Rosacea (Adult)

1. Clinical Overview

Summary

Rosacea is a chronic inflammatory facial skin condition characterised by episodic or persistent central facial erythema, telangiectasia, inflammatory papules and pustules, and in advanced cases, phymatous tissue remodelling. It predominantly affects fair-skinned adults over 30 years of age and follows a relapsing-remitting course with identifiable triggers. [1] The condition has significant psychosocial impact, with quality of life impairment comparable to moderate-to-severe acne and psoriasis. [2]

Unlike acne vulgaris, rosacea is characterised by the absence of comedones (blackheads/whiteheads) and a distinct pathophysiology involving neurovascular dysregulation, innate immune activation, and microbial dysbiosis. [3]

Key Facts

Clinical Pearls

Clinical Pearl: "It's NOT Acne": The complete absence of comedones (blackheads/whiteheads) is the single most important feature distinguishing rosacea from acne vulgaris. If you see comedones, it's not pure rosacea.

Clinical Pearl: Eye Examination is Mandatory: Up to 58% of patients have ocular involvement, and in 20% of cases, ocular symptoms precede cutaneous manifestations. [4] Always ask: "Do your eyes feel dry, gritty, or irritated?"

Clinical Pearl: Rhinophyma ≠ Alcoholism: While alcohol is a trigger, rhinophyma (phymatous nose) is NOT caused by alcohol abuse. This is a harmful misconception. Rhinophyma occurs almost exclusively in men due to androgen-mediated sebaceous gland hypertrophy. [5]

Clinical Pearl: Steroid Rosacea: Prolonged use of topical corticosteroids on the face can cause steroid-induced (iatrogenic) rosacea or exacerbate existing disease. Always take a detailed topical medication history.

Clinical Pearl: Trigger Diary: Encourage patients to keep a "flush diary" to identify personal triggers. Common triggers include UV exposure, hot drinks, spicy food, alcohol (especially red wine), temperature extremes, and emotional stress. [6]

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2. Epidemiology

Prevalence & Demographics

Age and Gender Distribution

Risk Factors

Exam Detail: Genetic Factors [8]

• Strong familial clustering: 30-40% have affected first-degree relatives
• HLA-DRB1*03 association in some populations
• GWAS identified loci near genes involved in immune regulation (HLA region, BTNL2)
• Twin studies suggest 46% heritability

Phenotypic Risk Factors

Environmental and Lifestyle Triggers

Occupational and Social Factors

• Outdoor workers: Increased UV exposure (farmers, construction workers, mariners)
• High-temperature occupations: Chefs, bakers, industrial workers
• Psychosocial burden: 76% report reduced self-confidence; 69% report embarrassment [2]
• Correlation with migraine: Increased prevalence in rosacea patients (OR 1.92) [9]

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3. Aetiology and Pathophysiology

Rosacea is a multifactorial disorder involving innate immune dysregulation, neurovascular hyperreactivity, microbial dysbiosis, and environmental triggers. [1,3]

Pathophysiological Model

┌─────────────────────────────────────────────────────────────┐
│         GENETIC PREDISPOSITION + ENVIRONMENTAL TRIGGERS      │
│         (Fair skin, HLA-DRB1*03, UV, heat, alcohol)         │
└────────────────────┬────────────────────────────────────────┘
                     ↓
┌─────────────────────────────────────────────────────────────┐
│              INNATE IMMUNE DYSREGULATION                     │
│   • Abnormal cathelicidin processing → LL-37 peptide        │
│   • Upregulation of TLR-2 (Toll-like receptor 2)            │
│   • Increased kallikrein 5 (KLK5) serine protease           │
└────────────────────┬────────────────────────────────────────┘
                     ↓
┌─────────────────────────────────────────────────────────────┐
│           NEUROVASCULAR HYPERREACTIVITY                      │
│   • TRPV (transient receptor potential vanilloid) channels  │
│   • Enhanced vasodilation response                          │
│   • Vascular endothelial growth factor (VEGF) upregulation  │
│   • Lymphangiogenesis and angiogenesis                      │
└────────────────────┬────────────────────────────────────────┘
                     ↓
┌─────────────────────────────────────────────────────────────┐
│                 MICROBIAL DYSBIOSIS                          │
│   • Demodex folliculorum overgrowth (10-20× normal)         │
│   • Bacillus oleronius (Demodex-associated bacteria)        │
│   • Staphylococcus epidermidis biofilms                     │
└────────────────────┬────────────────────────────────────────┘
                     ↓
┌─────────────────────────────────────────────────────────────┐
│              CLINICAL PHENOTYPES OF ROSACEA                  │
│   • Erythematotelangiectatic (flushing, erythema)           │
│   • Papulopustular (inflammatory lesions)                   │
│   • Phymatous (tissue remodelling, rhinophyma)              │
│   • Ocular (blepharitis, keratitis)                         │
└─────────────────────────────────────────────────────────────┘

