Shams ElDoha G . E . M Zaiema - Profile on Academia.edu (original) (raw)

Papers by Shams ElDoha G . E . M Zaiema

Scientific Reports , 2025

The expression of CD38 by cancer cells may mediate an immune-suppressive effect by producing Extr... more The expression of CD38 by cancer cells may mediate an immune-suppressive effect by producing Extracellular Adenosine (ADO) acting through G-protein-coupled cell surface receptors on cellular components and tumor cells. This can increase PD-1 expression and interaction with PD-L1, suppressing CD8 + cytotoxic T cells. This study examines the impact of heightened CD38 expression and extracellular ADO on various hematological and clinical parameters in patients with mature B-cell lymphoma, alongside their correlation with the soluble counterparts of the PD-1/PD-L1 axis. Our study was conducted on 90 patients, CD38-positive and CD38-negative (measured by flow cytometry), with mature B-cell lymphoma divided into CLL and B-NHL subtypes. Their serum ADO, soluble PD-1, and PD-L1 levels were measured using a sandwich ELISA. Our study revealed a positive correlation between CD38 expression, sADO, sPD-1, and sPD-L1 in mature B-cell lymphoma patients. CD38positive patients had higher sADO, sPD-1, and sPD-L1 levels. Higher CD38 expression and extracellular ADO negatively affected HB level and PLT count and positively correlated with the higher risk stratification in mature B-cell lymphoma patients. This study explored the potential impact of CD38 expression and elevated extracellular ADO on B-cell lymphoma alongside their link with the PD-1/ PD-L1 axis. Our findings underscore the influence of extracellular ADO on the neoplastic process of mature B-cell lymphoma. We also propose targeting the CD38-induced-ADO formation pathway, which could serve as a promising therapeutic immune target with multifaceted effects within mature B-cell neoplasms.

Springer Nature, 2025

Background Lupus nephritis is one of the major causes of ESRD, which may necessitate renal replac... more Background Lupus nephritis is one of the major causes of ESRD, which may necessitate renal replacement therapy, especially hemodialysis. Evaluating post-HD lupus flares in LN patients is pivotal in improving their outcomes. This issue is still under consideration by researchers. This research analyzed lupus activity in LN patients with ESRD treated with HD. Methods A number of 70 LN patients diagnosed by renal biopsy were divided into age-and sex-matched two groups: They were divided into two groups: the HD Group, which were LN patients who progressed to ESRD treated with HD (n = 35), and the CKD Group, which contains LN patients' stage III, IV by renal biopsies and HD free (n = 35). The non-renal systemic lupus erythematosus (SLE) disease activity index (nrSLEDAI) score was used to estimate lupus flares in both groups regardless of the stage of renal affection. The HD group exhibited considerably declined lupus activity compared to the CKD group, irrespective of the progression of renal pathology. With long-term period maintenance on HD, there was an obvious remission in both clinical and serological parameters of SLE recorded by the nrSLEDAI scoring system. Current doses of oral corticosteroids were less in the HD group than in the CKD group. Using the nrSLEDAI score, our current research provides evidence of a reverse association between the longevity of hemodialysis (HD) and lupus activity, a "Cut-down phenomenon. " We believe that performing clinical trials and developing new post-HD evidence-based treat-to-target management guidelines for LN patients is now mandatory to improve their clinical outcomes and quality of life.

The Egyptian Journal of Internal Medicine/The Egyptian Journal of Internal Medicine, Mar 5, 2024

