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218 results on '"Mellouli, Fethi"'

4. Inherited GATA2 Deficiency Is Dominant by Haploinsufficiency and Displays Incomplete Clinical Penetrance

Author

Oleaga-Quintas, Carmen, de Oliveira-Júnior, Edgar Borges, Rosain, Jérémie, Rapaport, Franck, Deswarte, Caroline, Guérin, Antoine, Sajjath, Sairaj Munavar, Zhou, Yu Jerry, Marot, Stéphane, Lozano, Claire, Branco, Lidia, Fernández-Hidalgo, Nuria, Lew, Dukhee Betty, Brunel, Anne-Sophie, Thomas, Caroline, Launay, Elise, Arias, Andrés Augusto, Cuffel, Alexis, Monjo, Vanesa Cunill, Neehus, Anna-Lena, Marques, Laura, Roynard, Manon, Moncada-Vélez, Marcela, Gerçeker, Bengü, Colobran, Roger, Vigué, Marie-Gabrielle, Lopez-Herrera, Gabriela, Berron-Ruiz, Laura, Méndez, Nora Hilda Segura, O’Farrill Romanillos, Patricia, Le Voyer, Tom, Puel, Anne, Bellanné-Chantelot, Christine, Ramirez, Kacy A., Lorenzo-Diaz, Lazaro, Alejo, Noé Ramirez, de Diego, Rebeca Pérez, Condino-Neto, Antonio, Mellouli, Fethi, Rodriguez-Gallego, Carlos, Witte, Torsten, Restrepo, José Franco, Jobim, Mariana, Boisson-Dupuis, Stéphanie, Jeziorski, Eric, Fieschi, Claire, Vogt, Guillaume, Donadieu, Jean, Pasquet, Marlène, Vasconcelos, Julia, Ardeniz, Fatma Omur, Martínez-Gallo, Mónica, Campos, Regis A., Jobim, Luiz Fernando, Martínez-Barricarte, Rubén, Liu, Kang, Cobat, Aurélie, Abel, Laurent, Casanova, Jean-Laurent, and Bustamante, Jacinta

Published
2021
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8. Hypomorphic homozygous mutations in phosphoglucomutase 3 (PGM3) impair immunity and increase serum IgE levels

Author

Sassi, Atfa, Lazaroski, Sandra, Wu, Gang, Haslam, Stuart M, Fliegauf, Manfred, Mellouli, Fethi, Patiroglu, Turkan, Unal, Ekrem, Ozdemir, Mehmet Akif, Jouhadi, Zineb, Khadir, Khadija, Ben-Khemis, Leila, Ben-Ali, Meriem, Ben-Mustapha, Imen, Borchani, Lamia, Pfeifer, Dietmar, Jakob, Thilo, Khemiri, Monia, Asplund, A Charlotta, Gustafsson, Manuela O, Lundin, Karin E, Falk-Sörqvist, Elin, Moens, Lotte N, Gungor, Hatice Eke, Engelhardt, Karin R, Dziadzio, Magdalena, Stauss, Hans, Fleckenstein, Bernhard, Meier, Rebecca, Prayitno, Khairunnadiya, Maul-Pavicic, Andrea, Schaffer, Sandra, Rakhmanov, Mirzokhid, Henneke, Philipp, Kraus, Helene, Eibel, Hermann, Kölsch, Uwe, Nadifi, Sellama, Nilsson, Mats, Bejaoui, Mohamed, Schäffer, Alejandro A, Smith, CI Edvard, Dell, Anne, Barbouche, Mohamed-Ridha, and Grimbacher, Bodo

Subjects
Biomedical and Clinical Sciences, Immunology, Clinical Research, Genetics, Rare Diseases, Emerging Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Adult, Amino Acid Substitution, Cell Proliferation, Child, Chromosomes, Human, Pair 6, Female, Genetic Diseases, Inborn, Genetic Linkage, Glycosylation, Homozygote, Humans, Immunity, Immunoglobulin E, Infant, Job Syndrome, Male, Mutation, Missense, Phosphoglucomutase, T-Lymphocytes, Tunisia, Hyper-IgE syndrome, glycosylation, Staphylococcus aureus, signal transducer and activator of transcription 3, dedicator of cytokinesis 8, phosphoglucomutase 3, Allergy
Abstract

BackgroundRecurrent bacterial and fungal infections, eczema, and increased serum IgE levels characterize patients with the hyper-IgE syndrome (HIES). Known genetic causes for HIES are mutations in signal transducer and activator of transcription 3 (STAT3) and dedicator of cytokinesis 8 (DOCK8), which are involved in signal transduction pathways. However, glycosylation defects have not been described in patients with HIES. One crucial enzyme in the glycosylation pathway is phosphoglucomutase 3 (PGM3), which catalyzes a key step in the synthesis of uridine diphosphate N-acetylglucosamine, which is required for the biosynthesis of N-glycans.ObjectiveWe sought to elucidate the genetic cause in patients with HIES who do not carry mutations in STAT3 or DOCK8.MethodsAfter establishing a linkage interval by means of SNPchip genotyping and homozygosity mapping in 2 families with HIES from Tunisia, mutational analysis was performed with selector-based, high-throughput sequencing. Protein expression was analyzed by means of Western blotting, and glycosylation was profiled by using mass spectrometry.ResultsMutational analysis of candidate genes in an 11.9-Mb linkage region on chromosome 6 shared by 2 multiplex families identified 2 homozygous mutations in PGM3 that segregated with disease status and followed recessive inheritance. The mutations predict amino acid changes in PGM3 (p.Glu340del and p.Leu83Ser). A third homozygous mutation (p.Asp502Tyr) and the p.Leu83Ser variant were identified in 2 other affected families, respectively. These hypomorphic mutations have an effect on the biosynthetic reactions involving uridine diphosphate N-acetylglucosamine. Glycomic analysis revealed an aberrant glycosylation pattern in leukocytes demonstrated by a reduced level of tri-antennary and tetra-antennary N-glycans. T-cell proliferation and differentiation were impaired in patients. Most patients had developmental delay, and many had psychomotor retardation.ConclusionImpairment of PGM3 function leads to a novel primary (inborn) error of development and immunity because biallelic hypomorphic mutations are associated with impaired glycosylation and a hyper-IgE-like phenotype.

