Evidence map›Paper›PMID 34191092›Full record

ReviewSeminars in immunopathology2021

Halting targeted and collateral damage to red blood cells by the complement system.

M Jalink, E C W de Boer, D Evers, M Q Havinga, J M I Vos, S Zeerleder, M de Haas, I Jongerius

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

M Jalink *Sanquin Research, Center for Clinical Transfusion Research, Plesmanlaan 125, 1066, CX, Amsterdam, The Netherlands.
E C W de Boer *Sanquin Research, Department of Immunopathology, and Landsteiner Laboratory, Amsterdam University Medical Centre, Amsterdam Infection and Immunity Institute, Amsterdam, The Netherlands.
D EversDepartment of Hematology, Radboud University Medical Center, Nijmegen, The Netherlands.
M Q HavingaSanquin Research, Department of Immunopathology, and Landsteiner Laboratory, Amsterdam University Medical Centre, Amsterdam Infection and Immunity Institute, Amsterdam, The Netherlands.
J M I VosDepartment of Hematology, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
S ZeerlederSanquin Research, Department of Immunopathology, and Landsteiner Laboratory, Amsterdam University Medical Centre, Amsterdam Infection and Immunity Institute, Amsterdam, The Netherlands.
M de HaasSanquin Research, Center for Clinical Transfusion Research, Plesmanlaan 125, 1066, CX, Amsterdam, The Netherlands.
I JongeriusSanquin Research, Department of Immunopathology, and Landsteiner Laboratory, Amsterdam University Medical Centre, Amsterdam Infection and Immunity Institute, Amsterdam, The Netherlands. i.jongerius@sanquin.nl.ORCID 0000-0002-7759-9897
Sanquin · NLLeiden University Medical Center · NLRadboud University Nijmegen · NLUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system is an important defense mechanism against pathogens; however, in certain pathologies, the system also attacks human cells, such as red blood cells (RBCs). In paroxysmal nocturnal hemoglobinuria (PNH), RBCs lack certain complement regulators which sensitize them to complement-mediated lysis, while in autoimmune hemolytic anemia (AIHA), antibodies against RBCs may initiate complement-mediated hemolysis. In recent years, complement inhibition has improved treatment prospects for these patients, with eculizumab now the standard of care for PNH patients. Current complement inhibitors are however not sufficient for all patients, and they come with high costs, patient burden, and increased infection risk. This review gives an overview of the underlying pathophysiology of complement-mediated hemolysis in PNH and AIHA, the role of therapeutic complement inhibition nowadays, and the high number of complement inhibitors currently under investigation, as for almost every complement protein, an inhibitor is being developed. The focus lies with novel therapeutics that inhibit complement activity specifically in the pathway that causes pathology or those that reduce costs or patient burden through novel administration routes.

Indexed as

Hemoglobinuria, ParoxysmalComplement Inactivating AgentsComplement System ProteinsErythrocytesHemolysisHumansComplement Inactivating AgentsComplement System ProteinsAutoimmune hemolytic anemiaComplementComplement inhibitorsComplement therapeuticsParoxysmal nocturnal hemoglobinuria

Identifiers

PMID34191092
PMCPMC8243056
OpenAlexW3175597564

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.