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Acute Lichenoid Pityriasis

Acute Lichenoid Pityriasis (PLEVA) — Comprehensive Disease Characteristics Report

2026-05-04
Falcon MONDO:0024250 Model: Edison Scientific Literature 39 citations

Acute Lichenoid Pityriasis (PLEVA) — Comprehensive Disease Characteristics Report

Target disease

Acute lichenoid pityriasis is most consistently used in the clinical literature as a synonym for pityriasis lichenoides et varioliformis acuta (PLEVA), the acute pole of the pityriasis lichenoides (PL) spectrum; some sources also refer to PLEVA as Mucha–Habermann disease, and the most severe ulceronecrotic systemic variant as febrile ulceronecrotic Mucha–Habermann disease (FUMHD). (jung2020systematicreviewof pages 1-2, ma2024diagnosticchallengesof pages 1-3, fatturi2024pityriasislichenoidesassessment pages 1-2)

Table (click to expand)
Domain Key points (with numbers) Evidence type (review/series/case report) Citation IDs Publication year URL/DOI
Definitions / synonyms Acute lichenoid pityriasis corresponds to pityriasis lichenoides et varioliformis acuta (PLEVA); also called Mucha-Habermann disease in some sources. It is the acute pole of the pityriasis lichenoides spectrum; severe ulceronecrotic variant = febrile ulceronecrotic Mucha-Habermann disease (FUMHD). Review; case report (jung2020systematicreviewof pages 1-2, ma2024diagnosticchallengesof pages 1-3, fatturi2024pityriasislichenoidesassessment pages 1-2) 2020, 2024 https://doi.org/10.1111/bjd.18977 ; https://doi.org/10.70672/bcfbzp08 ; https://doi.org/10.1016/j.jped.2024.03.011
Epidemiology stats Rare disease; one review cites incidence around 0.05% with slight male predominance and onset in late childhood/young adulthood. Pediatric review noted slight male predominance 56%. Pediatric Brazilian series: 41 patients total, 5/41 PLEVA (12.2%), 32/41 PLC (78.0%). Thai pediatric series: 43 patients, 10/43 PLEVA (23.3%), male:female 1.3:1, common onset age 4–7 years. A 2013 pediatric review summarized series with PLEVA frequencies ranging 25% to 57.3% among PL cohorts. Review; retrospective pediatric series (jung2020systematicreviewof pages 1-2, ma2024diagnosticchallengesof pages 1-3, fatturi2024pityriasislichenoidesassessment pages 1-2, rujimethapass2025pityriasislichenoidesin pages 5-6, boos2013pityriasislichenoidesand pages 1-2) 2020, 2024, 2025, 2013 https://doi.org/10.1111/bjd.18977 ; https://doi.org/10.70672/bcfbzp08 ; https://doi.org/10.1016/j.jped.2024.03.011 ; https://doi.org/10.35755/jmedassocthai.2025.5.377-383-02606 ; https://doi.org/10.1007/s13671-013-0054-x
Key clinical features and course Acute eruption of erythematous papules/papulovesicles that may become hemorrhagic/necrotic and heal with varioliform scarring. Lesions often involve trunk and extremities; pruritus common; lesions resolve over weeks but recur in crops. Thai series: PLEVA disease duration 1–20 months, mean about 4 ± 2 months; diagnosis lag about 1.5 months in PLEVA vs 3 months in PLC. Systemic symptoms (e.g., fever, hepatomegaly) were more common in PLEVA; varioliform scars were seen only in PLEVA. Severe FUMHD may include mucosal lesions, high fever, sepsis, cardiomyopathy, pulmonary involvement. Review; retrospective series; case report (ma2024diagnosticchallengesof pages 1-3, rujimethapass2025pityriasislichenoidesin pages 5-6, boos2013pityriasislichenoidesand pages 1-2, marinhernandez2023acutelichenoidand pages 1-2) 2024, 2025, 2013, 2023 https://doi.org/10.70672/bcfbzp08 ; https://doi.org/10.35755/jmedassocthai.2025.5.377-383-02606 ; https://doi.org/10.1007/s13671-013-0054-x ; https://doi.org/10.24875/bmhim.22000043