Published
2014

11. Diagnostic challenge in a series of eleven patients with hyper IgE syndromes

Author

Yaakoubi, Roukaya, primary, Mekki, Najla, additional, Ben-Mustapha, Imen, additional, Ben-Khemis, Leila, additional, Bouaziz, Asma, additional, Ben Fraj, Ilhem, additional, Ammar, Jamel, additional, Hamzaoui, Agnès, additional, Turki, Hamida, additional, Boussofara, Lobna, additional, Denguezli, Mohamed, additional, Haddad, Samir, additional, Ouederni, Monia, additional, Bejaoui, Mohamed, additional, Chan, Koon Wing, additional, Lau, Yu Lung, additional, Mellouli, Fethi, additional, Barbouche, Mohamed-Ridha, additional, and Ben-Ali, Meriem, additional

Published
2023
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12. The extended clinical phenotype of 64 patients with dedicator of cytokinesis 8 deficiency

Author

Engelhardt, Karin R., Gertz, Michael E., Keles, Sevgi, Schäffer, Alejandro A., Sigmund, Elena C., Glocker, Cristina, Saghafi, Shiva, Pourpak, Zahra, Ceja, Ruben, Sassi, Atfa, Graham, Laura E., Massaad, Michel J., Mellouli, Fethi, Ben-Mustapha, Imen, Khemiri, Monia, Kilic, Sara Sebnem, Etzioni, Amos, Freeman, Alexandra F., Thiel, Jens, Schulze, Ilka, Al-Herz, Waleed, Metin, Ayse, Sanal, Özden, Tezcan, Ilhan, Yeganeh, Mehdi, Niehues, Tim, Dueckers, Gregor, Weinspach, Sebastian, Patiroglu, Turkan, Unal, Ekrem, Dasouki, Majed, Yilmaz, Mustafa, Genel, Ferah, Aytekin, Caner, Kutukculer, Necil, Somer, Ayper, Kilic, Mehmet, Reisli, Ismail, Camcioglu, Yildiz, Gennery, Andrew R., Cant, Andrew J., Jones, Alison, Gaspar, Bobby H., Arkwright, Peter D., Pietrogrande, Maria C., Baz, Zeina, Al-Tamemi, Salem, Lougaris, Vassilios, Lefranc, Gerard, Megarbane, Andre, Boutros, Jeannette, Galal, Nermeen, Bejaoui, Mohamed, Barbouche, Mohamed-Ridha, Geha, Raif S., Chatila, Talal A., and Grimbacher, Bodo

Published
2015
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13. Phenotypic and molecular genetic analysis of Pyruvate Kinase deficiency in a Tunisian family

Author

Jaouani Mouna, Hamdi Nadia, Chaouch Leila, Kalai Miniar, Mellouli Fethi, Darragi Imen, Boudriga Imen, Chaouachi Dorra, Bejaoui Mohamed, and Abbes Salem

Subjects
Pyruvate Kinase deficiency, Phenotypic and molecular investigation, Hemolytic anemia, Hydrops fetalis, PKLR mutation, Medicine (General), R5-920, Genetics, QH426-470
Abstract

Pyruvate Kinase (PK) deficiency is the most frequent red cell enzymatic defect responsible for hereditary non-spherocytic hemolytic anemia. The disease has been studied in several ethnic groups. However, it is yet an unknown pathology in Tunisia. We report here, the phenotypic and molecular investigation of PK deficiency in a Tunisian family. This study was carried out on two Tunisian brothers and members of their family. Hematological, biochemical analysis and erythrocyte PK activity were performed. The molecular characterization was carried out by gene sequencing technique. The first patient died few hours after birth by hydrops fetalis, the second one presented with neonatal jaundice and severe anemia necessitating urgent blood transfusion. This severe clinical picture is the result of a homozygous mutation of PKLR gene at exon 8 (c.1079G>A; p.Cys360Tyr). Certainly, this research allowed us to correlate the clinical phenotype severity with the identified mutation. Moreover, this will help in understanding the etiology of unknown anemia in our country.

Published
2016
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18. X-Linked Agammagobulinemia in a Large Series of North African Patients: Frequency, Clinical Features and Novel BTK Mutations

Author

Aadam, Zahra, Kechout, Nadia, Barakat, Abdelhamid, Chan, Koon-Wing, Ben-Ali, Meriem, Ben-Mustapha, Imen, Zidi, Fethi, Ailal, Fatima, Attal, Nabila, Doudou, Fatouma, Abbadi, Mohamed-Cherif, Kaddache, Chawki, Smati, Leila, Touri, Nabila, Chemli, Jalel, Gargah, Tahar, Brini, Ines, Bakhchane, Amina, Charoute, Hicham, Jeddane, Leila, El Atiqi, Sara, El Hafidi, Naïma, Hida, Mustapha, Saile, Rachid, Alj, Hanane Salih, Boukari, Rachida, Bejaoui, Mohamed, Najib, Jilali, Barbouche, Mohamed-Ridha, Lau, Yu-Lung, Mellouli, Fethi, and Bousfiha, Ahmed Aziz

Published
2016
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21. Report of the Tunisian Registry of Primary Immunodeficiencies: 25-Years of Experience (1988–2012)

Author

Mellouli, Fethi, Mustapha, Imen Ben, Khaled, Monia Ben, Besbes, Habib, Ouederni, Monia, Mekki, Najla, Ali, Meriem Ben, Larguèche, Beya, Hachicha, Mongia, Sfar, Tahar, Gueddiche, Neji, Barsaoui, Siheme, Sammoud, Azza, Boussetta, Khadija, Becher, Saida Ben, Meherzi, Ahmed, Guandoura, Najoua, Boughammoura, Lamia, Harbi, Abdelaziz, Amri, Fethi, Bayoudh, Fethi, Jaballah, Najla Ben, Tebib, Neji, Bouaziz, Asma, Mahfoudh, Abdelmajid, Aloulou, Hajer, Mansour, Lamia Ben, Chabchoub, Imen, Boussoffara, Raoudha, Chemli, Jalel, Bouguila, Jihène, Hassayoun, Saida, Hammami, Saber, Habboul, Zakia, Hamzaoui, Agnès, Ammar, Jamel, Barbouche, Mohamed-Ridha, and Bejaoui, Mohamed

Published
2015
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23. Molecular characterization of a novel homozygous deletion in β-globin cluster causing (δβ) 0 -Thalassemia among Tunisian family.

