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2
Pathophys.
2
Histopath.
4
Phenotypes
3
Pathograph
2
Treatments
3
Differentials
6
References
1
Deep Research

Pathophysiology

2
Desmosomal Autoantibody-Mediated Acantholysis
Autoantibodies against desmosomal adhesion proteins in keratinocytes, especially desmoglein 1 and sometimes desmoglein 3, disrupt epidermal cell-cell adhesion. The resulting acantholysis produces superficial intraepidermal fluid collections and fragile bullae or erosions.
Keratinocyte link
Cell Adhesion link ↓ DECREASED Immunoglobulin Production link ↑ INCREASED
Show evidence (1 reference)
PMID:38957191 SUPPORT Human Clinical
"The autoantigens are desmoglein 3, desmoglein 1, and desmosomal adhesion proteins in keratinocytes. When these bonds are disrupted, it causes acantholysis of keratinocytes, leading to the fluid collection between layers."
This case report abstract directly links desmoglein/desmosomal autoantigens to keratinocyte acantholysis and intraepidermal fluid collection in Senear-Usher syndrome.
Dermal-Epidermal Junction Immune Complex and Complement Deposition
Pemphigus erythematosus includes lupus-band-like immunopathology, modeled as immunoglobulin-associated immune complex and complement deposition at the dermal-epidermal junction. This event distinguishes the disorder from plain superficial pemphigus foliaceus and helps explain the lupus erythematosus overlap.
Humoral immune response mediated by circulating immunoglobulin link Classical complement activation link
Show evidence (1 reference)
PMID:33609053 SUPPORT Human Clinical
"Pemphigus erythematosus (PE) is a rare autoimmune skin condition with clinical, histopathological, and serological features that show overlap between lupus erythematosus and pemphigus foliaceus."
The case series and literature review defines the disorder by overlap across clinical, histopathologic, and serologic dimensions.

Histopathology

2
Superficial Acantholysis
Superficial or subcorneal acantholysis is the pemphigus foliaceus-like microscopic component of pemphigus erythematosus and explains the shallow blistering pattern.
Show evidence (2 references)
PMID:38957191 SUPPORT Human Clinical
"When these bonds are disrupted, it causes acantholysis of keratinocytes, leading to the fluid collection between layers."
The abstract supports acantholysis as a histopathologic correlate of desmosomal disruption and intraepidermal fluid collection.
PMID:33609053 PARTIAL Human Clinical
"Pemphigus erythematosus (PE) is a rare autoimmune skin condition with clinical, histopathological, and serological features that show overlap between lupus erythematosus and pemphigus foliaceus."
The Hobbs abstract supports histopathology as a defining axis of the pemphigus foliaceus overlap, although the abstract does not spell out each microscopic criterion.
Direct Immunofluorescence IgG/C3 Deposition Pattern
Direct immunofluorescence is expected to show pemphigus-type intercellular epidermal IgG/C3 staining together with lupus-band-like IgG and/or C3 along the dermal-epidermal junction.
Show evidence (1 reference)
PMID:33609053 PARTIAL Human Clinical
"Clinical, histopathological, and serological features were consistent with what has been reported in the literature"
The cached abstract supports the combined histopathologic and serologic diagnostic axis; the detailed DIF pattern comes from the Falcon-summarized full-text review and is modeled conservatively here.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Pemphigus Erythematosus Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

4
Cardiovascular 1
Erythematous Scaly Plaques Erythema (HP:0010783)
Well-demarcated erythematous, scaly, crusted, or hyperkeratotic plaques are typical and often occur in seborrheic or photo-exposed areas such as the malar face, scalp, chest, upper trunk, and elbows.
Show evidence (2 references)
PMID:33609053 SUPPORT Human Clinical
"It typically presents with erythematous, scaly plaques and has a female predominance."
The literature review identifies erythematous scaly plaques as the typical clinical presentation.
PMID:38957191 SUPPORT Human Clinical
"We report the case of a 21-year-old female presenting to us with multiple hyperkeratotic plaques, mainly on the seborrheic areas, including the face, chest, and elbows."
This case report supports seborrheic-area plaques involving the face, chest, and elbows.
Integument 2
Superficial Cutaneous Blistering Abnormal blistering of the skin (HP:0008066)
Fragile superficial bullae may rupture quickly, leaving crusting and scaling.
Show evidence (1 reference)
PMID:38957191 SUPPORT Human Clinical
"Hence, the patient will present clinically with small flaccid bullae with crusting and scaling, mainly on the seborrheic areas."
The abstract explicitly describes flaccid bullae with crusting and scaling in seborrheic areas.
Cutaneous Photosensitivity Cutaneous photosensitivity (HP:0000992)
Photosensitivity and photo-distributed lesions are repeatedly discussed in pemphigus erythematosus, but the exact frequency is not well established in cache-backed abstracts.
Other 1
Uncommon Mucosal Involvement
Pemphigus erythematosus is primarily cutaneous; Falcon research summarized low pooled oral involvement, so mucosal disease is noted here as uncommon rather than modeled as a core high-frequency feature.
💊

Treatments

2
Topical Anti-Inflammatory Therapy and Photoprotection
Action: supportive care MAXO:0000950
Localized disease may be approached with strict photoprotection and topical anti-inflammatory therapy. This entry keeps the treatment general because the cache-backed abstracts do not provide detailed PE-specific regimen outcomes for topical corticosteroids.
Systemic Immunosuppression
Action: immunosuppressive therapy Ontology label: Immunosuppressive Therapy NCIT:C15261
More extensive or refractory disease may require systemic immunosuppression, including corticosteroids and steroid-sparing agents, selected according to severity and overlap features.
Show evidence (2 references)
PMID:38957191 SUPPORT Human Clinical
"The patient was then managed using immunosuppressant therapy, and the entire course has been detailed in this case report."
This case report documents management of Senear-Usher syndrome using immunosuppressant therapy.
PMID:38817480 PARTIAL Human Clinical
"we highlight the effectiveness of topical treatment in managing SP, contrary to the systemic therapy often required for PE."
This seborrheic pemphigus report contrasts SP with pemphigus erythematosus, noting that systemic therapy is often required for PE.
🌍

Environmental Factors

1
Ultraviolet Exposure
Ultraviolet exposure is treated as a plausible exacerbating factor based on the photo-distributed pattern emphasized in Falcon research and the MONDO/Orphanet definition, but this page does not assign a stronger causal claim without an abstract-backed quote.
🔬

