Coexistence of Helicobacter pylori and Giardia duodenalis causes severe iron deficiency anaemia in an adult male: a case report.

INTRODUCTION: Iron deficiency anaemia (IDA), the most prevalent type of anaemia, is recognised as a significant global health concern that affects individuals of all ages. CASE PRESENTATION: Herein, we present a case involving an adult male coinfected with Helicobacter pylori and Giardia duodenalis, which precipitated severe IDA. RESULTS: A 24-year-old male presented with symptoms including fatigue, dizziness, headache, abdominal pain, and diarrhoea persisting for four weeks. Thorough blood tests, including complete blood counts, blood film, and iron studies, conclusively established the presence of severe IDA. Furthermore, his faecal sample was collected and subjected to analysis of common bacterial and parasitic gastrointestinal infections. Examination of upper and lower gastrointestinal pathogens indicated that the severe IDA was most likely a result of coinfection with H. pylori and G. duodenalis. The patient received treatment involving antibiotics and iron replacement therapy, which resulted in an improvement in both his symptoms and laboratory results. CONCLUSIONS: The present report provides crucial insights into the synergistic effect of concurrent H. pylori and G. duodenalis infections, highlighting their potential to induce severe IDA in infected patients.

An overview of qualitative and quantitative platelet abnormalities in schistosomiasis.

Schistosomiasis is a neglected tropical disease referring to the infection with blood parasitic trematodes of the genus Schistosoma. It impacts millions of people worldwide, primarily in low-to-middle-income countries. Patients infected with schistosomiasis often exhibit a distinct hematological profile, including anemia, eosinophilia, thrombocytopenia, and coagulopathy. Platelets, essential components of the hemostatic system, play a crucial role in the pathogenesis of schistosomiasis. Schistosomes secrete serine proteases and express ectoenzymes, such as calpain protease, alkaline phosphatase (SmAP), phosphodiesterase (SmNPP5), ATP diphosphohydrolase (SmATPDase1), serine protease Sk1, SmSP2, and Sm22.6, which can interfere with platelet normal functioning. This report provides comprehensive, up-to-date information on platelet abnormalities observed in patients with schistosomiasis, highlighting their importance in the disease progression and complications. It delves into the interactions between platelets and schistosomes, including the impact of platelet dysfunction on hemostasis and immune responses, immune-mediated platelet destruction, and the potential mechanisms by which schistosome tegumental ectoenzymes affect platelets. Furthermore, the report clarifies the relationship between platelet abnormalities and clinical manifestations such as thrombocytopenia, coagulation disorders, and the emergence of portal hypertension and gastrointestinal bleeding. Understanding the complex interplay between platelets and schistosomes is crucial for improving patient management and outcomes in schistosomiasis, particularly for those with platelet alterations. This knowledge contributes to improved diagnostic methods, innovative treatment strategies, and global efforts to control and eliminate schistosomiasis.

The impact of wet cupping on haematological and inflammatory parameters in a sample of Jordanian team players.

Background/objective: The practice of complementary and alternative medicine has significantly gained acceptance worldwide, such as Al-Hijama, also known as cupping therapy. Despite the growing popularity of therapeutic cupping among athletes, little is known about the impact of cupping therapy on sports fields. The current study was designed to explore the effect of wet cupping therapy on the haematological and inflammatory parameters in Jordanian national team players. Methods: The procedure was carried out at a specialized centre for cupping in Amman on the morning of the 19th Rajab. The data were obtained from 14 healthy male participants aged between 21 and 22 years. The haematological and inflammatory parameters were assessed by comparing venous blood components before and after four weeks of wet cupping. Results: Complete blood count (CBC) analysis of venous blood samples four weeks after wet cupping showed a significant increase in the values of total white blood cells (WBCs), neutrophils, lymphocytes, red blood cells (RBCs), haematocrit, and haemoglobin as compared with venous blood samples before cupping. Blood film examination of venous blood samples post-cupping revealed normocytic normochromic RBCs; WBCs and platelets were unremarkable. Analysis of inflammatory markers post cupping showed a significant decrease in the monocyte/lymphocyte ratio (MLR) and platelet/lymphocyte ratio (PLR) but no differences in neutrophil/lymphocyte ratio (NLR). Conclusion: The findings of this study suggest that wet cupping has an indispensable influence on haematological and immunological parameters in athletes, where it reinforces cellular immunity, generates younger blood cells, and reduces inflammation markers. It is probable, therefore, that cupping improves sports performance and achievement. The evidence from this research adds to a growing body of literature on cupping therapy in sports.

