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9 results on '"Alwahadneh, Adel"'

2. Real-World Effectiveness of Four Types of COVID-19 Vaccines

Author

Abdel-Qader, Derar H., primary, Abdel-Qader, Hasan, additional, Silverthorne, Jennifer, additional, Kongkaew, Chuenjid, additional, Meslamani, Ahmad Z. Al, additional, Hayajneh, Wail, additional, Alwahadneh, Adel M., additional, Hamadi, Salim, additional, Abu-Qatouseh, Luay, additional, Awad, Riad, additional, Al Nsour, Mohannad, additional, Alhariri, Abdallah, additional, Shnewer, Khaldoun, additional, Da’ssan, Mohammad, additional, Obeidat, Nathir M., additional, Nusair, Khaldoon E., additional, Jalamdeh, Mothafer S., additional, Hawari, Feras, additional, Asad, Mohammad, additional, and AbuRuz, Salah, additional

Published
2023
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3. Inherited DOCK2 Deficiency in Patients with Early-Onset Invasive Infections

Author

Dobbs, Kerry, Domínguez Conde, Cecilia, Zhang, Shen-Ying, Parolini, Silvia, Audry, Magali, Chou, Janet, Haapaniemi, Emma, Keles, Sevgi, Bilic, Ivan, Okada, Satoshi, Massaad, Michel J., Rounioja, Samuli, Alwahadneh, Adel M., Serwas, Nina K., Capuder, Kelly, Çiftçi, Ergin, Felgentreff, Kerstin, Ohsumi, Toshiro K., Pedergnana, Vincent, Boisson, Bertrand, Haskoloğlu, Şule, Ensari, Arzu, Schuster, Michael, Moretta, Alessandro, Itan, Yuval, Patrizi, Ornella, Rozenberg, Flore, Lebon, Pierre, Saarela, Janna, Knip, Mikael, Petrovski, Slavé, Goldstein, David B., Parrott, Roberta E., Savas, Berna, Schambach, Axel, Tabellini, Giovanna, Bock, Christoph, Chatila, Talal A., Comeau, Anne Marie, Geha, Raif S., Abel, Laurent, Buckley, Rebecca H., İkincioğullar, Aydan, Al-Herz, Waleed, Helminen, Merja, Doğu, Figen, Casanova, Jean-Laurent, Boztuğ, Kaan, and Notarangelo, Luigi D.

Published
2015
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6. Pattern and diagnostic evaluation of systemic autoinflammatory diseases other than familial Mediterranean fever among Arab children: a multicenter study from the Pediatric Rheumatology Arab Group (PRAG).

Author

Al-Mayouf, Sulaiman M., Almutairi, Abdulaziz, Albrawi, Safiya, Fathalla, Basil M., Alzyoud, Raed, AlEnazi, Abdullatif, Abu-shukair, Mohammed, Alwahadneh, Adel, Alsonbul, Abdullah, Zlenti, Mabruka, Khawaja, Ebtisam, Abushhaiwia, Awatif, Khawaja, Khulood, AlMosawi, Zakiya, Madan, Wafa, Almuatiri, Muna, and Almuatiri, Nora

Subjects
FAMILIAL Mediterranean fever, PEDIATRIC rheumatology, COGNITION disorders, PEDIATRIC clinics, AGE of onset
Abstract

To define the spectrum and phenotypic characteristics of systemic autoinflammatory diseases (SAIDs) other than familial Mediterranean fever (FMF) in Arab children and to delineate diagnostic evaluation. Data retrospectively collected on patients with clinical and/or genetically proven SAIDs other than FMF at 10 tertiary Arab pediatric rheumatology clinics from 1990 to 2018. The collected data comprised the clinical findings and diagnostic evaluation including genetic testing, the provided treatment and the accrual damage related to SAIDs. A total of 144 patients (93 female) with a median age at onset of 2.5 (range 0.1–12) years were enrolled. The initial diagnosis was inaccurate in 49.3%. Consanguinity rate among parents was 74.6%. The median time-to-diagnosis for all SAIDs was 2.5 (range 0.1–10) years. There were 104 patients (72.2%) with a confirmed diagnosis and 40 patients with suspected SAIDs. Seventy-two had monogenic and 66 patients with multifactorial SAIDs while six patients had undifferentiated SAIDs. The most frequent monogenic SAIDs were LACC1 mediated monogenic disorders (n = 23) followed by CAPS (12), TRAPS (12), HIDS (12), and Majeed's syndrome (6). The most frequent multifactorial SAIDs was CRMO (34), followed by PFAPA (18), and early onset sarcoidosis (EOS) (14). Genetic analysis was performed in 69 patients; 50 patients had genetically confirmed disease. Corticosteroid used for 93 patients while biologic agents for 96 patients. Overall, growth failure was the most frequent accrual damage (36%), followed by cognitive impairment (13%). There were three deaths because of infection. This study shows a heterogenous spectrum of SAIDs with a high number of genetically confirmed monogenic diseases; notably, LACC1 associated diseases. Hopefully, this work will be the first step for a prospective registry for SAIDs in Arab countries. [ABSTRACT FROM AUTHOR]