Author

Kalai, Miniar, Moumni, Imen, Ouragini, Houyem, Ben Fraj, Ilhem, Mellouli, Fethi, Ouederni, Monia, Chaouachi, Dorra, Boudriga, Imen, and Menif, Samia

Subjects
FETAL hemoglobin, DELETION mutation, TUNISIANS, CAPILLARY electrophoresis, MOLE fraction, DATABASES
Abstract

Background: Deletions in the β-globin cluster are uncommon and cause thalassemia (thal) with hereditary persistence of fetal hemoglobin. They constitute a heterogenous group of disorders characterized by absent or reduced synthesis of adult hemoglobin (Hb A) and increased synthesis of fetal hemoglobin (Hb F). Although the clinical severity of these disorders are asymptomatic owing to the increased Hb F levels, the molecular basis is very heterogenous due to the large deletions in the β-globin cluster spanning both HBD and HBB genes. Here, we describe a Tunisian family carrying a novel deletion mutation causing (δβ)°-thalassemia. Methods: The amounts of hemoglobin fractions were measured by capillary electrophoresis of hemoglobin. Amplification and sequencing of different regions on the β-gene cluster were performed by Sanger method. Results: Family study and genetic analysis revealed a large deletion mutation in the β-globin cluster of 14.5 kb (NG_000,007.3:g. 58,253 to g.72837del14584) at the homozygous state in the patient and at heterozygous state at the other members of the family. This deletion removes the HBD and HBB genes. Conclusions: In our knowledge, this new large deletion is described for the first time in the Tunisian population and in the world, designed Tunisian(δβ)0 in Ithanet database (IthaID: 3971). Therefore, it is important to identify the deletion leading to δβ-thalassemia carriers at the molecular level, to highlight the importance of recognizing the clinical features and implementing appropriate testing to clarify the diagnosis and manage the condition. [ABSTRACT FROM AUTHOR]

Published
2023
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24. Diagnostic challenge in a series of eleven patients with hyper IgE syndromes.

Author

Roukaya Yaakoubi, Mekki, Najla, Ben-Mustapha, Imen, Ben-Khemis, Leila, Bouaziz, Asma, Fraj, Ilhem Ben, Ammar, Jamel, Hamzaoui, Agnès, Turki, Hamida, Boussofara, Lobna, Denguezli, Mohamed, Haddad, Samir, Ouederni, Monia, Bejaoui, Mohamed, Koon Wing Chan, Yu Lung Lau, Mellouli, Fethi, Barbouche, Mohamed-Ridha, and Ben-Ali, Meriem

Subjects
GUANINE nucleotide exchange factors, JOB'S syndrome, IMMUNOGLOBULIN E, PULMONARY eosinophilia, RESOURCE-limited settings, GENETIC testing
Abstract

Hyper IgE syndromes (HIES) is a heterogeneous group of Inborn Errors of Immunity characterized by eczema, recurrent skin and lung infections associated with eosinophilia and elevated IgE levels. Autosomal dominant HIES caused by loss of function mutations in Signal transducer and activator of transcription 3 (STAT3) gene is the prototype of these disorders. Over the past two decades, advent in genetic testing allowed the identification of ten other etiologies of HIES. Although Dedicator of Cytokinesis 8 (DOCK8) deficiency is no more classified among HIES etiologies but as a combined immunodeficiency, this disease, characterized by severe viral infections, food allergies, autoimmunity, and increased risk of malignancies, shares some clinical features with STAT3 deficiency. The present study highlights the diagnostic challenge in eleven patients with the clinical phenotype of HIES in a resource-limited region. Candidate gene strategy supported by clinical features, laboratory findings and functional investigations allowed the identification of two heterozygous STAT3 mutations in five patients, and a biallelic DOCK8 mutation in one patient. Whole Exome Sequencing allowed to unmask atypical presentations of DOCK8 deficiency in two patients presenting with clinical features reminiscent of STAT3 deficiency. Our study underlies the importance of the differential diagnosis between STAT3 and DOCK8 deficiencies in order to improve diagnostic criteria and to propose appropriate therapeutic approaches. In addition, our findings emphasize the role of NGS in detecting mutations that induce overlapping phenotypes. [ABSTRACT FROM AUTHOR]

Published
2023
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27. FANCA Gene Mutations in North African Fanconi Anemia Patients

Author

Ben Haj Ali, Abir, primary, Messaoud, Olfa, additional, Elouej, Sahar, additional, Talmoudi, Faten, additional, Ayed, Wiem, additional, Mellouli, Fethi, additional, Ouederni, Monia, additional, Hadiji, Sondes, additional, De Sandre-Giovannoli, Annachiara, additional, Delague, Valérie, additional, Lévy, Nicolas, additional, Bogliolo, Massimo, additional, Surrallés, Jordi, additional, Abdelhak, Sonia, additional, and Amouri, Ahlem, additional

Published
2021
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30. Genetic Approaches for Definitive Diagnosis of Agammaglobulinemia in Consanguineous Families

Author

Ben-Ali, Meriem, primary, Kechout, Nadia, additional, Mekki, Najla, additional, Yang, Jing, additional, Chan, Koon Wing, additional, Barakat, Abdelhamid, additional, Aadam, Zahra, additional, Gamara, Jouda, additional, Gargouri, Lamia, additional, Largueche, Beya, additional, BelHadj-Hmida, Nabil, additional, Nedri, Amel, additional, Ameur, Houcine Ben, additional, Mellouli, Fethi, additional, Boukari, Rachida, additional, Bejaoui, Mohamed, additional, Bousfiha, Aziz, additional, Ben-Mustapha, Imen, additional, Lau, Yu-Lung, additional, and Barbouche, Mohamed-Ridha, additional

Published
2019
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33. Myocardial and liver iron overload, assessed using T2* magnetic resonance imaging with an excel spreadsheet for post processing in Tunisian thalassemia major patients

Author

Ouederni, Monia, Ben Khaled, Monia, Mellouli, Fethi, Ben Fraj, Elhem, Dhouib, Nawel, Abbes, Selem, Ben Yakoub , Ismehen, Mnif, Najla, Bejaoui, Mohamed, Yakoub, Ismehen Ben, Faculty of Medicine of Tunis, Université de Tunis El Manar (UTM), Department of Peadiatric Immuno-Haematology, National Bone Marrow Transplantation, Laboratoire d'hématologie moléculaire et cellulaire (LR11IPT07), Institut Pasteur de Tunis, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Department of Radiology, and Hôpital Charles Nicolle [Tunis]