Molecular and Cellular Mechanisms

Exam Detail: #### 1. Innate Immune Dysregulation

Cathelicidin and LL-37 Antimicrobial Peptide [10]

Rosacea patients have:

• Elevated levels of cathelicidin (antimicrobial peptide) in facial skin
• Abnormal processing by kallikrein 5 (KLK5) protease → pathogenic LL-37 peptide fragments
• LL-37 triggers:
  • Neutrophil chemotaxis → inflammatory papules/pustules
  • Angiogenesis → telangiectasia
  • Vasodilation → erythema and flushing

Toll-Like Receptor 2 (TLR-2) Upregulation

• TLR-2 recognises Demodex-associated antigens and bacterial lipoproteins
• Activation → pro-inflammatory cytokines (IL-1β, IL-6, TNF-α)
• Increased matrix metalloproteinases (MMPs) → dermal matrix degradation

2. Neurovascular Dysregulation

TRPV Channels (Transient Receptor Potential Vanilloid) [11]

• TRPV1 and TRPV4 channels are temperature- and chemical-sensitive ion channels
• Activated by: heat, capsaicin (spicy food), alcohol, UV radiation
• Overexpression in rosacea → exaggerated vasodilation response
• Release of neuropeptides:
  • Substance P → vasodilation, mast cell degranulation
  • Calcitonin gene-related peptide (CGRP) → neurogenic inflammation

Vascular Endothelial Growth Factor (VEGF)

• Upregulated in rosacea skin [12]
• Promotes angiogenesis (new blood vessel formation) → telangiectasia
• Lymphangiogenesis → persistent oedema

3. Microbial Dysbiosis

Demodex folliculorum [13]

• Mite density 10-20× higher in rosacea patients vs controls
• Concentrated in pilosebaceous units of central face
• Proposed mechanisms:
  • "Mechanical: Follicular obstruction, physical irritation"
  • "Immunological: Chitin exoskeleton triggers innate immune responses (TLR-2)"
  • "Microbial: Harbours bacteria (Bacillus oleronius) that provoke immune reactions"

Bacillus oleronius

• Gram-negative bacterium living symbiotically within Demodex mites
• Antigens trigger B-cell and T-cell responses in rosacea patients
• May explain efficacy of antibiotics (immunomodulatory > antimicrobial effects)

Skin Microbiome Alterations

• Reduced microbial diversity compared to healthy controls
• Increased Staphylococcus epidermidis biofilms
• Dysbiosis → pro-inflammatory skin environment

4. Sebaceous Gland Dysfunction (Phymatous Subtype)

Sebaceous Gland Hyperplasia and Fibrosis

• Chronic inflammation → sebaceous gland hypertrophy
• Androgen sensitivity (explains male predominance of rhinophyma)
• Fibroblast proliferation, collagen deposition → tissue remodelling
• Advanced phymatous changes: disfiguring nasal enlargement (rhinophyma)

Summary of Key Pathophysiological Features

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4. Classification and Subtypes

The 2017 Global Rosacea Consensus (ROSCO) updated classification from "subtypes" to phenotypic presentations, recognising that features often overlap. [14]

Traditional Four Subtypes (Historical Classification)

Modern Phenotypic Classification (ROSCO 2017)

Recognises diagnostic features and major features:

Diagnostic Features (Either one is sufficient for diagnosis):

1. Persistent centrofacial erythema (≥3 months)
2. Phymatous changes

Major Features (Support diagnosis but not individually diagnostic):

• Papules and pustules (inflammatory)
• Flushing (transient erythema)
• Telangiectasia
• Ocular manifestations

Patients can have multiple phenotypic features simultaneously.

