ArticleClinical genetics2016
Glanzmann thrombasthenia in Pakistan: molecular analysis and identification of novel mutations.
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.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Flow cytometric analysis of platelet surface glycoproteins in the diagnosis of thirty-two Turkish patients with Glanzmann thrombasthenia: a multicenter experienceTurkish journal of medical sciences · 2021Article
- Article
- In silico analysis of structural modifications in and around the integrin αIIb genu caused by ITGA2B variants in human platelets with emphasis on Glanzmann thrombasthenia.Molecular genetics & genomic medicine · 2018Article
- Levonorgestrel-releasing intrauterine system for treatment of heavy menstrual bleeding in adolescents with Glanzmann's Thrombasthenia: illustrated case series.BMC women's health · 2018Article
- The Glanzmann's Thrombasthenia in Tunisia: A Cohort Study.Journal of hematology · 2017Article
- Utility of the ISTH bleeding assessment tool (BAT) in diagnosis of Glanzmann Thrombasthenia patients.Pakistan journal of medical sciencesArticle
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
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.
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