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8. Insuffisance antéhypophysaire : et si c’était un déficit immunitaire ?

Author

Fraj, I. Ben, Jelassi, O., Rekaya, S., Hamdi, R., Khaled, M. Ben, Ferchichi, L., Bettaieb, A., Bejaoui, M., Mellouli, F., and Ouederni, M.

Abstract

Le syndrome de DAVID est une association rare entre une insuffisance antéhypophysaire (IAH) et un déficit immunitaire commun variable (DICV). Ce diagnostic pourrait être méconnu quand les manifestations infectieuses ne sont pas au premier plan.

Published
2024
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15. EGFR targeting of [177Lu] gold nanoparticles to colorectal and breast tumour cells: Affinity, duration of binding and growth inhibition of Cetuximab-resistant cells

Author

Rekaya Shabbir, Marco Mingarelli, Gema Cabello, Marcel van Herk, Ananya Choudhury, and Tim A.D. Smith

Subjects
Gold nanoparticles, EGFR, Cetuximab, Targeted radiotherapy, Xenografts, 177Lu, Science (General), Q1-390
Abstract

Objective: Radioimmunotherapy (RIT) is a systemic therapy currently used in the treatment of patients with lymphoma. RIT complexes consist of a targeting molecule, commonly an antibody, radionuclide chelates and a linker which can be a nanoparticle platform. Nanoparticles facilitate the attachment of multiple radionuclides and targeting groups to a single complex. Here the target affinity, duration of target association and inhibition of colony formation of Cetuximab-resistant tumour cells with Cetuximab-targeted [177Lu]-AuNPs were investigated. Dose distribution in xenografts derived from EGFR-overexpressing cells was also determined. Methods: Cetuximab-targeted [177Lu]-AuNPs were generated by functionalising 15nm AuNPs with the chelator DOTA and Cetuximab and radiolabelling with 177LuCl3. KDis, a measure of affinity, was determined by competitive binding to EGFR expressing cells. Radio-sensitivity was determined in EGFR expressing tumour cells including the Cetuximab resistant cell line HCT116 using a colony formation assay. Dose distribution was measured in sections from xenografts grown in nude mice using autoradiography. Results: KDis for the complex binding to EGFR on MDA-MB-468 cells was 20 nM. Loss of cell associated [177Lu] activity was biphasic with loss of about 50% of activity in about 4 h. Remaining activity dissociated over a period of about 4 days. HCT8 and MDA-MB-468, but not HCT116 cells were sensitive to the growth inhibitory effect of Cetuximab. However, treatment with Cetuximab-targeted [177Lu]-AuNPs inhibited colony formation in all 3 cell lines. Dose distribution across sections from xenografts was found to demonstrate a co-efficient of variation of 15%. Conclusion: Cetuximab-targeted [177Lu]-AuNPs demonstrate high affinity for EGFR and could be an effective treatment for Cetuximab-resistant colorectal cancer cells. A strategy involving pre-treatment with receptor targeted[177Lu] to improve RIT therapeutic ratios has the potential to enhance clinical outcomes.

Published
2021
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19. Piezoelectric field effects on electron density in a d-doped AlGaAs/InyGa1-yAs/GaAs pseudomorphic HEMT.

Author

Bouzaïene, L., Rekaya, S., Sghaier, H., Sfaxi, L., and Maaref, H.

Subjects
PIEZOELECTRICITY, HETEROSTRUCTURES, ELECTRON distribution, LOW temperatures, SEMICONDUCTORS, CRYSTALS
Abstract

We have calculated the low-temperature electron density in a d-doped AlGaAs/InGaAs/GaAs heterostructure in the presence of a piezoelectric field. Growth of a strained InGaAs layer on (N11) GaAs substrates causes a piezoelectric field to be built into the quantum well of a pseudomorphic high electron mobility transistor (HEMT). The presence of this field modifies the electronic properties of strained-layer heterostructures. A self-consistent analysis is made of these d-doping systems to solve simultaneously the Schrödinger and Poisson equations taking into account exchange-correlation and strain effects. Thus, we have found the confining potential, the electron density, the subband energies, the eigenenvelope wavefunctions, and the Fermi-energy level in the quantum well. We have studied the effects of the InGaAs channel width and the indium composition on the electron density. Our results show a larger increase of the electron density when the calculated value is for a (111) GaAs substrate rather than for equivalent (001) and (311) substrates. We have also investigated the effects of the environmental Al concentration seen by the Si d-doped on the electron density. [ABSTRACT FROM AUTHOR]

Published
2005
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20. Influence of high-index GaAs substrates on the 2D electron density of δ-doped pHEMT with an additional InxGa1-xAs (x > 0.15) thin layer embedded in the channel

Author

Bouzaïene, L., Rekaya, S., Sfaxi, L., and Maaref, H.

Abstract

In this paper, we report the theoretical predictions of a high-index GaAs substrate ((111)A and (311)A) on the subband structure and thereafter on the 2D electron density of Si δ-doped Al0.33Ga0.67As/In0.15Ga0.85As/GaAs pseudomorphic high electron mobility transistor (pHEMT) with an additional InxGa1-xAs (x> 0.15) thin layer embedded in the channel. We have seen that the electronic structures and the electron density are quite sensitive to the additional InxGa1-xAs (x> 0.15) layer thickness, indium composition and to their position in the channel. An optimal position of the additional InxGa1-xAs layer was found to be corresponding to the maximum of the first eigen envelope function for the different growth directions. We report that the optimised electron density is obtained in the structure grown on (111)A GaAs substrate. In this case the electron transfer is significantly higher than those grown on (311)A and (001) GaAs substrates respectively.

Published
2005
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21. Influence of high-index GaAs substrates on the 2D electron density of <formula notation="TeX">$\delta $</formula>-doped pHEMT with an additional In<formula notation="TeX">$\mathsf{_{x}Ga_{1-x}As ~(x > 0.15)}$</formula> thin layer embedded in the channel

Author

Bouzaïene, L., Rekaya, S., Sfaxi, L., and Maaref, H.

