Rosacea

Meet the patient

A 48-year-old woman of Celtic descent — Fitzpatrick I, flushes with red wine and hot rooms — arrives with two years of flushing and fresh crops of small red papules across her cheeks and nose. Her GP called it acne and prescribed benzoyl peroxide; her skin burned and worsened. Last week a colleague asked whether she had lupus.^[1]

Two questions frame every rosacea viva, and they frame hers: is this acne, lupus, or rosacea? and which phenotype am I treating? Answer both and the therapy writes itself.^[1][3]

One disease, four faces — the phenotype face-off

Rosacea wears four faces on one patient; learn the one-line discriminator for each. The 2002 National Rosacea Society subtypes are scaffolding now, not scripture — the 2017 ROSCO panel rebuilt care around phenotypes rather than rigid boxes — but the four faces remain the fastest bedside shorthand and the spine of every viva answer.^[1]

^{[1] [3]}

The number rule: four faces, two diagnostic. ROSCO names only two phenotypes as sufficient for diagnosis on their own — persistent centrofacial erythema that intensifies periodically, and phymatous change. The rest (papules, pustules, flushing, telangiectasia, ocular features) are supporting phenotypes that overlap and fluctuate, so treatment is matched to the predominant feature, not to a subtype label.^[1]

The classic trap: patients carry more than one phenotype at once, and the mix shifts over years. A woman can start ETR, accumulate papules, and later develop ocular disease — each demanding its own treatment. Naming one subtype and stopping is how patients get undertreated.^[1][4]

The discriminator that wins the viva — no comedones

If you can see a comedone, it is not papulopustular rosacea. That single sentence is the most reproduced discriminator in dermatology exams, and the examiner will test it within the first minute. PPR papules sit on a red, flushing, centrofacial background; acne comedones are the diagnostic lesion of acne and they do not belong here.^[1]

The face-off the examiner expects, reproduced exactly:^[1]

^{[1] [2] [22]}

The classic trap: reaching for benzoyl peroxide and a retinoid in a patient whose face burns at the touch of water. Acne topicals are irritants, and PPR skin is exquisitely sensitive — the patient worsens, the diagnosis is questioned, and a steroid gets added on top. Recognise PPR first, and ivermectin or metronidazole becomes obvious.^[1]

Why it flushes — TLR2, KLK5 and LL-37

Rosacea is an innate-immune fire fed by Demodex and fanned by nerves. The four pillars are innate immune dysregulation, neurovascular hyper-reactivity, microbiome change and barrier dysfunction in a genetically primed host.^[7]

The axis the examiner wants, in one chain: a trigger or rising Demodex density switches on Toll-like receptor 2 (TLR2) on keratinocytes; TLR2 drives kallikrein-related peptidase 5 (KLK5); KLK5 cleaves the cathelicidin precursor into the pro-inflammatory peptide LL-37; and LL-37 ignites cytokine release, neutrophil recruitment, vasodilation and angiogenesis — the erythema, papules and pustules you see.^[5][6]

The deep mechanism — why LL-37 is the molecule that mattersShowHide

Yamasaki and colleagues showed rosacea skin carries abnormally high serine protease activity and cathelicidin, and that LL-37 alone reproduces the inflammatory phenotype. The same group then showed TLR2 is overexpressed in rosacea keratinocytes and itself amplifies KLK5 — a positive feedback loop. The neurovascular arm runs through transient receptor potential (TRP) channels: TRPV1 transduces heat and capsaicin, TRPA1 transduces stress and irritants, and neuropeptides (substance P, CGRP, VIP) drive vasodilation and mast-cell activation. Demodex folliculorum overgrowth initiates or amplifies TLR2 and LL-37 signalling — which is exactly why an antiparasitic, ivermectin, calms an "inflammatory" disease.^[5][6][7]

^[7]

The mantra: trigger hits TLR2, KLK5 cuts cathelicidin to LL-37, and the face catches fire. Demodex pours petrol on it; ivermectin takes the petrol away.^[1][7]

Etymology for viva gold: rhinophyma — from the Greek rhis, nose, and phyma, growth. The bulbous "drinker's nose" of caricature is phymatous rosacea, and the historians of dermatology have long agreed that alcohol is a trigger, not the cause.^[1]

What lights the fire — the trigger list

Triggers are remarkably consistent across patients, and avoidance is half the treatment. Hand every newly diagnosed patient a symptom diary for two to four weeks. The National Rosacea Society data and the ROSCO update converge on a small, memorable set:^[1][2]

