Background Coronavirus disease 2019 (COVID-19) was announced in early December 2019. The pandemic situation is declared. This study aimed to evaluate the role of biomarkers in estimating the severity and predicting the prognosis of COVID-19. Results A total of 116 confirmed patients were included in this study. The patients were evaluated clinically. The disease severity was assessed. The measured and calculated laboratory tests were done. The primary outcome is the 30-day mortality. Patients were assigned to the severe (14.7%) and non-severe (85.3%) groups. At IL-6 level of 32.3 pg/mL (the highest Youden’s index = 0.77), IL-6 can differentiate severe from non-severe patients with 82.4% sensitivity and 94.4% specificity. IL-6 can predict the severity [odds ratio of 87.7 (95% CI = 18.9-408.2) (P < 0.0001)]. After adjustment to the significant clinical and laboratory parameters, IL-6 had an adjusted odds ratio of 30.8 (95% CI = 1.1-728.3) (P = 0.046). A high CRP/albumin ratio of > 11.4 was associated with COVID-19 mortality [hazard ratio = 59.9 (95% CI = 7.4–488.3) (P < 0.0001)]. High CRP/albumin ratio had an adjusted hazard ratio of 26.5 (95% CI = 2.6-270.7) after adjustment of age and presence of co-morbidities (P = 0.006). Conclusion IL-6 level could effectively discriminate COVID-19 severity. CRP/albumin ratio was an independent risk factor for 30-day mortality rate in patients with COVID-19. IL-6 and CRP/albumin ratio seem to be valuable biomarkers in evaluating the severity and prognosis of COVID-19, respectively.

BackgroundEffective empirical antibiotic therapy for community acquired pneumonia (CAP), based on frequently updated data about the pattern of bacterial distribution and their antimicrobial susceptibilities, is mandatory.AimTo identify the bacterial etiology of CAP in adults and their antibiotic susceptibility patterns and to evaluate the response to initial empirical antibiotic therapy in an Egyptian university hospital.Settings and designA cross-sectional hospital-based study.Patients and methodsCAP cases were selected by systemic random sampling from those admitted to the chest department. All were evaluated at admission and 4 days after starting empiric therapy. Typical bacteria were isolated, identified and tested for their antibiotic susceptibility. An indirect IF assay was used to diagnose atypical bacteria. Clinical response to initial empiric antibiotic therapy was clinically, laboratory and radiologically evaluated.ResultsTwo hundred and seventy CAP patients were included. Bacteria represented 50.4% of them. Klebsiella pneumoniae was the most prevalent bacterium (10.37%) followed by Streptococcus pneumoniae and P. aeruginosa (7.78% each). Overall, 76.2% of isolates showed a multidrug resistant phenotype: 82.61% (19/23) S. pneumoniae, 89.66 % (26/29) K. pneumoniae, 65.22% (15/23) Pseudomonas aeruginosa, 87.50% (7/8) Escherichia coli and 81.25 % (13/16) Staphylococcus aureus. Broad spectrum β-lactams, especially carbapenems, and moxifloxacin showed in vitro efficacy on most of the tested isolates. Forty-three cases (15.9%) were nonresponders, 37 (86%) of them showed bacterial etiology. The highest rate of nonresponsiveness (30.43%) was observed in cases receiving antipseudomonal/antipneumococcal β-lactam plus a fluoroquinolone for suspected P. aeruginosa infection.ConclusionMultidrug resistance in bacteria causing CAP and high frequency of isolation of hospital pathogens are prominent features of this study. Azithromycin containing regimens were associated with the lowest rates of nonresponsiveness. Development and implementation of an antibiotic stewardship program are highly recommended for CAP management.

Cyclophosphamide (CP) is a chemotherapeutic agent which is extensively used in the treatment of multiple neoplastic and nonneoplastic diseases like breast cancer, lymphomas, systemic lupus erythematosus, and multiple sclerosis. Dose‐limiting side effects, mainly nephrotoxicity is a major problem hindering its use in the clinical practice. CP induces nephrogenic syndrome of inappropriate antidiuresis mostly via the activation of arginine vasopressin V 2 receptors. Moreover, CP produces reactive metabolites which is responsible for augmentation of lipid peroxidation and oxidative stress. Tolvaptan (TOL) is a selective vasopressin V 2 receptor antagonist used in the treatment of clinically significant hyponatremia, volume overload in heart failure, and liver cirrhosis with edema. The present study aimed to investigate the potential protective effect of TOL in CP‐induced nephrotoxicity. Twenty‐four adult male albino rats were randomly divided into four groups: the control group, TOL group that treated daily with tolvaptan (10 mg/kg/d, orally), CP group where CP was administered intraperitoneally 75 mg/kg on days 3, 4, 5, 19, 20, and 21 of study, and the CP + TOL group where animals were treated with TOL daily with (10 mg/kg/d, orally) for 22 days with concomitant administration of CP as described before. Coadministration of TOL with CP induces significant improvement in the level of urine volume, serum Na+, serum osmolarity, urinary creatinine, and free water clearance in addition to significant reduction of body weight, serum creatinine, urea, serum K+, blood pressure, urine osmolarity, and the fractional excretion of sodium as compared to CP‐treated group. In addition, coadministration of TOL significantly reduced MDA, the marker of lipid peroxidation, and different pro‐inflammatory cytokines. Histopathological changes showed improvement in the signs of nephrotoxicity with the coadministration of TOL. Also, co‐treatment with TOL significantly decreased the level of markers of apoptosis as caspase‐3 and Bax with increased expression of antiapoptotic Bcl‐2 in renal tissue as compared to CP‐treated group.

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The usefulness of cyclophosphamide (CP) in the treatment of multiple human malignancies and immunological diseases is hindered by the danger of developing nephrotoxicity. The toxic metabolites of CP are suggested to be responsible for oxidative stress resulted from the production of reactive oxygen species (ROS) and stimulation of lipid peroxidation. Nebivolol (NEB) is a third‐generation selective B1 adrenoceptor antagonist, but it has also various pharmacological properties such as anti‐inflammation, anti‐apoptotic, and antioxidant activities. Thus, the present study aims to explore the potential protective effect of NEB against CP‐induced nephrotoxicity. A cumulative dose of CP (75 mg/kg) was administered to albino rats by intraperitoneal injection. The protective effect of NEB was investigated by co‐administration of NEB (10 mg/kg orally daily). Administration of NEB with CP significantly improved renal functions and reduced the oxidative renal changes induced by CP injection. Co‐administration of NEB ameliorated apoptosis and inflammatory markers that were markedly exaggerated by CP. Our results indicated that NEB could be used as a protective agent against CP‐induced nephrotoxicity.