Abstract

In this paper, we report the theoretical predictions of a high-index GaAs substrate ((111)A and (311)A) on the subband structure and thereafter on the 2D electron density of Si $\delta $-doped Al$_{0.33}$Ga$_{0.67}$As/In$_{0.15}$Ga$_{0.85}$As/GaAs pseudomorphic high electron mobility transistor (pHEMT) with an additional In$_{x}$Ga$_{1-x}$As ($x > 0.15$) thin layer embedded in the channel. We have seen that the electronic structures and the electron density are quite sensitive to the additional In$_{x}$Ga$_{1-x}$As ($x > 0.15$) layer thickness, indium composition and to their position in the channel. An optimal position of the additional In$_{x}$Ga$_{1-x}$As layer was found to be corresponding to the maximum of the first eigen envelope function for the different growth directions. We report that the optimised electron density is obtained in the structure grown on (111)A GaAs substrate. In this case the electron transfer is significantly higher than those grown on (311)A and (001) GaAs substrates respectively.

Published
2005

22. 46th Medical Maghrebian Congress. November 9-10, 2018. Tunis

Author

Alami Aroussi, A., Fouad, A., Omrane, A., Razzak, A., Aissa, A., Akkad, A., Amraoui, A., Aouam, A., Arfaoui, A., Belkouchi, A., Ben Chaaben, A., Ben Cheikh, A., Ben Khélifa, A., Ben Mabrouk, A., Benhima, A., Bezza, A., Bezzine, A., Bourrahouat, A., Chaieb, A., Chakib, A., Chetoui, A., Daoudi, A., Ech-Chenbouli, A., Gaaliche, A., Hassani, A., Kassimi, A., Khachane, A., Labidi, A., Lalaoui, A., Masrar, A., Mchachi, A., Nakhli, A., Ouakaa, A., Siati, A., Toumi, A., Zaouali, A., Condé, A. Y., Haggui, A., Belaguid, A., abdelkader jalil el hangouche, Gharbi, A., Mahfoudh, A., Bouzouita, A., Aissaoui, A., Ben Hamouda, A., Hedhli, A., Ammous, A., Bahlous, A., Ben Halima, A., Belhadj, A., Blel, A., Brahem, A., Banasr, A., Meherzi, A., Saadi, A., Sellami, A., Turki, A., Ben Miled, A., Ben Slama, A., Daib, A., Zommiti, A., Chadly, A., Jmaa, A., Mtiraoui, A., Ksentini, A., Methnani, A., Zehani, A., Kessantini, A., Farah, A., Mankai, A., Mellouli, A., Touil, A., Hssine, A., Ben Safta, A., Derouiche, A., Jmal, A., Ferjani, A., Djobbi, A., Dridi, A., Aridhi, A., Bahdoudi, A., Ben Amara, A., Benzarti, A., Ben Slama, A. Y., Oueslati, A., Soltani, A., Chadli, A., Aloui, A., Belghuith Sriha, A., Bouden, A., Laabidi, A., Mensi, A., Sabbek, A., Zribi, A., Green, A., Ben Nasr, A., Azaiez, A., Yeades, A., Belhaj, A., Mediouni, A., Sammoud, A., Slim, A., Amine, B., Chelly, B., Jatik, B., Lmimouni, B., Daouahi, B., Ben Khelifa, B., Louzir, B., Dorra, A., Dhahri, B., Ben Nasrallah, C., Chefchaouni, C., Konzi, C., Loussaief, C., Makni, C., Dziri, C., Bouguerra, C., Kays, C., Zedini, C., Dhouha, C., Mohamed, C., Aichaouia, C., Dhieb, C., Fofana, D., Gargouri, D., Chebil, D., Issaoui, D., Gouiaa, D., Brahim, D., Essid, D., Jarraya, D., Trad, D., Ben Hmida, E., Sboui, E., Ben Brahim, E., Baati, E., Talbi, E., Chaari, E., Hammami, E., Ghazouani, E., Ayari, F., Ben Hariz, F., Bennaoui, F., Chebbi, F., Chigr, F., Guemira, F., Harrar, F., Benmoula, F. Z., Ouali, F. Z., Maoulainine, F. M. R., Bouden, F., Fdhila, F., Améziani, F., Bouhaouala, F., Charfi, F., Chermiti Ben Abdallah, F., Hammemi, F., Jarraya, F., Khanchel, F., Ourda, F., Sellami, F., Trabelsi, F., Yangui, F., Fekih Romdhane, F., Mellouli, F., Nacef Jomli, F., Mghaieth, F., Draiss, G., Elamine, G., Kablouti, G., Touzani, G., Manzeki, G. B., Garali, G., Drissi, G., Besbes, G., Abaza, H., Azzouz, H., Said Latiri, H., Rejeb, H., Ben Ammar, H., Ben Brahim, H., Ben Jeddi, H., Ben Mahjouba, H., Besbes, H., Dabbebi, H., Douik, H., El Haoury, H., Elannaz, H., Elloumi, H., Hachim, H., Iraqi, H., Kalboussi, H., Khadhraoui, H., Khouni, H., Mamad, H., Metjaouel, H., Naoui, H., Zargouni, H., Elmalki, H. O., Feki, H., Haouala, H., Jaafoura, H., Drissa, H., Mizouni, H., Kamoun, H., Ouerda, H., Zaibi, H., Chiha, H., Saibi, H., Skhiri, H., Boussaffa, H., Majed, H., Blibech, H., Daami, H., Harzallah, H., Rkain, H., Ben Massoud, H., Jaziri, H., Ben Said, H., Ayed, H., Harrabi, H., Chaabouni, H., Ladida Debbache, H., Harbi, H., Yacoub, H., Abroug, H., Ghali, H., Kchir, H., Msaad, H., Manai, H., Riahi, H., Bousselmi, H., Limem, H., Aouina, H., Jerraya, H., Ben Ayed, H., Chahed, H., Snéne, H., Lahlou Amine, I., Nouiser, I., Ait Sab, I., Chelly, I., Elboukhani, I., Ghanmi, I., Kallala, I., Kooli, I., Bouasker, I., Fetni, I., Bachouch, I., Bouguecha, I., Chaabani, I., Gazzeh, I., Samaali, I., Youssef, I., Zemni, I., Bachouche, I., Bouannene, I., Kasraoui, I., Laouini, I., Mahjoubi, I., Maoudoud, I., Riahi, I., Selmi, I., Tka, I., Hadj Khalifa, I., Mejri, I., Béjia, I., Bellagha, J., Boubaker, J., Daghfous, J., Dammak, J., Hleli, J., Ben Amar, J., Jedidi, J., Marrakchi, J., Kaoutar, K., Arjouni, K., Ben Helel, K., Benouhoud, K., Rjeb, K., Imene, K., Samoud, K., El Jeri, K., Abid, K., Chaker, K., Bouzghaîa, K., Kamoun, K., Zitouna, K., Oughlani, K., Lassoued, K., Letaif, K., Hakim, K., Cherif