Literature DB >> 28916186

Clinical, immunologic, and genetic spectrum of 696 patients with combined immunodeficiency.

Hassan Abolhassani1, Janet Chou2, Wayne Bainter2, Craig D Platt2, Mahmood Tavassoli3, Tooba Momen3, Marzieh Tavakol4, Mohammad Hossein Eslamian5, Mohammad Gharagozlou6, Masoud Movahedi6, Mohsen Ghadami7, Amir Ali Hamidieh8, Gholamreza Azizi9, Reza Yazdani10, Mohsen Afarideh11, Alireza Ghajar11, Arash Havaei11, Zahra Chavoshzadeh12, Seyed Alireza Mahdaviani13, Taher Cheraghi14, Nasrin Behniafard15, Reza Amin16, Soheila Aleyasin16, Reza Faridhosseini17, Farahzad Jabbari-Azad17, Mohammamd Nabavi18, Mohammad Hassan Bemanian18, Saba Arshi18, Rasol Molatefi19, Roya Sherkat20, Mahboubeh Mansouri21, Mehrnaz Mesdaghi12, Delara Babaie12, Iraj Mohammadzadeh22, Javad Ghaffari23, Alireza Shafiei24, Najmeddin Kalantari25, Hamid Ahanchian17, Maryam Khoshkhui17, Habib Soheili26, Abbas Dabbaghzadeh22, Afshin Shirkani27, Rasoul Nasiri Kalmarzi28, Seyed Hamidreza Mortazavi29, Javad Tafaroji30, Abbas Khalili31, Javad Mohammadi32, Babak Negahdari33, Mohammad-Taghi Joghataei34, Basel K Al-Ramadi35, Capucine Picard36, Nima Parvaneh11, Nima Rezaei37, Talal A Chatila2, Michel J Massaad2, Sevgi Keles2, Lennart Hammarström38, Raif S Geha39, Asghar Aghamohammadi40.   

Abstract

BACKGROUND: Combined immunodeficiencies (CIDs) are diseases of defective adaptive immunity with diverse clinical phenotypes. Although CIDs are more prevalent in the Middle East than Western countries, the resources for genetic diagnosis are limited.
OBJECTIVES: This study aims to characterize the categories of patients with CIDs in Iran clinically and genetically.
METHODS: Clinical and laboratory data were obtained from 696 patients with CIDs. Patients were subdivided into those with syndromic (344 patients) and nonsyndromic (352 patients) CIDs. Targeted DNA sequencing was performed on 243 (34.9%) patients.
RESULTS: The overall diagnostic yield of the 243 sequenced patients was 77.8% (189 patients). The clinical diagnosis of hyper-IgE syndrome (P < .001), onset of disease at greater than 5 years (P = .02), and absence of multiple affected family members (P = .04) were significantly more frequent in the patients without a genetic diagnosis. An autosomal recessive disease was found in 62.9% of patients, reflecting the high rate of consanguinity in this cohort. Mutations impairing VDJ recombination and DNA repair were the most common underlying causes of CIDs. However, in patients with syndromic CIDs, autosomal recessive mutations in ataxia-telangiectasia mutated (ATM), autosomal dominant mutations in signal transducer and activator of transcription 3 (STAT3), and microdeletions in 22q11.21 were the most commonly affected genomic loci. Patients with syndromic CIDs had a significantly lower 5-year survival rate rather than those with nonsyndromic CIDs.
CONCLUSIONS: This study provides proof of principle for the application of targeted next-generation sequencing panels in countries with limited diagnostic resources. The effect of genetic diagnosis on clinical care requires continued improvements in therapeutic resources for these patients.
Copyright © 2017 American Academy of Allergy, Asthma & Immunology. All rights reserved.

Entities:  

Keywords:  Combined immunodeficiencies; next-generation DNA sequencing; targeted gene panel sequencing; whole-exome sequencing

Mesh:

Substances:

Year:  2017        PMID: 28916186     DOI: 10.1016/j.jaci.2017.06.049

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  32 in total

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7.  Fourth Update on the Iranian National Registry of Primary Immunodeficiencies: Integration of Molecular Diagnosis.

Authors:  Hassan Abolhassani; Fatemeh Kiaee; Marzieh Tavakol; Zahra Chavoshzadeh; Seyed Alireza Mahdaviani; Tooba Momen; Reza Yazdani; Gholamreza Azizi; Sima Habibi; Mohammad Gharagozlou; Masoud Movahedi; Amir Ali Hamidieh; Nasrin Behniafard; Mohammamd Nabavi; Mohammad Hassan Bemanian; Saba Arshi; Rasol Molatefi; Roya Sherkat; Afshin Shirkani; Reza Amin; Soheila Aleyasin; Reza Faridhosseini; Farahzad Jabbari-Azad; Iraj Mohammadzadeh; Javad Ghaffari; Alireza Shafiei; Arash Kalantari; Mahboubeh Mansouri; Mehrnaz Mesdaghi; Delara Babaie; Hamid Ahanchian; Maryam Khoshkhui; Habib Soheili; Mohammad Hossein Eslamian; Taher Cheraghi; Abbas Dabbaghzadeh; Mahmoud Tavassoli; Rasoul Nasiri Kalmarzi; Seyed Hamidreza Mortazavi; Sara Kashef; Hossein Esmaeilzadeh; Javad Tafaroji; Abbas Khalili; Fariborz Zandieh; Mahnaz Sadeghi-Shabestari; Sepideh Darougar; Fatemeh Behmanesh; Hedayat Akbari; Mohammadreza Zandkarimi; Farhad Abolnezhadian; Abbas Fayezi; Mojgan Moghtaderi; Akefeh Ahmadiafshar; Behzad Shakerian; Vahid Sajedi; Behrang Taghvaei; Mojgan Safari; Marzieh Heidarzadeh; Babak Ghalebaghi; Seyed Mohammad Fathi; Behzad Darabi; Saeed Bazregari; Nasrin Bazargan; Morteza Fallahpour; Alireza Khayatzadeh; Naser Javahertrash; Bahram Bashardoust; Mohammadali Zamani; Azam Mohsenzadeh; Sarehsadat Ebrahimi; Samin Sharafian; Ahmad Vosughimotlagh; Mitra Tafakoridelbari; Maziar Rahimi; Parisa Ashournia; Anahita Razaghian; Arezou Rezaei; Setareh Mamishi; Nima Parvaneh; Nima Rezaei; Lennart Hammarström; Asghar Aghamohammadi
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8.  Global report on primary immunodeficiencies: 2018 update from the Jeffrey Modell Centers Network on disease classification, regional trends, treatment modalities, and physician reported outcomes.

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10.  Human STAT3 variants underlie autosomal dominant hyper-IgE syndrome by negative dominance.

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