Detailed Subtype Descriptions

Exam Detail: #### Erythematotelangiectatic Rosacea (ETR)

Clinical Features:

• Flushing: Episodic, triggered by heat, emotion, alcohol, spicy food
• Persistent erythema: Non-transient centrofacial redness (cheeks, nose, chin, central forehead)
• Telangiectasia: Visible, dilated superficial blood vessels
• Burning and stinging: Heightened skin sensitivity
• Dry, rough skin: Impaired barrier function

Distribution: Central convex facial areas (spares nasolabial folds)

Examination Findings:

• Diffuse erythema (blanchable with diascopy)
• Fine telangiectatic vessels (especially nasal bridge, medial cheeks)
• No papules, pustules, or comedones

Papulopustular Rosacea (PPR)

Clinical Features:

• Papules: Erythematous, dome-shaped, 1-5 mm
• Pustules: Sterile, pus-filled (culture negative for bacteria)
• Background erythema: Persistent centrofacial erythema
• No comedones: Critical distinguishing feature from acne
• Episodic flares: Relapsing-remitting course

Distribution: Cheeks, nose, chin, glabella; spares perioral and periocular areas

Examination Findings:

• Inflammatory papules and pustules on erythematous base
• May have associated telangiectasia
• Absence of open/closed comedones

Phymatous Rosacea

Clinical Features:

• Skin thickening: Fibrotic tissue expansion
• Irregular contour: Nodular surface
• Prominent pores: Sebaceous gland hypertrophy
• Rhinophyma: Phymatous change of nose (90% of phymatous cases)
• Other sites: chin (gnathophyma), forehead (metophyma), ears (otophyma), eyelids (blepharophyma)

Rhinophyma (Phymatous Nose):

• Almost exclusively in males (androgen-mediated)
• Bulbous, enlarged nose with irregular surface
• Telangiectasia prominent
• Not caused by alcohol (common misconception)
• Progression: Gradual over years; can be disfiguring
• Risk: Basal cell carcinoma can develop within rhinophyma tissue

Examination Findings:

• Thickened, fibrotic skin with loss of normal contours
• Dilated follicular openings
• Surface irregularities, nodularity

Ocular Rosacea

Prevalence: 50-58% of rosacea patients; precedes cutaneous disease in 20%

Clinical Features:

Ocular Examination Findings:

Red Flag: Ocular rosacea with keratitis can cause corneal scarring and vision loss if untreated.

Overlap and Spectrum Concept

• 60% of patients have features of more than one subtype [14]
• Spectrum concept: Rosacea is a continuum rather than discrete subtypes
• Evolution over time: ETR may progress to PPR; PPR may develop phymatous changes

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5. Clinical Presentation

History Taking: Key Questions

Clinical Pearl: Focused Rosacea History:

1. Symptoms: "Do you experience facial flushing, redness, or burning?"
2. Distribution: "Where on your face does this occur?"
3. Duration: "How long have you had these symptoms?"
4. Pattern: "Is the redness constant or does it come and go?"
5. Triggers: "What makes it worse?" (heat, alcohol, spicy food, stress, sun)
6. Ocular symptoms: "Do your eyes feel dry, gritty, or irritated?"
7. Previous treatments: "What have you tried? Any steroid creams?"
8. Cosmetics: "What products do you use on your face?"
9. Impact: "How does this affect your daily life and confidence?"
10. Family history: "Does anyone in your family have rosacea?"

Symptoms by Subtype

Clinical Examination Approach

Inspection (Good Lighting Essential):

1. General facial inspection:

   • Distribution of erythema (central face vs diffuse)
   • Presence of telangiectasia
   • Papules, pustules (look for absence of comedones)
   • Skin texture, thickening, irregularities

2. Specific site examination:

   • Nose: Rhinophyma? Surface irregularities?
   • Cheeks: Erythema, telangiectasia, papulopustules?
   • Forehead: Central forehead involvement?
   • Chin: Erythema, phymatous changes?
   • Nasolabial folds: Should be spared (if involved, consider seborrheic dermatitis or lupus)

3. Ocular examination:

   • Eyelid margin: Telangiectasia, crusting (blepharitis)?
   • Conjunctiva: Injection, hyperaemia?
   • Cornea: Clarity (if keratitis suspected → urgent ophthalmology referral)
   • Meibomian gland expression (lid margin)

4. Palpation:

   • Texture: Smooth vs thickened, fibrotic
   • Temperature: Warmth (active inflammation)

Examination Findings by Subtype

Exam Detail: #### Erythematotelangiectatic Rosacea (ETR)

Papulopustular Rosacea (PPR)

Phymatous Rosacea

Ocular Rosacea

Common Triggers (Patient-Reported)

Exam Detail: Evidence-Based Triggers [6]

Dietary Triggers (Evidence Mixed):

• Histamine-rich foods (aged cheese, fermented foods)
• Cinnamaldehyde-containing foods (tomatoes, citrus, cinnamon)
• Caffeine (may exacerbate flushing via vasodilation)

Note: Triggers are highly individualised; trigger diaries are recommended.