Alami, L., Benhmidoune, L., Boumhil, L., Bouzgarrou, L., Dhidah, L., Ifrine, L., Kallel, L., Merzougui, L., Errguig, L., Mouelhi, L., Sahli, L., Maoua, M., Rejeb, M., Ben Rejeb, M., Bouchrik, M., Bouhoula, M., Bourrous, M., Bouskraoui, M., El Belhadji, M., Essakhi, M., Essid, M., Gharbaoui, M., Haboub, M., Iken, M., Krifa, M., Lagrine, M., Leboyer, M., Najimi, M., Rahoui, M., Sabbah, M., Sbihi, M., Zouine, M., Chefchaouni, M. C., Gharbi, M. H., El Fakiri, M. M., Tagajdid, M. R., Shimi, M., Touaibia, M., Jguirim, M., Barsaoui, M., Belghith, M., Ben Jmaa, M., Koubaa, M., Tbini, M., Boughdir, M., Ben Salah, M., Ben Fraj, M., Ben Halima, M., Ben Khalifa, M., Bousleh, M., Limam, M., Mabrouk, M., Mallouli, M., Rebeii, M., Ayari, M., Belhadj, M., Ben Hmida, M., Boughattas, M., Drissa, M., El Ghardallou, M., Fejjeri, M., Hamza, M., Jaidane, M., Jrad, M., Kacem, M., Mersni, M., Mjid, M., Serghini, M., Triki, M., Ben Abbes, M., Boussaid, M., Gharbi, M., Hafi, M., Slama, M., Trigui, M., Taoueb, M., Chakroun, M., Ben Cheikh, M., Chebbi, M., Hadj Taieb, M., Ben Khelil, M., Hammami, M., Khalfallah, M., Ksiaa, M., Mechri, M., Mrad, M., Sboui, M., Bani, M., Hajri, M., Mellouli, M., Allouche, M., Mesrati, M. A., Mseddi, M. A., Amri, M., Bejaoui, M., Bellali, M., Ben Amor, M., Ben Dhieb, M., Ben Moussa, M., Chebil, M., Cherif, M., Fourati, M., Kahloul, M., Khaled, M., Machghoul, M., Mansour, M., Abdesslem, M. M., Ben Chehida, M. A., Chaouch, M. A., Essid, M. A., Meddeb, M. A., Gharbi, M. C., Elleuch, M. H., Loueslati, M. H., Sboui, M. M., Mhiri, M. N., Kilani, M. O., Ben Slama, M. R., Charfi, M. R., Nakhli, M. S., Mourali, M. S., El Asli, M. S., Lamouchi, M. T., Cherti, M., Khadhraoui, M., Bibi, M., Hamdoun, M., Kassis, M., Touzi, M., Ben Khaled, M., Fekih, M., Khemiri, M., Ouederni, M., Hchicha, M., Ben Attia, M., Yahyaoui, M., Ben Azaiez, M., Bousnina, M., Ben Jemaa, M., Ben Yahia, M., Daghfous, M., Haj Slimen, M., Assidi, M., Belhadj, N., Ben Mustapha, N., El Idrissislitine, N., Hikki, N., Kchir, N., Mars, N., Meddeb, N., Ouni, N., Rada, N., Rezg, N., Trabelsi, N., Bouafia, N., Haloui, N., Benfenatki, N., Bergaoui, N., Yomn, N., Maamouri, N., Mehiri, N., Siala, N., Beltaief, N., Aridhi, N., Sidaoui, N., Walid, N., Mechergui, N., Mnif, N., Ben Chekaya, N., Bellil, N., Dhouib, N., Achour, N., Kaabar, N., Mrizak, N., Chaouech, N., Hasni, N., Issaoui, N., Ati, N., Balloumi, N., Haj Salem, N., Ladhari, N., Akif, N., Liani, N., Hajji, N., Trad, N., Elleuch, N., Marzouki, N. E. H., Larbi, N., M Barek, N., Rebai, N., Bibani, N., Ben Salah, N., Belmaachi, O., Elmaalel, O., Jlassi, O., Mihoub, O., Ben Zaid, O., Bouallègue, O., Bousnina, O., Bouyahia, O., El Maalel, O., Fendri, O., Azzabi, O., Borgi, O., Ghdes, O., Ben Rejeb, O., Rachid, R., Abi, R., Bahiri, R., Boulma, R., Elkhayat, R., Habbal, R., Tamouza, R., Jomli, R., Ben Abdallah, R., Smaoui, R., Debbeche, R., Fakhfakh, R., El Kamel, R., Gargouri, R., Jouini, R., Nouira, R., Fessi, R., Bannour, R., Ben Rabeh, R., Kacem, R., Khmakhem, R., Ben Younes, R., Karray, R., Cheikh, R., Ben Malek, R., Ben Slama, R., Kouki, R., Baati, R., Bechraoui, R., Fradi, R., Lahiani, R., Ridha, R., Zainine, R., Kallel, R., Rostom, S., Ben Abdallah, S., Ben Hammamia, S., Benchérifa, S., Benkirane, S., Chatti, S., El Guedri, S., El Oussaoui, S., Elkochri, S., Elmoussaoui, S., Enbili, S., Gara, S., Haouet, S., Khammeri, S., Khefecha, S., Khtrouche, S., Macheghoul, S., Mallouli, S., Rharrit, S., Skouri, S., Helali, S., Boulehmi, S., Abid, S., Naouar, S., Zelfani, S., Ben Amar, S., Ajmi, S., Braiek, S., Yahiaoui, S., Ghezaiel, S., Ben Toumia, S., Thabeti, S., Daboussi, S., Ben Abderahman, S., Rhaiem, S., Ben Rhouma, S., Rekaya, S., Haddad, S., Kammoun, S., Merai, S., Mhamdi, S., Ben Ali, R., Gaaloul, S., Ouali, S., Taleb, S., Zrour, S., Hamdi, S., Zaghdoudi, S., Ammari, S., Ben Abderrahim, S., Karaa, S., Maazaoui, S., Saidani, S., Stambouli, S., Mokadem, S., Boudiche, S., Zaghbib, S., Ayedi, S., Jardek, S., Bouselmi, S., Chtourou, S., Manoubi, S., Bahri, S., Halioui, S., Jrad, S., Mazigh, S., Ouerghi, S., Toujani, S., Fenniche, S., Aboudrar, S., Meriem Amari, S., Karouia, S., Bourgou, S., Halayem, S., Rammeh, S., Yaïch, S., Ben Nasrallah, S., Chouchane, S., Ftini, S., Makni, S., Miri, S., Saadi, S., Manoubi, S. A., Khalfallah, T., Mechergui, T., Dakka, T., Barhoumi, T., M Rad, T. E. B., Ajmi, T., Dorra, T., Ouali, U., Hannachi, W., Ferjaoui, W., Aissi, W., Dahmani, W., Dhouib, W., Koubaa, W., Zhir, W., Gheriani, W., Arfa, W., Dougaz, W., Sahnoun, W., Naija, W., Sami, Y., Bouteraa, Y., Elhamdaoui, Y., Hama, Y., Ouahchi, Y., Guebsi, Y., Nouira, Y., Daly, Y., Mahjoubi, Y., Mejdoub, Y., Mosbahi, Y., Said, Y., Zaimi, Y., Zgueb, Y., Dridi, Y., Mesbahi, Y., Gharbi, Y., Hellal, Y., Hechmi, Z., Zid, Z., Elmouatassim, Z., Ghorbel, Z., Habbadi, Z., Marrakchi, Z., Hidouri, Z., Abbes, Z., Ouhachi, Z., Khessairi, Z., Khlayfia, Z., Mahjoubi, Z., and Moatemri, Z.