• Sunlight (UVA and UVB) — the single most consistent trigger; broad-spectrum SPF 30–50 daily is non-negotiable for every phenotype.
• Heat — saunas, hot showers, steamy kitchens, hot drinks, exertion in warm weather.
• Cold wind and temperature swings — a winter trap; barrier creams and a scarf help.
• Alcohol — red wine (histamine, congeners) is the classic offender; spirits and white wine are often better tolerated but not always.
• Spicy food and hot drinks — capsaicin fires TRPV1 directly; even hot black coffee can flush.
• Strenuous exercise — desirable for health but flushes; split sessions, cool with a damp cloth, avoid peak heat.
• Stress and emotion — adrenergic flushing via TRPA1; treating anxiety and depression helps the skin.
• Drugs and cosmetics — topical steroids (the classic iatrogenic trap), nicotinic acid, vasodilators, benzoyl peroxide, retinoids, fragrances, astringents.
• Hormonal change — perimenopausal and pregnancy flushing; distinguish from true menopausal flushing.
• Microbial drivers — upper respiratory infections, unrecognised Helicobacter pylori, surges in Demodex density. ^[1]

^{[2] [4]}

Who gets it, and what travels with it

Rosacea affects roughly 5 percent of adults worldwide, with peak prevalence in fair-skinned women aged 30–50 and a striking sex split by phenotype. ETR and PPR run in women; phymatous disease, especially rhinophyma, runs in older men. Celtic and Northern European stock (Fitzpatrick I–II) is the textbook demographic, but rosacea is underdiagnosed in darker phototypes, where erythema is subtler and post-inflammatory hyperpigmentation dominates.^[1]

Risk factors to run on autopilot: family history and HLA associations, Demodex folliculorum density, the trigger list above, neurovascular and hormonal stimuli, and topical or systemic corticosteroid exposure.^[1]

Rosacea travels with more than its face. Associations worth screening for — not investigating exhaustively in everyone — include migraine, cardiovascular disease, gastrointestinal disease (H. pylori, small intestinal bacterial overgrowth, inflammatory bowel disease), anxiety and depression, and higher rates of type 1 diabetes, coeliac disease and multiple sclerosis in some cohorts.^[1][4]

The mimics you must exclude

Rosacea is a clinical diagnosis, and the job of tests is to exclude its mimics — not to confirm the obvious. Biopsy only when the picture is atypical, granulomatous, or lupus or lymphoma is plausible.^[1]

^{[1] [2]}

The classic trap: the patient whose "rosacea" is actually cutaneous lupus. A malar rash plus photosensitivity plus oral ulceration is lupus until ANA and histology say otherwise — and the wrong call commits the patient to years of the wrong cream. A granulomatous variant (yellow-brown papules, sometimes extrafacial, with histologic granulomas) also warrants biopsy when the phenotype is atypical.^[1]

How you measure severity

Measure, do not eyeball. Severity anchors both treatment choice and trial endpoints, and the same instruments appear across every pivotal rosacea trial:^[1]

^{[1] [2]}

Quality of life is often disproportionate to what you can see, because the face is public. A patient with objectively mild disease may have disabling anxiety; the DLQI catches what the photograph misses.^[1]

The first move — skincare, sunscreen, a diary

Before any drug, prescribe a routine. Sunscreen, gentle skincare and trigger avoidance are foundational for every phenotype, and they are the intervention patients under-value most.^[1]

• Sun protection — broad-spectrum SPF 30–50 daily; UV is a near-universal trigger.
• Gentle skincare — non-soap cleanser, fragrance-free moisturiser, barrier repair; ban astringents, scrubs and irritant cosmeceuticals.
• Trigger diary — two to four weeks to personalise the list above.
• Cooling — tepid water, fans, avoidance of hot environments.
• Psychological support — screen for anxiety and depression; visible facial redness carries real burden. ^[1]

^{[2] [4]}

Phenotype-directed therapy — match the drug to the face

Match the drug to the dominant phenotype, never to a subtype label. The decision ladder below holds the doses the examiner expects.^[1]

^{[8] [9] [15] [17] [21] [23]}

The topical ladder, with mechanism and the trials behind each agent:^[1]

^[2]

