Iron deficiency anemia (IDA) is one of the commonest clinical scenarios especially in children, women of childbearing age, and elders. The crux of this review was revisiting iron homeostasis, mechanism of iron absorption, causes, laboratory diagnosis, and management of IDA. This narrative review is compiled after a relevant literature search from electronic databases including, but not limited to, Google, Google Scholar, PMC, PubMed, Science Direct, and Scopus. The key words used for searching relevant literature include iron, iron deficiency, iron deficiency anemia, iron metabolism, hepcidin, transferrin, causes of iron deficiency anemia, and laboratory diagnosis of iron deficiency anemia. Reference hema-tology books were also consulted. According to the published literature, about one mg of iron is required daily which equals its loss, although the iron requirement increases in pregnancy and lactating mothers. Dietary non heme iron (oxidized Fe3+) is reduced to the ferrous (Fe2+) form by ferrireductase present in the brush border of duodenal enterocytes. Ferrous iron is absorbed in the brush border of duodenal enterocytes through a carrier protein, divalent metal transporter 1 (DMT1). Heme iron is absorbed by the duodenal enterocytes through a mechanism that is not well understood or a receptor yet to be discovered. Transferrin receptor helps in the internalization of iron in the cells. Hepcidin acts as a gatekeeper and controls iron absorption by enterocytes and macrophages. IDA may be caused by decreased intake of iron, increased iron requirements or loss of iron from the body. Iron deficiency anemia is the most common nutritional anemia that affects large numbers of people in developed as well as in developing countries. It is estimated that approximately 2 billion people around the world have IDA. Microcytosis with marked reduction in serum iron, decreased % saturation of transferrin, low ferritin, and reduced or even undetectable hepcidin are the laboratory features of IDA. In addition, total iron binding capacity and soluble transferrin receptors increase significantly in IDA. Management of IDA is incomplete if the underlying cause is not ruled out and left untreated.

Purpose: Anemia is one of the most common disorders affecting the population in both low-income and developing countries. This study aimed to determine the prevalence of anemia and iron deficiency in apparently normal male and female students of Jazan University, Saudi Arabia. Material and Methods: This cross-sectional study was conducted at the Faculty of Applied Medical Sciences, Jazan University, Gizan, Saudi Arabia. One hundred thirty-four (85 males and 49 females) healthy students with no outward signs of illness were recruited. A specific questionnaire related to sociodemographic and health characteristics was designed and validated. The collected samples were analyzed for complete blood count, serum iron, and serum ferritin. Results: In the male group, 81 participants (95.3%) were nonanemic with normal hemoglobin (14.99 ± 1.11g/dl), whereas only 4 males were anemic (hemoglobin < 13.0 g/dl). On the other hand, anemia was more prevalent in female students, as 67.35% had hemoglobin values less than 12.0 g/dl. In addition, 26.54% of the anemic females had low serum iron and serum ferritin, indicating iron-deficiency anemia. Although the majority of male participants had normal hemoglobin levels, 37.6% of them had low mean cell volume (MCV), low mean cell hemoglobin (MCH), low mean cell hemoglobin concentration (MCHC), and high red blood cell (RBC) counts, suggesting thalassemia. Conclusion: Anemia, in particular iron-deficiency anemia, was found to be highly prevalent in females, whereas more than one-third of the male participants might be carriers of alpha or beta thalassemia. Additionally, low dietary iron intake and irregular meal consumption could be two of the possible causes of anemia in the study population. Conducting this study on a large scale of male and female students from different faculties of Jazan University will provide in-depth details about the prevalence and types of anemia among them.

Background: Diabetes mellitus (DM) is a major health burden affecting 537 million adults worldwide, characterized by chronic metabolic disorder and various complications. This case control study aimed to assess the impact of type 2 diabetes mellitus (T2DM), including hyperglycemia levels, on hematological parameters and complete blood count (CBC) derived parameters. Methods: A total of 250 known diabetic patients from the Jazan Diabetic Center, Saudi Arabia, between January 2021 and December 2022, along with 175 healthy adult controls were recruited from Jazan Hospital’s blood donation center. Demographic characteristics, medical histories, and relevant factors such as gender, age, BMI, treatment, disease duration, and comorbidities were collected with informed consent. Results: The results of the red blood cell (RBC) count, RBC indices, and mean platelet volume showed significant differences between patients and controls, while the white cell (WBC) and platelet count were comparable between the two groups. CBC-derived parameters, especially neutrophil/lymphocyte ratio (NLR), and platelet/neutrophil ratio (PNR) exhibited significant differences. Conclusion: CBC and derived parameters serve as inexpensive tools for T2DM patients monitoring, indicating early blood cell alterations and potential development of anemia. Further studies are needed to explore their role in predicting T2DM pathogenesis and progression, aiming to reduce severe complications, mortality and morbidity.