The transformation of acute myeloid leukemia with translocation (16;16) (p13; q22) from AML M2 to... more The transformation of acute myeloid leukemia with translocation (16;16) (p13; q22) from AML M2 to acute monocytic leukemia (AML M5) during therapy is a rare clinical occurrence, and this is the first time it has been reported. A 19-year-old male patient was admitted for severe fatigue with anemic manifestation and weight loss, for more than 1 month, with exacerbation of the condition in the last 2 days. Diagnosis A primary diagnosis was made for AML M2 with t (16;16) (p13; q22) established on bone marrow (BM) morphology. A consequential detection of FLT-3 ITD mutation was done. At day 28 follow-up after induction and maintenance therapy, the diagnosis of AML M2 was maintained with a high bone marrow (BM) blast count, prompting the initiation of a more aggressive treatment protocol. After 1 month of implementing the recent protocol, the patient remains morphologically resistant with a notable transformation of bone marrow infiltration by an abnormal monocytic population (monoblasts and promonocytes). The final diagnosis of transforming FLT3-mutated AML with t (16;16) (p13; q22) was established. Intervention After the initial diagnosis of AML M2 with t (16;16) (p13; q22), the patient received the 3 + 7 induction protocol. The 2nd induction protocol initiated after the second evaluation and morphological resistance was the FLAG Adrian protocol. The 3rd protocol after transformation to AML M5 was 1 cycle of the MEC protocol. Anti-FLT3 treatment was considered. The patient was maintained on the 3rd protocol of chemotherapy. Unfortunately, he was admitted to the ICU unit complaining of neutropenic fever and severe sepsis where he died before final re-evaluation and the anti-FLT3 treatment initiation. Conclusion AML with t (16;16) (p13; q22) characterized by favorable outcome. However, identifying additional chromosome abnormality or genetic aberration, especially FLT3 gene mutation, is recognized as an important factor influencing final disease outcome. Therefore, early detection of FLT3 mutations will allow comprehensive disease course prediction and targeted therapy that might achieve longer and more durable remissions.

Thrombosis journal, Mar 28, 2024

Antiphospholipid syndrome (APLS) is a systemic immune dysregulation distinguished by repetitive c... more Antiphospholipid syndrome (APLS) is a systemic immune dysregulation distinguished by repetitive complications and pregnancy loss in the absence of definite etiology. Most research focuses on the laboratory detection and clinical features of APLS, but its precise etiology remains to be deeply explored. NETosis is a newly developed theory in the pathophysiology of APLS which may serve as the missing bridge between coagulation and inflammation reaching the disease progression and severity. We aimed in this study to navigate the prognostic role of NETosis in thrombotic APLS. Our study included 49 newly diagnosed APLS patients (both 1ry and 2ry) who met clinical and laboratory criteria as per the international consensus statement on the update of the classification criteria for definite APLS and were sub-classified according to the occurrence of thrombotic events in thrombotic and non-thrombotic types. In addition, 20 sex and age-matched reactive subjects and 20 sex and age-matched healthy volunteer controls were enrolled. NETosis formation was assessed by measuring serum Myeloperoxidase (MPO) and Histones level using the enzyme-linked immunosorbent assay (ELISA) technique. Both MPO and Histones levels were able to discriminate among APLS cases from normal controls, showing significant cutoffs of > 2.09 ng/ml for MPO and > 1.45 ng/ml for Histones (AUC values were 0.987and 1.000, respectively). These values can be used as predictors for NETosis pathophysiology in APLS patients. Additionally, these markers demonstrated a significant association with several prognostic indicators, including thrombosis, higher PT and INR, and lower hemoglobin (Hb) levels which are supposed to be ameliorated by using NETs inhibitors. In conclusion, we suggest that measuring NETosis markers, MPO, and Histones, in the early course of APLS using proposed cutoff values will facilitate the timely initiation of anti-NETosis therapy and improve the overall prognosis, particularly for patients with thrombotic APLS.

Annals of Hematology, 2019

Since iron overload is the commonest cause of morbidity and mortality in β thalassemia major (β-T... more Since iron overload is the commonest cause of morbidity and mortality in β thalassemia major (β-TM), it represents one major target in therapeutic management of the disease. The recently discovered erythroid regulator, erythroferrone (ERFE), governed by high levels of erythropoietin, was found to suppress hepcidin expression, thus increasing iron availability for developing erythroid progenitors. We aimed to investigate ERFE levels in Egyptian β-TM patients as an attempt to understand its role in the prediction of iron overload states. Our study included 70 β-TM patients, divided into two subgroups according to the degree of iron overload, and 30 sex and age-matched healthy subjects. ERFE gene expression was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), and serum hepcidin was measured using enzyme-linked immunosorbent assay (ELISA) technique. Both ERFE gene expression levels and transferrin saturation (TS%) values were able to discriminate among cases with different degrees of iron overload, in contrast to hepcidin. TS% was acknowledged as the best predictor of iron overload (AUC 0.893) in comparison with serum hepcidin and ERFE gene levels (AUC 0.807 and 0.677, respectively), and ERFE gene expression was an independent predictor for the estimated TS%. In conclusion, we suggest that using the ERFE gene expression, combined with serum hepcidin estimation, can substantiate the role of estimated TS% as a promising tool in screening for iron overload in β-TM patients.