Histopathology / diagnostics / differentials Diagnosis is clinicopathologic and usually confirmed by skin biopsy. Reported findings: parakeratosis, spongiosis, lichenoid/interface dermatitis, dyskeratotic keratinocytes, erythrocyte extravasation, focal epidermotropism, epidermal necrosis, hemorrhagic crusting/ulceration; one pediatric case showed lymphocytic vasculitis with focal epidermal necrosis. DIF may be negative for IgG/IgA/IgM/C3. Important differentials: guttate psoriasis, varicella, pityriasis rosea, secondary syphilis, and occasionally mycosis fungoides. Review; case report; diagnostic image/table extraction (ma2024diagnosticchallengesof pages 1-3, ma2024diagnosticchallengesof pages 3-9, boos2013pityriasislichenoidesand pages 1-2, marinhernandez2023acutelichenoidand pages 1-2, ma2024diagnosticchallengesof media c2c2a990) 2024, 2013, 2023 https://doi.org/10.70672/bcfbzp08 ; https://doi.org/10.1007/s13671-013-0054-x ; https://doi.org/10.24875/bmhim.22000043
Triggers / etiology hypotheses Etiopathogenesis remains uncertain. Main hypotheses: T-cell dyscrasia / lymphoproliferative process, immune-complex hypersensitivity, or inflammatory reaction to antigenic stimuli. Reported infectious associations include EBV, HIV, VZV, HSV-2, Toxoplasma gondii, group A streptococcus, parvovirus B19, HHV-8. Reported exposure triggers include drugs (e.g., antidepressants, statins, anti-TNF agents), subcutaneous immunoglobulin, and vaccines (including MMR; case reports after COVID-19 vaccination also reported in the literature). Pediatric review cited preceding URI in 33% and drug/vaccination exposure in 20%. Review; case report; pediatric review (ma2024diagnosticchallengesof pages 1-3, boos2013pityriasislichenoidesand pages 1-2) 2024, 2013 https://doi.org/10.70672/bcfbzp08 ; https://doi.org/10.1007/s13671-013-0054-x
Treatments and reported response / remission rates No standardized guideline-supported regimen. Systematic review of 27 studies (502 participants) found phototherapy had the highest proportion of complete remissions; NB-UVB often recommended first-line. Pediatric Brazilian series: overall remission 71.9% (23 patients); remission with antibiotics 56.6% (17 patients) and with phototherapy 80% (4 patients). Thai series: erythromycin used in 95.3%, prednisolone 9.3%, methotrexate 9.3%; one FUMHD patient responded to methylprednisolone plus methotrexate. Review/case sources list oral erythromycin ± topical corticosteroids and low-dose methotrexate as common second-line options; refractory disease/FUMHD has been treated with methotrexate, acitretin, dapsone, cyclosporine, and other immunomodulators. One case resolved after 2 months of oral plus topical corticosteroids. Systematic review; retrospective pediatric series; case report (jung2020systematicreviewof pages 1-2, fatturi2024pityriasislichenoidesassessment pages 1-2, rujimethapass2025pityriasislichenoidesin pages 5-6, ma2024diagnosticchallengesof pages 3-9, ma2024diagnosticchallengesof pages 1-3) 2020, 2024, 2025 https://doi.org/10.1111/bjd.18977 ; https://doi.org/10.1016/j.jped.2024.03.011 ; https://doi.org/10.35755/jmedassocthai.2025.5.377-383-02606 ; https://doi.org/10.70672/bcfbzp08
Prognosis / CTCL progression signals Usually benign and self-limited/relapsing, but persistent monitoring is advised. Long-term PL-to-MF progression appears uncommon but documented: one study found 3/58 (5.2%) developed mycosis fungoides after 3–11 years; another pediatric cohort reported 1/43 (2.3%) later diagnosed with MF. In non-MF-associated PL, 85% (35/41) reported lasting complete remissions in one series. Signals concerning for CTCL evolution include prolonged clinical course, appearance of patches/larger plaques, increased lymphocytic atypia, reduced apoptotic keratinocytes, reduced CD7+/CD8+ cells, and clonal TCR rearrangement. Molecular clinicopathologic study; pediatric series; review (rujimethapass2025pityriasislichenoidesin pages 5-6, rujimethapass2025pityriasislichenoidesin pages 6-7) 2025 https://doi.org/10.35755/jmedassocthai.2025.5.377-383-02606
Immunopathogenesis / clonality signals Data are mixed and not disease-defining. A pediatric review summarized one study reporting monoclonal TCR rearrangement in 57% of PLEVA vs 8% of PLC, while another found only 1/23 positive, underscoring uncertainty. Overall interpretation in reviews: clonality can occur in PLEVA/PL and does not by itself establish lymphoma; clinicopathologic correlation remains essential. Review summarizing molecular studies (boos2013pityriasislichenoidesand pages 1-2) 2013 https://doi.org/10.1007/s13671-013-0054-x

