Introduction: Iron deficiency anaemia (IDA) is a worldwide nutritional problem; it accounts for about half of the world’s anaemia burden. Globally, Helicobacter pylori (H. pylori) is becoming an increasingly troublesome economic and public health problem. The colonization of the organism in gastric mucosa may impair iron uptake and increase iron loss, potentially leading to iron deficiency anaemia. The mechanisms by which H. pylori is postulated to cause IDA are H. pylori -associated chronic gastritis resulting in hypo/or achlorhydria, reduced ascorbic acid secretion and reduced intestinal iron absorption, occult blood loss due to chronic erosive gastritis, and sequestration and utilization of iron by Helicobacter pylori. Aims: To detect H. pylori–related IDA prevalence among asymptomatic cases of anaemia and to address the possibility that such infection may play a detrimental role in their blood picture, serum iron and ferritin levels and total iron binding capacity (TIBC) Study Design & Methods: Facility based cross-sectional study was conducted in the period from December 2018 to May 2019. Screening was done for asymptomatic attendants of a   number of private laboratories in Beheira, Alexandria and Gharbiya governorates. Three hundreds of whom were proved to be cases of IDA and were further tested for H. pylori antigen in stool. Results: Helicobacter pylori Ag test in stool was positive in 180 out of 300 cases of iron deficiency anaemia. The infection significantly affected the haemoglobin level, MCV, MCH and RDW in studied cases (p<0.05). Infection with H. pylori also significantly affected the serum iron, serum ferritin and TIBC in the studied cases of IDA (p<0.05). Conclusion: A significant association between H. pylori infection and IDA. Screening for H. pylori among unexplained cases of IDA is recommended.

Background: Acute myeloid leukemia (AML) can modulate toll-like receptor-9 (TLR9) expression and activation. This study was conducted to elucidate the expression of TLR9 in AML patients and its relation to the prognosis of the disease. Results: The study included 40 newly diagnosed AML patients managed in the hospital in addition to 20 sex and age matched normal volunteers as control. TLR9 expression assay was conducted on peripheral blood samples of AML cases before the start of treatment as well as the controls by immunophenotyping. TLR9 expression was ranging from 0.10 to 2.40% in AML patients with higher expression among the control, ranging from 0.94 to 8.25%. The median TLR9 expression in AML patients was significantly lower with advanced cytogenetic risk score. It is not significantly differing in relation to patients' sex, age group, and FAB type of AML. However, significant lower median expression was found in relation to clinical outcome. TLR9 expression ≤ 1% showed lower median overall survival time when compared to those with > 1% expression. Conclusion: This study concluded that AML patients express TLR9 in leukemic cells with very low percentage. This expression was negatively related to the clinical outcome.