Subjects
Adult, Male, medicine.medical_specialty, Liver Iron Concentration, Iron Overload, Tunisia, Adolescent, [SDV]Life Sciences [q-bio], Thalassemia, Gastroenterology, 030218 nuclear medicine & medical imaging, Cohort Studies, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, Liver iron, Child, Serum ferritin, ComputingMilieux_MISCELLANEOUS, Hematology, medicine.diagnostic_test, business.industry, Myocardium, beta-Thalassemia, Serum ferritin level, Transfusion Reaction, Magnetic resonance imaging, General Medicine, medicine.disease, Magnetic Resonance Imaging, 3. Good health, Surgery, Liver, Cohort, Female, business, Software, Follow-Up Studies, 030215 immunology
Abstract

Thalassemia is a common genetic disorder in Tunisia. Early iron concentration assessment is a crucial and challenging issue. Most of annual deaths due to iron overload occurred in underdeveloped regions of the world. Limited access to liver and heart MRI monitoring might partially explain these poor prognostic results. Standard software programs are not available in Tunisia. This study is the first to evaluate iron overload in heart and liver using the MRI T2* with excel spreadsheet for post processing. Association of this MRI tool results to serum ferritin level, and echocardiography was also investigated. One hundred Tunisian-transfused thalassemia patients older than 10 years (16.1 ± 5.2) were enrolled in the study. The mean myocardial iron concentration (MIC) was 1.26 ± 1.65 mg/g dw (0.06-8.32). Cardiac T2* (CT2*) was under 20 ms in 30 % of patients and under 10 ms in 21 % of patients. Left ventricular ejection function was significantly lower in patients with CT2*10 ms. Abnormal liver iron concentration (LIC3 mg/g dw) was found in 95 % of patients. LIC was over 15 mg/g dw in 25 % of patients. MIC was more correlated than CT2* to LIC and serum ferritin. Among patients with SF1000 μg/l, 13 % had CT2*20 ms. Our data showed that 30 % of the Tunisian thalassemia major patients enrolled in this cohort had myocardial iron overload despite being treated by iron chelators. SF could not reliably predict iron overload in all thalassemia patients. MRI T2* using excel spreadsheet for routine follow-up of iron overload might improve the prognosis of thalassemia major patients in developing countries, such as Tunisia, where standard MRI tools are not available or expensive.

Published
2016

35. Oral HPV infection and MHC class II deficiency (A study of two cases with atypical outcome)

Author

Guirat-Dhouib Naouel, Baccar Yemen, Mustapha Imène, ouederni Monia, Chouaibi Sameh, El Fekih Nadia, Barbouche Mohamed, Fezaa Bassima, Kouki Ridha, Hmida Slama, Mellouli Fethi, and Bejaoui Mohamed

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Major histocompatibility complex class II deficiency, also referred to as bare lymphocyte syndrome is a rare primary Immunodeficiency disorder characterized by a profondly deficient human leukocyte antigen class II expression and a lack of cellular and humoral immune responses to foreign antigens. Clinical manifestations include extreme susceptibility to viral, bacterial, and fungal infections. The infections begin in the first year of life and involve usually the respiratory system and the gastrointestinal tract. Severe malabsorption with failure to thrive ensues, often leading to death in early childhood. Bone marrow transplantation is the curative treatment. Case reports Here we report two cases with a late outcome MHC class II deficiency. They had a long term history of recurrent bronchopulmonary and gastrointestinal infections. Bone marrow transplantation could not be performed because no compatible donor had been identified. At the age of 12 years, they developed oral papillomatous lesions related to HPV (human papillomavirus). The diagnosis of HPV infection was done by histological examination. HPV typing performed on the tissue obtained at biopsy showed HPV type 6. The lesions were partially removed after two months of laser treatment. Conclusions Viral infections are common in patients with MHC class II and remain the main cause of death. Besides warts caused by HPV infection do not exhibit a propensity for malignant transformation; they can cause great psychosocial morbidity.

Published
2012
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36. Kaposi’s sarcoma in a child with Wiskott-Aldrich syndrome

Author

Picard, Capucine, Mellouli, Fethi, Duprez, Renan, Chédeville, Gaëlle, Neven, Bénédicte, Fraitag, Sylvie, Delaunay, Jean, Le Deist, Françoise, Fischer, Alain, Blanche, Stéphane, Bodemer, Christine, Gessain, Antoine, Casanova, Jean-Laurent, and Bejaoui, Mohamed

Published
2006
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40. A founder mutation underlies a severe form of phosphoglutamase 3 (PGM3) deficiency in Tunisian patients

Author

Ben-Khemis, Leila, primary, Mekki, Najla, additional, Ben-Mustapha, Imen, additional, Rouault, Karen, additional, Mellouli, Fethi, additional, Khemiri, Monia, additional, Bejaoui, Mohamed, additional, Essaddam, Leila, additional, Ben-Becher, Saayda, additional, Boughamoura, Lamia, additional, Hassayoun, Saida, additional, Ben-Ali, Meriem, additional, and Barbouche, Mohamed-Ridha, additional

Published
2017
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41. Phenotypic and molecular genetic analysis of Pyruvate Kinase deficiency in a Tunisian family

Author

Kalai Miniar, Bejaoui Mohamed, Chaouachi Dorra, Abbes Salem, Chaouch Leila, Boudriga Imen, Mellouli Fethi, Hamdi Nadia, Jaouani Mouna, and Darragi Imen

Subjects
Hemolytic anemia, lcsh:QH426-470, Anemia, Biology, medicine.disease_cause, 03 medical and health sciences, Exon, 0302 clinical medicine, Phenotypic and molecular investigation, Hydrops fetalis, medicine, Pyruvate Kinase deficiency, Genetics(clinical), Genetics (clinical), Genetics, lcsh:R5-920, Mutation, Jaundice, medicine.disease, lcsh:Genetics, PKLR mutation, 030220 oncology & carcinogenesis, Immunology, medicine.symptom, lcsh:Medicine (General), Pyruvate kinase, 030215 immunology, Pyruvate kinase deficiency
Abstract