23. Sideroblastic anemia in children: challenges in diagnosis and management in three cases.

Author

Rekaya S, Ben Fraj I, Hamdi R, Ben Taieb A, Merdassi A, Jouini H, Zarrouk H, Zaiter I, Kouki R, Bejaoui M, Mellouli F, Ben Khaled M, and Ouederni M

Abstract

Sideroblastic anemias (SAs) represent a heterogeneous group of rare hematological disorders characterized by iron accumulation in mitochondria of erythroblasts with ineffective erythropoiesis. SAs are categorized into acquired and congenital forms. Acquired, secondary, and clonal, SA is rare in pediatric populations. Congenital SA (CSA) is classified into syndromic and non-syndromic forms. Herein, we describe three cases of pediatric patients with SA. The diagnosis of SA was based on the presence of type 3 sideroblasts on BM aspirate smear (greater than 15%) and genetic tests. In the first case, the diagnosis of myelodysplastic syndrome with ring sideroblasts (MDS-RS) with somatic SF3B1 mutation was made at the age of 11 years. A whole exome sequencing did not reveal any germinal predisposition for MDS. A wait-and-see strategy was adopted. After one year- of follow-up, no blood transfusion was needed and no further cytopenia occurred. The two other children had presented anemia at an early age and were diagnosed with CSA. The first case was a girl with SCL25A38 gene mutation. For the second one, the diagnosis of aminolevulinic acid synthase 2 deficiency was considered the most plausible given the family history and the favourable response to pyridoxine. Iron overload occurred in both patients with CSA, requiring chelation therapy. In conclusion, Perls' stain remains a valuable tool for guiding the diagnosis of unexplained anemia in pediatric patients. Genetic testing is crucial for the characterization of congenital sideroblastic anemias. The incidence of myeloid neoplasms with ring sideroblasts is exceptional in children, and the long-term prognosis remains undefined., Competing Interests: Declarations. Ethical approval: Informed consent was obtained from the patients for the publication of any potentially identifiable data included in this article. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Published
2025
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25. Incidence and risk factors for osteonecrosis of the femoral head in five hundred and ten sickle cell disease paediatric patients.

Author

Ouederni M, Rouag H, Ben Fraj I, Rekaya S, Kouki R, Lamouchi T, Zaiter I, Mellouli F, Bejaoui M, and Ben Khaled M

Subjects
Humans, Child, Retrospective Studies, Incidence, Femur Head, Risk Factors, Volatile Organic Compounds, Anemia, Sickle Cell complications, Anemia, Sickle Cell epidemiology, Femur Head Necrosis etiology, Femur Head Necrosis complications
Abstract