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6. Differential Diagnosis

Centrofacial erythema and papulopustular lesions have a broad differential. [15]

Key Differentiating Features

Detailed Comparison: Rosacea vs Acne Vulgaris

Detailed Comparison: Rosacea vs Lupus (Malar Rash)

When to Investigate Further

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7. Investigations

Diagnosis

Rosacea is a clinical diagnosis based on history and examination. No specific laboratory tests or imaging are required for typical presentations. [1,14]

Diagnostic Criteria (ROSCO 2017)

At least ONE of the following diagnostic features:

1. Persistent centrofacial erythema (≥3 months, with or without periodic intensification)
2. Phymatous changes (thickening skin, irregular contour)

Supported by major features:

• Papules and pustules (inflammatory)
• Flushing
• Telangiectasia
• Ocular manifestations

When to Perform Investigations

Exam Detail: #### Skin Biopsy (Rarely Required)

Indications:

• Atypical presentation
• Diagnostic uncertainty (e.g., possible lupus, dermatomyositis)
• Suspected malignancy (basal cell carcinoma in rhinophyma)

Histological Findings in Rosacea:

• Dermal perivascular and perifollicular lymphocytic infiltrate
• Vascular dilatation (telangiectasia)
• Solar elastosis (UV-induced dermal damage)
• Follicular Demodex mites (may be visible, but non-specific)
• Sebaceous gland hyperplasia (phymatous subtype)
• Granulomatous inflammation (granulomatous rosacea variant, rare)

Autoimmune Screen (If Lupus Suspected)

Ophthalmology Referral

Indications:

• Urgent: Suspected keratitis (corneal involvement)
• Routine: Ocular rosacea with inadequate response to treatment
• Screening: Severe cutaneous rosacea (50-58% have ocular involvement)

Ophthalmology Investigations:

• Slit-lamp examination (lid margin, meibomian glands, cornea)
• Tear break-up time (TBUT) – reduced in dry eye disease
• Fluorescein staining (punctate keratopathy)
• Schirmer test (tear production)

Microbiology (Culture)

Not routinely required – pustules in rosacea are sterile (culture-negative).

Consider if:

• Suspected secondary bacterial infection (e.g., impetigo, folliculitis)
• Atypical presentation with systemic features (fever, malaise)

Demodex Mite Examination

Standardised skin surface biopsy (SSSB) or skin scraping can quantify Demodex density.

• Normal: less than 5 mites/cm²
• Rosacea: 10-20× higher (50-100 mites/cm²)

Clinical relevance:

• Not routinely required for diagnosis
• May guide ivermectin therapy (anti-Demodex agent)

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8. Management

Management of rosacea is individualised based on predominant subtype, severity, and patient preferences. A stepwise approach is recommended. [14,16]

General Principles (All Subtypes)

Clinical Pearl: Foundation of Rosacea Management:

1. Trigger avoidance: Identify and avoid personal triggers (trigger diary)
2. Sun protection: Broad-spectrum SPF 30-50+, physical blockers (zinc oxide, titanium dioxide)
3. Gentle skincare: Fragrance-free, hypoallergenic cleansers and moisturisers
4. Avoid irritants: Alcohol-based products, physical exfoliants, harsh scrubs
5. Temperature regulation: Avoid extremes (hot baths, saunas, icy wind)
6. Cosmetic camouflage: Green-tinted makeup to neutralise redness (supportive)

General Measures (All Patients)

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Treatment by Subtype

Exam Detail: #### 1. Erythematotelangiectatic Rosacea (ETR)

Goal: Reduce flushing, persistent erythema, and telangiectasia.

Topical Therapies

Note: Vasoconstrictors provide temporary symptom relief but do not modify disease course.

Laser and Light-Based Therapies (For Persistent Telangiectasia)

Patient Selection: Fair skin (Fitzpatrick I-III) ideal; darker skin at risk of dyspigmentation.

Side Effects: Transient purpura (PDL), erythema, hyperpigmentation (darker skin).

Systemic Therapies (Severe, Refractory ETR)

2. Papulopustular Rosacea (PPR)

Goal: Reduce inflammatory papules and pustules.

First-Line Topical Therapies

Choice of First-Line Agent:

• Ivermectin: Preferred for moderate-severe PPR (superior efficacy)
• Metronidazole: Well-tolerated; established safety profile
• Azelaic acid: Useful for erythema + papulopustules

Systemic Therapies (Moderate-Severe PPR)

Duration of Systemic Therapy:

• Doxycycline: 12-16 weeks; then step down to topical maintenance
• Isotretinoin: 4-6 months (low-dose); longer if phymatous changes

Combination Therapy (Severe PPR)

Approach: Oral doxycycline 40 mg MR + topical ivermectin/metronidazole

• Faster response than monotherapy
• Step down to topical maintenance once controlled

3. Phymatous Rosacea (Including Rhinophyma)

Goal: Halt progression; surgical remodelling for established disease.

