Evidence map›Paper›PMID 26096001›Full record

ArticleClinical genetics2016

Glanzmann thrombasthenia in Pakistan: molecular analysis and identification of novel mutations.

A Haghighi, M Borhany, A Ghazi, N Edwards, A Tabaksert, A Haghighi, N Fatima, T S Shamsi, J A Sayer

Open access · hybridAbstract read
In one paragraph

Article in Clinical genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 19 citations in OpenAlex.

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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

9 authors at 5 institutions in 4 countries.

A HaghighiDepartment of Genetics, Harvard Medical School, Boston, MA, USA.
M BorhanyDepartment of Hematology, Hemostasis & Thrombosis of National Institute of Blood Disease & Bone Marrow Transplantation, Karachi, Pakistan.
A GhaziChronic Pain Clinic, Wilderman Medicine Professional Corporation, Toronto, Canada.
N EdwardsInstitute of Genetic Medicine, Newcastle University, Newcastle, UK.
A TabaksertInstitute of Genetic Medicine, Newcastle University, Newcastle, UK.
A HaghighiToronto General Hospital, University of Toronto, Toronto, Canada.
N FatimaDepartment of Hematology, Hemostasis & Thrombosis of National Institute of Blood Disease & Bone Marrow Transplantation, Karachi, Pakistan.
T S ShamsiDepartment of Hematology, Hemostasis & Thrombosis of National Institute of Blood Disease & Bone Marrow Transplantation, Karachi, Pakistan.
J A SayerInstitute of Genetic Medicine, Newcastle University, Newcastle, UK.
Brigham and Women's Hospital · USNational Institute Of Blood Disease and Bone Marrow Transplantation · PKNewcastle University · GBUniversity of Toronto · CAWorld Wildlife Fund Canada · CA

Funding

Wellcome Trust
6 · The paper itself

Abstract

Glanzmann thrombasthenia (GT) is an inherited genetic disorder affecting platelets, which is characterized by spontaneous mucocutaneous bleeding and abnormally prolonged bleeding in response to injury or trauma. The underlying defect is failure of platelet aggregation due to qualitative and/or quantitative deficiency of platelet integrin αIIbβ3 resulting from molecular genetic defects in either ITGA2B or ITGB3. Here, we examine a Pakistani cohort of 15 patients with clinical symptoms of GT who underwent laboratory and molecular genetic analysis. In patients with a broad range of disease severity and age of presentation, we identified pathogenic mutations in ITGA2B in 11 patients from 8 different families, including 2 novel homozygous mutations and 1 novel heterozygous mutation. Mutations in ITGB3 were identified in 4 patients from 3 families, two of which were novel homozygous truncating mutations. A molecular genetic diagnosis was established in 11 families with GT, including 5 novel mutations extending the spectrum of mutations in this disease within a region of the world where little is known about the incidence of GT. Mutational analysis is a key component of a complete diagnosis of GT and allows appropriate management and screening of other family members to be performed.

Indexed as

AdolescentChildChild, PreschoolCohort StudiesFemaleHumansInfantInfant, NewbornMaleModels, MolecularMutation, MissensePakistanThrombastheniableeding disorderconsanguineousintegrinITGA2BITGB3Pakistan

Identifiers

PMID26096001
PMCPMC4737203
OpenAlexW1511083160

What OpenQuestion holds

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LicenceCC BY
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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.