Pyruvate Kinase (PK) deficiency is the most frequent red cell enzymatic defect responsible for hereditary non-spherocytic hemolytic anemia. The disease has been studied in several ethnic groups. However, it is yet an unknown pathology in Tunisia. We report here, the phenotypic and molecular investigation of PK deficiency in a Tunisian family. This study was carried out on two Tunisian brothers and members of their family. Hematological, biochemical analysis and erythrocyte PK activity were performed. The molecular characterization was carried out by gene sequencing technique. The first patient died few hours after birth by hydrops fetalis, the second one presented with neonatal jaundice and severe anemia necessitating urgent blood transfusion. This severe clinical picture is the result of a homozygous mutation of PKLR gene at exon 8 (c.1079G>A; p.Cys360Tyr). Certainly, this research allowed us to correlate the clinical phenotype severity with the identified mutation. Moreover, this will help in understanding the etiology of unknown anemia in our country. Keywords : Pyruvate Kinase deficiency; Phenotypic and molecular investigation; Hemolytic anemia; Hydrops fetalis; PKLR mutation

Published
2016

42. Abstracts from the 3rd International Genomic Medicine Conference (3rd IGMC 2015)

Author

Jerry W. Shay, Noriko Homma, Ruyun Zhou, Muhammad Imran Naseer, Adeel G. Chaudhary, Mohammed Al-Qahtani, Nobutaka Hirokawa, Maryam Goudarzi, Albert J. Fornace, Saleh Baeesa, Deema Hussain, Mohammed Bangash, Fahad Alghamdi, Hans-Juergen Schulten, Angel Carracedo, Ishaq Khan, Hanadi Qashqari, Nawal Madkhali, Mohamad Saka, Kulvinder S. Saini, Awatif Jamal, Jaudah Al-Maghrabi, Adel Abuzenadah, Adeel Chaudhary, Mohammed Al Qahtani, Ghazi Damanhouri, Heba Alkhatabi, Anne Goodeve, Laura Crookes, Nikolas Niksic, Nicholas Beauchamp, Adel M. Abuzenadah, Jim Vaught, Bruce Budowle, Mourad Assidi, Abdelbaset Buhmeida, Leena Merdad, Sudhir Kumar, Sayaka Miura, Karen Gomez, Mahmood Rasool, Ahmed Rebai, Sajjad Karim, Hend F. Nour Eldin, Heba Abusamra, Elham M. Alhathli, Nada Salem, Mohammed H. Al-Qahtani, Hossam Faheem, Ashok Agarwa, Eberhard Nieschlag, Joachim Wistuba, Oliver S. Damm, Mohd A. Beg, Taha A. Abdel-Meguid, Hisham A. Mosli, Osama S. Bajouh, Serdar Coskun, Muhammad Abu-Elmagd, Ashraf Dallol, Sahar Hakamy, Wejdan Al-Qahtani, Asia Al-Harbi, Shireen Hussain, Burak Ozkosem, Rick DuBois, Safia S. Messaoudi, Maryam T. Dandana, Touhami Mahjoub, Wassim Y. Almawi, S. Abdalla, M. Nabil Al-Aama, Asmaa Elzawahry, Tsuyoshi Takahashi, Sachiyo Mimaki, Eisaku Furukawa, Rie Nakatsuka, Isao Kurosaka, Takahiko Nishigaki, Hiromi Nakamura, Satoshi Serada, Tetsuji Naka, Seiichi Hirota, Tatsuhiro Shibata, Katsuya Tsuchihara, Toshirou Nishida, Mamoru Kato, Sajid Mehmood, Naeem Mahmood Ashraf, Awais Asif, Muhammad Bilal, Malik Siddique Mehmood, Aadil Hussain, Qazi Mohammad Sajid Jamal, Mughees Uddin Siddiqui, Mohammad A. Alzohairy, Mohammad A. Al Karaawi, Taoufik Nedjadi, Heba Al-Khattabi, Adel Al-Ammari, Ahmed Al-Sayyad, Hédia Zitouni, Nozha Raguema, Marwa Ben Ali, Wided Malah, Raja Lfalah, Wassim Almawi, Mohammed Elanbari, Andrey Ptitsyn, Sana Mahjoub, Rabeb El Ghali, Bechir Achour, Nidhal Ben Amor, Brahim N’siri, Hamid Morjani, Esam Azhar, Vera Chayeb, Maryam Dendena, Hedia Zitouni, Khedija Zouari-Limayem, Bassem Refaat, Ahmed M. Ashshi, Sarah A. Batwa, Hazem Ramadan, Amal Awad, Ahmed Ateya, Adel Galal Ahmed El-Shemi, Ahmad Ashshi, Mohammed Basalamah, Youjin Na, Chae-Ok Yun, Adel Galal El-Shemi, Osama Kensara, Amr Abdelfattah, Batol Imran Dheeb, Mohammed M. F. Al-Halbosiy, Rghad Kadhim Al lihabi, Basim Mohammed Khashman, Djouhri Laiche, Chaudhary Adeel, Nedjadi Taoufik, Hani Al-Afghani, Maria Łastowska, Haya H. Al-Balool, Harsh Sheth, Emma Mercer, Jonathan M. Coxhead, Chris P. F. Redfern, Heiko Peters, Alastair D. Burt, Mauro Santibanez-Koref, Chris M. Bacon, Louis Chesler, Alistair G. Rust, David J. Adams, Daniel Williamson, Steven C. Clifford, Michael S. Jackson, Mala Singh, Mohmmad Shoab Mansuri, Shahnawaz D. Jadeja, Hima Patel, Yogesh S. Marfatia, Rasheedunnisa Begum, Amal M. Mohamed, Alaa K. Kamel, Nivin A. Helmy, Sayda A. Hammad, Hesham F. Kayed, Marwa I. Shehab, Assad El Gerzawy, Maha M. Ead, Ola M. Ead, Mona Mekkawy, Innas Mazen, Mona El-Ruby, S. M. A. Shahid, J. M. Arif, Mohtashim Lohani, Moumni Imen, Chaouch Leila, Ouragini Houyem, Douzi Kais, Chaouachi Dorra Mellouli Fethi, Bejaoui Mohamed, Abbes Salem, Areeg Faggad, Amanuel T. Gebreslasie, Hani Y. Zaki, Badreldin E. Abdalla, Maha S. AlShammari, Rhaya Al-Ali, Nader Al-Balawi, Mansour Al-Enazi, Ali Al-Muraikhi, Fadi Busaleh, Ali Al-Sahwan, Francis Borgio, Abdulazeez Sayyed, Amein Al-Ali, Sadananda Acharya, Maha S. Zaki, Hala T. El-Bassyouni, Mohammed F. Elshal, Kaleemuddin M., Alia M. Aldahlawi, Omar Saadah, J. Philip McCoy, Adel E. El-Tarras, Nabil S. Awad, Abdulla A. Alharthi, Mohamed M. M. Ibrahim, Haneen S. Alsehli, Abdullah M. Gari, Mohammed M. Abbas, Roaa A. Kadam, Mazen M. Gari, Mohmmed H. Alkaff, Mamdooh A. Gari, Hend F. Nour eldin, Fatima A. Moradi, Omran M. Rashidi, Zuhier A. Awan, Ibrahim Hamza Kaya, Olfat Al-Harazi, Dilek Colak, Nabila A. Alkousi, Takis Athanasopoulos, Afnan O. Bahmaid, Etimad A. Alhwait, Mohammed H. Alkaf, Roaa Kadam, Gauthaman Kalamegam, Elham Alhathli, Salma