Papulopustular rosacea — ivermectin first

Ivermectin 1% cream once daily is the first-line topical for PPR, because it does two jobs at once: it is anti-inflammatory and it clears Demodex. Two pivotal phase III trials showed superior inflammatory lesion reduction over vehicle, and the ATTRACT extension showed ivermectin held remission better than metronidazole 0.75% cream over 36 weeks.^[8][9]

Metronidazole 0.75–1% twice daily and azelaic acid 15–20% are the workhorses when ivermectin is unavailable or poorly tolerated; azelaic acid can sting on sensitive skin, so introduce it slowly.^[1]

For moderate-to-severe PPR, add oral doxycycline 40 mg modified-release once daily — a subantibiotic, anti-inflammatory dose. Two phase III trials found greater inflammatory lesion reduction than placebo at 16 weeks, and 52-week data show a lower relapse rate than placebo.^[15][17]

• Alternatives — the DOMINO trial found minocycline 100 mg non-inferior to doxycycline 40 mg over 16 weeks, with longer remission at follow-up and no significant difference in safety; minocycline is an option when doxycycline is not tolerated.^[18]
• Biomarker evidence — doxycycline 40 mg MR reduces cathelicidin and serine protease activity, which is exactly the mechanism the disease runs on. ^[16]

^[2]

For severe PPR, combine topical and systemic: in severe rosacea (IGA 4), ivermectin 1% cream plus doxycycline 40 mg MR beat ivermectin plus placebo over 12 weeks, with faster onset and higher clear rates.^[10]

Persistent erythema — vasoconstrictors, with a rebound warning

Persistent centrofacial erythema is treated with topical vasoconstrictors — brimonidine or oxymetazoline — because no anti-inflammatory clears background redness.^[1]

Brimonidine 0.33% gel once daily is an alpha-2-adrenergic agonist with onset around 30 minutes and an effect lasting about 9–12 hours. Pivotal trials of once-daily brimonidine (0.5% tartrate gel formulation history) established efficacy for moderate-to-severe facial erythema, and patient-reported outcomes improve rapidly.^[12][13][14] A one-year open-label study confirmed long-term safety and sustained efficacy, and patient satisfaction tracks the standard clinical endpoints closely.^[19][20]

Oxymetazoline 1% cream once daily (an alpha-1a agonist) beat vehicle on composite erythema success in the REVEAL pivotal trial and is a reasonable alternative or add-on.^[23]

The classic trap: rebound erythema. Brimonidine can paradoxically worsen redness in roughly 10% of patients, sometimes beyond baseline. Warn the patient before the first application; if rebound appears, stop the drug rather than escalate.^[12]

When a patient has both erythema and papules, combine agents — ivermectin 1% cream plus brimonidine 0.33% gel is safe and effective for simultaneous inflammatory lesions and background redness.^[11]

Severe and refractory — low-dose isotretinoin

Low-dose oral isotretinoin (0.3 mg/kg/day) is an off-label option for severe, refractory papulopustular or phymatous rosacea unresponsive to the ladder above. In a randomized dose-finding study of 573 patients, 0.3 mg/kg beat placebo and matched doxycycline, cutting lesions by around 90 percent over 12 weeks.^[21]

Alternatives when tetracyclines are contraindicated include oral metronidazole or clarithromycin, and oral carvedilol (a beta-blocker with alpha-blocking activity) has been reported for severe refractory flushing and erythema, though the evidence base is thin.^[1]

Phymatous rosacea — surgery, not creams

Once tissue has remodelled, medicine stops working. Rhinophyma — bulbous, nodular, sebaceous enlargement of the distal nose with patulous follicular ostia and a ruddy hue — is the canonical phymatous lesion; gnathophyma (chin), metophyma (forehead), otophyma (ears) and eyelid involvement are less common. It favours older men with long disease duration and high cumulative inflammation.^[1]

Definitive treatment is CO2 or Er:YAG laser, electrosurgery, dermabrasion or scalpel sculpting, performed by dermatologic or plastic surgeons. Recurrence is common if background inflammation is not controlled, so keep the medical therapy running alongside the debulking.^[1]

Ocular rosacea — ask about the eyes every visit

Up to half of rosacea patients have ocular signs on slit-lamp, yet only a minority volunteer eye symptoms — so ask, every time. The screening question is one sentence: are your eyes dry, gritty, red or light-sensitive?^[1]