Purpose: Osteonecrosis of the femoral head (ONFH) is a degenerative and progressive disorder that mainly affects people with sickle cell disease (SCD). Herein, we aimed to search for a better understanding of markers that can act as risk factors for ONFH in patients with SCD., Methods: We conducted a retrospective study including 510 SCD patients followed over 23 years. Patients were divided into the ONFH group and the no-ONHF control group. Univariate and multivariate logistic regression analyses were performed to identify risk factors., Results: Among 510 SCD patients, 41(8%) were diagnosed with ONFH at a mean age of 167 months ± 64 (72-288). The cumulative incidence of ONHF increased from 2.3% at ten years to 18.3% at 20 years of age. The radiological grade 3 ONHF was predominant. No significant differences in sex, age at diagnosis of SCD, and Hb genotype were found between groups. The patient age and the time since diagnosis of SCD were statistically higher in patients with ONHF in univariate and multivariate analysis. ONHF was also associated with higher creatinine level (p = 0.001) lower LDH level (p = 0.006), and higher number of vaso-occlusive crisis (VOC)/patient/year (p < 0.001). The cumulative incidence of ONHF in patients having more than 3 VOC/year was significantly higher (43% versus 18.9% at 20 years, p < 0.001). In addition, infections, gallstones, growth delay, delayed initiation of hydroxyurea, and a higher transfusion rate were significantly associated with ONFH., Conclusion: These findings confirm that ONFH is closely related to the age, severity, and duration of SCD. Better management of this disease prevents acute and chronic complications, and early screening of the ONFH as soon as the first signs of the severity of the disease are detected provides a better functional prognosis., (© 2023. The Author(s) under exclusive licence to SICOT aisbl.)

Published
2023
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26. Clinical features and predictors of osteoarticular manifestations in common variable immunodeficiency.

Author

Ben Khaled M, Merdassi A, Rekaya S, Fraj IB, Lamouchi T, Zaiter I, Kouki R, Bejaoui M, Mellouli F, and Ouederni M

Subjects
Humans, Child, Retrospective Studies, Hepatomegaly, Diarrhea, Body Weight, Autoimmunity, Common Variable Immunodeficiency complications, Common Variable Immunodeficiency diagnosis, Common Variable Immunodeficiency epidemiology, Iron Deficiencies
Abstract

Introduction: This study aimed to assess osteoarticular manifestations in patients with common variable immunodeficiency (CIVD) and to identify the predictive factors., Methods: This was a retrospective and prognostic study conducted in the pediatrics: immuno-hematology and stem cell transplantation department, including patients who fit the definition of CVID. A Cox model analysis was used to identify predictive factors., Results: A total of 36 patients were enrolled. Osteoarticular involvement was noted in 15 patients (42%) with a cumulative incidence of 90% after a median follow-up of 25 years. Non-infectious manifestations were reported in 14 patients (39%). The cumulative risk of inflammatory or autoimmune osteoarticular etiology was 74%. Well-characterized rheumatic diseases were retained in six patients and unlabeled autoimmune or inflammatory mechanism in five cases. Bone mineral density revealed osteoporosis in six cases leading to a cumulative risk of degenerative complications of 72%. The cumulative incidence of infectious complications was 17%. In multivariate analysis, predictors of osteoarticular complications were low body weight (HR = 8.67, CI: 1.496-50.278, p = 0.01) and hepatomegaly at diagnosis (HR = 6.2, CI: 1.537-25.075, p = 0.01). Reduced CD4 cells rate < 600 cells/mm 3 and hepatomegaly were predictors of autoimmune or inflammatory complications, while chronic diarrhea and iron deficiency were associated with degenerative manifestations., Conclusions: Osteoarticular manifestations have emerged as a real health problem for CVID patients. Risk increases with low body weight, hepatomegaly, chronic diarrhea, iron deficiency, and CD4 cells rate under 600 cell/mm 3 . Elucidating the mechanisms of these complications in CVID is important for developing preventive strategies. Key Points • This retrospective and prognostic study described the clinical characteristics of osteoarticular manifestations in 36 patients with CVID to ensure better recognition and understanding of this association by clinicians. • Identification of predictive factors of osteoarticular complications according to its etiology is crucial to establish appropriate, optimal and early management of patients at risk., (© 2023. The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR).)

Published
2023
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27. Long-Term Observational Study of Chronic Granulomatous Disease About 41 Patients From Tunisia and Comparison to Other Long-Term Follow-Up Studies.

Author

Mellouli F, Ksouri H, Lajhouri M, Ben Khaled M, Rekaya S, Ben Fraj E, Ouederni M, Barbouche MR, and Bejaoui M

Subjects
Child, Preschool, Follow-Up Studies, Humans, Leukocytes, Mononuclear, Quality of Life, Tunisia epidemiology, Anti-Infective Agents, Granulomatous Disease, Chronic complications, Granulomatous Disease, Chronic diagnosis
Abstract

Chronic granulomatous disease (CGD) is an inherited autosomal recessive or X-Linked primitive immunodeficiency (PID), due to a defective nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex impairing anti-infectious and anti-inflammatory role of peripheral blood mononuclear cells. It is characterized by severe bacterial and fungal infections and by excessive inflammation leading to granulomatous complications. This work was made over a period of 34 years on 41 Tunisian patients suffering from CGD. Cumulative follow-up of patients was 2768.5 months, median 31 months. Survival was studied by survival curves according to Kaplan-Meier method. Lymphatic nodes, pulmonary and cutaneous infections predominate as revealing manifestations and as infectious events during patients' monitoring. At study end 12 patients died mainly of invasive pulmonary aspergillosis and septicemia. Median age of death was 30 months. CGD remains compatible with a decent quality of life. Early diagnosis, anti-infectious prophylaxis, and initiation of adequate management, as soon as complication is perceived, promote pretty good evolution.

Published
2022
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28. Containment of Local COVID-19 Outbreak Among Hematopoietic Stem Cell Transplant Recipients and Healthcare Workers in a Pediatric Stem Cell Unit.

Author

Ouederni M, Rekaya S, Bouabdallah O, Ben Fradj I, Kouki R, Chebbi Y, Ammar SB, Lamouchi T, Lachiheb A, Zekri N, Laajili S, Zaiter I, Hamzaoui A, Bejaoui M, Mellouli F, Achour W, and Ben Khaled M

Subjects
COVID-19 therapy, Disease Outbreaks, Hematopoietic Stem Cell Transplantation, Hospitals, Pediatric, Humans, Transplant Recipients, Tunisia epidemiology, COVID-19 epidemiology, Health Personnel, SARS-CoV-2 physiology
Published
2021
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29. Prevalence and predictive factors of splenic sequestration crisis among 423 pediatric patients with sickle cell disease in Tunisia.

