Evidence map›Paper›PMID 19395674›Full record

ReviewBlood2009

The ITP syndrome: pathogenic and clinical diversity.

Douglas B Cines, James B Bussel, Howard A Liebman, Eline T Luning Prak

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04113915 (Viral Hepatitis B and C Infection in Patients With Idiopathic Thrombocytopenic Purpura Treated With Triple Therapy), which is not on this map. Cited by 290 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
290citing papers in PubMed, 6 pooled it
20.1field-weighted citation impact, top 1% 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.

NCT04113915 unknown statusnot on this mapstarted 2019, after this paper: background citation

Viral Hepatitis B and C Infection in Patients With Idiopathic Thrombocytopenic Purpura Treated With Triple Therapy

TypeobservationalSponsorSafaa AA KhaledRan2019 to 2020Enrolled150ConditionsITP - Immune Thrombocytopenic Purpura, Viral HepatitisArmstriple therapy, Steroids
3 · Its place in the literature

Who cites it

290 citing papers in PubMed, 6 syntheses or guidelines pooled it, 798 citations in OpenAlex.

  1. Evaluation ofFrontiers in medicine · 2026
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  11. Efficacy and safety of a new intravenous immunoglobulin (PanzygaTransfusion medicine (Oxford, England) · 2019
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230 more citing papers are in PubMed but not listed here.

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 1 country.

Douglas B CinesDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, 513A Stellar-Chance, 422 Curie Blvd, Philadelphia, PA 19104, USA. dcines@mail.med.upenn.edu
James B Bussel
Howard A Liebman
Eline T Luning Prak
Cornell University · USUniversity of Pennsylvania · USUniversity of Southern California · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024996 · NCRR · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2007 to 2011
$49.6M
THE ROLE OF SEMA4D/CD100 AND ITS RECEPTORS IN PLATELET BIOLOGY AND THROMBOSISP50HL081012 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BRASS, LAWRENCE · 2006 to 2010
$11.9M
B-Lymphocyte Immunotherapy in Islet TransplantationU01DK070430 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI NAJI, ALI · 2004 to 2011
$10.1M
B Cells in Murine Sjogren's SyndromeR01DE017590 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI COHEN, PHILIP L · 2006 to 2010
$2.4M
Novel Therapies in Hemostasis and Transfusion MedicineU01HL072196 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI BUSSEL, JAMES BRUCE · 2002 to 2012
$2.1M
NCRR NIH HHS UL1 RR024996NHLBI NIH HHS 1U01 HL72196-01NHLBI NIH HHS 1U01 HL72196-01-05NHLBI NIH HHS HL081012NHLBI NIH HHS P50 HL081012NHLBI NIH HHS U01 HL072196NIDCR NIH HHS R01 DE017590NIDDK NIH HHS U01 DK 070430NIDDK NIH HHS U01 DK070430
6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is mediated by platelet autoantibodies that accelerate platelet destruction and inhibit their production. Most cases are considered idiopathic, whereas others are secondary to coexisting conditions. Insights from secondary forms suggest that the proclivity to develop platelet-reactive antibodies arises through diverse mechanisms. Variability in natural history and response to therapy suggests that primary ITP is also heterogeneous. Certain cases may be secondary to persistent, sometimes inapparent, infections, accompanied by coexisting antibodies that influence outcome. Alternatively, underlying immune deficiencies may emerge. In addition, environmental and genetic factors may impact platelet turnover, propensity to bleed, and response to ITP-directed therapy. We review the pathophysiology of several common secondary forms of ITP. We suggest that primary ITP is also best thought of as an autoimmune syndrome. Better understanding of pathogenesis and tolerance checkpoint defects leading to autoantibody formation may facilitate patient-specific approaches to diagnosis and management.

Indexed as

AdultAntigens, Human PlateletAutoantibodiesAutoimmune DiseasesBlood PlateletsChildCommunicable DiseasesDisease SusceptibilityHematologic NeoplasmsHemorrhageHumansIncidenceLymphocyte SubsetsPostoperative ComplicationsPurpura, Thrombocytopenic, IdiopathicSelf ToleranceAntigens, Human PlateletAutoantibodies

Identifiers

PMID19395674
PMCPMC2710913
OpenAlexW2097591338

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.