Table: This table compacts the main disease-characteristics evidence for acute lichenoid pityriasis (PLEVA), including epidemiology, phenotype, diagnosis, triggers, treatment outcomes, and prognosis. It is useful as a quick-reference scaffold for a disease knowledge base entry with source-linked claims.

1. Disease information

Overview / definition (current understanding)

PLEVA is an uncommon inflammatory papulosquamous dermatosis characterized clinically by crops of erythematous papules/papulovesicles that may become necrotic/hemorrhagic and can heal with varioliform scarring, with recurrences over time. (ma2024diagnosticchallengesof pages 1-3, jung2020systematicreviewof pages 1-2, marinhernandez2023acutelichenoidand pages 1-2)

Key identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

Within the retrieved primary and review sources in this run, ICD-10/ICD-11, MeSH, OMIM, Orphanet, and MONDO identifiers were not explicitly provided, so they cannot be safely asserted from the evidence base assembled here. (ma2024diagnosticchallengesof pages 1-3, jung2020systematicreviewof pages 1-2)

Common synonyms / alternative names

Evidence provenance

Evidence is primarily derived from aggregated disease-level resources (systematic reviews and cohort/case series) and supplemented by individual case reports. (jung2020systematicreviewof pages 1-2, marinhernandez2023acutelichenoidand pages 1-2, fatturi2024pityriasislichenoidesassessment pages 1-2)

2. Etiology

Disease causal factors (mechanistic hypotheses)

Etiopathogenesis remains uncertain. Frequently cited hypotheses include: 1) T-cell dyscrasia / lymphoproliferative process (i.e., antigen-driven clonal/oligoclonal T-cell expansion in skin), and 2) immune-complex hypersensitivity reaction to infectious/drug antigens. (ma2024diagnosticchallengesof pages 1-3, boos2013pityriasislichenoidesand pages 1-2, fatturi2024pityriasislichenoidesassessment pages 1-2)

Risk factors / triggers (2023–2024 emphasis)

Evidence supports PLEVA/PL being triggered (not proven caused) by infections, drugs, or vaccines in some patients.

In a 2024 pediatric series (n=41), triggers were documented in 11/41 (26.8%) patients, including fever (3), COVID-19 infection (2), and single cases of sun exposure, HIV, parotitis, tonsillitis, cold weather, and COVID-19 vaccination. (fatturi2024pityriasislichenoidesassessment pages 2-4)

A 2024 diagnostic-focused report lists reported infectious triggers (e.g., EBV, HIV, varicella-zoster virus, HSV-2, Toxoplasma gondii, group A streptococcus) and notes drug and vaccine triggers in the literature (including anti-TNF and vaccination). (ma2024diagnosticchallengesof pages 1-3)