Author

Ben Khaled M, Ouederni M, Mankai Y, Rekaya S, Ben Fraj I, Dhouib N, Kouki R, Mellouli F, and Bejaoui M

Subjects
Acute Disease, Anemia, Sickle Cell diagnosis, Biomarkers, Child, Child, Preschool, Female, Humans, Incidence, Infant, Male, Phenotype, Prevalence, Prognosis, Public Health Surveillance, Risk, Splenic Diseases diagnosis, Splenomegaly, Tunisia epidemiology, Anemia, Sickle Cell complications, Anemia, Sickle Cell epidemiology, Splenic Diseases epidemiology, Splenic Diseases etiology
Abstract

This study was aimed to identify the predictors of splenic sequestration crisis (SSC) among pediatric patients with sickle cell disease (SCD). This prognosis study was carried out in the pediatric immuno-hematology unit, over 20 years (1998 to 2017), enrolling patients with SCD. The cox model was used in multivariate analysis. Among 423 patients with SCD (240 S/S phenotype, 128 S/B0, 30 S/B+, 14 S/O arab and 11 S/C), 150(35.4%) had at least one episode of SSC. The average age of patients at the first episode was 48.3 months ± 32.4(2-168). Recurrence of SSC was observed in 117 patients (78%). Spleen size ≥3 cm at baseline was the strongest predictor of SSC occurrence (HR = 7.27, CI: 4.01-13.20, p = 0.05) and recurrence (HR = 6.37, CI: 1,46-27.83, p = 0.01). Pallor revealing the disease, age at onset of symptoms <24 months and reticulocytosis ≥300,000/mm 3 increased the risk of SSC. Pain crisis revealing the disease as well as neutrophilia was associated with a lower risk of SSC. In conclusion, this study confirmed the high prevalence of SSC in SCD and the high frequency of recurrence after a first episode. The SSC occurrence and recurrence were intimately linked to the presence of splenomegaly, chronic pallor revealing the disease as well as reticulocytosis., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Published
2020
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30. Predictors of autoimmune hemolytic anemia in beta-thalassemia patients with underlying red blood cells autoantibodies.

Author

Khaled MB, Ouederni M, Sahli N, Dhouib N, Abdelaziz AB, Rekaya S, Kouki R, Kaabi H, Slama H, Mellouli F, and Bejaoui M

Subjects
ABO Blood-Group System, Adult, Blood Transfusion methods, Coombs Test, Female, Humans, Leukocyte Reduction Procedures, Longitudinal Studies, Male, Medical History Taking, Middle Aged, Prognosis, Risk Factors, Splenectomy, Tunisia, beta-Thalassemia surgery, beta-Thalassemia therapy, Anemia, Hemolytic, Autoimmune etiology, Autoantibodies blood, Erythrocytes immunology, beta-Thalassemia complications
Abstract

In beta-thalassemia patients, erythrocyte autoantibodies can remain silent or lead to Autoimmune Hemolytic Anemia (AIHA).The aim of this study was to identify predictors of AIHA in beta-thalassemia patients with positive Direct Antiglobulin Test (DAT), in Tunisia. This longitudinal prognosis study was carried out on beta-thalassemia patients with a positive confirmed DAT. Predictors of AIHA were identified the Kaplan-Meier method. A Cox model analysis was used to identify independent predictors. Among 385 beta thalassemia patients, 87 developed positive DAT (22.6%). Autoimmune hemolytic anemia was occurred in 25 patients. Multivariate analysis showed that AIHA was independently associated with beta-thalassemia intermedia and similar family history of AIHA. Splenectomy in patients with positive DAT was independently associated with an increased risk of AIHA (HR = 6.175, CI: 2.049-18.612, p < 0.001). The risk of developing AIHA was higher during the first 72 transfusions. Autoimmune hemolytic anemia was significantly associated with polyspecific DAT (anti-complement and anti-IgG), blood group AB and prior alloimmunization. Whereas transfusion by phenotypic and leukoreduced blood was a protective factor. In summary, splenectomy after autoimmunization, prior alloimmunization, DAT specificity (IgG with complement), thalassemia intermedia, AB blood group and family history of AIHA were strongly associated with AIHA. Leukoreduced blood transfusion had a proven preventive role., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Published
2019
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31. 46th Medical Maghrebian Congress. November 9-10, 2018. Tunis.

