Blood Products Management and Safety During COVID-19: a Public Health Challenge.

BACKGROUND: Blood products are essential therapeutics that are pivotal in saving and improving millions of lives worldwide. A sufficient and safe blood supply is necessary for efficient healthcare services to provide effective patient care in various acute and chronic conditions. Blood donations are the main source of blood products in almost all nations of the world. The coronavirus 2019 (COVID-19) pandemic negatively impacted blood product management worldwide and has added stress to the already stressed healthcare system. Most of the earlier months of 2020 witnessed a decrease in blood donations as donors were highly apprehensive about their safety, and the isolation practices implemented to contain the virus spread discouraged donor participation. Because of the spread of the virus, blood collection centers and regulatory bodies have undertaken numerous strategic steps to prevent any viral transmission at the blood collection centers while aiming to increase donor participation. Maintaining extra sterilization in all the processes involved in blood product management and the modified criteria for participating donors changed the entire paradigm of blood product management. This review discusses various challenges and modifications adopted by different roles of participants involved in blood product availability to maintain an adequate and safe blood supply during the emerging COVID-19 pandemic. METHODS: An extensive online search was done to obtain the necessary information regarding various scenarios concerning blood product crises, advisories, and availability. RESULTS: A change in how the blood supply chain works that has overcome and prevented a crisis in blood demand and supply during the COVID-19 pandemic world over was observed. CONCLUSIONS: Blood products are critical for medical and surgical procedures. The COVID-19 pandemic has led to a crisis in the availability of blood products with decreased participation of donors. It has become the prime re-sponsibility of the blood collection centers and government agencies to change strategies, so that blood stocks do not become exhausted and create another crisis.

Endothelial Nitric Oxide Synthase Gene Polymorphisms Increase Risk of Deep Vein Thrombosis by Altering Homocysteine Levels.

BACKGROUND: Deep Vein Thrombosis (DVT) is a multicausal disease involving both acquired as well as genetic factors. Nitric oxide is an influential endogenous factor having its role in the development of deep vein thrombosis. It maintains the vascular integrity and any alterations in its levels may lead to a thrombotic event. It may also modulate homocysteine metabolism to cause hyperhomocysteinemia, which is a prominent risk factor for thrombosis. The objective of the study was to study if endothelial nitric oxide gene polymorphisms, 894G/T, and 2479G/A alter the plasma nitric oxide and homocysteine levels which may eventually increase the risk of deep vein thrombosis. METHODS: One hundred Doppler ultrasonography and computerized tomography confirmed (for cerebral venous thrombosis), non-related DVT patients (M:F = 58:42; age range = 18 to 61 years) served as the study population. Two hundred hospital staff and their relatives or unrelated attendants of the patients served as the controls. Nitric oxide levels were determined by measuring its metabolites (NOx), and EIA was used to measure homocysteine levels. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for detecting the eNOS polymorphisms 894G/T and 2479G/A. RESULTS: In total, DVT subjects have 25% higher plasma levels of homocysteine and 37% lower levels of NOx in their circulation when compared to controls. In tertile analysis of nitric oxide and homocysteine levels, 894G/T and 2479G/A polymorphisms were associated with plasma nitric oxide and homocysteine levels. The increased risk of deep vein thrombosis was associated with endothelial nitric oxide gene polymorphisms and nitric oxide levels, but homocysteine levels were not a risk for deep vein thrombosis. CONCLUSION: The present study demonstrates that 894G/T and 2479G/A polymorphisms interact with lower levels of nitric oxide and higher levels of homocysteine that may possess the risk of deep vein thrombosis.

Case Report: Hyperbilirubinemia in Gilbert Syndrome Attenuates Covid-19-Induced Metabolic Disturbances.

Gilbert syndrome (GS) is a liver disorder characterized by non-hemolytic unconjugated hyperbilirubinemia. On the other hand, Coronavirus disease 2019 (Covid-19) is a recent viral infectious disease presented as clusters of pneumonia, triggered by the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). Little is known on the association between SARS-CoV-2 and GS, despite different studies have recently stated a link between hyperbilirubinemia and SARS-CoV-2 severity. In this case-report study we described a 47-year-old man, a known case of GS since the age of 4, presented to the emergency department with fever (39.8°C), dry cough, dyspnea, headache, myalgia, sweating and jaundice diagnosed with Covid-19-induced pneumonia. Interestingly, GS patient exhibited a rapid clinical recovery and short hospital stay compared to other SARS-CoV-2 positive patient, seeming that hyperbilirubinemia may exert a protective effect of against Covid-19 induced-cardiometabolic disturbances. Data obtained here underlines that the higher resistance against Covid-19 evidenced by the GS patient seems to be due to the antioxidant, anti-inflammatory, and antiviral effects of unconjugated bilirubin.

Melatonin Ameliorates BPA Induced Oxidative Stress in Human Red Blood Cells: An In vitro Study.