A pediatric review summarizes that a preceding upper respiratory infection was reported in 33% and drug/vaccination exposure in 20% in one summarized series. (boos2013pityriasislichenoidesand pages 1-2)

Protective factors

No validated genetic or environmental protective factors were identified in the retrieved evidence. (jung2020systematicreviewof pages 1-2, fatturi2024pityriasislichenoidesassessment pages 1-2)

Gene–environment interactions

No specific gene–environment interaction findings were available in the retrieved full text, although one systematic review explicitly calls for future work on “understanding the interplay between genetic predisposition and environmental factors.” (everettUnknownyear…forpityriasisa pages 61-64)

3. Phenotypes

Core clinical phenotypes (with suggested HPO terms)

Key phenotypes include: * Crops of erythematous papules/papulovesicles, sometimes necrotic/hemorrhagic (suggested HPO: Papule [HP:0200031], Vesicle [HP:0100796], Skin ulcer [HP:0001053]) (ma2024diagnosticchallengesof pages 1-3, marinhernandez2023acutelichenoidand pages 1-2) * Crusting/necrosis and potential ulceration (HPO: Skin necrosis [HP:0001032], Crusting [HP:0030799]) (ma2024diagnosticchallengesof pages 1-3) * Pruritus (HPO: Pruritus [HP:0000989]) (rujimethapass2025pityriasislichenoidesin pages 5-6, boos2013pityriasislichenoidesand pages 1-2) * Varioliform scarring (HPO: Abnormal scar [HP:0100699]) (rujimethapass2025pityriasislichenoidesin pages 5-6, marinhernandez2023acutelichenoidand pages 1-2) * Post-inflammatory dyspigmentation (HPO: Hypopigmentation of the skin [HP:0001042]) (marinhernandez2023acutelichenoidand pages 1-2, rujimethapass2025pityriasislichenoidesin pages 5-6)

Age of onset

Onset often occurs in childhood/young adulthood; pediatric cohorts show onset peaks around preschool/early school ages. (jung2020systematicreviewof pages 1-2, rujimethapass2025pityriasislichenoidesin pages 5-6, fatturi2024pityriasislichenoidesassessment pages 1-2)

Severity and progression/course

PLEVA is typically acute/subacute and may recur in crops; a Thai pediatric cohort reported PLEVA duration range 1–20 months with mean ~4±2 months. (rujimethapass2025pityriasislichenoidesin pages 5-6)

Severe FUMHD can present with mucosal involvement, high fever, and systemic complications (e.g., sepsis, cardiomyopathy, pulmonary involvement). (ma2024diagnosticchallengesof pages 1-3)

Frequency among affected individuals

In pediatric PL cohorts, PLEVA frequency varies widely by setting and referral patterns; for example, in a 2024 pediatric Brazilian cohort PLEVA was 5/41 (12.2%). (fatturi2024pityriasislichenoidesassessment pages 1-2)

Quality of life impact

Formal HRQoL instruments were not reported in retrieved primary sources; however, a 2024 diagnostic report notes misdiagnosis can lead to substantial emotional/psychological stress (qualitative impact). (ma2024diagnosticchallengesof pages 1-3)

4. Genetic/molecular information

Causal genes / pathogenic variants

No causal genes or pathogenic germline variants were identified in the retrieved literature; PLEVA is generally treated as a complex inflammatory dermatosis rather than a monogenic disorder in these sources. (jung2020systematicreviewof pages 1-2, fatturi2024pityriasislichenoidesassessment pages 1-2)

Molecular findings (limited)

Immunophenotyping can show T-cell–predominant infiltrates. A 2023 pediatric case reported lesional IHC including CD3+, CD4+++, CD8+, CD7+++, and CD20−. (marinhernandez2023acutelichenoidand pages 1-2)

T-cell receptor clonality is variably detected and is not diagnostic of lymphoma by itself; a pediatric review summarized one study with monoclonal TCR rearrangement in 57% of PLEVA vs 8% of PLC, while another series found only 1/23 positive, emphasizing heterogeneity and uncertain clinical significance. (boos2013pityriasislichenoidesand pages 1-2)