N. Alsayed, Fawziah H. Aljohani, Samaher M. Habeeb, Rawan A. Almashali, Sulman Basit, Samia M. Ahmed, Rakesh Sharma, Ashok Agarwal, Damayanthi Durairajanayagam, Luna Samanta, Edmund S. Sabanegh, Zhihong Cui, Alaa A. Alboogmi, Nuha A. Alansari, Maha M. Al-Quaiti, Fai T. Ashgan, Afnan Bandah, Hasan S. Jamal, Abdullraheem Rozi, Zeenat Mirza, Ahmad J. Al Sayyad, Hasan M. A. Farsi, Jaudah A. Al-Maghrabi, Reem Alotibi, Alaa Al-Ahmadi, Alaa A. Albogmi, Rasha A. Ebiya, Samia M. Darwish, Metwally M. Montaser, Vladimir B. Bajic, Wafaey Gomaa, Mehenaz Hanbazazh, Mahmoud Al-Ahwal, Saher Hakamy, Ghali Baba, Abdullah Al-Harbi, Ghalia Baba, Hend Nour Eldin, Aisha A. Alyamani, Rawan Gadi, Saadiah M. Alfakeeh, Rubi Ghazala, Shilu Mathew, M. Haroon Hamed, Ishtiaq Qadri, Lobna Mira, Manal Shaabad, Mikhlid H. Almutairi, Angie Ambers, Jennifer Churchill, Jonathan King, Monika Stoljarova, Harrell Gill-King, Muhammad Al-Qatani, Farid Ahmed, Taha Abo Almagd, Muhammad Al-Qahtani, Abdelbaset Buhmaida, Rukhsana Satar, Waseem Ahmad, Nazia Nazam, Mohamad I. Lone, Muhammad I. Naseer, Mohammad S. Jamal, Syed K. Zaidi, Peter N. Pushparaj, Mohammad A. Jafri, Shakeel A. Ansari, Mohammed H. Alqahtani, Hanan Bashier, Abrar Al Qahtani, Amal M. Nour, Adel M. Abu Zenadah, Muhammed Al Qahtani, Muhammad Faheem, Shiny Mathew, Peter Natesan Pushparaj, Mohammad H. Al-Qahtani, Hani A. Alhadrami, Ibtessam R. Hussein, Rima S. Bader, Randa Bassiouni, Maha Alquaiti, Fai Ashgan, Hans Schulten, Mohamed Nabil Alama, Mohammad H. Al Qahtani, Mohammad I. Lone, Nazia Nizam, Muhammed H. Al-Qahtani, Eradah Alshihri, Lina Alharbi, Peter Pushparaj Natesan, Fazal Khan, Khalid Hussain Wali Sait, Nisreen Anfinan, Lobna S. Mira, Mohammed H. AlQahtani, Sameera Sogaty, Randa I. Bassiouni, Abdulrahman M. S. Sibiani, Mohiuddin K. Warsi, null Rubi, Kundan Kumar, Ahmad A. T. Naqvi, Faizan Ahmad, Md I. Hassan, Ashraf Ali, Jummanah Jarullah, Abdelbasit Buhmeida, Shahida Khan, Ghufrana Abdussami, Maryam Mahfooz, Mohammad A. Kamal, Ghazi A. Damanhouri, Bushra Jarullah, Mohammad S. S. Jarullah, Osama Bajouh, Abdulah E. A. Mathkoor, Hashim M. A. Alsalmi, Anas M. M. Oun, Ghazi A. Damanhauri, Adeel G. Chudhary, Yousif A. Abutalib, Daniele Merico, Susan Walker, Christian R. Marshall, Mehdi Zarrei, Stephen W. Scherer, Fai Talal Ashgan, Syed Kashif Zaidi, Mohammed M. Jan, Maryam Al-Zahrani, Sahira Lary, Emmanuel Dermitzakis, Abeer A. Al-refai, Mona Saleh, Rehab I. Yassien, Mahmmoud Kamel, Rabab M. Habeb, Najlaa Filimban, Nadia Ghannam, Adel Mohammed Abuzenadah, Fehmida Bibi, Sana Akhtar, Esam I. Azhar, Muhammad Yasir, Muhammad I. Nasser, Asif A. Jiman-Fatani, Ali Sawan, Ruaa A. Lahzah, Asho Ali, Syed A. Hassan, Seyed E. Hasnain, Iftikhar A. Tayubi, Hamza A. Abujabal, Alaa O. Magrabi, Adel Abuzenada, Taha Abduallah Kumosani, Elie Barbour, Manal Shabaad, Adnan Merdad, Kalamegam Gauthaman, Mamdooh Gari, Hani M. A. Aljahdali, Reham Al Nono, Haneen Alsehli, Mohammed Abbas, Mohammed Sarwar Jamal, Shakeel Ansari, Mansour A. Alghamdi, Magdy Shamy, Max Costa, Mamdouh I. Khoder, Najla Kharrat, Sabrine Belmabrouk, Rania Abdelhedi, Riadh Benmarzoug, Mohammed H. Al Qahtani, Ghazi Dhamanhouri, Abdelwahab Noorwali, Mohammad Khalid Alwasiyah, Afnan Bahamaid, Saadiah Alfakeeh, Aisha Alyamani, Ali Mobasheri, Mohammad Sarwar Jamal, Raziuddin Khan, Kanchan Bhatia, Saif Ahmad, Iftikhar AslamTayubi, Manish Tripathi, Syed Asif Hassan, Rahul Shrivastava, Syed Hassan, Hamza A. S. Abujabal, Ishani Shah, Ishfaq A. Sheikh, Ejaz Ahmad, Mohd Rehan, Samera F. AlBasri, Rola F. Turki, Sahar A. F. Hammoudah, Khalid M. AlHarbi, Lama M. El-Attar, Ahmed M. Z. Darwish, Sara M. Ibrahim, Hani Choudhry, Jalaludden Awlia, Imran khan, Sameera Al-basri, Taha Kumosani, Heba M. EL Sayed, Eman A. Hafez, Aisha Hassan Elaimi, Randa Ibrahim Bassiouni, Richard F. Wintle, Vikram Gopalakrishna Pillai, Sujata Sharma, Punit Kaur, Alagiri Srinivasan, Tej P. Singh, Fatima Al-Adwani, Deema Hussein, Mona Al-Sharif, Fahad Al-Ghamdi, Saleh S. Baeesa, Taha Abdullah Kumosani, Faisal A. Al-Allaf, Zainularifeen Abduljaleel, Abdullah Alashwal, Mohiuddin M. Taher, Abdellatif Bouazzaoui, Halah Abalkhail, Faisal A. Ba-Hammam, Mohammad Athar, Khalid HussainWali Sait, Naira Ben Mami, Yosr Z. Haffani, Mouna Medhioub, Lamine Hamzaoui, Ameur Cherif, Msadok Azouz, Mohammed Imran Nasser, Shereen A. Turkistany, Lina M. Al-harbi, Jamal Sabir, Basmah Al-Madoudi, Bayan Al-Aslani, Khulud Al-Harbi, Rwan Al-Jahdali, Hanadi Qudaih, Emad Al Hamzy, Asad M. Ilyas, Youssri Ahmed, Mohammed Alqahtani, Alaa Alamandi, Ohoud Subhi, Nadia Bagatian, Adel Al-Johari, Osman Abdel Al-Hamour, Hosam Al-Aradati, Abdulmonem Al-Mutawa, Faisal Al-Mashat, Mohammad Al-Qahtani, Muhammad W. shah, Esam I Azhar, Saad Al-Masoodi, Emna Khamla, Chaima Jlassi, Ahmed S. Masmoudi, Lassaad Belbahri, Shadi Al-Khayyat, Roba Attas, Atlal Abu-Sanad, Mohammed Abuzinadah, Habib Bouazzi, Carlos Trujillo, Maha Alotaibi, Rami Nassir, Essam H. Jiffri, Ghulam M. Ashraf, Mohammad A. Aziz, Rizwan Ali, Nusaibah Samman, Sathish Periyasamy, Mohammed Aldress, Majed Al Otaibi, Zeyad Al Yousef, Mohamed Boudjelal, Ibrahim AlAbdulkarim, Mohd Suhail, Abid Qureshi, Adil Jamal, Mahmoud Z. El-Readi, Safaa Y. Eid, Michael Wink, Ahmed M. Isa, Lulu Alnuaim, Johara Almutawa, Basim Abu-Rafae, Saleh Alasiri, Saleh Binsaleh, and Mohamed H. Alqahtani

