage phymatous changes — thickening without nodularity — may stabilize or slightly improve with topical retinoids and oral isotretinoin. Established rhinophyma generally requires procedural treatment.

Treatment approach for phymatous features:

1. Treat the underlying inflammatory rosacea aggressively to minimize ongoing phymatous progression. PPR-style treatment (topical ivermectin, oral doxycycline) is often appropriate.
2. Topical retinoids and oral isotretinoin for early phymatous changes. Isotretinoin at low dose has evidence for stabilizing and modestly improving early rhinophyma, but does not reverse established disease.
3. Procedural debulking for established rhinophyma. Options include CO₂ laser ablation, electrosurgical excision (loop or wire), dermabrasion, and surgical paring. Outcomes are generally good in experienced hands; recurrence is possible if the underlying rosacea is not controlled.
4. Daily mineral sunscreen and standard supportive care as for any rosacea phenotype.

For a focused discussion of nasal phymatous changes, see our rosacea on the nose / rhinophyma overview. For changes inside the nose, see rosacea inside the nose.

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Subtype 4 — Ocular rosacea

Ocular rosacea affects the eyes and eyelids. It is dramatically underdiagnosed — many patients are managed for years for “dry eye” or “blepharitis” without the connection to facial rosacea being made.

Hallmark features:

• Dryness and burning sensation in the eyes
• Gritty or foreign-body sensation (“like there’s something in my eye”)
• Watery eyes / reflex tearing
• Light sensitivity (photophobia)
• Recurrent styes (hordeola) and chalazia
• Blepharitis — inflammation along the lid margins, often with crusting
• Telangiectasias along the lid margins
• Conjunctival injection — visible redness in the whites of the eyes
• In advanced cases: corneal involvement (keratitis), which can produce blurred vision and is sight-threatening

Ocular rosacea can occur with or without significant facial rosacea. Around 50–60% of facial rosacea patients have at least some ocular involvement, but only a fraction of them recognize it. Conversely, around 20% of ocular rosacea patients have minimal facial features.

Mechanism. Ocular rosacea is driven by meibomian gland dysfunction (MGD) — the small oil glands that line the eyelid margins become inflamed, blocked, and produce abnormal oil. The unstable tear film that results is what produces the dryness, gritty feeling, and reflex tearing. The same inflammatory mechanisms that drive facial rosacea appear to drive the meibomian gland involvement.

Treatment approach for ocular rosacea:

1. Lid hygiene. Daily warm compresses (5–10 minutes) followed by gentle lid-margin cleaning with a commercial lid wipe or diluted baby shampoo on a clean cotton tip. This is the cornerstone treatment — most ocular rosacea improves substantially with consistent lid hygiene alone.
2. Artificial tears. Preservative-free artificial tears used 4+ times daily provide symptomatic relief and support tear film stability.
3. Topical or oral antibiotics under ophthalmologic supervision. Topical erythromycin or azithromycin ointment, or oral doxycycline at sub-antimicrobial dose (40 mg modified-release), are standard escalations.
4. Topical cyclosporine or lifitegrast for the dry-eye component in patients with significant inflammation.
5. Referral to ophthalmology for any patient with vision changes, severe photophobia, or signs of corneal involvement. Corneal keratitis from rosacea is a vision-threatening complication that requires urgent care.

For the full ocular rosacea discussion including how to distinguish it from other causes of dry eye, see our ocular rosacea standalone guide.

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The phenotype model — how real patients actually look

In real practice, almost no rosacea patient presents as a clean single subtype. The typical patient has some combination — diffuse erythema with a few papulopustules; persistent erythema with telangiectasias and ocular irritation; mild phymatous changes on the nose with background ETR features.

The 2017 ROSCO phenotype model addresses this by reorganizing the classification around features rather than subtypes. The diagnostic features defined by ROSCO are:

Diagnostic features (presence of either feature establishes the diagnosis):

1. Persistent erythema in a centrofacial distribution that may periodically intensify
2. Phymatous changes

Major features (any combination supports the diagnosis but is not by itself diagnostic):

1. Flushing / transient erythema
2. Inflammatory papules and pustules
3. Telangiectasia
4. Ocular manifestations: lid margin telangiectasia, conjunctival injection, anterior blepharitis, keratitis/keratoconjunctivitis/sclerokeratitis

Secondary features:

1. Burning sensation
2. Stinging sensation
3. Edema
4. Dry sensation

The phenotype model says: identify which features your patient has, then assemble a treatment plan from the menu of interventions matched to those features. If the patient has flushing and telangiectasia (ETR-type features), the plan includes vascular laser and topical alpha-agonists. If the patient has papulopustules (PPR-type features), the plan includes topical ivermectin or azelaic acid and possibly oral doxycycline. If the patient has both, the plan includes both — running in parallel rather than sequential.

