Evidence map›Paper›PMID 30221035›Full record

ArticleExperimental hematology & oncology2018

Temporality of heparin-induced antibodies: a retrospective study in outpatients undergoing hemodialysis on unfractionated heparin.

Satish Maharaj, Simone Chang, Karan Seegobin, James Morales, Agnes Aysola, Fauzia Rana, Marwan Shaikh

Open access · goldAbstract read
In one paragraph

Article in Experimental hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Heparin-Induced Thrombocytopenia in Chronic Hemodialysis Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Review
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

7 authors at 2 institutions in 1 country.

Satish Maharaj1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.ORCID 0000-0002-2872-3011
Simone Chang2University of Miami Health System, Miami, FL USA.
Karan Seegobin1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.
James Morales1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.
Agnes Aysola1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.
Fauzia Rana1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.
Marwan Shaikh1Division of Hematology and Medical Oncology, Department of Internal Medicine, University of Florida College of Medicine-Jacksonville, UF Health Jacksonville, 653 W 8th St, Jacksonville, FL 32209 USA.
University of Florida Health · USUniversity of Miami Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeparin-induced antibodies (HIA) are responsible for causing heparin-induced thrombocytopenia and thrombosis. Research has shown that the temporality of heparin-induced antibodies does not follow the classic immunologic response. The immunobiology of HIA generation remains unclear with varying in vitro and in vivo data. Outpatients undergoing hemodialysis (HD) are exposed to heparin chronically. The HIA immune response can therefore be investigated in vivo in this population.

methodsWe examined the time between the start of HD using unfractionated heparin and HIA levels in 212 outpatients during a 6-year period. Antibodies were detected on enzyme-linked immunosorbent assay. HIA levels were analyzed to determine significance of the trend over time. HIA subgroups were also analyzed for correlation with subsequent thrombotic events and platelet count during follow up.

resultsOverall, the HIA response in HD was found to peak early with waning antibody response despite continued exposure to heparin. The peak prevalence of a strong immune response (optical density > 1.000) was early and short lived, while weaker immune response (optical density 0.400-1.000) persisted for the first 6 months then declined. The mean follow-up time per patient was 2.3 ± 1.4 years. Despite circulating HIA, including high titers, no patients developed HIT in this sample. There was no association between HIA and thrombocytopenia. There was increased incidence of thrombosis in patients with strong HIA compared to other groups, but this did not achieve statistical significance.

conclusionsThe data suggest a significant temporal pattern of HIA in outpatients undergoing HD using unfractionated heparin. Positive HIA was not found to be significantly associated with thrombocytopenia or thrombosis risk in these patients. However, while not achieving statistical significance, subsequent thrombotic events occurred most frequently in the strong positive HIA group (optical density > 1.000). Further research into HIA and risk of thrombosis in this population is needed.

Indexed as

AntibodiesHemodialysisHeparinHITThrombocytopeniaThrombosis

Identifiers

PMID30221035
PMCPMC6137914
OpenAlexW2891833541

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LicenceCC BY
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Registered trials

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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.