Evidence map›Paper›PMID 29844251›Full record

ReviewInternational journal of molecular sciences2018

Human Fibrinogen: Molecular and Genetic Aspects of Congenital Disorders.

Giovanni Luca Tiscia, Maurizio Margaglione

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. The Molecular Pathology of Non-Malignant Haematological Disease.British journal of biomedical science · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. [Congenital dysfibrinogenemia: current status and challenges in diagnosis and treatment].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024
    Review
  12. Article
  13. Article
  14. TheFrontiers in neurology · 2024
    Article
  15. Article
  16. Review
  17. Article
  18. Article
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  20. 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

2 authors.

Giovanni Luca TisciaAtherosclerosis and Thrombosis Unit, I.R.C.C.S. "Casa Sollievo della Sofferenza", 71013 San Giovanni Rotondo, Italy. g.tiscia@operapadrepio.it.
Maurizio MargaglioneMedical Genetics, Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy. maurizio.margaglione@unifg.it.ORCID 0000-0001-5627-9221

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital fibrinogen disorders can be quantitative (afibrinogenemia, hypofibrinogenemia) or functional (dysfibrinognemia). To date, several genetic variants have been identified in individuals with fibrinogen disorders. The complexity of the fibrinogen molecules, formed by three non-identical chains and with a trinodal organization, renders the identification of molecular causes and of clinical and biochemical phenotypes very challenging. However, the acknowledgement of the type of molecular defect is crucial for a safer therapy, which is going to improve the clinical management of these patients. In this review, some aspects concerning molecular and clinical findings available on congenital fibrinogen disorders will be discussed.

Indexed as

AfibrinogenemiaFibrinogenHumansFibrinogenafibrinogenemiadysfibrinogenemiahypofibrinogenemia

Identifiers

PMID29844251
PMCPMC6032319

What OpenQuestion holds

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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.