This is more useful than the subtype model because it matches reality. The subtype model implicitly suggested patients fit one bucket; the phenotype model acknowledges that they don’t.

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Are there other rosacea variants worth knowing?

Beyond the four classical subtypes, several variants and rosacea-adjacent conditions are described in the literature:

Granulomatous rosacea. Originally classified as a variant by the 2002 framework. Characterized by hard, monomorphic, brown-red papules on the central face, often with minimal background erythema. Histology shows granulomatous inflammation. Treatment overlaps with PPR but often requires longer courses and may include oral isotretinoin.

Neurogenic rosacea. A proposed variant characterized by burning, stinging, and flushing that is disproportionate to the visible erythema, often with associated psychiatric symptoms (anxiety, depression). The classification is debated; some authors consider it a severe ETR variant rather than a separate entity. Treatment is challenging and often involves a combination of topical alpha-agonists, low-dose neuromodulators (gabapentin, low-dose tricyclics), and trigger management.

Steroid rosacea. A rosacea-like eruption produced by prolonged use of topical corticosteroids on the face. Often improves dramatically when the steroid is withdrawn (with a transient worsening during the withdrawal phase known as topical steroid withdrawal). Strictly speaking, steroid rosacea is not classical rosacea but is treated similarly once the steroid is stopped.

Perioral dermatitis. A separate condition often grouped clinically with rosacea because it presents with similar small papules around the mouth, nose, and eyes. Strongly associated with topical steroid use, fluorinated toothpaste, and certain cosmetics. Treatment is similar (topical metronidazole, ivermectin, or pimecrolimus) but the entity is distinct.

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Common mistakes when self-classifying

Calling adult acne “rosacea.” The presence of comedones (blackheads, closed-comedone whiteheads) effectively rules out rosacea. PPR has papules and pustules but not comedones. If you have blackheads, you have acne (or both acne and rosacea), not pure rosacea.

Ignoring eye symptoms because the redness is on the face. Ocular rosacea is dramatically underdiagnosed because patients and clinicians don’t connect the eye complaints to the facial rosacea. Gritty eyes, recurrent styes, and reflex tearing in a rosacea patient are ocular rosacea until proven otherwise.

Assuming nose redness equals rhinophyma. Erythema on the nose is most often ETR, not phymatous rosacea. Phymatous rosacea involves visible thickening, irregular surface, and enlarged follicles — not just redness.

Treating ETR features with anti-inflammatory antibiotics. Patients with pure flushing-and-telangiectasia rosacea sometimes get prescribed long courses of oral doxycycline or topical metronidazole that don’t work. The mechanisms don’t match. ETR responds to vasoconstrictors and laser, not to anti-inflammatory antibiotics.

Assuming you can self-classify without a clinical exam. The visual diagnosis of rosacea subtype is more reliable than most patient self-assessments. If you’ve been guessing for months and not improving, an evaluation is the highest-leverage step you haven’t taken.

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When to see a dermatologist for classification

Bring your rosacea questions to a dermatologist if:

• You’re not sure whether your facial redness is rosacea or something else (perioral dermatitis, contact dermatitis, lupus-related malar rash, photodamage, polycythemia, carcinoid)
• You have papules and pustules that haven’t responded to OTC azelaic acid after 8 weeks
• You have any visible thickening on the nose or central face
• You have eye symptoms — gritty feeling, recurrent styes, blurred vision, light sensitivity
• Your flushing pattern is severe, sudden-onset, asymmetric, or accompanied by systemic symptoms (palpitations, diarrhea, weight loss)
• You’re considering vascular laser or IPL for telangiectasias
• You’ve been treated for “rosacea” for over a year without meaningful improvement

For more on what to bring to the appointment and what to expect, see when to see a rosacea dermatologist. For the full treatment landscape, see our companion rosacea treatment pillar and our patient-action-oriented how to treat rosacea guide.

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Frequently asked questions

Can you have more than one type of rosacea at the same time?