Zeb1 maintains long-term adult hematopoietic stem cell function and extramedullary hematopoiesis.

Emerging evidence implicates the epithelial-mesenchymal transition transcription factor Zeb1 as a critical regulator of hematopoietic stem cell (HSC) differentiation. Whether Zeb1 regulates long-term maintenance of HSC function remains an open question. Using an inducible Mx-1-Cre mouse model that deletes conditional Zeb1 alleles in the adult hematopoietic system, we found that mice engineered to be deficient in Zeb1 for 32 weeks displayed expanded immunophenotypically defined adult HSCs and multipotent progenitors associated with increased abundance of lineage-biased/balanced HSC subsets and augmented cell survival characteristics. During hematopoietic differentiation, persistent Zeb1 loss increased B cells in the bone marrow and spleen and decreased monocyte generation in the peripheral blood. In competitive transplantation experiments, we found that HSCs from adult mice with long-term Zeb1 deletion displayed a cell autonomous defect in multilineage differentiation capacity. Long-term Zeb1 loss perturbed extramedullary hematopoiesis characterized by increased splenic weight and a paradoxical reduction in splenic cellularity that was accompanied by HSC exhaustion, lineage-specific defects, and an accumulation of aberrant, preleukemic like c-kit+CD16/32+ progenitors. Loss of Zeb1 for up to 42 weeks can lead to progressive splenomegaly and an accumulation of Gr-1+Mac-1+ cells, further supporting the notion that long-term expression of Zeb1 suppresses preleukemic activity. Thus, sustained Zeb1 deletion disrupts HSC functionality in vivo and impairs regulation of extramedullary hematopoiesis with potential implications for tumor suppressor functions of Zeb1 in myeloid neoplasms.

Vitamin B12 insufficiency and deficiency: a review of nondisease risk factors.

Vitamin B12 deficiency and insufficiency can lead to both hematological and neurological impairments. This review examines nondisease causes and risk factors associated with dietary availability, such as eating habits, food processing, cooking techniques, and bioavailability, as well as increased physiological needs and iatrogenic factors linked to medication use or surgical procedures. As a result of these nondisease influences, groups at higher risk include vegans, vegetarians, older adults, individuals with limited diets, breastfed and preterm infants, and those who primarily consume foods prepared or cooked in ways that reduce vitamin B12 content, as well as individuals on certain medications or who have undergone specific surgeries. Recognizing these diverse risk factors helps develop strategies for prevention and intervention to minimize the adverse health effects related to B12 deficiency and insufficiency.

The Role of NOTCH1, GATA3, and c-MYC in T Cell Non-Hodgkin Lymphomas.

Lymphomas are heterogeneous malignant tumours of white blood cells characterised by the aberrant proliferation of mature lymphoid cells or their precursors. Lymphomas are classified into main types depending on the histopathologic evidence of biopsy taken from an enlarged lymph node, progress stages, treatment strategies, and outcomes: Hodgkin and non-Hodgkin lymphoma (NHL). Moreover, lymphomas can be further divided into subtypes depending on the cell origin, and immunophenotypic and genetic aberrations. Many factors play vital roles in the progression, pathogenicity, incidence, and mortality rate of lymphomas. Among NHLs, peripheral T cell lymphomas (PTCLs) are rare lymphoid malignancies, that have various cellular morphology and genetic mutations. The clinical presentations are usually observed at the advanced stage of the disease. Many recent studies have reported that the expressions of NOTCH1, GATA3, and c-MYC are associated with poorer prognosis in PTCL and are involved in downstream activities. However, questions have been raised about the pathological relationship between these factors in PTCLs. Therefore, in this review, we investigate the role and relationship of the NOTCH1 pathway, transcriptional factor GATA3 and proto-oncogene c-MYC in normal T cell development and malignant PTCL subtypes.

Flow Cytometry Analysis of Hematopoietic Stem/Progenitor Cells and Mature Blood Cell Subsets in Atherosclerosis.

Advancing age causes physiologic decline in tissue function. In the hematopoietic system this manifests as a progressive reduction in blood or immune cell function and clonal hematopoiesis, where a mutated hematopoietic stem cell can dominate blood cell production and confer an increased propensity for myeloid malignancy. In the aging cardiovascular system, atherosclerosis causes an inflammatory cell- driven accumulation of lipid-derived plaques in major arteries which constrains blood flow and can lead to myocardial infarction and stroke. Clonal hematopoiesis in the elderly has recently been associated with a substantially increased risk of atherosclerosis-related cardiovascular disease. However, the direct association between deregulated hematopoiesis in clonal hematopoiesis and atherosclerosis is poorly defined. Herein, we describe a flow cytometry method to prospectively analyze the crucial hematopoietic stem/progenitor, inflammatory and lymphoid cell participants in atherosclerosis. This analysis can be applied to decipher the complex relationship between hematopoietic cell types involved in clonal hematopoiesis and atherosclerosis in mouse models.

