Comparison between clinical characteristics and laboratory findings among patients with complicated and noncomplicated SARS-CoV-2 infection: A single-center experience from Shebin Al-Kom, Egypt.

BACKGROUND: Coronavirus disease 2019 (COVID-19) infection is considered a serious highly infectious disease caused by severe acute respiratory syndrome coronavirus 2, resulting in more than 6.27 million deaths worldwide. AIM OF THE STUDY: The study aimed to compare clinical characteristics and laboratory findings of COVID-19 patients with complications and without complications and discriminate the important risk factors for the complications and deaths. SUBJECTS AND METHODS: This cross-sectional study included 75 confirmed COVID-19 positive patients; out of which 49 were severely-ill cases. Analysis of all patients' clinical and laboratory information on admission including serum ferritin, thrombotic activity (d-dimer), lactate dehydrogenase (LDH), C-reactive protein (CRP), creatinine, aspartate aminotransferase, and alanine aminotransferase were done. RESULTS: Lymphopenia, tachycardia, tachypnea, elevated CRP, d-dimer, serum ferritin, LDH, and decreased SpO2 were significantly associated with complicated cases (p < .05 for all). By using multivariate logistic regression analysis models, elevated serum ferritin and tachycardia were significantly correlated with the increased odds of complicated COVID-19 cases (odds ratio [confidence interval 95%] = 10.42 [2.32-46.89] and 8.01 [1.17-55.99]; respectively) (p = .002 and .007, respectively). CONCLUSION: Lymphocytopenia, d-dimer, LDH, and CRP levels, which were significantly linked to the severity of COVID-19, were the prognostic biomarkers to predict the disease severity.

Vitamin D Insufficiency is Not Associated With Pediatric and Adolescent Immune Thrombocytopenia: A Study in Conjunction With its Receptor Genetic Polymorphisms.

Idiopathic thrombocytopenic purpura (ITP) is a heterogeneous immunologic disorder. Vitamin D has immune-modulatory effects. The pleiotropic effects of vitamin D are exerted via vitamin D receptor (VDR) and its genetic alterations could influence its functions. In our study, we measured the serum 25-hydroxyvitamin D levels in 98 Pediatric and Adolescent ITP patients, in addition to 100 apparently healthy controls. Genetic polymorphisms of the VDR gene FokI, BsmI, ApaI, and TaqI were tested using specific restriction enzymes for each polymorphism. Vitamin D deficiency in the studied Pediatric age was a dominant factor, but it was found not to be associated with Pediatric ITP. However, patients carrying the FokI CC genotype had statistically higher vitamin D levels compared with those carrying other genotypes (P=0.036). Patients who were carriers of the BsmI G allele had a nearly 2-fold higher risk of ITP (odds ratio: 2.203; 95% confidence interval: 1.467-3.309). Therefore, the BsmI polymorphism of VDR could be considered a molecular risk factor for ITP.

L-Selectin P213S and Integrin Alpha 2 C807T Genetic Polymorphisms in Pediatric Sickle Cell Disease Patients.

Sickle cell disease (SCD) is an autosomal recessive hemoglobinopathy characterized by increased cellular adhesiveness. Vaso-occlusion (VOC) is the most prevalent disease complication of SCD that could be altered by genetic factors. L-Selectin and integrin alpha 2 (ITGA2) are 2 adhesion molecules linked to vasculopathy and inflammation. The current study aimed at detecting the prevalence of genetic variants of L-selectin and ITGA2 as possible molecular modulators and novel therapeutic targets in a cohort of pediatric SCD patients. Genotyping was performed by polymerase chain reaction restriction fragment length polymorphism technique for 100 SCD patients and 100 age and gender-matched unrelated healthy controls. The homomutant genotype of ITGA2 C807T was significantly higher in SCD patients compared with controls (P=0.001) and confirmed almost a 3-fold increased risk of moderate and severe attacks of VOC. There are significant adverse effects caused by the polymorphisms of ITGA2, and hence Egyptian SCD patients could benefit from the targeted therapies specifically against ITGA2 to ameliorate the severe course of the disease and improve the quality of life. However, further studies of genotypes and expression levels of these adhesion molecules during the attacks of VOC are recommended.

Digging more in the genetic risk prediction of hepatitis C virus epidemic in Egypt: Apoptosis genes polymorphisms in the susceptibility of hepatitis C virus and association with viral load.

Egypt is confronted with the highest hepatitis C virus (HCV) epidemic. Apoptosis and cellular immune responses are crucial to the clearance or persistence of viral infections. This case-control study was carried out to detect whether apoptosis genes single nucleotide polymorphisms (SNPs) confer risk to HCV in a cohort of Egyptian patients and to explore their association with viral load. One hundred and ninety six blood samples were withdrawn from 96 HCV patients and 100 controls. The Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) -1525G>A and FasL-844T>C SNPs were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Hepatitis C viral load was measured using Real time PCR. Results Genotypes distributions of TRAIL -1525G>A and FasL-844 T>C polymorphisms in controls were in accordance with Hardy-Weinberg equilibrium (p>0.05). The study showed a statistically significant difference in the distribution of the TRAIL -1525G>A polymorphism genotypes and the FasL-844 T>C polymorphism genotypes between the HCV patients and the controls (p=0.001 and 0.02 respectively), with association of the -1525GA genotype and -844 TT genotype with increased risk of HCV infection (OR=2.68, 1.942 respectively, 95% CI=1.482-4.846, 1.1-3.43, respectively). No significant association was detected between TRAIL, FasL and the viral load. Our results suggest that the FasL -844T>C SNP is implicated in the susceptibility to HCV in Egyptian patients and firstly report the involvement of TRAIL gene polymorphism in the risk of the disease. Therefore we recommend national programs to delineate genetic factors that may put individuals at risk for contracting HCV.