Ain Shams Medical Journal

Background: Among the more complex tests for the diagnostic workup of acute leukemia (AL), automa... more Background: Among the more complex tests for the diagnostic workup of acute leukemia (AL), automated hematology cell counters provide leucocyte cell population data (CPD) parameters along with the basic complete blood count (CBC) that have the ability to recognize morphological changes in these cells. Aim of the work: Assessment of the efficiency of CPD research parameters obtained by Sysmex XN-1000 auto-analyzer to predict the diagnosis of AL and its subclassification into acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Patients and methods: Cell population data (CPD) parameters from 103 newly diagnosed AL samples were processed on Sysmex XN-1000 auto-analyzer and compared with 101 age-matched controls (51 healthy and 50 reactive subjects). Results: We found significant differences in many CPD neutrophilic, monocytic, and lymphocytic population together with parameters between AL patients and both healthy and reactive controls, particularly those related to the width of dispersion of the parameters related to neutrophil side scatter intensity, neutrophil forward scatter intensity, lymphocyte side scatter intensity, monocyte side scatter intensity and monocyte side fluorescence intensity. To differentiate AML from ALL, the most significant differences were found in the median values of monocyte side scatter and monocyte side fluorescence along with the neutrophil forward scatter area distribution width and neutrophil forward scatter. Conclusion: The CPD parameters generated from Sysmex XN-1000 auto-analyzer during CBC analysis could be a useful tool for the prediction of AL and its lineage.

Erythroferrone, the new iron regulator: evaluation of its levels in Egyptian patients with beta thalassemia, 2020

Unpredicted transformation of acute myeloid leukemia with translocation (16;16) (p13; q22): a case report and review of the literature, 2024

Introduction The transformation of acute myeloid leukemia with translocation (16;16) (p13; q22) f... more Introduction The transformation of acute myeloid leukemia with translocation (16;16) (p13; q22) from AML M2 to acute monocytic leukemia (AML M5) during therapy is a rare clinical occurrence, and this is the first time it has been reported. Clinical complain A 19-year-old male patient was admitted for severe fatigue with anemic manifestation and weight loss, for more than 1 month, with exacerbation of the condition in the last 2 days. Diagnosis A primary diagnosis was made for AML M2 with t (16;16) (p13; q22) established on bone marrow (BM) morphology. A consequential detection of FLT-3 ITD mutation was done. At day 28 follow-up after induction and maintenance therapy, the diagnosis of AML M2 was maintained with a high bone marrow (BM) blast count, prompting the initiation of a more aggressive treatment protocol. After 1 month of implementing the recent protocol, the patient remains morphologically resistant with a notable transformation of bone marrow infiltration by an abnormal monocytic population (monoblasts and promonocytes). The final diagnosis of transforming FLT3-mutated AML with t (16;16) (p13; q22) was established. Intervention After the initial diagnosis of AML M2 with t (16;16) (p13; q22), the patient received the 3 + 7 induction protocol. The 2nd induction protocol initiated after the second evaluation and morphological resistance was the FLAG Adrian protocol. The 3rd protocol after transformation to AML M5 was 1 cycle of the MEC protocol. Anti-FLT3 treatment was considered. Outcomes The patient was maintained on the 3rd protocol of chemotherapy. Unfortunately, he was admitted to the ICU unit complaining of neutropenic fever and severe sepsis where he died before final re-evaluation and the anti-FLT3 treatment initiation. Conclusion AML with t (16;16) (p13; q22) characterized by favorable outcome. However, identifying additional chromosome abnormality or genetic aberration, especially FLT3 gene mutation, is recognized as an important factor influencing final disease outcome. Therefore, early detection of FLT3 mutations will allow comprehensive disease course prediction and targeted therapy that might achieve longer and more durable remissions.