Biochemical Markers

1
ANA and anti-dsDNA positivity (PRESENT)
Context: Lupus-overlap serologic finding reported in Senear-Usher syndrome.
Show evidence (1 reference)
PMID:38957191 SUPPORT Human Clinical
"the diagnosis of pemphigus erythematosus associated with anti-double-stranded deoxyribonucleic acid (anti-dSDNA) and anti-nuclear antibody (ANA) positivity was made."
The case report directly supports ANA and anti-dsDNA positivity as a lupus-overlap serologic finding in this patient.
🔀

Differential Diagnoses

3

Conditions with similar clinical presentations that must be differentiated from Pemphigus Erythematosus:

Pemphigus foliaceus
Distinguishing Features
  • Pemphigus foliaceus lacks the defining lupus-like clinical or serologic overlap expected in pemphigus erythematosus.
Show evidence (1 reference)
PMID:33609053 SUPPORT Human Clinical
"Pemphigus erythematosus (PE) is a rare autoimmune skin condition with clinical, histopathological, and serological features that show overlap between lupus erythematosus and pemphigus foliaceus."
The overlap definition supports pemphigus foliaceus as a close diagnostic comparator rather than an identical concept.
Seborrheic pemphigus
Distinguishing Features
  • Seborrheic pemphigus may resemble pemphigus erythematosus clinically but is framed as a localized superficial pemphigus foliaceus variant without the same lupus-overlap framing.
Show evidence (1 reference)
PMID:38817480 SUPPORT Human Clinical
"Additionally, SP may be conceptually confused with pemphigus erythematosus (PE) due to historical terminology and overlapping clinical features."
The abstract directly identifies confusion between seborrheic pemphigus and pemphigus erythematosus.
Cutaneous lupus erythematosus
Distinguishing Features
  • Cutaneous lupus erythematosus can share malar or photo-distributed plaques, but pemphigus erythematosus also has pemphigus-type acantholysis and desmosomal autoantigens.
Show evidence (1 reference)
PMID:33609053 SUPPORT Human Clinical
"Pemphigus erythematosus (PE) is a rare autoimmune skin condition with clinical, histopathological, and serological features that show overlap between lupus erythematosus and pemphigus foliaceus."
The overlap definition supports lupus erythematosus as a differential diagnosis that must be separated from the pemphigus component.
{ }

