What is Rowell syndrome?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: November 9, 2025View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

What is Rowell Syndrome?

Rowell syndrome is a rare autoimmune disorder characterized by the simultaneous occurrence of lupus erythematosus (LE), erythema multiforme (EM)-like skin lesions, and specific immunological abnormalities including speckled pattern antinuclear antibodies. 1

Diagnostic Criteria

The diagnosis requires meeting all three major criteria plus at least one minor criterion 2, 3:

Major Criteria (All Required):

  • Lupus erythematosus (systemic, discoid, or subacute cutaneous forms) 3
  • Erythema multiforme-like skin lesions with target or annular patterns, often with hemorrhagic crusts 4
  • Speckled pattern antinuclear antibodies (ANA) on indirect immunofluorescence 5

Minor Criteria (At Least One Required):

  • Chilblains 2
  • Positive anti-Ro/SSA or anti-La/SSB antibodies 3
  • Positive rheumatoid factor 5

Clinical Presentation

The skin lesions typically appear as erythematous infiltrated plaques with annular or target patterns, predominantly affecting sun-exposed areas including the neck, chest, upper back, and shoulders 4. The lesions characteristically form hemorrhagic crusts and scales at the margins, while mucous membranes are usually spared 4.

Associated systemic symptoms include:

  • Fatigability and myalgia 2
  • Arthritis (lupus arthritis) 4
  • Constitutional symptoms related to underlying lupus 1

Triggering Factors

Multiple precipitating factors have been identified 1:

  • Medications (most common drug-induced triggers):

    • Proton pump inhibitors (omeprazole, esomeprazole) 4, 2
    • Oral antifungals (terbinafine) 2
    • Antibiotics (norfloxacin) 4
    • Anticonvulsants (sodium valproate) 4
  • Infections:

    • Herpes simplex virus type 1 3
    • Bacterial infections (Pseudomonas aeruginosa) 4
  • Environmental factors:

    • Prolonged sun exposure 3
    • COVID-19 vaccination 1

Laboratory Findings

Essential laboratory evaluation includes 1, 4:

  • Positive speckled ANA (often >1:1280 titers) 4
  • Anti-Ro/SSA antibodies (>200 U/mL) 4
  • Anti-La/SSB antibodies (>200 U/mL) 4
  • Rheumatoid factor (may be positive) 5
  • Complete blood count with differential 1
  • 24-hour urine protein (to assess for lupus nephritis) 4

Direct immunofluorescence from lesional skin typically shows granular C3 deposits at the dermo-epidermal junction 4.

Histopathological Features

Skin biopsy reveals overlapping features of both lupus erythematosus and erythema multiforme 4:

  • Epidermal atrophy with vacuolar degeneration of the basal layer 4
  • Sparse perivascular lymphocytic infiltrate in the dermis 4
  • Single eosinophilic necrotic keratinocytes (characteristic of EM) 4

Treatment Approach

Systemic corticosteroids serve as first-line therapy, with hydroxychloroquine as the cornerstone of long-term management 1, 5:

Initial Management:

  • Methylprednisolone 0.5 mg/kg/day for acute flares 2
  • Hydroxychloroquine 200-400 mg/day for maintenance 4, 5
  • Immediate discontinuation of suspected triggering medications 4

Additional Therapeutic Options:

  • Azathioprine 50 mg/day for steroid-sparing immunosuppression 2
  • Topical corticosteroids (fluticasone propionate 0.05% cream) 2
  • Topical calcineurin inhibitors 3
  • Rituximab for refractory cases (showing favorable outcomes) 1

Supportive Measures:

  • Gastroprotection with H2-receptor antagonists (famotidine 20 mg/day) if PPIs must be avoided 4
  • Potassium supplementation (1 g/day) when on systemic corticosteroids 2
  • Treatment of superimposed infections (ceftriaxone 2 g/day for bacterial infections) 4

Important Clinical Pitfalls

The latency period between drug initiation and syndrome onset can exceed one year, making causality assessment challenging 4. This is particularly true for proton pump inhibitors and diuretics, which have longer latency periods compared to antifungals or chemotherapeutics 4.

Clinical improvement typically occurs within one month after discontinuing the offending agent and optimizing immunosuppressive therapy 4. However, the existence of Rowell syndrome as a distinct entity versus a coincidental overlap remains debated in the literature 4.

Sun protection is critical as sun-exposed areas are preferentially affected, and UV exposure can trigger or exacerbate lesions 3.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.