Evidence map›Paper›PMID 31359133›Full record

ArticleEuropean journal of pediatrics2019

Genotype phenotype correlation in a pediatric population with antithrombin deficiency.

Mirjana Kovac, Gorana Mitic, Iva Djilas, Milos Kuzmanovic, Olivera Serbic, Danijela Lekovic, Branko Tomic, Zsuzsanna Bereczky

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in European journal of pediatrics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.8field-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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Hereditary Antithrombin Deficiency in Pediatric Patients: Pathophysiology, Clinical Features, Diagnosis, and Antithrombin Replacement Therapy.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

8 authors at 4 institutions in 3 countries.

Mirjana KovacFaculty of Medicine, University of Belgrade, Belgrade, Serbia. mkovac008@gmail.com.ORCID http://orcid.org/0000-0001-6676-0561
Gorana MiticInstitute of Laboratory Medicine, Clinical Center of Vojvodina, Faculty of Medicine Novi Sad, University of Novi Sad, Novi Sad, Serbia.
Iva DjilasBlood Transfusion Institute of Serbia, Hemostasis Department, Sv. Save 39, Belgrade, 11000, Serbia.
Milos KuzmanovicFaculty of Medicine, University of Belgrade, Belgrade, Serbia.
Olivera SerbicInstitute for Health Care of Mother and Child of Serbia Dr Vukan Cupic, Belgrade, Serbia.
Danijela LekovicFaculty of Medicine, University of Belgrade, Belgrade, Serbia.
Branko TomicInstitute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia.
Zsuzsanna BereczkyDivision of Clinical Laboratory Research, Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
University of Belgrade · RSInstitute of Public Health of Serbia · RSUniversity of Debrecen · HUUniversity of Novi Sad · RS

Funding

Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja 173008the Hungarian National Research Fund (OTKA K116228) and by the Ministry of National Economy, Hungary OTKA K116228,GINOP-2.3.2-15-2016-00039
6 · The paper itself

Abstract

Inherited antithrombin (AT) deficiency is a rare autosomal dominant disorder, caused by mutations in the AT gene (SERPINC1). Considering that the genotype phenotype relationship in AT deficiency patients remains unclear, especially in pediatric patients, the aim of our study was to evaluate genotype phenotype correlation in a Serbian pediatric population. A retrospective cohort study included 19 children younger than 18 years, from 15 Serbian families, with newly diagnosed AT deficiency. In 21% of the recruited families, mutations affecting exon 4, 5, and 6 of the SERPINC1 gene that causes type I AT deficiency were detected. In the remaining families, the mutation in exon 2 causing type II HBS (AT Budapest 3) was found. Thrombosis events were observed in 1 (33%) of those with type I, 11 (85%) of those with AT Budapest 3 in the homozygous respectively, and 1(33%) in the heterozygous form. Recurrent thrombosis was observed only in AT Budapest 3 in the homozygous form, in 27% during initial treatment of the first thrombotic event. Abdominal venous thrombosis and arterial ischemic stroke, observed in almost half of the children from the group with AT Budapest 3 in the homozygous form, were unprovoked in all cases.Conclusion: Type II HBS (AT Budapest 3) in the homozygous form is a strong risk factor for arterial and venous thrombosis in pediatric patients. What is Known: • Inherited AT deficiency is a rare autosomal dominant disorder, caused by mutations in the SERPINC1gene. • The genotype phenotype correlation in AT deficiency patients remains unclear, especially in pediatric patients. What is New: • The genetic results for our paediatric population predominantly showed the presence of a single specific mutation in exon 2, that causes type II HBS deficiency (AT Budapest 3). • In this group thrombosis mostly occurred as unprovoked, in almost half of them as abdominal thrombosis or stroke with high incidence of recurrent thrombosis, in 27% during initial treatment.

Indexed as

Antithrombin IIIAdolescentAntithrombin III DeficiencyChildChild, PreschoolFemaleHeterozygoteHumansInfantMaleMutationPedigreePhenotypeRetrospective StudiesSerbiaVenous ThrombosisAntithrombin IIISERPINC1 protein, humanAntithrombin deficiencyPediatric populationSERPINC1 mutations

Identifiers

PMID31359133
OpenAlexW2964860006

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.