5. Environmental information

Environmental contributors are mainly reported as triggering exposures (infections, drugs, vaccines) rather than chronic toxic or occupational exposures. (ma2024diagnosticchallengesof pages 1-3, fatturi2024pityriasislichenoidesassessment pages 2-4)

6. Mechanism / pathophysiology

Proposed causal chain (current consensus framing)

A common mechanistic framing is: antigenic stimulus (infectious agent, drug, vaccine) → cutaneous immune activation with T-cell–predominant interface/lichenoid dermatitis → keratinocyte injury/necrosis and vascular/inflammatory changes → papulonecrotic lesions with crusting → post-inflammatory dyspigmentation or varioliform scarring. (ma2024diagnosticchallengesof pages 1-3, marinhernandez2023acutelichenoidand pages 1-2, boos2013pityriasislichenoidesand pages 1-2)

Cellular processes and pathways (ontology suggestions)

Because the retrieved sources do not provide pathway-specific transcriptomic/proteomic findings, ontology terms are suggested at a high level based on clinicopathology: * GO biological processes: T cell activation, inflammatory response, keratinocyte apoptotic process, leukocyte migration (supported conceptually by interface/lichenoid pattern and T-cell infiltrates) (ma2024diagnosticchallengesof pages 1-3, marinhernandez2023acutelichenoidand pages 1-2) * Cell types (Cell Ontology): T cell (CL:0000084); plausible involvement of CD4-positive, alpha-beta T cell (CL:0000624) and CD8-positive, alpha-beta T cell (CL:0000625) consistent with reported IHC (marinhernandez2023acutelichenoidand pages 1-2)

Immune system involvement

PLEVA lesions show interface/lichenoid dermatitis with epidermotropism in some cases, and PLEVA may represent a benign clonal or oligoclonal T-cell–driven process in a subset. (ma2024diagnosticchallengesof pages 3-9, boos2013pityriasislichenoidesand pages 1-2)

7. Anatomical structures affected

Organ and tissue level

Primary involvement is the skin (UBERON: skin [UBERON:0002097]), with lesions commonly on trunk and extremities. (marinhernandez2023acutelichenoidand pages 1-2, ma2024diagnosticchallengesof pages 1-3)

Severe FUMHD can involve mucosa and systemic organs (cardiopulmonary involvement described). (ma2024diagnosticchallengesof pages 1-3)

Subcellular level

Not resolved in retrieved evidence.

8. Temporal development

9. Inheritance and population

PLEVA is not presented as a Mendelian disorder in the retrieved sources; inheritance pattern and penetrance are not established. (jung2020systematicreviewof pages 1-2)

Epidemiology statistics (available)

Because these numbers come from different sources with different contexts, they should be treated as approximate. (jung2020systematicreviewof pages 1-2, marinhernandez2023acutelichenoidand pages 1-2)

10. Diagnostics

Clinical evaluation

PLEVA can mimic multiple papulovesicular/papulosquamous eruptions. Diagnostic work-up typically relies on clinical morphology and distribution plus biopsy confirmation. (ma2024diagnosticchallengesof pages 1-3, jung2020systematicreviewof pages 1-2)

Histopathology

Commonly described findings include lichenoid/interface dermatitis, parakeratosis, spongiosis, erythrocyte extravasation, epidermal necrosis, subepidermal blistering, and sometimes focal epidermotropism; one pediatric case highlighted lymphocytic vasculitis with focal epidermal necrosis. (ma2024diagnosticchallengesof pages 1-3, ma2024diagnosticchallengesof pages 3-9, marinhernandez2023acutelichenoidand pages 1-2)

Direct immunofluorescence may be negative for immune deposits at the dermal–epidermal junction (IgG/IgA/IgM/C3 negative in a reported case). (ma2024diagnosticchallengesof pages 1-3)