BACKGROUND: Bisphenol A (BPA) is a xenobiotic that causes oxidative stress in various organs in living organisms. Blood cells are also an endpoint where BPA is known to cause oxidative stress. Blood cells, especially red blood cells (RBCs), are crucial for maintaining homeostasis and overall wellbeing of the organism. They are highly susceptible to oxidative stress induced by xenobiotics. However, there is limited data about the oxidative stress induced by BPA in blood, especially in red blood cells. This study was carried out to evaluate BPA induced oxidative stress in human RBCs in vitro and its amelioration by melatonin. OBJECTIVE: To find if melatonin exerts a protective effect on the oxidative stress induced by the BPA in human red blood cells in vitro. METHODS: The erythrocyte suspensions (2 ml) were divided into six groups and treated with 0, 50, 100, 150, 200, and 250 µg/ml of BPA. Another set of erythrocyte suspension with similar BPA treatment and 50 µM Melatonin per group was also set. Incubations lasted for 12 hrs in the dark. Lipid peroxidation, glutathione, glutathione reductase, catalase, and superoxide dismutase were measured as indicators of oxidative stress. RESULTS: BPA caused a significant increase in lipid peroxidation. A decrease in GSH levels was also observed. The activities of all the studied antioxidants also decreased with BPA treatment. Melatonin was seen to mitigate the oxidative stress induced by BPA. CONCLUSION: Treatment of red blood cells with BPA caused an increase in oxidative stress, while melatonin decreased the induced oxidative stress.

Inhibiting Effect of Zinc Oxide Nanoparticles on Advanced Glycation Products and Oxidative Modifications: a Potential Tool to Counteract Oxidative Stress in Neurodegenerative Diseases.

Advanced glycation end products (AGEs) are implicated in several central nervous system (CNS) pathologies including Alzheimer and Parkinson's diseases. In the face-off of AGE menace, we have attempted to investigate the zinc oxide nanoparticle (ZnONP) role in inhibition of AGE formation. Synthesized ZnONPs were used to investigate the inhibitory effects on AGE formation. The inhibitory effects of ZnONPs on AGE formation were determined by biophysical immunological and biochemical techniques. The results showed that ZnONP is a potential anti-glycating agent inhibiting AGE formation as well as protecting the protein structure from change. Therefore, our findings suggest ZnONPs may be used as a therapeutic in resolving the AGE role in CNS-related complications.

Protein oxidation: an overview of metabolism of sulphur containing amino acid, cysteine.

The available data suggest that among cellular constituents, proteins are the major target for oxidation primarily because of their quantity and high rate of interactions with ROS. Proteins are susceptible to ROS modifications of amino acid side chains which alter protein structure. Among the amino acids, Cysteine (Cys) is more prone to oxidation by ROS because of its high nucleophilic property. The reactivity of Cys with ROS is due to the presence of thiol group. In the oxidised form, Cys forms disulfide bond, which are primary covalent cross-link found in proteins, and which stabilize the native conformation of a protein. Indirect evidence suggests that thiol modifications by ROS may be involved in neurodegenerative disorders, but the significance and precise extent of the contributions are poorly understood. Here, we review the role of oxidized Cys in different pathological consequences and its biochemistry may increase the research in the discovery of new therapies. The purpose of this review is to re-examine the role and biochemistry of oxidised Cys residues.

The effect of repeated blood donations on the iron status of male Saudi blood donors.

BACKGROUND: Regular blood donation can lead to iron deficiency. Screening donors' serum ferritin levels at the time of first donation and subsequently once every year is a very rational way to pick up iron deficiency in a voluntary blood donor population. The aim of this study was to determine the effect of blood donation and the prevalence of erythropoiesis with iron deficiency (sideropenia) in Saudi male blood donors. MATERIALS AND METHODS: The study was prospectively conducted, between December 2008 and March 2009, on 182 male native Saudi blood donors at King Fahd Central Hospital in Jazan region, Saudi Arabia. Each donor gave 450 ± 50 mL of whole blood. Following the donation, samples were removed into 2.5 mL EDTA tubes for measurement of mean cell volume (MCV) and mean corpuscular haemoglobin (MCH) and into 7.5 mL plain tubes for estimation of iron and serum ferritin concentrations. The blood donors were divided into five groups, according to the number of donations they had given in the preceding 3 years. The blood donors in group I were first-time donors, with no previous history of blood donation. Group II donors had donated once in the last 3 years. Subjects in groups III, IV and V had donated more than once in the preceding 3 years and were considered regular donors. RESULTS: The mean serum iron was significantly higher among subjects with no previous history of blood donation (group I) than among regular donors who had donated twice or more. The difference in serum ferritin concentration was statistically significant (p<0.05) when comparing regular donors in group III (72.4 µg/L), group IV (67.4 µg/L) and group V (26.2 µg/L) with first-time blood donors (131.4 µg/L). In contrast, the difference in the concentration of serum ferritin between subjects in group II (98.9 µg/L), who had donated once in the last 3 years, and in first-time blood donors (131.4 µg/L) was not statistically significant (p<0.131). None of the group I donors suffered from iron deficiency, whereas 2.8% of the donors who had donated between two to five times had iron deficiency. The prevalence of erythropoiesis with iron deficiency in regular blood donors was 4.3%. CONCLUSION: The results of this study show that an increase in the number of donations results in an increase in the frequency of depleted iron stores and subsequently in erythropoiesis with iron deficiency, although the level of haemoglobin remained acceptable for blood donation. This result may indicate the need to review the guidelines on acceptance of donors.