Gata2 haploinsufficiency promotes proliferation and functional decline of hematopoietic stem cells with myeloid bias during aging.

During aging, hematopoietic stem cell (HSC) function wanes with important biological and clinical implications for benign and malignant hematology, and other comorbidities, such as cardiovascular disease. However, the molecular mechanisms regulating HSC aging remain incompletely defined. GATA2 haploinsufficiency driven clinical syndromes initially result in primary immunodeficiencies and routinely evolve into hematologic malignancies on acquisition of further epigenetic mutations in both young and older patients. Using a conditional mouse model of Gata2 haploinsufficiency, we discover that during aging Gata2 promotes HSC proliferation, monocytosis, and loss of the common lymphoid progenitor. Aging of Gata2 haploinsufficient mice also offsets enhanced HSC apoptosis and decreased granulocyte-macrophage progenitor number normally observed in young Gata2 haploinsufficient mice. Transplantation of elderly Gata2 haploinsufficient HSCs impairs HSC function with evidence of myeloid bias. Our data demonstrate that Gata2 regulates HSC aging and suggest the mechanisms by which Gata2 mediated HSC aging has an impact on the evolution of malignancies in GATA2 haploinsufficiency syndromes.

Zeb1 modulates hematopoietic stem cell fates required for suppressing acute myeloid leukemia.

Zeb1, a zinc finger E-box binding homeobox epithelial-mesenchymal transition (EMT) transcription factor, confers properties of "stemness," such as self-renewal, in cancer. Yet little is known about the function of Zeb1 in adult stem cells. Here, we used the hematopoietic system as a well-established paradigm of stem cell biology to evaluate Zeb1-mediated regulation of adult stem cells. We employed a conditional genetic approach using the Mx1-Cre system to specifically knock out (KO) Zeb1 in adult hematopoietic stem cells (HSCs) and their downstream progeny. Acute genetic deletion of Zeb1 led to rapid-onset thymic atrophy and apoptosis-driven loss of thymocytes and T cells. A profound cell-autonomous self-renewal defect and multilineage differentiation block were observed in Zeb1-KO HSCs. Loss of Zeb1 in HSCs activated transcriptional programs of deregulated HSC maintenance and multilineage differentiation genes and of cell polarity consisting of cytoskeleton-, lipid metabolism/lipid membrane-, and cell adhesion-related genes. Notably, epithelial cell adhesion molecule (EpCAM) expression was prodigiously upregulated in Zeb1-KO HSCs, which correlated with enhanced cell survival, diminished mitochondrial metabolism, ribosome biogenesis, and differentiation capacity and an activated transcriptomic signature associated with acute myeloid leukemia (AML) signaling. ZEB1 expression was downregulated in AML patients, and Zeb1 KO in the malignant counterparts of HSCs - leukemic stem cells (LSCs) - accelerated MLL-AF9- and Meis1a/Hoxa9-driven AML progression, implicating Zeb1 as a tumor suppressor in AML LSCs. Thus, Zeb1 acts as a transcriptional regulator in hematopoiesis, critically coordinating HSC self-renewal, apoptotic, and multilineage differentiation fates required to suppress leukemic potential in AML.

Gata2 as a Crucial Regulator of Stem Cells in Adult Hematopoiesis and Acute Myeloid Leukemia.

Subversion of transcription factor (TF) activity in hematopoietic stem/progenitor cells (HSPCs) leads to the development of therapy-resistant leukemic stem cells (LSCs) that drive fulminant acute myeloid leukemia (AML). Using a conditional mouse model where zinc-finger TF Gata2 was deleted specifically in hematopoietic cells, we show that knockout of Gata2 leads to rapid and complete cell-autonomous loss of adult hematopoietic stem cells. By using short hairpin RNAi to target GATA2, we also identify a requirement for GATA2 in human HSPCs. In Meis1a/Hoxa9-driven AML, deletion of Gata2 impedes maintenance and self-renewal of LSCs. Ablation of Gata2 enforces an LSC-specific program of enhanced apoptosis, exemplified by attenuation of anti-apoptotic factor BCL2, and re-instigation of myeloid differentiation--which is characteristically blocked in AML. Thus, GATA2 acts as a critical regulator of normal and leukemic stem cells and mediates transcriptional networks that may be exploited therapeutically to target key facets of LSC behavior in AML.