The spectrum runs from blepharitis, meibomian gland dysfunction, conjunctival hyperaemia and dry eye through recurrent styes and episcleritis to, at the severe end, keratitis with corneal vascularisation, ulceration and — rarely — perforation. Ocular disease can appear with little or no skin disease, so a red gritty eye with no facial rash is still rosacea until excluded.^[1]

Management starts with ocular hygiene and trigger avoidance. The treatments with the best evidence are oral doxycycline and topical cyclosporine or azithromycin for the dry-eye and blepharitis components; combination treatment is common.^[22]

Procedural options — the right laser for the right lesion

Vascular lasers and light treat what topicals cannot — established telangiectasia, fixed erythema and rhinophyma. Match the modality to the target:^[1]

^{[2] [4]}

Special populations

Pregnancy. Avoid tetracyclines, isotretinoin and oral retinoids. Topical azelaic acid, metronidazole and ivermectin are generally considered safe at the lowest effective potency over limited areas; brimonidine and oxymetazoline have limited systemic absorption, so discuss risk and benefit.^[1]

Children. Rosacea is uncommon — think first of steroid-induced dermatitis, periorificial dermatitis or Demodex. Tetracyclines are contraindicated under 8 years (tooth discolouration); use erythromycin if systemic therapy is essential.^[1]

Steroid-induced rosacea — the iatrogenic trap

Potent topical steroids on the face cause rosacea-like dermatitis, and stopping them abruptly causes rebound. The history is the diagnosis: weeks to months of a potent steroid on the face, followed by worsening erythema, telangiectasia and papulopustules. Management is gradual steroid withdrawal layered onto standard rosacea therapy, and the patient must be warned that things will get worse before they get better.^[1]

This is the single most preventable rosacea mimic, and the rule that prevents it is one sentence: do not prescribe potent topical steroids for the face.^[1]

Comorbidities — the face is not the whole patient

Rosacea is increasingly read as a systemic inflammatory condition, and the associations matter for holistic care even when they do not drive every investigation:^[1]

^[1]

Use these associations to prompt a risk-factor conversation — not to send every patient for an autoimmune screen.^[4]

Prognosis and follow-up

Rosacea is chronic and relapsing; there is no cure, but excellent control is the rule with combination therapy. Treatment goals are control of inflammation, fewer flares, improved quality of life and prevention of complications — phymatous change, ocular damage and psychological morbidity.^[1]

• Topical therapy — review at 8 to 12 weeks.
• Systemic therapy — review at 6 to 12 weeks; many step down or stop after 3 to 6 months onto topical maintenance.
• Maintenance — long-term topical ivermectin, azelaic acid or intermittent brimonidine is often needed.
• Relapse — common after stopping; treat-to-target with planned re-treatment beats reactive rescue. ^[1]

^{[2] [9] [17]}

How rosacea patients come to harm — the preventable list

• Sight loss from undiagnosed ocular rosacea with keratitis — the preventable harm.^[1]
• Potent topical steroids on the face creating a worse disease than the one they were meant to treat.^[1]
• Cutaneous lupus labelled rosacea and treated with the wrong cream for years.^[1]
• Benzoyl peroxide and retinoids burning sensitive PPR skin because no one checked for comedones.^[1]
• Brimonidine rebound misread as treatment failure and escalated rather than stopped.^[12]
• Tetracyclines or isotretinoin prescribed in pregnancy.^[1]
• Rhinophyma left to disfigure because medical therapy was tried and "failed" instead of referring for surgery.^[1]
• Untreated anxiety and depression behind "just a red face".^[1]

Evidence, guidelines and the trials that matter

The framework is globally consistent and phenotype-directed, anchored by three documents and a handful of pivotal trials:^[1]

• ROSCO (2017) — moved the field from subtypes to phenotypes; named persistent centrofacial erythema and phymatous change as the two diagnostic phenotypes.^[1]
• National Rosacea Society Expert Committee (2019 update) — phenotype-based management across topical, systemic and procedural therapy.^[2]
• BAD rosacea guideline (2021) — UK consensus on trigger avoidance, skincare, topical and systemic therapy, and laser or IPL for the right phenotypes.
• Del Rosso 2024 — names the diagnostic and therapeutic gaps that still lose patients.^[4]

The trials an examiner expects you to cite:^[2]