Source YAML

click to show
name: Pemphigus Erythematosus
creation_date: "2026-05-07T02:02:04Z"
updated_date: "2026-05-07T02:16:00Z"
category: Autoimmune
parents:
- Autoimmune Disease
- Skin Disease
disease_term:
  preferred_term: Pemphigus Erythematosus
  term:
    id: MONDO:0019323
    label: pemphigus erythematosus
description: >-
  Pemphigus erythematosus, also called Senear-Usher syndrome, is a rare
  superficial autoimmune blistering disorder with clinical, histopathologic, and
  serologic overlap between pemphigus foliaceus and lupus erythematosus. It is
  modeled here as a localized pemphigus spectrum disorder with seborrheic and
  photo-distributed cutaneous lesions, not as generic pemphigus or mucosal-
  dominant pemphigus vulgaris.
references:
- reference: DOI:10.5114/ada.2024.139233
  title: Senear-Usher syndrome in a 5-year-old girl
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
- reference: DOI:10.7759/cureus.59389
  title: "Seborrheic Pemphigus: A Misunderstood Variant of Pemphigus Foliaceus"
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
- reference: DOI:10.1111/cup.13992
  title: >-
    Pemphigus erythematosus: A case series from a tertiary academic center and
    literature review
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
- reference: DOI:10.1016/j.cger.2023.09.002
  title: Diagnosis and Management of Bullous Disease
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
- reference: DOI:10.5070/d3241037928
  title: Unusually extensive scalp ulcerations manifested in pemphigus erythematosus
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
- reference: DOI:10.7759/cureus.49268
  title: A Case Report on Senear-Usher Syndrome
  found_in:
  - Pemphigus_Erythematosus-deep-research-falcon.md
pathophysiology:
- name: Desmosomal Autoantibody-Mediated Acantholysis
  description: >-
    Autoantibodies against desmosomal adhesion proteins in keratinocytes,
    especially desmoglein 1 and sometimes desmoglein 3, disrupt epidermal
    cell-cell adhesion. The resulting acantholysis produces superficial
    intraepidermal fluid collections and fragile bullae or erosions.
  cell_types:
  - preferred_term: Keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  biological_processes:
  - preferred_term: Cell Adhesion
    term:
      id: GO:0007155
      label: cell adhesion
    modifier: DECREASED
  - preferred_term: Immunoglobulin Production
    term:
      id: GO:0002377
      label: immunoglobulin production
    modifier: INCREASED
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The autoantigens are desmoglein 3, desmoglein 1, and desmosomal adhesion
      proteins in keratinocytes. When these bonds are disrupted, it causes
      acantholysis of keratinocytes, leading to the fluid collection between
      layers.
    explanation: >-
      This case report abstract directly links desmoglein/desmosomal
      autoantigens to keratinocyte acantholysis and intraepidermal fluid
      collection in Senear-Usher syndrome.
  downstream:
  - target: Dermal-Epidermal Junction Immune Complex and Complement Deposition
    description: >-
      Desmosomal autoimmunity co-occurs with lupus-like immunopathology at the
      dermal-epidermal junction in pemphigus erythematosus.
    causal_link_type: UNKNOWN
- name: Dermal-Epidermal Junction Immune Complex and Complement Deposition
  description: >-
    Pemphigus erythematosus includes lupus-band-like immunopathology, modeled as
    immunoglobulin-associated immune complex and complement deposition at the
    dermal-epidermal junction. This event distinguishes the disorder from plain
    superficial pemphigus foliaceus and helps explain the lupus erythematosus
    overlap.
  biological_processes:
  - preferred_term: Humoral immune response mediated by circulating immunoglobulin
    term:
      id: GO:0002455
      label: humoral immune response mediated by circulating immunoglobulin
  - preferred_term: Classical complement activation
    term:
      id: GO:0006958
      label: complement activation, classical pathway
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Pemphigus erythematosus (PE) is a rare autoimmune skin condition with
      clinical, histopathological, and serological features that show overlap
      between lupus erythematosus and pemphigus foliaceus.
    explanation: >-
      The case series and literature review defines the disorder by overlap
      across clinical, histopathologic, and serologic dimensions.
  downstream:
  - target: Erythematous Scaly Plaques
    description: >-
      Lupus-like cutaneous immune deposition contributes to the erythematous,
      scaly plaque phenotype in seborrheic or photo-distributed skin.
    causal_link_type: INDIRECT_UNKNOWN_INTERMEDIATES
histopathology:
- name: Superficial Acantholysis
  diagnostic: true
  description: >-
    Superficial or subcorneal acantholysis is the pemphigus foliaceus-like
    microscopic component of pemphigus erythematosus and explains the shallow
    blistering pattern.
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      When these bonds are disrupted, it causes acantholysis of keratinocytes,
      leading to the fluid collection between layers.
    explanation: >-
      The abstract supports acantholysis as a histopathologic correlate of
      desmosomal disruption and intraepidermal fluid collection.
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Pemphigus erythematosus (PE) is a rare autoimmune skin condition with
      clinical, histopathological, and serological features that show overlap
      between lupus erythematosus and pemphigus foliaceus.
    explanation: >-
      The Hobbs abstract supports histopathology as a defining axis of the
      pemphigus foliaceus overlap, although the abstract does not spell out each
      microscopic criterion.
- name: Direct Immunofluorescence IgG/C3 Deposition Pattern
  diagnostic: true
  description: >-
    Direct immunofluorescence is expected to show pemphigus-type intercellular
    epidermal IgG/C3 staining together with lupus-band-like IgG and/or C3 along
    the dermal-epidermal junction.
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Clinical, histopathological, and serological features were consistent with
      what has been reported in the literature
    explanation: >-
      The cached abstract supports the combined histopathologic and serologic
      diagnostic axis; the detailed DIF pattern comes from the Falcon-summarized
      full-text review and is modeled conservatively here.
phenotypes:
- name: Erythematous Scaly Plaques
  category: Dermatologic
  notes: >-
    Well-demarcated erythematous, scaly, crusted, or hyperkeratotic plaques are
    typical and often occur in seborrheic or photo-exposed areas such as the
    malar face, scalp, chest, upper trunk, and elbows.
  phenotype_term:
    preferred_term: Erythematous scaly plaques
    term:
      id: HP:0010783
      label: Erythema
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      It typically presents with erythematous, scaly plaques and has a female
      predominance.
    explanation: >-
      The literature review identifies erythematous scaly plaques as the typical
      clinical presentation.
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      We report the case of a 21-year-old female presenting to us with multiple
      hyperkeratotic plaques, mainly on the seborrheic areas, including the
      face, chest, and elbows.
    explanation: >-
      This case report supports seborrheic-area plaques involving the face,
      chest, and elbows.
- name: Superficial Cutaneous Blistering
  category: Dermatologic
  notes: >-
    Fragile superficial bullae may rupture quickly, leaving crusting and scaling.
  phenotype_term:
    preferred_term: Superficial cutaneous blistering
    term:
      id: HP:0008066
      label: Abnormal blistering of the skin
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Hence, the patient will present clinically with small flaccid bullae with
      crusting and scaling, mainly on the seborrheic areas.
    explanation: >-
      The abstract explicitly describes flaccid bullae with crusting and scaling
      in seborrheic areas.
- name: Cutaneous Photosensitivity
  category: Dermatologic
  notes: >-
    Photosensitivity and photo-distributed lesions are repeatedly discussed in
    pemphigus erythematosus, but the exact frequency is not well established in
    cache-backed abstracts.
  phenotype_term:
    preferred_term: Cutaneous photosensitivity
    term:
      id: HP:0000992
      label: Cutaneous photosensitivity
- name: Uncommon Mucosal Involvement
  category: Oral
  notes: >-
    Pemphigus erythematosus is primarily cutaneous; Falcon research summarized
    low pooled oral involvement, so mucosal disease is noted here as uncommon
    rather than modeled as a core high-frequency feature.
biochemical:
- name: ANA and anti-dsDNA positivity
  presence: PRESENT
  context: Lupus-overlap serologic finding reported in Senear-Usher syndrome.
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      the diagnosis of pemphigus erythematosus associated with anti-double-stranded
      deoxyribonucleic acid (anti-dSDNA) and anti-nuclear antibody (ANA)
      positivity was made.
    explanation: >-
      The case report directly supports ANA and anti-dsDNA positivity as a
      lupus-overlap serologic finding in this patient.
diagnosis:
- name: Integrated Clinicopathologic Diagnosis
  description: >-
    Diagnosis relies on correlating clinical distribution with histopathology,
    direct immunofluorescence, and serology to distinguish pemphigus
    erythematosus from pemphigus foliaceus, seborrheic dermatitis, and cutaneous
    lupus erythematosus.
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Clinical, histopathological, and serological features were consistent with
      what has been reported in the literature
    explanation: >-
      The case series and literature review demonstrates that diagnosis is
      grounded in concordant clinical, histopathologic, and serologic features.
- name: Desmoglein Autoantibody Serology
  description: >-
    Desmoglein autoantibody testing can support the pemphigus component of the
    diagnosis, with desmoglein 1 expected to dominate in superficial pemphigus
    patterns while some cases also show desmoglein 3 reactivity.
  markers: anti-desmoglein 1, anti-desmoglein 3
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The autoantigens are desmoglein 3, desmoglein 1, and desmosomal adhesion
      proteins in keratinocytes.
    explanation: >-
      The abstract identifies desmoglein 1 and desmoglein 3 as relevant
      autoantigens for Senear-Usher syndrome.
environmental:
- name: Ultraviolet Exposure
  presence: PRESENT
  description: >-
    Ultraviolet exposure is treated as a plausible exacerbating factor based on
    the photo-distributed pattern emphasized in Falcon research and the
    MONDO/Orphanet definition, but this page does not assign a stronger causal
    claim without an abstract-backed quote.
  effect: Exacerbating factor for photo-distributed cutaneous lesions.
treatments:
- name: Topical Anti-Inflammatory Therapy and Photoprotection
  description: >-
    Localized disease may be approached with strict photoprotection and topical
    anti-inflammatory therapy. This entry keeps the treatment general because
    the cache-backed abstracts do not provide detailed PE-specific regimen
    outcomes for topical corticosteroids.
  treatment_term:
    preferred_term: supportive care
    term:
      id: MAXO:0000950
      label: supportive care
- name: Systemic Immunosuppression
  description: >-
    More extensive or refractory disease may require systemic immunosuppression,
    including corticosteroids and steroid-sparing agents, selected according to
    severity and overlap features.
  treatment_term:
    preferred_term: immunosuppressive therapy
    term:
      id: NCIT:C15261
      label: Immunosuppressive Therapy
  evidence:
  - reference: PMID:38957191
    reference_title: A Case Report on Senear-Usher Syndrome.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The patient was then managed using immunosuppressant therapy, and the
      entire course has been detailed in this case report.
    explanation: >-
      This case report documents management of Senear-Usher syndrome using
      immunosuppressant therapy.
  - reference: PMID:38817480
    reference_title: >-
      Seborrheic Pemphigus: A Misunderstood Variant of Pemphigus Foliaceus.
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      we highlight the effectiveness of topical treatment in managing SP,
      contrary to the systemic therapy often required for PE.
    explanation: >-
      This seborrheic pemphigus report contrasts SP with pemphigus
      erythematosus, noting that systemic therapy is often required for PE.
differential_diagnoses:
- name: Pemphigus foliaceus
  distinguishing_features:
  - Pemphigus foliaceus lacks the defining lupus-like clinical or serologic overlap
    expected in pemphigus erythematosus.
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Pemphigus erythematosus (PE) is a rare autoimmune skin condition with
      clinical, histopathological, and serological features that show overlap
      between lupus erythematosus and pemphigus foliaceus.
    explanation: >-
      The overlap definition supports pemphigus foliaceus as a close diagnostic
      comparator rather than an identical concept.
- name: Seborrheic pemphigus
  distinguishing_features:
  - Seborrheic pemphigus may resemble pemphigus erythematosus clinically but is
    framed as a localized superficial pemphigus foliaceus variant without the
    same lupus-overlap framing.
  evidence:
  - reference: PMID:38817480
    reference_title: >-
      Seborrheic Pemphigus: A Misunderstood Variant of Pemphigus Foliaceus.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Additionally, SP may be conceptually confused with pemphigus
      erythematosus (PE) due to historical terminology and overlapping clinical
      features.
    explanation: >-
      The abstract directly identifies confusion between seborrheic pemphigus
      and pemphigus erythematosus.
- name: Cutaneous lupus erythematosus
  distinguishing_features:
  - Cutaneous lupus erythematosus can share malar or photo-distributed plaques,
    but pemphigus erythematosus also has pemphigus-type acantholysis and
    desmosomal autoantigens.
  evidence:
  - reference: PMID:33609053
    reference_title: >-
      Pemphigus erythematosus: A case series from a tertiary academic center and
      literature review.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Pemphigus erythematosus (PE) is a rare autoimmune skin condition with
      clinical, histopathological, and serological features that show overlap
      between lupus erythematosus and pemphigus foliaceus.
    explanation: >-
      The overlap definition supports lupus erythematosus as a differential
      diagnosis that must be separated from the pemphigus component.
📚