Author

Alami Aroussi A, Fouad A, Omrane A, Razzak A, Aissa A, Akkad A, Amraoui A, Aouam A, Arfaoui A, Belkouchi A, Ben Chaaben A, Ben Cheikh A, Ben Khélifa A, Ben Mabrouk A, Benhima A, Bezza A, Bezzine A, Bourrahouat A, Chaieb A, Chakib A, Chetoui A, Daoudi A, Ech-Chenbouli A, Gaaliche A, Hassani A, Kassimi A, Khachane A, Labidi A, Lalaoui A, Masrar A, McHachi A, Nakhli A, Ouakaa A, Siati A, Toumi A, Zaouali A, Condé AY, Haggui A, Belaguid A, El Hangouche AJ, Gharbi A, Mahfoudh A, Bouzouita A, Aissaoui A, Ben Hamouda A, Hedhli A, Ammous A, Bahlous A, Ben Halima A, Belhadj A, Bezzine A, Blel A, Brahem A, Banasr A, Meherzi A, Saadi A, Sellami A, Turki A, Ben Miled A, Ben Slama A, Daib A, Zommiti A, Chadly A, Jmaa A, Mtiraoui A, Ksentini A, Methnani A, Zehani A, Kessantini A, Farah A, Mankai A, Mellouli A, Zaouali A, Touil A, Hssine A, Ben Safta A, Derouiche A, Jmal A, Ferjani A, Djobbi A, Dridi A, Aridhi A, Bahdoudi A, Ben Amara A, Benzarti A, Ben Slama AY, Oueslati A, Soltani A, Chadli A, Aloui A, Belghuith Sriha A, Bouden A, Laabidi A, Mensi A, Ouakaa A, Sabbek A, Zribi A, Green A, Ben Nasr A, Azaiez A, Yeades A, Belhaj A, Mediouni A, Sammoud A, Slim A, Amine B, Chelly B, Jatik B, Lmimouni B, Daouahi B, Ben Khelifa B, Louzir B, Dorra A, Dhahri B, Ben Nasrallah C, Chefchaouni C, Konzi C, Loussaief C, Makni C, Dziri C, Bouguerra C, Kays C, Zedini C, Dhouha C, Mohamed C, Aichaouia C, Dhieb C, Fofana D, Gargouri D, Chebil D, Issaoui D, Gouiaa D, Brahim D, Essid D, Jarraya D, Trad D, Ben Hmida E, Sboui E, Ben Brahim E, Baati E, Talbi E, Chaari E, Hammami E, Ghazouani E, Ayari F, Ben Hariz F, Bennaoui F, Chebbi F, Chigr F, Guemira F, Harrar F, Benmoula FZ, Ouali FZ, Maoulainine FMR, Bouden F, Fdhila F, Améziani F, Bouhaouala F, Charfi F, Chermiti Ben Abdallah F, Hammemi F, Jarraya F, Khanchel F, Ourda F, Sellami F, Trabelsi F, Yangui F, Fekih Romdhane F, Mellouli F, Nacef Jomli F, Mghaieth F, Draiss G, Elamine G, Kablouti G, Touzani G, Manzeki GB, Garali G, Drissi G, Besbes G, Abaza H, Azzouz H, Said Latiri H, Rejeb H, Ben Ammar H, Ben Brahim H, Ben Jeddi H, Ben Mahjouba H, Besbes H, Dabbebi H, Douik H, El Haoury H, Elannaz H, Elloumi H, Hachim H, Iraqi H, Kalboussi H, Khadhraoui H, Khouni H, Mamad H, Metjaouel H, Naoui H, Zargouni H, Elmalki HO, Feki H, Haouala H, Jaafoura H, Drissa H, Mizouni H, Kamoun H, Ouerda H, Zaibi H, Chiha H, Kamoun H, Saibi H, Skhiri H, Boussaffa H, Majed H, Blibech H, Daami H, Harzallah H, Rkain H, Ben Massoud H, Jaziri H, Ben Said H, Ayed H, Harrabi H, Chaabouni H, Ladida Debbache H, Harbi H, Yacoub H, Abroug H, Ghali H, Kchir H, Msaad H, Ghali H, Manai H, Riahi H, Bousselmi H, Limem H, Aouina H, Jerraya H, Ben Ayed H, Chahed H, Snéne H, Lahlou Amine I, Nouiser I, Ait Sab I, Chelly I, Elboukhani I, Ghanmi I, Kallala I, Kooli I, Bouasker I, Fetni I, Bachouch I, Bouguecha I, Chaabani I, Gazzeh I, Samaali I, Youssef I, Zemni I, Bachouche I, Youssef I, Bouannene I, Kasraoui I, Laouini I, Mahjoubi I, Maoudoud I, Riahi I, Selmi I, Tka I, Hadj Khalifa I, Mejri I, Béjia I, Bellagha J, Boubaker J, Daghfous J, Dammak J, Hleli J, Ben Amar J, Jedidi J, Marrakchi J, Kaoutar K, Arjouni K, Ben Helel K, Benouhoud K, Rjeb K, Imene K, Samoud K, El Jeri K, Abid K, Chaker K, Abid K, Bouzghaîa K, Kamoun K, Zitouna K, Oughlani K, Lassoued K, Letaif K, Hakim K, Cherif Alami L, Benhmidoune L, Boumhil L, Bouzgarrou L, Dhidah L, Ifrine L, Kallel L, Merzougui L, Errguig L, Mouelhi L, Sahli L, Maoua M, Rejeb M, Ben Rejeb M, Bouchrik M, Bouhoula M, Bourrous M, Bouskraoui M, El Belhadji M, El Belhadji M, Essakhi M, Essid M, Gharbaoui M, Haboub M, Iken M, Krifa M, Lagrine M, Leboyer M, Najimi M, Rahoui M, Sabbah M, Sbihi M, Zouine M, Chefchaouni MC, Gharbi MH, El Fakiri MM, Tagajdid MR, Shimi M, Touaibia M, Jguirim M, Barsaoui M, Belghith M, Ben Jmaa M, Koubaa M, Tbini M, Boughdir M, Ben Salah M, Ben Fraj M, Ben Halima M, Ben Khalifa M, Bousleh M, Limam M, Mabrouk M, Mallouli M, Rebeii M, Ayari M, Belhadj M, Ben Hmida M, Boughattas M, Drissa M, El Ghardallou M, Fejjeri M, Hamza M, Jaidane M, Jrad M, Kacem M, Mersni M, Mjid M, Sabbah M, Serghini M, Triki M, Ben Abbes M, Boussaid M, Gharbi M, Hafi M, Slama M, Trigui M, Taoueb M, Chakroun M, Ben Cheikh M, Chebbi M, Hadj Taieb M, Kacem M, Ben Khelil M, Hammami M, Khalfallah M, Ksiaa M, Mechri M, Mrad M, Sboui M, Bani M, Hajri M, Mellouli M, Allouche M, Mesrati MA, Mseddi MA, Amri M, Bejaoui M, Bellali M, Ben Amor M, Ben Dhieb M, Ben Moussa M, Chebil M, Cherif M, Fourati M, Kahloul M, Khaled M, Machghoul M, Mansour M, Abdesslem MM, Ben Chehida MA, Chaouch MA, Essid MA, Meddeb MA, Gharbi MC, Elleuch MH, Loueslati MH, Sboui MM, Mhiri MN, Kilani MO, Ben Slama MR, Charfi MR, Nakhli MS, Mourali MS, El Asli MS, Lamouchi MT, Cherti M, Khadhraoui M, Bibi M, Hamdoun M, Kassis M, Touzi M, Ben Khaled M, Fekih M, Khemiri M, Ouederni M, Hchicha M, Kassis M, Ben Attia M, Yahyaoui M, Ben Azaiez M, Bousnina M, Ben Jemaa M, Ben Yahia M, Daghfous M, Haj Slimen M, Assidi M, Belhadj N, Ben Mustapha N, El Idrissislitine N, Hikki N, Kchir N, Mars N, Meddeb N, Ouni N, Rada N, Rezg N, Trabelsi N, Bouafia N, Haloui N, Benfenatki N, Bergaoui N, Yomn N, Ben Mustapha N, Maamouri N, Mehiri N, Siala N, Beltaief N, Aridhi N, Sidaoui N, Walid N, Mechergui N, Mnif N, Ben Chekaya N, Bellil N, Dhouib N, Achour N, Kaabar N, Mrizak N, Mnif N, Chaouech N, Hasni N, Issaoui N, Ati N, Balloumi N, Haj Salem N, Ladhari N, Akif N, Liani N, Hajji N, Trad N, Elleuch N, Marzouki NEH, Larbi N, M'barek N, Rebai N, Bibani N, Ben Salah N, Belmaachi O, Elmaalel O, Jlassi O, Mihoub O, Ben Zaid O, Bouallègue O, Bousnina O, Bouyahia O, El Maalel O, Fendri O, Azzabi O, Borgi O, Ghdes O, Ben Rejeb O, Rachid R, Abi R, Bahiri R, Boulma R, Elkhayat R, Habbal R, Rachid R, Tamouza R, Jomli R, Ben Abdallah R, Smaoui R, Debbeche R, Fakhfakh R, El Kamel R, Gargouri R, Jouini R, Nouira R, Fessi R, Bannour R, Ben Rabeh R, Kacem R, Khmakhem R, Ben Younes R, Karray R, Cheikh R, Ben Malek R, Ben Slama R, Kouki R, Baati R, Bechraoui R, Fakhfakh R, Fradi R, Lahiani R, Ridha R, Zainine R, Kallel R, Rostom S, Ben Abdallah S, Ben Hammamia S, Benchérifa S, Benkirane S, Chatti S, El Guedri S, El Oussaoui S, Elkochri S, Elmoussaoui S, Enbili S, Gara S, Haouet S, Khammeri S, Khefecha S, Khtrouche S, Macheghoul S, Mallouli S, Rharrit S, Skouri S, Helali S, Boulehmi S, Abid S, Naouar S, Zelfani S, Ben Amar S, Ajmi S, Braiek S, Yahiaoui S, Ghezaiel S, Ben Toumia S, Thabeti S, Daboussi S, Ben Abderahman S, Rhaiem S, Ben Rhouma S, Rekaya S, Haddad S, Kammoun S, Merai S, Mhamdi S, Ben Ali R, Gaaloul S, Ouali S, Taleb S, Zrour S, Hamdi S, Zaghdoudi S, Ammari S, Ben Abderrahim S, Karaa S, Maazaoui S, Saidani S, Stambouli S, Mokadem S, Boudiche S, Zaghbib S, Ayedi S, Jardek S, Bouselmi S, Chtourou S, Manoubi S, Bahri S, Halioui S, Jrad S, Mazigh S, Ouerghi S, Toujani S, Fenniche S, Aboudrar S, Meriem Amari S, Karouia S, Bourgou S, Halayem S, Rammeh S, Yaïch S, Ben Nasrallah S, Chouchane S, Ftini S, Makni S, Manoubi S, Miri S, Saadi S, Manoubi SA, Khalfallah T, Mechergui T, Dakka T, Barhoumi T, M'rad TEB, Ajmi T, Dorra T, Ouali U, Hannachi W, Ferjaoui W, Aissi W, Dahmani W, Dhouib W, Koubaa W, Zhir W, Gheriani W, Arfa W, Dougaz W, Sahnoun W, Naija W, Sami Y, Bouteraa Y, Elhamdaoui Y, Hama Y, Ouahchi Y, Guebsi Y, Nouira Y, Daly Y, Mahjoubi Y, Mejdoub Y, Mosbahi Y, Said Y, Zaimi Y, Zgueb Y, Dridi Y, Mesbahi Y, Gharbi Y, Hellal Y, Hechmi Z, Zid Z, Elmouatassim Z, Ghorbel Z, Habbadi Z, Marrakchi Z, Hidouri Z, Abbes Z, Ouhachi Z, Khessairi Z, Khlayfia Z, Mahjoubi Z, and Moatemri Z