• Yamasaki 2007 — increased serine protease activity and raised cathelicidin drive the inflammation.^[5]
• Yamasaki 2011 — TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes.^[6]
• Stein 2014 — two randomized, double-blind, vehicle-controlled studies of ivermectin 1% cream in PPR.^[8]
• Fowler 2013 — once-daily brimonidine tartrate gel 0.5% for moderate to severe facial erythema, two randomized vehicle-controlled studies.^[12]
• Del Rosso 2007 — two randomized phase III trials of doxycycline 40 mg once daily.^[15]
• DOMINO 2017 — minocycline 100 mg non-inferior to doxycycline 40 mg over 16 weeks, with longer remission at follow-up.^[18]

The mantra, and the mnemonic

^[1]

The mantra: no comedones, four faces, match the drug to the phenotype — and never put a potent steroid on a red face.^[1][2]

Ward-round test — three stems, thirty seconds each

Stem 1 — the woman from the top of the topic (answer)ShowHide

The 48-year-old Celtic woman with two years of flushing, new papules on her cheeks and nose, and worsening after benzoyl peroxide. What went wrong, and what is the first prescription? Model: Benzoyl peroxide worsened her sensitive skin, and the diagnosis slipped because acne was assumed. Stop the benzoyl peroxide, start gentle skincare and daily sunscreen, and prescribe ivermectin 1% cream once daily. If inflammation is moderate to severe, add doxycycline 40 mg modified-release once daily. Screen her eyes, and exclude lupus if photosensitivity or systemic features appear.^[8][15]

Stem 2 — the red face that worsened on brimonidine (answer)ShowHide

A patient returns two weeks after starting brimonidine 0.33% gel with redness worse than baseline, spreading beyond the application site. What happened, and what do you do? Model: This is rebound erythema — reported in roughly 10% of brimonidine users, sometimes beyond baseline. Stop the brimonidine rather than escalate; switch to oxymetazoline 1% cream or move to pulsed dye laser for the fixed erythema. Warn her before any future vasoconstrictor, and re-examine for an overlapping inflammatory component that needs ivermectin or doxycycline rather than a redness drug.^[12]

Stem 3 — the gritty eye and the missed diagnosis (answer)ShowHide

A 55-year-old man with intermittent facial flushing is referred for conjunctivitis that has not responded to three courses of antibiotic drops. Slit-lamp shows blepharitis, meibomian gland dysfunction and peripheral corneal vascularisation. What is the diagnosis, the risk, and the management? Model: This is ocular rosacea — ocular disease can occur with little or no skin disease, and the unresponsive conjunctivitis is the giveaway. Corneal vascularisation needs same-day ophthalmology assessment. Start ocular hygiene and oral doxycycline, add topical treatment for the dry-eye component, and treat any skin phenotype in parallel. The preventable harm here is permanent visual impairment from delayed recognition.^[22]