Medical Therapy

Surgical/Procedural Therapies (Established Rhinophyma)

Post-Procedure:

• Wound care: Petroleum-based ointments, non-adherent dressings
• Re-epithelialisation: 2-3 weeks
• Avoid sun exposure during healing

Red Flag: Basal cell carcinoma can develop within rhinophyma tissue; biopsy suspicious lesions.

4. Ocular Rosacea

Goal: Relieve ocular symptoms; prevent corneal complications.

First-Line (Mild Ocular Rosacea)

Systemic Therapy (Moderate-Severe Ocular Rosacea)

Topical Ophthalmic Therapies

Ophthalmology Referral (Indications)

• Urgent: Keratitis, corneal involvement, vision changes
• Routine: Inadequate response to first-line therapy; recurrent styes/chalazia

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Treatment Algorithm (Simplified)

┌─────────────────────────────────────────────────────────────┐
│                  ROSACEA DIAGNOSIS CONFIRMED                 │
└────────────────────┬────────────────────────────────────────┘
                     ↓
         ┌───────────────────────────┐
         │ Identify Predominant      │
         │ Subtype(s)                │
         └───────────┬───────────────┘
                     ↓
    ┌────────────────┼────────────────────┬─────────────────┐
    ↓                ↓                    ↓                 ↓
┌─────────┐  ┌──────────────┐  ┌──────────────┐  ┌────────────────┐
│   ETR   │  │     PPR      │  │  Phymatous   │  │     Ocular     │
└────┬────┘  └──────┬───────┘  └──────┬───────┘  └────────┬───────┘
     ↓              ↓                  ↓                   ↓
┌─────────────┐ ┌──────────────────┐ ┌──────────┐ ┌──────────────────┐
│ Topical     │ │ Mild: Topical    │ │ Early:   │ │ Mild: Lid        │
│ brimonidine │ │ (ivermectin,     │ │ Oral     │ │ hygiene +        │
│ or          │ │ metronidazole)   │ │ isotret. │ │ artificial tears │
│ oxymetazoline│ └──────┬───────────┘ │          │ └──────┬───────────┘
└─────┬───────┘        ↓              │ Establ.: │        ↓
      ↓         ┌──────────────────┐  │ CO₂      │ ┌──────────────────┐
┌─────────────┐ │ Moderate-Severe: │  │ laser/   │ │ Moderate-Severe: │
│ Persistent  │ │ Oral doxycycline │  │ surgery  │ │ Oral doxycycline │
│ telangiect.:│ │ 40 mg MR +       │  └──────────┘ │ 40-100 mg        │
│ IPL/PDL     │ │ topical          │               └──────┬───────────┘
└─────────────┘ └──────────────────┘                      ↓
                                                  ┌──────────────────┐
                                                  │ Keratitis?       │
                                                  │ → URGENT Ophthal.│
                                                  │ referral         │
                                                  └──────────────────┘

Maintenance Therapy

Once acute flare controlled:

• Topical maintenance: Metronidazole, ivermectin, or azelaic acid (continue long-term)
• Trigger avoidance: Ongoing
• Sun protection: Daily SPF 30-50+
• Review: 3-6 months; adjust therapy as needed

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9. Prognosis and Outcomes

Natural History

Prognosis by Subtype

Complications

Exam Detail: | Complication | Frequency | Management | |--------------|-----------|------------| | Ocular keratitis | 5-10% of ocular rosacea | Urgent ophthalmology referral; topical steroids + systemic antibiotics; risk of corneal scarring | | Corneal neovascularisation | Rare; end-stage ocular rosacea | Vision-threatening; ophthalmology-led management | | Rhinophyma | ~5% of rosacea patients (males >> females) | Disfiguring; requires CO₂ laser or surgical excision | | Basal cell carcinoma in rhinophyma | Rare; case reports | Biopsy suspicious lesions; standard BCC management | | Steroid-induced (iatrogenic) rosacea | Common with prolonged topical steroid use | Taper steroids; treat with rosacea-specific therapy | | Psychological impact | 70-90% report reduced quality of life [2] | Acknowledge impact; consider referral to dermatology psychology services if severe |

Quality of Life Impact

Evidence from validated studies: [2]