References & Deep Research

References

6
Senear-Usher syndrome in a 5-year-old girl
No top-level findings curated for this source.
Seborrheic Pemphigus: A Misunderstood Variant of Pemphigus Foliaceus
No top-level findings curated for this source.
Pemphigus erythematosus: A case series from a tertiary academic center and literature review
No top-level findings curated for this source.
Diagnosis and Management of Bullous Disease
No top-level findings curated for this source.
Unusually extensive scalp ulcerations manifested in pemphigus erythematosus
No top-level findings curated for this source.
A Case Report on Senear-Usher Syndrome
No top-level findings curated for this source.

Deep Research

1
Falcon
1. Disease Information
Edison Scientific Literature 19 citations 2026-05-06T22:13:21.026109

1. Disease Information

1.1 Concise overview (current understanding)

Pemphigus erythematosus is a rare autoimmune blistering disorder with overlapping clinical, histopathologic, and immunologic features of pemphigus foliaceus and lupus erythematosus, often presenting as erythematous, scaly/crusted plaques and/or superficial flaccid blisters on seborrheic and photoexposed sites (especially malar face/scalp/upper trunk). (hobbs2021pemphiguserythematosusa pages 1-2, onalajaunderwood2024diagnosisandmanagement pages 1-3)

A central clinicopathologic concept is that PE demonstrates pemphigus-type intraepidermal acantholysis plus a lupus-band–like direct immunofluorescence pattern along the dermal–epidermal junction (DEJ). (chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 1-2)

1.2 Key identifiers (knowledge-base fields)

  • ICD-10 / ICD-11: Not available in retrieved evidence. (hobbs2021pemphiguserythematosusa pages 1-2)
  • MeSH: Not available in retrieved evidence. (hobbs2021pemphiguserythematosusa pages 1-2)
  • Orphanet: Not available in retrieved evidence. (hobbs2021pemphiguserythematosusa pages 1-2)
  • OMIM: Not available in retrieved evidence. (hobbs2021pemphiguserythematosusa pages 1-2)
  • MONDO: Not available in retrieved evidence. (hobbs2021pemphiguserythematosusa pages 1-2)

1.3 Evidence source type

The disease-specific information in this report is derived mainly from aggregated disease-level synthesis (a tertiary-center case series + literature review) and recent case reports/reviews rather than EHR-scale datasets. (hobbs2021pemphiguserythematosusa pages 1-2, arasiewicz2024senearushersyndromein pages 1-3, jangid2023acasereport pages 1-4)


2. Etiology

2.1 Disease causal factors (mechanistic)

PE is caused by an autoimmune response against desmosomal adhesion molecules (most prominently desmoglein-1), leading to impaired keratinocyte–keratinocyte adhesion (acantholysis) and superficial intraepidermal blistering. (onalajaunderwood2024diagnosisandmanagement pages 1-3, chandan2018unusuallyextensivescalp pages 1-4)

2.2 Risk factors

Genetic (susceptibility): A genetic predisposition via HLA haplotypes has been suggested; a pediatric PE report mentions HLA haplotypes including A10/A26 and DRW6 in the context of susceptibility. (arasiewicz2024senearushersyndromein pages 1-3)

Environmental (exacerbating/triggering): - Ultraviolet (UV) exposure/sunlight is repeatedly described as an exacerbating factor; a PE case report review notes UV can contribute mechanistically (including desmoglein-1 ectodomain cleavage and immune deposition at the DEJ in UV-exposed skin). (chandan2018unusuallyextensivescalp pages 4-5, onalajaunderwood2024diagnosisandmanagement pages 1-3)

Medication triggers (class effect for pemphigus; PE-specific evidence limited): A 2024 bullous disease review lists multiple medications associated with pemphigus (e.g., penicillamine, captopril, propranolol) while discussing pemphigus foliaceus and variants including PE, supporting consideration of drug triggers in susceptible individuals, though PE-specific causal attribution is not established in the retrieved PE-focused data. (onalajaunderwood2024diagnosisandmanagement pages 3-7)

2.3 Protective factors

No protective genetic or environmental factors were identified in the retrieved evidence set. (hobbs2021pemphiguserythematosusa pages 1-2)

2.4 Gene–environment interactions

A plausible gene–environment interaction is HLA-associated susceptibility combined with UV exposure as a clinical and mechanistic aggravator, but direct studies in PE were not available in the retrieved evidence set. (arasiewicz2024senearushersyndromein pages 1-3, chandan2018unusuallyextensivescalp pages 4-5)


3. Phenotypes

3.1 Core clinical phenotype spectrum

Across a tertiary-center case series and literature review (87 literature cases summarized), common anatomic distributions included trunk (62%), face (51.7%), extremities (39%), scalp (35.6%). (hobbs2021pemphiguserythematosusa pages 2-5)