References23ShowHide

1. [1]Tan J, Almeida LMC, Bewley A, et al. Updating the diagnosis, classification and assessment of rosacea: recommendations from the global ROSacea COnsensus (ROSCO) panel Br J Dermatol, 2017.PMID 27718519
2. [2]Thiboutot D, Anderson R, Cook-Bolden F, et al. Standard management options for rosacea: The 2019 update by the National Rosacea Society Expert Committee J Am Acad Dermatol, 2020.PMID 32035944
3. [3]Barakji YA, Rønnstad ATM, Christensen MO, et al. Assessment of Frequency of Rosacea Subtypes in Patients With Rosacea: A Systematic Review and Meta-analysis JAMA Dermatol, 2022.PMID 35385049
4. [4]Del Rosso J, Baldwin H, Bhatia N, et al. A Review of the Diagnostic and Therapeutic Gaps in Rosacea Management: Consensus Opinion Dermatol Ther (Heidelb), 2024.PMID 38194021
5. [5]Yamasaki K, Di Nardo A, Bardan A, et al. Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea Nat Med, 2007.PMID 17676051
6. [6]Yamasaki K, Kanada K, Macleod DT, et al. TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes J Invest Dermatol, 2011.PMID 21107351
7. [7]Wang H, Zhou C Advances in the pathogenesis of rosacea Front Immunol, 2025.PMID 41646975
8. [8]Stein L, Kircik L, Fowler J, et al. Efficacy and safety of ivermectin 1% cream in treatment of papulopustular rosacea: results of two randomized, double-blind, vehicle-controlled pivotal studies J Drugs Dermatol, 2014.PMID 24595578
9. [9]Taieb A, Khemis A, Ruzicka T, et al. Maintenance of remission following successful treatment of papulopustular rosacea with ivermectin 1% cream vs. metronidazole 0.75% cream: 36-week extension of the ATTRACT randomized study J Eur Acad Dermatol Venereol, 2016.PMID 26691278
10. [10]Schaller M, Kemény L, Havlickova B, et al. A randomized phase 3b/4 study to evaluate concomitant use of topical ivermectin 1% cream and doxycycline 40-mg modified-release capsules, versus topical ivermectin 1% cream and placebo in the treatment of severe rosacea J Am Acad Dermatol, 2020.PMID 31150711
11. [11]Gold LS, Papp K, Lynde C, et al. Treatment of Rosacea With Concomitant Use of Topical Ivermectin 1% Cream and Brimonidine 0.33% Gel: A Randomized, Vehicle-controlled Study J Drugs Dermatol, 2017.PMID 28915286
12. [12]Fowler J Jr, Jackson M, Moore A, et al. Efficacy and safety of once-daily topical brimonidine tartrate gel 0.5% for the treatment of moderate to severe facial erythema of rosacea: results of two randomized, double-blind, and vehicle-controlled pivotal studies J Drugs Dermatol, 2013.PMID 23839181
13. [13]Fowler J, Jarratt M, Moore A, et al. Once-daily topical brimonidine tartrate gel 0·5% is a novel treatment for moderate to severe facial erythema of rosacea: results of two multicentre, randomized and vehicle-controlled studies Br J Dermatol, 2012.PMID 22050040
14. [14]Layton AM, Schaller M, Homey B, et al. Brimonidine gel 0.33% rapidly improves patient-reported outcomes by controlling facial erythema of rosacea: a randomized, double-blind, vehicle-controlled study J Eur Acad Dermatol Venereol, 2015.PMID 26416154
15. [15]Del Rosso JQ, Webster GF, Jackson M, et al. Two randomized phase III clinical trials evaluating anti-inflammatory dose doxycycline (40-mg doxycycline, USP capsules) administered once daily for treatment of rosacea J Am Acad Dermatol, 2007.PMID 17367893
16. [16]Di Nardo A, Holmes AD, Muto Y, et al. Improved clinical outcome and biomarkers in adults with papulopustular rosacea treated with doxycycline modified-release capsules in a randomized trial J Am Acad Dermatol, 2016.PMID 26951940
17. [17]Del Rosso JQ, Brantman S, Baldwin H Long-term inflammatory rosacea management with subantibiotic dose oral doxycycline 40 mg modified-release capsules once daily Dermatol Ther, 2022.PMID 34713539
18. [18]van der Linden MMD, van Ratingen AR, van Rappard DC, et al. DOMINO, doxycycline 40 mg vs. minocycline 100 mg in the treatment of rosacea: a randomized, single-blinded, noninferiority trial, comparing efficacy and safety Br J Dermatol, 2017.PMID 27797396
19. [19]Moore A, Kempers S, Murakawa G, et al. Long-term safety and efficacy of once-daily topical brimonidine tartrate gel 0.5% for the treatment of moderate to severe facial erythema of rosacea: results of a 1-year open-label study J Drugs Dermatol, 2014.PMID 24385120
20. [20]Fowler J, Tan J, Jackson JM, et al. Treatment of facial erythema in patients with rosacea with topical brimonidine tartrate: correlation of patient satisfaction with standard clinical endpoints of improvement of facial erythema J Eur Acad Dermatol Venereol, 2015.PMID 25074756
21. [21]Gollnick H, Blume-Peytavi U, Szabó EL, et al. Systemic isotretinoin in the treatment of rosacea - doxycycline- and placebo-controlled, randomized clinical study J Dtsch Dermatol Ges, 2010.PMID 20337772
22. [22]Malagón-Liceaga A, Recillas-Gispert C, Ruiz-Quintero NC, et al. Treatment of ocular rosacea: A practical review from an interdisciplinary approach Arch Soc Esp Oftalmol (Engl Ed), 2023.PMID 37696488
23. [23]Baumann L, Goldberg DJ, Stein Gold L, et al. Pivotal Trial of the Efficacy and Safety of Oxymetazoline Cream 1.0% for the Treatment of Persistent Facial Erythema Associated With Rosacea: Findings from the Second REVEAL Trial J Drugs Dermatol, 2018.PMID 29537447