Published
2020
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8. DOCK2 and a Recessive Immunodeficiency with Early-Onset Invasive Infections

Author

Dobbs, Kerry, Domínguez Conde, Cecilia, Zhang, Shen-Ying, Parolini, Silvia, Audry, Magali, Chou, Janet, Haapaniemi, Emma, Keles, Sevgi, Bilic, Ivan, Okada, Satoshi, Massaad, Michel J., Rounioja, Samuli, Alwahadneh, Adel M., Serwas, Nina K., Capuder, Kelly, Ciftci, Ergin, Felgentreff, Kerstin, Ohsumi, Toshiro K., Pedergnana, Vincent, Boisson, Bertrand, Haskoloğlu, Sule, Ensari, Arzu, Schuster, Michael, Moretta, Alessandro, Itan, Yuval, Patrizi, Ornella, Rozenberg, Flore, Lebon, Pierre, Saarela, Janna, Knip, Mikael, Petrovski, Slavé, Goldstein, David B., Parrott, Roberta E., Savas, Berna, Schambach, Axel, Tabellini, Giovanna, Bock, Christoph, Chatila, Talal, Comeau, Anne Marie, Geha, Raif S., Abel, Laurent, Buckley, Rebecca H., Ikincioğullari, Aydan, Al-Herz, Waleed, Helminen, Merja, Doğu, Figen, Casanova, Jean-Laurent, Boztuğ, Kaan, and Notarangelo, Luigi D.

Subjects
Male, rac1 GTP-Binding Protein, B-Lymphocytes, T-Lymphocytes, GTPase-Activating Proteins, Genetic Diseases, Inborn, Hematopoietic Stem Cell Transplantation, Immunologic Deficiency Syndromes, Infant, Genes, Recessive, Article, Pedigree, Killer Cells, Natural, Fatal Outcome, Child, Preschool, Mutation, Guanine Nucleotide Exchange Factors, Humans, Female
Abstract

Background Combined immunodeficiencies are marked by inborn errors of T-cell immunity in which the T cells that are present are quantitatively or functionally deficient. Impaired humoral immunity is also common. Patients have severe infections, autoimmunity, or both. The specific molecular, cellular, and clinical features of many types of combined immunodeficiencies remain unknown. Methods We performed genetic and cellular immunologic studies involving five unrelated children with early-onset invasive bacterial and viral infections, lymphopenia, and defective T-cell, B-cell, and natural killer (NK)-cell responses. Two patients died early in childhood; after allogeneic hematopoietic stem-cell transplantation, the other three had normalization of T-cell function and clinical improvement. Results We identified biallelic mutations in the dedicator of cytokinesis 2 gene (DOCK2) in these five patients. RAC1 activation was impaired in the T cells. Chemokine-induced migration and actin polymerization were defective in the T cells, B cells, and NK cells. NK-cell degranulation was also affected. Interferon-α and interferon-λ production by peripheral-blood mononuclear cells was diminished after viral infection. Moreover, in DOCK2-deficient fibroblasts, viral replication was increased and virus-induced cell death was enhanced; these conditions were normalized by treatment with interferon alfa-2b or after expression of wild-type DOCK2. Conclusions Autosomal recessive DOCK2 deficiency is a new mendelian disorder with pleiotropic defects of hematopoietic and nonhematopoietic immunity. Children with clinical features of combined immunodeficiencies, especially with early-onset, invasive infections, may have this condition. (Supported by the National Institutes of Health and others.).

Published
2015

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