Subjects
Africa, Northern epidemiology, Anatomy education, Education, Medical history, Education, Medical methods, Education, Medical organization & administration, History, 21st Century, Humans, Internship and Residency standards, Internship and Residency trends, Job Satisfaction, Pathology, Clinical education, Tunisia epidemiology, Education, Medical trends, Medicine methods, Medicine organization & administration, Medicine trends
Published
2019

32. A nine-month-old-boy with Atypical Hemophagocytic Lymphohistiocytosis.

Author

Ouederni M, Ben Khaled M, Rekaya S, Ben Fraj I, Mellouli F, and Bejaoui M

Abstract

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammation caused by uncontrolled proliferation of activated lymphocytes and histiocytes. Often, HLH is an acquired syndrome. We report a case of a nine month-old-boy presented with hepatosplenomegaly, severe anemia, thrombocytopenia, hypertriglyceridemia and high hyperferritinemia. These clinical features of HLH prompted a wide range of infectious and auto-immune tests to be performed. After an extensive diagnostic workup, he was referred to the immune-hematologic unit for HLH suspicion with an unknown cause. Primary HLH due to familial lymphohistiocytosis (FLH) was first evoked in front of consanguinity, probable HLH in the family, early onset, and in the absence of a causative pathology like infection or cancer. However, functional tests were normal. Atypical features like the: absence of fever, hypotonia, recurrent diarrhea since diversification, hematuria, and proteinuria suggested an inborn metabolism error with gastrointestinal involvement. Specific tests were performed to reach a final diagnosis., Competing Interests: Competing interests: The authors have declared that no competing interests exist.

Published
2017
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