Evidence map›Paper›PMID 28427966›Full record

ArticleChest2017

IVIg for Treatment of Severe Refractory Heparin-Induced Thrombocytopenia.

Anand Padmanabhan, Curtis G Jones, Shannon M Pechauer, Brian R Curtis, Daniel W Bougie, Mehraboon S Irani, Barbara J Bryant, Jack B Alperin, Thomas G Deloughery, Kevin P Mulvey and 4 more

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in Chest, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
14.4field-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.

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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Guideline
  2. Classification of Platelet-Activating Anti-Platelet Factor 4 Disorders.International journal of laboratory hematology · 2026
    Review
  3. Review
  4. Thrombocytopenia in Sepsis.Life (Basel, Switzerland) · 2025
    Review
  5. Review
  6. Approaches to management of HIT in complex scenarios, including cardiac surgery.Hematology. American Society of Hematology. Education Program · 2024
    Review
  7. How We Interpret Thrombosis with Thrombocytopenia Syndrome?International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Autoimmune Heparin-Induced Thrombocytopenia.Journal of clinical medicine · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. FcFrontiers in cardiovascular medicine · 2023
    Review
  19. Article
  20. Vaccine-induced immune thrombotic thrombocytopenia.Best practice & research. Clinical haematology · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 1 country.

Anand PadmanabhanMedical Sciences Institute, BloodCenter of Wisconsin, Milwaukee, WI; Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI. Electronic address: anand.padmanabhan@bcw.edu.
Curtis G JonesMedical Sciences Institute, BloodCenter of Wisconsin, Milwaukee, WI.
Shannon M PechauerBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI.
Brian R CurtisPlatelet and Neutrophil Immunology Laboratory, BloodCenter of Wisconsin, Milwaukee, WI.
Daniel W BougieBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI.
Mehraboon S IraniMedical Sciences Institute, BloodCenter of Wisconsin, Milwaukee, WI; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI.
Barbara J BryantDepartment of Pathology, University of Texas Medical Branch, Galveston, TX.
Jack B AlperinDepartment of Pathology, University of Texas Medical Branch, Galveston, TX; Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX.
Thomas G DelougheryKnight Cancer Center, Oregon Health & Science University, Portland, OR.
Kevin P MulveyDepartment of Medicine, Kootenai Health, Coeur d'Alene, ID.
Binod DhakalDepartment of Medicine, Medical College of Wisconsin, Milwaukee, WI.
Renren WenBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI.
Demin WangBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI.
Richard H AsterBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI.
Versiti Blood Center of Wisconsin · USThe University of Texas Medical Branch at Galveston · USKootenai Medical Center · USMedical College of Wisconsin · USOregon Health & Science University · US

Funding

HEMORRHAGIC DISEASESR01HL013629 · NHLBI · VERSITI WISCONSIN, INC. · PI ASTER, RICHARD HERBERT · 1985 to 2019
$8.7M
Hemorrhagic DiseasesR56HL013629 · NHLBI · VERSITI WISCONSIN, INC. · PI ASTER, RICHARD HERBERT · 2008 to 2008
$440k
HEMORRHAGIC DISEASESR37HL013629 · NHLBI · BLOODCENTER OF WISCONSIN, INC. · PI ASTER, RICHARD HERBERT · 1989 to 1998
–
NHLBI NIH HHS R01 HL013629NHLBI NIH HHS R37 HL013629NHLBI NIH HHS R56 HL013629
6 · The paper itself

Abstract

backgroundHeparin-induced thrombocytopenia (HIT) complicated by severe thrombocytopenia and thrombosis can pose significant treatment challenges. Use of alternative anticoagulants in this setting may increase bleeding risks, especially in patients who have a protracted disease course. Additional therapies are lacking in this severely affected patient population.

methodsWe describe three patients with HIT who had severe thromboembolism and prolonged thrombocytopenia refractory to standard treatment but who achieved an immediate and sustained response to IVIg therapy. The mechanism of action of IVIg was evaluated in these patients and in five additional patients with severe HIT. The impact of a common polymorphism (H/R 131) in the platelet IgG receptor FcγRIIa on IVIg-mediated inhibition of platelet activation was also examined.

resultsAt levels attained in vivo, IVIg inhibits HIT antibody-mediated platelet activation. The constant domain of IgG (Fc) but not the antigen-binding portion (Fab) is required for this effect. Consistent with this finding, IVIg had no effect on HIT antibody binding in a solid-phase HIT immunoassay (platelet factor 4 enzyme-linked immunoassay). The H/R131 polymorphism in FcγRIIa influences the susceptibility of platelets to IVIg treatment, with the HH131 genotype being most susceptible to IVIg-mediated inhibition of antibody-induced activation. However, at high doses of IVIg, activation of platelets of all FcγRIIa genotypes was significantly inhibited. All three patients did well on long-term anticoagulation therapy with direct oral anticoagulants.

conclusionsThese studies suggest that IVIg treatment should be considered in patients with HIT who have severe disease that is refractory to standard therapies.

Indexed as

AgedAnticoagulantsFemaleHeparinHumansImmunoglobulins, IntravenousImmunologic FactorsMaleMiddle AgedReceptors, IgGThrombocytopeniaAnticoagulantsFc gamma receptor IIAHeparinImmunoglobulins, IntravenousImmunologic FactorsReceptors, IgGDOACheparinHITIVIgthrombocytopeniathrombosis

Identifiers

PMID28427966
PMCPMC5812774
OpenAlexW2605638326

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.