Background: Despite the importance of epidemiological studies in the development of effective control strategies and provision of basic health services for refugees and internally displaced persons (IDPs), data on the prevalence of malaria are limited. Thus, this study was conducted to estimate the molecular prevalence of malaria amongst the displaced population in Ardamata IDP camp in Al-Geneina City, Sudan.Methods: A cross-sectional study was conducted from July 2018 to December 2018 to estimate malaria prevalence amongst the displaced population in Ardamata IDP camp in Al-Geneina City, Sudan. A total of 380 patients with suspected malaria were recruited. Nested polymerase chain reaction (nPCR) assays were performed to detect thePlasmodiumgenus and species.Results: Of 380 patients, 232 (61.1%) were positive for malaria.Plasmodium falciparumwas the only prevalent species detected amongst the study population. nPCR analysis revealed that none of the samples hadPlasmodium vivax,Plasmodium ovaleorPlasmodium malariae. The malaria prevalence rate was higher amongst males (67.1%) than in females (56.8%), and gender was the only risk factor that was significantly associated with malaria infection (p = .042).Conclusions: Despite control programmes, malaria remains a significant cause of illness amongst a displaced population. The high prevalence of malaria infection in this study indicates that additional health facilities and control strategies should be implemented in displaced camps and the surrounding areas.

Thrombosis plays a crucial role in the morbidity and mortality of coronavirus disease-19 (COVID-19). About one-third of COVID-19 patients experience a thrombotic event, most commonly pulmonary embolism. Based on published data, the mechanism of thrombosis in COVID-19 patients seems to be multi-factorial. In this article, we reviewed the publsihed data concerning with thrombosis in COVID-19 and summarized the predisposing factors and the mechanisms behind COVID-19 related thrombosis. Inflammatory response to SARS-CoV-2 and the consequent hyperviscosity thought to cause endothelial damage and initiate coagulation. Furthermore, inflammation promotes platelet activation and exerts a pathogenic effect on endothelial cells. The presence of anticardiolipin and anti–β2-glycoprotein antibodies in some patients with COVID-19 suggests that SARS-CoV-2, like many other viral infections, induces the formation of antiphospholipid antibodies, which provoke hypercoagulability. Thrombophilic mutations, mainly factor V Leiden and prothrombin G20201A mutations, can be a contributing factor in the development of thrombosis in COVID-19 patients, and they are associated with increased disease severity and pulmonary embolism. However, the research concerning with the association of thrombophilic mutations with COVID-19 related thrombosis showed conflict results. The mechanism of thrombosis in COVID-19 patients seems to be multifactorial. Endothelial damage, antiphospholipid antibodies, inflammation, hyperviscosity, and thrombophilic mutations are the main factors that predispose COVID-19 patients to. thrombosis.

To assess the clinical presentation and hematological profile among young (≤ 55 years) and old (> 55 years) chronic lymphocytic leukemia patients in Sudan. In the present cross-sectional descriptive study, out of 110 cases studied, among them 31 (28.2%) were young (≤ 55 years) patients with mean age 48 years, and 79 (71.8%) were elder patients (> 55 years) with mean age 66 years, the overall mean age was 62.97 ± 12.06 with range (22–85 years), and 79 (71.8%) were males and 31 (28.2%) were females (M:F = 2.6:1) (P = 0.000). (7.3%) were asymptomatic, 61 (55.5%) presented with nonspecific complains. Generalized lymphadenopathy was seen in 52 (47.27%) with elder predominance (P = 0.03). Splenomegaly, hepatomegaly, thrombocytopenia and anemia were seen in 54 (49.1%), 14 (12.7%), 43 (39.1%) and 38 (34.5%) of patients respectively with male predominance. 54 (49.1%) and 42 (38.18%) of patients presented at Rai high risk and Binet C stages respectively with nearly same age and sex distribution. CLL in Sudan is a disease of elders, same as seen in literature, with high male to female ratio. In general hematological parameters means were noted to be distributed equally according to age and sex groups. Majority of patients were presented with nonspecific symptoms and nearly half of patients presented at late stages as reported in most developing countries.

TNF–α influences lymphomagenesis by upregulating proinflammatory and antiapoptotic pathways. In this study, we evaluated the frequency of TNF–α rs1800629 (–308 G>A) polymorphism in newly diagnosed adult patients with acute lymphoblastic leukemia (ALL) and its correlation with age at diagnosis, gender and subtype of ALL. In this case control study, a total of 330 individuals were recruited, including 165 newly diagnosed adult patients with ALL, from the Radiation and Isotope Center in Khartoum (RICK) and 165 healthy normal controls. TNF–α rs1800629 polymorphism was tested through allele-specific polymerase chain reaction (PCR) assay. The frequency of the rs1800629 GA genotype was high (70.9% vs. 60%, OR = 1.84) in the patient group as compared to healthy controls, whereas GG and AA genotypes did not exhibit any statistically significant difference between controls and patients. Based on subtype, GG and GA rs1800629 genotypes showed increased risk of B-ALL (OR 0.46 and 2.12, respectively), whereas rs1800629 GG, GA and AA genotypes did not show any disease association with T-ALL (p > 0.05). Age at diagnosis and gender did not exhibit any association of rs1800629 with ALL in the patient group. In conclusion, rs1800629 is associated with high risk of adult B-ALL, with an insignificant effect of age at diagnosis and gender.

Purpose: Glutathione S-transferases (GSTT1 and GSTM1) are instrumental in detoxification process of activated carcinogens. Nucleotide excision repair is carried out by DNA helicase encoded by xeroderma pigmentosum group D (XPD) genes and aberrations in the XPD gene predisposes to increased risk of cancer. The present study aimed to investigate GSTT1, GSTM1 and XPD polymorphisms in newly diagnosed chronic myeloid leukemia (CML) patients and to examine the association of these polymorphisms with the risk of developing CML. Patients and Methods: This case–control study was carried out from June 2019 to August 2021 involving 150 newly diagnosed patients with CML and an equal number of randomly selected age- and sex-matched healthy individuals. A multiplex-PCR assay was used to genotype GSTT1 null and GSTM1 null polymorphisms. XPD gene polymorphism was detected by PCR-RFLP using predesigned gene-specific primers. Results: GSTT1 and GSTM1 null polymorphisms were detected in 42.7% and 61.3% of cases, respectively, compared to 18% and 35.3% for controls. The combination of both GST null polymorphisms revealed a significant association with CML. Frequencies of XPD Lys751Gln genotypes in cases were 62.7% heterozygous Lys/Gln, 24% homozygous Lys/Lys and 13.3% homozygous Gln/Gln, while in the controls were 74.7%, 20%, and 5.3%, respectively. Significant differences were also noted regarding the combination of GSTT1/GSTM1 null with XPD Lys/Lys, and GSTM1 null with XPD Lys/Lys. Conclusion: In conclusion, GSTT1 null, GSTM1 null and XPD polymorphisms showed positive association with the risk of development of CML. Furthermore, age and gender did not exhibit any association with the studied polymorphisms, while CML phases were associated with GSTT1 null polymorphism.