• 76% report reduced self-confidence
• 69% report embarrassment
• 56% avoid social situations
• Quality of life impairment comparable to moderate-severe acne and psoriasis
• DLQI (Dermatology Life Quality Index) scores: Mean 8-12 (moderate-large effect on life)

Long-Term Management

Rosacea is a chronic disease requiring long-term management:

1. Maintenance topical therapy: Continue indefinitely (metronidazole, ivermectin, or azelaic acid)
2. Trigger avoidance: Lifelong
3. Sun protection: Daily, year-round
4. Monitoring: 3-6 monthly reviews; adjust therapy for flares
5. Patient education: Realistic expectations; disease control, not cure

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10. Prevention and Patient Education

Primary Prevention

No proven primary prevention strategies (genetic predisposition).

Secondary Prevention (Reduce Flares)

Clinical Pearl: Patient Education: "The Rosacea Five"

1. Sun protection EVERY day – SPF 30-50+, physical blockers
2. Identify YOUR triggers – keep a flush diary for 4 weeks
3. Gentle skincare ONLY – fragrance-free, non-irritating products
4. Avoid temperature extremes – cool down hot drinks, avoid saunas
5. Medication adherence – topical therapy takes 4-8 weeks to work; persist!

Trigger Avoidance Strategies

Skincare Recommendations

DO:

• Use gentle, fragrance-free cleansers (e.g., Cerave, Cetaphil)
• Apply non-comedogenic moisturisers (ceramide-containing preferred)
• Use broad-spectrum SPF 30-50+ daily (physical blockers: zinc oxide, titanium dioxide)
• Apply green-tinted primers before makeup (neutralises redness)

DON'T:

• Avoid harsh scrubs, physical exfoliants, astringents
• Avoid alcohol-based toners and products
• Avoid fragranced cosmetics
• Avoid topical retinoids (can exacerbate irritation)

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11. Guidelines and Key Evidence

Major Guidelines

Landmark Studies and High-Quality Evidence

Exam Detail: | Study | Design | Key Finding | Citation | |-------|--------|-------------|----------| | Ivermectin vs Metronidazole (Taieb et al., 2015) | RCT, n=962 | Ivermectin 1% superior to metronidazole 0.75% for inflammatory lesion reduction (83% vs 73.7% improvement) | [19] | | Doxycycline 40 mg MR (Del Rosso et al., 2008) | RCT, n=269 | Sub-antimicrobial dose (40 mg MR) as effective as 100 mg but fewer GI side effects; no resistance | [20] | | IPL for Erythema (Papageorgiou et al., 2008) | RCT, n=30 | 70% improvement in erythema vs 10% placebo; well-tolerated | [18] | | Cathelicidin/LL-37 Pathogenesis (Yamasaki et al., 2007) | Mechanistic study | Abnormal cathelicidin processing → LL-37 → inflammation, angiogenesis | [10] | | TRPV Channels (Sulk et al., 2012) | Mechanistic study | TRPV1/4 overexpression in rosacea → enhanced vasodilation | [11] | | Demodex Density (Forton et al., 2005) | Case-control, n=60 | 10-20× higher Demodex density in rosacea vs controls | [13] | | Quality of Life (van Zuuren, 2017) | Systematic review | Significant QoL impairment (DLQI mean 8-12); comparable to acne/psoriasis | [2] |

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12. Examination Focus: Viva Voce / Oral Exam Scenarios

Exam Detail: ### Scenario 1: Papulopustular Rosacea

Examiner: "This 45-year-old woman presents with a 6-month history of facial redness and spots. Describe your approach."

Model Answer:

1. History:

   • Duration, distribution, triggers (heat, alcohol, spicy food, sun)
   • Symptoms: Flushing, burning, stinging?
   • Previous treatments, especially topical steroids
   • Ocular symptoms (dry, gritty eyes)
   • Impact on quality of life

2. Examination:

   • Central facial erythema (cheeks, nose, chin)
   • Inflammatory papules and pustules
   • Absence of comedones (key feature)
   • Telangiectasia
   • Ocular examination (lid margins, conjunctiva)

3. Diagnosis: Papulopustular rosacea (PPR)

4. Differential:

   • Acne vulgaris (comedones present, younger age)
   • Perioral dermatitis (perioral distribution)
   • Seborrheic dermatitis (greasy scale, nasolabial folds)

5. Investigations: Clinical diagnosis; no tests required

6. Management:

   • General: Trigger avoidance, sun protection (SPF 30-50+), gentle skincare
   • First-line topical: Ivermectin 1% cream once daily OR metronidazole 0.75% gel BD
   • Moderate-severe: Add oral doxycycline 40 mg MR once daily × 12-16 weeks
   • Maintenance: Continue topical long-term
   • Review: 8-12 weeks

Examiner Follow-Up: "What if topical steroids worsen it?"

