Evidence map›Paper›PMID 27379854›Full record

ReviewWiener medizinische Wochenschrift (1946)2017

Pyoderma gangrenosum-a novel approach?

Anastasia Atanasova Chokoeva, José Carlos Cardoso, Uwe Wollina, Georgi Tchernev

Abstract readReview
PubMed Publisher
In one paragraph

Review in Wiener medizinische Wochenschrift (1946), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
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

4 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. A Comprehensive Review of Neutrophilic Diseases.Clinical reviews in allergy & immunology · 2018
    Review
  4. Global dermatology: challenges and changes?Wiener medizinische Wochenschrift (1946) · 2017
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Anastasia Atanasova ChokoevaOnkoderma - Policlinic for Dermatology and Dermatologic surgery, 26 General Scobelev, Sofia, Bulgaria. assia_chokoeva@abv.bg.
José Carlos CardosoDermatology Department, University Hospital of Coimbra, Praceta Mota Pinto, 3000075, Coimbra, Portugal.
Uwe WollinaDepartment of Dermatology and Allergology, Academic Teaching Hospital Dresden-Friedrichstadt, Friedrichstraße 41, 01067, Dresden, Germany.
Georgi TchernevOnkoderma - Policlinic for Dermatology and Dermatologic surgery, 26 General Scobelev, Sofia, Bulgaria.
Krankenhaus Dresden-Friedrichstadt · DEMilitary Medical Academy · BGUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyoderma gangrenosum (PG) represents a rare skin disorder, with several clinical variants and still not fully understood ethiopathogenesis. Often associated with inflammatory or neoplastic disease, PG is nowadays considered an inflammatory neutrophilic disease with common underlying morbidity. Modern treatment options are oriented towards key mechanisms underlying the pathogenesis of the disease, namely inflammatory mediators, and seem to be the most effective treatment currently available. Although promising, the results are not invariable and these treatments are sometimes surrounded by controversy, as recent studies have reported cases that are refractory to therapy with biological agents. It is possible that refractoriness to the use of biological agents as monotherapy stems from the fact that a single agent is not able to affect the entire inflammatory cascade, or to simultaneously influence all of its levels. Based on the pathogenesis of inflammation, we can suggest that an ideal targeted therapy should be able to induce the following changes: 1) reduction of the secretion of interleukin (IL)-1a/b from the inflammasome with subsequent blocking of its biological effect (by therapy with IL-1 receptor antagonists); 2) blocking of the activation of the secreted procytokines in their active form (by therapy with caspase-1 inhibitors; 3) blocking of the effect of the already released active cytokines (by therapy with tumour necrosis factor alpha, TNF-α, inhibitors); 4) blocking of the effector action of the cytokines on the target intracellular molecules (by therapy with kinase inhibitors). The specific therapy should aim to attack more than one link in the inflammatory cascade, in order to achieve maximum therapeutic effectiveness. Most surely, this could be achieved with combined therapy with different groups of biological agents (for example a combined therapy with IL-1 receptor antagonist and a TNF-α inhibitor). Currently, no data in the literature exist to support this statement, and there are no safety data relating to such approaches. We focus this review on the novel etiopathogenetic concepts of PG and the future therapeutic approaches based on blocking different levels of the inflammatory cascade, which seems to be the most promising weapon in the target-oriented treatment options.

Indexed as

Drug ResistanceDrug Therapy, CombinationHumansInflammasomesInflammation MediatorsProtein Kinase InhibitorsPyoderma GangrenosumReceptors, Interleukin-1SerpinsTumor Necrosis Factor-alphaViral ProteinsInflammasomesInflammation Mediatorsinterleukin-1beta-converting enzyme inhibitorProtein Kinase InhibitorsReceptors, Interleukin-1SerpinsTNF protein, humanTumor Necrosis Factor-alphaViral ProteinsBiological agentsEtiopathogenesisNeutrophilic disordersPyoderma gangrenosumTreatment

Identifiers

PMID27379854
OpenAlexW2474965496

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.