Mucosal involvement is uncommon; pooled oral involvement was ~9.2%. (hobbs2021pemphiguserythematosusa pages 2-5)

Common morphologies include erythematous scaly/crusted plaques, superficial erosions, and fragile/flaccid blisters that rupture with crusting. (jangid2023acasereport pages 1-4, hobbs2021pemphiguserythematosusa pages 10-11)

Course: A 2024 review characterizes PE as generally chronic and localized to malar and other seborrheic areas. (onalajaunderwood2024diagnosisandmanagement pages 3-7)

3.2 Suggested HPO terms (mapping suggestions)

(These are ontology suggestions; the retrieved articles do not provide HPO codes.) - Erythematous scaly plaques / erythema: HP:0020116 (Erythema) (suggested) (hobbs2021pemphiguserythematosusa pages 2-5) - Blistering: HP:0030057 (Blistering of the skin) (suggested) (jangid2023acasereport pages 1-4) - Skin erosions/crusting: HP:0100717 (Skin erosion); HP:0200042 (Crusting of skin lesions) (suggested) (arasiewicz2024senearushersyndromein pages 1-3, jangid2023acasereport pages 1-4) - Photosensitivity: HP:0000992 (Photosensitivity) (suggested) (hobbs2021pemphiguserythematosusa pages 10-11, onalajaunderwood2024diagnosisandmanagement pages 3-7) - Positive Nikolsky sign (clinical sign; HPO mapping may vary): (suggested) (onalajaunderwood2024diagnosisandmanagement pages 1-3)

3.3 Quality-of-life impact

Disease-specific QoL instrument data were not identified for PE in the retrieved evidence set; however, PE is described as causing symptomatic, visible lesions and is discussed as requiring integrated assessment in case-report literature. (jangid2023acasereport pages 6-7)


4. Genetic/Molecular Information

4.1 Causal genes

PE is not a monogenic disorder in the retrieved evidence set; no single causal gene/variant is established. Evidence supports HLA-associated susceptibility (immunogenetic predisposition) rather than Mendelian inheritance. (arasiewicz2024senearushersyndromein pages 1-3)

4.2 Autoantigens / molecular targets (key disease molecules)

  • Desmoglein 1 (DSG1): Central autoantigen; a 2024 review describes PF (and variants including PE) as mediated by IgG4 autoantibodies against desmoglein-1. (onalajaunderwood2024diagnosisandmanagement pages 1-3)
  • Desmoglein 3 (DSG3): Some PE cases have anti-Dsg3 antibodies; PE case reports mention Dsg1 and Dsg3 and other desmosomal proteins. (arasiewicz2024senearushersyndromein pages 1-3, jangid2023acasereport pages 1-4)

4.3 Pathogenic variants / allele frequencies

Not applicable based on retrieved evidence; PE evidence focuses on autoantibodies and HLA associations rather than pathogenic variants. (hobbs2021pemphiguserythematosusa pages 1-2)


5. Environmental Information

Key environmental factor

  • UV exposure / sunlight: recurrently described as worsening PE, including a mechanistic explanation involving UV-associated effects on desmoglein-1 and deposition at the DEJ. (chandan2018unusuallyextensivescalp pages 4-5, onalajaunderwood2024diagnosisandmanagement pages 3-7)

No specific infectious trigger was identified in the retrieved evidence set for PE. (hobbs2021pemphiguserythematosusa pages 1-2)


6. Mechanism / Pathophysiology

6.1 Causal chain (current model)

1) Autoantibody production against desmosomal proteins (especially DSG1, sometimes DSG3) occurs in susceptible individuals. (onalajaunderwood2024diagnosisandmanagement pages 1-3, jangid2023acasereport pages 1-4) 2) Binding of autoantibodies to keratinocyte adhesion molecules leads to loss of intercellular adhesion (acantholysis), producing superficial intraepidermal blistering and erosions. (chandan2018unusuallyextensivescalp pages 1-4, hobbs2021pemphiguserythematosusa pages 2-5) 3) PE uniquely shows lupus-like immunopathology, commonly featuring DEJ immune deposits (IgG/C3) on direct immunofluorescence (“lupus-band”-like), especially in photoexposed skin. (chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 10-11) 4) Clinically this yields erythematous scaly/crusted plaques and superficial erosions in seborrheic/photoexposed distributions with relatively infrequent mucosal involvement. (hobbs2021pemphiguserythematosusa pages 2-5, onalajaunderwood2024diagnosisandmanagement pages 3-7)

6.2 Key immune components

  • IgG4-class autoantibodies to DSG1 are emphasized in PF/variant pathogenesis. (onalajaunderwood2024diagnosisandmanagement pages 1-3)
  • Complement (C3) deposition is a common DIF feature (intercellular and along DEJ). (hobbs2021pemphiguserythematosusa pages 10-11)

6.3 Suggested GO and CL ontology terms (mapping suggestions)

(These are ontology suggestions; the retrieved articles do not provide GO/CL codes.) - GO biological processes: keratinocyte cell–cell adhesion; complement activation; humoral immune response; inflammatory response in skin. (suggested) (hobbs2021pemphiguserythematosusa pages 10-11, onalajaunderwood2024diagnosisandmanagement pages 1-3) - CL cell types: keratinocyte; B cell/plasma cell (autoantibody production). (suggested) (onalajaunderwood2024diagnosisandmanagement pages 1-3)

6.4 Molecular profiling / omics

No transcriptomic/proteomic/metabolomic PE-specific profiling was identified in the retrieved evidence set. (hobbs2021pemphiguserythematosusa pages 1-2)


7. Anatomical Structures Affected

7.1 Organ/tissue level

  • Primary: skin, especially seborrheic and photoexposed regions (malar face, scalp, upper trunk). (onalajaunderwood2024diagnosisandmanagement pages 3-7, hobbs2021pemphiguserythematosusa pages 2-5)
  • Mucosa: uncommon oral involvement (~9.2% in pooled review). (hobbs2021pemphiguserythematosusa pages 2-5)

7.2 Suggested UBERON terms (mapping suggestions)

  • Skin (UBERON:0002097), face (UBERON:0001456), scalp (UBERON:0001135), trunk (UBERON:0002100), oral mucosa (UBERON:0000344) (suggested). (hobbs2021pemphiguserythematosusa pages 2-5)

7.3 Subcellular level

  • Desmosomes/cell junctions are implicated via autoantibody targeting of desmosomal cadherins (desmogleins). (onalajaunderwood2024diagnosisandmanagement pages 1-3)