Subjects
0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Differentially expressed genes, Gene expression, Genetics, Feature selection, Computational biology, Biology, Cluster analysis, Classifier (UML), Biotechnology
Published
2016

44. Restriction mapping of βS locus among tunisian sickle-cell patients

Author

Zorai Amine, Moumni Imen, Mellouli Fethi, Ben Mansour Mosbehi Ikbel, Abbes Salem, Chaouch Leila, and Bejaoui Mohamed

Subjects
Male, Tunisia, Adolescent, DNA Mutational Analysis, Restriction Mapping, Population, Locus (genetics), Anemia, Sickle Cell, beta-Globins, Biology, Restriction map, Gene cluster, Genetics, Humans, Child, education, Gene, Fetal Hemoglobin, Ecology, Evolution, Behavior and Systematics, education.field_of_study, Haplotype, Infant, Chromosome, Very high frequency, Emigration and Immigration, Haplotypes, Child, Preschool, Multigene Family, Anthropology, Female, Anatomy, Polymorphism, Restriction Fragment Length
Abstract

Objectives: The polymorphism of the β-globin gene haplotypes and frameworks is useful in the determination of the unicentric and multicentric origin of a mutational event. In our study, the haplotypes linked to the Tunisian βS mutation are determined to improve our knowledge of the chromosomal background of the β-globin gene in sickle-cell anemia in Tunisia. Methods: The authors have investigated 242 unrelated individuals. Haplotype analysis was carried out by polymerase chain reaction-restriction fragment length polymorphism-based methods. Seven polymorphic sites in the β-globin gene cluster were examined. The correlation of these various haplotypes with Hb F expression was studied. Results: The Benin haplotype (Ben) was largely predominant (60.54%) followed by the Atypical haplotype A (8.43%) and Bantu (Ban) (2.71%) haplotypes. A total of 94 chromosomes had atypical haplotypes, 78 (23.49%) had A1 [−−−−−++], 11 (3.31%) had A2 [−−−−−−−], and five (1.5%) had B1 [−−+−−++]. The Benin haplotype is associated with a fairly low HbF levels. Conclusion: The very high frequency of the Benin haplotype in our study suggests that the βS mutation present in Tunisia may have originated from the Benin region and was brought to Tunisia along the slave trade routes. However, another atypical haplotype observed a new emergence in our population and could be considered as specific to Tunisian chromosome βS. Am. J. Hum. Biol., 2011. © 2011 Wiley-Liss, Inc.

