Pemphigus Erythematosus

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

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.