Answer: Steroid-induced (iatrogenic) rosacea. Taper steroids gradually; treat with rosacea-specific therapy (ivermectin, metronidazole). Educate patient to avoid topical steroids on face.

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Scenario 2: Rhinophyma

Examiner: "This 65-year-old man has progressive nasal enlargement over 10 years. What is your assessment?"

Model Answer:

1. Examination Findings:

   • Bulbous, enlarged nose with irregular, nodular surface
   • Dilated follicles, prominent telangiectasia
   • Skin thickening, loss of normal nasal contours
   • Diagnosis: Rhinophyma (phymatous rosacea)

2. Pathophysiology:

   • Chronic inflammation → sebaceous gland hypertrophy, fibrosis
   • Androgen-mediated (explains male predominance)
   • Advanced stage of rosacea

3. Misconception:

   • NOT caused by alcohol (common myth)
   • Alcohol is a trigger but not causative

4. Red Flag: Basal cell carcinoma can develop within rhinophyma; biopsy suspicious lesions

5. Management:

   • Early phymatous changes: Oral isotretinoin 0.5-1 mg/kg/day may slow progression
   • Established rhinophyma: Medical therapy ineffective; requires surgical remodelling
   • Surgical options: CO₂ laser ablation (gold standard), electrosurgery, scalpel excision
   • Post-op: Wound care, avoid sun, re-epithelialisation 2-3 weeks

Examiner Follow-Up: "Does isotretinoin reverse rhinophyma?"

Answer: No. Isotretinoin may reduce early sebaceous hyperplasia and slow progression, but does not reverse established rhinophyma. Surgery/laser is required for tissue remodelling.

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Scenario 3: Ocular Rosacea

Examiner: "A 50-year-old woman with facial rosacea complains of gritty, dry eyes. What is your approach?"

Model Answer:

1. Ocular Rosacea – affects 50-58% of rosacea patients

2. Symptoms:

   • Dry, gritty, burning eyes
   • Photophobia
   • Blurred vision (transient; tear film instability)
   • Recurrent styes/chalazia

3. Examination:

   • Lid margin telangiectasia
   • Blepharitis (lid margin inflammation, crusting)
   • Meibomian gland dysfunction (inspissated secretions)
   • Conjunctival injection
   • Red flag: Punctate keratopathy, keratitis (fluorescein +ve)

4. Management:

   • Mild: Lid hygiene (warm compresses BD, lid massage), artificial tears (preservative-free)
   • Moderate-severe: Oral doxycycline 40-100 mg once daily × 12-16 weeks
   • Adjuncts: Omega-3 fatty acids 1000-2000 mg/day
   • Ophthalmology referral:
     • Urgent: Keratitis, corneal involvement, vision changes
     • Routine: Inadequate response to first-line therapy

5. Complications: Keratitis → corneal scarring → vision loss (if untreated)

Examiner Follow-Up: "Why doxycycline for eyes?"

Answer: Doxycycline has anti-inflammatory effects (↓ MMPs, ↓ IL-1) and improves meibomian gland function. At 40-100 mg daily, it's primarily anti-inflammatory rather than antimicrobial.

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High-Yield Viva Topics

1. Rosacea vs Acne: Absence of comedones (rosacea); age (rosacea > 30 years)
2. Pathophysiology: Cathelicidin/LL-37, TRPV channels, Demodex, innate immunity
3. Rhinophyma: Male predominance, androgen-mediated, NOT caused by alcohol, CO₂ laser treatment
4. Ocular rosacea: 50% prevalence, keratitis = red flag, doxycycline + lid hygiene
5. Steroid-induced rosacea: Prolonged topical steroid use → worsening; taper + treat
6. Doxycycline 40 mg MR: Sub-antimicrobial, anti-inflammatory dose; no resistance
7. Ivermectin: Anti-Demodex + anti-inflammatory; superior to metronidazole
8. Triggers: UV, alcohol, spicy food, heat; trigger diary recommended

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13. Patient / Layperson Explanation

For Patients: Understanding Rosacea

What is rosacea?

Rosacea is a common long-term skin condition that causes redness, flushing, and sometimes spots on the face. It usually affects the cheeks, nose, chin, and forehead. It's not contagious, not caused by poor hygiene, and can't be "cured," but it can be well-controlled with the right treatment.

