Evidence map›Paper›PMID 41553945›Full record

ArticleDermatology (Basel, Switzerland)2026

Clinical Phenotype Transition in Pemphigus May Suggest Undertreatment with Rituximab: Findings from a Retrospective Single-Centre Analysis of Relapsed Patients.

Anne-Lise Strandmoe, Marjolein A J Hiel, Joost M Meijer, Laura L van Nijen-Vos, A Miranda Nijenhuis, L Joost van Pelt, Gonnie H J Meijer, Peter Heeringa, Gilles F H Diercks, Jeroen Bremer and 1 more

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Article in Dermatology (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

11 authors.

Anne-Lise StrandmoeDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands, a.l.strandmoe@umcg.nl.
Marjolein A J HielDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
Joost M MeijerDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
Laura L van Nijen-VosDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
A Miranda NijenhuisDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
L Joost van PeltDepartment of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Gonnie H J MeijerDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
Peter HeeringaDepartment of Medical Biology and Pathology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Gilles F H DiercksDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
Jeroen BremerDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.
Barbara HorváthDepartment of Dermatology, University of Groningen, University Medical Center Groningen, UMCG Center of Expertise for Blistering Diseases, European Reference Network for Rare Skin Diseases (ERN SKIN), Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

<p>Introduction: Pemphigus is an autoimmune bullous disease caused by autoantibodies against desmoglein (DSG) 1 and/or 3 and comprises two main subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). PV affects the skin and/or mucosa and includes two forms: mucocutaneous PV (mcPV; anti-DSG1 and anti-DSG3) and mucosal PV (mPV; anti-DSG3). PF, characterized by anti-DSG1 autoantibodies, is limited to the skin. Pemphigus is effectively treated with rituximab, a B-cell-depleting therapy. However, about half of patients relapse, with a subset exhibiting a shift in clinical subtype following relapse, known as clinical phenotype transition. This study aimed to investigate clinical phenotype transition in relapsed pemphigus patients following rituximab treatment.

methodsA single-centre, exploratory retrospective cohort study was conducted, reviewing the medical records of patients with pemphigus who received at least one treatment cycle of rituximab between December 2006 and December 2023. Clinical and immunological data were collected at several time points during the first cycle of rituximab treatment.

resultsA total of 109 patients were included, of whom 44% (48/109) achieved sustained complete remission, while 56% (61/109) experienced relapse. Among the 61 patients who relapsed, 26% (16/61) experienced a clinical phenotype transition. All had an initial diagnosis of mcPV. Among these, 75% (12/16) transitioned from mcPV to mPV and 25% (4/16) from mcPV to PF. Clinical phenotype transitioned patients often remained seropositive for anti-DSG3 at clinical remission, a pattern not observed in patients who did not experience a clinical phenotype transition.

conclusionsClinical phenotype transition was observed exclusively in mcPV patients, suggesting that such changes do not represent a true alteration in disease subtype but rather reflect persistent activity of the same pathogenic autoantibody due to suboptimal B-cell depletion, suggesting undertreatment with rituximab. These findings support the need to refine rituximab treatment regimens to achieve complete B-cell depletion, reduce relapse rates, and optimize long-term disease control in pemphigus. </p>.

Indexed as

Immunologic FactorsPemphigusRituximabAdultAgedAutoantibodiesDesmoglein 1Desmoglein 3FemaleHumansMaleMiddle AgedPhenotypeRecurrenceRetrospective StudiesAutoantibodiesDesmoglein 1Desmoglein 3Immunologic FactorsRituximabAutoimmune bullous diseaseImmunobullous diseasePemphigusPhenotype transitionRituximab

Identifiers

PMID41553945
PMCPMC12991809

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