8. Temporal Development

8.1 Onset

In the Hobbs literature review, age ranged from 5–84 years (mean ~51.77 years, median 57), supporting predominantly adult onset but possible pediatric presentation. (hobbs2021pemphiguserythematosusa pages 2-5)

8.2 Progression/course

PE is described as generally chronic; disease duration in reviewed literature ranged 1–60 months (mean 18.2 months; median 11 months). (onalajaunderwood2024diagnosisandmanagement pages 3-7, hobbs2021pemphiguserythematosusa pages 5-5)


9. Inheritance and Population

9.1 Epidemiology

Epidemiology is not well established; a recent pediatric report states epidemiology is unknown and cites a prevalence estimate of 4.4 cases/million. (arasiewicz2024senearushersyndromein pages 1-3)

9.2 Demographics

  • Sex distribution: literature review in Hobbs found female:male = 45:36, suggesting mild female predominance. (hobbs2021pemphiguserythematosusa pages 2-5)
  • Race/ethnicity: Hobbs’ center case series (n=5) had 4/5 Black (80%), higher than literature reporting where race was available (~20% Black), though this may reflect referral/catchment characteristics rather than true population risk. (hobbs2021pemphiguserythematosusa pages 1-2)

9.3 Genetic etiology (inheritance)

No Mendelian inheritance is supported; risk appears multifactorial with HLA-linked susceptibility reported. (arasiewicz2024senearushersyndromein pages 1-3)


10. Diagnostics

10.1 Clinical criteria and standard diagnostic approach

In Hobbs et al., diagnostic criteria required (i) pemphigus foliaceus-like histopathology plus (ii) DIF evidence of epidermal intercellular IgG and (iii) IgG and/or C3 along the DEJ. (hobbs2021pemphiguserythematosusa pages 1-2)

A 2024 review emphasizes that when a blistering disorder is suspected, clinicians should obtain a lesional biopsy for H&E and a perilesional biopsy for DIF, with the DIF specimen taken from immediately adjacent uninvolved skin and sent in Michel medium. (onalajaunderwood2024diagnosisandmanagement pages 1-3)

10.2 Histopathology

Typical histology includes superficial/subcorneal or intraepidermal acantholysis, often with dyskeratosis and lymphocytic dermal inflammation. (hobbs2021pemphiguserythematosusa pages 2-5, hobbs2021pemphiguserythematosusa pages 10-11)

10.3 Direct immunofluorescence (DIF)

DIF typically demonstrates intercellular space IgG/C3 deposition plus a linear/granular DEJ (lupus-band–like) IgG/C3 pattern. (chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 10-11)

10.4 Serology / biomarkers

  • Anti-DSG1: frequently elevated in pooled reports; Hobbs notes reported anti-DSG1 levels were elevated in available reports. (hobbs2021pemphiguserythematosusa pages 10-11)
  • ANA: variable; cited range 30–80% across literature, with one PE case series showing ANA elevated in 1/5 (20%). (jangid2023acasereport pages 1-4, hobbs2021pemphiguserythematosusa pages 2-5)

10.5 Differential diagnosis

PE is repeatedly discussed in diagnostic context as overlapping lupus erythematosus and pemphigus foliaceus and may be confused with seborrheic dermatitis and other seborrheic eruptions; accurate diagnosis hinges on histology and immunopathology. (espadas2024seborrheicpemphigusa pages 1-3, hobbs2021pemphiguserythematosusa pages 1-2)


11. Outcome / Prognosis

PE is often described as more benign/easier to manage than pemphigus vulgaris in case literature, but robust survival or long-term morbidity statistics were not available from the retrieved evidence set. (chandan2018unusuallyextensivescalp pages 4-5)

Complications reported/mentioned include secondary infection and severe erythroderma in individual cases. (arasiewicz2024senearushersyndromein pages 1-3)


12. Treatment

12.1 Current applications / real-world implementation

A 2024 review provides practical management framing: “Localized disease can typically be managed by potent topical steroids”, while more extensive disease may require systemic therapy including prednisone and steroid-sparing agents such as azathioprine, mycophenolate mofetil, rituximab, or dapsone. (onalajaunderwood2024diagnosisandmanagement pages 3-7)

Case-based evidence includes use of hydroxychloroquine + systemic prednisone + dapsone with clinical response in pediatric PE, supporting real-world use of antimalarial and anti-neutrophil/anti-inflammatory adjunct approaches in overlap-like presentations. (arasiewicz2024senearushersyndromein pages 1-3)

12.2 Treatment outcomes (data points)

  • Case-series summaries cited in recent case-report literature describe remission outcomes (e.g., “three of four complete remission at mean six months” in one small series summary), though these are not controlled studies and likely heterogeneous in severity and therapy. (jangid2023acasereport pages 4-6)
  • Hobbs literature review notes cases treated with rituximab achieving prolonged resolution (example: 3-year complete resolution reported). (hobbs2021pemphiguserythematosusa pages 10-11)

12.3 MAXO terms (mapping suggestions)

  • Topical corticosteroid therapy; systemic glucocorticoid therapy; immunosuppressive therapy (azathioprine, mycophenolate); anti-CD20 monoclonal antibody therapy (rituximab); dapsone therapy; antimalarial therapy (hydroxychloroquine); photoprotection counseling (suggested). (onalajaunderwood2024diagnosisandmanagement pages 3-7, arasiewicz2024senearushersyndromein pages 1-3)

12.4 Expert opinion / guideline-like synthesis

  • The geriatric bullous disease review serves as an expert synthesis emphasizing biopsy + DIF as core diagnostics and stratifying therapy by extent (topical for localized; systemic immunosuppression/biologics for extensive). (onalajaunderwood2024diagnosisandmanagement pages 1-3, onalajaunderwood2024diagnosisandmanagement pages 3-7)

13. Prevention

Evidence-based PE-specific prevention strategies were not identified beyond avoidance of known aggravating factors, especially sunlight/UV exposure given repeated associations with photosensitivity and worsening. (onalajaunderwood2024diagnosisandmanagement pages 3-7, chandan2018unusuallyextensivescalp pages 4-5)


14. Other Species / Natural Disease

No natural disease reports in non-human species specific to pemphigus erythematosus were identified in the retrieved evidence set. (hobbs2021pemphiguserythematosusa pages 1-2)


15. Model Organisms

No PE-specific model organism systems were identified in the retrieved evidence set. Mechanistic work in pemphigus broadly often uses antibody transfer/ex vivo skin systems, but such details were not retrieved here for PE specifically. (hobbs2021pemphiguserythematosusa pages 1-2)


Recent developments and latest research (prioritizing 2023–2024)