Yes — and most patients do. The subtype framework was descriptive shorthand; in real clinical practice, the typical rosacea patient shows features of two or three subtypes simultaneously. The current ROSCO phenotype-based classification was developed specifically to handle this overlap by matching treatment to features rather than to subtype labels.

What is the difference between subtypes and phenotypes?

Subtypes are a four-bucket classification (ETR, PPR, phymatous, ocular) that asks “which type does this patient have?” Phenotypes are a feature-based classification that asks “which features does this patient show?” The phenotype model is the current international consensus because it better matches how rosacea actually presents — most patients have features from multiple subtypes simultaneously.

Which type of rosacea is the most common?

Erythematotelangiectatic features (flushing and persistent central erythema) are the most prevalent across the rosacea population, followed by papulopustular features. Phymatous rosacea is the least common subtype. Ocular involvement is more common than usually recognized — likely 50% or more of facial rosacea patients have at least some ocular features, though many don’t connect their eye symptoms to their facial rosacea.

Does rosacea progress from one subtype to another?

Not in a strict ladder. Phymatous changes generally appear later in the rosacea course (years or decades after initial onset) and are dramatically more common in men. Otherwise, the features any individual patient shows tend to remain similar over time, though severity fluctuates. ETR-only patients do not predictably “progress” to PPR or to phymatous disease; some develop additional features over time, many do not.

What is granulomatous rosacea?

A variant characterized by hard, monomorphic brown-red papules on the central face with minimal background erythema. Histology shows granulomatous inflammation rather than the typical perifollicular inflammatory infiltrate of papulopustular rosacea. It’s often treated like papulopustular rosacea but may require longer courses, and oral isotretinoin is sometimes used.

How is ocular rosacea different from regular dry eye?

The mechanism is meibomian gland dysfunction — the oil glands of the eyelid margins become inflamed and dysfunctional, producing an unstable tear film. Other causes of dry eye (autoimmune dry eye in Sjögren’s syndrome, age-related, environmental) have different mechanisms. Ocular rosacea is also distinguished by the typical features of lid margin telangiectasia, recurrent styes, and chalazia. Many patients are managed for years for “blepharitis” or “dry eye” without the rosacea connection being made.

Can you have rosacea on parts of the body other than the face?

Classical rosacea is centrofacial — confined to the convexities of the central face. The neck, chest, and scalp can be involved in some patients but this is less common and warrants more careful diagnostic consideration to rule out other conditions (poikiloderma of Civatte on the neck, photoaging, lupus). Rosacea in non-facial distributions should be evaluated in person.

Is granulomatous rosacea contagious?

No. Rosacea of any subtype is not contagious. The Demodex mite associated with rosacea is a normal commensal organism present on virtually all human skin; the issue in rosacea is the host inflammatory response, not transmission of the mite.

Why is phymatous rosacea so much more common in men?

The mechanism is not fully understood. Androgens are believed to play a role — testosterone may contribute to the sebaceous gland hypertrophy that’s part of the phymatous process. The male predominance is striking (12:1 to 30:1 in different series), and rhinophyma in particular is overwhelmingly a male presentation.

Can rosacea ever go away on its own?

Rosacea is a chronic condition; a true permanent remission without treatment is uncommon. Many patients have natural fluctuations in severity, with quieter periods that can last months or years, but the underlying tendency persists. The realistic goal is good control with a sustainable routine, not cure.

Does rosacea affect skin of color?

Yes. Rosacea is most often described in fair-skinned populations, but it occurs in all skin tones. In darker skin, the erythema can be subtle or appear violaceous rather than red, which contributes to underdiagnosis. The diagnostic features (centrofacial distribution, characteristic triggers, papulopustules without comedones) are the same; the recognition just requires more careful examination.

How do I know if my redness is rosacea or something else?

Some distinguishing features: rosacea is centrofacial (cheeks, nose, central forehead, chin), tends to flare with classic triggers (heat, alcohol, spicy food, sun, stress), is symmetric, and develops gradually over months to years. Sudden onset, asymmetric distribution, involvement away from the central face, or association with systemic symptoms argues for a non-rosacea cause and warrants evaluation. See our redness 101: rosacea vs. irritation primer for the most common alternatives.

Sources

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Educational content. Not a substitute for individualized medical advice. If you have any of the red-flag symptoms above, see a dermatologist for evaluation.