Purpose: Sickle cell disease (SCD) and thalassemia are common inherited blood disorders in Saudi Arabia, especially in Jazan Province. Patients with these disorders require multiple blood transfusions, which may lead to alloimmunization because of mismatched blood group antigens. In this study, we examined the alloimmunization and autoimmunization rates in patients with SCD and thalassemia together with the involved antibodies. Patients and Methods: A cross-sectional study was conducted to review the transfusion history records of patients with SCD and thalassemia at Prince Mohammed bin Nasser Hospital, Jazan Province, Saudi Arabia. Results: Four-hundred thirty-eight patients (385 with SCD, 52 with β-thalassemia, and 1 with α-thalassemia) were received leukoreduced red cell transfusions. The alloimmunization and autoimmunization rates in patients with SCD were 12.98% and 0.52%, respectively. In patients with thalassemia, the alloimmunization and autoimmunization rates were 13.21% and 3.77%, respectively. The most prevalent antibodies in the study population were anti-E (17.19%) and anti-K (14.06%). Conclusion: The alloimmunization and autoimmunization rates were determined in patients with SCD and thalassemia in Jazan Province, Saudi Arabia. The results highlight the need for extended phenotyping to include ABO, RH (D, C, c, E, e), K, Fy^a, Fy^b, Jk^a and Jk^b antigens in the screening panel. This will benefit patients to ensure better transfusion practices.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common inherited metabolic abnormality of red blood cells (RBCs), affecting 400 million individuals worldwide. Patients with G6PD deficiency anemia might exhibit severe clinical manifestations, including acute hemolytic anemia (AHA), neonatal hyperbilirubinemia (jaundice), favism, and chronic non-spherocytic hemolytic anemia (CNSHA). The aim of the current review is to report the prevalence and genetic variants of G6PD deficiency anemia in Saudi Arabia. The scientific literature was reviewed for reports on G6PD deficiency in Saudi Arabia. The incidence rate of G6PD deficiency is very high in Saudi Arabia and varies from Province to Province. As reported by the Ministry of Health, the prevalence of G6PD deficiency in Saudi Arabia is 8.4% among males. The pattern and distribution of the genetic mutations also vary. Some of the genetic mutations of G6PD deficiency have been associated with clinical manifestations including hemolysis, especially in neonates. Several studies have reported known common variants such as Mediterranean and A–, as well as rare variants such as Nara, Sibiri, and Viangchan in the Saudi population. Early detection, characterization, and understanding of the phenotypic and molecular patterns of G6PD deficiency in Saudi Arabia are needed for better management and control of the disease. Thus, neonatal screening for G6PD deficiency, family counseling, and public awareness of the disease should be established.

Advanced mitochondrial multi-omics indicate a multi-facet involvement of mitochondria in the physiology of the cell, changing the perception of mitochondria from being just the energy-generating organelles to organelles that highly influence cell structure, function, signaling, and cell fate. This sets mitochondrial dysfunction in the centerstage of numerous acquired and genetic diseases. Sickle cell disease is also being increasingly associated with mitochondrial anomalies and the pathophysiology of sickle cell disease finds mitochondria at crucial intersections in the pathological cascade. Altered mitophagy, increased ROS, and mitochondrial DNA all contribute to the condition and its severity. Such mitochondrial aberrations lead to consequent mitochondrial retention in red blood cells in sickle cell diseases, increased oxidation in the cellular environment, inflammation, worsened vaso-occlusive crisis, etc. There are increasing studies indicating mitochondrial significance in sickle cell disease, consequently providing an opportunity to target it for improving the outcomes of treatment. Identification of the impaired mitochondrial attributes in sickle cell disease and their modulation by therapeutic interventions can impart a better management of the disease. This review aims to describe the mitochondria in the perspective of sicke cell disease so as to provide the reader an overview of the emerging mitochondrial stance in sickle cell disease.