Differential diagnosis

A differential table extracted from a 2024 diagnostic paper highlights confusion with guttate psoriasis, varicella, pityriasis rosea, and secondary syphilis. (ma2024diagnosticchallengesof media c2c2a990)

Histopathology figures supporting interface dermatitis and focal epidermotropism are available from the same report. (ma2024diagnosticchallengesof media 72391849, ma2024diagnosticchallengesof media 01b2711c)

Omics/genetic testing

Routine genetic testing is not described for PLEVA in the retrieved sources. (jung2020systematicreviewof pages 1-2)

11. Outcome / prognosis

General prognosis

PLEVA is generally benign/self-limited but can be relapsing. (jung2020systematicreviewof pages 1-2, rujimethapass2025pityriasislichenoidesin pages 5-6)

Risk of progression to cutaneous T-cell lymphoma (CTCL)

Progression risk is debated; in a Thai pediatric cohort, 1/43 (2.3%) was later diagnosed as mycosis fungoides on repeat biopsy. (rujimethapass2025pityriasislichenoidesin pages 5-6)

Clinical concern for MF/CTCL is heightened when clinical morphology changes or the course is prolonged; a 2023 pediatric case illustrates diagnostic overlap when an initial biopsy was read as suggestive of mycosis fungoides but was later revised to PLEVA with lymphocytic vasculitis. (marinhernandez2023acutelichenoidand pages 1-2)

12. Treatment

Evidence quality (expert appraisal)

A 2020 systematic review (British Journal of Dermatology) notes: “The current literature consists almost entirely of uncontrolled studies, and none provides compelling data to support an evidence-based approach to PL treatment.” (May 2020). (jung2020systematicreviewof pages 1-2)

First-line and second-line approaches (real-world implementations)

Across reviews and recent summaries, narrow-band UVB (NB-UVB) phototherapy is commonly recommended as first-line, with oral erythromycin or low-dose methotrexate (± topical corticosteroids) used as second-line options. (ma2024diagnosticchallengesof pages 3-9, feschuk2023pityriasislichenoidesfollowing pages 1-3)

Quantitative treatment outcomes

Phototherapy (systematic review evidence): In a 2020 systematic review, complete response rates were reported as 75.0% (102/136) for NB-UVB and 69% (25/36) for PUVA, with relapse after phototherapy in 25.7% (66/257). (jung2020systematicreviewof pages 2-4)

Pediatric real-world outcomes (2024 series): In a 2024 pediatric cohort, overall remission was 71.9%; among antibiotic-treated patients remission was 56.6% (17/30); among phototherapy-treated patients remission was 80% (4/5). (fatturi2024pityriasislichenoidesassessment pages 1-2)

Pediatric phototherapy-focused evidence: A pediatric phototherapy literature review reported initial clearance rates of 89.6% for BB-UVB (with 23.1% recurrence), 73% for NB-UVB (with no recurrence), and 83% for PUVA (with 60% recurrence), with generally mild erythema as the main side effect. (maranda2016phototherapyforpityriasis pages 1-2)

Systemic therapy for severe disease (FUMHD)

FUMHD may require systemic immunosuppression; methotrexate is repeatedly cited as important in refractory PLEVA/FUMHD. (ma2024diagnosticchallengesof pages 3-9, rujimethapass2025pityriasislichenoidesin pages 5-6)

MAXO (Medical Action Ontology) suggestions

Clinical trials

A ClinicalTrials.gov search in this run returned no relevant interventional trials for PLEVA; retrieved NCT records were unrelated false positives. (clinical trial search output not relevant to PLEVA; no citeable PLEVA trial context IDs available)

13. Prevention

No evidence-based primary prevention strategies were identified in retrieved sources; because triggers are inconsistent and causality is unproven, prevention is limited to pragmatic measures (avoidance of suspected individual triggers when reproducibly associated) and close follow-up for severe/systemic features suggestive of FUMHD. (ma2024diagnosticchallengesof pages 1-3, ma2024diagnosticchallengesof pages 3-9)