Who gets it?

Rosacea typically starts after age 30 and is most common in fair-skinned people of Northern European descent. Women are more likely to get it, but men tend to have more severe symptoms, especially thickening of the nose (rhinophyma).

What causes it?

The exact cause isn't fully understood, but rosacea involves:

• Overactive blood vessels in the face (causing redness and flushing)
• An exaggerated inflammatory response
• Tiny mites called Demodex that live on everyone's skin but are found in higher numbers in people with rosacea
• Genetic factors (it runs in families)

What are the triggers?

Common triggers that make rosacea worse include:

• Sun exposure (the most common trigger)
• Hot drinks and spicy foods
• Alcohol (especially red wine)
• Temperature extremes (hot weather, cold wind, saunas)
• Stress and embarrassment
• Certain skincare products (especially those with fragrance or alcohol)

Keeping a "flush diary" can help you identify your personal triggers.

What are the symptoms?

Rosacea has different types (subtypes) with different symptoms:

1. Flushing and redness (Erythematotelangiectatic): Facial flushing, persistent redness, visible blood vessels
2. Spots (Papulopustular): Red bumps and pus-filled spots (but no blackheads or whiteheads – that's acne, not rosacea)
3. Thickened skin (Phymatous): Skin becomes thick and bumpy, especially on the nose (rhinophyma)
4. Eye symptoms (Ocular): Dry, gritty, irritated eyes; this affects about half of people with rosacea

How is it treated?

Treatment depends on which type you have:

For redness and flushing:

• Creams that temporarily reduce redness (brimonidine, oxymetazoline)
• Laser or light therapy (IPL, pulsed dye laser) to reduce visible blood vessels

For spots:

• Creams (ivermectin, metronidazole, azelaic acid) – apply daily
• Tablets (low-dose doxycycline) if creams aren't enough

For thickened skin (rhinophyma):

• Tablets (isotretinoin) may help early changes
• Surgery or laser treatment for established thickening

For eye symptoms:

• Warm compresses and lid hygiene
• Artificial tears
• Tablets (doxycycline) if symptoms are moderate or severe
• See an eye specialist if your vision is affected

What can I do to help myself?

1. Protect your skin from the sun: Use SPF 30-50+ sunscreen every day (even when cloudy)
2. Avoid your triggers: Keep a diary to work out what makes your rosacea worse
3. Use gentle skincare: Fragrance-free, non-irritating products only; avoid scrubs and harsh cleansers
4. Stay cool: Let hot drinks cool down; avoid saunas and very hot baths
5. Stick with treatment: Creams can take 4-8 weeks to work – don't give up!

Will it go away?

Rosacea is a chronic (long-term) condition, so it won't go away completely. However, with the right treatment and by avoiding triggers, most people can keep it well-controlled and live normal lives.

When should I see a doctor urgently?

• If your eyes are very painful, red, or your vision is affected (this could be keratitis, which needs urgent treatment)
• If you develop a sudden, severe flare that doesn't respond to usual treatment

Can I wear makeup?

Yes! Use non-comedogenic (won't block pores), fragrance-free makeup. Green-tinted primers can help neutralise redness before applying foundation.

Is it true that rhinophyma is caused by drinking alcohol?

No, this is a myth. Alcohol can trigger flushing and worsen rosacea, but it does not cause rhinophyma. Rhinophyma is caused by long-term inflammation and enlargement of oil glands in the nose.

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14. References

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17. Fowler J Jr, Jackson JM, 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;12(6):650-656.

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19. Taieb A, Ortonne JP, Ruzicka T, et al. Superiority of ivermectin 1% cream over metronidazole 0·75% cream in treating inflammatory lesions of rosacea: a randomized, investigator-blinded trial. Br J Dermatol. 2015;172(4):1103-1110. doi:10.1111/bjd.13408

20. 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;56(5):791-802. doi:10.1016/j.jaad.2006.11.021

21. Sbidian E, Vicaut E, Chidiack H, et al. A randomized-controlled trial of oral low-dose isotretinoin for difficult-to-treat papulopustular rosacea. J Invest Dermatol. 2016;136(6):1124-1129. doi:10.1016/j.jid.2016.01.025

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23. Quarterman MJ, Johnson DW, Abele DC, Lesher JL Jr, Hull DS, Davis LS. Ocular rosacea. Signs, symptoms, and tear studies before and after treatment with doxycycline. Arch Dermatol. 1997;133(1):49-54. doi:10.1001/archderm.1997.03890370051007

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