1) Clinical recognition and pediatric presentations: Recent case reports highlight that PE can occur in children (e.g., a 2024 report in a 5-year-old), reinforcing that the age range includes pediatric-onset disease even if adult-onset is more typical. (arasiewicz2024senearushersyndromein pages 1-3)

2) Refined diagnostic workflows in bullous disease practice: A 2024 expert review reinforces practical details for DIF sampling (perilesional biopsy, Michel medium) and emphasizes ELISA availability for desmoglein autoantibodies, reflecting continuing standardization and accessibility of serologic testing in clinical practice. (onalajaunderwood2024diagnosisandmanagement pages 1-3)

3) Therapeutic positioning: A 2024 review frames PE management within modern pemphigus care, including topical steroids for localized disease and systemic immunosuppression and biologics (including rituximab) for more extensive disease, consistent with current real-world practice patterns. (onalajaunderwood2024diagnosisandmanagement pages 3-7)


Evidence-backed statistics (selected)

  • Common site distribution (pooled literature review): trunk 62%, face 51.7%, extremities 39%, scalp 35.6%. (hobbs2021pemphiguserythematosusa pages 2-5)
  • Oral involvement (pooled): ~9.2%. (hobbs2021pemphiguserythematosusa pages 2-5)
  • Sex ratio (pooled): female:male 45:36. (hobbs2021pemphiguserythematosusa pages 2-5)
  • Age distribution (pooled): range 5–84; mean ~51.77; median 57. (hobbs2021pemphiguserythematosusa pages 2-5)
  • ANA positivity: widely cited 30–80% in literature; one center series 1/5 (20%). (jangid2023acasereport pages 1-4, hobbs2021pemphiguserythematosusa pages 2-5)
  • Prevalence estimate (single cited figure): 4.4 cases/million. (arasiewicz2024senearushersyndromein pages 1-3)

Summary table

Domain Key finding Supporting citations
Definition / disease concept Pemphigus erythematosus (PE), also called Senear–Usher syndrome, is a rare autoimmune blistering disorder generally regarded as a localized variant of pemphigus foliaceus with clinical, histologic, and immunologic overlap with cutaneous lupus erythematosus. (arasiewicz2024senearushersyndromein pages 1-3, jangid2023acasereport pages 1-4, hobbs2021pemphiguserythematosusa pages 1-2, onalajaunderwood2024diagnosisandmanagement pages 3-7)
Typical clinical distribution Lesions are usually erythematous, scaly or crusted plaques / superficial flaccid bullae in seborrheic and photoexposed areas, especially the malar face, scalp, upper trunk, and back; face involvement was 80% in one center series and 51.7% in the pooled literature review. (arasiewicz2024senearushersyndromein pages 1-3, hobbs2021pemphiguserythematosusa pages 1-2, hobbs2021pemphiguserythematosusa pages 2-5, onalajaunderwood2024diagnosisandmanagement pages 3-7, onalajaunderwood2024diagnosisandmanagement pages 1-3)
Mucosal involvement Mucosal disease is uncommon; oral/pharyngeal/vulvar mucosa are often spared, and pooled oral involvement was ~9.2% in Hobbs et al. (arasiewicz2024senearushersyndromein pages 1-3, hobbs2021pemphiguserythematosusa pages 2-5, onalajaunderwood2024diagnosisandmanagement pages 1-3)
Key autoantigens Main autoantigen is desmoglein 1 (Dsg1); some reports also describe Dsg3 and other desmosomal adhesion proteins / plakins. PF-variant pathogenesis is linked to IgG4 against Dsg1. (arasiewicz2024senearushersyndromein pages 1-3, jangid2023acasereport pages 1-4, chandan2018unusuallyextensivescalp pages 1-4, onalajaunderwood2024diagnosisandmanagement pages 1-3)
Histology Characteristic pathology is superficial/subcorneal or intraepidermal acantholysis, often with dyskeratosis; inflammatory infiltrates may be lymphocytic or mixed, with papillary dermal edema/perivascular infiltrates in some cases. (arasiewicz2024senearushersyndromein pages 1-3, chandan2018unusuallyextensivescalp pages 1-4, hobbs2021pemphiguserythematosusa pages 2-5, hobbs2021pemphiguserythematosusa pages 10-11)
Direct immunofluorescence (DIF) Classic DIF shows intercellular epidermal IgG/C3 deposition plus IgG and/or C3 along the dermal–epidermal junction ("lupus-band"-like pattern). PE diagnostic criteria in Hobbs et al. required PF histology plus these DIF findings. (chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 1-2, hobbs2021pemphiguserythematosusa pages 10-11, jangid2023acasereport pages 4-6)
ANA / lupus serology ANA positivity is variably reported, commonly cited as ~30%–80% of cases; in the Hobbs center series ANA was elevated in 1/5 patients (20%). Additional lupus-associated serologies reported in case literature include anti-dsDNA, anti-Ro/SSA, anti-Sm, and anti-RNP. (jangid2023acasereport pages 1-4, hobbs2021pemphiguserythematosusa pages 1-2, hobbs2021pemphiguserythematosusa pages 2-5)
Epidemiology Epidemiology is poorly defined. One cited prevalence estimate is 4.4 cases/million. In Hobbs et al., the literature review found mean age 51.77 years (median 57; range 5–84) and female:male ratio 45:36; the center series had mean age 43.8 years and 3/5 female. Oral involvement in the pooled review was ~9.2%. (arasiewicz2024senearushersyndromein pages 1-3, hobbs2021pemphiguserythematosusa pages 1-2, hobbs2021pemphiguserythematosusa pages 2-5)
Triggers / exacerbating factors Ultraviolet exposure / sunlight is a recognized exacerbating factor; photosensitivity is a recurring clinical feature and UV may contribute to DEJ immune deposition in PE. Medication-associated pemphigus triggers are also discussed in broader reviews, though PE-specific evidence is limited. (chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 10-11, onalajaunderwood2024diagnosisandmanagement pages 3-7, onalajaunderwood2024diagnosisandmanagement pages 1-3)
Common treatments Localized disease can often be treated with potent topical corticosteroids. More extensive disease is treated with systemic corticosteroids plus steroid-sparing agents such as azathioprine, mycophenolate mofetil, dapsone, methotrexate, cyclophosphamide, or rituximab; hydroxychloroquine has also been used in overlap-style cases. (arasiewicz2024senearushersyndromein pages 1-3, chandan2018unusuallyextensivescalp pages 4-5, hobbs2021pemphiguserythematosusa pages 10-11, onalajaunderwood2024diagnosisandmanagement pages 3-7, jangid2023acasereport pages 1-4)

Table: This table condenses the main disease-characteristics evidence for pemphigus erythematosus (Senear–Usher syndrome), including defining overlap features, phenotype, diagnostics, epidemiology, triggers, and treatment. It is useful as a quick-reference summary mapped directly to the gathered citation IDs.