14. Other species / natural disease

No evidence was found in the retrieved sources for naturally occurring PLEVA in other species or zoonotic considerations. (maranda2016phototherapyforpityriasis pages 1-2, ma2024diagnosticchallengesof pages 3-9)

15. Model organisms

No explicit model organism systems or animal models for PLEVA were described in the retrieved, PLEVA-focused texts in this run. (maranda2016phototherapyforpityriasis pages 1-2, ma2024diagnosticchallengesof pages 3-9)

Recent developments and latest research highlights (prioritize 2023–2024)

1) SARS-CoV-2 infection/vaccination temporal association literature (2023): A 2023 review of 14 cases reported that 9/14 (64.3%) followed vaccination and 4/14 (28.6%) followed infection; 12/14 (85.7%) had marked improvement or complete resolution at follow-up, and the authors state “Naranjo’s ADRPS suggests SARS-CoV-2 may be a ‘probable’ cause of PL,” while emphasizing uncertainty and possible coincidence. (Jan 2023; https://doi.org/10.1007/s13671-023-00380-1). (feschuk2023pityriasislichenoidesfollowing pages 3-4)

2) Pityriasis eruptions after COVID-19 vaccination (systematic review, 2023): A systematic review identified 94 patients with pityriasis/pityriasis-like eruptions after vaccination; PLEVA accounted for 7.4% of reported cases; biopsy was performed in 41/94. (Aug 2023; https://doi.org/10.4081/dr.2023.9742). (duzett2023pityriasisfollowingcovid19 pages 2-3)

3) Large pediatric series with quantified remission predictors (2024): A 2024 pediatric cohort reported documented triggers in 26.8% and remission rates by therapy (antibiotics vs phototherapy), and found remission odds were higher with onset after age 5 (OR 13.33). (Sep 2024; https://doi.org/10.1016/j.jped.2024.03.011). (fatturi2024pityriasislichenoidesassessment pages 2-4, fatturi2024pityriasislichenoidesassessment pages 1-2)

4) Diagnostic pitfalls and histopathology emphasis (2024): A 2024 diagnostic report underscores clinical overlap with guttate psoriasis/varicella/pityriasis rosea/secondary syphilis and provides histopathology examples (subepidermal blistering, interface dermatitis, focal epidermotropism) to support biopsy confirmation. (Nov 2024; https://doi.org/10.70672/bcfbzp08). (ma2024diagnosticchallengesof media c2c2a990, ma2024diagnosticchallengesof media 72391849, ma2024diagnosticchallengesof media 01b2711c)

References

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  2. (ma2024diagnosticchallengesof pages 1-3): Abd Rahman MA, Jamani NA, Abdul Halim S, and Zainun N. Diagnostic challenges of pityriasis lichenoides et varioliformis acuta (pleva). Asian Journal of Medicine & Health Sciences, 7:279-287, Nov 2024. URL: https://doi.org/10.70672/bcfbzp08, doi:10.70672/bcfbzp08. This article has 0 citations.

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  6. (marinhernandez2023acutelichenoidand pages 1-2): Eduardo Marín-Hernández, Laura N. Escobar-García, Martha G. Contreras, Alfredo Valero-Gómez, and Georgina A. Siordia-Reyes. Acute lichenoid and varioliform pityriasis in a pediatric patient. Boletín Médico del Hospital Infantil de México, Jun 2023. URL: https://doi.org/10.24875/bmhim.22000043, doi:10.24875/bmhim.22000043. This article has 5 citations.

  7. (ma2024diagnosticchallengesof pages 3-9): Abd Rahman MA, Jamani NA, Abdul Halim S, and Zainun N. Diagnostic challenges of pityriasis lichenoides et varioliformis acuta (pleva). Asian Journal of Medicine & Health Sciences, 7:279-287, Nov 2024. URL: https://doi.org/10.70672/bcfbzp08, doi:10.70672/bcfbzp08. This article has 0 citations.

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