Published
2011

45. GROWTH AND ENDOCRINE FUNCTION IN TUNISIAN THALASSEMIA MAJOR PATIENTS

Author

Dhouib, Naouel Guirat, Ben Khaled, Monia, Ouederni, Monia, Besbes, Habib, Kouki, Ridha, Mellouli, Fethi, and Bejaoui, Mohamed

Subjects
Delayed puberty, medicine.medical_specialty, Thalassemic Syndromes , endocrine disorders, Thalassemia, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Adrenal insufficiency, Endocrine system, Glucose homeostasis, Thalassemic syndromes, lcsh:RC633-647.5, business.industry, 05 social sciences, 050301 education, lcsh:Diseases of the blood and blood-forming organs, Hematology, medicine.disease, Infectious Diseases, Hypoparathyroidism, Endocrine disorders, Original Article, medicine.symptom, business, 0503 education, 030215 immunology, Endocrine gland, Hormone
Abstract

Beta-thalassemia major (TM) is among prevalent hereditary disorders imposing high expenses on health-care system worldwide. The patient’s survival is dependent on lifetime blood transfusion which leads to iron overload and its toxicity on various organs including endocrine glands. This article provides an overview of endocrine disorders in beta-TM patients. This single center investigation enrolled 28 beta-TM patients (16 males, 12 females) regularly transfused with packed red cell since early years of life. For each patient were determined: age, sex, number of transfusions received, history of splenectomy and anthropometric parameters. Evaluation for hormonal status including growth, gonadal, thyroid, adrenal cortex, and parathyroid glands was done for all patients. Dual energy X-ray absorptiometry was used to diagnose osteoporosis. Assessment of iron overload status was performed by measuring the serum ferritin concentration and the results of magnetic resonance imaging T2*. Growth retardation was found in 16 of the 28 studied patients (57 %).Thirteen among them had delayed puberty. Spontaneous puberty was achieved in 16 cases. Growth hormone (GH) deficiency was found in 10 cases (35 %). Seventeen among the studied patients (60 %) developed disorders of glucose homeostasis. Subclinical hypothyroidism was found in six patients (21 %). Intensive chelation therapy had allowed the reversibility of this complication in five cases. Adrenal Insufficiency was found in 9 cases (32%). Hypoparathyroidism has occurred in one case. Ten of the 28 studied patients had osteoporosis (35%). Twenty-three of the 28 studied patients (82%) had at least one endocrine complication.

Published
2018

49. The extended clinical phenotype of 64 patients with DOCK8 deficiency

Author

Engelhardt, Karin R., Gertz, E. Michael, Keles, Sevgi, Schäffer, Alejandro A., Sigmund, Elena C., Glocker, Cristina, Saghafi, Shiva, Pourpak, Zahra, Ceja, Ruben, Sassi, Atfa, Graham, Laura E., Massaad, Michel J., Mellouli, Fethi, Ben-Mustapha, Imen, Khemiri, Monia, Kilic, Sara Sebnem, Etzioni, Amos, Freeman, Alexandra F., Thiel, Jens, Schulze, Ilka, Al-Herz, Waleed, Metin, Ayse, Sanal, Özden, Tezcan, Ilhan, Yeganeh, Mehdi, Niehues, Tim, Dueckers, Gregor, Weinspach, Sebastian, Patiroglu, Turkan, Unal, Ekrem, Dasouki, Majed, Yilmaz, Mustafa, Genel, Ferah, Aytekin, Caner, Kutukculer, Necil, Somer, Ayper, Kilic, Mehmet, Reisli, Ismail, Camcioglu, Yildiz, Gennery, Andrew R., Cant, Andrew J., Jones, Alison, Gaspar, H. Bobby, Arkwright, Peter D., Pietrogrande, Maria C., Baz, Zeina, Al-Tamemi, Salem, Lougaris, Vassilios, Lefranc, Gerard, Megarbane, Andre, Boutros, Jeannette, Galal, Nermeen, Bejaoui, Mohamed, Barbouche, Mohamed-Ridha, Geha, Raif S., Chatila, Talal A., and Grimbacher, Bodo

Subjects
Adult, CD4-Positive T-Lymphocytes, Male, STAT3 Transcription Factor, Support Vector Machine, Adolescent, CD8-Positive T-Lymphocytes, Skin Diseases, Article, Guanine Nucleotide Exchange Factors, Humans, Lymphocyte Count, Child, Antigens, Viral, Antigens, Bacterial, Infant, Bacterial Infections, Immunoglobulin E, Middle Aged, Survival Analysis, Eosinophils, Phenotype, Immunoglobulin M, Virus Diseases, Child, Preschool, Mutation, Female, Job Syndrome
Abstract

Mutations in dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autosomal recessive (AR) hyper-IgE syndrome (HIES). Recognizing patients with CID/HIES is of clinical importance because of the difference in prognosis and management.We sought to define the clinical features that distinguish DOCK8 deficiency from other forms of HIES and CIDs, study the mutational spectrum of DOCK8 deficiency, and report on the frequency of specific clinical findings.Eighty-two patients from 60 families with CID and the phenotype of AR-HIES with (64 patients) and without (18 patients) DOCK8 mutations were studied. Support vector machines were used to compare clinical data from 35 patients with DOCK8 deficiency with those from 10 patients with AR-HIES without a DOCK8 mutation and 64 patients with signal transducer and activator of transcription 3 (STAT3) mutations.DOCK8-deficient patients had median IgE levels of 5201 IU, high eosinophil levels of usually at least 800/μL (92% of patients), and low IgM levels (62%). About 20% of patients were lymphopenic, mainly because of low CD4(+) and CD8(+) T-cell counts. Fewer than half of the patients tested produced normal specific antibody responses to recall antigens. Bacterial (84%), viral (78%), and fungal (70%) infections were frequently observed. Skin abscesses (60%) and allergies (73%) were common clinical problems. In contrast to STAT3 deficiency, there were few pneumatoceles, bone fractures, and teething problems. Mortality was high (34%). A combination of 5 clinical features was helpful in distinguishing patients with DOCK8 mutations from those with STAT3 mutations.DOCK8 deficiency is likely in patients with severe viral infections, allergies, and/or low IgM levels who have a diagnosis of HIES plus hypereosinophilia and upper respiratory tract infections in the absence of parenchymal lung abnormalities, retained primary teeth, and minimal trauma fractures.

Published
2015

50. Novel and recurrent AID mutations underlie prevalent autosomal recessive form of HIGM in consanguineous patients

Author

Ouadani, Hanen, primary, Ben-Mustapha, Imen, additional, Ben-ali, Meriem, additional, Ben-khemis, Leila, additional, Larguèche, Beya, additional, Boussoffara, Raoudha, additional, Maalej, Sonia, additional, Fetni, Ilhem, additional, Hassayoun, Saida, additional, Mahfoudh, Abdelmajid, additional, Mellouli, Fethi, additional, Yalaoui, Sadok, additional, Masmoudi, Hatem, additional, Bejaoui, Mohamed, additional, and Barbouche, Mohamed-Ridha, additional

Published
2015
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