Key direct quotes (from retrieved sources)

  • 2024 review statement: “Localized disease can typically be managed by potent topical steroids.” (onalajaunderwood2024diagnosisandmanagement pages 3-7)
  • 2024 review epidemiologic framing: “Represents 10% of all cases of pemphigus foliaceus, with features of lupus erythematosus.” (onalajaunderwood2024diagnosisandmanagement pages 1-3)

Limitations of this report (data gaps)

  • Curated identifiers (ICD/MeSH/Orphanet/MONDO/OMIM) were not found in the retrieved full-text evidence set, so they cannot be provided with citations here. (hobbs2021pemphiguserythematosusa pages 1-2)
  • PE-specific controlled trial data and PE-specific QoL instruments/statistics were not identified in the retrieved evidence; most treatment/outcome information is case-based and extrapolated from broader pemphigus management frameworks. (hobbs2021pemphiguserythematosusa pages 10-11, onalajaunderwood2024diagnosisandmanagement pages 3-7)

References

  1. (arasiewicz2024senearushersyndromein pages 1-3): Hubert Arasiewicz, Joanna Czuwara, Michał Dec, and Lilianna Leśniak-Jakubiec. Senear-usher syndrome in a 5-year-old girl. Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii, 41:242-244, Apr 2024. URL: https://doi.org/10.5114/ada.2024.139233, doi:10.5114/ada.2024.139233. This article has 1 citations.

  2. (espadas2024seborrheicpemphigusa pages 1-3): Diana Gallegos Espadas, Arely Gissell Ramirez Cibrian, and Jesús Iván Martínez-Ortega. Seborrheic pemphigus: a misunderstood variant of pemphigus foliaceus. Cureus, Apr 2024. URL: https://doi.org/10.7759/cureus.59389, doi:10.7759/cureus.59389. This article has 2 citations.

  3. (hobbs2021pemphiguserythematosusa pages 1-2): Landon K. Hobbs, Mary‐Margaret B. Noland, Shyam S. Raghavan, and Alejandro A. Gru. Pemphigus erythematosus: a case series from a tertiary academic center and literature review. Journal of Cutaneous Pathology, 48:1038-1050, Mar 2021. URL: https://doi.org/10.1111/cup.13992, doi:10.1111/cup.13992. This article has 12 citations and is from a peer-reviewed journal.

  4. (onalajaunderwood2024diagnosisandmanagement pages 3-7): Amanda A. Onalaja-Underwood, Maria Yadira Hurley, and Olayemi Sokumbi. Diagnosis and management of bullous disease. Clinics in Geriatric Medicine, 40:37-74, Feb 2024. URL: https://doi.org/10.1016/j.cger.2023.09.002, doi:10.1016/j.cger.2023.09.002. This article has 4 citations and is from a peer-reviewed journal.

  5. (onalajaunderwood2024diagnosisandmanagement pages 1-3): Amanda A. Onalaja-Underwood, Maria Yadira Hurley, and Olayemi Sokumbi. Diagnosis and management of bullous disease. Clinics in Geriatric Medicine, 40:37-74, Feb 2024. URL: https://doi.org/10.1016/j.cger.2023.09.002, doi:10.1016/j.cger.2023.09.002. This article has 4 citations and is from a peer-reviewed journal.

  6. (chandan2018unusuallyextensivescalp pages 4-5): Neha Chandan, Eden P Lake, and Lawrence S Chan. Unusually extensive scalp ulcerations manifested in pemphigus erythematosus. Dermatology Online Journal, Feb 2018. URL: https://doi.org/10.5070/d3241037928, doi:10.5070/d3241037928. This article has 7 citations and is from a peer-reviewed journal.

  7. (jangid2023acasereport pages 1-4): Shivani D Jangid, Bhushan Madke, Adarshlata Singh, Drishti M Bhatt, and Arshiya Khan. A case report on senear-usher syndrome. Cureus, Nov 2023. URL: https://doi.org/10.7759/cureus.49268, doi:10.7759/cureus.49268. This article has 1 citations.

  8. (chandan2018unusuallyextensivescalp pages 1-4): Neha Chandan, Eden P Lake, and Lawrence S Chan. Unusually extensive scalp ulcerations manifested in pemphigus erythematosus. Dermatology Online Journal, Feb 2018. URL: https://doi.org/10.5070/d3241037928, doi:10.5070/d3241037928. This article has 7 citations and is from a peer-reviewed journal.

  9. (hobbs2021pemphiguserythematosusa pages 2-5): Landon K. Hobbs, Mary‐Margaret B. Noland, Shyam S. Raghavan, and Alejandro A. Gru. Pemphigus erythematosus: a case series from a tertiary academic center and literature review. Journal of Cutaneous Pathology, 48:1038-1050, Mar 2021. URL: https://doi.org/10.1111/cup.13992, doi:10.1111/cup.13992. This article has 12 citations and is from a peer-reviewed journal.

  10. (hobbs2021pemphiguserythematosusa pages 10-11): Landon K. Hobbs, Mary‐Margaret B. Noland, Shyam S. Raghavan, and Alejandro A. Gru. Pemphigus erythematosus: a case series from a tertiary academic center and literature review. Journal of Cutaneous Pathology, 48:1038-1050, Mar 2021. URL: https://doi.org/10.1111/cup.13992, doi:10.1111/cup.13992. This article has 12 citations and is from a peer-reviewed journal.

  11. (jangid2023acasereport pages 6-7): Shivani D Jangid, Bhushan Madke, Adarshlata Singh, Drishti M Bhatt, and Arshiya Khan. A case report on senear-usher syndrome. Cureus, Nov 2023. URL: https://doi.org/10.7759/cureus.49268, doi:10.7759/cureus.49268. This article has 1 citations.

  12. (hobbs2021pemphiguserythematosusa pages 5-5): Landon K. Hobbs, Mary‐Margaret B. Noland, Shyam S. Raghavan, and Alejandro A. Gru. Pemphigus erythematosus: a case series from a tertiary academic center and literature review. Journal of Cutaneous Pathology, 48:1038-1050, Mar 2021. URL: https://doi.org/10.1111/cup.13992, doi:10.1111/cup.13992. This article has 12 citations and is from a peer-reviewed journal.

  13. (jangid2023acasereport pages 4-6): Shivani D Jangid, Bhushan Madke, Adarshlata Singh, Drishti M Bhatt, and Arshiya Khan. A case report on senear-usher syndrome. Cureus, Nov 2023. URL: https://doi.org/10.7759/cureus.49268, doi:10.7759/cureus.49268. This article has 1 citations.